POPULARITY
2 episodes with myelination
3 episodes with myelination
3 episodes with myelination
2 episodes with myelination
2 episodes with myelination
6 episodes with myelination
In this episode, we review the high-yield topic of Diseases of Myelination from the Neurology section.FollowMedbullets on social media:Facebook: www.facebook.com/medbulletsInstagram: www.instagram.com/medbulletsofficialTwitter: www.twitter.com/medbullets
In this episode of the NeuroNoodle Podcast,
Here Is How to Stop Stuttering and Say What You Want with Michael Williams
Learn how to reduce stuttering anxiety by applying two powerful laws that can transform your speech into smooth, confident communication. In this video, we discuss practical strategies to help you manage speech pressure, minimize stuttering, and improve your fluency. Michael Williams shares his personal journey of overcoming stuttering and offers actionable tips you can implement today. Don't miss this opportunity to enhance your speech and build lasting confidence. Grab our Labor Day Special Now: https://www.pro90d.com/start-speaking-smoothly-in-3-months#section-3b91bc4b Do you think these guys regret investing in their speech: https://www.pro90d.com/before-and-after-pro90d Here are the chapters with each one on its own line: 0:00 Introduction and Survey on Perfectionism 0:13 Discussing Perfectionism and Speech Fluency 1:08 Understanding Perfectionism in Speech 1:49 Handling Disfluencies and Expectations 2:46 Coping with Criticism and Self-Judgment 3:33 Addressing Anxiety and Nervousness Before Speaking 5:12 Identifying Triggers of Speech Anxiety 7:22 Introduction to the Law of Relaxation 8:28 Personal Experience and the Law of Relaxation 10:07 Strategies to Refocus and Avoid Negative Thinking 11:39 Shifting Focus from Negative Anticipation to Positive Preparation 13:33 Utilizing Opportunities to Shine in Public Speaking 15:18 Replacing Negative Thoughts with Positive, Constructive Ones 17:24 Patterns and Habits in Thinking and Speaking 18:24 Importance of Believing in the Science Behind Speech Transformation 19:38 Neuroplasticity and Rewiring the Brain for Fluent Speech 21:19 Replacing Negative Patterns with Positive Ones 22:23 The Power of Preparation Over Worrying 24:59 The Role of Being Present in Conversations 25:20 Managing Expectations and Being Present 29:31 Dealing with Speech Dips and How to Improve 30:26 Leaning into Practice During Speech Dips 31:59 The Science Behind Speech Patterns and Myelination 33:03 Structuring Presentations to Reduce Pressure 34:19 Applying the 80-20 Rule to Presentations 35:08 Visualizing Positive Outcomes in Speaking 36:29 Recording Yourself for Improvement 38:05 The Impact of Recording and Tweaking Speech 40:28 Dealing with the Pressure of Speaking in Front of an Audience 42:47 Applying Vic and Rick Techniques in Conversations 44:15 The Importance of Emptying the Mind During Conversations 46:22 Continuing Exercises Even When Results Aren't Immediate 47:52 The Science Behind Persistence in Speech Exercises 51:06 Introduction to the Law of Flexibility and Fluidity 52:44 Applying Flexibility in Speech Situations 55:26 The Concept of Speech Flowing Like Water 57:49 Reducing Pressure by Creating Speech Flow 59:24 Overcoming Speech Barriers with Flexibility 1:01:00 Success Breeds Success in Speech Practice 1:02:12 Using the PIES Method for Speech Improvement 1:05:23 Overcoming the Challenges of Scripted Speech 1:07:23 Modeling Speech Without Mimicking Exactly 1:09:23 Avoiding the Traps of Scripted Speech 1:10:22 The Role of Pausing and Breathing in Speech 1:11:55 Handling Hard Words in Speech Progress 1:15:11 Measuring Short-Term and Long-Term Speech Progress 1:18:28 The Importance of Immersion in Speech Practice 1:21:04 Addressing the Challenges of New vs. Old Speaking Styles 1:22:47 Identity Shifts in Different Speaking Situations 1:24:39 Explaining Speech Style Changes to Family Members 1:26:08 Adapting to New Speaking Styles in Various Contexts 1:28:45 Encouragement to Apply Learned Techniques 1:30:02 Final Thoughts and Encouragement to Invest in Speech Improvement Let me know if this format works for you! #stuttering #fluentspeech #speechanxiety #overcomestuttering #speechtherapy #confidencebuilding #michaelwilliams #smoothspeech #speechimprovement #labordaysale PRO90D SMOOTH SPEECH PROGRAMS: ✅ Private Laser-Focused Coaching: https://bit.ly/laser-focused-coaching-michael ✅ Ultimate Smooth Speech Self-Study Course: https://bit.ly/pro90d-self-study ✅ 7-Step Program: https://www.pro90d.com/7steps
Here Is How to Stop Stuttering and Say What You Want with Michael Williams
Learn how to effectively overcome stuttering and improve your communication skills with Michael Williams in this comprehensive Pro90D Change Series. Discover three crucial steps to define your speech goals, implement consistent practices, and overcome resistance, leading to smoother, more confident speech. Transform your stuttering challenges into strengths with proven techniques. Chapters: 00:01 Introduction to the Series on Three Steps to Create Change 00:11 Step One: Defining What You Want to Change 00:50 Importance of Clarity in Defining Change 01:06 Recap of Previous Steps and Introduction to the Final Step 01:15 Step Three: How to Implement Change 02:03 The Roadmap for Speech Improvement 02:31 Three Key Areas to Focus on for Speech Improvement 03:33 Four Principles of Change 03:44 Principle One: Awareness 04:41 Principle Two: Consistency 09:23 Principle Three: Resistance 13:31 Explanation of Myelination and Habit Formation 14:30 Principle Four: Self-Talk 18:19 Importance of Cognitive Breathing Space 23:33 Invitation to Join the Pro90D Virtual Speech Masters Club #overcomestuttering #stutteringsolutions #speechimprovement #pro90d #michaelwilliams #smoothspeech #confidencebuilding #selfimprovement #changeseries #speechtherapy Explore how the Pro90d Smooth Speech System can assist you on this journey: PRO90D SMOOTH SPEECH PROGRAMS: ✅ Private Laser-Focused Coaching: https://bit.ly/laser-focused-coaching-michael ✅ Ultimate Smooth Speech Self-Study Course: https://bit.ly/pro90d-self-study ✅ 7-Step Program: https://www.pro90d.com/7steps
Myelination is one of the last events during mammalian brain development and is thought to continue into young adulthood in humans. Even in adulthood, ongoing low-level myelination is essential for neural homeostasis, and for dynamic processes such as learning and memory. Deficits in myelination resulting in abnormal white matter and disruption of neuronal function are observed in a wide variety of disorders of the CNS. One strategy for alleviating these deficits is to enhance the genesis of myelin-forming oligodendrocytes from their upstream precursor parents, oligodendrocyte precursor cells (OPCs). However, the capability of these OPCs to contribute to remyelination in injury or disease in the adult CNS remains unclear. To better understand adult oligodendrogenesis and remyelination, our guests today characterized and compared murine OPCs during early postnatal myelination with those from adult injury-induced adult remyelination. Their findings identify two developing OPC groups subserving distinct postnatal functions and suggest that neonatal and adult OPC-mediated oligodendrogenesis are fundamentally different, The findings have important implications for therapeutic interventions aimed at myelin repair. GuestsFreda Miller, PhD, Michael Smith Laboratories, The University of British Columbia Beatrix Wang, BSC, PhD candidate, The University of British Columbia and The University of Toronto Supporting ContentSingle-cell approaches define two groups of mammalian oligodendrocyte precursor cells and their evolution over developmental time, Stem Cell ReportsAbout Stem Cell ReportsStem Cell Reports is the open access, peer-reviewed journal of the International Society for Stem Cell Research communicating basic discoveries in stem cell research, in addition to translational and clinical studies. Stem Cell Reports focuses on original research with conceptual or practical advances that are of broad interest to stem cell biologists and clinicians. X: @StemCellReportsAbout ISSCRWith nearly 5,000 members from 75+ countries, the International Society for Stem Cell Research (@ISSCR) is the preeminent global, cross-disciplinary, science-based organization dedicated to stem cell research and its translation to the clinic. The ISSCR mission is to promote excellence in stem cell science and applications to human health.ISSCR StaffKeith Alm, Chief Executive OfficerYvonne Fisher, Managing Editor, Stem Cell ReportsKym Kilbourne, Director of Media and Strategic CommunicationsJack Mosher, Scientific AdvisorVoice WorkBen Snitkoff
In this episode, we discuss common genetic and proteins implicated with Autism. This episode is all about preparing for a future episode about Excitation and Inhibition imbalance- a known phenomena with Autism. I play Tug-of-War with Barbed-Wire and talk about a critical factor of our environment implicating proteins and development- This is huge, and necessary. Genomic Architecture of Autism https://www.cell.com/cell/pdf/S0092-8674(22)01324-1.pdfPTEN and mTOR https://www.cell.com/cell-reports/fulltext/S2211-1247(22)01435-8?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2211124722014358%3Fshowall%3Dtrue16p11.2, Serotonin, and Possible Social Deficit Rescueshttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824539/https://www.nature.com/articles/s41586-018-0416-4https://www.nature.com/articles/s41386-021-01091-6https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7606557/Dr. Jack Kruse on Autism https://jackkruse.com/category/autism/Cullin 3 / Cul3 https://pubmed.ncbi.nlm.nih.gov/31455858/SHANK3 https://pubmed.ncbi.nlm.nih.gov/?term=shank3Neurexin and Neuroligin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120877/https://www.sciencedirect.com/science/article/pii/S0092867414006734(0:00) Introduction; Excitation and Inhibition; (3:15) Phosphate and Tensin- Pten; Synapses, Soma Size, Migration, Cellular Spine Density, Dendritic Overgrowth, Myelination; mTOR (Rapamycin) and hope; Are cells doing what they should? (10:18) 16p11.2; Serotonin; Raphe and Nucleus Accumbens; Possible Therapeutic Help;(13:40) NEED TO KNOW INFORMATION; Tryptophan, Aromatic Amino Acids, UV-B Light and Proteins; Changes in our Light Environment and Implications to our Biology and Modern Health Concerns; Photoreceptors and Brain and Skin Connection- Neuroectoderm; Circadian Mismatch;(19:24) Back to 16p11.2 and Cortical Development;(22:00) Cullin 3 and Cul3 and Implications to Socialness and Sensory-Gating; Causes of Stereotypic Behaviors; Neuronal Excitability;(24:09) SHANK3; Tissues and Brain; Synaptic Implications; more Spine and Dendritic formation; Sensory Processing; Repetitive Behaviors; Anxiety; Social Deficits; Poor Motor Coordination;(25:59) Neurexin and Neuroligin; Synaptic development and action; Myelination; E/I and Spine; CNTNAP2 and mPFC(29:25) Wrap Up and Contact Informationemail: info.fromthespectrum@gmail.com
References Developmental Cell 2022. Volume 57, Issue 6, 28 March Pages 691-706 Cell Rep. 2014 Feb 13; 6(3): 541–552. Dr Guerra: graduate lecture notes Mozart, WA 1791.Requiem in D Minor, K 626 https://youtu.be/YaH3zI0bYkM?si=X1yv50zY6nKTZmV9 Lennon/McCartney.1964 "I Don't Want to Spoil the Party" https://youtu.be/zqVDvLDLsjI?si=K1ve_5zJLZjqclsb --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
References Dr Guerra-Graduate lipid biochemistry lectures Biochem J. 2022 Sep 30; 479(18): 1917–1940 Front Cell Dev Biol. 2022; 10: 946393. Nat Commun. 2019; 10: 97. Lennon-McCartney 1965. "Ive Just Seen a Face" https://youtu.be/m8LbJfC0SYM?si=gl_URu_yPTn9iZSd McShee, J./Traditional/Pentangle.1969 "Light Flight" https://youtu.be/2tyVezuUtCA?si=THxBJ0reUETkwDLa Mozart, WA. 1785.Piano Concerto No. 21 in C Major, K. 467 https://youtu.be/whTEVQ2OizI?si=YDMhOhlwmpKYqK-t --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
References Front Cell Dev Biol. 2022; 10: 946393. Adv Exp Med Biol. 2024:1440:149-161 Mozart, WA..1786.Horn Concerto in E-flat major # 4 KV 495 https://youtu.be/MMjqU461WpI?si=o2OWIijoe-mbF-pM Sebastian, J. 1968 She's a Lady https://youtu.be/xyFdzevDOHg?si=wgmv5z_jGrtA9x7c --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support
Laia Fibla and John Spencer discuss their paper, “Language exposure and brain myelination in early development”, published in Vol. 43, Issue 23 of JNeurosci, with Reviewing Editor Elana Zion-Golumbic. Find our upcoming webinar schedule here. With special guests: Laia Fibla and John Spencer On Neuro Current, we delve into the stories and conversations surrounding research published in the journals of the Society for Neuroscience. Through its publications, JNeurosci, eNeuro, and the History of Neuroscience in Autobiography, SfN promotes discussion, debate, and reflection on the nature of scientific discovery, to advance the understanding of the brain and the nervous system. Find out more about SfN and connect with us on Twitter, Instagram, and LinkedIn.
The drug clemastine and other compounds that fortify the protective sheath around neurons may prove therapeutic for some genetic neurodevelopmental conditions.
The drug clemastine and other compounds that fortify the protective sheath around neurons may prove therapeutic for some genetic neurodevelopmental conditions.
In this episode:We dive deep into some groundbreaking new research from the Duke-NUS Medical School and the National University of Singapore that could potentially revolutionize how we understand the development and aging of the brain.We introduce you to a 'superhero' protein called Mfsd2a and its role as a transporter of a lipid containing an omega-3 fatty acid, known as lysophosphatidylcholine (LPC), which is vital for the process of myelination.We explore the implications of this research for those living with MS and other neurological disorders. The potential therapeutic benefits of LPC omega-3 lipids could help maintain or even improve myelination in the aging brain.We discuss the future of this research as the team now aims to conduct further preclinical studies to see if dietary LPC omega-3 can help re-myelinate damaged axons in the brain.Referenced Article: https://www.sciencedaily.com/releases/2023/05/230505101659.htmTune in again for more exciting updates from the world of MS research. Remember, you're not alone on this journey, and together, we can make a difference.Enjoyed the show? Please leave us a review and share it with someone who might benefit from it.Stay connected and let us know your thoughts via our social media channels. Until next time, keep the hope alive!https://www.sciencedaily.com/releases/2023/05/230505101659.htmThe Just MS (Multiple Sclerosis) Show, w host Justin Loizos, is a podcast that connects, educates and tries to uplift others living with multiple sclerosis. It provides real-life stories, interviews, and information about DMTs (disease modification therapies) and updates on research developments.www.justmultiplesclerosis.com
Discover the power of mindset in healing! In this enlightening conversation with Mindset Expert, Jane Hogan, she shares her personal journey from structural designer to wellness engineer, overcoming rheumatoid arthritis. She explains how pain and illness are signals for change, and dives into the role of beliefs in the healing process. Jane reveals the transformative practice of breathwork to activate the parasympathetic state and promote well-being. Tap into the potential of your mind and body and an empowering perspective on wellness and personal growth!Jane Hogan, 'The Wellness Engineer,' blends leading-edge science and ancient spiritual practices to help people release chronic pain using the mind, body and breath so they can become empowered creators of their own health. TUNE IN00:00 - Intro04:32 - The life event that forced Jane to pivot into the health space19:10 - Tap into your intuition13:12 - Opening others to new belief systems18:00 - Knowing transcends belief23:08 - Stress26:52 - Myelination, mindset & re-engineering your mind31:16 - Where do our emotions & beliefs come from?33:25 - Change your subconscious beliefs: affirmations, EFT tapping, blink therapy39:06 - Balancing control & surrender during the healing process42:47 - Overcoming overwhelm?46:52 - How to regulating your nervous system50:56 - Meditation technique to calm the parasympathetic NS58:47 - Connect with Jane HoganLISTEN & SUBSCRIBE TO THE PODCASTSpotify: https://open.spotify.com/show/2HJCflVnHRDmvNtI8r2a65?si=692723d115ce4ef2/Apple Podcasts: https://podcasts.apple.com/au/podcast/inspired-evolution/id1272090974/CONNECT WITH JANE HOGANWebsite: https://thewellnesssengineer.com/YouTube: https://www.youtube.com/@JaneHoganHealth/Instagram: https://www.instagram.com/janehoganhealth/Facebook: https://www.facebook.com/janehoganhealth/TikTok: @thewellnessengineerLinkedIn: https://linkedin.com/in/jane-hogan-5609b83a/Podcast: https://thewellnessengineer.com/podcasts/wellness-by-design/JOIN THE INSPIRED EVOLUTION COMMUNITYWebsite: https://www.inspiredevolution/YouTube: https://www.youtube.com/@inspiredevolution/Instagram: https://www.instagram.com/inspired_evolution/Facebook: https://www.facebook.com/inspiredevolution/STAY INSPIRED & KEEP EVOLVINGYEWSupport this show http://supporter.acast.com/inspiredevolution. Hosted on Acast. See acast.com/privacy for more information.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.02.530800v1?rss=1 Authors: Grotheer, M., Bloom, D., Kruper, J., Richie-Halford, A., Zika, S., Aguilera Gonzalez, V. A., Yeatman, J. D., Grill-Spector, K., Rokem, A. Abstract: The formation of myelin, the fatty sheath that insulates nerve fibers, is critical for healthy brain function. A fundamental open question is what is the impact of being born on myelin growth. To address this question, we evaluated a large (n=300) cross-sectional sample of newborns from the Developing Human Connectome Project (dHCP). First, we developed new software for the automated identification of 20 white matter bundles in individuals that is well-suited for large samples. Next, we fit linear models that quantify T1w/T2w, a myelin-sensitive imaging contrast, increases along bundles. We found faster growth of T1w/T2w along the lengths of all bundles before birth than right after birth. Further, in a separate longitudinal sample of preterm infants (N=34), we found lower T1w/T2w at term-equivalent age than in full-term peers. By applying the linear models fit on the cross-section sample to the longitudinal sample of preterm infants, we find that their delay in T1w/T2w growth is well explained by the amount of time preterm infants spend developing in utero and ex utero. These results suggest that being born slows the rate of myelin growths. This reduction in the rate of myelin growth at birth, in turn, explains lower myelin content in individuals born preterm, and could account for long-term cognitive, neurological, and developmental consequences of preterm birth. We hypothesize that closely matching the environment of infants born preterm to what they would have experienced in the womb may reduce delays in myelin growth and hence improve developmental outcomes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.27.530298v1?rss=1 Authors: Grove, M., Kim, H., Pang, S., Amaya, J. P., Hu, G., Zhou, J., Lemay, M., Son, Y.-J. Abstract: The hippo pathway transcriptional effectors, YAP/TAZ, are crucial for Schwann cells (SCs) to myelinate axons but the mechanisms are poorly defined. Although TEAD1 has been implicated as a partner transcription factor, how it supports the transcriptional regulation of myelination and which aspects of the process it affects are unknown. Here, using conditional and inducible knockout mice, we report that TEAD1 is essential for SCs to develop, grow, and regenerate myelin sheaths. TEAD1/2/3/4 are present in SCs, but YAP/TAZ strongly favors TEAD1. It promotes myelination by positively and negatively regulating SC proliferation, enabling Krox20/Egr2 to upregulate myelin proteins, and upregulating the cholesterol biosynthetic enzymes FDPS and IDI1. We also show stage-dependent redundancy of TEAD1 and that non-myelinating SCs have a unique requirement for TEAD1 to enwrap nociceptive axons in Remak bundles. Our findings establish TEAD1 as a crucial partner of YAP/TAZ in developmental myelination and functional nerve regeneration and as a novel transcription factor regulating Remak bundle integrity. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.04.527112v1?rss=1 Authors: Brancaccio, A., Tabarelli, D., Belardinelli, P. Abstract: Healthy aging affects both grey and white matter. However, the trajectories of regional specific degeneration are not fully understood. Here we investigate the effects of aging on cortical thickness and myelin concentration in a large cohort of healthy participants (N = 610) aged between 18 and 89 years' old who underwent single-site T1-weighted, T2-weighted and MTI sequences in the context of the Cam-CAN project. Participants were subdivided in three age groups representative of young, middle and late adulthood. The large size of the dataset allowed us to minimize the impact of sample variance without relying on multi-site acquisition protocols. We assessed linear changes in cortical thickness and cortical myelin concentration; the latter was assessed using both T1w/T2w ratio and MTR proxies, to evaluate which is the most stable metrics. Our results do not fit with either the anterior-posterior gradient or the last-in/first-out hypothesis. We demonstrate that aging patterns are more complex than just depending on a spatial gradient or the temporally reversed order of regional development. Moreover, we show a dissociation in aging patterns between somatosensory and motor regions both in terms of cortical thickness and myelin concentration. Finally, comparing T1w/T2w and MTR results of cortical myelination, we found the latter being a more stable and reliable proxy. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.12.523740v1?rss=1 Authors: Tiane, A., Schepers, M., Reijnders, R. A., van Veggel, L., Chenine, S., Rombaut, B., Dempster, E., Verfaillie, C., Wasner, K., Grunewald, A., Prickaerts, J., Pishva, E., Hellings, N., van den Hove, D., Vanmierlo, T. Abstract: Introduction: In the progressive phase of multiple sclerosis (MS), the hampered differentiation capacity of oligodendrocyte precursor cells (OPCs) eventually results in remyelination failure. We have previously shown that DNA methylation of Id2/Id4 is highly involved in OPC differentiation and remyelination. In this study, we took an unbiased approach by determining genome-wide DNA methylation patterns within chronically demyelinated MS lesions and investigated how certain epigenetic signatures relate to OPC differentiation capacity. Methods: We compared genome-wide DNA methylation and transcriptional profiles between chronically demyelinated MS lesions and matched normal-appearing white matter (NAWM), making use of post-mortem brain tissue (n=9/group). DNA methylation differences that inversely correlated with mRNA expression of their corresponding genes were validated for their cell-type specificity in laser-captured OPCs using pyrosequencing. The CRISPR-dCas9-DNMT3a/TET1 system was used to epigenetically edit human-iPSC-derived oligodendrocytes to assess the effect on cellular differentiation. Results: Our data show hypermethylation of CpGs within genes that cluster in gene ontologies related to myelination and axon ensheathment. Cell type-specific validation indicates a region-dependent hypermethylation of MBP, encoding for myelin basic protein, in OPCs obtained from white matter lesions compared to NAWM-derived OPCs. By altering the DNA methylation state of specific CpGs within the promotor region of MBP, using epigenetic editing, we show that cellular differentiation can be bidirectionally manipulated using the CRISPR-dCas9-DNMT3a/TET1 system in vitro. Conclusion: Our data indicate that OPCs within chronically demyelinated MS lesions acquire an inhibitory phenotype, which translates into hypermethylation of crucial myelination related genes. Altering the epigenetic status of MBP can restore the differentiation capacity of OPCs and possibly boost (re)myelination. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.11.523655v1?rss=1 Authors: Rowe, E., Zhang, Y., Garrido, M. Abstract: Conscious visual motion information follows a cortical pathway from the retina to the lateral geniculate nucleus (LGN) and on to the primary visual cortex (V1) before arriving at the middle temporal visual area (MT/V5). Alternative subcortical pathways that bypass V1 are thought to convey unconscious visual information. One flows from the retina to the pulvinar (PUL) and on to MT; while the other directly connects the LGN to MT. Evidence for these pathways comes from non-human primates and modest-sized studies in humans with brain lesions. Thus, the aim of the current study was to reconstruct these pathways in a large sample of neurotypical individuals and to determine the degree to which these pathways are myelinated, suggesting information flow is rapid. We used the publicly available 7T (N = 98; 'discovery') and 3T (N = 381; 'validation') diffusion MRI datasets from the Human Connectome Project to reconstruct the PUL-MT and LGN-MT pathways. We found more fibre tracts with greater density in the left hemisphere. Although the left PUL-MT path was denser, the bilateral LGN-MT tracts were more heavily myelinated, suggesting faster signal transduction. We suggest that this apparent discrepancy may be due to 'adaptive myelination' caused by more frequent use of the LGN-MT pathway that leads to greater myelination and faster overall signal transmission. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.10.523413v1?rss=1 Authors: Pinatel, D., Pearlstein, E., Bonetto, G., Goutebroze, L., Karagogeos, D., Crepel, V., Faivre-Sarrailh, C. Abstract: The role of myelination for axonal conduction is well-established in projection neurons but little is known about its significance in GABAergic interneurons. Myelination is discontinuous along interneuron axons and the mechanisms controlling myelin patterning and segregation of ion channels at the nodes of Ranvier have not been elucidated. Protein 4.1B is implicated in the organization of the nodes of Ranvier as a linker between paranodal and juxtaparanodal membrane proteins to the spectrin cytoskeleton. In the present study, 4.1B KO mice are used as a genetic model to analyze the functional role of myelin in Lhx6-positive parvalbumin and somatostatin neurons, two major classes of GABAergic neurons in the hippocampus. We show that deletion of 4.1B induces disruption of juxtaparanodal K+ channel clustering and mislocalization of nodal or heminodal Na+ channels. Strikingly, 4.1B-deficiency causes loss of myelin in GABAergic axons in the hippocampus. In particular, stratum oriens O-LM cells display severe axonal dysmyelination and a reduced excitability. This reduced excitability is associated with a decrease in occurrence probability of small amplitude synaptic inhibitory events on pyramidal cells. In contrast, stratum pyramidale fast-spiking basket cells do not appear affected. The aberrant myelination of hippocampal interneurons is also correlated with impairment of spatial memory in 4.1B KO mice. In conclusion, our results indicate a class-specific effect of dysmyelination on the excitability of hippocampal interneurons associated with a functional alteration of inhibitory drive and impairment of spatial memory. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.03.522525v1?rss=1 Authors: Hu, X., Zhu, Q., Lou, T., Hu, Q., Niu, X., He, L., Huang, H., Xu, Y., Qiu, M., Shen, Y., Jia, J.-M., Tao, Y. Abstract: White matter abnormalities are an emerging feature of schizophrenia, yet the underlying pathophysiological mechanisms are largely unknown. Disruption of ErbB signaling that is essential for peripheral myelination has been genetically associated with schizophrenia and white matter lesions in schizophrenic patients. However, the roles of ErbB signaling in oligodendrocytes remain elusive. Here, we used a pan-ErbB inhibition strategy and demonstrated the synergistic functions of endogenous ErbB receptors in oligodendrocytes. Through analyses of the cellular, histological, biochemical, behavioral, and electrophysiological differences in mice with manipulation of ErbB activities in oligodendrocytes at different differentiation stages, we found that ErbB signaling regulates myelination and aerobic glycolysis in oligodendrocytes, and both functions are required for working memory. ErbB inhibition in oligodendrocytes at early differentiation stages induces hypomyelination by suppressing the differentiation of newly-formed oligodendrocytes. In contrast, ErbB inhibition in mature oligodendrocytes alters neither myelination nor oligodendrocyte numbers, but accelerates axonal conduction decline under energy stress. Mechanistically, mature oligodendrocytes with ErbB inhibition reduce the expression of lactate dehydrogenase A, failing to provide lactate to electrically active axons. Supplementation of L-lactate restores axonal conduction and working memory capacity that are suppressed by ErbB inhibition in mature oligodendrocytes. These findings reveal the indispensable roles of ErbB signaling in white matter integrity and function, and provide insights into the multifaceted contributions of white matter abnormalities to cognitive impairment. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Summary In this episode, Dr. Peter reviews the limitations of current Catholic resources on anger, and then reviews secular resources, including interpersonal neurobiology and the structural theory of dissociation. We examine the role of the body in anger responses, and discuss more wholistic ways of working constructive with parts that experience anger, rather than trying to dismiss anger, suppress it or distract from it. Lead-in William Blake, A Poison Tree: I was angry with my friends; I told my wrath, my wrath did end. I was angry with my foe: I told it not, my wrath did grow. We've all experienced anger and we've all experienced angry people We know it's a problem. And global data suggest that it's getting worse. Gallup world poll from 2021: 140 countries Did you experience the following feelings during a lot of the day yesterday? How about anger? 17% of US respondents agreed 26% of women worldwide up from 20% from 10 years ago 20% of men -- flat from 10 years ago. Harm can come from anger Mark Twain “Anger is an acid that can do more harm to the vessel in which it is stored than to anything on which it is poured.” CCC 2302 By recalling the commandment, "You shall not kill," our Lord asked for peace of heart and denounced murderous anger and hatred as immoral. Anger is a desire for revenge. "To desire vengeance in order to do evil to someone who should be punished is illicit," but it is praiseworthy to impose restitution "to correct vices and maintain justice." If anger reaches the point of a deliberate desire to kill or seriously wound a neighbor, it is gravely against charity; it is a mortal sin. The Lord says, "Everyone who is angry with his brother shall be liable to judgment." "Everyone who is angry with his brother shall be liable to judgment." And who hasn't been angry -- including Jesus himself?. We have got to unpack this There is so much misunderstanding about anger in the Catholic world, so much of the way that Catholics have approached anger has been limited, misinformed, and misguided When I think about why the Catholic Church in the US, in Canada, in Europe and Australia, in the entire Western World, there are many factors. Brandon Vogt New Stats on Why Young People Leave the Church based on his book Return: How to Draw Your Child Back to the Church One critical factor is that cradle Catholics, especially young Catholics do not believe that the Church can help them with their problems. Diocese of Springfield Exit Surveys (2014) 68% – Spiritual needs not met67% – Lost interest over time Only 7% of Millennials raised Catholic still actively practice their faith today (weekly Mass, pray a few times each week, say their faith is “extremely” or “very” important) 6.5 people leave the Catholic Church for every one that joins 66% of “nones” agree that “religion causes more problems than it solves” That's why so many fall away from the Faith. The Church doesn't seem relevant to them because she doesn't seem like she has the answers to the real issues they face. 10% of American adults are former Catholics Nearly half of those who fall away from the Church become "nones" And another quarter become Evangelical Christians. 79% of former Catholics leave the Church before age 23. 50% of Millennials raised Catholic no longer identify as Catholic today And it's about topics like anger -- we are not doing a good job meeting the needs that Catholics have today, human formation needs. Intro I am Dr. Peter Malinoski, a.k.a. Dr. Peter, clinical psychologist, trauma therapist, podcaster, blogger, cofounder and president of Souls and Hearts -- but most of all I am a beloved little son of God, a passionate Catholic who wants to help you to taste and see the height and depth and breadth and warmth and the light of the love of God, especially God the Father and Mary our Mother, our spiritual parents, our primary parents. To really absorb your identity as a little child of God and Mary. I want you to enter much more deeply into an intimate, personal, loving relationship with the three Persons of the Trinity and with our Lady. That is what this Interior Integration for Catholics podcast is all about, that is what Souls and Hearts is all about – all about shoring up the natural foundation for the spiritual life of intimacy with God, all about overcoming the natural human formation deficits and obstacles to contemplative union with God our Father and our Lady, our Mother We are on an adventure of love together. And one thing, one major, big, huge thing that gets in the way of being loved by God and Mary and loving in return is anger. Anger. This is Episode 103 of Interior Integration for Catholics. Interior Integration for Catholics is part of Souls and Hearts, our online outreach, check us out at soulsandhearts.com. Anger: one of the seven deadly sins, one the lethal vices that can kill your soul. Anger. So much confusion about anger. The Burden of Anger: June 10, 2021 Catholic-daily-reflections.com The first level of sin is simply to be “angry” interiorly. The sin of anger is an interior attitude of disgust toward another. Jesus says that the consequence of having anger toward another is that you will be “liable to judgment.” Humility. I could be wrong. The offerings from Five Catholic writers on anger are a case in point. The most popular book Fr. T.G. Morrow, Overcoming Sinful Anger 303 Amazon Review, mostly positive, #16 on the list of bestsellers in Catholic Theology, put out by Sophia Press in 2015 And it's not very good. I can't recommend it. First off, Fr. Morrow admits that he doesn't understand why people get angry We've all encountered people who explode when they feel angry. It baffles me how often the sort of anger rears its ugly head in marriages – even in allegedly Christian marriages. (p. 9). I am often surprised to discover Christians who pray ardently, receive the sacraments regularly, we've and attend Mass daily, and yet have an anger problem. (p. 10) Presumes a homogeneous, single personality. Easy to explain with part. Why do people explode in anger? There are many reasons, but I think the top three are power and control, a refusal to take responsibility, and habit. (p. 13). Very simplistic view of psychology, and no consideration of neurology, traumatology, Confusion about the causal chain in anger. Where anger fits in a sequence of events Little genuine interest in anger. Anger is something to essentially get rid of. Not much consideration of the unconscious and unconscious anger. Acknowledges that suppressing anger is problematic, but there still is an assumption that if I'm not feeling anger, it's not there. Disconnect. "Irrational anger" Very focused on the will and will training -- naïve assumptions about sympathetic arousal. Nike Spirituality -- Just do it. Romans 7:15: I do not understand my own actions. For I do not do what I want, but I do the very thing I hate. Spiritual Bypassing Definitions John Welwood: American clinical psychologist, psychotherapist, teacher, and author, known for integrating psychological and spiritual concepts Using “spiritual ideas, words and practices to sidestep or avoid personal, emotional ‘unfinished business,' to shore up a shaky sense of self, or to belittle basic needs, feelings, psychological wounds and developmental tasks.” Blogger Rose Hahn: Spiritual Bypassing: What It Is & How To Avoid It Bypassing occurs when spiritual ideals get elevated to the realm of absolute truth in such a way that our real, lived experience is somehow denied. Rather than doing the work of healing deep wounds, we may use these ideals to deny, devalue, or avoid meeting our more human needs – such as emotional bonding, love, and esteem. In other words, rather than risk opening ourselves to real human connection, and possibly get hurt, we adopt a more enlightened, spiritual way of relating to the world that doesn't rely on human relationship. Not a lot from a specifically Catholic perspective, but this is from Katharina, who styles herself "The Bohemian Catholic" We are supposed to uplift each other, and treat each other with love and respect - like icons of Christ, as God's creation… BUT if you find yourself trying to tell someone that their faith should keep them "happy" all the time, then you aren't helping them. Using spiritual words, spiritual means, spiritual concepts -- all to whitewash or put a Band-Aid on significant psychological or emotional problems in the natural realm Bypassing the natural realm and going to the spiritual realm. Essentially saying -- You should not feel this way. Which is what Fr. Morrow is saying. He promises to "I will offer some ideas, which I consider quite novel, on how to avoid angry explosions." (p.4) Tips So, as a first step in overcoming passive-aggressive anger keep reminding yourself that you want to be a Christian, and therefore you can't take revenge anymore. (p. 9). First, take the time to calm down and figure out why you're angry…. One of the tactics often recommended is to count to ten before deciding what to do. (p. 20). Better still, say a short prayer before acting. The next step is to ask yourself if your angry feeling is been caused by something significant. Most angry fights in marriage are caused by trifling things. (p. 20). Or perhaps use humor to make your point.(p. 20). Offering your angry feeling as a sacrifice is not suppressing it but doing something with it. It is making a bad situation into a beneficial one. That is what it means to embrace the cross. (p. 23-24). If we can forgive others, we can pull the rug out from beneath our anger most of the time. Unforgiveness is the main culprit behind anger. (p. 25). … Refocus your thoughts away from the things that made you angry to some very positive thoughts. For example, thank God for the beautiful weather for the ability to read or buy things you need. (p. 30). I often encourage people with an anger problem to daily for humility. It works. (p. 36). Chapter 7: Thanking God, praising God Consider your future. One key way to change her behaviors to work on in your mind just what your life will be like if you don't change your angry behavior. (pp. 72-73) If you struggle with an anger problem write on an index card all the negatives of continuing your anger and read that list several times a day. (p. 74). Fr. Joseph Esper, Saintly Solutions to Life's Common Problems 99 reviews on amazon. #138 in Roman Catholicism. 2001 Book -- First Chapter is on anger. St. Thomas of Villanova: "Dismiss all anger and look into yourself a little." (p. 7) "St. Francis de Sales advises that, to avoid the sin of anger, you must quickly ask God to give peace to your heart when you're angered and then turn your thoughts to something else. Don't discuss the matter at hand or make decisions or correct other person while you're angry. When a person angers you, St. Francis advises, consider the person's good qualities rather than the words or actions you find objectionable." (p. 7) When we have to speak to someone with whom we are angry, we should first pray for the Lord's guidance and help. It's often more effective to speak in terms of asking favors, rather than making demands or giving orders…" (p. 5-6) ...rehearse possible responses and evaluate which ones which might help you. (p. 7) Tommy Tighe St. Dymphna's Playbook: A Catholic Guide to Finding Mental and Emotional Well-Being 2021 book, #57 in Christian Pastoral Counseling, 66 reviews, mostly positive. Doesn't discuss anger. Discusses irritability as a symptom of depression and resentment as a problem in relationships "However, the more I have experienced depression in my own life and in my work as a clinician, the more I have seen the symptoms of irritability and anger is predominant features of depression." (p. 13). That's one way, not the only way. So often depression results from Recommendations "…go for a walk, take some time to meditate, watch or read something that lightens our mood. (p. 13) "Keeping a diary of our emotions and reactions to those emotions is a great place to start… Look back on a situation, slow it down, and examine what exactly happened….We might ask ourselves: What is it that has led to my irritability? Is it because I'm depressed and trying to stuff that feeling down rather than address it? What am I thinking in that situation? (p. 15). "We draw this all out on paper, examine what was really behind our emotional response, and then explore ways of thinking that will restructure our reactions and response. And we write these down! Simply thinking about these things isn't going to help. The whole point is to get them out of our head and onto paper so that we can work them out. Consider it an emotional "show your work" kind of exercise." (p. 15). Then, after a really brief introspective process, we can catch that the real reason for our irritability is our depressed mood, and we can interject coping skills for depression to stave off our irritability. (p. 16). Changing the focus of our thinking is key when we try to battle against depression and irritability that inevitably rears its ugly head. You've probably heard people suggest keeping a gratitude list to help you feel more positive, much along the same lines as St. Paul's advice. It works. (p. 18). Steps in the process Visualize yourself from the perspective of compassionate observer. Notice from the outside whole feelings xare upsetting you and how they are reflected in your appearance. Try to let the warm feeling of compassion and desire to help arise within you. Say to yourself: "It is understandable that you feel that way. You are experiencing a natural response to depressing thoughts. But I'm going to help you." Visualize putting your hand on your shoulder or hugging yourself to soothe and comfort yourself. Give yourself a friendly smile. Think about if there are other things you want to tell yourself that would energize and encourage you to cheer up. Taking time to say those things. When you feel it is appropriate, begin saying goodbye to yourself and remind yourself that you come back anytime you want. (p. 16-17). For resentment: Active listening Tommy Tighe: to fend off resentment, we have to communicate with things are important to us and why. We can't expect our partner to read her mind. We have to tell them the things we value, what things we have grown to expect in relationships because of our past experiences and we have to tell them why. (p 113) Rhonda Chevrin Taming the Lion Within: 5 Steps from Anger to Peace 2017 16 ratings is a Catholic author, international speaker and Professor of Philosophy. She is the author of over 60 books concerning the matters of Catholic thought, practice and spirituality, Take a secure thought -- use your imagination to think of ways out of annoying or enraging situations Avoid exceptionality. Accept the averageMove your musclesHumor is your best friendF.I.S.T. Feelings, Impulses, Sensations, Thoughts: What it signifies is that we can control our immediate impulses and sensations when hurt or frustrated, but if we control our thoughts we can control her impulses.Put your mental health firstPeace over power: Many times you can't win, and it doesn't matter if you lose. It's not worth the effort to put up a fight. They are not doing it to you; they're just doing it! – Much is not done on purposeNot a 911 Not everything is an emergency,.Be Group minded Anger at GodForgiveness Fr. Spitzer Angry with God? Here's Fr. Spitzer's Advice on How to Overcome Anger God understands your anger. Don't dwell on it. Don't go there. Choose instead to: Three step process in the YouTube clip Angry with God: Stop comparing to the way you once were. Stop comparing yourself to others. Stop having expectations for your suffering. Offer it up. Stop the questioning. Saints' behaviors Meg Hunter-Kilmer - published on 09/28/17Aleteia September 28, 2017, What We Probably Don't Know about St. Jerome Is Just What We Need to Know St. Jerome was known to carry around a stone that he would hit himself with every time he lost his temper. If these are helpful to you, great. I don't want to put up roadblocks. Might be helpful to many people. As a Catholic psychologist, I am not comfortable recommending any of these Catholic sources Very simplistic view of psychology, and no consideration of neurology, traumatology, Confusion about the causal chain in anger. Where anger fits in a sequence of events Little genuine interest in anger. Anger is something to essentially get rid of. Very focused on the will and will training -- naïve assumptions about sympathetic arousal. And they don't get that anger has a protective function -- to protect us against shame. Not one of those sources connects anger to shame. And that's the primary connection we need to understand if we want to resolve anger, not just try to shoo it away. What are we talking about when we discuss anger -- let's get into definitions of Anger Focused on vengeance secondary to a desire -- more than an emotion. Written discussions of anger in the western canon go back as far as fourth-century BC in Greece when the philosopher Aristotle (384-322 B.C.) argued that anger is a rational and natural reaction to being offended and thus is closely associated with reason. In the Rhetoric (1991, p. 1380) he defined anger as “a belief that we, or our friends, have been unfairly slighted, which causes in us both painful feelings and a desire or impulse for revenge.” 1907 Catholic Encyclopedia: Anger: The desire of vengeance. Its ethical rating depends upon the quality of the vengeance and the quantity of the passion. When these are in conformity with the prescriptions of balanced reason, anger is not a sin. It is rather a praiseworthy thing and justifiable with a proper zeal. It becomes sinful when it is sought to wreak vengeance upon one who has not deserved it, or to a greater extent than it has been deserved, or in conflict with the dispositions of law, or from an improper motive. The sin is then in a general sense mortal as being opposed to justice and charity. It may, however, be venial because the punishment aimed at is but a trifling one or because of lack of full deliberation. Likewise, anger is sinful when there is an undue vehemence in the passion itself, whether inwardly or outwardly. Ordinarily it is then accounted a venial sin unless the excess be so great as to go counter seriously to the love of God or of one's neighbor. CCC 2302 By recalling the commandment, "You shall not kill," our Lord asked for peace of heart and denounced murderous anger and hatred as immoral. Anger is a desire for revenge. "To desire vengeance in order to do evil to someone who should be punished is illicit," but it is praiseworthy to impose restitution "to correct vices and maintain justice." If anger reaches the point of a deliberate desire to kill or seriously wound a neighbor, it is gravely against charity; it is a mortal sin. The Lord says, "Everyone who is angry with his brother shall be liable to judgment." Contradiction that aggression (or vengeance) and anger have to go together Lot of research to tease about anger and aggression: Ephesians 4:26: Be angry but do not sin; do not let the sun go down on your anger APA Dictionary of Psychology: an emotion characterized by tension and hostility arising from frustration, real or imagined injury by another, or perceived injustice. It can manifest itself in behaviors designed to remove the object of the anger (e.g., determined action) or behaviors designed merely to express the emotion (e.g., swearing). Anger is distinct from, but a significant activator of, aggression, which is behavior intended to harm someone or something. Despite their mutually influential relationship, anger is neither necessary nor sufficient for aggression to occur. Psychologist Paul Ekman. (1999). Basic emotions. In T. Dalgleish & M. J. Power (Eds.), Handbook of cognition and emotion (pp. 45–60). John Wiley & Sons Ltd Due to its distinct and widely recognizable pattern of face expression, anger has always been included in the repertoire of basic emotions. Benefits of Anger Farzaneh Pahlavan Multiple Facets of Anger: Getting Mad or Restoring Justice? Chapter 3: The Neurobiology of RAGE and Anger & Psychiatric Implications with a Focus on Depression Daniel J. Guerra1, Valentina Colonnello and Jaak Panksepp As a basic emotion, anger emerges early in life and has a unique adaptive function in motivating, organizing, and regulating behavior. No other emotion can match the consistency and vigor of anger in mobilizing high-level energy and sustaining goal-directed activity. Anger serves a variety of regulatory functions in physiological and psychological processes related to self-defense as well as to interpersonal and societal behaviors. Through socialization processes, it plays an important role in the development of personality and individual differences in responding to environmental challenges, which can be more or less adaptive. (p. v). Aristotle: Aristotle: Nichomachean Ethics: It is easy to fly into a passion – anybody can do that – but to be angry with the right person into the right extent and at the right time and with the right object in the right way – that is not easy, and it is not everyone who can do it In themselves passions are neither good nor evil. They are morally qualified only to the extent that they effectively engage reason and will….It belongs to the perfection of the moral or human good that the passions be governed by reason. CCC 1767 CCMMP: Catholic-Christian Meta-Model of the Person DMU Paul Vitz, William Nordling, Paul Craig Titus. p. (294) to remain in the virtuous middle ground requires being disposed to a righteous anger that will stand up to injustice, and use a good measure of anger in ways that are corrective of the evil, preventive of further injustice, and indicative of a balance to mean between extremes. Emotions are good when, as reactions antecedent to reasoning, they make us conscious of reality and prepare us for a more complete reaction and moral action. Emotion and choice then serve moral flourishing (e.g., when we have an appropriate spontaneous reaction of anger at injustice). Second, emotions are good as felt reactions that also follow the intellectual evaluation of the situation. Emotions can be expressive of rational decisions. Emotions can thus participate in our life of reason and will (Gondreau, 2013). For example, when we choose to rectify and injustice, a balanced expression of anger can help us to act decisively will being restrained enough that we do not overreact. Through a righteous or just expression of anger, we entered rectify injustice, will finding a just and rational mean between excessively weak or exceedingly strong emotional displays. (p. 650). Emotions are viewed as informing people about their cares and concerns. To prepare the body for action, directing our thoughts to ways that will appropriately address the issues at hand. They can signal and manipulate other people in ways that suit the person's emotional needs (Parrott, 2001). Being disconnected from emotional experience, therefore, means being cut off from adaptive information (Pos et al., 2003). (pp. 650-651). Digression into justification of secular sources Question may arise, "OK, Dr. Peter, as you already noted, anger has been recognized for a long time, going all the way back to Aristotle and way before that in Sacred Scripture. You emphasize that you are a Catholic psychologist, so why are you even looking at these secular sources like the American Psychological Association? There is a lot about anger in Scripture, in the Church Fathers and the saints about anger in the spiritual life. Discalced Carmelite Abbott Marc Foley in his excellent book The Context of Holiness: Psychological and Spiritual Reflections on the Life of St. Therese of Lisieux "One…misconception is that the spiritual life is an encapsulated sphere, cloistered from the realities of daily living….we have only one life composed of various dimensions. Our emotional life, intellectual life, social life, work life, sex life, spiritual life are simple ways of speaking of the different facets of our one life. (p. 1). We have one life. One life. We don't have a spiritual life that is separate from our emotional life. We have one life. If we are angry, that affects our whole life. The Church herself encourages us to look to all branches of knowledge and glean what is best from them in order to live our one life better. From the CCC, paragraph 159 "Though faith is above reason, there can never be any real discrepancy between faith and reason. Since the same God who reveals mysteries and infuses faith has bestowed the light of reason on the human mind, God cannot deny himself, nor can truth ever contradict truth." "Consequently, methodical research in all branches of knowledge, provided it is carried out in a truly scientific manner and does not override moral laws, can never conflict with the faith, because the things of the world and the things of faith derive from the same God. The humble and persevering investigator of the secrets of nature is being led, as it were, by the hand of God in spite of himself, for it is God, the conserver of all things, who made them what they are." And from the Vatican II document, the Pastoral Constitution of the Church in the Modern World, paragraph 62 reads: In pastoral care, sufficient use must be made not only of theological principles, but also of the findings of the secular sciences, especially of psychology and sociology, so that the faithful may be brought to a more adequate and mature life of faith. Remember that we are embodied beings -- we are composites of a soul and a body. The 17th Century Philosopher Rene Descartes' popularized what is called mind-body dualism. Mind-body dualism is the idea that the body and the mind operate in separate spheres, and neither can be assimilated into the other. And that is false. Demonstrably false in a lot of ways, be we so often assume it to be true. We have one life. In the last several years we are realizing just how much of our mental life and our psychological well-being is linked in various ways to our neurobiology -- the ways that our nervous systems function. And the relationship between our embodied brain and our minds is reciprocal -- each affects the other in complex ways that we are just beginning to understand. In other words, brain chemistry affects our emotional states. And our emotional states and our behaviors affect brain chemistry. It's not just our minds and it's not just our bodies and it's not just our souls -- it's all of those, all of what makes me who I am, body, mind, soul, spirit, all of it. And since Scripture, the Early Church Fathers, the Catechism and so on are silent on neurobiology, neurochemistry, neurophysiology and so many other areas that impact our minds and our well-being, as a Catholic psychologist I am going to look elsewhere, I'm going to look into secular sources. I just don't think it's reasonable to expect the United States Conference of Catholic Bishops or the Congregation for the Doctrine of the Faith in the Vatican to be experts in these areas -- it's not their calling, it's not their expertise. St. John of the Cross in his Prologue of Ascent of Mt. Carmel: "I will not rely on experience or science…[but] I will not neglect whatever possible use I can make of them. Fr. Marc Foley, OCD : The Context of Holiness: As St. Thomas wrote of St. Augustine's use of Platonic philosophy in the Summa: "whenever Augustine, who was imbued with the doctrines of the Platonists, found in their teaching anything consistent with the faith, he adopted it and those things which he found contrary to the faith he amended." (ST I, q. 84,a. 5) p.4 And St. Thomas himself drew on so much of Aristotle's thought in his writings, bringing it into his body of work. Abbot Marc Foley. In short, we should never swallow the school of thought whole; we should sift the wheat from the chaff, separate truth from falsehood. p.4 We want the best from all sources. Emphasis on biological processes: From Heidi Crockett Anger Management with Interpersonal Neurobiology Discussed Interpersonal Neurobiology at length in Episode 92 of this podcast Understanding and Healing your Mind through IPNB In interpersonal neurobiology, anger as an emotion is viewed from the perspective of cognitive neuroscience. And cognitive neuroscience states that cognition and emotion are dynamically combined with physical arousal. When anger is induced as an emotion in humans, it can unconsciously affect physiological and neural resources. Affective states of anger are subsequently expressed in the brain as well as the body, and these neural and physiological changes can influence the cognitive processes. Many studies and resources have been expended on studying the emotions of happiness, sadness, and fear, which align with psychopathological states of hypomania, depression, and anxiety. Kathy Steele, Suzette Boon, Onno van der Hart: Treating Trauma-Related Dissociation: A Practical, Integrative Approach: Anger is an affect to derived from activation of the sympathetic nervous system, geared to energize the body for maximum effort to fend off perceived danger. Psychologically, it protects from awareness of vulnerability and lack of control, and therefore from shame. And fight mode, we are all primed to perceive cues of danger rather than cues of safety and relational connection. In such a heightened state of arousal, it is easy to misunderstand the intentions of others. (p.332). Polyvagal theory and anger A critical period for experience-dependent development of the feelings of safety during early infancy: A polyvagal perspective on anger and psychometric tools to assess perceived safety Frontiers in Integrative Neuroscience July 2022 article Andrea Poli, Angelo Gemignani, Carlo Chiorri and Mario Miccoli Brief primer here on some neurology. Don't worry. I will keep it simple. Neurons are specialized cells that receive and send signals to other cells through fragile and thin cellular extensions called axons. Myelination: a membrane or a sheath around the axons on neurons. Myelinated axons often have a larger diameter Myelinated axons are insulated Myelination allows for much faster transmission of electric impulses Presence of safety during the critical period (first year of life). Decreased unmyelinated/myelinated cardioinhibitory fibers ratio in adulthood Ventral Vagal complex is able to have a greater impact on reducing the Sympathetic Nervous System arousal -- decreasing anger VVC is able to have a greater impact on reducing Dorsal Vagal Complex fear and shutdown responses -- the freeze response. Greater capacity for self-regulation. Absence of safety during the critical period Increased unmyelinated/myelinated cardioinhibitory fibers ratio in adulthood Ventral Vagal complex has a lesser impact on reducing the Sympathetic Nervous System arousal -- less able to decrease sympathetic arousal, including anger VVC has a lesser impact on reducing Dorsal Vagal Complex fear and shutdown responses -- less able to reduce the freeze response. Less capacity for self-regulation. Dampened VVC activity reduces the capacity of adaptive inhibition of SNS and DVC (Dorsal Vagal Complex), and emotional self-regulation. Hence, environmental detection of unsafety cues may preferentially trigger SNS-mediated anger in order to avoid DVC-mediated immobilization with fear. Young children exposed to five or more significant adverse experiences in the first three years of childhood face a 76% likelihood of having one or more delays in their language, emotional or brain development. (6) As the number of traumatic events experienced during childhood increases, the risk for the following health problems in adulthood increases: depression; alcoholism; drug abuse; suicide attempts; heart and liver diseases; pregnancy problems; high stress; uncontrollable anger; and family, financial, and job problems. (6) 7 ways childhood adversity changes a child's brain Donna Jackson Nakazawa Acestoohigh.com website September 8, 2016 Epigenetic Shifts gene methylation, in which small chemical markers, or methyl groups, adhere to the genes involved in regulating our stress response, and prevent these genes from doing their jobs. Size and Shape of the Brain stress releases a hormone that actually shrinks the size of the hippocampus, an area of our brain responsible for processing emotion and memory and managing stress. Chronic neuroinflammation can lead to changes that reset the tone of the brain for life Brain connectivity: Dr. Ryan Herringa, neuropsychiatrist and assistant professor of child and adolescent psychiatry at the University of Wisconsin, found that children and teens who'd experienced chronic childhood adversity showed weaker neural connections between the prefrontal cortex and the hippocampus. Girls also displayed weaker connections between the prefrontal cortex and the amygdala. The prefrontal-cortex-amygdala relationship plays an essential role in determining how emotionally reactive we're likely to be to the things that happen to us in our day-to-day life, and how likely we are to perceive these events as stressful or dangerous. Including anger. Wiring of the brain and nervous system matter -- they matter a lot Brain activation in anger Distinct Brain Areas involved in Anger versus Punishment during Social Interactions Olga M. Klimecki, David Sander & Patrik Vuilleumier Scientific Reports 2018. 25 men fMRI study anger induced in an in inequality game designed to be unfair. In the present study, we found that the intensity of experienced anger when seeing the face of the unfair other was parametrically related to activations in amygdala, STS (superior temporal sulcus), and fusiform gyrus (related to facial recognition). The STS has been shown to produce strong responses when subjects perceive stimuli in research areas that facial recognition Farzaneh Pahlavan Multiple Facets of Anger: Getting Mad or Restoring Justice? Chapter 3: The Neurobiology of RAGE and Anger & Psychiatric Implications with a Focus on Depression Daniel J. Guerra1, Valentina Colonnello and Jaak Panksepp Rage emerges when specific environmental stimuli arouse the neural circuitry of the RAGE system. Even if the anger-thoughts and the related expression are modulated and regulated by higher cortico-cognitive areas, the human basic circuitry of anger is still subcortical. Since the early description of rage in decorticated cats (Dusser De Barenne, 1920) and dogs (Rothmann, 1923) and their responses to inoffensive stimuli, it was clear that the rage expression is i) dependent on subcortical areas, i.e. the ancient regions play a crucial role more than the higher neocortical regions; ii) independent of an intact cortex. p. 11 Among the higher limbic regions of this network, the medial nucleus, the basal complex, and central and lateral nuclei of the amygdala play a key role in the modulation of RAGE. p. 1 All this happens far away from the frontal cortex in the limbic system of your brain. Kathy Steele, Suzette Boon, Onno van der Hart: Treating Trauma-Related Dissociation: A Practical, Integrative Approach Why of Chronic anger. Anger is the primary emotion of the "fight" defense. When (parts of) the patient become stuck in this defense, anger becomes chronic. Thus, the first intervention is safety. 332 As long as a fight reaction remains unresolved, anger will remain chronic. (p.332). Almost no one seems to understands that anger is a defense against fear and shame. It's a way of trying to protect oneself. There are several reasons that anger and hostility become chronic in dissociative patients. First, patients typically have been severely invalidated, ignored, heard, betrayed, and sometimes even tortured over extended periods of time, while helpless to stop it. In itself, this is enough to generate enormous rage in anyone as part of the naturally occurring fight defense. Second, as children, patients often had little to no help in learning how to regulate and appropriately express normal anger, much less how to cope with it. Often it was unacceptable for many patients to express any kind of anger as children, while the adults around them were uncontained and highly destructive with their anger. Others had no limit set on their angry behaviors. (p. 330). Angry dissociative parts are feared and avoided internally by most other parts, particularly those that function in daily life. After all, angry behaviors toward self and others may interfere with functioning in a variety of personal and social ways. An ongoing vicious cycle of rage and shame ensues internally: the more patients avoid their angry and destructive dissociative parts, the angry these parts become, and the more they shame other parts and are shamed by them. (p. 331). … Angry parts have a deep shame and are highly defended against the strong belief that they are very bad. Their defense is reinforced by the shame of patients that such parts of themselves even exist. These parts of the patient are terrified of attachment to the therapist and you the relationship is dangerous, mainly because they are afraid that the therapist will never accept them. (p. 331-332). Whether the anger is part of a fight response or not, it is often a secondary emotion that protects the patient from feelings of sadness, extreme powerlessness, shame, guilt, and loss. (p. 333). (add grief) Parts of the patient that developed controlling-punitive strategies will be angry with others to get what they need, while those that have controlling-caregiving strategies will punish themselves for being angry or having needs. (p. 333). This is often the case in hostile parts such as those of self-injure or encourage other parts to self-harm, prostitute themselves, abuse drugs or alcohol, or engage in other self-destructive behaviors. They are often stuck in destructive and harmful behaviors that are an "attack self" defense against shame. (p.333). Finally, the rage of the perpetrator is often an embodied experience from which patients cannot yet escape without sufficient realization and further integration. Some dissociative parts imitate perpetrators internally, repeating the family dynamics from the past with other parts in a rather literal way. (p.333). "Getting the anger out" is not really useful, as the problem is that the patient needs to learn how to effectively express anger verbally rather than physically, and in socially appropriate and contained ways, so the patient can be heard by others. It is less the fact that patients express anger, but how they do so and whether that expression allows him to remain grounded in the present, to retain important relationships, and to avoid being self-destructive. (p. 334). Expression of anger is not necessarily therapeutic in itself. It is how (parts of) the patient experience and express it that is important; whether it is within a window of tolerancex in a socially appropriate and safe. Therapist must learn when expression of anger is therapeutic and when containment of anger is more helpful. (p. 334). Working with anger an angry parts (p.335). Take the time to educate the patient as a whole about the functions of anger and angry parts. Although they may seem like "troublemakers," they can be understood as attempting to solve problems with ineffective or insufficient tools. Encourage all parts of the patient understand, accept, and listen to angry parts, instead of avoiding them. Make efforts to understand what provokes angry parts. There are many potential triggers. Not direct quotes Do all parts feel the same way as the angry part? If not, can those parts listen to and accept angry parts perspective? Would the angry part be willing to listen to the other internal perspectives? Invite other parts to watch and listen if possible. Can set limits with the angry part the angry part and all parts need to learn that healthy relationships do not include punishment, humiliation, or force Use titration, helping the person experienced as a small amount of anger will remain grounded in the present Parts and imitate a perpetrator often literally experience themselves in our experienced by other parts as the actual perpetrator. Thus they understandably induce fear and shame within a patient as a whole, and sometimes fearing the therapist. (p. 345). The functions of perpetrator-imitating parts are (1) protect the patient against threats of the perpetrator, which continue to be experienced as real in the present; (2) defend the patient against unbearable realizations of being helpless and powerless as a child, (3) re-enact traumatic memories from the perspective of the perpetrator, as mentalize by the child; (4) serve as a defense against shame through attacking the patient and avoiding inner experiences of shame; (5) provide an outlet for the patient's disowned sadistic and punitive tendencies; and (6) hold unbearable traumatic memories. (p. 346). Suzette Boon, Kathy Steele, Onno van der Hart 2011 book Coping with Trauma-Related Dissociation: Skills Training for Patients and Therapists Destructive expressions of anger include persistent revenge fantasies or actions, hurting self or others, "taking it out" on innocent people (or animals), or destruction of property. (p. 265). Dissociative parts of a person that are stuck in anger may experience this feeling as vehement and overwhelming, often without words. They may have irresistible urges to act aggressively and have great difficulty thinking and reflecting on their feelings before acting. Angry parts have not learned how to experience or express anger and helpful ways. There are two types of anger dissociative parts. The first are parts that are stuck in a defensive fight mode, ready to protect you. Their anger at original injustices may be legitimate and naturally accompanies a tendency to strike out and fight, which is an essential survival strategy. However, such parts have become stuck in anger, unable to experience much else. They rigidly perceived threat and ill-will everywhere and they react with anger and aggression as their only option of response. Although these parts of you may not yet realize it, anger is often a protection against vulnerable feelings of shame, fear, hurt, despair, powerlessness, and loss. The second type of angry part may seem very much like the original perpetrator. They imitate those who hurt them in the past, and they can be experienced internally as the actual perpetrator. This experience can be particularly frightening, disorienting, and shameful. But be assured this is a very common way of dealing with being traumatized. In fact, although these parts may have some similarities to those who hurt you, they also significant differences: they are parts of you as a whole person, who is trying to cope with unresolved traumatic experiences. (p. 267) Tips for coping with anger (p, 269 to 271) recognize how to make distinctions among the many gradations of anger, from mild irritation to rage, so that you can intervene more rapidly. Understand your tells around anger, which may include a tight or tense feeling in your body, clenched jaw's or fists, feeling flushed or shaky, breathing heavily, heart racing, a feeling of heat, a surge of energy. Empathize with her angry parts, recognizing they have very limited coping skills, and very limited vision. They've been shunned by other parts, left alone with their hurt, fear, shame, in isolation. This does not mean you have to accept their impulses toward inappropriate behavior Once you start feeling some compassion toward these parts you can begin to communicate with them, listening with an intention, with curiosity to understand what lies underneath the anger Angry parts have a strength, that they could transferred to use and more positive ways Become more curious about why anger is happening. Try creative and healthy nonverbal ways of expressing your anger, such as writing, drawing, painting, making a collage Physical exercise may help as an outlet for the physical energy generated by the physiology of anger Work on understanding your anger, by reflecting on it, rather than just experiencing it, being immersed in it. You might imagine observing yourself from a distance, and getting curious about why you feel the way you do. Give yourself a time-out, that is, walk away from the situation if you're getting too angry. Counseling to 10, or even 200 before you say or do something you might regret later. Calm breathing may help Listen to each part of you, about what might help that part with anger. You can have in her conversations with parts of yourself about anger and how to express it. Small and safe ways to express anger can be negotiated that are agreeable to all parts of you Watch safe people in your life and seal they handle their own anger. Do they accept being angry? Are they are respectful and appropriate with her anger? Are there particular strategies that they use that you could practice for yourself? Healthy anger can get positive strength and energy. It can help you be appropriately assertive, set clear boundaries, and confront wrongs in the world. Anger can pave the way to other emotions, leading to the resolution relational conflicts. We learn the most common triggers of your anger. Once you learn these triggers, you can be more aware when they occur and more able to prevent an automatic reaction of anger. Establish intercommunication among parts of yourself to recognize triggers and negotiate possible helpful strategies to cope with them rather than just reacting. You can try allowing yourself to experience just a small amount of anger from another part of yourself: a drop, a teaspoon, 1% or 2%. In exchange you can share with angry parts feelings of calm and safety. Inner safe spaces can be very helpful for childlike parts that feel terrified My parts Feisty Part-- defends against shame -- Melancholio. Good Boy Challenger Creative-distracting me. Closing Mark your calendars. Next Live Experience of the IIC podcast will be on Friday, January 13, 2023 from 2:00 PM to 3:00 PM Eastern time on Zoom (repeat) -- All about Anger -- dealing with your anger. Going beyond what books can do. Experiential exercise. Links to register have gone out in our emailed Wednesday Reflections. Can get the link on the IIC landing page as well, SoulsandHearts.com/iic December 28, 2022 Reflection at soulsandhearts.com/blog From Rejecting to Embracing Aging Reach out to me Crisis@soulsandhearts.com Conversation hours: cell is 317.567.9594 conversation hours 4:30 PM to 5:30 PM Eastern Time Every Tuesday and Thursday. Resilient Catholic Community -- you do not have to be alone. Why a deep intimate personal relationship with God our Father, Mary our Mother -- spiritual parents By claiming our identity as beloved daughters and sons of God the Father and Mary our Mother. Identity is freely given. How By dealing with the natural level issues we have, the human formation issues we have that have spiritual consequences. Grace perfects nature So many spiritual problems have their roots in the natural realm, in human formation. If this kind of exercise is helpful to you, we have nearly 100 of them in the Resilient Catholics Community. 120 Catholics like you already on board, already on the pilgrimage -- just had 47 apply for the December 2022 cohort, excited to get to know our new applicants. Closed December 31 -- wait list should be up soon for the June 2023 Cohort. Get to know your own parts Get to love your own parts If interested, contact me. Crisis@soulsandhearts.com 317.567.9594 conversation hours 4:30 PM to 5:30 PM Eastern Time Every Tuesday and Thursday.
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.31.522394v1?rss=1 Authors: Zhang, T., Bae, H.-G., Bhambri, A., Zhang, Y., Barbosa, D., Xue, J., Wazir, S., Mulinyawe, S. B., Kim, J. H., Sun, L. O. Abstract: Oligodendrocytes are the sole myelin producing cells in the central nervous system. Oligodendrocyte numbers are tightly controlled across diverse brain regions to match local axon type and number, but the underlying mechanisms and functional significance remain unclear. Here, we show that autophagy, an evolutionarily conserved cellular process that promotes cell survival under canonical settings, elicits premyelinating oligodendrocyte apoptosis during development and regulates critical aspects of nerve pulse propagation. Autophagy flux is increased in premyelinating oligodendrocytes, and its genetic blockage causes ectopic oligodendrocyte survival throughout the entire brain. Autophagy acts in the TFEB-Bax/Bak pathway and elevates PUMA mRNA levels to trigger premyelinating oligodendrocyte apoptosis cell-autonomously. Autophagy continuously functions in the myelinating oligodendrocytes to limit myelin sheath numbers and fine-tune nerve pulse propagation. Our results provide in vivo evidence showing that autophagy promotes apoptosis in mammalian cells under physiological conditions and reveal key intrinsic mechanisms governing oligodendrocyte number. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.08.519209v1?rss=1 Authors: Fazal, S. V., Mutschler, C., Chen, C., Turmaine, M., Chen, C.-Y., Hsueh, Y.-P., Loreto, A., Casillas-Bajo, A., Cabedo, H., Franklin, R. J., Barker, R. A., Monk, K., Steventon, B., Coleman, M., Gomez-Sanchez, J. A., Arthur-Farraj, P. Abstract: SARM1 is a central regulator of programmed axon death and is required to initiate axon self-destruction after traumatic and toxic insults to the nervous system. Abnormal activation of this axon degeneration pathway is increasingly recognized as a contributor to human neurological disease and SARM1 knockdown or inhibition has become an attractive therapeutic strategy to preserve axon loss in a variety of disorders of the peripheral and central nervous system. Despite this, it remains unknown whether Sarm1/SARM1 is present in myelinating glia and whether it plays a role in myelination in the PNS or CNS. It is important to answer these questions to understand whether future therapies inhibiting SARM1 function may have unintended deleterious impacts on myelination. Here we show that Sarm1 mRNA is present in oligodendrocytes in zebrafish but only detectable at low levels in Schwann cells in both zebrafish and mice. We find SARM1 protein is readily detectable in murine oligodendrocytes in vitro and in vivo and activation of endogenous SARM1 in oligodendrocytes induces cell death. In contrast, SARM1 protein is not detectable in Schwann cells and satellite glia in the adult murine nervous system. Cultured Schwann cells contain negligible functional SARM1 and are insensitive to specific SARM1 activators. Using zebrafish and mouse Sarm1 mutants, we show that SARM1 is not required for initiation of myelination nor myelin sheath maintenance by oligodendrocytes and Schwann cells. Thus, strategies to inhibit SARM1 function in the nervous system to treat neurological disease are unlikely to perturb myelination in humans. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.20.512802v1?rss=1 Authors: Fotiadis, P., Cieslak, M., He, X., Caciagli, L., Ouellet, M., Satterthwaite, T. D., Shinohara, R. T., Bassett, D. S. Abstract: Recent work has demonstrated that the relationship between structural and functional connectivity varies regionally across the human brain, with reduced coupling emerging along the sensory-association cortical hierarchy. The biological underpinnings driving this expression, however, remain largely unknown. Here, we postulated that intracortical myelination and excitation-inhibition (EI) balance mediate the heterogeneous expression of structure-function coupling (SFC) and its temporal variance across the cortical hierarchy. We employed atlas- and voxel-based connectivity approaches to analyze neuroimaging data acquired from two groups of healthy participants. Our findings were consistent across processing pipelines: 1) increased myelination and lower EI-ratio associated with more rigid SFC and restricted moment-to-moment SFC fluctuations; 2) a gradual shift from EI-ratio to myelination as the principal predictor of SFC occurred when traversing from granular to agranular cortical regions. Collectively, our work delivers a novel framework to conceptualize structure-function relationships in the human brain, paving the way for an improved understanding of how demyelination and/or EI-imbalances induce reorganization in brain disorders. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.23.509146v1?rss=1 Authors: Chang, Y., Zhu, J., Nie, C., Lu, Y., Ren, F., Cao, X., Li, J., Wang, C., Yang, C., Li, T., Liang, Y., Qi, S., Kang, X., Kong, E. Abstract: Cell adhesion molecule 4 (Cadm4) plays important roles on plasma membrane (PM) to regulate myelin formation and the downregulation of Cadm4 is a prominent feature in many demyelination diseases. However, how Cadm4 maintains its level on PM has been elusive. Here, we identify that Cadm4 is palmitoylated at cysteine-347 (C347) and palmitoylation regulates the stable localization of Cadm4 on PM, as blocking palmitoylation by mutating C347 into alanine (C347A) results in the dissociation of Cadm4 from PM and targeting for degradation. Intriguingly, blocking Cadm4 palmitoylation by introducing C347A (Cadm4-KI) causes myelin abnormalities in CNS, characterized by loss of myelination, myelin infoldings and hypermyelination. Moreover, it is uncovered that Cadm4 palmitoylation is catalyzed by DHHC3, reducing Cadm4 palmitoylation by the deletion of DHHC3 renders the redistribution of Cadm4 for degrading. Consistently, the genetic deletion of DHHC3 leads to downregulated Cadm4 palmitoylation and defects in CNS myelination, virtually phenocopies that of the Cadm4-KI mice. Our findings suggest a mechanism that the stable localization of Cadm4 on PM regulated by protein palmitoylation is vital for myelination in CNS. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.21.508765v1?rss=1 Authors: Iram, T., Garcia, M. A., Amand, J., Kaur, A., Iyer, M., Lam, M., Ambiel, N., Keller, A., Wyss-Coray, T., Kern, F., Zuchero, J. B. Abstract: Myelination of neuronal axons is essential for nervous system development. Myelination requires dramatic cytoskeletal dynamics in oligodendrocytes, but how actin is regulated during myelination is poorly understood. We recently identified serum response factor (SRF), a transcription factor known to regulate expression of actin and actin regulators in other cell types, as a critical driver of myelination in the aged brain. Yet, a major gap remains in understanding the fundamental role of SRF in oligodendrocyte lineage cells. Here we show that SRF is required cell autonomously in oligodendrocytes for myelination during development. Combining ChIP-seq with RNA-seq identifies SRF-target genes in OPCs and oligodendrocytes that include actin and other key cytoskeletal genes. Accordingly, SRF knockout oligodendrocytes exhibit dramatically reduced actin filament levels early in differentiation, consistent with its role in actin-dependent myelin sheath initiation. Together, our findings identify SRF as a transcriptional regulator that controls the expression of cytoskeletal genes required in oligodendrocytes for myelination. This study identifies a novel pathway regulating oligodendrocyte biology with high relevance to brain development, aging, and disease. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.15.508143v1?rss=1 Authors: Rowland, M. E., Jiang, Y., Shafiq, S., Ghahramani, A., Pena-Ortiz, M. A., Dumeaux, V., Berube, N. G. Abstract: Neurodevelopmental disorders are often characterized by abnormal production of myelin, an extension of the oligodendrocyte plasma membrane wrapped around axons to facilitate nerve conduction. However, the molecular mechanisms that control myelination during brain development are incompletely resolved. Here, we provide evidence that loss of ATRX, encoded by the gene mutated in the ATR-X intellectual disability syndrome, leads to myelin deficits in the mouse CNS. While postnatal systemic thyroxine administration can improve myelination, the rescue is incomplete, pointing to additional roles of ATRX in this process. We show that targeted inactivation of ATRX in postnatal oligodendrocyte progenitor cells (OPCs), but not in neurons, also leads to myelination deficits, demonstrating cell-intrinsic effects of ATRX deficiency. A subset of ATRX-null OPCs express lower levels of oligodendrocyte specification and differentiation markers, including the basic helix-loop-helix Olig2 transcription factor. Mechanistically, we provide evidence that ATRX occupies genomic sites in OPCs marked by H3K27Ac, CHD7 and CHD8 and demonstrate that reduced Olig2 expression is associated with decreased H3K27Ac. Finally, our data suggest that ATRX-null OPCs acquire a more plastic state and can exhibit astrocyte-like features in vitro and in vivo, supporting a model in which ATRX regulates the onset of myelination by promoting OPC identity and suppressing astrogliogenesis. These previously unrecognized functions of ATRX might explain white matter pathogenesis in ATR-X syndrome patients. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer
Multiple Sclerosis News Today's multimedia associate, Price Wooldridge, reads a news article on a study aimed at developing precise markers of myelination in people with MS. He also reads “To Everything There Is a Season': Coping With Grief, Loss, and MS”, a column by Teresa Wright-Johnson. =================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/
Array Cast - July 8, 2022 Show Notes[01] 00:01:15 Dyalog Problem /solving Contest https://contest.dyalog.com/?goto=welcome[02] 00:01:35 Dyalog Early Bird Discount https://www.dyalog.com/user-meetings/dyalog22.htm[03] 00:02:40 Jeremy Howard wikipedia https://en.wikipedia.org/wiki/Jeremy_Howard_(entrepreneur) Fastmail https://www.fastmail.com/ Optimal Decisions Group https://www.finextra.com/newsarticle/18047/choicepoint-acquires-insurance-analytics-firm-optimal-decisions[04] 00:04:30 APL Study Group https://forums.fast.ai/t/apl-array-programming/97188[05] 00:05:50 McKinsey and Company https://en.wikipedia.org/wiki/McKinsey_%26_Company[06] 00:10:20 AT Kearney https://en.wikipedia.org/wiki/AT_Kearney[07] 00:12:33 MKL (Intel) https://en.wikipedia.org/wiki/Math_Kernel_Library[08] 00:13:00 BLAS http://www.netlib.org/blas/[09] 00:13:11 Perl BQN https://mlochbaum.github.io/BQN/running.html[10] 00:14:06 Raku https://en.wikipedia.org/wiki/Raku_%28programming_language%29[11] 00:15:45 kaggle https://www.kaggle.com/ kaggle competition https://www.kaggle.com/competitions/unimelb/leaderboard[12] 00:16:52 R https://en.wikipedia.org/wiki/R_(programming_language)[13] 00:18:50 Neural Networks https://en.wikipedia.org/wiki/Artificial_neural_network[14] 00:19:50 Enlitic https://www.enlitic.com/[15] 00:20:01 Fast.ai https://www.fast.ai/about/[16] 00:21:02 Numpy https://numpy.org/[17] 00:21:26 Leading Axis Theory https://aplwiki.com/wiki/Leading_axis_theory[18] 00:21:31 Rank Conjunction https://code.jsoftware.com/wiki/Vocabulary/quote[19] 00:21:40 Einstein notation https://en.wikipedia.org/wiki/Einstein_notation[20] 00:22:30 GPU https://en.wikipedia.org/wiki/Graphics_processing_unit[21] 00:22:55 CUDA https://en.wikipedia.org/wiki/CUDA[22] 00:23:30 Map https://en.wikipedia.org/wiki/Map_(higher-order_function)[23] 00:24:05 Data Science https://en.wikipedia.org/wiki/Data_science[24] 00:25:15 First Neural Network https://en.wikipedia.org/wiki/Frank_Rosenblatt[25] 00:28:51 Numpy Another Iverson Ghost https://dev.to/bakerjd99/numpy-another-iverson-ghost-9mc[26] 00:30:11 Pivot Tables https://en.wikipedia.org/wiki/Pivot_table[27] 00:30:36 SQL https://en.wikipedia.org/wiki/SQL[28] 00:31:25 Larry Wall "The three chief virtues of a programmer are: Laziness, Impatience and Hubris." From the glossary of the first Programming Perl book.[29] 00:32:00 Python https://www.python.org/[30] 00:36:25 Regular Expressions https://en.wikipedia.org/wiki/Regular_expression[31] 00:36:50 PyTorch https://pytorch.org/[32] 00:37:39 Notation as Tool of Thought https://www.jsoftware.com/papers/tot.htm[33] 00:37:55 Aaron Hsu codfns https://scholarworks.iu.edu/dspace/handle/2022/24749[34] 00:38:40 J https://www.jsoftware.com/#/[35] 00:39:06 Eric Iverson on Array Cast https://www.arraycast.com/episodes/episode10-eric-iverson[36] 00:40:18 Triangulation Jeremy Howard https://www.youtube.com/watch?v=hxB-rEQvBeM[37] 00:41:48 Google Brain https://en.wikipedia.org/wiki/Google_Brain[38] 00:42:30 RAPIDS https://rapids.ai/[39] 00:43:40 Julia https://julialang.org/[40] 00:43:50 llvm https://llvm.org/[41] 00:44:07 JAX https://jax.readthedocs.io/en/latest/notebooks/quickstart.html[42] 00:44:21 XLA https://www.tensorflow.org/xla[43] 00:44:32 MILAR https://www.tensorflow.org/mlir[44] 00:44:42 Chris Lattner https://en.wikipedia.org/wiki/Chris_Lattner[45] 00:44:53 Tensorflow https://www.tensorflow.org/[46] 00:49:33 torchscript https://pytorch.org/tutorials/beginner/Intro_to_TorchScript_tutorial.html[47] 00:50:09 Scheme https://en.wikipedia.org/wiki/Scheme_(programming_language)[48] 00:50:28 Swift https://en.wikipedia.org/wiki/Swift_(programming_language)[49] 00:51:10 DragonBox Algebra https://dragonbox.com/products/algebra-12[50] 00:52:47 APL Glyphs https://aplwiki.com/wiki/Glyph[51] 00:53:24 Dyalog APL https://www.dyalog.com/[52] 00:54:24 Jupyter https://jupyter.org/[53] 00:55:44 Jeremy's tweet of Meta Math https://twitter.com/jeremyphoward/status/1543738953391800320[54] 00:56:37 Power function https://aplwiki.com/wiki/Power_(function)[55] 01:03:06 Reshape ⍴ https://aplwiki.com/wiki/Reshape[56] 01:03:40 Stallman 'Rho, rho, rho' https://stallman.org/doggerel.html#APL[57] 01:04:20 APLcart https://aplcart.info/ BQNcrate https://mlochbaum.github.io/bqncrate/[58] 01:06:12 J for C programmers https://www.jsoftware.com/help/jforc/contents.htm[59] 01:07:54 Transpose episode https://www.arraycast.com/episodes/episode29-transpose[60] 01:10:00 APLcart video https://www.youtube.com/watch?v=r3owA7tfKE8[61] 01:12:28 Functional Programming https://en.wikipedia.org/wiki/Functional_programming[62] 01:13:00 List Comprehensions https://docs.python.org/3/tutorial/datastructures.html#list-comprehensions[63] 01:13:30 BQN to J https://mlochbaum.github.io/BQN/doc/fromJ.html BQN to Dyalog APL https://mlochbaum.github.io/BQN/doc/fromDyalog.html[64] 01:18:15 Einops https://cgarciae.github.io/einops/1-einops-basics/[65] 01:19:30 April Fools APL https://ci.tc39.es/preview/tc39/ecma262/sha/efb411f2f2a6f0e242849a8cc8d7e21bbcdff543/#sec-apl-expression-rules[66] 01:20:35 Flask library https://flask.palletsprojects.com/en/2.1.x/[67] 01:21:22 JuliaCon 2022 https://juliacon.org/2022/[68] 01:28:05 Myelination https://en.wikipedia.org/wiki/Myelin[69] 01:29:15 Sanyam Bhutani interview https://www.youtube.com/watch?v=g_6nQBsE4pU&t=2150s[70] 01:31:27 Jo Boaler Growth Mindset https://www.youcubed.org/resource/growth-mindset/[71] 01:33:45 Discovery Learning https://en.wikipedia.org/wiki/Discovery_learning[72] 01:37:05 Iverson Bracket https://en.wikipedia.org/wiki/Iverson_bracket[73] 01:39:14 Radek Osmulski Meta Learning https://rosmulski.gumroad.com/l/learn_machine_learning[74] 01:40:12 Top Down Learning https://medium.com/@jacksonbull1987/top-down-learning-4743f16d63d3[75] 01:41:20 Anki https://apps.ankiweb.net/[76] 01:43:50 Lex Fridman Interview https://www.youtube.com/watch?v=J6XcP4JOHmk Deep Talks #54 https://www.youtube.com/watch?v=n7YVlPszaWc0
Apologies for the absolute chaos that is this episode. Today I wanted to cover some foundational background concepts, including how a signal travel within a neuron from dendrites to the tip of the axon and how that neuron then communicates to other neurons and parts of the body. Curious? Come and listen to find out more!!!Please rate, review, and subscribe and if you have any questions, comments, concerns, queries, or complaints, please email me at neuroscienceamateurhour@gmail.com or DM me at NeuroscienceAmateurHour on Instagram.Also if you have the means/desire to financially support this podcast - please go to https://www.buymeacoffee.com/neuroscienceI really appreciate it!!!Citations and relevant papers are below! Guy-Evans O. What Is a Neuron? Function, Parts, Structure, and Types | Simply Psychology. www.simplypsychology.org. Published February 15, 2021. https://www.simplypsychology.org/neuron.htmlKhan Academy. Neuron action potentials: The creation of a brain signal. Khan Academy. Published 2016. https://www.khanacademy.org/test-prep/mcat/organ-systems/neuron-membrane-potentials/a/neuron-action-potentials-the-creation-of-a-brain-signalPurves D, Augustine GJ, Fitzpatrick D, et al. Increased Conduction Velocity as a Result of Myelination. Neuroscience 2nd edition. Published online 2001. https://www.ncbi.nlm.nih.gov/books/NBK10921/#:~:text=By%20acting%20as%20an%20electricalChen I, Forshing Lui. Neuroanatomy, Neuron Action Potential. Nih.gov. Published August 27, 2019. https://www.ncbi.nlm.nih.gov/books/NBK546639/Guy-Evans O. Synapse Definition and Function | Simply Psychology. www.simplypsychology.org. Published February 21, 2021. https://www.simplypsychology.org/synapse.htmlmy brainnnnnnnnnSupport the show
On Episode 54 I sat down with Dominique Stasulli of Zeal Endurance Coaching located in Boulder, Colorado. I familiarized myself with Dominique and her work by reading a great article on skill acquisition called The Neuroscience of skill acquisition. Much of the first portion of our conversation centers around many of the theoretical models you see referenced in that article, as I have grown as a prep coach I've increasingly become more interested in how preparatory methods translate in regards to retention for specific purposes. To do more and actually achieve less is not only a waste of time, it leaves you with an athlete or person who did not reach their optimal state due to the arrangement of practice or other preparatory methods. Dominique shares according to Fitts and Posner that skill development follows a three step model. The Cognitive stage is what we associate with novice learners and is where thought and introspection are very involved in the process. At this stage, motor skills and the display of skills are rough and more exposure is needed to reach the next level. The associative level is where you begin to see a refinement of skills and association with other movement options, more efficient models are constructed in this portion. Lastly is the autonomous stage where motor skills are subconscious, this is the level of mastery and there appears to be an uninterrupted flow to the display of skills. We begin to talk about exposure and one of the big conundrums you discover in the building of skills is that myelination determines the motor pathways which we choose to activate to display a certain set of skills. Myelination occurs through repetition, the only problem with mind numbing repetition is that it lacks the variance of many of the dynamic settings that skills will have to displayed within. Dominique shares the difference between random order and blocked practices and how random order practices provide greater variance and opportunity for the growth and retention of a given set of skills. Throughout the conversation Dominique shares multiple examples of different categories of constraints and you can see how it is easy to wisely construct constraints to tailor training to the needs of a given athletic or certain subset of athletes. Dominique shares how she likes to utilize variance in the task specific constraints to arrange meaningful and efficient sessions with her runners. She discusses how she switches up warmups, changes paces, changes energy system work, etc. to keep athletes on their toes. She also rationalizes why she includes sprinting with her distance runners, she states that it shows intent and also has a promotes feel for the runner to a greater degree. She shares how she utilizes hills to help build more efficient runners. The last portion of the conversation deals with the 3 most common lower body deficits that she encounters among the athletes that she works with. They are 1) Poor Proprioception, 2) Core stability/Pelvic stability 3) Poor hip extension. Dominique shares how she helps to bring up these deficits and make her athletes less prone to injury and more resilient in the process. Zeal Endurance Insta Zeal Endurance Web From The Ground Up Web
Today, Amy and Cheryl are joined by Becca Ribbing. Becca is a life coach, writer, and author of The Clarity Journal. They discuss about the importance of journaling, the clarity it gives and how it helps people to be more aware of themselves. They also talk about covid19's different effects in people's lives and how pushing through everything is not really the right way to live by. In This Episode: 01:13 – Becca tells people a bit about herself and her book, The Clarity Journal, and helping people find their paths (or their next paths) in life. 01:50 – Getting “unstuck”. Why the answers need to come from within ourselves. 03:38 –How people went inward during COVID and many of us emerged with unique and different experiences. 06:35 –Becca discusses the importance of clarity and timing when making major decisions. 07:30 – The difficulty of making decisions when the world keeps changing. 08:20 – Why to avoid big decisions in the face of trauma. 09:20 – Making choices based upon your own inner voice verses what others feel you should do. 11:50 – Becca shares the reasons why she wrote her book and gives some tips for journaling. 13:30 – Your process needs to be authentic to you. 16:50 – The importance of change and friction for growth. 21:23 – Myelination and the benefit of creating new neural pathways. 22:00 – The importance of self-compassion. 25:20 – The benefits of maintaining some level of simplification in our lives and our schedules. 27:50 – Things that people can do to nurture themselves. 28:15 – Naming the different parts of your mind. (Have an inner-coach, an inner-best friend, an inner-mom, etc.) To learn more about Becca Ribbing, her services, and her books, visit www.beccaribbing.com.
In this episode, we review the high-yield topic of Diseases of Myelination from the Neurology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message
Guest Sims Brar, a third year student in the physician-scientist program at Rensselaer Polytechnic Institute, elaborates on her research on myelination within the peripheral nervous system. We discuss animal training as she uses mice in lab for her particular project, and Sims provides some very helpful insight into navigating her initial difficulties over handling live animals. Want to join our team? Submit research? Join the podcast? Website link: eruditenurj.org Apply link: eruditenurj.org/apply Submit link: eruditenurj.org/submit Podcast: eruditenurj.org/podcast Give us a like and follow on our social media: @EruditeNURJ on Facebook, Twitter, Instagram and LinkedIn
Marching to the Middle of the alphabet Merits a Mega episode to Memorialize the Momentous Milestone! So, Meet Jake & David from ‘Life Is Unfair’, the Malcolm in the Middle podcast that we Mention in Most episodes, who Match Minds with us as we discuss the Marvelous Movies: The Matrix (David), Mean Girls (Jake), Memento (Eric), and Moulin Rouge! (Dylan). A Myriad of tangents awaits! Much More than usual, Mentioning: How getting punched in the face will Make you forever associate certain Movie characters with their real-life wannabe counterparts; David Mentors us on Myelination; Where we were as Members of high school cliques; Being Mall rats and Moments we were kicked out of Megastores; Jake’s Mindful insights into the deeper Meaning of Tina Fey’s Magnum Opus; Eric’s Military naivete and lamentable reason for being there; Dylan’s utter lack of knowledge of Months or Maps; and Much Much More! You can find Jake & David’s show ‘Life Is Unfair’ wherever you find your podcasts: iTunes: https://podcasts.apple.com/us/podcast/life-is-unfair/id1497467628 Spotify: https://open.spotify.com/show/47IG2aqEpsDRqCfwHe4o9G?si=JC29Xy9FQy2WZaU2AF4bEw They stream video games and add their wit, charm, and general awesomeness for all to experience on their Twitch channel https://twitch.tv/lpdeathray And you should follow their Twitter accounts: @unfair_podcast @LPDeathRay @yearofalgorithm You can follow File Under: Entertainment on Twitter @FileUnderPod, and/or e-mail us at fileunderpod@gmail.com More to come, Merry band of Misfits!
Broccoli compound extends lifespan in worm model University of Heidelberg (Germany), February 5 2021. An article published on January 20, 2021 in Aging reported the findings of a team from the University of Heidelberg in Germany of an association between the intake of the compound sulforaphane derived from broccoli and other Brassicaceae family vegetables and longer survival of the roundworm Caenorhabditiselegans. “Several studies have described the isolation of natural substances from food plants and characterized them as suitable anti-aging agents; such substances include the phenol resveratrol from grapes and berries, the phenol curcumin from turmeric, the alkaloid berberine found in plants used in traditional Chinese medicine (TCM), the polyphenol chlorogenic acid from coffee and tea, and chlorophyll from green vegetables, among others,” wrote Zhimin Qi and colleagues. “We asked whether sulforaphane may influence the lifespan and health span of C. elegans.” Adding sulforaphane to the worms’ diets increased the lifespan of various strains of C. elegans by an average of 17%. The mechanism of action was attributed to inhibition of abnormal dauer formation protein 2 (DAF-2)-mediated insulin and insulin-like growth factor signaling and its downstream targets, which positively affected other factors. (DAF-2 is part of a metabolic pathway that regulates the rate of aging.) Sulforaphane also increased health span, resulting in a delay in aging-associated physiologic decline. Mobility, appetite and food intake were greater in worms that received sulforaphane, while the accumulation of the aging-associated pigment lipofuscin was reduced. Other experiments revealed that sulforaphane enhanced oxidative stress resistance. "We are the first to report that sulforaphane prolongs the lifespan and increases the health span of C. elegans through the inhibition of DAF- 2/insulin/IGF-1 signaling and the activation of DAF- 16/FOXO nuclear transcription in C. elegans,” the authors announced. “Our study provides a promising hint regarding the suitability of sulforaphane as a new anti-aging drug.” Oral N-acetylglucosamine may be neuroprotective in demyelinating diseases like MS University of California at Irvine, January 31, 2021 According to news reporting originating in Irvine, California, research stated, “Myelination plays an important role in cognitive development and in demyelinating diseases like multiple sclerosis (MS), where failure of remyelination promotes permanent neuro-axonal damage. Modification of cell surface receptors with branched N-glycans coordinates cell growth and differentiation by controlling glycoprotein clustering, signaling, and endocytosis.” The news reporters obtained a quote from the research from the University of California Irvine, “GlcNAc is a rate-limiting metabolite for N-glycan branching. Here we report that GlcNAc and N-glycan branching trigger oligodendrogenesis from precursor cells by inhibiting platelet-derived growth factor receptor-alpha cell endocytosis. Supplying oral GlcNAc to lactating mice drives primary myelination in newborn pups via secretion in breast milk, whereas genetically blocking N-glycan branching markedly inhibits primary myelination. In adult mice with toxin (cuprizone)-induced demyelination, oral GlcNAc prevents neuro-axonal damage by driving myelin repair. In MS patients, endogenous serum GlcNAc levels inversely correlated with imaging measures of demyelination and microstructural damage.” According to the news reporters, the research concluded: “Our data identify N-glycan branching and GlcNAc as critical regulators of primary myelination and myelin repair and suggest that oral GlcNAc may be neuroprotective in demyelinating diseases like MS.” This research has been peer-reviewed. Happiness really does come for free: study McGill University (Quebec), February 9, 2021 Economic growth is often prescribed as a sure way of increasing the well-being of people in low-income countries, but a study led by McGill and the Institute of Environmental Sciences and Technologies at the Universitat Autònoma de Barcelona (ICTA-UAB) suggests that there may be good reason to question this assumption. The researchers set out to find out how people rate their subjective well-being in societies where money plays a minimal role, and which are not usually included in global happiness surveys. They found that the majority of people reported remarkably high levels of happiness. This was especially true in the communities with the lowest levels of monetization, where citizens reported a degree of happiness comparable to that found in Scandinavian countries which typically rate highest in the world. The results suggest that high levels of subjective well-being can be achieved with minimal monetization, challenging the perception that economic growth will automatically raise life satisfaction among low-income populations. Measuring happiness To explore how monetization affects people's sense of well-being, the researchers spent time in several small fishing communities, with varying degrees of monetization, in the Solomon Islands and Bangladesh, two very low-income countries. Over a period of a few months, with the help of local translators, they interviewed citizens in both rural and urban areas a number of times. The interviews, which took place both in person and through phone calls at unexpected moments, were designed to elicit information about what constituted happiness for the study subjects, as well as to get a sense of their passing moods, their lifestyle, fishing activities, household income, and level of market integration. In all, the researchers interviewed 678 people, ranging in age between their mid-twenties and early fifties, with an average age of about 37. Almost 85 % of the study participants were male. The disproportionate number of men in the study was due to the fact that cultural norms in Bangladesh made it difficult to interview women. In the Solomon Islands, responses to the study questions from men and women were not significantly different. However, this is not necessarily applicable to the situation in Bangladesh, as men and women's social realities and lifestyles differ so much. Further research will need to address whether gender-related societal norms impact the association found in this study. Early stages of monetization may be detrimental to happiness The researchers found that in the communities where money was in greater use, such as in urban Bangladesh, residents reported lower levels of happiness. "Our study hints at possible ways of achieving happiness that are unrelated to high incomes and material wealth," says Eric Galbraith, a professor in McGill's Department of Earth and Planetary Sciences and the senior author on the study, which was recently published in PLOS One. "This is important, because if we replicate these results elsewhere and can pinpoint the factors that contribute to subjective well-being, it may help us circumvent some of the environmental costs associated with achieving social well-being in the least developed nations." "In less monetized sites, we found that people reported a greater proportion of time spent with family and contact with nature as being responsible for making them happy," explains Sara Miñarro, the lead author on the study who is a Postdoctoral Research Fellow at (ICTA-UAB). "But with increasing monetization, we found that the social and economic factors commonly recognized in industrialized countries played a bigger role. Overall, our findings suggest that monetization, especially in its early stages, may actually be detrimental to happiness." Interestingly, while other research has found that technology and access to information from faraway cultures with different lifestyles may affect people's sense of their own well-being by offering standards to which people compare their own lives, this did not appear to be the case in these communities. "This work adds to a growing realization that important supports for happiness are not in principle related to economic output," adds Chris Barrington-Leigh, a professor in McGill's Bieler School of the Environment. "When people are comfortable, safe, and free to enjoy life within a strong community, they are happy—regardless of whether or not they are making any money." Depressed moms who breastfeed boost babies' mood, neuroprotection and mutual touch Study first to show EEG patterns shift as a result of feeding method and affectionate touch in depressed and non-depressed moms and babies Florida Atlantic University, February 10, 2021 About 1 in 9 mothers suffers from maternal depression, which can affect the mother-infant bond as well as infant development. Touch plays an important role in an infant's socio-emotional development. Mothers who are depressed are less likely to provide their babies with soothing touch, less able to detect changes in facial expressions, and more likely to have trouble regulating their own emotions. In addition, infants of depressed mothers exhibit similar brain functioning patterns as their depressed mothers, which also are linked to temperament characteristics. Infants of depressed mothers are at a high risk of atypical and potentially dysregulated social interaction. A first-of-its-kind study by researchers at Florida Atlantic University's Charles E. Schmidt College of Science examined the developing mother-infant relationship by studying feeding method (breastfeeding and/or bottle-feeding) and affectionate touch patterns in depressed and non-depressed mother-infant dyads as well examining the infant's electroencephalogram activity (EEG) during development. Affectionate touch was coded during the mother-infant feeding context and included stroking, massaging and caressing initiated by either mother or infant. For the study, researchers evaluated 113 mothers and their infants and assessed maternal depressive symptoms, feeding and temperament or mood. They collected EEG patterns (asymmetry and left and right activity) from infants at 1 and 3 months old and videotaped mother-infant dyads during feeding to assess affectionate touch patterns in both mother and baby. They specifically focused on alterations in EEG activation patterns in infants across development to determine whether feeding and maternal depression are interactively related to changes in resting frontal EEG asymmetry and power. Data from EEG activity, published in the journal Neuropsychobiology, revealed that mother-infant affectionate touch differed as a function of mood and feeding method (breastfeeding vs. bottle-feeding), affecting outcomes for infants of depressed mothers compared to non-depressed mothers. Researchers observed a reduction in infant touch toward their mothers only with the infants in the depressed and bottle-fed group. Affectionate touch of mothers and infants varied by depression interacting with feeding type, with breastfeeding having a positive effect on both maternal and infant affectionate touch. Infants of depressed and breastfeeding mothers showed neither behavioral nor brain development dysregulation previously found in infants of depressed mothers. "We focused on mother-infant affectionate touch patterns during feeding in our study because touch is a form of mutual interaction established in early infancy, used to communicate needs, soothe, and downregulate stress responses, and because mothers and infants spend a significant amount of time feeding across the first three months postpartum," said Nancy Aaron Jones, Ph.D., lead author, an associate professor, and director of the FAU WAVES Emotion Laboratory in the Department of Psychology in the Charles E. Schmidt College of Science, and a member of the FAU Brain Institute. "As experience with maternal mood and feeding pervade the infant's early environment, we chose to examine how these factors interact to affect mother-infant affectionate touch, focusing fastidiously on the key roles of individual variation in temperament and EEG activation patterns." Asymmetry patterns in certain infant populations, such as those of depressed mothers differ from the asymmetry patterns of typically developing infants and children. While EEG asymmetry measures the balance of the right and left hemisphere activity, infants of depressed mothers exhibit patterns of right frontal asymmetry, due in part to hypoactivation of the left hemisphere within the frontal region. This pattern of brain activation (greater right asymmetry) is similar to the pattern observed in depressed adults and is thought to represent heightened negative affect as well as motor tendencies for withdrawal and inhibited approach behaviors. In addition to the tactile behavior changes, the infants in this study displayed differential brain activation patterns as a function of maternal depression and feeding group status. Not only were the infants' EEG patterns affected by their mother's depression status, stable breastfeeding experience also interacted with the depression group to impact EEG patterns across early development. Left frontal asymmetry in infants was associated with having a non-depressed mother and infant care experiences in the form of stable breastfeeding. Left frontal activity has been associated with advancing maturation, positive emotions, as well as higher order processing skills. Notably, EEG patterns of infants of depressed mothers showed right frontal asymmetry; however, shifts to greater left frontal activation (left frontal hyperactivation change) were found in those infants with stable breastfeeding experiences. Analysis from the study also revealed that infant breastfeeding duration and positive temperamental characteristics predicted infant affectionate touch patterns, suggesting that early infant experiences, and more broadly, their underlying neurochemical regulatory processes during feeding could influence the development of infant physiology and behavior, even for infants of depressed mothers. "Ultimately, our study provides evidence that the sensitive caretaking that occurs, even for mothers with postnatal depression in the context of more predominant breastfeeding, may redirect neurophysiological, temperamental, and socio-emotional risk through dyadic tactile experiences across early development," said Aaron Jones. Vitamin D supplementation: possible gain in life years combined with cost savings German Cancer Research Center, February 11, 2021 In recent years, three meta-analyses of clinical studies have come to the conclusion that vitamin D supplementation was associated with a reduction in the mortality rate from cancer of around 13 percent. Scientists at the German Cancer Research Center (DKFZ) have now transferred these results to the situation in Germany and calculated: If all Germans over the age of 50 were to take vitamin D supplements, up to 30,000 cancer deaths per year could possibly be avoided and more than 300,000 years of life could be gained - in addition, health care costs could be saved. For several years now, scientists have been investigating the influence of an adequate supply of vitamin D on the prognosis of numerous diseases. The focus is particularly on inflammatory diseases, diabetes, respiratory diseases and cancer. Three meta-analyses of large clinical studies have been published in recent years on the question of how vitamin D supply affects cancer mortality rates. The studies* came to the same conclusion: cancer mortality is reduced by around 13 percent with vitamin D supplementation - across all cancers. Only methodologically high-quality randomized trials from all parts of the world were included in the meta-analyses. Exactly what biological mechanisms might underlie this is not yet clear. "In many countries around the world, the age-adjusted rate of cancer mortality has fortunately declined over the past decade," says Hermann Brenner, an epidemiologist at the German Cancer Research Center (DKFZ). "However, given the often considerable costs of many new cancer drugs, this success has often come at a high price. Vitamin D, on the other hand, is comparatively inexpensive in the usual daily doses." Vitamin D deficiency is common in the elderly population and especially among cancer patients. Brenner and colleagues now calculated what costs would be incurred by vitamin D supplementation of the entire population of Germany from the age of 50. They contrasted this sum with the potential savings for cancer therapies, which are often associated with costs in the range of several 10,000 euros, particularly in the case of advanced cancers during the last months of patients' lives. The scientists based this calculation on a daily administration of 1,000 international units of vitamin D at a cost of 25 euros per person per year. In 2016, approximately 36 million people over the age of 50 lived in Germany, resulting in annual supplementation costs of 900 million euros. The researchers took the cost of cancer treatment from the scientific literature, assuming mean additional treatment costs of €40,000 for the last year of life. A 13 percent reduction in cancer mortality in Germany corresponded to approximately 30,000 fewer cancer-related deaths per year, the treatment costs of which amounted to €1.154 billion in the model calculation. Compared with the costs of vitamin supplementation, this model calculates an annual saving of €254 million. The researchers determined the number of years of life lost at the time of cancer death using data from the German Federal Statistical Office. Brenner considers the costs and effort of a routine determination of the individual vitamin D level to be dispensable, since an overdose is not to be feared with a supplementation of 1000 international units. Such a prior testing had not been made in the clinical trials either. "In view of the potentially significant positive effects on cancer mortality - additionally combined with a possible cost saving - we should look for new ways to reduce the widespread vitamin D deficiency in the elderly population in Germany. In some countries, foods have even been enriched with vitamin D for many years - for example, in Finland, where cancer mortality rates are about 20 percent lower than in Germany. Not to mention that there is mounting evidence of other positive health effects of adequate vitamin D supply, such as in lung disease mortality rates," says Brenner, adding, "Finally, we consider vitamin D supplementation so safe that we even recommend it for newborn babies to develop healthy bones." To improve one's vitamin D levels at absolutely no cost, DKFZ's Cancer Information Service recommends spending time outdoors in the sunshine, two to three times a week for about twelve minutes. Face, hands and parts of arms and legs should be uncovered and without sunscreen for this period of time. Poor fitness linked to weaker brain fiber, higher dementia risk University of Texas Medical Center, February 14, 2021 Scientists have more evidence that exercise improves brain health and could be a lifesaving ingredient that prevents Alzheimer's disease. In particular, a new study from UT Southwestern's O'Donnell Brain Institute suggests that the lower the fitness level, the faster the deterioration of vital nerve fibers in the brain. This deterioration results in cognitive decline, including memory issues characteristic of dementia patients. "This research supports the hypothesis that improving people's fitness may improve their brain health and slow down the aging process," said Dr. Kan Ding, a neurologist from the Peter O'Donnell Jr. Brain Institute who authored the study. White matter The study published in the Journal of Alzheimer's Disease focused on a type of brain tissue called white matter, which is comprised of millions of bundles of nerve fibers used by neurons to communicate across the brain. Dr. Ding's team enrolled older patients at high risk to develop Alzheimer's disease who have early signs of memory loss, or mild cognitive impairment (MCI). The researchers determined that lower fitness levels were associated with weaker white matter, which in turn correlated with lower brain function. Distinctive tactics Unlike previous studies that relied on study participants to assess their own fitness, the new research objectively measured cardiorespiratory fitness with a scientific formula called maximal oxygen uptake. Scientists also used brain imaging to measure the functionality of each patient's white matter. Patients were then given memory and other cognitive tests to measure brain function, allowing scientists to establish strong correlations between exercise, brain health, and cognition. Lingering mysteries The study adds to a growing body of evidence pointing to a simple yet crucial mandate for human health: Exercise regularly. However, the study leaves plenty of unanswered questions about how fitness and Alzheimer's disease are intertwined. For instance, what fitness level is needed to notably reduce the risk of dementia? Is it too late to intervene when patients begin showing symptoms? Some of these topics are already being researched through a five-year national clinical trial led by the O'Donnell Brain Institute. The trial, which includes six medical centers across the country, aims to determine whether regular aerobic exercise and taking specific medications to reduce high blood pressure and cholesterol levels can help preserve brain function. It involves more than 600 older adults at high risk to develop Alzheimer's disease. "Evidence suggests that what is bad for your heart is bad for your brain. We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer's disease," said Dr. Rong Zhang of UT Southwestern, who oversees the clinical trial and is Director of the Cerebrovascular Laboratory in the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas, where the Dallas arm of the study is being carried out. Prior findings The research builds upon prior investigations linking healthy lifestyles to better brain function, including a 2013 study from Dr. Zhang's team that found neuronal messages are more efficiently relayed in the brains of older adults who exercise. In addition, other teams at the O'Donnell Brain Institute are designing tests for the early detection of patients who will develop dementia, and seeking methods to slow or stop the spread of toxic proteins associated with the disease such as beta-amyloid and tau, which are blamed for destroying certain groups of neurons in the brain. "A lot of work remains to better understand and treat dementia," said Dr. Ding, Assistant Professor of Neurology & Neurotherapeutics. "But, eventually, the hope is that our studies will convince people to exercise more." A systematic review and meta-analysis of impact of red wine polyphenols on vascular health University of Birmingham (UK), February 4, 2021 According to news reporting originating from Birmingham, United Kingdom, research stated, “Red wine polyphenols (RWP) are plant-based molecules that have been extensively studied in relation to their protective effects on vascular health in both animals and humans. The aim of this review was to quantify and compare the efficacy of RWP and pure resveratrol on outcomes measures of vascular health and function in both animals and humans.” Our news editors obtained a quote from the research from the University of Birmingham, “Comprehensive database searches were carried out through PubMed, Web of Science and OVID for randomised, placebo-controlled studies in both animals and humans. Meta-analyses were carried out on acute and chronic studies of RWP in humans, alongside sub-group analysis where possible. Risk-of-bias assessment was carried out for all included studies based on randomisation, allocation, blinding, outcome data reporting, and other biases. Results 48 animal and 37 human studies were included in data extraction following screening. Significant improvements in measures of blood pressure and vascular function following RWP were seen in 84% and 100% of animal studies, respectively. Human studies indicated significant improvements in systolic blood pressure overall (- 2.6 mmHg, 95% CI: [- 4.8, - 0.4]), with a greater improvement in pure-resveratrol studies alone (- 3.7 mmHg, 95% CI: [- 7.3, - 0.0]). No significant effects of RWP were seen in diastolic blood pressure or flow-mediated dilation (FMD) of the brachial artery.” According to the news editors, the research concluded: “RWP have the potential to improve vascular health in at risk human populations, particularly in regard to lowering systolic blood pressure; however, such benefits are not as prevalent as those observed in animal models.” This research has been peer-reviewed.
Andrew Henry MA LPC and Paul Krauss MA LPC discuss many concepts related to Intuition, Stoicism, the Present Moment and the intersections with the practice of Psychotherapy. Paul and Andrew elaborate on the philosophy of Stoicism, Reality Therapy, ways to enhance your meditation or mindfulness practice, and methods for getting more out of psychotherapy. Andrew's book The Gift, an Unconscious Intuitive Mind! is available on Apple Books. Andrew discusses the power of the unconscious intuitive mind, and how it can help a person better understand them self, and those around them. Andrew stated: All people are born with a powerful alley: the unconscious and intuitive mind. Tapping into this vital internal resource is as important as knowing the route to your next destination. Andrew discusses the history of Stoicism and how this philosophy can help us decrease our anxiety and also help us be more present. Andrew also discusses how the concept of personal responsibility being grounded in the now can help a person in their journey. Paul goes on to discuss the concepts of Reality Therapy (William Glasser). Andrew also discuses the concept of cynicism as well. Paul discusses some existential concepts illustrated by Irvin Yalom. Andrew goes on to discuss the values of struggle in people's transformation. Andrew also discusses his first book and some exercises in dialectics that people can do from their home. Also discussed: Neurobiology, Trauma, Jordan Peterson, Personal Struggles, Carl Jung, Micro vs. Macro, Control, Imperfect Systems, How to make a difference, Don Miguel Ruiz, Incremental Changes lead to larger changes, Myelination, Neurological Wiring, triggers, Relapses, Personal difficulties, Positive Psychology, Blame, Individual Strengths, Self-Reflection, Unconscious Mind, Adverse Experiences, problems that are out of time, Stuck Points, Crystalline Structures, Trauma-Informed Therapy, Schema, Self-Construct, the fantasy of the future and the past, emotional dysregulation, “time capsules”, ego states, different concepts of time, Alchemy, Dialectics, Mindfulness Skills, Imagination, Colors, Symbols, James Hillman, what a person can do at home to help themselves, amygdala, the negative bias, survival, adaptation, the prefrontal cortex, seeing a therapist, Hypnosis, and more. Andrew Henry, MA, LPC is a licensed professional counselor in private practice located in Mesa Arizona. Andrew is an EMDRIA certified clinician, and Andrew has 16 years of experience in the field of counseling. In addition to being an author, Andrew taught Masters level counseling as an adjunct professor at Grand Canyon University in Phoenix Arizona. He continues to work in private practice utilizing Jungian methods, Hypnosis, EMDR, elements of DBT, energy psychology, mindfulness, and CBT. Andrew is currently open to guest lecturing on campuses via video, and teaching national and international workshops on the topics of Hypnosis and Jungian methods via video. Andrew graduated with a Masters degree in professional counseling plus the certificate in advance graduate studies in 2004 from Ottawa University in Phoenix Arizona. Andrew has an undergraduate degree in Sociology from Arizona State University in Tempe Arizona 1996. Andrew volunteers his time in Kathmandu Nepal providing therapeutic treatment. Learn more about Andrew Henry here: www.CounselingbyAndrew.com aehlpc@icloud.com Get Andrew Henry's Book Here. Paul Krauss MA LPC is the Clinical Director of Health for Life Grand Rapids, home of The Trauma-Informed Counseling Center of Grand Rapids. Paul is also a Private Practice Psychotherapist, EMDRIA Consultant in Training (CIT), host of the Intentional Clinician podcast, Behavioral Health Consultant, Clinical Trainer, and Counseling Supervisor. Paul is now offering consulting for a few individuals and organizations. Paul is the creator of the National Violence Prevention Hotline (in progress) as well as the Intentional Clinician Training Program for Counselors. Questions? Call the office at 616-200-4433. If you are looking for EMDRIA consulting groups, Paul Krauss MA LPC is now hosting weekly online and in-person groups. For details, click here. For general behavioral and mental health consulting for you or your organization. Follow Health for Life Grand Rapids: Instagram | Facebook | Youtube Original Music: ”Shades of Currency" [Instrumental] from Archetypes by PAWL (Spotify) "Nivedan" from Healing the Divide by Anousha Shankar (Spotify) “Geometry of Lawns” from Strange Geometry by The Clientele (Spotify) Support your local bookstore by shopping at https://bookshop.org/ (You can order online from the comfort of your own home, while supporting local businesses near you).
In this episode, we look at why smoking is so much easier than working out. Sponsor: http://andstillivote.org The Problem We all know the “right” things to do. If you want to lose weight, eat better and exercise. If you want to get out of debt, live below your means and save your money. If you want to improve your relationship, create lines of open communication with each other. Chances are if you have a goal for your life you are also FULLY aware of how to accomplish it. And even if you aren’t 100% positive on the exact formula, you at least know what direction to go in. And even more, let’s pretend that you have a goal and have absolutely no idea at all how to accomplish it. There are plenty of resources like this podcast, google, or books to help you out. My point is that we have absolutely no problem figuring out what to do to make progress. Digging Deeper Researchers over the years have come up with a reliable theory on how habits are formed. We’ve discussed this in past episodes but as a bit of a refresher, a habit requires 3 things in order to be created. First it needs a trigger, this is the external thing that your behavior is responding to. Second it needs a behavior, this is the core activity of the habit, finally it needs some kind of reward. Once the trigger happens, if we take the behavior our brains use a process called Myelination to reinforce the circuitry responsible. This allows the response to the initial trigger to become much faster. We essentially become more efficient in order to use less energy the next time. The Solution Honestly this is a difficult question to answer. There is no way to get results from the gym faster. There is no way to reduce the pleasures of engaging in bad habits. Since we can’t change this dynamic between good habits and bad habits there is really only one thing we can do. Accept that building good habits is going to suck. Like seriously suck. And it sucks for a reason, your brain wants there to be a clear reward from that activity. That’s how it tricks you into doing it. If you work out for long enough you will start to feel that reward in the release of neurochemicals. You’ll start to see that reward in your body. But you’ve gotta make it to that point before you can take advantage of it. --- This episode is sponsored by · Anchor: The easiest way to make a podcast. https://anchor.fm/app
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.10.334656v1?rss=1 Authors: Micheva, K. D., Kiraly, M., Perez, M. M., Madison, D. V. Abstract: Parvalbumin-containing (PV+) basket cells in mammalian neocortex are fast-spiking interneurons that regulate the activity of local neuronal circuits in multiple ways. Even though PV+ basket cells are locally projecting interneurons, their axons are myelinated. Can this myelination contribute in any significant way to the speed of action potential propagation along such short axons? We used dual whole cell recordings of synaptically connected PV+ interneurons and their postsynaptic target in acutely-prepared neocortical slices from adult mice to measure the amplitude and latency of single presynaptic action potential-evoked inhibitory postsynaptic currents (IPSCs). These same neurons were then imaged with immunofluorescent array tomography, the synaptic contacts between them identified and a precise map of the connections was generated, with the exact axonal length and extent of myelin coverage. Our results support that myelination of PV+ basket cells significantly increases conduction velocity, and does so to a degree that can be physiologically relevant. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.09.289223v1?rss=1 Authors: Hu, X., Xiao, G., He, L., Zhu, Q., Niu, X., Li, H., Xu, Q., Wei, Z., Huang, H., Luan, Y., Qiu, M., Tanaka, K. F., Shen, Y., Tao, Y. Abstract: White matter abnormalities are an emerging pathological feature of schizophrenia. However, their attributions to the disease remain largely elusive. ErbB receptors and their ligands, some of which are essential for peripheral myelination, confer susceptibility to schizophrenia. By synergistically manipulating ErbB receptor activities in a oligodendrocyte-stage-specific manner in mice after early development, we demonstrate the distinct effects of ErbB signaling on oligodendrocytes at various differentiation states. ErbB overactivation, in mature oligodendrocytes, induces necroptosis causing demyelination, whereas in oligodendrocyte precursor cells, induces apoptosis causing hypomyelination. In contrast, ErbB inhibition increases oligodendrocyte precursor cell proliferation but induces hypomyelination by suppressing the myelinating capabilities of newly-formed oligodendrocytes. Remarkably, ErbB inhibition in mature oligodendrocytes diminishes axonal conduction under energy stress and impairs working memory capacity independently of myelin pathology. This study reveals the etiological implications of oligodendrocyte vulnerability induced by ErbB dysregulation, and elucidates the pathogenetic mechanisms for variable structural and functional white matter abnormalities. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.28.271593v1?rss=1 Authors: Almeida, R. G., Williamson, J. M., Madden, M. E., Early, J. J., Voas, M. G., Talbot, W. S., Bianco, I. H., Lyons, D. A. Abstract: To study activity-regulated myelination, we imaged synaptic vesicle fusion along single axons in living zebrafish, and found, surprisingly, that axonal synaptic vesicle fusion is driven by myelination. This myelin-induced axonal vesicle fusion was enriched along the unmyelinated domains into which newly-formed sheaths grew, and was promoted by neuronal activity, which in turn accelerated sheath growth. Our results indicate that neuronal activity consolidates sheath growth along axons already selected for myelination. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.23.263681v1?rss=1 Authors: Yang, S. M., Michel, K., Jokhi, V., Nedivi, E., Arlotta, P. Abstract: Myelination plasticity plays a critical role in neurological function, including learning and memory. However, it is unknown whether this plasticity is enacted through uniform changes across all neuronal subtypes, or whether myelin dynamics vary between neuronal classes to enable fine-tuning of adaptive circuit responses. We performed in vivo two-photon imaging to investigate the dynamics of myelin sheaths along single axons of both excitatory callosal projection neurons and inhibitory parvalbumin+ interneurons in layer 2/3 of adult mouse visual cortex. We find that both neuron types show dynamic, homeostatic myelin remodeling under normal vision. However, monocular deprivation results in experience-dependent adaptive myelin remodeling only in parvalbumin+ interneurons, but not in callosal projection neurons. Monocular deprivation induces an initial increase in elongation events in myelin segments of parvalbumin+ interneurons, followed by a contraction phase affecting a separate cohort of segments. Sensory experience does not alter the generation rate of new myelinating oligodendrocytes, but can recruit pre-existing oligodendrocytes to generate new myelin sheaths. Parvalbumin+ interneurons also show a concomitant increase in axonal branch tip dynamics independent from myelination events. These findings suggest that adaptive myelination is part of a coordinated suite of circuit reconfiguration processes, and demonstrate that distinct classes of neocortical neurons individualize adaptive remodeling of their myelination profiles to diversify circuit tuning in response to sensory experience. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.20.260083v1?rss=1 Authors: Knowles, J. K., Soane, C., Frost, E., Tam, L. T., Fraga, D., Xu, H., Batra, A., Ni, L., Villar, K., Saucedo, T., Huguenard, J., Monje, M. Abstract: Neuronal activity can influence the generation of new oligodendrocytes (oligodendrogenesis) and myelination. In health, this is an adaptive process that can increase synchrony within distributed neuronal networks and contribute to cognitive function. We hypothesized that in seizure disorders, aberrant neuronal activity may promote maladaptive myelination that contributes to pathogenesis. Absence epilepsy is a disease defined by increasingly frequent behavioral arrest seizures over time, thought to be due to thalamocortical network hypersynchrony. We tested the hypothesis that activity-dependent myelination resulting from absence seizures promotes epileptogenesis. Using two distinct models of absence epilepsy, Wag/Rij rats and Scn8a+/mut mice, we found increased oligodendrogenesis and myelination specifically within the absence seizure network. These changes are evident only after seizure onset in both models and are prevented with pharmacological inhibition of seizures. Genetic blockade of activity-dependent myelination during epileptogenesis markedly decreased seizure frequency in the Scn8a+/mut mouse model of absence epilepsy. Taken together, these findings indicate that activity-dependent myelination driven by absence seizures contributes to seizure kindling during epileptogenesis. Copy rights belong to original authors. Visit the link for more info
Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.02.130625v1?rss=1 Authors: Gonzalez, S., Cazevieille, C. Abstract: Schwann cells produce myelin sheath around peripheral nerve axons. Myelination is critical for rapid propagation of action potentials, as illustrated by the large number of acquired and hereditary peripheral neuropathies, such as diabetic neuropathy or Charcot-Marie-Tooth (CMT) diseases, that are commonly associated with a process of demyelination. Peripheral neuropathy is a major complication of diabetes, and the pathomechanism of the disease remains poorly studied. Here, we studied the progressive demyelinating process, hearing impairment and blindness observed in the CMT1A mouse model C3. Our results confirm that these mice represent a robust and validated model to study the peripheral neuropathy induced by CMT disorder allowing to determine the efficacy of new pharmacological candidates targeting demyelinating diseases such as CMT1A disorder. Copy rights belong to original authors. Visit the link for more info
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Michael was off this week, which means Matt and Michelle were left alone running episode 103. Matt found TikTok and he can't stop watching short videos about everything and anything and he cant get over the effects contouring has on women's makeup. Michelle was looking for suggestions to make a diaper cake. The crew talks the importance of praise in therapy, the link between myelination and autism, dysphagia and cues from the Informed SLP, and Interstate Compacts as well as the shoutouts and due process. ----more---- The Discord is up and ready for people to interact with the crew 24/7. SSPOD Shoutout: We want to know your #SSPODSHOUTOUT. This week, the crew recognizes the SLPs who started their own Teletherapy group, Expressable. SSPOD Due Process: Do you have a complaint or need to vent, then you want to participate in the #SSPODDUEPROCESS. There were no due processes this week. Article #1: Praising your students can lead to improved results. Teachers and students report up to a 30% improvement thanks to using positive reinforcement over negative or punitive reinforcers. Article #2: What if the myelination in the brain had an impact on autism? A recent study reported in NPR, researchers from Johns Hopkins believe they have found a link between myelination and autism. What does this look like for the future of diagnoses? Interview: The mission of Adam's Camp is to realize the potentials and develop the strengths of children and young adults by bringing together individuals and families with professionals and volunteers to collaboratively provide customized, intensive therapy, family support, and recreation in a camp environment. Michelle spoke with Kim Kelleher, Therapy Manager from Adam's Camp, about what they do and the up-coming summer camp schedules. The Informed SLP: What does the timing of your cue have to do with the safety of a swallow? The Informed SLP's Stephanie Muñoz breaks down the latest research. ASHA Spotlight: Time to make plans for ASHA Connect. Hot Take: Michelle looks at the Interstate Compact and why hasn't it already come to fruition? Contact Email: speechsciencepodcast@gmail.com Voicemail: (614) 681-1798 Discord: https://discord.gg/3Tm5jrS New Episode and Interact here: www.speechsciencepodcast.com podcast.speechsciencepodcast.com Support Patreon – https://www.patreon.com/speechsciencepodcast Rate and Review: https://podcasts.apple.com/us/podcast/speechscience-org-podcast/id1224862476?fbclid=IwAR3QRzd5K4J-eS2SUGBK1CyIUvoDrhu8Gr4SqskNkCDVUJyk5It3sa26k3Y&ign-mpt=uo%3D8&mt=2 Credits Intro Music: Please Listen Carefully by Jahzzar is licensed under a Attribution-ShareAlike License. Bump Music: County Fair Rock, copyright of John Deku, at soundcloud.com/dirtdogmusic The Informed SLP: At The Count by Broke For Free is licensed under a Creative Commons Attribution License Closing Music: Slow Burn by Kevin MacLeod is licensed under a Creative Commons Attribution License. Show Links The Informed SLP https://www.theinformedslpmembers.com/reviews-adults/is-the-timing-of-your-cue-hurting-your-patients-swallow https://link.springer.com/article/10.1007%2Fs00455-019-10050-9 Expressable https://www.expressable.io/about-us/ Reinforcement: https://www.cnn.com/2020/01/30/health/teacher-praise-wellness/index.html?fbclid=IwAR3qktKF9nqD5zRtS-AtSe4KrH7Lm7lvLLJfyzNULZPMfuXr21XD639K7k8 Autism and Myelination https://www.npr.org/sections/health-shots/2020/02/03/802215344/researchers-link-autism-to-a-system-that-insulates-brain-wiring?fbclid=IwAR2crTzbJa5xIsteBBJbaBuw2rXUmnw1SP6i-AItKWb5nDzg3FUYGzHWAwA Adam's Camp https://adamscamp.org/ ASHA Spotlight https://www.asha.org/events/connect/?utm_source=ASHA&utm_medium=twitter&utm_campaign=connect20&fbclid=IwAR0YrhEb99-AMkwv4DaF4CeX6i9_OQvJizYM3LA9OxuFzF8Pk1AYVm0S9ek Intro Music: Please Listen Carefully by Jahzzar is licensed under a Attribution-ShareAlike License. Bump Music: County Fair Rock, copyright of John Deku, at soundcloud.com/dirtdogmusic The Informed SLP: At The Count by Broke For Free is licensed under a Creative Commons Attribution License Closing Music: Slow Burn by Kevin MacLeod is licensed under a Creative Commons Attribution License. Speech Science Powered by: You!
In new and exciting research, scientists have found that autistic individuals exhibited a significant reduction in myelination and myelin producing glial cells. Let us review what we know about myelination and how we can RE-myelinate.
Myelination is an important neurological process that impacts almost everything I care about in my child: motor coordination, learning, focus, moods. And there are some easy ways to impact Myelination: Practice, Nutrition, and one more key mindset. Yes, it is actually a mindset.
Elizabeth Vosseller is a speech therapist and founder of S2C (Spelling to Communicate). She talks to me this week about how motor issues can seem like cognitive disorders. "What we observe often is the body. We can't really observe intelligence directly." Tune in to listen to how powerful using motor appropriately can be.
program #115 59:30 Artist: Jean Claude Jones The free improviser and double bass player Jean-Claude Jones was born in Tunisia and lives in Jerusalem. A Music teacher, former head of the jazz department at the Jerusalem Academy of Music and Dance in the late 1990s. In 2005 Jones founded "Kadima" - a collective of free improvising musicians and visual artists, and the artistic label KCR. In the open project Myelination, Jean-Claude Jones creates a meeting space for his fellow musicians along with the disease of multiple sclerosis from which he has been suffering since the mid 80s. The encounter takes place via sound and it has been documented in three separate performances and albums so far. They are based on the artists' communication with the sounds of myelin - a fatty substance that isolates the nerve fibres and assists in the transfer of electrical currents between the nerve cells. Multiple sclerosis, a chronic disease of the nervous system, impacts the normal function of nerve cells by damaging and reducing myelin. Myelin protein is based on a long chain of molecules called amino acids. Jean-Claude Jones's friend, chemist Andy Shipway, programmed and slowed the vibration of each molecule in the chain to an audible frequency band. And so the sound of the myelin was born, the core of the project. Featuring: Harold Rubin-clarinet and voice, Stephen Hornstein-baritone saxophone, Yoni Silver-bass clarinet, Ariel Shibolet-soprano saxophone, Yael Thai-Voice, Hagai Fershtman-percussion, And jazz poet Jake Marmer, in the first part of the project, 2011. myelination 2, 2013 with Meira Asher-voice and electronics, recorded live at the Uganda Bar, Jerusalem. myelination 3, 2014 featuring vocal artists Anat Pick, Ayelet Lerman and Joseph Sprinzak, recorded live at the Mazkeka, Jerusalem. Mix and Mastering by Jean Claude Jones. Playlist: > myelination (2011): 18Aas, Inducing One, Arihag > myelination 2 (2013): One Out, Two In, Four In > myelination (2011): JC's remix, Voices > myelination 2 (2013): Seven Out, Three Out > myelination 3 (2014)
It is extremely powerful to combine leadership and gratitude. For starters, gratitude helps you feel generally better. Choosing to recognize and acknowledge all the good things in life (which is what gratitude practices help you do), creates a more positive outlook. In addition, when you establish a true gratitude practice you're able to anchor that feeling of gratefulness and positivity into your body. This anchoring creates an emotional reserve you'll be able to call on later.Another gratitude superpower is that it gives you the edge you need to be able to pivot quickly, especially in times of stress or conflict. By pausing and implementing a gratitude practice, you give your mind and body a chance to recalibrate. This will help you realign and refocus. It also helps you find hidden opportunities to be grateful. So, rather than only thinking of gratitude during holidays, we can use the entire year to store up a reserve of gratitude! And as you'll see below, just a little bit of gratitude can go a long way. My executive coaching clients have found that the gratitude practice I teach is really practical and beneficial.Close your eyes.Focus on a blessing in your life - something you're thankful for.See an image of this blessing in your mind's eye.Offer a silent thank-you to the person or object of your blessing.Relax into the feeling of gratitude. Take a deep breath, and feel more gratitude. (Think of turning the volume up.)The latest research shows that 6 doses of feeling 30 seconds of gratitude daily actually enables your neurons to fire together and wire together around gratitude in as little as two weeks! This means that practicing gratitude (and naturally having a more grateful mindset) will become more natural and be achieved more easily.When I first learned, I started doing it. Now, I wake up each morning and automatically and easily think "thank you". It's right there, because I've grown my own personal practice of gratitude. This practice reinforced gratitude as second nature, and also increases myelination. (Grab the handy infographic here: https://www.smarttribesinstitute.com/myelination-practice/)All of these results, in under 3 minutes a day! That's an ROI that's hard to argue with.If you want to learn more about cultivating an attitude of gratitude, check out the annual retreat, Beyond Your Brain at https://www.smarttribesinstitute.com/stiretreat/.Resources Mentioned:Beyond Your Brain Retreat: https://www.smarttribesinstitute.com/stiretreat/Myelination: https://www.smarttribesinstitute.com/myelination-practice/Contact Christine: https://smarttribesinstitute.com/contact/You’re busy growing. Let’s have a strategy session when it makes sense, which means you are…· Committed to getting better results and finding out how awesome your performance can truly be· Ready to make this a priority and get started in the next few months· Allocating budget to improving the leadership, culture and results of you and your company· Able to make the decision to move forward (or can convince the person who can)https://smarttribesinstitute.com/strategy-session/Ready? Great! Please fill out the form here. If not, check out our resources and subscribe to receive news and more tools as they become available, and we’ll work together when the time is right. See acast.com/privacy for privacy and opt-out information.
Myelination Support with Tara Hunkin by Tara Hunkin
Few features of humanity are more fascinating than creativity; and few fields are more dynamic now than neuroscience. Rex Jung is a neuropsychologist who puts the two together. He’s working on a cutting edge of science, exploring the differences and interplay between intelligence and creativity. He and his colleagues unsettle long-held beliefs about who is creative and who is not. And they’re seeing practical, often common-sense connections between creativity and family life, aging, and purpose.
Rex Jung is an Assistant Professor of Neurosurgery at the University of New Mexico in Albuquerque. He’s a Distinguished Senior Advisor to the Positive Neuroscience Project, based at the University of Pennsylvania. This interview is edited and produced with music and other features in the On Being episode “Rex Jung — Creativity and the Everyday Brain.” Find more at onbeing.org.
Medizinische Fakultät - Digitale Hochschulschriften der LMU - Teil 18/19
Neuregulin-1 (NRG1) type III is a growth factor on the surface of neurons in the peripheral nervous system (PNS). It is required for initial myelination of nerves by Schwann cells after birth and for remyelination after injury. Neuregulin-1 type III is activated by cleavage (shedding) in its extracellular juxtamembrane region generating a membrane-bound N-terminal fragment (NTF) that contains a bioactive epidermal growth factor (EGF)-like domain. This domain signals to neighboring Schwann cells in a contact-dependent manner prompting the cells to initiate myelination. The β-site APP cleaving enzyme 1 (BACE1) was identified as the enzyme that cleaves NRG1 type III and promotes myelination. Consequently, loss of BACE1 cleavage results in dramatically reduced myelin sheaths around nerves in the PNS of BACE1 knockout mice. Besides its role in myelination, BACE1, better known as β-secretase, is also involved in the generation of the neurotoxic amyloid β-peptide (Aβ) which is the main component of amyloid plaques in the brain of patients suffering from Alzheimer’s disease (AD). The Aβ peptide is derived through sequential cleavage of the amyloid precursor protein APP, first by BACE1 in the extracellular domain and subsequently by the γ-secretase in the transmembrane domain (TMD). Inhibition of BACE1 and γ-secretase is therefore considered a promising therapeutic strategy for AD. However, this approach harbors the risk of mechanism-based side effects due to impaired processing of substrates beside APP such as NRG1 type III which is not only a substrate for BACE1 but like APP is also cleaved in its TMD by the γ-secretase. Adding another layer of complexity, ADAM10 and ADAM17, the so-called α-secretases of AD, also cleave NRG1 type III. In the first part of this study, the proteolytic processing of NRG1 type III in its ectodomain was investigated in detail. The precise juxtamembrane shedding sites of BACE1, ADAM10 and ADAM17 were determined by mass spectrometry and two novel cleavage sites of BACE1 and ADAM17 N-terminal of the EGF-like domain were discovered. Cleavage at these novel sites by ADAM17 and BACE1 results in the secretion of the EGF-like domain from NRG1 type III as α-sEGF and β-sEGF, respectively. Using novel monoclonal antibodies generated against the identified cleavage sites the processing of NRG1 type III could also be confirmed in primary neurons. The soluble EGF-like domains were found to be functionally active and induced signaling pathways required for myelination in cultured Schwann cells. Furthermore, β-sEGF rescued the myelination deficit in the PNS of a zebrafish model lacking BACE1, thereby demonstrating its activity in vivo. Using cell culture and the zebrafish model the effects of BACE1- and ADAM17-mediated shedding on the activity of the soluble EGF-like domains were carefully dissected. In contrast to published evidence, however, both the BACE1- as well as the ADAM17-shed sEGF were found to be equally active and to promote myelination in vivo. Together this suggests that NRG1 type III dependent myelination is not only controlled by membrane-retained NRG1 type III but also in a contact-independent manner via proteolytic liberation of the EGF-like domain. The second part of this study investigates the processing of the C-terminal fragment (CTF) which remains after shedding of NRG1 type III. Intramembranous cleavage of the CTF by the γ-secretase was previously shown to release the NRG1 intracellular domain, which acts as transcriptional regulator of proteins involved in neuronal maturation and brain plasticity. Interestingly, a mutation within the TMD of NRG1 type III is associated with an increased risk of schizophrenia linking γ-secretase processing of NRG1 type III to this neurological disorder. Using a novel antibody against the N-terminus of the NRG1 CTF it was possible to detect a NRG1 β-peptide that is secreted during γ-secretase cleavage and could potentially serve as marker for this processing. Moreover, by means of mass spectrometry, the precise cleavage sites within the TMD of NRG1 could be identified. Strikingly, the ɛ-like cleavage site was found to be located exactly at the position of the schizophrenia-associated mutation providing a possible mechanism for the reported interference of this mutation with γ-secretase cleavage. The evidence presented unambiguously establishes NRG1 type III as a γ-secretase substrate and provides a basis for further investigation of the mechanisms which link its processing to the development of schizophrenia. In summary and with regard to BACE1 and γ-secretase being prime targets for a potential AD therapy, the results of this work call for further careful investigation of the consequences of altered NRG1 type III signaling due to chronic treatment with inhibitors.
Will Talbot discusses how collagen binds to and activates the orphan receptor GPR126.
Listen to Bridget Shafit-Zagardo discuss her latest ASN NEURO paper on how Gas6 enhances axonal ensheathment by MBP+ membranous processes in human DRG/OL promyelinating co-cultures.
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