Podcasts about sod2

In this episode, I break down the results of my Smart Nutrition methylation and nutrigenomics test — and how it's helped me finally understand the root cause of my inflammation, energy crashes, IBS symptoms, and persistent neck and eye issues. I share my exact results, including key gene variations like MTHFR, CBS, COMT, MAOA, and SOD2, and how these are impacting my: – Stress response and emotional regulation – Ability to clear toxins, sulphur, and ammonia – Digestion, sleep, and protein metabolism – Histamine sensitivity and inflammation Based on my profile, I'm now supplementing with: – Methylated B-complex (B12, B2, B6, 5-MTHF) – Buffered vitamin C – Choline (350mg with each main meal) – Glycine powder (with every protein meal) – Dicalcium Malate (to support mineral balance and inflammation control) – Omega-3 DHA/EPA – Magnesium glycinate (evening) – Marine collagen (evening) – Liposomal glutathione – Quercetin (for histamine and eye/neck inflammation) I'm also following a low FODMAP, ketogenic-style diet, spacing my protein evenly across the day, and using cold exposure and vagal tone exercises for nervous system support. You can order your own personalised DNA test and consultation here: https://smartnutrition.co.uk/methylation-test Book a consultation call: https://calendly.com/garygunn/consultation Work on your dating success for only £10.79/$13.50 per month with my Advanced Dating System and 100-Day Dating Challenge: https://social-attraction-courses.teachable.com/p/small-bundle Access all of my digital products for only £24.96/$33.20 per month: https://social-attraction-courses.teachable.com/p/gary-gunn-big-bundle View all of my digital courses here: https://social-attraction-courses.teachable.com/ My TikTok account: https://www.tiktok.com/@garygunnshow Follow me on Instagram: https://www.instagram.com/garygunnshow/ Access my podcast with over 200 episodes: https://soundcloud.com/garygunn Subscribe to my YouTube channel: https://www.youtube.com/c/GaryGunn?sub_confirmation=1 This video is for entertainment purposes only. Any action you take upon the information provided is strictly at your own risk, and we will not be responsible for any losses or damages in connection with the use of this video. The selection of techniques, opinions, programs, products, services, tools, templates, or manuals is not a guarantee of income or success. You are fully responsible for the effort you put in and the results you achieve by following the information in this video. All content, materials, and techniques delivered are proprietary and cannot be used, disclosed, or duplicated without permission. This video is for informational purposes only and does not form a professional relationship. Visit our website if you wish to hire us on a professional basis. #datingadviceformen #datingtipsformen #datingcoachformen

In this episode of the RWS Clinician's Corner, Margaret Floyd Barry sits down with Dr. Robert Whitfield, a world-renowned holistic plastic surgeon and leading expert in breast implant illness (BII). Together, Margaret and Dr. Whitfield unpack the complexities of BII—what it is, how to recognize it in clients, and the critical intersection between surgical expertise and functional health support. Dr. Whitfield shares his personal journey that led him to specialize in BII, the science behind chronic inflammation related to implants, and what functional practitioners need to know when helping clients navigate unexplained fatigue, hormonal imbalance, detox challenges, and much more.   In this interview, we discuss:    -Dr. Whitfield's transition from cancer reconstruction to explant surgeries   -Recognizing and assessing breast implant illness   -Various surgical approaches and controversies   -The functional approach: assessing genetics, methylation, and toxicity   -Dr. Whitfield's “SHARP” protocol: holistic pre- and post-op recovery program   -Detoxification Do's and Don'ts & Lymphatic post-operative support The Clinician's Corner is brought to you by Restorative Wellness Solutions.  Follow us: https://www.instagram.com/restorativewellnesssolutions/   Connect with Dr. Robert Whitfield: Website: www.drrobertwhitfield.com YouTube: @breastimplantillnessexpert Instagram: @breastimplantillnessexpert Facebook: @drrobertwhitfield TikTok: @drrobertwhitfield   To book a discovery call: https://www.drrobertwhitfield.com/discovery-call/   Timestamps:  00:00 Breast Implant Illness Insight 05:16 Breast Cancer Treatment Access Challenges 10:38 Breast Implants and Chronic Inflammation 20:03 Navigating Complex Health Evaluations 21:03 Guidance on Medical Device Removal 30:19 Hormonal Imbalance Detection in Bloodwork 32:18 Understanding Hormone Impact on Recovery 41:15 Managing Environmental Toxins for Health 45:23 Breast Surgery and Surveillance Concerns 47:44 Support for Clients Undergoing Explants 53:11 Detoxing: Recognizing When to Slow Down 01:02:38 "Clinicians Corner Podcast Callout" Speaker bio: Dr. Robert Whitfield, M.D., is a world-renowned holistic plastic surgeon certified by the American Board of Plastic Surgery. He is an author and the leading expert in Breast Implant Illness (BII), known for his pioneering surgical techniques and groundbreaking "No-Cut" Facelift. With a deep specialization in oncology and microsurgery, Dr. Whitfield is at the forefront of advanced breast explant procedures, delivering exceptional patient outcomes worldwide.   Dr. Whitfield received his medical degree from the University of Las Vegas School of Medicine. He then completed six years of surgical training and a plastic surgery residency at Indiana University Medical Center. He returned to Nevada for a microsurgery fellowship before settling down to practice and teach at the Medical College of Wisconsin for seven years. In 2012, Dr. Whitfield came to Austin and became renowned for his breast surgery expertise. He entered private practice in 2017. In 2019, Dr. Whitfield was chosen to speak at the FDA hearings on breast implants and their safety. In 2024, he published his first book, SHARP (Strategic Holistic Accelerated Recovery Program), to share his protocol and expertise in holistic surgical preparation and recovery. The same year, he published his first scientific paper on microbial communities and associated biofilm in breast augmentation failure.   Dr. Whitfield's work has earned him consistent recognition on the Texas Super Doctors list as one of the "Best Doctors in America." As the host of the popular podcast "Breast Explant Surgery & Recovery," he shares patient stories, explores cutting-edge treatments, and discusses the latest advancements in plastic surgery, further solidifying his status as a trusted authority in the field.   Keywords: breast implant illness, explant surgery, functional medicine, detox pathways, plastic surgery, chronic inflammation, genetic testing, microbial communities, biofilm, capsular contracture, holistic recovery, autoimmune symptoms, estrogen toxicity, oxylipin 10-HOME, fatigue, mold exposure, hormone imbalance, fat transfer, gut health, food sensitivities, toxicity burden, liposomal supplements, cellcore detox, dietary protocols, GI-MAP testing, inflammation markers, SOD2 enzyme, impaired methylation, Vibrant Wellness testing, Sharp program   Disclaimer: The views expressed in the RWS Clinician's Corner series are those of the individual speakers and interviewees, and do not necessarily reflect the views of Restorative Wellness Solutions, LLC. Restorative Wellness Solutions, LLC does not specifically endorse or approve of any of the information or opinions expressed in the RWS Clinician's Corner series. The information and opinions expressed in the RWS Clinician's Corner series are for educational purposes only and should not be construed as medical advice. If you have any medical concerns, please consult with a qualified healthcare professional. Restorative Wellness Solutions, LLC is not liable for any damages or injuries that may result from the use of the information or opinions expressed in the RWS Clinician's Corner series. By viewing or listening to this information, you agree to hold Restorative Wellness Solutions, LLC harmless from any and all claims, demands, and causes of action arising out of or in connection with your participation. Thank you for your understanding.  

BUFFALO, NY — April 7, 2025 — A new #research paper was #published in Aging (Aging-US) on March 18, 2025, in Volume 17, Issue 3, titled “Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness.” Researchers from the University of Arkansas for Medical Sciences, led by first author Ana Resende-Coelho and corresponding authors Melda Onal and Maria Almeida, investigated why bones become less responsive to exercise as people age. They studied two well-known aging-related cellular changes: oxidative stress (a buildup of harmful molecules inside cells) and reduced autophagy (a slowdown in the cell's ability to clean out and recycle damaged parts) to determine whether these could explain the decline in bone strength. Their findings revealed that these changes alone are not enough to account for the reduced bone-building response seen with aging. Physical activity is known to strengthen bones by creating mechanical stress, which activates bone cells like osteocytes to promote new bone formation. However, this process becomes less effective with age, increasing the risk of bone loss and fractures in older adults. The study aimed to uncover why this response weakens over time by focusing on specific age-related changes inside bone-forming cells. “The bone response to loading is less effective with aging, but the cellular and molecular mechanisms responsible for the impaired mechanoresponsiveness remain unclear.” The research team used a well-established mouse model in which pressure was applied to the tibia, simulating the effects of exercise. As expected, bones from older mice showed a weaker response compared to those of younger mice. However, when the researchers examined younger mice genetically modified to have either high oxidative stress or impaired autophagy, as seen in aging, their bones still responded normally to mechanical loading. The researchers also found that damage to the bone's osteocyte network, a system of cells that helps sense and respond to mechanical forces, did not prevent a healthy bone-building response in mice with autophagy deficiencies. This challenges the long-standing idea that deterioration of this cell network is a main cause of age-related bone decline. These results are significant because they eliminate two widely suspected causes of the aging skeleton's reduced responsiveness to exercise. While oxidative stress and autophagy dysfunction are common in older bone, they are not solely responsible for its reduced ability to grow stronger under physical stress. The authors suggest that future studies should explore other possible factors, such as changes in energy metabolism or how bone cells communicate. Overall, this study shows that bone aging is more complex than previously thought. Protecting bone health in older adults may require new strategies that go beyond targeting oxidative stress or autophagy. DOI - https://doi.org/10.18632/aging.206213 Corresponding authors - Melda Onal - MOnal@uams.edu, and Maria Almeida - schullermaria@uams.edu Video short - https://www.youtube.com/watch?v=fHQhA6rOaDc Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206213 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Atg7, tibia compressive loading, Sod2, Osx1-Cre, osteocytes Please visit our website at https://www.Aging-US.com​​ and connect with us: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

A new paper entitled “Isorhamnetin protects porcine oocytes from zearalenone-induced reproductive toxicity through the PI3K/Akt signaling pathway” investigated the effects of a natural flavonoid called isorhamnetin on the damage caused by a toxin called Zearalenone (ZEA) to pig oocytes (immature egg cells). Zearalenone (ZEA) is a harmful mycotoxin found in moldy grain like corn, oats, and millet that can cause irreversible damage to the reproductive system of animals and humans. It can cause reproductive disorders by binding to estrogen receptors and has been shown to impair the development of sperm and oocytes in humans and animals. ZEA can cause oxidative stress that leads to the production of reactive oxygen species (ROS), which can be harmful and contribute to cell death. ZEA can also disrupt pregnancy, inhibit the meiosis of oocytes, and induce mitochondrial damage and stress in the maturation of oocytes. Since ZEA is heat-stable and cannot be completely eliminated from the food chain, it is important to explore potential compounds that can protect against ZEA-induced damage to oocytes. In recent years, natural substances called flavonoids, which have antioxidant properties, have gained attention for their ability to support the development of oocytes. For example, quercetin has been found to increase the proportion of porcine oocytes developing into blastocysts, while kaempferol has shown potential in reducing the negative effects of aging on the development of porcine oocytes by improving mitochondrial function and reducing oxidative stress. Isorhamnetin is a compound found in the herb ginkgo biloba and in foods like pears, onions, and peanuts. It has various pharmacological activities, such as being an antioxidant, anti-inflammatory, and antiviral.     Isorhamnetin acts as an antioxidant by decreasing the production of reactive oxygen species (ROS) and increasing the expression of SOD2 protein, which helps protect against oxidative stress. This study found that isorhamnetin can protect the oocytes from ZEA-induced damage by improving their development, reducing oxidative stress, preventing mitochondrial dysfunction, and inhibiting apoptosis. This research provides a potential solution for reproductive toxicity caused by ZEA and treating female infertility. Mold Toxicity and Ginkgo Biloba Clinical Applications Ginkgo biloba is rich in isorhamnetin as well as other powerful flavonoids like quercetin, kaempferol, and luteolin which makes it the perfect herb for patients with mold toxicity. Ginkgo biloba has many benefits including anti-inflammatory, antioxidant, antiviral, anticoagulant, anti-obesity, hypolipidemic, hypotensive, anti-diabetic, anti-cancer, adaptogenic, and it protects the brain, eye, inner ear, heart, liver, cardiovascular system, reproductive system, lungs, and kidneys. Patients with mold toxicity tend to have reactivated herpes viruses like EBV, CMV, and HHV-6 and ginkgo biloba is effective against these types of viruses as explained in this article. I use VascuSelect from Moss Nutrition which contains 120 mg of standardized ginkgo biloba extract along with grape seed extract and mango extract to further support microcirculation. 120 mg of ginkgo biloba twice a day is the usual dose for this versatile herbal medicine. If you're a practitioner who sees patients with mold toxicity and/or infertility, then VascuSelect should be considered an important part of your protocol. Click here to learn more about the Hedberg Institute Membership to take your functional medicine practice to the next level.

This episode is the third and final installment of a 3-part series on ADHD and genetics. In previous episodes, explore the role of genetics in ADHD and the significance of MTHFR in the ADHD and Autism conversation. Tune in to this episode to learn more about detoxification and oxidative stress and how these things affect ADHD symptoms.  Sign up for my free ADHD masterclass and discover how to reduce ADHD symptoms naturally, sometimes in as little as 60-90 days here  - https://info.adhdthriveinstitute.com/live Learn more about one of our favorite DNA tests here - https://shop.adhdthriveinstitute.com/the-dna-company-360-report.html    Key Takeaways: [2:30] What is detoxification, and why is it important for managing ADHD? [4:26] What is oxidative stress? [6:08] Genes that affect detoxification [6:29] The gene GSTT1 [8:35] The gene GSTM1 [9:42] The gene GSTP1 [11:23] Genes that relate to antioxidation — SOD2 and GPX [17:01] Strategies you can do to optimize detoxification in the body [19:21] A word of caution about detoxification [19:53] The importance of regular bowel movements in detoxification [21:00] The benefits of detox baths, infrared saunas, milk thistle, essential oils, and skin brushing   Memorable Moments: ”Toxins are pretty much everywhere, and while our bodies are built to handle some level of detoxification, the sheer volume of exposure can be overwhelming, especially for individuals with ADHD who may already have sensitive systems.” ”Detoxification and antioxidation are a really important part of naturally reducing ADHD symptoms.” ”It's not just about one gene's results. It's how they come together for that overall picture in that child's body.” ”Oxidative stress can exacerbate symptoms by affecting neurotransmitter regulation and neural development.” ”An efficient detox system can help manage ADHD symptoms more effectively.” ”The more you know about your genetic makeup, the better equipped you'll be to navigate the complexities of ADHD.” ”Water is essential for every cellular process in your body, including detoxification.” ”One of the most straightforward ways to help your child detox is to ensure they're having regular bowel movements.” ”[Infrared] Saunas are the finest single additional modality for toxic metal elimination and detoxification.” ”Milk thistle is another natural detoxifier that supports liver, kidney, and gallbladder function.” ”Essential oils can also be a powerful tool for detoxification.” ”The skin is our largest organ and plays a vital role in detoxification.”   Dana Kay Resources: Website: https://adhdthriveinstitute.com/  Facebook: https://www.facebook.com/ADHDThriveInstitute/  Instagram: https://www.instagram.com/adhdthriveinstitute/  YouTube: https://www.youtube.com/c/ADHDThriveInstitute  LinkedIn: https://www.linkedin.com/company/adhd-thrive-institute/mycompany/  Pinterest: https://www.pinterest.ph/adhdthriveinstitute/  Tiktok: https://www.tiktok.com/@adhd_thriveinstitute  International Best Selling Book, Thriving with ADHD – https://adhdthriveinstitute.com/book/  Free Reduce ADHD Symptoms Naturally Masterclass - https://bit.ly/3GAbFQl  ADHD Parenting Course – https://info.adhdthriveinstitute.com/parentingadhd ADHD Thrive Method 4 Kids Program – https://adhdthriveinstitute.com/packages/

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 6, entitled, “Knockout of AMD-associated gene POLDIP2 reduces mitochondrial superoxide in human retinal pigment epithelial cells.” Genetic and epidemiologic studies have significantly advanced our understanding of the genetic factors contributing to age-related macular degeneration (AMD). In particular, recent expression quantitative trait loci (eQTL) studies have highlighted POLDIP2 as a significant gene that confers risk of developing AMD. However, the role of POLDIP2 in retinal cells such as retinal pigment epithelium (RPE) and how it contributes to AMD pathology are unknown. In this new study, researchers Tu Nguyen, Daniel Urrutia-Cabrera, Luozixian Wang, Jarmon G. Lees, Jiang-Hui Wang, Sandy S.C. Hung, Alex W. Hewitt, Thomas L. Edwards, Sam McLenachan, Fred K. Chen, Shiang Y. Lim, Chi D. Luu, Robyn Guymer, and Raymond C.B. Wong from Royal Victorian Eye and Ear Hospital, University of Melbourne, St Vincent's Institute of Medical Research, University of Tasmania, and The University of Western Australia report the generation of a stable human RPE cell line ARPE-19 with POLDIP2 knockout using CRISPR/Cas, providing an in vitro model to investigate the functions of POLDIP2. “We conducted functional studies on the POLDIP2 knockout cell line and showed that it retained normal levels of cell proliferation, cell viability, phagocytosis and autophagy. Also, we performed RNA sequencing to profile the transcriptome of POLDIP2 knockout cells.” Their results highlighted significant changes in genes involved in immune response, complement activation, oxidative damage and vascular development. They showed that loss of POLDIP2 caused a reduction in mitochondrial superoxide levels, which is consistent with the upregulation of the mitochondrial superoxide dismutase SOD2. In conclusion, this study demonstrates a novel link between POLDIP2 and SOD2 in ARPE-19, which supports a potential role of POLDIP2 in regulating oxidative stress in AMD pathology. “In summary, we have generated a POLDIP2 knockout ARPE-19 cell line using CRISPR/Cas9 and studied the biological functions of POLDIP2. To our knowledge, this is the first functional study of POLDIP2 in retinal cells to understand its potential role in AMD.” DOI: https://doi.org/10.18632/aging.204522 Corresponding Author: Raymond C.B. Wong - wongcb@unimelb.edu.au Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204522 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, age-related macular degeneration, retina, CRISPR/Cas, mitochondria superoxide, POLDIP2 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.02.01.526349v1?rss=1 Authors: Harbin, N. H., Lustberg, D. J., Hurst, C., Pare, J.-F., Crotty, K. M., Waters, A. L., Yeligar, S. M., Smith, Y., Seyfried, N. T., Weinshenker, D., Hepler, J. R. Abstract: RGS14 is a complex multifunctional scaffolding protein that is highly enriched within pyramidal cells (PCs) of hippocampal area CA2. There, RGS14 suppresses glutamate-induced calcium influx and related G protein and ERK signaling in dendritic spines to restrain postsynaptic signaling and plasticity. Previous findings show that, unlike PCs of hippocampal areas CA1 and CA3, CA2 PCs are resistant to a number of neurological insults, including degeneration caused by temporal lobe epilepsy (TLE). While RGS14 is protective against peripheral injury, similar roles for RGS14 during pathological injury in hippocampus remain unexplored. Recent studies show that area CA2 modulates hippocampal excitability, generates epileptiform activity and promotes hippocampal pathology in animal models and patients with TLE. Because RGS14 suppresses CA2 excitability and signaling, we hypothesized that RGS14 would moderate seizure behavior and early hippocampal pathology following seizure activity. Using kainic acid (KA) to induce status epilepticus (KA-SE) in mice, we show loss of RGS14 (RGS14 KO) accelerated onset of limbic motor seizures and mortality compared to wild type (WT) mice, and that KA-SE upregulated RGS14 protein expression in CA2 and CA1 PCs of WT. Utilizing proteomics, we saw loss of RGS14 impacted the expression of a number of proteins at baseline and after KA-SE, many of which associated unexpectedly with mitochondrial function and oxidative stress. RGS14 was shown to localize to the mitochondria in CA2 PCs of mice and reduce mitochondrial respiration in vitro. As a readout of oxidative stress, we found RGS14 KO dramatically increased 3-nitrotyrosine levels in CA2 PCs, which was greatly exacerbated following KA-SE and correlated with a lack of superoxide dismutase 2 (SOD2) induction. Assessing for hallmarks of seizure pathology in RGS14 KO, we observed worse neuronal injury in area CA3 (but none in CA2 or CA1), and a lack of microgliosis in CA1 and CA2 compared to WT. Together, our data demonstrates a newly appreciated neuroprotective role for RGS14 against intense seizure activity in hippocampus. Our findings are consistent with a model where, after seizure, RGS14 is upregulated to support mitochondrial function and prevent oxidative stress in CA2 PCs, limit seizure onset and hippocampal neuronal injury, and promote microglial activation in hippocampus. 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/2023.02.01.526688v1?rss=1 Authors: Sanz-Alcazar, A., Britti, E., Delaspre, F., Medina-Carbonero, M., Pazos-Gil, M., Tamarit, J., ROS, J., Cabiscol, E. Abstract: Friedreich ataxia (FA) is a rare, recessive neuro-cardiodegenerative disease caused by deficiency of the mitochondrial protein frataxin. Mitochondrial dysfunction, a reduction in the activity of iron-sulfur enzymes, iron accumulation, and increased oxidative stress have been described. However, the mechanisms causing such cellular disturbances in mammals are not completely understood. Dorsal root ganglion (DRG) sensory neurons are among the cellular types most affected in the early stages of this disease. We have previously demonstrated that frataxin depletion in primary cultures of DRG neurons results in calcium dysregulation, neurite degeneration and apoptotic cell death. However, its effect on mitochondrial function remains to be elucidated. In the present study, we found that in primary cultures of DRG neurons as well as in DRGs from the FXNI151F mouse model, frataxin deficiency resulted in lower activity and levels of the electron transport complexes, mainly complexes I and II. As a consequence, the NAD+/NADH ratio was reduced and SirT3, a mitochondrial NAD+-dependent deacetylase, was impaired. We identified alpha tubulin as the major acetylated protein from DRG homogenates whose levels were increased in FXNI151F mice compared to WT mice. Mitochondrial superoxide dismutase (SOD2), a SirT3 substrate, displayed increased acetylation in frataxin-deficient DRG neurons. Since SOD2 acetylation inactivates the enzyme, and higher levels of mitochondrial superoxide anion were detected, oxidative stress markers were analyzed. Elevated levels of hydroxynonenal bound to proteins and mitochondrial Fe2+ accumulation were detected when frataxin decreased. Honokiol, a SirT3 activator, restores mitochondrial respiration. Altogether, these results provide the molecular bases to understand mitochondria dysfunction in sensory neurons which have greater susceptibility to frataxin deficiency compared to other tissues. 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/2022.12.21.521533v1?rss=1 Authors: Montgomery-Song, A., Ashraf, S., Santerre, P., Kandel, R. Abstract: Senescence, particularly in the nucleus pulposus (NP) cells, has been implicated in the pathogenesis of disc degeneration, however, the mechanism(s) of annulus fibrosus (AF) cell senescence is still not well understood. Both TNF and H2O2, have been implicated as contributors to the senescence pathways, and their levels are increased in degenerated discs when compared to healthy discs. This the objective of this study is to identify factor(s) that induces inner AF (iAF) cell senescence Under TNF exposure, at a concentration that can induce senescence in NP cells, bovine iAF cells did not undergo senescence, indicated by their ability to continue to proliferate as demonstrated by Ki67 staining and growth curves and lack of expression of the senescent markers, p16 and p21. Unlike iAF cells, NP cells treated with TNF accumulated more intracellular ROS and secreted more H2O2. Following TNF treatment, only iAF cells had increased expression of the superoxide scavengers SOD1 and SOD2 whereas NP cells had increased NOX4 gene expression, an enzyme that can generate H2O2. Treating iAF cells with low dose H2O2 (50 M) induced senescence, however unlike TNF, H2O2 did not induce degenerative-like changes as there was no difference in COL2, ACAN, MMP13, or IL6 gene expression or number of COL2 and ACAN immunopositive cells compared to untreated controls. The latter result suggests that iAF cells have distinct degenerative and senescent phenotypes. To evaluate paracrine signalling, iAF and TNF-treated NP cells were co-cultured. In contact co-culture the NP cells did induce iAF senescence. Thus, senescent NP cells may secrete soluble factors that induce degenerative and senescent changes within the iAF. This may contribute to a positive feedback loop of disc degeneration, and these processes could include H2O2 and cytokines (TNF). Further studies will investigate if human disc cells respond similarly. 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/2022.11.07.515395v1?rss=1 Authors: Takenaka, Y., Inoue, I., Hirasaki, M., Ikeda, M., Kakinuma, Y. Abstract: We previously developed a stress-induced premature senescence (SIPS) model in which normal human fibroblast MRC-5 cells were treated with either the proteasome inhibitor MG132 or the V-ATPase inhibitor bafilomycin A1 (BAFA1). To elucidate the involvement of mitochondrial function in our SIPS model, we treated cells with an inhibitor of electron transport chain (ETC) complexes I, III, or a mitochondrial uncoupler reagent along with MG132 or BAFA1 and evaluated the induction of premature senescence. SIPS induced by MG132 or BAFA1 was partially attenuated by co-treatment with antimycin A (AA) and rotenone, but not carbonyl cyanide 3-chlorophenylhydrazone (CCCP), in which intracellular reactive oxygen species (ROS) levels, acute mitochondrial unfolded protein responses, and accumulation of protein aggregates were remarkably suppressed. Co-treatment with AA also reversed the temporal depletion of SOD2 in the mitochondrial fraction on day 1 of MG132 treatment. Furthermore, co-treatment with AA suppressed the induction of mitophagy in MG132-treated cells and enhanced mitochondrial biogenesis. These findings provide evidence that the temporal inhibition of mitochondrial respiration exerts protective effects against the progression of premature senescence caused by impaired proteostasis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Health optimisation often involves a good diet, sleep, and exercise. But do we know how to implement practices that are compatible with our bodies? For some people, intense exercise can lead to more oxidative stress and inflammation! Not only that, some of us take medication and pills to treat pain and hormones, but are these really helping?   Small actions today can lead to big problems in the future.     Kashif Khan from The DNA Company joins us in this episode to talk about how understanding our DNA can help us make better choices for our health. Diseases can be prevented with healthy habits. But before you try any DNA testing, you should understand the nuances within the genetic industry. With Kashif's advice, you can learn to choose a provider that can help you take actionable steps. If you want to know more about the science behind DNA testing for health optimisation, then this episode is for you!   Get Customised Guidance for Your Genetic Make-Up For our epigenetics health programme, all about optimising your fitness, lifestyle, nutrition and mind performance to your particular genes, go to  https://www.lisatamati.com/page/epigenetics-and-health-coaching/.   Customised Online Coaching for Runners CUSTOMISED RUN COACHING PLANS — How to Run Faster, Be Stronger, Run Longer  Without Burnout & Injuries Have you struggled to fit in training in your busy life? Maybe you don't know where to start, or perhaps you have done a few races but keep having motivation or injury troubles? Do you want to beat last year's time or finish at the front of the pack? Want to run your first 5-km or run a 100-miler? ​​Do you want a holistic programme that is personalised & customised to your ability, goals, and lifestyle?  Go to www.runninghotcoaching.com for our online run training coaching.   Health Optimisation and Life Coaching If you are struggling with a health issue and need people who look outside the square and are connected to some of the greatest science and health minds in the world, then reach out to us at support@lisatamati.com, we can jump on a call to see if we are a good fit for you. If you have a big challenge ahead, are dealing with adversity, or want to take your performance to the next level and want to learn how to increase your mental toughness, emotional resilience, foundational health, and more, then contact us at support@lisatamati.com.   Order My Books My latest book Relentless chronicles the inspiring journey about how my mother and I defied the odds after an aneurysm left my mum Isobel with massive brain damage at age 74. The medical professionals told me there was absolutely no hope of any quality of life again, but I used every mindset tool, years of research and incredible tenacity to prove them wrong and bring my mother back to full health within three years. Get your copy here: https://shop.lisatamati.com/collections/books/products/relentless. For my other two best-selling books Running Hot and Running to Extremes, chronicling my ultrarunning adventures and expeditions all around the world, go to https://shop.lisatamati.com/collections/books.   Lisa's Anti-Ageing and Longevity Supplements  NMN: Nicotinamide Mononucleotide, an NAD+ precursor Feel Healthier and Younger* Researchers have found that Nicotinamide Adenine Dinucleotide or NAD+, a master regulator of metabolism and a molecule essential for the functionality of all human cells, is being dramatically decreased over time. What is NMN? NMN Bio offers a cutting edge Vitamin B3 derivative named NMN (beta Nicotinamide Mononucleotide) that can boost the levels of NAD+ in muscle tissue and liver. Take charge of your energy levels, focus, metabolism and overall health so you can live a happy, fulfilling life. Founded by scientists, NMN Bio offers supplements of the highest purity and rigorously tested by an independent, third party lab. Start your cellular rejuvenation journey today. Support Your Healthy Ageing We offer powerful, third party tested, NAD+ boosting supplements so you can start your healthy ageing journey today. Shop now: https://nmnbio.nz/collections/all NMN (beta Nicotinamide Mononucleotide) 250mg | 30 capsules NMN (beta Nicotinamide Mononucleotide) 500mg | 30 capsules 6 Bottles | NMN (beta Nicotinamide Mononucleotide) 250mg | 30 Capsules 6 Bottles | NMN (beta Nicotinamide Mononucleotide) 500mg | 30 Capsules Quality You Can Trust — NMN Our premium range of anti-ageing nutraceuticals (supplements that combine Mother Nature with cutting edge science) combats the effects of aging while designed to boost NAD+ levels. Manufactured in an ISO9001 certified facility Boost Your NAD+ Levels — Healthy Ageing: Redefined Cellular Health Energy & Focus Bone Density Skin Elasticity DNA Repair Cardiovascular Health Brain Health  Metabolic Health   My  ‘Fierce' Sports Jewellery Collection For my gorgeous and inspiring sports jewellery collection, 'Fierce', go to https://shop.lisatamati.com/collections/lisa-tamati-bespoke-jewellery-collection.   Here are three reasons why you should listen to the full episode: Discover how our bodies are a whole system of processes and how our genes can be affected by many factors such as lifestyle and behaviour. Learn the differences in DNA testing companies and how you can get the best value out of your reports. Understand how to boost your immunity and prevent diseases!      Resources Gain exclusive access and bonuses to Pushing the Limits Podcast by becoming a patron!  Harness the power of NAD and NMN for anti-aging and longevity with NMN Bio.  A new program, BoostCamp, is coming this September at Peak Wellness! Past episodes with Dr Mansoor Mohammed: Episode 181 - Understanding Your Genetic Hormone Pathways Episode 160 - Understanding Your Own DNA   Connect with Kashif: LinkedIn I Twitter I Facebook      Know how you can change your lifestyle based on your genes. Learn more on The DNA Company.  Tiny Habits by Dr. BJ Fogg Books by Peter Diamandis and Steven Kotler The Future Is Faster Than You Think  Bold Abundance    Episode Highlights [04:09] Understanding What Your DNA Means Every process in your body is being driven by genetic instructions. Kashif's company set out to make these instructions more actionable for their clients. You can do a quick online search of ‘DNA testing near me' and get many hits, but you won't get the results you want out of these. Many of our diseases are preventable; consistently making the wrong choices can lead us to develop these illnesses.     Those choices will not be the same for everyone. You can look at your genetics to see what the right choices are for you.  [08:11] Know What You're Testing For Most companies offering DNA testing tend to make conclusions based on a single gene. However, the body is more complex than that.  Many of these DNA tests don't really dive deep into your health. To make their business model profitable, many businesses in the genetic industry sell their patient's data to pharmaceutical companies. The genetic industry has been used as a data collection machine. Kashif's vision for their company is to turn this situation around and derive key insights for their consumers.  [12:35] The Role of Hormones in Health  Kashif observes that their company has had the biggest impact on women's healthcare.  This is due to the massive gap between what women need and what is provided by traditional healthcare.  There is a widespread belief that women are supposed to have hormone-related issues like PMS. However, this should not be the case. Tune in to the full episode to find out how Kashif helped pinpoint his niece's hormone issues using DNA testing and analysis. [19:26] Covering Up the Symptoms The healthcare industry tends to look at a problem in isolation and try to treat it with medication.  Treating hormonal issues is not as simplistic as prescribing pills for the hormones a patient lacks. Listen to the full episode to hear more insights on this topic! For instance, we're led to believe that women are prone to breast cancer when they reach menopause. However, this condition is preventable.      [24:01] Applying AI to DNA Testing Kashif's company found it challenging to train clinicians to interpret results from DNA testing.  To remedy this problem, they are using AI technology to create personalised reports and recommendations.  As a result, their reports are now much more comprehensive. It even analyses your mood and behaviour—crucial factors when it comes to dealing with your health. [30:05] Understanding Your Mood and Behaviour   Lisa's high adrenaline and lack of dopamine receptors manifest in an action-oriented behaviour.  Kashif shares that having low dopamine receptors can also lead to addiction or depression. That's because you are predisposed to not experience reward and pleasure.  Curious to know how your genes affect your mood? Find out how DNA testing can shed a light on this in the full episode!  You can view your gene expressions two-fold: a weakness and a superpower. For instance, you may think that you are irritable. But that also makes you detail-oriented. [35:50] Change Takes Effort Kashif's company is focused on solving and preventing problems.  People may get great recommendations, but the real challenge lies in implementation and change.  Community and accountability are important to help people stay on track. Group accountability with people in similar situations can increase motivation and persistence.  [42:21] Prevention is the Key The current healthcare system is based on a reactive model rather than a preventive one.  Diseases can be prevented; we don't need to reach a point of crisis until we take action.  In the US, the Center for Disease Control created a Diabetes Prevention Program, the first of its kind in the country.  [47:31] Health at the Cellular Level Diseases are born from inflammation, which is based on cellular health. Cellular health depends on the body's capacity for detoxification and oxidative stress.  Simple activities like golfing can have long term effects. Kashif shares that golfers may be in danger of inhaling pesticides in golf courses.  Exercise may work for some people. However, people with weaker SOD2 are prone to oxidative stress and more toxicity in the blood.  Your genetics will dictate what kind and how much exercise you should do. Listen to the full episode to learn more! [56:34] The Future of Healthcare  Beyond DNA testing and analysis, it's important to have someone knowledgeable on your end. They can help patients get the most value out of the reports. New technologies tend to go through different phases. These involve deception, disruption, dematerialisation, demonetisation, and democratisation.  The technology in the genetic industry is becoming more accessible. It is now near the latter phases of technology development.    7 Powerful Quotes ‘We didn't go study DNA. There's enough science out there already. We studied people. We said, “Let's start at what's wrong with this person? What are they expressing as a symptom? Let's drill down genetically to see where is the system failing.”' ‘Of all the things we do, female hormone health is where we had the biggest impact. Not because we're the greatest, but because it's the worst experience in current healthcare.' ‘The DNA world looks at things in terms of disease. So you can speak at it that way. But there's so much more to it than that if you know how to interpret it.' ‘We believe coaching is primarily around accountability. So we have coaches we train that understand the reports, that can help.' ‘We're all coming out of the same model, I suppose this reactive healthcare model. Really, we're inventing the future of healthcare.‘ ‘That's only then when you have that persistence and the resilience to actually go through with these changes that you're actually going to get new results.' ‘This reactive system that we're living in at the moment and the current model is just bloody bandaids on festering wounds.'   About Kashif Kashif Khan is the founder and CEO of The DNA Company, a functional genomics company. They help people understand their unique genetic code and how to unlock their physical potential. If you're looking for ‘DNA testing near me', their company is the one to call. They ensure actionable advice through a comprehensive genomic profile.  Kashif is also the co-founder and CEO of Younutrients. Their company provides supplement formulations personalised to people's unique needs. In addition, he is also an investor and serial entrepreneur. He has helped build, scale, and run several businesses across different industries. He has advised early-stage startups and Fortune 500 companies including the Royal Bank of Canada and Cirque du Soleil.  Interested in Kashif's work? Check out The DNA Company.  You can also reach out to Kashif on LinkedIn, Twitter, and Facebook.          Enjoyed This Podcast? If you did, be sure to subscribe and share it with your friends! Post a review and share it! If you enjoyed tuning in, then leave us a review. You can also share this with your family and friends so they can be inspired to search for ‘DNA testing near me' and optimise their health.  Have any questions? You can contact me through email (support@lisatamati.com) or find me on Facebook, Twitter, Instagram and YouTube. For more episode updates, visit my website. You may also tune in on Apple Podcasts. To pushing the limits, Lisa

A 45-year-old female who is inquiring about bio-identical hormones for depression, anxiety, and weight gain.  Patient's top objectives  1. Hormones 2. Mood 3. Weight   COMT Val/Val (wild type) COMT met/met (homozygous)   Cognitive Panel: ·       COMT (rs4680)   Detox Panel: ·       COMT (rs4680) (Estrogen Metabolism) ·       GSTP1 (rs1695)  (Glutathione Peroxidase) ·       SOD2 (rs4880) (Antioxidant Enzymes)   Vitamins/Minerals/Omega 3s: ·       PEMT (rs7946) (Choline)   Resources Nutrigenomics Case Study Events 2021  GMOTG Events Line-up PureGenomics Schedule a complimentary 1:1 Welcome to PureGenomics coaching session

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.05.078691v1?rss=1 Authors: Sullivan, M. N., Brill, S. A., Mangus, L. M., Jeong, Y. J., Solis, C. V., Knight, A. C., Colantuoni, C., Keceli, G., Paolocci, N., Queen, S. E., Mankowski, J. L. Abstract: HIV-associated neurocognitive disorders (HAND) remain prevalent despite implementation of antiretroviral therapy (ART). Development of HAND is linked to mitochondrial dysfunction and oxidative stress in the brain; therefore, upregulation of antioxidant defenses is critical to curtail neuronal damage. Superoxide dismutase 2 (SOD2) is a mitochondrial antioxidant enzyme essential for maintaining cellular viability. We hypothesized that SOD2 was upregulated during retroviral infection. Using a simian immunodeficiency virus (SIV)-infected macaque model of HIV, quantitative PCR showed elevated SOD2 mRNA in cortical gray (GM, 7.6-fold for SIV vs. uninfected) and white matter (WM, 77-fold for SIV vs. uninfected) during SIV infection. Further, SOD2 immunostaining was enhanced in GM and WM from SIV-infected animals. Double immunofluorescence labeling illustrated that SOD2 primarily co-localized with astrocyte marker glial fibrillary acidic protein (GFAP) in SIV-infected animals. Interestingly, in ART-treated SIV-infected animals, brain SOD2 RNA levels were similar to uninfected animals. Additionally, using principal component analysis in a transcriptomic approach, SOD2 and GFAP expression separated SIV-infected from uninfected brain tissue. Projection of these data into a HIV dataset revealed similar expression changes, thereby validating the clinical relevance. Together, our findings suggest that novel SOD2-enhancing therapies may delay the onset or reduce severity of HAND seen in ART-treated HIV-infected patients. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.04.26.062380v1?rss=1 Authors: El Kodsi, D. N., Tokarew, J. M., Sengupta, R., Lengacher, N. A., Ng, A. C., Boston, H., Jiang, Q., Palmberg, C., Pileggi, C., Shutinoski, B., Li, J., Nguyen, A. P., Fehr, T. K., Im, D. S., Callaghan, S., Park, D. S., LaVoie, M. J., Chan, J. A., Takanashi, M., Hattori, N., Ratan, R. R., Zecca, L., Puente, L., Shaw, G. S., Harper, M.-E., Holmgren, A., Tomlinson, J. J., Schlossmacher, M. G. Abstract: We recently hypothesized that parkin plays a role in redox homeostasis and provided evidence that it directly reduces hydrogen peroxide (H2O2) in vitro. Here, we examined this anti-oxidant activity in vivo. Informed by findings in human brain, we demonstrate that elevated oxidative stress promotes parkin insolubility in mice. In normal mouse brain parkin was partially oxidized, e.g., at cysteines 195 and 252, which was augmented by oxidative stress. Although under basal conditions H2O2 levels were unchanged in adult prkn-/- brain, a parkin-dependent reduction of cytosolic H2O2 was observed when mitochondria were impaired, either due to neurotoxicant exposure (MPTP) or Sod2 haploinsufficiency. In accordance, markers of oxidative stress, e.g., protein carbonylation and nitrotyrosination, were elevated in the cytosol but not in mitochondria from prkn-/- mice. This rise in oxidative stress was associated with altered glutathione homeostasis. In parkin's absence reduced glutathione concentrations were increased in cells, murine brain and human cortex. This compensation was not due to new glutathione synthesis but attributed to elevated oxidized glutathione (GSSG)-reductase activity. Moreover, we discovered that parkin also recycled GSSG to its reduced form. With this reaction, parkin became S-glutathionylated, e.g., at cysteines 59 and human-specific 95. This oxidative modification was reversed by glutaredoxin. Our results demonstrate that cytosolic parkin mediates anti-oxidant reactions including H2O2 reduction and glutathione regeneration. These reducing activities lead to a range of oxidative modifications in parkin itself. In parkin-deficient brain oxidative stress rises despite changes to maintain redox balance. Copy rights belong to original authors. Visit the link for more info

State of Decay 2 has another update?? Let’s see if these quality of life improvements are worth coming back to the game. We also dive into spoilers and exotic impressions of the “Division 2”.

Welcome to The Blaise XPerience, the podcast where you XPerience a variety of games from every angle. Today Derreck is back once again to talk more State of Decay 2! This time he invites Geoffrey Card from Undead Labs back on the podcast to discuss the latest patch 10.0 in SOD2. Derreck and Geoffrey go over briefly the new bounty broker part of this update in which we get a new trader in Cash Beaumont and a new bounty system with him. However, this will be gone over more in depth on a future episode. Then Derreck and Geoffrey go over the rest of the patch in full including some things that weren't able to be covered on the Undead Labs stream. Geoffrey does a great job going in detail on all of the notes of this patch and what they entail for the community. So Come check it out and let us know what you think! Thank you so much as always for listening to The Blaise XPerience! Links to follow us on: Our Patreon--www.patreon.com/blaisexperience Our twitter-- @BlaiseXPerience Our email-- theblaisexperience@gmail.com Our discord--https://discord.gg/kyA9Bq6 Our mixer(streaming)--www.mixer.com/blaisexperience Derreck's Xbox Live gamertag--BlaiseXPerience Our Youtube (the podcast is now here as well)-- https://www.youtube.com/channel/UClzmSAjzgjUTMKmW8j-0JOQ?view_as=subscriber OurFacebook Group--https://www.facebook.com/groups/330934434348977/ Listen Notes Interview with Host/Founder Derreck Blaise (this is an interview with the host giving insight into his perspectives, motivations, and process for creating the podcast...go check it out!) -- https://www.listennotes.com/r/8eb505c493f54d929c3772b875421c7b/derreck-blaise/ Our Apple podcasts link- https://itunes.apple.com/us/podcast/the-blaise-xperience/id1358494878 Our Current Website/Castette http://theblaisexperience.cast.rocks Our Intro/Outro Song: sonicsushi.com by NNNNNNNNNN https://nnnnnnnnnn.bandcamp.com/track/sonicsushi-com Podcast NH Network: www.podcastnh.com Contact Info Mentioned this Episode: Geoffrey Card twitter: @rangutang twitch: http://twitch.tv/derangutang Special Thanks to our patrons including: Maximiliankolbe Niahcyan MfnJuggernaut Meader Thank you and I hope you enjoy--The Blaise XPerience

Welcome to The Blaise XPerience, the podcast where you XPerience a variety of games from every angle. Today Derreck is back once again and this time we are back for more State of Decay 2. In fact, its been ONE YEAR since this amazing game came out! To celebrate we are doing a special episode highlighting the top 10 changes to SOD2 in year one. Derreck is joined by Coconutkid123 making his 2nd appearance and Falloutgurl4 on her first appearance. We all compiled our own lists of what we think are the top changes to the game we love in the first year after release. There are some differences and some overlap in our list, but what ensues is a great discussion of the hard work that the team at Undead Labs has put together over the first year. In addition, lots of laughs and jokes at our expense are had in good fun making for a very enjoyable listen. Thank you again to the team at Undead Labs for all your hard work this past year! So Come check it out and let us know what you think! Thank you so much as always for listening to The Blaise XPerience! Links to follow us on: Our Patreon--www.patreon.com/blaisexperience Our twitter-- @BlaiseXPerience Our email-- theblaisexperience@gmail.com Our discord--https://discord.gg/kyA9Bq6 Our mixer(streaming)--www.mixer.com/blaisexperience Derreck's Xbox Live gamertag--BlaiseXPerience Our Youtube (the podcast is now here as well)-- https://www.youtube.com/channel/UClzmSAjzgjUTMKmW8j-0JOQ?view_as=subscriber OurFacebook Group--https://www.facebook.com/groups/330934434348977/ Listen Notes Interview with Host/Founder Derreck Blaise (this is an interview with the host giving insight into his perspectives, motivations, and process for creating the podcast...go check it out!) -- https://www.listennotes.com/r/8eb505c493f54d929c3772b875421c7b/derreck-blaise/ Our Apple podcasts link- https://itunes.apple.com/us/podcast/the-blaise-xperience/id1358494878 Our Current Website/Castette http://theblaisexperience.cast.rocks Our Intro/Outro Song: sonicsushi.com by NNNNNNNNNN https://nnnnnnnnnn.bandcamp.com/track/sonicsushi-com Podcast NH Network: www.podcastnh.com Places Mentioned this Episode: Falloutgurl4 contact info: streaming: twitch.tv/falloutgurl4 twitter: @falloutgurl4 Coconutkid123 contact info: twitter: @brickbasher14 Special Thanks to our patrons including: Maximiliankolbe Niahcyan MfnJuggernaut Meader Thank you and I hope you enjoy--The Blaise XPerience

Welcome to The Blaise XPerience, the podcast where you XPerience a variety of games from every angle. Today Derreck is back once again to talk about State of Decay 2. In this Episode Derreck is back for a solo episode to discuss the top 10 enclave bonuses in SOD2. Derreck begins by going over all 37 enclave benefits both original and the new ones post update 6.0. He discusses what ones might be good or bad touching on each one briefly at least. Then Derreck gives his opinion on the bottom 3 benefits on the list that you should avoid using. Finally, he gets into his list of top 10 enclave benefits and goes through them revealing what he thinks the best ones are in the game. So Come check it out and let us know what you think! Thank you so much as always for listening to The Blaise XPerience! Thank you so much for listening to the podcast. We appreciate each and every listener. Please rate and subscribe on Apple podcasts and leave feedback for the podcast. Any feedback you give will help the cast become better. If you want to send feedback you can always interact with the podcast in the following ways: Our twitter-- @BlaiseXPerience Our email-- theblaisexperience@gmail.com Our discord--https://discord.gg/kyA9Bq6 Our mixer(streaming)--www.mixer.com/blaisexperience Derreck's Xbox Live gamertag--BlaiseXPerience Our Youtube (the podcast is now here as well)-- https://www.youtube.com/channel/UClzmSAjzgjUTMKmW8j-0JOQ?view_as=subscriber Our New Facebook Group--https://www.facebook.com/groups/330934434348977/ Derreck's Xbox Live gamertag--BlaiseXPerience Listen Notes Interview with Host/Founder Derreck Blaise (this is an interview with the host giving insight into his perspectives, motivations, and process for creating the podcast...go check it out!) -- https://www.listennotes.com/r/8eb505c493f54d929c3772b875421c7b/derreck-blaise/ The best way to help the podcast is by giving us a review on apple podcasts. These reviews help expose the podcast to more people and help the podcast grow. Any review is greatly appreciated! Our Apple podcasts link- https://itunes.apple.com/us/podcast/the-blaise-xperience/id1358494878 Our Current Website/Castette http://theblaisexperience.cast.rocks Our Intro/Outro Song: sonicsushi.com by NNNNNNNNNN https://nnnnnnnnnn.bandcamp.com/track/sonicsushi-com Other places mentioned this episode: Undead Trials Information: Undead Trials Discord: https://discord.gg/GxcfkbF (this link never expires

The E3 hangover from hell concludes with Paul, James, and Trevor talking up the Game Critics E3 Awards and announcing the best games of the first half of 2018 in the Perfect List. Meanwhile, we didn’t get access to the rub and tug edition of SoD2, we didn’t get to play Anthem, and there’s too much email. SALT AVALANCHE! Also covered: HORRIBLE single player games like God of War. Also, Shawn did NOT invite us over. --- Send in a voice message: https://anchor.fm/pressxtopodcast/message

Ponies Turn On Nxtgen720 XB1 S Running SOD2 Better Than XBOX ONE X E3 LEAKS

Tonight we are down both an Ashgar and a Kodra… and the intro felt really weird to start with Grace.  Tonight we had one of those nights where we felt like we didn’t have an awful lot to talk about… but then wound up running over time anyways.  Bel talks about his experiences with State of Decay 2 on both Xbox One and PC and how it has changed from the original. Grace talks about her experiences with the Warmind Destiny 2 expansion that then spawns a discussion about why we feel D2 has a bad attach rate.  Bel and Grace talk about how not excited they are for Battle for Azeroth in World of Warcraft, but how otherwise generally awesome the experience of leveling alts has become. Tam and Thalen talk about their further experiences with Battletech and coming to terms with the random headshots. Featured Topics: State of Decay 2 Destiny 2 Warmind Bad Progression Design World of Warcraft Battle for Azeroth Angst Excellent Alt Leveling BattleTech

This week we look at two genes that form part of our antioxidant needs section of the our nutrition reports, called CAT and GPX1. The gene that carries the most weight in this section is SOD2, which we have looked at previously in this series. If you can’t remember that far back, SOD2 is an antioxidant enzyme, and small changes in the SOD2 gene can lead to that enzyme working better or worse, which can increase how much of the antioxidant nutrients you require. CAT and GPX1 play a supportive role here.   CAT GPX1 CC Good enzyme activity – standard antioxidant intake required. Good enzyme activity – standard antioxidant intake required. CT Moderately reduced levels of enzyme activity – ensure slightly higher intake of antioxidants. Moderately reduced levels of enzyme activity – ensure slightly higher intake of antioxidants and selenium. TT Lowest level of enzyme activity – should increase intake of antioxidants. Lowest level of enzyme activity – should increase intake of antioxidants, especially selenium. Resources & Studies Mentioned https://www.ncbi.nlm.nih.gov/pubmed/16538174  

Apply for My DNA Coach's Academy by clicking here - SOD2 is the gene that creates Manganese Superoxide Dismutase-2 (MnSOD2), an antioxidant found in the mitochondria – small “cells within our cells” which are where our body produces energy for both movement and everyday life. The enzyme helps to convert free radicals, which can cause damage to the mitochondria, into oxygen and hydrogen peroxide.This prevents the free radicals from causing too much damage, but hydrogen peroxide in and of itself can also damage the mitochondria. Our body then has to further break down this hydrogen peroxide to water, and two other enzymes help in this process, called catalase and glutathione peroxidase. A single nucleotide polymorphism (SNP) in the SOD2 gene can change the structure of the protein found in the MnSOD2 enzyme, which can make it more or less efficient. The more efficient this enzyme is, the better you are at reducing free radicals to hydrogen peroxide and water. Whilst this might sound good, it has a secondary effect of increasing the amount of hydrogen peroxide that will be present, which, as already mentioned, can be damaging. Because the other enzymes, catalase and glutathione peroxidase, are supported by antioxidants, low intakes of antioxidants will lead to an increase in hydrogen peroxide build up, which will damage the mitochondria. So, whilst having a more efficient MnSOD2 enzyme might sound good, if your overall antioxidant intake is low, it can actually increase risk over time.   What we know from a number of different studies is that the C allele of SOD2 is associated with a more efficient MnSOD2 enzyme – so if antioxidant intake is high, this is good, but if it is low, this is not ideal. We see this from studies such as this one by Li and colleagues, published in 2005. In this study, they looked at 567 people who developed prostate cancer, and compared them to 764 people who didn’t. They compared SOD2 genotype between the groups, and also how many antioxidants each person consumed on a regular basis. What they found was that, when antioxidant intake was low, those with the CC genotype had a much higher risk of developing prostate cancer compared to the CT & TT genotypes – about 2.5 times higher. However, if antioxidant intake was high, their risk dropped, significantly, to around half that of those with the CT & TT genotypes. This is a really good example of how genes aren’t good or bad, just dependent on the situation; in this example, the CC genotype carries the risk if antioxidant intake is low, but is protective if antioxidant intake is high. We take a food first approach, so if you see you have a raised need for antioxidants, we think it’s a good idea to get this from fruits and vegetables, as these foods are highest in these nutrients. The most common forms of antioxidants are vitamin A (found in carrots and sweet potato), vitamin C (found in broccoli, peppers and oranges), and vitamin E (found in almonds and sunflower seeds). There are also other antioxidant compounds, such as carotenoids (found in colourful fruits and vegetables) and polyphenols (found in teas, coffee, wine and chocolate – it’s not all bad news!). All of these nutrients are important, so for those of you with a raised need, we recommend eating a wide range of fruits and vegetables per day, along with different teas, coffee, and maybe a few squares of dark chocolate with a glass of wine in the evening – depending on your fat loss goals of course.

Thu, 6 Oct 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/13654/ https://edoc.ub.uni-muenchen.de/13654/1/Weber_Franziska.pdf Weber, Franziska

Background: Coliform bacteria are the most common etiologic agents in severe mastitis of cows. Escherichia coli infections are mostly restricted to a single udder quarter whereas neighboring quarters stay clinically inapparent, implicating the presence of a systemic defense reaction. To address its underlying mechanism, we performed a transcriptome study of mammary tissue from udder quarters inoculated with E. coli (6 h and 24 h post infection), from neighboring quarters of the same animals, and from untreated control animals. Results: After 6 h 13 probe sets of differentially expressed genes (DEG) were detected in infected quarters versus control animals. Eighteen hours later 2154 and 476 DEG were found in infected and in neighboring quarters vs. control animals. Cluster analysis revealed DEG found only in infected quarters (local response) and DEG detected in both infected and neighboring quarters (systemic response). The first group includes genes mainly involved in immune response and inflammation, while the systemic reaction comprises antigen processing and presentation, cytokines, protein degradation and apoptosis. Enhanced expression of antimicrobial genes (S100A8, S100A9, S100A12, CXCL2, GNLY), acute phase genes (LBP, SAA3, CP, BF, C6, C4BPA, IF), and indicators of oxidative stress (GPX3, MT1A, MT2A, SOD2) point to an active defense reaction in infected and neighboring healthy quarters. Its early onset is indicated by increased transcription of NFIL3 at 6 h. NFIL3 is a predicted regulator of many genes of the systemic response at 24 h. The significance of our transcriptome study was evidenced by some recent findings with candidate gene based approaches. Conclusions: The discovery and holistic analysis of an extensive systemic reaction in the mammary gland significantly expands the knowledge of host-pathogen interactions in mastitis which may be relevant for the development of novel therapies and for genetic selection towards mastitis resistance.