Podcasts about dlk

A Little More Conversation with Ben O’Hara-Byrne

Play Episode Listen Later Nov 29, 2023 71:41

Den mäktiga basisten Frida i The Baboon Show slog sig ner i poddens hytt på Östersjön för att ta sig ett snack om DLK, baslirandet, lite gearsnack, klubb kontra festivalgig, att gå hem i många läger, olika influenser och otrendkänslighet. Vidare till seriefigurerna, steal the thunder, Tallinn, djuren, Spiders, DULL, Clowns från Melbourne, Tina Turner, Beyond Pink, Allvaret, Twin Pigs, 90-tals-grunge och Världen Brinner.

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MLK

Tre inte så visa män

Play Episode Listen Later Aug 28, 2023 69:46

Förti Kå, MLK, DLK?

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065: State Fair, Summer Bounty

DonnaLonna Kitchen Show

Play Episode Listen Later Jul 27, 2023 47:16

Tomatoes and sweet corn - fresh from the garden. We look ahead to the Iowa State Fair and DLK's upcoming cooking demonstration at the fair. Donna reviews the recipes. We celebrate Iowa food with polenta with candied tomatoes and lard pound cake with berries and whipped cream. Also some thoughts on gazpacho, zucchini, carrot top pesto and elderberries. Lonna reads about the Automat, a short food history from the book Food of a Younger Land.

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World's first fully electric flying car approved to begin test runs in U.S.

Play Episode Listen Later Jul 7, 2023 94:19

Office vacancy rates rising to highest levels ever in Canada Guest: Susan Thompson, Associate Director, Research, Colliers Is it time to get rid of the often misunderstood best before dates on food? Guest: Mike von Massow, OAC chair in food system leadership and a food economics professor at the University of Guelph New survey shows 25% of Britons have never boiled an egg: Are basic cooking skills a bit of a dying art? Guest: Jonathan Kinney, Culinary Instructor and Co-Owner, Northwest Culinary Academy of Vancouver 150 restaurants past and present that shaped Canada and the way we eat Guest: Gabby Peyton, food & travel writer and author of Where We Ate: A Field Guide to Canada's Restaurants, Past and Present World's first fully electric flying car approved to begin test runs in U.S. Guest: Jim Dukhovny, CEO, Alef Aeronautics Myths we believe and mistakes we make when it comes to sunscreen Guest: Dr. Lisa Kellett, dermatologist, owner of DLK on Avenue

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The axonal localization of Dual Leucine Zipper Kinase defines its protein-turnover

Play Episode Listen Later Apr 19, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.18.537392v1?rss=1 Authors: Kim, S., Quagraine, Y., Singh, M., Kim, J. H. Abstract: Subcellular protein localization plays critical roles in diverse neuronal functions. Dual Leucine Zipper Kinase (DLK) mediates neuronal stress responses including neuronal loss in multiple neurodegenerative disorders. DLK is axonally expressed, and its expression is constantly suppressed under normal conditions. However, little is known about how and why DLK is localized in axons. We found that Wallenda (Wnd), the Drosophila ortholog of DLK, is highly enriched in the axon terminals and this localization is necessary for the Highwire-mediated suppression of Wnd protein levels. We further found that a palmitoylation on Wnd plays an essential role in its axonal localization. Inhibiting axonal localization of Wnd resulted in dramatically increased protein levels of Wnd, which led to excessive stress signaling including neuronal loss. Our study demonstrates that subcellular protein localization is coupled with regulated protein turnover in neuronal stress response. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Bonus: Winter, Spring and In Between

DonnaLonna Kitchen Show

Play Episode Listen Later Feb 23, 2023 50:03

The content of this DLK show was originally aired in February 2019. Donna and Lonna give their thoughts on cabin fever, discuss the history of CSAs, talk about an onion jam recipe, winter greens, backyard edibles and share some insect news.

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DLK-dependent mitochondrial fission drives axon degeneration and neuronal cell death

Play Episode Listen Later Feb 2, 2023

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.30.526132v1?rss=1 Authors: Gomez Deza, J., Nebiyou, M., Alkaslasi, M. R., Somasundaran, P., Slavutsky, A. L., Ward, M. E., Watkins, T. A., Le Pichon, C. E. Abstract: Currently there are no effective treatments for an array of neurodegenerative disorders to a large part because cell-based models fail to recapitulate disease. Here we developed a robust human IPSC-based model where laser axotomy causes retrograde axon degeneration leading to neuronal cell death. Time-lapse confocal imaging revealed that damage triggers a wave of mitochondrial fission proceeding from the site of injury to the soma. We demonstrated that mitochondrial fission and resultant cell death is entirely dependent on phosphorylation of dynamin related protein 1 (DRP1) by dual leucine zipper kinase (DLK). Importantly, we show that CRISPR mediated Drp1 depletion protected mouse retinal ganglion neurons from mitochondrial fission and degeneration after optic nerve crush. Our results provide a powerful platform for studying degeneration of human neurons, pinpoint key early events in damage related neural death and new focus for therapeutic intervention. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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Keine Lust auf Vereinsarbeit?

Brand Punkt On Air

Play Episode Listen Later Feb 1, 2023 18:44

Einsatzabteilung / Verein Früh schon hatte ich den Eindruck, dass der Verein ein notwendiges Übel in der Feuerwehr ist. Ich wollte Einsätze, Übungen, Technik, Action, DLK, RW, HLF und noch viel mehr. Aus der Jugendfeuerwehr kommend hat mich das ganze Vereinsgedöns nicht interessiert. Wieso haben wir eigentlich einen Verein? Irgendwie gab das richtig Zoff mit meinem Vater der Chef war und mich zu überzeugen versuchte, dass ich aktiv im Verein mitwirken soll. Also wurde ich Schriftführer im Verein, weil ich beruflich in der Verwaltung war. Interessiert hat mich das trotzdem nicht. Manchmal hasste ich den Verein. Wie ist das Vereinswesen entstanden? Brandschutz gab es schon in grauer Vorzeit. Bei den Römern wurden Sklaven eingesetzt und im Mittelalter wurden die Bürger verpflichtet, sich am Brandschutz zu beteiligen. Vereine aber entstanden erst später. Feuerwehrvereine finanzieren sich in der Regel durch Spenden und Mitgliedsbeiträge. Von diesen Geldern werden oft Anschaffungen im Sinne der Kameradschaft, aber auch Zuschüsse zur Ausrüstung gegeben. Die Erlöse aus Veranstaltungen sind eine wesentliche Finanzierungshilfe für die öffentlich-rechtliche Abteilung. Also dann doch beide Institutionen? Feuerwehrvereine sind z.B. Mitglied im Vereinsring und haben dadurch Einfluss. Auch unsere Feuerwehrverbände haben die wichtige Aufgabe, das Feuerwehrwesen innerhalb ihrer Region zu fördern und zu vertreten. Als ich dann Führungskraft wurde, habe ich bemerkt, wie uns durch die Vereinsseite manchmal der Rücken gestärkt wurde und das nicht nur im Bereich Finanzen, sondern auch und vor allem nach außen. Wir wünschen dir viel Spaß mit dieser Podcast-Folge. Dein Team von Brand Punkt, Hermann und Carina _____________________________ Blogbeitrag der Podcastfolge: https://brand-punkt.de/219-keine-lust-auf-vereinsarbeit/ Presseartikel in der FNP vom 31.01.2023: https://brand-punkt.de/interview-mit-der-frankfurter-neuen-presse-mehr-mensch-hinter-dem-visier/ Live Session am 06.02.23 um 19:00 Uhr Thema: Thema: Verbrennungen durch Silvesterböller - wohin mit der Wut? https://us02web.zoom.us/webinar/register/WN_J_RAHVE9QkKanuPiz_rYuw _____________________________ Brauchst du bei einem Thema, dass dich mental belastet Unterstützung? Nimm gerne Kontakt zu uns auf: https://brand-punkt.de/kontakt/ Mehr Infos über uns und unsere Arbeit: www.brand-punkt.de Mehr Infos über fireproof360° - dem E-Learning Programm für mental starke und motivierte Feuerwehreinsatzkräfte: https://brand-punkt.de/e-learning-fireproof360 Teile diese Podcastfolge und hilf deinen Kamerad:innen: Vielleicht befindet sich ein Kamerad oder Kameradin in einer Situation, bei der genau diese Folge eine wertvolle Unterstützung sein kann - deshalb bitten wir dich: Teile diese Folge und helfe somit auch denjenigen, die diesen kostenfreien Podcast noch nicht kennen.

Membrane association is required for Stmn2-mediated axon protection

Play Episode Listen Later Dec 23, 2022

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.23.521801v1?rss=1 Authors: Thornburg-Suresh, E. J. C., Richardson, J. E., Summers, D. W. Abstract: Axon integrity is essential for functional connectivity in the nervous system. The degeneration of stressed or damaged axons is a common and sometimes initiating event in neurodegenerative disorders. Cellular factors that preserve axon integrity have an important influence on the fate of a damaged axon. Stathmin-2 (Stmn2) is an axon maintenance factor that is depleted in Amyotrophic Lateral Sclerosis and replenishment of Stmn2 can restore neurite outgrowth in diseased neurons. Stathmins have a well-documented role in microtubule dynamics during neurodevelopment, yet mechanisms responsible for Stmn2-mediated axon maintenance in injured neurons are not known. We demonstrate that membrane association of Stmn2 is critical for its axon-protective activity. Axonal enrichment of Stmn2 is driven by palmitoylation as well as tubulin interaction. We discover that another Stathmin, Stmn3, co-migrates with Stmn2-containing vesicles and undergoes regulated degradation through DLK-JNK signaling. The Stmn2 membrane targeting domain is both necessary and sufficient for localization to a specific vesicle population and confers sensitivity to DLK-dependent degradation. Our findings reveal a broader role for DLK in tuning the local abundance of palmitoylated Stathmins in axon segments. Moreover, palmitoylation is a critical component of Stathmin-mediated axon protection and defining the Stmn2-containing vesicle population will provide important clues toward mechanisms of axon maintenance. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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November 2022 Discover Circ Res

Discover CircRes

Play Episode Listen Later Nov 17, 2022 28:13

This month on Episode 42 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the October 28 and November 11th issues of Circulation Research. This episode also features an interview with Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson from University of California San Diego about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformations. Article highlights: Jia, et al. Prohibitin2 Maintains VSMC Contractile Phenotype Rammah, et al. PPARg and Non-Canonical NOTCH Signaling in the OFT Wang, et al. Histone Lactylation in Myocardial Infarction Katsuki, et al. PCSK9 Promotes Vein Graft Lesion Development Cindy St. Hilaire: Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's Journal, Circulation Research. I'm your host, Dr Cindy St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today, I'm going to be highlighting articles from our October 28th and our November 11th issues of Circ Res. I'm also going to have a chat with Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson, about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformations. But, before I get into the interviews, here are a few article highlights. Cindy St. Hilaire: The first article is from our October 28th issue, and the title is, PHB2 Maintains the Contractile Phenotype of Smooth Muscle Cells by Counteracting PKM Splicing. The corresponding author is Wei Kong, and the first authors are Yiting Jia and Chengfeng Mao, and they are all from Peking University. Insults to blood vessels, whether in the form of atherosclerosis, physical injury, or inflammation, can trigger vascular smooth muscle cells to transition from a contractile state to a proliferative and migratory one. Accompanying this conversion is a switch in the cells' metabolism from the mitochondria to glycolysis. But what controls this switch? To investigate, this group compared the transcriptomes of contractile and proliferative smooth muscle cells. Among the differentially expressed genes, more than 1800 were reciprocally up and down regulated. Of those, six were associated with glucose metabolism, including one called Prohibitin-2, or PHB2, which the team showed localized to the artery wall. In cultured smooth muscle cells, suppression of PHB2 reduced expression of several contractile genes. While in rat arteries, injury caused a decrease in production of PHB2 itself, and of contractile markers. Furthermore, expression of PHB2 in proliferative smooth muscle cells could revert these cells to a contractile phenotype. Further experiments revealed PHB2 controlled the splicing of the metabolic enzyme to up-regulate the phenotypic switch. Regardless of mechanism, the results suggest that boosting PHB2 might be a way to reduce adverse smooth muscle cell overgrowth and conditions such as atherosclerosis and restenosis. Cindy St. Hilaire: The second article I'm going to highlight is also from our October 28th issue, and the first authors are Mayassa Rammah and Magali Theveniau-Ruissy. And the corresponding authors are Francesca Rochais and Robert Kelly. And they are all from Marseille University. Abnormal development of the heart's outflow track, which ultimately forms the bases of the aorta and the pulmonary artery, accounts for more than 30% of all human congenital heart defects. To gain a better understanding of outflow tract development, and thus the origins of such defects, this group investigated the role of transcription factors thought to be involved in specifying the superior outflow tract, or SOFT, which gives rise to the subaortic myocardium, and the inferior outflow tract, which gives rise to the subpulmonary myocardium. Transcription factor S1 is over-expressed in superior outflow tract cells and the transcription factors, TBX1 and PPAR gamma, are expressed in inferior outflow tract cells. And now this group has shown that TBX1 drives PPAR gamma expression in the inferior outflow tract, while Hess-1 surpasses PPAR gamma expression in the superior outflow tract. Indeed, in mouse embryos lacking TBX1, PPAR gamma expression was absent in the outflow tract. While in mouse embryos lacking Hess-1, PPAR gamma expression was increased and PPAR gamma positive cells were more widespread in the outflow tract. The team also identified that signaling kinase DLK is an upstream activator of Hess-1 and a suppressor of PPAR gamma. In further detailing the molecular interplay regulating outflow tract patterning, the work will shed light on congenital heart disease etiologies, and inform potential interventions for future therapies. Cindy St. Hilaire: The third article I want to highlight is from our November 11th issue of Circulation Research, and the title is Histone Lactylation Boosts Reparative Gene Activation Post Myocardial Infarction. The first author is Jinjin Wang and the corresponding author is Maomao Zhang, and they're from Harbin Medical University. Lactylation of histones is a recently discovered epigenetic modification that regulates gene expression in a variety of biological processes. In inflammation, for example, a significant increase in histone lactylation is responsible for switching on reparative genes and macrophages when pro-inflammatory processes give way to pro-resolvin ones. The role of histone lactylation in inflammation resolution has been shown in a variety of pathologies, but has not been examined in myocardial infarction. Wang and colleagues have now done just that. They isolated monocytes from the bone marrow and the circulation of mice at various time points after induced myocardial infarctions, and examined the cells' gene expression patterns. Within a day of myocardial infarction, monocytes from both bone marrow and the blood had begun upregulating genes involved in inflammation resolution. And, concordant with this, histone lactylation was dramatically increased in the cells, specifically at genes involved in repair processes. The team went on to show that injection of sodium lactate into mice boosted monocyte histone lactylation and improved heart function after myocardial infarction, findings that suggest further studies of lactylation's pro-resolving benefits are warranted. Cindy St. Hilaire: The last article I want to highlight is titled, PCSK9 Promotes Macrophage Activation via LDL Receptor Independent Mechanisms. The first authors are Shunsuke Katsuki and Prabhash Kumar Jha, and the corresponding author is Masanori Aikawa, and they are from Brigham and Women's Hospital in Harvard. Statins are the go-to drug for lowering cholesterol in atherosclerosis patients. But the more recently approved PCSK9 inhibitors also lower cholesterol and can be used to augment or replace statins in patients where these drugs are insufficient. PCSK9 is an enzyme that circulates in the blood and destroys the LDL receptor, thereby impeding the removal of bad cholesterol. The enzyme also appears to promote inflammation, thus potentially contributing to atherosclerosis in two ways. This group now confirms that PCSK9 does indeed promote pro-inflammatory macrophage activation and lesion development, and does so independent of its actions on the LDL receptor. The team assessed PCSK9-induced lesions in animals with saphenous vein grafts, which are commonly used in bypass surgery but are prone to lesion regrowth. They found that LDL receptor lacking graft containing mice had greater graft macrophage accumulation and lesion development when PCSK9 activity was boosted than when it was not. The animal's macrophages also had higher levels of the pro-inflammatory factor expression. Together, this work shows that PCSK9 inhibitors provide a double punch against atherosclerosis and might be effective drugs for preventing the all too common failure of saphenous vein grafts. Cindy St. Hilaire: So, today with me I have Dr Miguel Lopez-Ramirez and undergraduate student Bliss Nelson from the University of California in San Diego, and we're going to talk about their study, Neuroinflammation Plays a Critical Role in Cerebral Cavernous Malformation Disease, and this article is in our November 11th issue of Circulation Research. Thank you both so much for joining me today. Before we talk about the science, want to just maybe tell me a little bit about yourselves? Bliss Nelson: My name is Bliss Nelson. I'm a member of Miguel Lopez-Ramirez's lab here at UC San Diego at the School of Medicine. I'm an undergraduate student here at UC San Diego. I'm actually a transfer student. I went to a community college here in California and I got involved in research after I transferred. Cindy St. Hilaire: What's your major? Bliss Nelson: I'm a cognitive science major. Cindy St. Hilaire: Excellent. You might be the first undergrad on the podcast, which is exciting. Bliss Nelson: Wow. What an honor. Thank so much. Cindy St. Hilaire: And Miguel, how about you? Miguel Lopez-Ramirez: Yes, thank you. Well, first thank you very much for the opportunity to present our work through this media. It's very exciting for us. My name is Miguel Alejandro Lopez-Ramirez, and I'm an assistant professor in the Department of Medicine and Pharmacology here at UCSD. Cindy St. Hilaire: Wonderful. I loved your paper, because, well, first, I don't think I've talked about cerebral cavernous malformations. So what are CCMs, and why are they so bad? Bliss Nelson: Cerebral cavernous malformations, or CCMs for short, are common neurovascular lesions caused by a loss of function mutation in one of three genes. These genes are KRIT1, or CCM1, CCM2 and PDCD10, or CCM3, and generally regarded as an endothelial cell autonomous disease found in the central nervous system, so the brain and the spinal cord. The relevance of CCMs is that it affects about one in every 200 children and adults, and this causes a lifelong risk of chronic and acute hemorrhaging. CCMs can be quiescent or dynamic lesions. If they are dynamic, they can enlarge, regress, or behave progressively, producing repetitive hemorrhaging and exacerbations of the disease. Other side effects of the disease could be chronic bleedings, focal neurological deficits, headaches, epileptic seizures and, in some cases, death. There's no pharmacological treatment for CCMs. There's only one type of option some patients may have, which would be to have surgery to cut out the lesions. But of course this depends on where the lesion or lesions are in the central nervous system, if that's even an option. So sometimes there's no option these patients have, there's no treatment, which is what propels our lab to towards finding a pharmacological treatment or uncovering some of the mechanisms behind that. Cindy St. Hilaire: Do people who have CCM know that they have them or sometimes it not detected? And when it is detected, what are the symptoms? Bliss Nelson: Sometimes patients who have them may not show any symptoms either ever in their lifetime or until a certain point, so really the only way to find out if you were to have them is if you went to go get a brain scan, if you went to go see a doctor, or if you started having symptoms. But also, one of the issues with CCMs is that they're very hard to diagnose, and in the medical community there's a lack of knowledge for CCMs, so sometimes you may not get directed to the right specialist in time, or even ever, and be diagnosed. Miguel Lopez-Ramirez: I will just add a little bit. It is fabulous, what you're doing. I think this is very, very good. But yes, that's why they're considered rare disease, because it's not obvious disease, so sometimes most of the patient, they go asymptomatic even when they have one lesions, but there's still no answers of why patients that are asymptomatics can become symptomatics. And there is a lot in neuro study, this study that we will start mentioning a little bit more in detail. We try to explain these transitions from silent or, quiescent, lesion, into a more active lesion that gives the disability to the patient. Some of the symptoms, it can start even with headaches, or, in some cases, they have more neurological deficits that could be like weakness in the arms or loss of vision. In many cases also problems with the speech or balance. So it depends where the lesion is present, in the brain or in the spinal cord, the symptoms that the patient will experience. And some of the most, I will say, severe symptoms is the hemorrhagic stroke and the vascular thrombosis and seizure that the patients can present. Those would be the most significant symptoms that the patient will experience. Cindy St. Hilaire: What have been some limitations in the study of CCMs? What have been limitations in trying to figure out what's going on here? Bliss Nelson: The limitations to the disease is that, well, one, the propensity for lesions, or the disease, to come about, isn't known, so a lot of the labs that work on it, just going down to the basic building blocks of what's even happening in the disease is a major problem, because until that's well established, it's really hard to go over to the pharmacological side of treating the disease or helping patients with the disease, without knowing what's going on at the molecular level. Cindy St. Hilaire: You just mentioned molecular level. Maybe let's take a step back. What's actually going on at the cellular level in CCMs? What are the major cell types that are not happy, that shift and become unhappy cells? Which are the key players? Bliss Nelson: That's a great question and a great part of this paper. So when we're talking about the neuroinflammation in the disease, our paper, we're reporting the interactions between the endothelium, the astrocytes, leukocytes, microglia and neutrophils, and we've actually coined this term as the CaLM interaction. Cindy St. Hilaire: Great name, by the way. Bliss Nelson: Thank you. All props to Miguel. And if you look at our paper, in figure seven we actually have a great graphic that's showing this interaction in play, showing the different components happening and the different cell types involved in the CaLM interaction that's happening within or around the CCM lesions. Cindy St. Hilaire: What does a astrocyte normally do? I think our podcast listening base is definitely well versed in probably endothelial and smooth muscle cell and pericyte, but not many of us, not going to lie, including me, really know what a astrocyte does. So what does that cell do and why do we care about its interaction with the endothelium? Miguel Lopez-Ramirez: Well, the astrocytes play a very important role. Actually, there are more astrocytes than any other cells in the central nervous system, so that can tell you how important they are. Obviously play a very important role maintaining the neurological synapses, maintaining also the hemostasis of the central nervous system by supporting not only the neurons during the neural communication, but also by supporting the blood vessels of the brain. All this is telling us that also another important role is the inflammation, or the response to damage. So in this case, what also this study proposed, is that new signature for these reactive astrocytes during cerebral malformation disease. So understanding better how the vasculature with malformations can activate the astrocytes, and how the astrocytes can contribute back to these developing of malformations. It will teach us a lot of how new therapeutic targets can be implemented for the disease. This is part of this work, and now we extend it to see how it can also contribute to the communication with immune cells as Bliss already mentioned. Cindy St. Hilaire: Is it a fair analogy to say that a astrocyte is more similar to a pericyte in the periphery? Is that accurate? Miguel Lopez-Ramirez: No, actually there are pericytes in the central nervous system as well. They have different roles. The pericyte is still a neuron cell that give the shape, plays a role in the contractility and maintains the integrity of the vessels, while the astrocyte is more like part of the immune system, but also part of the supporting of growth factors or maintaining if something leaks out of the vasculature to be able to capture that. Cindy St. Hilaire: You used a handful of really interesting mouse models to conduct this study. Can you tell us a little bit about, I guess, the base model for CCM and then some of the unique tools that you used to study the cells specifically? Bliss Nelson: Yeah, of course. I do a lot of the animal work in the lab. I'd love to tell you about the mouse model. So to this study we use the animal model with CCM3 mutation. We use this one because it is the most aggressive form of CCM and it really gives us a wide range of options to study the disease super intricately. We use tamoxifen-regulated Cre recombinase under the control of brain endothelial specific promoter, driving the silencing of the gene CCM3, which we call the PDCD10 betco animal, as you can see in our manuscript. To this, the animal without the Cre system, that does not develop any lesions, that we use as a control, we call the PDCD10 plox. And these animals are injected with the tamoxifen postnatally day one, and then for brain collection to investigate, wcollected at different stages. So we do P15, which we call the acute stage, P50, which we term the progressive stage, and then P80, which is the chronocytes stage. And after enough brain collections, we use them for histology, gene expression, RNA analysis, flow cytometry, and different imaging to help us further look into CCMs. Cindy St. Hilaire: How similar is a murine CCM to a human CCM? Is there really good overlap or are there some differences? Miguel Lopez-Ramirez: Yes. So, actually, that's a very good question, and that's part of the work that we are doing. This model definitely has advantages in which the lesions of the vascular formations are in an adult and juvenile animals, which represent an advantage for the field in which now we will be able to test pharmacological therapies in a more meaningful, way where we can test different doses, different, again, approaches. But definitely, I mean, I think I cannot say that it's only one perfect model for to mimic the human disease. It's the complementary of multiple models that give us certain advantages in another, so the integration of this knowledge is what will help us to understand better the disease. Cindy St. Hilaire: That's great. I now want to hear a little bit about your findings, because they're really cool. So you took two approaches to study this, and the first was looking at the astrocytes and how they become these, what you're calling reactive astrocytes, and then you look specifically at the brain endothelium. So could you maybe just summarize those two big findings for us? Miguel Lopez-Ramirez: Yeah, so, basically by doing these studies we use trangenic animal in this case that they give us the visibility to obtain the transcripts in the astrocytes. And basically this is very important because we don't need to isolate the cells, we don't need to manipulate anything, we just took all the ribosomes that were basically capturing the mRNAs and we profile those RNAs that are specifically expressed in the astrocytes. By doing this, we actually went into looking at in depth the transcripts that were altered in the animals that developed the disease, in this case the cerebral cavernous malformation disease, and what we look at is multiple genes that were changing. Many of them were already described in our previous work, which were associated with hypoxia and angiogenesis. But what we found in this work is that now there were a lot of genes associated with inflammation and coagulation actually, which were not identified before. What we notice is that now these astrocytes, during the initial phase of the vascular malformation, may play a more important role in angiogenesis or the degradation of the vessels. Later during the stage of the malformation, they play a more important role in the thrombosis, in the inflammation, and recruitment of leukocyte That was a great advantage in this work by using this approach and looking in detail, these astrocytes. Also, we identified there were very important signature in these astrocytes that we refer as a reactive astrocytes with neuroinflammatory properties. In the same animals, basically, not in the same animal, but in the same basically the experimental approach, we isolated brain vasculature. And by doing the same, we actually identified not only the astrocyte but also the endothelium was quite a different pattern that we were not seeing before. And this pattern was also associated with inflammation, hypoxia and coagulation pathways. That lead us to go into more detail of what was relevant in this vascular malformations. And one additional part that in the paper this is novel and very impactful, is that we identify inflammasome as a one important component, and particularly in those lesions that are multi-cavernous. Now we have two different approaches. One, we see this temporality in which the lesions forms different patterns in which the initial phase maybe is more aneugenic, but as they become more progressive in chronocytes, inflammation and hypoxy pathways are more relevant for the recruitment of the inflammatory cells and also the precipitation of immunothrombosis. But also what we notice is that inflammasome in endothelial and in the leukocytes may play an important role in the multi-cavernous formation, and that's something that we are looking in more detail, if therapeutics or also interventions in these pathways could ameliorate the transition of phases between single lesions into a more aggressive lesions. Cindy St. Hilaire: That's kind of one of the follow up questions I was thinking about too is, from looking at the data that you have, obviously to get a CCM, there's a physical issue in the vessel, right? It's not formed properly. Does that form influence the activation of the astrocyte, and then the astrocytes, I guess, secrete inflammatory factors, target more inflammation in the vessel? Or is there something coming from the CCM initially that's then activating the astrocyte? It's kind of a chicken and the egg question, but do you have a sense of secondary to the malformation, what is the initial trigger? Miguel Lopez-Ramirez: The malformations in our model, and this is important in our model, definitely start by producing changes in the brain endothelial. And as you mention it, these endothelium start secreting molecules that actually directly affect the neighboring cells. One of the first neighboring cells that at least we have identified to be affected is the astrocytes, but clearly could be also pericytes or other cells that are in the neurovascular unit or form part of the neurovascular unit. But what we have seen now is that this interaction gets extended into more robust interactions that what you were referring as the CaLM interactions. Definitely I think during the vascular malformations maybe is the discommunication that we identify already few of those very strong iteration that is part of the follow up manuscript that we have. But also it could be the blood brain barrier breakdown and other changes in the endothelium could also trigger the activation of the astrocytes and brain cells. Cindy St. Hilaire: What does your data suggest about potential future therapies of CCM? I know you have a really intriguing statement or data that showed targeting NF-kappa B isn't likely going to be a good therapeutic strategy. So maybe tell us just a little bit about that, but also, what does that imply, perhaps, of what a therapeutic strategy could be? Bliss Nelson: Originally we did think that the inhibition of NF-kappa B would cause an improvement potentially downstream of the CCMs. And unexpectedly, to our surprise, the partial or total loss of the brain endothelial NF-kappa B activity in the chronic model of the mice, it didn't prevent or cause any improvement in the lesion genesis or neuroinflammation, but instead it resulted in a trend to increase the number of lesions and immunothrombosis, suggesting that the inhibition of it is actually worsening the disease and shouldn't be used as a target for therapeutical approaches. Miguel Lopez-Ramirez: Yes, particularly that's also part of the work that we have ongoing in which NF-kappa B may also play a role in preventing the further increase of inflammation. So that is something that it can also be very important. And this is very particular for certain cell types. It's very little known what the NF-kappa B actually is doing in the brain endothelial during malformations or inflammation per se. So now it's telling us that this is something that we have to consider for the future. Also, our future therapeutics of what we propose are two main therapeutic targets. One is the harmful hypoxia pathway, which involves activation, again, of the population pathway inflammation, but also the inflammasomes. So these two venues are part of our ongoing work in trying to see if we have a way to target with a more safe and basically efficient way this inflammation. However, knowing the mechanisms of how these neuroinflammation take place is what is the key for understanding the disease. And maybe even that inflammatory and inflammatory compounds may not be the direct therapeutic approach, but by understanding these mechanisms, we may come with new approaches that will help for safe and effective therapies. Cindy St. Hilaire: What was the most challenging part of this study? I'm going to guess it has something to do with the mice, but in terms of collecting the data or figure out what's going on, what was the most challenging? Bliss Nelson: To this, I'd like to say that I think our team is very strong. We work very well together, so I think even the most challenging part of completing this paper wasn't so challenging because we have a really strong support system among ourselves, with Miguel as a great mentor. And then there's also two postdocs in the lab who are also first authors that contributed a lot to it. Cindy St. Hilaire: Great. Well, I just want to commend both of you on an amazing, beautiful story. I loved a lot of the imaging in it, really well done, very technically challenging, I think, pulling out these specific sets of cells and investigating what's happening in them. Really well done study. And Bliss, as an undergraduate student, quite an impressive amount of work. And I congratulate both you and your team on such a wonderful story. Bliss Nelson: Thank you very much. Miguel Lopez-Ramirez: Thank you for Bliss and also Elios and Edo and Katrine, who all contributed enormously to the completion of this project. Cindy St. Hilaire: It always takes a team. Miguel Lopez-Ramirez: Yes. Cindy St. Hilaire: Great. Well, thank you so much, and I can't wait to see what's next for this story. Cindy St. Hilaire: That's it for the highlights from October 28th and November 11th issues of Circulation Research. Thank you so much for listening. Please check out the Circ Res Facebook page and follow us on Twitter and Instagram with the handle @circres and #discovercircres. Thank you to our guests, Dr Miguel Lopez-Ramirez and Bliss Nelson. This podcast is produced by Ashara Retniyaka, edited by Melissa Stoner, and supported by the editorial team of Circulation Research. Some of the copy text for our highlighted articles is provided by Ruth Williams. I'm your host, Dr Cindy St. Hilaire, and this is Discover CircRes, you're on the go source for the most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2022. The opinions expressed by speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, please visit ahagenerals.org.

#131: Was erwartet uns auf dem Deutschen Logistik Kongress 2022 in Berlin? (Christoph Meyer, Kai Althoff)

BVL.digital Podcast

Play Episode Listen Later Sep 7, 2022 30:16

In wenigen Wochen ist es soweit: vom 19.-21.Oktober öffnet der Deutsche Logistik Kongress 2022 in Berlin seine Pforten. Deshalb habe wir uns heute Christoph Meyer, Geschäftsführer der BVL und gleichzeitig Projektleiter für den DLK und Kai Althoff, CEO der 4flow AG, Mitglied im Beirat der BVL und zugleich Projektgruppenleiter des DLKs zu uns virtuelle Studio geladen. Gemeinsam mit unserem Host Boris Felgendreher sprechen die beiden darüber, was uns in diesem Jahr auf dem DLK erwartet, welche Themenschwerpunkte gesetzt werden, wie das Programm gestaltet ist, welche Möglichkeiten zum Netzwerken es gibt, auf welche Neuerungen wir uns in diesem Jahr freuen dürfen und vieles mehr. Hilfreiche Links: BVL: https://www.bvl.de/ Deutscher Logistik Kongress: https://www.bvl.de/dlk Autostore, der Sponsor der heutigen Sendung: www.autostoresystem.com

015: Summer is Here! The solstice, Cucumbers, Eggplant, Peaches and more

DonnaLonna Kitchen Show

Play Episode Listen Later Jun 27, 2022 50:59

Donna talks about the summer solstice. In a visit to the DLK archives, Donna and Lonna explore some of the joys of summer for a show about cicadas, trains, cucumbers, corn, and a flourless chocolate cake.

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#126 Genetika - Terezie Valčíková

Pejskárium

Play Episode Listen Later Jun 23, 2022 76:58

Bonusová část je k dispozici na Herohero.Genetiku si možná ze základky pamatujete jako to šíleně složité téma, které šlo úplně mimo vás. Přesto by ale každý majitel psa měl mít aspoň základní povědomí o hlavních pojmech a souvislostech, zejména potom když se chystá svého psa nebo fenu uchovnit a třeba odchovávat štěňata.Proto jsem se rozhodla jí věnovat samostatnou epizodu podcastu a pevně věřím, že se nám podařilo s Terezií Valčíkovou vybrat z téhle obrovsky široké oblasti ty zásadní věci a otázky, které si chovatelé psů kladou.V podcastu mimo jiné probíráme:– proč by se měl v základech genetiky orientovat každý majitel psa?– jak funguje genetické testování na konkrétní nemoci, co se dá testovat a co má smysl testovat?– základní genetické pojmy a jejich vysvětlení – gen, alela, fenotyp, genotyp a další– jsou voříšci opravdu zdravější než čistokrevní psi s PP?– jak to funguje s dědičností barev?– jak je to s dědičností DKK, DLK a dalších– co je to inbreeding, koeficient inbreedingu a proč by nás měl zajímat– jak vlastně probíhá genetické testováníLíbí se vám podcasty Pejskárium® a chcete je mít k dispozici ještě dříve včetně bonusů? Přidejte se do Pejskárium fanklubu na Herohero! To je česká platforma, díky které můžete v ceně jednoho kafíčka měsíčně podpořit moji tvorbu a vznik dalších dílů tohoto podcastu. Na oplátku dostanete vstup do kompletního archivu bonusových materiálů a spoustu dalších výhod :-).Jestli vás zajímá víc podobných příspěvků, článků a tipů do života se psem, budu se na vás těšit na www.pejskarium.cz!Za střih a úpravu podcastu děkuji Terezce, která stojí za projektem "Kreativní brejloun", její krásné psí ilustrace najdete na Instagramu.Podcast můžete v aplikaci Apple podcasts během pár vteřin ohodnotit a dát mi tak zpětnou vazbu, zda se vám rozhovory líbí.Poznámka pod čarou: Rozhovory v podcastech reprezentují také osobní názory hosta, které se vždy nemusí shodovat s tím, co šířím sama za sebe v rámci svých dalších kanálů.

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Dr Lisa Kellett: On Skincare For Every Day & Your Wedding Day

Aisle Seat

Play Episode Listen Later Jun 23, 2022 30:40

On this show we're exploring cosmetic dermatology with the Dr. Lisa Kellett, a board-certified dermatologist in both Canada and the United States. Dr. Kellett specializes in surgical, medical, laser and cosmetic dermatology at her Toronto-based clinic DLK on Avenue. In her own words, “your skin is a personal and precious possession As seen in my happy patients protecting and maintaining your skin at its optimal health an appearance will greatly contribute to your quality of life.” Dr. Kellett chats with host Alison McGill about the latest trends in cosmetic dermatology and wedding pre-juvenation treatments.

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148. Gorilla Killarna

Play Episode Listen Later May 11, 2022 124:51

Peter, Anders, Pontus, Fredrik och Martin i Gorilla Killarna slog sig ned framför mickarna för att snacka om varför de lade ned, tidigare band, Amiga 500, Zombiekrig, särskrivningen, Rock Of Bohuslän, spöken, MNW-killen, Kiss, Ebba Grön, DLK, nya inspelningar, Demonen, första fullängdaren, Binnike Bengt, punk, kassetten, pastorn, Bengt Perry, Jörlanda Bageri, Linda & Maria, Jurassic Park, Märvel och Ta.S.K.

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Fasting, Intermittent Fasting, and Keto #24, S.4

Tres Puntos, de McKinsey Colombia

Play Episode Listen Later Apr 9, 2022 26:33 Very Popular

Beginners often wonder if fasting, intermittent fasting, and keto go hand in hand. Are these strategies required? Will they help spur ketosis and weight loss? Don't be intimidated by the idea of I.F. (intermittent fasting). Though popular, this strategy is not a requirement for the keto diet. Fasting or Intermittent Fasting (I.F.) describes a planned period of time where a person does not eat. It can be executed in a variety of ways. The length of time, frequency, or allowable food/drinks during a fast? These variables can be customized to meet a person's individual needs or preferences on the keto diet. There are no hard and fast rules. Benefits of Fasting or Intermittent Fasting Folks who practice fasting or intermittent fasting report that it helps trigger ketosis. The body is given an opportunity to use up available carb storage before transitioning into fat-burning mode. Emotionally, many experience feelings of relief. Decisions about what to eat are set aside during a planned period of fasting. Should I Start Fasting or Intermittent Fasting? This is a personal question that only you can answer. There is no right or wrong answer. Fasting & Ketosis You can achieve ketosis with or without the practice of fasting. With DIRTY, LAZY, KETO, you can individualize your weight loss plan to fit your lifestyle. There are plenty of folks who have achieved amazing weight loss results on keto with, and without, this strategy. The decision to include fasting or intermittent fasting is up to you! Stephanie Laska is the USA Today bestselling author of the DIRTY, LAZY, KETO books with over 10,000 positive reviews on Amazon and Goodreads. Check out the many available keto diet resources to help you (available from online retailers like Amazon or Barnes & Noble or through your local library): DIRTY, LAZY, KETO Get Started Losing Weight While Breaking the Rules by Stephanie Laska (St. Martin's, 2020) The DIRTY, LAZY, KETO 5-Ingredient Cookbook: 100 Easy-Peasy Recipes Low in Carbs, Big on Flavor by Stephanie & William Laska (Simon & Schuster, 2021) The DIRTY, LAZY, KETO No Time to Cook Cookbook: 100 Easy Recipes Ready in Under 30 Minutes by Stephanie & William Laska (Simon & Schuster, 2021) The DIRTY, LAZY, KETO Dirt Cheap Cookbook: 100 Easy Recipes to Save Money & Time by Stephanie & William Laska (Simon & Schuster, 2020) The DIRTY, LAZY, KETO Cookbook: Bend the Rules to Lose the Weight by Stephanie & William Laska (Simon & Schuster, 2020) DIRTY, LAZY, KETO Fast Food Guide: 10 Carbs or Less by William & Stephanie Laska (2018) Free Keto Newsletter Sign up for the free keto newsletter full of low carb tips, keto recipes, and weight loss inspiration. The first email comes automatically and includes a free starter keto grocery list (can't find it? check your junk folder). There is no charge for the DLK motivational emails. Unsubscribe at any time. Related "Fasting and Intermittent Fasting" Resources: How to Jump-Start Ketosis and Weight Loss Need more support? Stephanie also leads a small group, premium keto support group on Facebook - for women only.

Paul & Sam Elliott (Drumderg Loyalists Keady)

Made to Parade

Play Episode Listen Later Mar 14, 2022 70:20

The brand new episode finds us in conversation with Paul Elliott from Drumderg Loyalists Keady FB. We are also joined by his son Sam in the episode as well.Drumderg Loyalists Keady, also known as the DLK are one of the most respected bands on the road today with a reputation for not only great playing, but for having one of the best colour party's on the road, their distinctive look and sound make them a must watch at every parade.Paul shares how he got involved with bands and the traditions he learned and how he is passing them on through his family. He also talks about how the band has developed over their nearly 100 years of existence, and the role that he has played in that.Paul brought his son Sam along for the recording of the episode and Sam shares why he loves being a member of the band and what he gets out of it.Talking to both Paul and Sam it is evident just how much of a positive influence the band has had on their whole family life and it was an absolute pleasure to have them both on to kick of this new season of Made to Parade.Make sure you join us next week when we will be joined by Les McMaster from Parkinson Accordion Band. You won't want to miss it.A big thank you as always to our sponsors British Drum Co, as well as all our supporters on Patreon, we also have some more sponsors joining the Made to Parade family and I will keep you updated on that as the season progresses.Make sure you check out our YouTube channel for video versions of the podcast and check out our website to subscribe to the audio only version of the podcast www.madetoparade.com

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#79: Berliner Momente genießen! Der Deutsche Logistik-Kongress kommt! (Christoph Meyer, Geschäftsführer, BVL)

BVL.digital Podcast

Play Episode Listen Later Sep 3, 2021 35:39

Der Deutsche Logistik-Kongress 2021 findet live vor Ort in Berlin und als Hybrid-Veranstaltung statt. Unser Gast heute ist Christoph Meyer, Geschäftsführer der BVL und Projektleier des DLK. Gemeinsam mit unserem Host Boris Felgendreher spricht er unter anderem über folgende Themen: - Die Learnings aus 2020 und was in diesem Jahr alles anders ist - Der Kongress als Präsenzveranstaltung vor Ort - Live Streaming: Was erwartet die Teilnehmer im Büro oder Home Office? - Die Fachausstellung - Das Netzwerken und die Rahmenveranstaltungen - Die Schwerpunkte, die Referenten und das Programm - Der Deutsche Logistik Preis 2021 - Das Hygienekonzept - Gibt es überhaupt noch Möglichkeiten für Aussteller oder Teilnehmer - und vieles mehr Links: Deutscher Logistik-Kongress 2021: https://www.bvl.de/dlk Das Programm: https://www.bvl.de/files/1951/2142/2835/BVL_Deutscher_Logistik-Kongress_2021_Programm.pdf Anmeldung: https://www.bvl.de/dlk-anmeldung BVL: https://www.bvl.de/ BVL.digital: http://bvl.digital/

¿Cómo ha cambiado la industria de la gastronomía?: Conversación con Jaime Escobar, fundador de DLK

Play Episode Listen Later Jun 2, 2021 28:02

En este episodio conversamos con Jaime Escobar sobre su trayectoria y experiencia en la industria de la gastronomía: desde los inicios de su empresa DLK, los retos y momentos difíciles que ha atravesado, hasta cómo se imagina el futuro de la industria. Santiago Carbonell y Jaime Escobar conversan sobre la innovación constante como pilar para la prosperidad y éxito dentro de la industria. Read more > Listen to the podcast (duration: 28:02) >

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¿Cómo ha cambiado la industria de la gastronomía?: Conversación con Jaime Escobar, fundador de DLK

Tres Puntos, de McKinsey Colombia

Play Episode Listen Later Jun 2, 2021 28:02

Read more > Listen to the podcast (duration: 28:02) > En este episodio conversamos con Jaime Escobar sobre su trayectoria y experiencia en la industria de la gastronomía: desde los inicios de su empresa DLK, los retos y momentos difíciles que ha atravesado, hasta cómo se imagina el futuro de la industria. Santiago Carbonell y Jaime Escobar conversan sobre la innovación constante como pilar para la prosperidad y éxito dentro de la industria.See www.mckinsey.com/privacy-policy for privacy information

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Easy Keto Desserts? Keto Chocolate on a Low Carb Diet #52, S.2 Free Keto Recipe -The DIRTY LAZY KETO No Time to Cook Cookbook

Play Episode Listen Later Dec 19, 2020 50:51

Chocolate Keto Desserts... Can you have chocolate on DIRTY, LAZY, KETO? Absolutely! Let me share a dozen (or more!) keto dessert suggestions that will help you curb a chocolate craving. In today's video, I'll do a little "show and tell" with sugar-free chocolate products. Some are home-runs (while others I'll tell you to avoid). As an added bonus, today's podcast includes a live cooking demo of a chocolate keto dessert recipe from The DIRTY, LAZY, KETO No Time to Cook Cookbook, Salty Pecan Bark. It's so fast and easy to make - plus it tastes delicious. This recipe is just 1 of 100 new DLK recipes you can make in under 30 minutes. I hope you'll order a copy today! Watch on YouTube or listen to an audio-only version on ApplePodcasts, Spotify, iHeartRadio, Pandora, Amazon Music... wherever you like to listen to podcasts. If you enjoyed the video, please like, comment, and subscribe to the DIRTY, LAZY, KETO YouTube channel. Turn on your notifications so you never miss an update. Follow along by printing out the below Salty Pecan Bark recipe. This excerpt from The DIRTY, LAZY, KETO No Time to Cook Cookbook by Stephanie & William Laska is provided below with permission from the publisher @Simon&Schuster (2021). Related Posts: Keto Baking Tips Is Carbquik Keto-Friendly? Keto Sweet Tooth - How to Manage Cravings

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110. The Sensitives

Play Episode Listen Later Dec 9, 2020 100:47

Magnus, Martin och Paulina i The Sensitives snackar om Peace And Love 2011, Falun, hoppbackar, Gruvpunx, Kupolen, nya plattan, Vilnius, hund & katthem, turnéminnen, punkfamiljen, sleazerock och recensioner. Vidare till 360-video, Raketklubben, King Albatross, Vånna Inget, punk, Against Me!, The Baboon Show, Misfits -97, turnéplaner, Death By Horse, Lucky Malice, DLK, Motörhead, GNR, Elin Callmer och Trubbel.

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Let’s Talk Turkey! FREE Easy Keto Recipe from The DIRTY, LAZY, KETO No Time to Cook Cookbook -NEW!

Play Episode Listen Later Nov 21, 2020 26:31

Looking for a FAST keto dinner recipe? Let's talk turkey! Low carb cooking doesn't have to take all day. You can make an easy keto meal in less than 30 minutes from start to finish. In today's cooking video, I teach you how to make my famous turkey leg recipe. It's a sneak peek recipe from my 3rd. cookbook, The DIRTY, LAZY, KETO No Time to Cook Cookbook! https://youtu.be/qnerpKyaC8k If you like making keto meals fast, you'll love the new book in the DLK series, The DIRTY, LAZY, KETO No Time to Cook Cookbook! *100 easy keto recipes *Ready in 30 minutes or less (including prep time!) *Weight loss inspiration, keto tips, and kitchen shortcuts I hope you enjoyed the video! Please give it a thumbs up, make a comment, and subscribe to the DIRTY, LAZY, KETO YouTube channel so you'll never miss a video update. You'll find tons of helpful videos on the channel. Did you catch the video about how to make a delicious keto-friendly green bean casserole? How about the chaffle recipe? Those are two of my favorites. As promised, you can download today's keto turkey recipe here. The DIRTY, LAZY, KETO No Time to Cook Cookbook by Stephanie & William Laska (Simon & Schuster, 2021). Reprinted with permission from the publisher. Keto Green Bean Recipe! Avoid Weight Gain Over the Holidays - Here is how! Holiday Cheat Meal?

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Palmitoylation Couples DLK to JNK3 to Facilitate Pro-degenerative Axon-to-Soma Signaling

Play Episode Listen Later Nov 17, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.17.387191v1?rss=1 Authors: Niu, J., Holland, S. M., Ketschek, A., Collura, K. M., Hayashi, T., Smith, G. M., Gallo, G., Thomas, G. Abstract: Dual Leucine-zipper Kinase (DLK, a MAP3K) mediates neuronal responses to diverse injuries and insults via c-Jun N-terminal Kinase (JNK) family Mitogen-activated Protein Kinases (MAPKs). It is unclear why DLK couples to JNKs in mammalian neurons versus other MAPKs, especially because some invertebrate DLK orthologs couple instead to the related p38 family MAPKs. Here we identify two mechanisms that potentially explain this DLK-JNK coupling. First, neural-specific JNK3, but not p38-MAPK, catalyzes positive feedback phosphorylation of DLK that further activates DLK and locks the DLK-JNK3 module in a highly active state. Furthermore, the pro-degenerative JNK2 and JNK3, but not the related JNK1, are endogenously palmitoylated. Moreover, palmitoylation targets both DLK and JNK3 to the same axonal vesicles and JNK3 palmitoylation is essential for pro-degenerative axonal retrograde signaling in vivo. These findings provide insights into DLK-JNK signaling relevant to multiple neuropathological conditions and answer long-standing questions regarding the selective pro-degenerative roles of JNK2/3. Copy rights belong to original authors. Visit the link for more info

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Green Bean Casserole? FREE Keto Recipe! from The DIRTY, LAZY, KETO No Time to Cook Cookbook

Play Episode Listen Later Nov 14, 2020 32:04

The holidays are just around the corner. It's time to plan easy keto recipes for the big family dinner. Today's podcast teaches you how to make a classic comfort food recipe - delicious Keto Green Bean Casserole! This free keto recipe is a sneak peek from the newest addition to the DIRTY, LAZY, KETO family: The DIRTY, LAZY, KETO No Time to Cook Cookbook: 100 Easy Recipes Ready in Under 30 Minutes. https://youtu.be/WQJ8mzdlegY Learn how to cook keto fast! This is the first of three recipes I'll be sharing with you from The DIRTY, LAZY, KETO No Time to Cook Cookbook. Learn keto meal prep short-cuts and share a laugh while learning how to make a mouth-watering, low carb meal with USA Today bestselling author, Stephanie Laska. Stephanie Laska lost 140 pounds and created DIRTY, LAZY, KETO. As shared on NBC's TODAY show, losing weight doesn't have to be so complicated, expensive, or take all day! Break the rules of the strict keto diet and have some fun. There is an easier way to keto and Stephanie will show you how! Dirty keto or lazy keto will help you get the same keto diet results. NEW! The DIRTY, LAZY, KETO No Time to Cook Cookbook: 100 Easy Recipes Ready in Under 30 Minutes (Simon & Schuster, 2021) is available for you to order now on Amazon, Barnes & Noble, or wherever you like to shop for books. If you enjoyed today's DIRTY, LAZY, KETO cooking video, please give it a thumbs up on YouTube, leave a comment, and subscribe to the DIRTY, LAZY, KETO channel. Turn on your notifications so you never miss an update! Thanks for watching and being part of the DLK community. The attached "Gobble Gobble Green Bean Casserole" is reprinted with permission from Adams Media, an imprint of Simon & Schuster, from The DIRTY, LAZY, KETO No Time to Cook Cookbook by Stephanie and William Laska (2021). Related episodes: Keto Christmas Gifts $20 or Less Holiday Cheat Meal? Should you Cheat on the Keto Diet?

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Fighting with My Family – Holiday Stress Can Lead to Family Fighting + Overeating #46 S.2

Play Episode Listen Later Nov 7, 2020 31:54

Fighting with My Family might be just a movie for some - but for many, it's a reality. Holiday stress often leads to family fighting. How do you deal? When stress levels are high, we use coping mechanisms to manage our feelings. These aren't always healthy, right? Overeating, spending too much money, drinking a lot... how we deal with stress isn't always healthy! In this week's DIRTY, LAZY, Girl podcast, we look at 6 ways to handle family drama and conflict. This holiday season, try using these dirty and lazy strategies to prevent family problems from getting out of hand. https://youtu.be/z0LtZ783hD4 Today's episode is sponsored by a new addition to the DLK family! Just in time for the perfect holiday gift, let me introduce you to The DIRTY, LAZY, KETO No Time to Cook Cookbook. This is the third cookbook in the DIRTY, LAZY, KETO series, each with a different twist. Readers have been asking for FAST recipes - easy keto meals they can make in a hurry. Help has arrived! I share 100 new delicious recipes that you can make in 30 minutes or less. That's fast! In each of the DIRTY, LAZY, KETO books, my goal is to chip away at the common excuses people use as to why they can’t lose weight. Keto is too complicated, too expensive, takes too much time… I’ve heard it all! The DIRTY, LAZY, KETO No Time to Cook Cookbook is here to help you cook healthy meals quickly. I share 100 amazing low carb recipes that you can easily make in under a half-hour, including prep time! Related Articles: Keto Cheat Meals Over the Holidays Family Support on Keto: Get the Help You Need

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Into The Void Podcast - Avsnittet om trallpunk

Into The Void Podcast

Play Episode Listen Later Sep 27, 2020 81:56

Magnus och Svempa pratar om musik som påverkar ens sätt att tänka när man är ung och hur mycket av det som sen stannar kvar. Vi snackar också om punken i början på 90-talet och om varför man måste sortera in saker i genrer. Och så har Magnus grävt i intervjuarkivet och klippt ihop en historia där medlemmar från Asta Kask, Strebers/Dia Psalma, DLK och Coca Carola berättar om trallpunkens uppgång och fall men det är också en betraktelse om betydelsen av musik när man är ung. Dessutom berättar vi om vad vi har lyssnat mest på den senaste tiden. Det hörs lite av: Om trallpunkenCharta 77 - Kungarna af stan IIStrebers - 39 stegAsdta Kask - De får aldrig migSterbers - Alla vackra barnCoca Carola - Ingenstanz (Live i Hallstahammar 9 mars 1996)Dia Psalma - Alla älskar digDLK - IshockeyfrisyrCoca Carola - Dimmornas land MusiktipsMarilyn Manson - We are chaosOrochen - In the city

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Coupled Control of Distal Axon Integrity and Somal Responses to Axonal Damage by the Palmitoyl Acyltransferase ZDHHC17

Play Episode Listen Later Sep 1, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.01.276287v1?rss=1 Authors: Niu, J., Sanders, S., Jeong, H.-K., Holland, S., Sun, Y., Collura, K., Hernandez, L., Huang, H., Hayden, M. R., Smith, G., Hu, Y., Jin, Y., Thomas, G. Abstract: After optic nerve crush (ONC), the cell bodies and distal axons of most retinal ganglion cells (RGCs) degenerate. RGC somal and distal axon degeneration were previously thought to be controlled by two distinct pathways, involving activation of the kinase DLK and loss of the axon survival factor NMNAT2, respectively. However, we found that mutual palmitoylation by the palmitoyl acyltransferase ZDHHC17 couples the DLK and NMNAT2 signals, which together form a 'trust, but verify system'. In healthy optic nerves, ZDHHC17-dependent palmitoylation ensures NMNAT-dependent distal axon integrity, while following ONC, ZDHHC17-dependent palmitoylation is critical for DLK-dependent somal degeneration. We found that ZDHHC17 also controls survival-versus-degeneration decisions in sensory neurons and identified motifs in NMNAT2 and DLK that govern their ZDHHC17-dependent regulation. These findings suggest that the control of somal and distal axon integrity should be considered as a single, holistic process, involving two palmitoylation-dependent pathways acting in concert. Copy rights belong to original authors. Visit the link for more info

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Episode 35 - Cuisine at Home + Dirty, Lazy, Keto

Must Love Food

Play Episode Listen Later Aug 25, 2020 38:53

Pam is joined by Stephanie Laska, author and founder of Dirty, Lazy, Keto (DLK). Stephanie is one of the authors featured in our Must Love Food Cookbook Summit. In her video, Stephanie shares her story of how, in her dirty, lazy, keto way, she lost 140 lb. and has kept it off for over seven years. In her video, she makes her taste-rockin' Friday-Night Wings with Big-Bang Sauce and shares some tips and products she's found to be helpful. Stephanie has written several DLK cookbooks and she also has a podcast, Dirty, Lazy, Girl. If you don't know Stephanie, or even if you do, she's quite inspirational, and fun(ny) — this is worth a listen (and her video is worth a watch)!

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Ep. 018: Is Laser Vision Correction Right For You? - with Curtin Kelley, MD

Healthy Eyes 101

Play Episode Listen Later Aug 16, 2020 41:31

Refractive eye surgery involves changing the refractive state of the eye to decrease one’s dependency on glasses or contact lenses. The first corneal refractive surgical procedure developed was radial keratotomy (RK). Corneal instability and progressive shifting of the refraction (glasses prescription) made this surgery obsolete. LASIK (Laser-Assisted In-Situ Keratomileusis) and PRK (PhotoRefractive Keratectomy) use the excimer laser to reshape the cornea to help focus the light rays onto the retina like glasses or contact lenses do. These laser vision correction (LVC) procedures can correct nearsightedness, farsightedness, and astigmatism.Patients who may not be good candidates for LVC:Thin corneasHigh glasses prescriptionsKeratoconusAutoimmune diseases like rheumatoid arthritisPerfectionistsPeople who need excellent nighttime vision, like truck drivers or airline pilotsCurrently on certain medications like Accutane/isotretinoin (or other acne medications)Large pupilsHistory of past corneal infectionsUnstable glasses prescriptionSevere dry eyesPresbyopia (decreased ability to see up close) starts in the mid-40s. If both eyes are lasered to correct their distance, then they will need reading glasses. Monovision is an option where one eye is set for distance and the other eye is set for or left with some nearsightedness.Nowadays, both eyes are usually lasered in the same sitting. The first step in LASIK is to use a femtosecond laser or a micro-keratome blade to make the corneal flap. In PRK, the top layer of cells (epithelium) is carefully scraped off. The excimer laser energy is then applied to the exposed cornea to reshape it. This laser may take up to ~50 seconds per eye. If PRK was performed, then a bandage contact lens is placed to help the epithelium to grow back and for pain control. With LASIK the vision may be fairly sharp immediately after the procedure. PRK has a slower recovery because the epithelium has to grow back onto the cornea. The final results of the PRK may not be seen for several weeks. PRK may be chosen because of thin corneas and for people who are in a profession where eye injuries can occur. LASIK has become the more popular procedure because of its quicker recovery and less discomfort.Complications may include corneal infections, intra-flap inflammation (diffuse lamellar keratitis (DLK)) in LASIK, halos at night, and difficulty driving at night. Ectasia (progressive thinning and warpage of the cornea) may be difficult to treat and the patient may need to wear hard contact lenses to improve their vision.The ICL (Implantable Contact Lens) is a refractive intraocular lens that is placed into the area behind the iris and the natural lens. This can treat high amounts of nearsightedness and astigmatism without having to sacrifice any corneal tissue.The SMILE (SMall Incision Lenticule Extraction) procedure utilizes the femtosecond laser to create a disc of corneal tissue that is removed. This procedure, which can correct nearsightedness and astigmatism, has not been used in the United States as much as in Europe and other countries.Here is another great resource on Laser Vision Correction.To find out more about Dr. Curtin Kelley, go to his practice website or follow his practice on Facebook. This is intended for informational and educational purposes only, and nothing in this podcast/blog is to be considered as recommending or rendering medical advice or treatment to a specific patient. Please consult your eye care specialist for proper diagnosis and treatment of any eye conditions that you may have.

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#26: Was erwartet uns auf dem Deutschen Logistik Kongress 2020 in Berlin? Mit Christoph Meyer (BVL)

BVL.digital Podcast

Play Episode Listen Later Aug 12, 2020 32:00

In dieser Folge des BVL.digital Podcast dreht sich alles um den Deutschen Logistik Kongress 2020. Dazu haben wir uns Christoph Meyer geladen, der bei der Bundesvereinigung Logistik (BVL) die Bereiche Forschung, Veranstaltungen, Inhalte, Wissen, Forschung und die Koordination des DLK verantwortet. Gemeinsam mit unserem Host Boris Felgendreher diskutiert Christoph Meyer unter anderem folgende Themen: - Was die BVL dazu bewegt hat, den DLK trotz Corona-Pandemie durchzuführen. - Welche Besonderheiten und Herausforderungen in der Organisation es in diesem ganz besonderen Jahr bisher gab. - Auf welche Änderungen sich Teilnehmer in diesem Jahr einstellen sollten. - Welche spannenden Möglichkeiten es geben wird, für Teilnehmer die diesmal nicht vor Ort sein können. - Ws es ist mit dem Jahresmotto "Nachhaltig gestalten - Winning the Next Decade" auf sich hat und warum es perfekt in diese Zeit passt. - Auf welche Themen, Highlights und Sprecher wir uns diesem Jahr freuen dürfen. - Und vieles mehr. Mehr Informationen zum Deutschen Logistik Kongress findet Ihr unter: https://www.bvl.de/dlk Das Programm zum DLK 2020 findet Ihr unter: https://www.bvl.de/files/1951/2142/2697/BVL_Deutscher_Logistik-Kongress_2020_Programm.pdf Mehr Informationen zu BVL.digital findet Ihr unter: www.bvl-digital.de

TIR-1SARM1 Inhibits Axon Regeneration

Play Episode Listen Later Jun 23, 2020

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.23.165852v1?rss=1 Authors: Julian, V., Byrne, A. B. Abstract: An injured axon has two choices, regenerate or degenerate. In many neurons, the result is catastrophic axon degeneration and a failure to regenerate. To coerce the injured nervous system to regenerate, the molecular mechanisms that regulate both axon regeneration and degeneration need to be defined. We found that TIR-1/SARM1, a key regulator of axon degeneration, inhibits regeneration of injured motor axons. Loss of tir-1 function both reduces the frequency with which severed axon fragments degenerate and increases the frequency of axon regeneration. The increased regeneration in tir-1 mutants is not a secondary consequence of its effects on degeneration. Rather, TIR-1 carries out each of these opposing functions cell autonomously by regulating independent downstream genetic pathways. While promoting axon degeneration with the DLK-1 mitogen activated protein kinase (MAPK) signaling cascade, TIR-1 inhibits axon regeneration by activating the NSY-1/ASK1 MAPK signaling cascade. Our finding that TIR-1 regulates both axon regeneration and degeneration provides critical insight into how axons coordinately regulate the two key responses to injury, consequently informing approaches to manipulate the balance between these responses towards repair. Copy rights belong to original authors. Visit the link for more info

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Room Decoration Ideas! Customize + Personalize #22 S.2

Play Episode Listen Later May 24, 2020 33:16

No matter what your goal is... you need an empowering space to get to work. I sure wish I had listened to this episode "back in the day." When I was writing the early drafts of DIRTY, LAZY, KETO, I had to fight to get a few minutes of peace and quiet on the family computer. I haven't had a space of my own since high school! I've wasted a lot of time and anguish over the years by not taking this topic seriously. Once you claim your space (for a home gym, DIRTY, LAZY, KETO cabinet in the kitchen, gardening shed, craft corner...), then it's time to set up shop. Pull out all the stops! Customize and personalize the space to make it more inviting. DIY room decoration can provide you with a surprising amount of motivation. Just look at what I was able to create below... I became motivated to create this DLK space thanks to this episode! With a little forethought and creativity, I transformed a noisy and crowded playroom into an inspiring and organized workspace. This project didn't cost an arm and a leg. I finished the transformation fast and on the cheap. Now that I have a quiet, inspirational place to work, I've become motivated to try making DIRTY, LAZY, KETO live videos. I hosted a virtual book launch party for DIRTY, LAZY, KETO Get Started Losing Weight While Breaking the Rules, and gave away dozens of sponsored prizes! But that's not all... I tried recording an upcoming podcast ON VIDEO (details to come on the DIRTY, LAZY, KETO YouTube channel!) and started a weekly FRIDAY LIVE Facebook Q/A for the Premium Supporters Group. Hopefully, listeners, you were able to “carve out some space” using the tips we shared in the last podcast episode, She-Shed – Cozy Corner episode. Now we are going to help you take your space to the next level with 5 Fast and Cheap DIY Tips to Customize and Personalize Your Space. The DIRTY, LAZY, Girl Podcast is a free resource provided by author Stephanie Laska to support you on your path to awesomeness (yup, that’s a word). Stephanie is the author and creator of DIRTY, LAZY, KETO. If you need a girlfriend to “tell it to you like it is”, check out the sassy and honest, DIRTY, LAZY, KETO Get Started Losing Weight While Breaking the Rules (St. Martin’s Press, 2020). Losing weight involves so much more than just changing what you eat. It’s a lifestyle change (or in my case, overhaul!). The DIRTY, LAZY, Girl Podcast is designed to support positive lifestyle changes and help get you to your goals. The DIRTY, LAZY, Girl podcast is available for you to download and subscribe (for free!) on ApplePodcasts, Spotify, IHeartRadio, GooglePodcasts, Stitcher, and even here on the website, www.DIRTYLAZYKETO.COM. Show your support of the program by leaving a positive review on ApplePodcasts. Here is how! On your iPhone, select the purple podcast icon. Using the search tool, type in DIRTY, LAZY, Girl. Click the thumbnail at the top (to open it up). Scroll down until you see the Ratings and Reviews section. Click on stars. Select five stars (I hope!). Scroll down and select “leave a review”. Add a snappy title, enter your review. Hit send. That’s IT! Thank you for your help. We might even read your review on the air! #KetoOn! Stephanie & Tamara, Co-Hosts of The DIRTY, LAZY, Girl Podcast

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87. Björnarna

Play Episode Listen Later Feb 4, 2020 116:42

Martin, Henke, Björn, Fredrik och Micke i bandet Björnarna snackar om kunglig behandling, Järncell, Sticky Fingers, starten, Östhammar, Uppsala, trallpunk, dialekter, Close Up-båten, Augustibuller, vuxenblöjpunk och Prescriptiondeath. Vidare till punk, trams, Radioaktiva Räker, Björn Afzelius, låtstöld, stekare, iPhone-inspelningar, DHL-bud, Nalles Ark, Lastkaj 14, Crashdïet, Strebers, DLK, Ebba Busch Thor och Fängelset.

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83. Kardborrebandet

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Play Episode Listen Later Dec 17, 2019 112:36

Gösta, Kim, Johanna, Jocke och Emil i bandet Kardborrebandet snackar om storyn, medlemsbyten, stage-gimpen Kulan, Eddie, Andy McCoy, 24 band i en text, Sörling, pingvin, fåglar, konflikter, Some Kind Of Monster, Radioaktiva Räker, ackord och Pastoratet. Vidare till punk, Falköping, Errol, portade i Göteborg, Sportlov, nya plattan Välkommen Till Fabriken, DLK, Close-Up-båten, tävling, Klagomuren, ZZ Top och Fat Mike.

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The Obstacle (Course Race) Is The Way with Scott Bennett

EXTRAordinary Podcast

Play Episode Listen Later Aug 13, 2019 66:32

How you do anything is how you do every thing Try Hard, Be Honest And Help other along the way. This is a Quote from Ryan Holliday’s book the Obstacle is the way. And it defines Scott Bennett. Scott also defines what I think of as a good ol’ boy from the hills of North Georgia. Although we are not related, he is my people. Everything from the way he talks to the way he walks. He is the thing I strive to be. Any given weekend you will find Scott packing in as many obstacle, trail or endurance races as time and travel will allow. That’s right, the weekends he only does one race are rare. And I'm not sure the last time he actually took a weekend off. Scott has made the obstacle his Way. He has learned that in every obstacle lies an opportunity. From planting grass seed with a spoon as a kid to torturous hour after hour on an OCR, how Scott does anything is exactly how he does everything. And the impact he has had on those around him definitely reflects that. his ability to see things through and overcome any obstacle is his most endearing quality. Learn how you too can make Your obstacle the way With Scott Bennett.

Avsnitt 115: Mart Hällgren från De Lyckliga Kompisarna

White Limo Rocks Podcast

Play Episode Listen Later Jul 6, 2019 27:06

I avsnitt 115 är Martin Hällgren från De Lyckliga Kompisarna gäst.Vi pratar bland annat om och att: Japan, Pokémon, trallpunksnerd, smaka räkskal, tågnerd, ha ett skrivbordsarbete, DLK, nya låtar, Tompa Eken, professionell, kapellmästare, behöva öva mer, Total Egon och så otroligt mycket mer. Avsnittet presenteras i samarbete med Strongstyle Clothing.Prenumerera, betygsätt och recensera podden på iTunes eller i din podapp så andra vet att vi finns.

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64. Skrammel

Play Episode Listen Later May 28, 2019 79:02

Daniel, Mathias, Martin och Viktor från bandet Skrammel snackar om medlemsbyten, dialekten, DLK, Räserbajs, Bad Religion, Slaveriet, Rör Mig Int och tvingande trall. Vidare till Millencolin, Winamp, Sommartider, Hoppborgen, tyska recensioner, HC, Västervik, musikaliskt geni, Hoola Bandoola, punk, Björnarna, gym, Kongressen, Grå Vardag, Sista Sekunden, Ett Liv Kvar, Myspace, Fredag Den 13:e och alla mammor!

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The Unexplained World 2019 relaunch with Edward Shanahan and Annette

The Unexplained World

Play Episode Listen Later Jan 7, 2019 60:00

The Unexplained World returns on January 6th 2019 with Edward Shanahan and Annette. This will be the 10th year of broadcasting The Unexplained World after taking a three year break from broadcasting the show. The past years of shows are being downloaded and now Edward and Annette bring a refreshed new show starting in 2019 with this broadcast. It will be a reintroduction of Chicago Psychic Medium and Paranormal Explorer Edward Shanahan and Pagan Truth Seeker Annette. Also Edward and Annette will discuss 'Vindication through the way of Spirits' and the coming broadcasts. Mr. David Kump joins the broadcast and what he will be providing on different broadcasts. Also the playing of song 'The Unimaginable Truth' by DLK and Captains of Liberty.

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50. Henke Brannerydh

Play Episode Listen Later Dec 26, 2018 125:16

Henke Brannerydh från Rockpoddden snackar om hur allt började, teknik och det första misstaget. Vidare till avsnitt, feedback, bli igenkänd på rösten, 100-festen, nervös för att intervjua punkare, DLK, In Flames, Johan Johansson och namnet på podden. Sämsta bandnamnet, ambulansförare, Migrationsverket, Bokassa, Metallica, Kjell-Arne, basist i badshorts, den bortrökta plattan, punk, Ramones, AC/DC, Biffen och massa tips.

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31. Trallpunk