Podcasts about cdc2

* Testing will never end, they're demanding MORE and charging to punish unvaccinated. But CDC wants to end PCR. What 2 billionaires will profit? And if the test can't distinguish between Covid and flu, how does it distinguish between “variants”?* Fauci pushes for masks on vaccinated children and knows that LOCAL CONTROL is the key to rolling out mandates — and also where WE STOP THEM* Senicide — the deliberate killing of the elderly — exposed by nurses* Another GOP politician Gov Ivey goes to war with the unvaccinated* Airsoft gun PHOTO panics plane crew and passengers * The limp Olympics - fear, loathing, virtue signaling & astronomical costs* NFL is modeling employer coercion, takes MORE steps to punish unvaccinatedTOPICS by TIMECODE2:11 FAA changes the rules to keep Bezos from getting his “astronaut” certification, LOL. Astronauts now have to be doing something “safety” related.4:41 Picture of an airsoft gun freaks out crew and passengers. Delays flight. Czech Republic moves to create a “2A” protection in their constitution but miss the central idea.9:37 Mississippi Attorney General begs Supreme Court to overturn Roe v Wade. When will we STOP doing the same thing over and over again? Judicial Supremacy is NOT Constitutional. Roe v Wade is NOT the “law of the land” as EVERY SCOTUS judge says, it's a key part of their power grab15:36 Pelosi: The Worth of Children Depends on YOUR Net Worth. For rich people like her, kids are a “blessing”. But for the poor, we should kill their kids in the name of “fairness”. She's embracing the ancient practice of child sacrifice to gain prosperity22:25 Limp Olympics — fear, loathing, virtue signaling, escalating astronomical costs — then there's the South Korean coverage41:09 39% Effective? 16% Effective — Actual Data. Remember the one-upmanship at the beginning? Now more data is in and it's not just “breakthrough” infections. It's useless — but dangerous. But as Dr. Astrid Stuckelberger points out, the vaccine slavery will NEVER end53:08 Latest report from CDC on Trump Shots and the children they're killing. And Gov Kay Ivey (GOP) wants to blame unvaccinated people for what politicians like her are doing to the country1:00:12 About the same number dying (they presume) as dying from cars. So the solution is to ban cars also1:04:31 Senicide? Deliberate murder of elderly documented by nurses.1:12:01 Letter from a nurse in Wyoming on the push by hospitals to coerce the jab — and the push back1:34:01 The NFL, whether or not you watch it, is being used to set the tone for draconian employer coercion. Every day they are adding new sanctions for unvaccinated — and firing unvaccinated staff1:44:51 “You might take the jab IF…”1:48:53 Fauci: Key to MASK Dictatorship is LOCAL Control. Local is where the rubber meets the road. And THAT will be the focus of “Mr. Science” and the CDC2:42:40 CDC Admits PCR Doesn't Work. Can't tell Covid from flu. So how can they distinguish “delta variant” from “lambda” or the original? And what 2 billionaires just bought a test company that will likely replace the PCR?Find out more about the show and where you can watch it at TheDavidKnightShow.comIf you would like to support the show and our family please consider subscribing monthly here: SubscribeStar https://www.subscribestar.com/the-david-knight-showOr you can send a donation throughZelle: @DavidKnightShow@protonmail.comCash App at:  $davidknightshowBTC to:  bc1qkuec29hkuye4xse9unh7nptvu3y9qmv24vanh7Mail: David Knight POB 1323 Elgin, TX 78621

Volume 11, Issue 25 of @Oncotarget reported that to examine the role of RSK in AML, the authors analyzed apoptosis and the cell cycle profile following treatment with BI-D1870, a potent inhibitor of RSK. BI-D1870 treatment increased the G2/M population and induced apoptosis in Acute Myeloid Leukemia cell lines and patient Acute Myeloid Leukemia cells. Therefore, the authors investigated whether BI-D1870 potentiates the anti-leukemic activity of vincristine by targeting mitotic exit. Combination treatment of BI-D1870 and vincristine synergistically increased mitotic arrest and apoptosis in acute leukemia cells. These data show that BI-D1870 induces apoptosis of AML cells alone and in combination with vincristine through blocking mitotic exit, providing a novel approach to overcoming vincristine resistance in AML cells. Dr. Kathleen M. Sakamoto from Stanford University School of Medicine said, "Acute myeloid leukemia (AML) is a genetically and phenotypically heterogeneous hematologic malignancy characterized by the accumulation of immature myeloid blasts with resultant peripheral blood cytopenia." Treatment of cells with microtubule targeting agents, including paclitaxel and the vinca alkaloid vincristine, blocks the proper formation of the mitotic spindle through inhibition of microtubule dynamics, resulting in the prolonged mitotic arrest of cancer cells. MTAs-treated mitotic arrested cells may undergo apoptosis in mitosis, however, the rapid degradation of Cyclin B due to an insufficient SAC leads to the mitotic slippage into tetraploid G1 stage in resistant cells. Though vinca alkaloid microtubule-destabilizing compounds have shown clinical efficacy against various hematological malignancies and were included in combination chemotherapy of the VAPA study, they are not currently used in induction chemotherapy for AML due to their high toxicity against lymphoid cells and rapid degradation by myeloperoxidase in AML cells. In this study, they demonstrate that BI-D1870, a potent inhibitor of RSK, induces mitotic arrest, and apoptosis in AML cells without inhibiting CDC2 and CDC25C. Furthermore, BI-D1870 synergizes with vinca alkaloid vincristine in AML cells, suggesting that inhibition of mitotic exit with BI-D1870 could be a promising novel approach for AML therapy in combination with MTAs. The Sakamoto Research Team concluded in their Oncotarget Research Paper that BI-D1870 is a reversible pan-RSK inhibitor, showing > 500-fold higher activity for RSK than other AGC kinases. BI-D1870 also inhibits the activity of PLK1, Aurora-B, MELK, PIM3, MST2, and GSK3β at higher concentrations than for RSK. BI-D1870 and BRD7389 have been reported to inhibit proliferation and significantly increase the G2/M population in melanoma cells. BI-D1870 does not have proper physicochemical properties for clinical application. Future structure-activity relationships study for BI-D1870 is required to improve solubility and pharmacokinetic profiles for in vivo preclinical and clinical studies. Sign up for free Altmetric alerts about this article DOI - https://doi.org/10.18632/oncotarget.27630 Full text - https://www.oncotarget.com/article/27630/text/ Correspondence to - Kathleen M. Sakamoto - kmsakamo@stanford.edu Keywords - acute myeloid leukemia, BI-D1870, RSK, vincristine, spindle assembly checkpoint About Oncotarget Oncotarget is a weekly, peer-reviewed, open access biomedical journal covering research on all aspects of oncology. To learn more about Oncotarget, please visit https://www.oncotarget.com or connect with: Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Oncotarget is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957x105

Fabienne Billat, plus connue sous le pseudo Fadouce, est consultante en communication digitale et en transformation numérique pour les entreprises. Speaker, elle accompagne également des dirigeants. Fabienne fait partie du board de la transformation digitale de la Caisse des Dépôts, le CDC2, et a crée la délégation Femmes du Numérique du Syntec Numérique pour Lyon et sa région. Fabienne partage ici sa réflexion sur la transformation numérique en entreprise, sous l'angle de l'implication des managers, des équipes.

Marriage is a stage designed to show forth the realities of the gospel. This seminar will set forth the biblical vision of marriage and give practical counsel of how we can reorient our hearts and actions so our marriages better reflect the profound realities they illustrate.

Is mental illness due to sin or disease? This session discusses the controversy on this topic, discusses biblical definitions of illness and sin and offers suggestions for how to be helpful in the midst of the controversy.

Many counselees are living with a prior psychological diagnosis. How can we help them with compassion and humility? This session will help you learn to speak biblically to heart and life issues of counselees regardless of diagnosis.

The gospel of grace needs to be at the heart of how we understand marriage roles. Both husband and wife have a unique part to play that shows forth the relationship of Christ with his church. This session will focus on the role of the husband in marriage.

The gospel of grace needs to be at the heart of how we understand marriage roles. Both husband and wife have a unique part to play that shows forth the relationship of Christ with his church. This session will focus on the role of the wife in marriage.

Marriage requires lifelong maintenance to keep it healthy and strong. It takes a lot of effort to guard and grow your marriage but the reward is more than worth it. This session will discuss many practical ways to preserve and strengthen your marriage.

God's revelation in Scripture is complete. While every believer is called to seek God's revealed moral will, some go beyond this and claim that God speaks to them. How does God guide us today? How are we to understand his will for our lives?

The goal of parenting is to make your children ready to live wisely on their own. Parents must recognize that their relationship with their adult child is very different from what it was when the child was small. One of the biggest mistakes made by Christian parents is to treat young adults as if they were still small children. How can parents foster healthy relationships with their adult children and pursue peace?

What should parents do when their children rebel? Christian parents must be aware of two extremes: giving up too soon because of personal hurt feelings, anger and bitterness ... and tolerating and enabling sin. How can we beware of not being manipulated and becoming enablers of their sinful lifestyle?

Those advocating formulas often assume a form of “parental determinism” – the (unbiblical) belief that how well you follow their formula determines how your kids turn out. Parents who depend on these can tend toward pharisaical pride, as if we can save our kids by our good works. Parenting is not about following an extra-biblical man-made formula; it is about the gospel.

Parents often look for a formula which will guarantee that their kids will turn out right. Many “Christian” approaches to parenting are legalistic. It is very important to distinguish between what Scripture commands versus one of many possible ways to fulfill our responsibilities to God. Some make their particular methodology “law”, while failing to acknowledge that other approaches are equally valid ways to fulfill biblical commands.

God designed marriage to be a lifelong covenant of companionship. Marriage is worth fighting for. Some are called by God to remain in hard marriages. Divorce (and remarriage) without biblical grounds is sinful and adulterous. This session unpacks the surrounding issues and questions about this difficult subject.

How can we make our sexual relationships in marriage all that they should be? We need to think about our marriage and sex lives through a gospel lens. Gracious sex gives to your spouse freely, just as God has given to you - treating him/her better than he/she deserves.

God created sex to be a blessing. It is part of God's perfect and holy creation but is often twisted sinfully. Idolatry, more than adultery, is the key to understanding sexual sin. Even something which is good can become sinfully idolatrous when we desire it more than we desire God, are willing to sin in order to get it, or react sinfully when we don’t get what we want.

God is the owner and source of all wealth. We need to maintain a balanced perspective on finances. Money can be good but it is also dangerous. Christians need to learn the secret of contentment as they work hard and smart to make a living. Make it your goal to be wise, not rich!

Every family experiences communication breakdown. The key to our relationships with each other is our relationship with God (and vice versa). We need to grant forgiveness when we have been wronged. We need to learn to listen in love. Are we more concerned about being heard, or hearing?

The main function of glucocorticoids in corticotroph cells is to suppress proopiomelanocortin, the precursor of the stress hormone adrenocorticotropin (ACTH). Cushing’s disease is a rare but severe neuroendocrine condition caused by partially glucocorticoid resistant corticotroph adenomas, which consequently secrete excessive amounts of ACTH in an uncontrolled fashion. The patients suffer from chronic hypercortisolism due to excessive stimulation of the adrenal glands by ACTH to produce glucocorticoids. Impairing mutations of the glucocorticoid receptor (GR) only sporadically explain the reduced glucocorticoid sensitivity in the adenomas – the molecular mechanism behind the partial resistance is poorly understood. The function of GR depends on direct interactions with the molecular chaperone Hsp90. Both the reduction and overexpression of Hsp90 impedes GR activity in different experimental settings. Therefore, the expression of the inducible Hsp90α isoform was determined in biopsy specimens of corticotroph pituitary adenomas from patients with Cushing’s disease. Its strong overexpression compared to normal human pituitary cells paved the way to study its role in the function of corticotroph adenomas using small molecules which target Hsp90. The three distinct Hsp90 inhibitors 17–AAG, Novobiocin and Silibinin showed antiproliferative effects in AtT–20 cells through the degradation of the oncogenic client kinase Cdc2, a hallmark of pharmacologic inhibition of Hsp90. Surprisingly, only the N–terminal Hsp90 inhibitor 17–AAG caused the degradation of GR, as was reported also for other Geldanamycin–based Hsp90 inhibitors. Neither Silibinin nor the C–terminal Hsp90 inhibitor Novobiocin affected GR protein levels. These converging effects led to the assumption that both compounds bind to the same domain in Hsp90. It was shown here that Novobiocin displaces Silibinin from the C–terminal domain of Hsp90, and that these compounds dissociate mature GR from Hsp90 at the biochemical level. As a result, increased levels of mature receptor were present in the cell able to bind glucocorticoids with high affinity. This novel molecular mechanism proved to potentiate GR transcriptional activity in AtT–20 cells. The potentiation in GR activity also led to enhanced suppression of ACTH elicited by low concentrations of Dexamethasone in AtT–20 cells and in primary cultures of human corticotroph adenomas from patients with Cushing’s disease. In contrast, Silibinin did not show effects on rat normal pituitary cells. Finally, Silibinin reduced tumor growth, partially reverted hormonal alterations, and alleviated symptoms in a mouse allograft model for Cushing’s disease. These results suggest that the regulation of GR sensitivity by overexpressed Hsp90 may represent a pharmacologically reversible mechanism in the pathogenesis of this disease. Together, a proof of principle is provided that the clinically safe Hsp90 inhibitor Silibinin potentially restores glucocorticoid sensitivity in corticotroph adenomas in vitro and in vivo, and that it might be used to treat Cushing’s patients in the future.

We have recently reported that a polymorphism in the cell division cycle (CDC2) gene, designated Ex6 + 7I/D, is associated with Alzheimer's disease (AD). The CDC2 gene is located on chromosome 10q21.1 close to the marker D10S1225 linked to AD. Active cdc2 accumulates in neurons containing neurofibrillary tangles (NFT), a process that can precede the formation of NFT. Therefore, CDC2 is a promising candidate susceptibility gene for AD. We investigated the possible effects of the CDC2 polymorphism on cerebrospinal fluid (CSF) biomarkers in AD patients. CDC2 genotypes were evaluated in relation to CSF protein levels of total tau, phospho-tau and beta-amyloid (1-42) in AD patients and control individuals, and in relation to the amount of senile plaques and NFT in the frontal cortex and in the hippocampus in patients with autopsy-proven AD and controls. The CDC2 Ex6 + 7I allele was associated with a gene dose-dependent increase of CSF total tau levels (F-2,F- 626 = 7.0, p = 0.001) and the homozygous CDC2Ex6 +7II genotype was significantly more frequent among AD patients compared to controls (p = 0.006, OR = 1.57, 95% CI 1.13-2.17). Our results provide further evidence for an involvement of cdc2 in the pathogenesis of AD. Copyright (C) 2005 S. Karger AG, Basel.

Cardiomyocytes cease to divide shortly after birth and an irreversible cell cycle arrest is evident accompanied by the downregulation of cyclin-dependent kinase activities. To get a better understanding of the cardiac cell cycle and its regulation, the effect of functional recovery of the mitosis-promoting factor (MPF) consisting of cyclin B1 and the cyclin-dependent kinase Cdc2 was assessed in primary cultures of postmitotic ventricular adult rat cardiomyocytes ( ARC). Gene transfer into ARC was achieved using the adenovirus-enhanced transferrinfection system that was characterized by the absence of cytotoxic events. Simultaneous ectopic expression of wild-type versions of cyclin B1 and Cdc2 was sufficient to induce MPF activity. Reestablished MPF resulted in a mitotic phenotype, marked by an abnormal condensation of the nuclei, histone H3 phosphorylation and variable degree of decay of the contractile apparatus. Although a complete cell division was not observed, the results provided conclusive evidence that cell cycle-related events in postmitotic cardiomyocytes could be triggered by genetic intervention downstream of the G1/S checkpoint. This will be of importance to design novel strategies to overcome the proliferation arrest in adult cardiomyocytes.