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CGM Academy Louisian Group

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Nikolai Kornilov
Nikolai Kornilov

Concerts During Nfr


The Thomas & Mack Center is the only place in Las Vegas for you to watch all of the rodeo action including bronco and bull busting of the Wrangler NFR. The arena transforms itself into a perfect place for the dirt to fly during the performances. Each night is sponsored by a different entity with giveaways at your seat and at the door when you enter. The sightlines at the arena are ideal for viewing all of the rodeo events and there is sure to be an entertaining clown or two to help keep the contestants safe. The arena offers numerous choices for food and drink with plenty of VIP seating available such as boxes and party suites. Get there early and take a stroll through the grounds where you can visit with contestants and their animals. Each is sure to bring all of the excitement that this world class event brings, so make sure you get in to watch the rodeo action.




Concerts During Nfr



The remarkable, and for decades untold, story of Elizebeth Smith Friedman. Her genius for breaking codes saved countless lives during WWll. I can't help but be amazed by this pioneer cryptanalyst. Directed by Chana Gazit.


Who was Chavela? Creating a new persona, she broke the mold of the traditional ranchera singer and opened a door for the LGBTQ community in Mexico and beyond. Co-directors Catherine Gund and Daresha Kyi examine the complicated life of a trailblazer. Her concerts were legendary and cathartic, which you will see when you watch this doc.


The first wave of the inducible gene network up-regulated by pathogen-stimulated mononuclear cells encodes a variety of effector proteins with pleitropic biological activities. This class of primary immediate early (IE) genes codes for potent pro-inflammatory cytokines and chemokines that play a prominent role during the manifestation of inflammatory response. In an attempt to better understand induction mechanisms for such genes, I have focused on those coding for human interleukin-1? (IL1B) and tumor necrosis factor ? (TNF), which exhibit both transient IE induction as well as cell-type restriction. Employing a combined approach using cell lines and primary cells, reporter transient transfection, chromatin conformational capture and immunoprecipitation, evaluation of transcript integrity, ectopic expression in a non-competent cell type, and comparison to mouse orthologs, I have determined that a complex array of mechanisms interplay in order to distinctly regulate the Toll-like receptor (TLR) signaling-dependent induction of these two important pro-inflammatory genes whose deregulation provides the etiology for numerous diseases. Prior to induction, TNF exhibited pre-bound TATA Binding Protein (TBP) and paused RNA Polymerase II (Pol II), which are the hallmarks of poised IE genes. In contrast, IL1B is stringently regulated by long-distance chromosome gyrations, multistep activation through a unique doubly-paused Pol II which, in association with the monocyte lineage factor Spi1/PU.1 (Spi1), maintains a low TBP and Pol II occupancy prior to activation. Activation and DNA binding of the transcription factors C/EBP? and NF-?B resulted in de novo recruitment of TBP and Pol II to IL1B in concert with a permissive state for elongation mediated by the recruitment of the positive elongation factor b (P-TEFb). This Spi1-dependent mechanism for IL1B transcription, which is unique for a rapidly-induced/poised IE gene, was more dependent upon P-TEFb than was the case for the TNF gene. Nucleosome occupancy and chromatin modification analyses of the IL1B and TNF promoters, revealed activation-specific changes in chromatin marks that are supportive for nucleosome clearance and formation of nucleosome free regions (NFR). Furthermore, ectopic expression of Spi1, along with a TLR surrogate (over-expressed TNF receptor associated factor 6, TRAF6), in a cell line incompetent for IL1B transcription, is observed to prime the cell's endogenous genome for IL1B induction by appropriately phasing promoter nucleosomes and recruiting paused Pol II in a manner reminiscent of that observed in competent monocytes. Here I report a novel connection between the metabolic state of cells and HIF-1? in regulating murine Il1b gene expression. With regard to the lipopolysaccharide (LPS) unresponsive state known as endotoxin tolerance, my data revealed that following transient induction, IL1B and TNF remained marked with paused Pol II complexes for up to 24 hours post-stimulation. Upon subsequent LPS exposure, tolerized TNF remained in an unresponsive paused state, while IL1B resumed transcription due to recruitment of positive elongation kinase P-TEFb. Emerging evidence suggests that inflammatory responses of LPS/TLR4 activated macrophages are interconnected with metabolic pathways, resulting in the shift of energy utilization by the cells. Here I report that inhibition of either phosphoinositide 3-kinase (PI3K) or glucose metabolism had a greater affect on the transcriptional response of Il1b than of Tnf. The differences between these two genes, especially for endotoxin tolerance, suggest that il1b may play a distinct role from tnf in chronic inflammation. 041b061a72


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