Podcasts about febs lett

References Biomolecules. 2020 Jul 7;10(7):1008. FEBS Lett 2021.595, Issue8. Pages 1107-1131 Cell Res. 2022 Mar 2;32(4):327–328. Cell Chem Biol.2024 Jul 18;31(7):1264-1276.e7.Peterson &Lesh. 1974. "Unbroken Chain" on [Live from the Mars Hotel} lp Grateful Dead https://youtu.be/T5FN06LFfHk?si=RgFd7kBKAAJ6YKK0 Hunter&Lesh1970 "Box of Rain" on [American Beauty] lp. https://youtu.be/nxjvo4BRf-Y?si=e9MyF6FdLM2ylZaG Schubert, F. 1826. (Liszt Variation thereof.). ""Standchen.D889. https://youtu.be/9h35VSz2Kkc?si=ch4W4TX9iefj0t1C --- Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

References Biomedicines 2023, 11(7), 1804 BMC Biology. 2011. 9:85 Cancer Res. 2011 Jan 15;71(2):293-7. FEBS Lett.2019.593.17:2428-2451 Verdi, G. 1841. Nabucco Overture https://youtu.be/OseGETWEnCo?si=LhiIQV-N0-_Z_s-s Lennon&McCartney. 1966 "For No One". Beatles: Revolver. https://youtu.be/sep5E3ssXLQ?si=WLtMrP-Xq279qZXl --- Send in a voice message: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/message Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support

Bone is not just a passive scaffold that supports our body. It is also an active endocrine organ that secretes hormones that regulate various aspects of our physiology, from energy metabolism to brain function. One of these hormones is osteocalcin, which has been extensively studied by Gerard Karsently and his team at Columbia University. In this podcast, we will explore the fascinating discoveries that Karsently and his colleagues have made about osteocalcin and its role in health and disease. Osteocalcin is a protein that is produced by bone cells called osteoblasts. It is then released into the bloodstream, where it can reach different organs and tissues and exert its effects. Osteocalcin has been shown to enhance insulin secretion by the pancreas, testosterone production by the testes, muscle function during exercise, memory formation and mood regulation by the brain, and even the ability to cope with stress. Osteocalcin also has anti-aging properties, as it can prevent or reverse some of the decline in physiological functions that occurs with age. The levels of osteocalcin in the blood are not constant. They vary depending on several factors, such as diet, exercise, stress and age. These interactions create a complex network of communication between bone and other organs that helps to maintain homeostasis and adapt to changing conditions. Karsently's research has opened new avenues for understanding the biology of bone and its impact on whole-body physiology. It has also revealed new potential therapeutic targets or strategies for treating or preventing various metabolic, reproductive, cognitive and emotional disorders. In this podcast, we will dive deeper into the fascinating world of osteocalcin and bone endocrinology with Gerard Karsently himself. Useful Links: Berger JM, Karsenty G. Osteocalcin and the physiology of danger. FEBS Lett. 2022;596(5):665-680. doi:10.1002/1873-3468.1425

Episode 347 is an updated guide to somatropic hormone and GOD did I go crazy on this one! I honestly want to know more about growth hormone than anyone alive and thus, begins this string of GH based guides! I DID finally discuss the MoA for how GH causes localized fat loss which really had me excited since no one in our industry has EVER talked about this so that definitely was an interesting avenue to go down! Below I am going to reference a lot of the literature for this hormone that I was read through over the past few years on this topic so please DO NOT TAKE MY WORD FOR THIS - READ THESE YOURSELF! Keep in mind this is a brief snippet of every bit of literature on the topic however. REFERENCES   Daughaday WH, Rotwein P. Insulin-like growth factors I and II. Peptide, messenger ribonucleic acid and gene structures, serum, and tissue concentrations. Endocr Rev. 1989;10:68–91. [PubMed] [Google Scholar] Jones JI, Clemmons DR. 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In questa puntata del podcast Pillole parliamo dell’aspetto scientifico dell’amore romantico.- - - - - - - - -Fonti:S. Zeki, The neurobiology of love, FEBS Lett, 2007Z. Zou, H. Song, Y. Zhang, X. Zhang, Romantic Love VS Drug Addiction May Inspire a New Treatment for Addiction, Front Psychol, 2016- - - - - - - - -Per ulteriori informazioni visita il sito web www.pillolepodcast.it

Episode 293 is your updated complete guide to injectable glutathione! Glutathione (GSH) has so much misunderstanding and misinformation in our industry that I want to ensure people understand a lot of the interactions and MoA going on with this compound. It has tremendous application as a "health", restoration, and progression tool when utilized in the proper setting. Sit back, take notes, and enjoy the references I'll attach to this episode!   REFERENCES Aniya Y., Imaizumi N. (2011). Mitochondrial glutathione transferases involving a new function for membrane permeability transition pore regulation. Drug Metab. Rev. 43 292–299 Arakane F., King S. R., Du Y., Kallen C. B., Walsh L. P., Watari H., et al. (1997). Phosphorylation of steroidogenic acute regulatory protein (StAR) modulates its steroidogenic activity. J. Biol. Chem. 272 32656–32662 10.1074/jbc.272.51.32656 Armeni T., Cianfruglia L., Piva F., Urbanelli L., Luisa Caniglia M., Pugnaloni A., et al. (2014). 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FEBS Lett. 579 2327–2333 10.1016/j.febslet.2005.03.027 Basso E., Fante L., Fowlkes J., Petronilli V., Forte M. A., Bernardi P. (2005). Properties of the permeability transition pore in mitochondria devoid of Cyclophilin D. J. Biol. Chem. 280 18558–18561 10.1074/jbc.C500089200 Beer S. M., Taylor E. R., Brown S. E., Dahm C. C., Costa N. J., Runswick M. J., et al. (2004). Glutaredoxin 2 catalyzes the reversible oxidation and glutathionylation of mitochondrial membrane thiol proteins: implications for mitochondrial redox regulation and antioxidant DEFENSE. J. Biol. Chem. 279 47939–47951 10.1074/jbc.M408011200 Benipal B., Lash L. H. (2013). Modulation of mitochondrial glutathione status and cellular energetics in primary cultures of proximal tubular cells from remnant kidney of uninephrectomized rats. Biochem. Pharmacol. 85 1379–1388 10.1016/j.bcp.2013.02.013 Brand M. D. (2010). The sites and topology of mitochondrial superoxide production. Exp. 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Hepatology 36 326–335 10.1053/jhep.2002.34943    •••SUPPORT OUR SPONSORS•••   (COACHING) Alex - www.theprepcoach.com   (FREE OPEN FORUM w/ EXCLUSIVE VIDEOS) http://www.theprepcoachforum.com   (SUPPLEMENTS) www.projectad.me___use discount code “BFR25” to save off your order!   (RESEARCH CHEMS) www.maresearchchems.net___use discount code “alex15” to save off your order!   (SPECIALTY SUPPS) www.masupps.com___use discount code “alex20” to save off your order!   (BULK SUPPLEMENTS) www.truenutrition.com___use discount code “AXK5” to save off your order!       •••FIND THE EPISODES•••   ITUNES:https://itunes.apple.com/us/podcast/beastfitness-radios-podcast/id1065532968   LIBSYN:http://beastfitnessradio.libsyn.com   VIMEO: www.vimeo.com/theprepcoach        •••PREP COACH APPAREL•••   https://teespring.com/stores/the-prep-coach-apparel    

This episode: Fruit fly gut microbes can mediate non-genetic traits passed from parents to offspring! Thanks to Dr. Per Stenberg for his contribution! Download Episode (10.0 MB, 10.9 minutes) Show notes: Microbe of the episode: Bifidobacterium breve News item Takeaways Heritability of traits is essential for evolution; if an ability can't be passed on from generation to generation, then natural selection can't act on it on a population-wide level. An organism's genome is the source of most heritable traits, as DNA gets passed on to offspring, but a number of other ways of passing on traits have been discovered, in the field of epigenetics. In this study, the gut microbes from fruit flies raised in one temperature could affect the gene expression of their offspring raised in a different temperature, compared to flies that had been kept at the latter temperature over both generations. While the effects on fly fitness or behavior are not yet known, these results suggest that gut microbes, transmitted from parents to offspring, could be another mechanism of heritability. Journal Paper: Zare A, Johansson A-M, Karlsson E, Delhomme N, Stenberg P. 2018. The gut microbiome participates in transgenerational inheritance of low-temperature responses in Drosophila melanogaster. FEBS Lett 592:4078–4086. Other interesting stories: Bacteria living in alfalfa plants seem to extend roundworm lifespans (paper) Whole fruit fly microbe community affects whether flies live longer or reproduce more Hot spring archaea have unusual membranes that help tolerate the heat   Email questions or comments to bacteriofiles at gmail dot com. Thanks for listening! Subscribe: Apple Podcasts, RSS, Google Play. Support the show at Patreon, or check out the show at Twitter or Facebook

Glimepiride is a novel sulfonylurea for the treatment of type II-diabetic patients exhibiting different receptor binding kinetics to β-cell membranes with 8–9-fold higher koff rate and 2.5–3-fold higher kon rate compared to glibenclamide (see accompanying paper (Müller, G. et al. (1994) Biochim. Biophys. Acta 1191, 267–277)). To elucidate the molecular basis for this differential behaviour of glimepiride and glibenclamide, direct photoaffinity labeling studies using β-cell tumor membranes were performed. [3H]Glimepiride was specifically incorporated into a membrane polypeptide of Mr = 65000 under conditions, which led to predominant labeling of a 140 kDa protein by [3H]glibenclamide (Kramer, W. et al. (1988) FEBS Lett. 229, 355–359). Labeling of the 140 kDa protein by [3H]glibenclamide was inhibited by unlabeled glimepiride and, vice versa, glibenclamide inhibited labeling of the 65 kDa protein by [3H]glimepiride. The 65 kDa protein was also specifically photolabeled by the sulfonylurea [125I]35623, whereas an 4-azidobenzoyl derivative of glibenclamide, N3-[3H]33055, exclusively labeled a 33 kDa protein. Competitive Scatchard analysis of [3H]glimepiride-binding and [3H]glibenclamide-binding to RINm5F cell membranes using glibenclamide and glimepiride, respectively, as heterologous displacing compounds yielded non-linear plots. These findings may be explained by cooperative interactions between the 140 and 65 kDa sulfonylurea-binding proteins. The possibility that sulfonylureas of different structure have different access to the 140 and 65 kDa receptor proteins due to the β-cell membrane barrier was investigated by photoaffinity labeling of solubilized β-cell membrane proteins. Interestingly, solubilization of β-cell tumor membranes led to a shift of specific [3H]glibenclamide binding from the 140 kDa to the 65 kDa binding protein, exclusively, and to an increased labeling of the 65 kDa protein by [3H]glimepiride. The labeling of a unique protein is in agreement with similar Kd values measured for both sulfonylurcas upon solubilization of β-cell tumor and RINm5F cell membranes (see accompanying paper). Furthermore, competitive Scatchard plots of [3H]glimepiride binding to solubilized RINm5F cell membrane proteins in the presence of glibenclamide and vice versa approximate linearity suggesting loss of cooperativity between the 140 kDa glibenclamide-binding and 65 kDa glimepiride-binding proteins upon solubilization. The physiological significance of the differential interaction of glimepiride and glibenclamide with different binding proteins was also substantiated by photoaffinity labeling of RINm5F cells leading to labeling of a 140 kDa protein by [3H]glibenclamide and of a 65 kDa protein by [3H]glimepiride. In conclusion, this report presents the first evidence that different sulfonylurea drugs bind to different components of the sulfonylurea receptor complex which are characterized by different accessibility for the drugs.

Cleavage of the disulfide bond linking the heavy and the light chains of tetanus toxin is necessary for its inhibitory action on exocytotic release ofcatecholamines from permeabi1ized chromaffin cells [(1989) FEBS Lett. 242, 245-248; (1989) J. Neurochern., in press]. The related botulinum A toxin also consists of a heavy and a light chain linked by a disulfide bond. The actions ofboth neurotoxins on exocytosis were presently compared using streptolysin O-permeabilized bovine adrenal chromaffin cells. Botulinum A toxin inhibited Ca2 +-stimulated catecholamine release from these cells. Addition of dithiothreitollowered the effective doses to values below 5 nM. Under the same conditions, the effective doses of tetanus toxin were decreased by a factor of five. This indicates that the interchain S-S bond of botulinum A toxin must also be split before the neurotoxin can exert its effect on exocytosis.