Podcasts about cd133

support dispatch: https://citadeldispatch.com/donate ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠EPISODE: 133BLOCK: 843588PRICE: 1540 sats per dollarTOPICS: exchange traded funds changed the paradigm, supporting open source, embracing transparencyproject website: https://bitwiseinvestments.com/crypto-funds/bitcoin new to nostr? check out https://primal.net website: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://citadeldispatch.comnostr live chat: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://citadeldispatch.com/stream⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠nostr account: ⁠https://primal.net/odell⁠youtube: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.youtube.com/@citadeldispatch⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠stream sats to the show: ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.fountain.fm/(00:00:04) WBD Intro(00:02:27) Introduction to Citadel Dispatch(00:03:01) Introduction of Hong Kim, cofounder and CTO of Bitwise, and discussion on Bitcoin ETFs(00:04:28) Challenges faced during the 6-year process of working on the Bitcoin ETF(00:07:35) Discussion on the approval process and timeline of Bitcoin ETFs by the SEC(00:15:16) Reflections on the significance of having a Bitcoin ETF and the impact on the community(00:22:36) Comparison of assets under management in the Bitcoin ETF market(00:28:26) Discussion on the model of funding open source contributors through profits from the Bitcoin ETF(00:34:41) Explanation of the long-term commitment and financial implications of funding open source contributors(00:38:04) Discussion on the success of a debut and comparison to an IPO moment(00:39:10) Comparison of the ETF moment to a state change rather than a singular event(00:40:01) Challenges faced by financial advisors in including a Bitcoin ETF in portfolios(01:18:56) Bitcoin ETFs in kind redemptions(01:19:30) Importance of Self-Custody for Bitcoiners(01:21:08) Advantages of Bitcoin ETFs and In-Kind Possibility(01:30:52) Discussion on eCash and Financial Privacy(01:46:39) Progress and Urgency in Financial Privacy

In the eLife Podcast this month, signs that bees are oblivious to pesticides in nectar, sea anemone stinging strategies, a new means of cell-cell communication to share growth factors and other signals, how plants make a comeback when ice sheets retreat, and how the world's biggest bird uses wind and waves to good effect to minimise the costs of takeoff... Get the references and the transcripts for this programme from the Naked Scientists website

BUFFALO, NY- October 11, 2023 – A new research paper was published in Oncotarget's Volume 14 on October 4, 2023, entitled, “Inhibiting BRAF/EGFR/MEK suppresses cancer stemness and drug resistance of primary colorectal cancer cells.” Drug resistance is a major barrier against successful treatments of cancer patients. Gain of stemness under drug pressure is a major mechanism that renders treatments ineffective. Identifying approaches to target cancer stem cells (CSCs) is expected to improve treatment outcomes for patients. In their new study, researchers Astha Lamichhane, Gary D. Luker, Seema Agarwal, and Hossein Tavana from The University of Akron, University of Michigan and Georgetown University aimed to elucidate the role of cancer stemness in resistance of colorectal cancer cells to targeted therapies. “[...] we developed spheroid cultures of patient-derived BRAFmut and KRASmut tumor cells and studied resistance mechanisms to inhibition of MAPK pathway through phenotypic and gene and protein expression analysis.” They found that treatments enriched the expression of CSC markers CD166, ALDH1A3, CD133, and LGR5 and activated PI3K/Akt pathway in cancer cells. The team examined various combination treatments to block these activities and found that a triple combination against BRAF, EGFR, and MEK significantly reduced stemness and activities of oncogenic signaling pathways. This study demonstrates the feasibility of blocking stemness-mediated drug resistance and tumorigenic activities in colorectal cancer. “Our approach to identify mechanisms of drug resistance of patient-derived cancer cells to targeted therapies and develop effective treatments is promising toward cancer precision medicine.” DOI - https://doi.org/10.18632/oncotarget.28517 Correspondence to - Hossein Tavana - tavana@uakron.edu Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.28517 Subscribe for free publication alerts from Oncotarget - https://www.oncotarget.com/subscribe/ Keywords - cancer, drug resistance, cancer stem cells, patient-derived tumor model, colorectal cancer, combination treatment About Oncotarget Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science. To learn more about Oncotarget, please visit https://www.oncotarget.com and connect with us: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ X - https://twitter.com/oncotarget Instagram - https://www.instagram.com/oncotargetjrnl/ YouTube - https://www.youtube.com/@OncotargetJournal LinkedIn - https://www.linkedin.com/company/oncotarget Pinterest - https://www.pinterest.com/oncotarget/ Reddit - https://www.reddit.com/user/Oncotarget/ Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Oncotarget published this trending research paper on May 1, 2018, entitled, "Treatment of ovarian cancer by targeting the tumor stem cell-associated carbohydrate antigen, Sialyl-Thomsen-nouveau" by researchers from the Massachusetts General Hospital, Boston, MA; Siamab Therapeutics, Inc., Newton, MA; Harvard Medical School, Boston, MA. Abstract: Recurrent ovarian cancer (OvCa) is thought to result in part from the inability to eliminate rare quiescent cancer stem cells (CSCs) that survive cytotoxic chemotherapy and drive tumor resurgence. The Sialyl-Thomsen-nouveau antigen (STn) is a carbohydrate moiety present on protein markers of CSCs in pancreatic, colon, and gastric malignancies. We have demonstrated that human OvCa cell lines contain varying levels of cells that independently express either STn or the ovarian CSC marker CD133. Here we determine co-expression of STn and CD133 in a subset of human OvCa cell lines. Analyses of colony and sphere forming capacity and of response to standard-of-care cytotoxic therapy suggest a subset of OvCa STn+ cells display some CSC features. The effect of the anti-STn antibody-drug conjugates (ADCs) S3F-CL-MMAE and 2G12-2B2-CL-MMAE on OvCa cell viability in vitro and in vivo was also assessed. Treatment with S3F-CL-MMAE reduced the viability of two of three OvCa cell lines in vitro and exposure to either S3F-CL-MMAE or 2G12-2B2-CL-MMAE reduced OVCAR3-derived xenograft volume in vivo, depleting STn+ tumor cells. In summary, STn+ cells demonstrate some stem-like properties and specific therapeutic targeting of STn in ovarian tumors may be an effective clinical strategy to eliminate both STn+ CSC and STn+ non-CSC populations. Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.25289 DOI - https://doi.org/10.18632/oncotarget.25289 Full text - https://www.oncotarget.com/article/25289/text/ Correspondence to - Bo R. Rueda - brueda@mgh.harvard.edu Keywords - ovarian cancer, sialyl-Tn, antibody-drug conjugate, cancer stem cell, tumor-associated carbohydrate antigen About Oncotarget Oncotarget is a bi-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: SoundCloud - https://soundcloud.com/oncotarget Facebook - https://www.facebook.com/Oncotarget/ Twitter - https://twitter.com/oncotarget YouTube - https://www.youtube.com/c/OncotargetYouTube/ 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 https://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact MEDIA@IMPACTJOURNALS.COM 18009220957

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.09.289488v1?rss=1 Authors: Kotani, N., Nakano, T. Abstract: COVID-19 represents a real threat to the global population, and understanding the biological features of the causative virus (SARS-CoV-2) is imperative to aid in mitigating this threat. Analyses of proteins such as primary receptors and co-receptors (co-factors) that are involved in SARS-CoV-2 entry into host cells will provide important clues to help control the virus. Here, we identified host cell membrane protein candidates that were present in proximity to the attachment sites of SARS-CoV-2 spike proteins through the use of proximity labeling and proteomics analysis. The identified proteins represent candidate key factors that may be required for viral entry. Our results indicated that a number of membrane proteins, including DPP4, Cadherin-17, and CD133, were identified to co-localize with cell membrane-bound SARS-CoV-2 spike proteins in Caco-2 cells that were used to expand the SARS-CoV-2 virion. We anticipate that the information regarding these protein candidates will be utilized for the future development of vaccines and antiviral agents against SARS-CoV-2. Copy rights belong to original authors. Visit the link for more info

En el 33º congreso anual de la Sociedad Europea de Reproducción Humana (ESHRE por sus siglas en inglés) celebrado en Ginebra se ha presentado un prometedor estudio en el que se han utilizado células madre para hacer crecer endometrios atróficos.El resumen del artículo se puede citar aquí:https://www.ncbi.nlm.nih.gov/m/pubmed/27005892/?i=1&from=CD133+%20bone%20marrow-derived%20Asherman’s%20syndrome%20and%20endometrial%20atrophy:%20a%20pilot%20cohort%20st

In a Presidential Election year when the Big Two Parties have selected widely disliked candidates, is it possible to vote None of the Above into the Presidency? In this episode, by learning how the electoral college works, we explore our options for realistically denying the Presidency to the chosen candidates of the Republican and Democratic Parties. *This episode has been updated from it's original version for information accuracy. Please support Congressional Dish: Click here to contribute with PayPal or Bitcoin; click the PayPal "Make it Monthly" checkbox to create a monthly subscription Click here to support Congressional Dish for each episode via Patreon Mail Contributions to: 5753 Hwy 85 North #4576 Crestview, FL 32536 Thank you for supporting truly independent media! United States Electoral College U.S. Electoral College: About the Electors, National Archives and Records Administration. The 2016 Presidential Election, National Archives and Records Administration. History of Faithless Electors, Fair Vote Democracy Directory of Representatives, United States House of Representatives State Control of Electors, Fair Vote Presidential Elections Reform Program Sound Clip Sources: FBI News Conference: FBI Director James Comey News Conference, Federal Bureau of Investigation, CSPAN, July 5, 2016. Video: Gary Johnson & Drones, YouTube, May 3, 2016. Television News Clip: Hillary Clinton in 2015: Email Server was Permitted, CNN, July 12, 2015. Video: Gary Johnson & Drones, YouTube, May 3, 2016. Videos: Video: The Trouble with the Electoral College By CGP Grey, YouTube, November 7, 2011. Recommended Congressional Dish Episodes Congressional Dish Episode 126: The Presidential Primary, By Jennifer Briney, May 23, 2016. Additional Reading Article: A Reminder of the Permanent Wars: Dozens of U.S. Airstrikes in Six Countries By Missy Ryan, The Washington Post, September 8, 2016. Article: US election: Why is Clinton's Foundation So Controversial? By Anthony Zurcher, BBC News, August 23, 2016. Article: Trump University: It's Worse Than You Think By John Cassidy, The New Yorker, June 2, 2016. Article: The Definitive Roundup of Trump’s Scandals and Business Failures By Celina Durgin, National Review, March 15, 2016. Article: Pew Research Center will Call 75% Cellphones for Surveys in 2016 By Kyley McGeeney, Pew Research Center, January 5, 2016. Article: Clintons Personally Paid State Department Staffer to Maintain Server By Rosalind S. Helderman and Carol D. Leonnig, The Washington Post, September 5, 2015. Additional Information Report by the Office of Inspector General: Office of the Secretary: Evaluation of Email Records Management and Cybersecurity Requirements Office of Evaluations and Special Projects, May 2016. Commission on Presidential Debates Polls Used by Commission on Presidential Debates 2000 Official Presidential General Election Results, State Elections Offices Election Polling Methodology, Pew Reseach Center. Music Presented in This Episode Intro & Exit: Tired of Being Lied To by David Ippolito (found on Music Alley by mevio) Cover Art Design by Only Child Imaginations, with a special thanks to photographer Dennis "Chunga" Cieklinski for the awesome photo of the Bennett School for Girls.

The vast majority of colorectal cancer (CRC)-related deaths is caused by the metastatic spread of tumor cells to distant organs rather than by the growth of the primary tumor. However, until today the mechanisms involved in CRC metastasis are not completely understood. For cancer cells the epithelial-mesenchymal transition (EMT) is thought to represent a prerequisite to invade adjacent tissue and form metastases at distant sites. Transcription factors, cytokines or oncogenic signaling pathways play an important role in the regulation of the EMT program. Recently, the oncoprotein c-MYC was shown to induce EMT, e.g. by enhancing SNAIL expression. Previously an interaction between c-MYC and the transcription factor ZNF281/ZBP-99 has been described. However, so far it remained elusive which upstream signals regulate ZNF281 levels or activity and furthermore, what functions are mediated by ZNF281, which may contribute to the c-MYC-mediated tumor progression. Here, it could be shown that SNAIL and miR-34a/b/c control the expression of ZNF281 in a coherent feed-forward-loop: the EMT-transcription factor SNAIL directly induced ZNF281 transcription and repressed miR-34a/b/c, thereby alleviating ZNF281 from direct down-regulation by miR-34. Moreover, p53 activation led to a miR-34a-dependent down-regulation of ZNF281 expression. Additionally, in CRC cells it could be demonstrated, that ectopic ZNF281 expression induces EMT. This process was mediated by and dependent on the direct induction of SNAIL. Furthermore, ectopic ZNF281 increased migration/invasion, and enhanced β-catenin activity. Expression of the stemness markers LGR5 was directly and CD133 indirectly induced by ectopic ZNF281 expression, which also increased sphere formation. Conversely, in CRC cells the experimental down-regulation of ZNF281 resulted in a mesenchymal-epithelial transition (MET), inhibited migration/invasion and decreased sphere formation. Additionally, repression of ZNF281 led to decreased formation of lung metastases by CRC cells in a xenograft mouse tumor model. Furthermore, ZNF281 protein expression was indirectly elevated by ectopic c-MYC expression. Inactivation of ZNF281 prevented the induction of EMT by c-MYC or SNAIL. The analysis of tumor samples revealed that ZNF281 expression increases during CRC progression and correlates with tumor recurrence. Taken together, the results identify ZNF281 as a new EMT-promoting transcription factor, which contributes to metastasis formation in CRC. In the future, this knowledge may be exploited for therapeutic and diagnostic purposes in cancer therapy.

Thu, 17 Jul 2014 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/17323/ https://edoc.ub.uni-muenchen.de/17323/1/Lechner_Axel.pdf Lechner, Axel ddc:610, ddc:600, Medizinische Fakul

In Anbetracht der nach wie vor verheerenden Prognose, der Patienten mit diagnostiziertem Pankreaskarzinom gegenüberstehen (Jemal, Siegel et al. 2008), ist die Entwicklung neuer Behandlungsansätze dringend erforderlich. Studien konnten zeigen, dass Pankreaskarzinome eine kleine Population undifferenzierter Zellen enthalten, die anhand der Expression von CD133 oder CD44/CD24 charakterisiert werden können (Hermann, Huber et al. 2007; Li, Heidt et al. 2007), die ausschließlich tumorigen sind und zudem hoch resistent gegenüber Chemotherapeutika (Hermann, Huber et al. 2007; Jimeno, Feldmann et al. 2009). Die Behandlung mit Gemcitabin führt demnach nicht zu einer Eliminierung der Tumorstammzellen, sondern vielmehr zu ihrer relativen Anreicherung, was zeigt, dass aktuelle Standardtherapeutika primär auf die differenzierteren und schnell proliferierenden Tumorzellen wirken. Daher wird, obwohl die differenzierteren Zellen Hauptbestandteil des Tumors sind, deren Auslöschung nicht zu einer Verminderung des tumorigenen Potenzials führen, welches von den Tumorstammzellen ausgeht. Die vorliegende Studie zeigt, dass eine alleinige Inhibition des Shh oder des mTOR Signalweges nicht ausreicht, den Tumorstammzell-Pool signifikant zu vermindern, eine Blockade beider Signalwege aber in Kombination mit Gemcitabin (CRG) durchaus. In der Tat führte eine Kombinationsbehandlung in vitro zu einem vollständigen Verlust des tumorigenen Potenzials, wie durch die anschließenden in vivo Transplantationsversuche bewiesen werden konnte. In Mäusen mit etablierten Pankreastumoren von kultivierten Zellen oder humanem Primärgewebe führte die Dreifach-Behandlung (CRG) in vivo zu einer Regression der Tumoren, einer Eliminierung der Tumorstammzellen und in der Folge zu einem deutlich verbesserten Langzeitüberleben.

Thu, 20 Jan 2011 12:00:00 +0100 https://edoc.ub.uni-muenchen.de/12644/ https://edoc.ub.uni-muenchen.de/12644/1/Damianoff_Karin.pdf Damianoff, Karin ddc:610, ddc:600, Medizinische

Astrocytes perform many functions in the adult brain and even act as neural stem cells after brain injury (Buffo et al., 2008) or in regions where neurogenesis persists, e.g. in the subependymal zone of the lateral ventricle. The stem cell astrocytes possess an apicobasal polarity as they are coupled by adherens junctions to neighbouring ependymal cells and possess an apical membrane domain with CD133 and Par complex proteins and a basolateral membrane domain including contact of processes to the basement membrane (BM). This is notably different from parenchymal astrocytes that only have contacts to the BM under physiological conditions. The major underlying question is how differences between neural stem cells and 'normal' astrocytes are generated and how polarity mechanisms may be involved in generating this difference. Here, I set out to determine the role of BM contact and the Par complex for astrocyte function in the normal brain parenchyma as well as in the neurogenic niche. First, I examined the influence of BM-mediated signaling by conditional deletion of β1-integrin, one of the major BM receptors in the CNS. The use of specific Cre lines resulted in a loss of β1-integrin protein only at postnatal stages either in both glia and neurons or specifically in neurons. Strikingly, only the former resulted in reactive gliosis, with the hallmarks of reactive astrocytes comprising astrocyte hypertrophy and upregulation of the intermediate filaments GFAP and Vimentin as well as pericellular components, such Tenascin-C and the 473HD proteoglycan. This reaction to the loss of β1-integrin was further accompanied by non-cell autonomous activation of microglial cells. However, neither reactive astrocytes nor microglia divided, suggesting that the loss of β1-integrin-mediated signaling is not sufficient to elicit proliferation of these cells. Interestingly, this partial reactive gliosis appeared in the absence of cell death and blood-brain barrier disturbances. As these effects did not appear after neuron-specific deletion of β1-integrin, we conclude that β1-integrin-mediated signaling in astrocytes is required to promote their acquisition of a mature, non-reactive state. Interestingly, neural stem cell astrocytes in the SEZ were not affected in their proliferation and fate, suggesting that β1-integrins are not involved in the regulation of these stem cell properties. However, loss of β1-integrins interfered with the normal dedifferentiation of astrocytes into stem cells after brain injury. Next, I examined the role of Cdc42, a key activator of the Par complex, but also a mediator of β1-integrin signalling in adult stem cell astrocytes. Therefore, I genetically deleted this small RhoGTPase in astroglia at adult stages. In contrast to what has been observed during development, loss of Cdc42 had no influence on proliferation or fate of subependymal zone astrocytes. These effects on adult astroglia-like stem cells differ profoundly from effects on parenchymal astrocytes upon injury. Here, deletion of Cdc42 resulted in severe defects of astrocyte polarity as measured by centrosome reorientation and oriented process extension in the scratch assay in vitro. In vivo, astrocytes could still orient towards the injury site suggesting the existence of compensating signaling pathways. However, the increase of astrocyte numbers around the injury site was reduced. Impaired proliferation certainly contributes to this phenotype. Most importantly, loss of Cdc42 resulted in a significantly increased size of brain injury enlightening the importance of this pathway in the wound reaction towards brain injury. Conversely, no effects were seen by Cdc42 deletion in astrocytes in the absence of injury, suggesting that integrin-mediated signaling from the BM maintains the hallmarks of mature non-reactive astrocytes while Cdc42, most likely via activation of the Par complex, regulates polarity and dedifferentiation after injury. Taken together, this work elucidated for the first time specific signaling pathways regulating the role of astrocytes as stem cells during wound reaction of the injured brain.

Adult neural stem cells, as the source of life-long neurogenesis, reside in the subependymal zone (SEZ) in the lateral wall of the lateral ventricles and in the dentate gyrus of the hippocampus. In both neurogenic regions, subsets of glial fibrillary acidic protein (GFAP) expressing astrocytes are found, that have been shown to act as neural stem cells. So far, it is not known how to distinguish these stem cell astrocytes from other astrocyte populations within the SEZ. Towards this end we decided to isolate a subpopulation of adult SEZ astrocytes that expresses the CD133 by FACS. GFP-positive cells in the SEZ from hGFAP/eGFP mice that were also CD133+ve comprised all neurosphere-initiating cells that were self-renewing and multipotent from the SEZ. Moreover, single cell neurosphere analysis showed 70% efficiency in neurosphere formation. Further more Cre-mediated fate mapping of this double-positive population showed their contribution to adult neurogenesis. Transcriptional profiling of the GFP/CD133-double-positive cells allowed us to a) determine their similarity at the transcriptome level to both ependymal cells AND astrocytes and b) to identify their unique molecular neural stem cell signature. We also discovered that astrocytes outside this neurogenic niche could go some way towards dedifferentiation into neural stem cells. We have previously described (Buffo et al., PNAS 2008) a population of astrocytes in the adult cerebral cortex after stab wound injury that dedifferentiates as far to form multipotent and self-renewing neurospheres. Now we succeeded to establish the factor responsible for this dedifferentiation and sufficient to elicit the dedifferentiation response even in cells that were not exposed to injury. These data will be presented. Taken together, our work allows for the first time, the identification and characterization of the astrocyte sub-types acting as neural stem cells.

ABCG2 is a transporter protein that has the ability to efflux many drugs and fluorescent dyes. Primitive haematopoietic stem cells highly express ABCG2 and the expression level decreases as these cells differentiate indicating a possible role of this transporter in HSC. In the present study, we have analyzed the role of ABCG2 in early haematopoietic stem cells by constitutively expressing ABCG2 in human CB derived CD133+ cells. This constitutive expression of ABCG2 demonstrated an enhancement of primary CFCs in vitro, including the most primitive clonogenic cells the CFU-GEMM (n=12, p