Podcasts about f344

It is an amazing time to be alive. We have more modern conveniences than the wealthiest person on Earth could have imagined just thirty years ago.We have an abundance of food, climate-controlled air, and flavors that surpass our wildest dreams.However, there is one downside. This life of comfort and convenience is detrimental to our health. We are more obese, metabolically unhealthy, and miserable than we have any right to be. Dr. Gus Vickery, M.D., has written a book to illustrate the path out of "Comforville."In this episode, Gus and I discuss what inspired him to write a book that offers a path out of this perilous life of extreme comfort.Escaping Comfortville: Dr. Gus Vickery's Guide to Health in the Modern WorldIn this episode of The Healthy CEO, Dr. Gus Vickery introduces his new book, 'Escape from Comfortville.' The book, inspired by his successful 'Authentic Health,' explores how modern comforts have negatively impacted health. Dr. Vickery shares his motivation behind writing the book and details its central themes, including nutrition, physical activity, sleep, breath, and stress management. He emphasizes the importance of creating healthier environments and fostering supportive communities. The book is presented as a compelling story aimed at simplifying health principles to make them accessible and impactful for a wide audience.00:00 Introduction: The Embarrassment of Promoting a Book01:00 Welcome Back to the Healthy CEO01:27 Discussing the New Book and Its Principles01:54 Book Recommendation: The Art of Resilience04:34 The Journey of Writing Authentic Health15:21 The Evolution of Health Principles21:51 The Story of Comfortville27:42 The Grueling Kenyan Rite of Passage29:33 Mental Toughness and Overcoming Obstacles29:55 The Value of Stress and Training30:27 The Comfort Crisis and Its Impact31:34 Inspiration to Pursue Health33:59 The Importance of Basic Health Fundamentals39:12 Introducing Authentic Health's Supplement Line39:52 The Essential Nutrients: F1, F2, and F344:37 The Role of Essential Amino Acids50:00 The Book: Escape from Comfortville54:48 Final Thoughts and Call to Action

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.05.327155v1?rss=1 Authors: Kozlova, A., Butler, R. R., Zhang, S., Ujas, T., Zhang, H., Steidl, S., Sanders, A. R., Pang, Z. P., Vezina, P., Duan, J. Abstract: Rodents are frequently used to model drug addiction, yet their genetic relevance to human addictive behaviors especially the mounting genome-wide association study (GWAS) findings is poorly understood. Considering a possible gateway drug role of nicotine (NIC), we modeled NIC addiction, specifically NIC sensitization (SST) and self-administration (SA), in F1 progeny of inbred Envigo rats (F344/BN) and conducted integrative genomics analyses. We unexpectedly observed male-specific NIC SST and a parental effect of SA only present in paternal F344 crosses. Transcriptional profiling in the ventral tegmental area (VTA) and nucleus accumbens (NAc) core and shell further revealed sex and brain region-specific transcriptomic signatures of SST and SA. We found that genes associated with SST and SA were enriched for those related to synaptic processes, myelin sheath, and tobacco use disorder or chemdependency. Interestingly, SST-associated genes were often downregulated in male VTA but upregulated in female VTA, and strongly enriched for smoking GWAS risk variants, possibly explaining the male-specific SST. For SA, we found widespread region-specific allelic imbalance of expression (AIE), of which genes showing AIE bias towards paternal F344 alleles in NAc core were strongly enriched for SA-associated genes and for GWAS risk variants of smoking initiation, likely contributing to the parental effect of SA. The transcriptional signatures of sex-specific nicotine SST and SA suggest a mechanistic link between genes underlying these processes and human nicotine addiction, providing a resource for understanding the biology underlying the GWAS findings on human smoking and other addictive phenotypes. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.08.05.238725v1?rss=1 Authors: Johnson, S. A., Zequeira, S., Turner, S. M., Maurer, A. P., Bizon, J. L., Burke, S. N. Abstract: Mnemonic similarity task performance, in which a known target stimulus must be distinguished from similar lures, is supported by the hippocampus and perirhinal cortex and is known to decline in advanced age. Interestingly, disrupting hippocampal activity leads to mnemonic discrimination impairments when lures are novel, but not when they are familiar. This observation suggests other brain structures can support discrimination abilities as stimuli are learned. The prefrontal cortex (PFC) is critical for retrieval of remote events and executive functions, such as working memory, and is also particularly vulnerable to dysfunction in aging. Importantly, the medial PFC is reciprocally connected to the perirhinal cortex and neuron firing in this region coordinates communication between lateral entorhinal and perirhinal cortices to presumably modulate hippocampal activity. This anatomical organization and function of the medial PFC suggests that it contributes to mnemonic discrimination; however, this notion has not been empirically tested. In the current study, young adult male and female F344 x Brown Norway F1 hybrid rats were trained on a rodent object-based mnemonic similarity task, and surgically implanted with guide cannulae targeting prelimbic and infralimbic regions of the medial PFC. Prior to mnemonic discrimination tests, rats received PFC infusions of the GABAA agonist muscimol. Analyses of expression of the neuronal activity-dependent immediate-early gene Arc in medial PFC and adjacent cortical regions confirmed muscimol infusions led to neuronal inactivation in the infralimbic and prelimbic cortices. Moreover, muscimol infusions in PFC impaired mnemonic discrimination performance relative to the vehicle control across all testing blocks when lures shared 50-90% feature overlap with the target. Thus, in contrast to prior results from rats given hippocampal muscimol infusions, PFC inactivation impaired target-lure discrimination regardless of the novelty or familiarity of the lures. These findings indicate the PFC plays a critical role in mnemonic similarity task performance, but the time course of PFC involvement is dissociable from that of the hippocampus. Copy rights belong to original authors. Visit the link for more info

Proteomics Reveals Acute Pro-inflammatory and Protective Responses in Rat Kupffer Cells and Hepatocytes after Chemical Initiation of Liver Cancer and after LPS and IL-6, Proteomic analysis of cells in the early stages of Herpes Simplex Virus Type-1 infection reveals widespread changes in the host cell proteome, Proteomic changes in the hypothalamus and retroperitoneal fat from male F344 rats subjected to repeated light-dark shifts

Proteomics Reveals Acute Pro-inflammatory and Protective Responses in Rat Kupffer Cells and Hepatocytes after Chemical Initiation of Liver Cancer and after LPS and IL-6, Proteomic analysis of cells in the early stages of Herpes Simplex Virus Type-1 infection reveals widespread changes in the host cell proteome, Proteomic changes in the hypothalamus and retroperitoneal fat from male F344 rats subjected to repeated light-dark shifts

The therapeutic potential of systemically or locally injected bone marrow cells (BMC) or mesenchymal stem cells in myocardial infarction (MI) is a very controversial issue. Using human placental alkaline phosphatase (hPLAP) as a genetic marker for cell tracking, we examined the therapeutic efficacy and the homing of intravenously administered, hPLAP labeled cells in marker tolerant, immunocompetent rats after induction of MI. The marker enzyme hPLAP provides superb histological detection quality in paraffin and plastic sections. The influx of bone marrow-derived cells during tissue repair was monitored in wild-type inbred Fischer 344 rats reconstituted with bone marrow from transgenic F344 rats expressing hPLAP under the control of the ubiquitous R26 promoter. Four months post-MI, we found that the mesenchymal cells in the scar tissue were almost exclusively of local origin. Intravenous administration of 1x107 BMC from hPLAP transgenic donors administered 1 week post-MI profoundly reduced the infiltration of the infarction site by bone marrow-derived cells, and also the infarction area. No differentiation of endogenous nor exogenous BMCs was observed. To examine the homing of intravenous hPLAP labeled BMC in MI we established a background-free syngeneic model for long-term histological cell tracking in the absence of immune-mediated rejection of labeled cells in immunocompetent animals. Skin grafts showed that neonatal exposure of wild-type F344 rats to hPLAP transgenic F344 cells results in lifelong tolerance to hPLAP expressing tissues and cells. Using this model of neonatally tolerized marker tolerant rats, we showed that only very few hPLAP labeled BMC injected intravenously one week post-MI homed to the infarction site. Therefore, we hypothesize that the beneficial effect of intravenous BMC on left ventricular remodeling after MI is caused by systemic immunomodulation.

Background: Immune- mediated rejection of labeled cells is a general problem in transplantation studies using cells labeled with any immunogenic marker, and also in gene therapy protocols. The aim of this study was to establish a syngeneic model for long-term histological cell tracking in the absence of immune-mediated rejection of labeled cells in immunocompetent animals. We used inbred transgenic Fischer 344 rats expressing human placental alkaline phosphatase (hPLAP) under the control of the ubiquitous R26 promoter for this study. hPLAP is an excellent marker enzyme, providing superb histological detection quality in paraffin and plastic sections. Results: Transplantation of cells from hPLAP transgenic (hPLAP-tg) F344 rats into wild-type ( WT) F344 recipients failed because of immune-mediated rejection. Here we show that this problem can be overcome by inducing tolerance to the marker gene by transplantation of bone marrow from hPLAP-tg F344 rats into WT F344 hosts after lethal irradiation, or by neonatal exposure of WT F344 rats to hPLAP-tg F344 cells. As proof-of-principle, we injected bone marrow cells (BMC) from hPLAP-tg rats into the knee joint of marker tolerant, bone marrow-transplanted WT rats, and found successful engraftment and differentiation of donor cells. In addition, hPLAP-tg BMC injected intravenously in neonatally tolerized WT F344 hosts could be traced in lymph nodes, 2 months post-injection. Conclusion: In combination with the excellent marker hPLAP, marker tolerant animals may open up new perspectives for all experiments requiring long-term histological tracking of genetically labeled cells.