Jsi 124 pathway
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1. The document presents the discovery of JSI-124, a selective inhibitor of the JAK/STAT3 pathway, which was identified from screening a library of compounds for inhibition of STAT3 phosphorylation in cancer cells. 2. JSI-124 was found to reduce phospho-STAT3 levels in multiple human cancer cell lines and block STAT3 DNA binding and gene transcription, inhibiting tumor growth. 3. JSI-124 selectively targeted STAT3 signaling over other pathways and showed potent antitumor activity against human tumor xenografts in mouse models, demonstrating its potential as an anticancer therapeutic targeting the STAT3 pathway.
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Proinflammatory Actions of Thromboxane Receptors to Enhance Cellular Immune R...Federal University of Bahia
TP receptors augment cellular immune responses and inflammatory tissue injury. Mice lacking the TP receptor, which binds thromboxane A2, show reduced T cell proliferation in response to mitogens and alloantigens. They also show attenuated tissue injury in a cardiac transplant model of inflammation. Thus, thromboxane signaling through the TP receptor enhances immune responses and inflammation, suggesting that specific inhibition of this receptor may reduce inflammation without the side effects of broad COX inhibition by NSAIDs.journal dental - gingival
This study examined the effects of cyclosporine A (CsA) on human gingival epithelial cells in vitro and the role of transforming growth factor beta 1 (TGF-β1). The results showed that CsA induced changes in cell morphology from cobblestone to spindle-shaped and altered protein and mRNA expression levels of epithelial-mesenchymal transition (EMT) markers. Pretreatment with a TGF-β1 inhibitor reversed the CsA-induced changes, suggesting CsA induces EMT in gingival cells dependent on or partially dependent on TGF-β1. The study provides further evidence that CsA can induce EMT in gingiva through altering EMT markers and effectors.
Lepow Day Poster 2
1) Researchers identified differential methylation of the GRIN2D gene in colon cancer cells using reduced representation bisulfite sequencing, finding it demethylated in approximately 60% of cell lines. 2) They confirmed this epigenetic alteration led to upregulated GRIN2D expression and assessed its role in the cancer phenotype. 3) Knockdown of GRIN2D expression in demethylated RKO colon cancer cells using shRNA corresponded to reduced cell growth, suggesting GRIN2D demethylation contributes to the tumor cell phenotype. Future replication of these findings is needed to fully understand the significance.
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This document discusses signal transduction in cells. It describes the three stages of cell signaling as extracellular receptors, intracellular receptors, and second messengers that transmit signals into cells to elicit physiological responses. It notes that integrin receptors on the cell membrane play a role in cell attachment and signaling from extracellular matrix components. Cooperative signaling between integrin receptors and receptor tyrosine kinases determines cellular processes like survival, apoptosis, proliferation and differentiation.
Cell signalling 1
Cell signaling involves communication between cells through extracellular signaling molecules that bind to receptor proteins on the cell surface or inside the cell. These receptors activate intracellular signaling pathways that lead to changes in target proteins and cell behavior. The major types of cellular signaling pathways are those using membrane receptors, including ion channel-linked receptors, enzyme-linked receptors, and G protein-coupled receptors, which activate intracellular signaling proteins upon ligand binding.
G protein signal
1. G-proteins bind GTP and control intracellular signaling pathways. They exist in two states - active when bound to GTP and inactive when bound to GDP.
2. G-proteins are tightly regulated by accessory proteins that modulate their cycling between GTP-bound and GDP-bound states.
3. The heterotrimeric G-proteins transmit signals from cell surface receptors to enzymes and channels. They are stimulated by receptors, act on effectors, and are regulated by nucleotide exchange and hydrolysis.
Cell signaling3
The document summarizes G protein-coupled receptor (GPCR) signaling. It discusses how different GPCRs are coupled to different G proteins that activate various downstream effectors like adenylyl cyclase, phospholipase C or ion channels. It provides examples of specific GPCRs like beta-adrenergic receptors and muscarinic acetylcholine receptor and their signaling mechanisms. It also describes the role of second messengers like cAMP, IP3 and DAG in GPCR signaling.
Cell signalling 2
This document discusses G protein-coupled receptors (GPCRs), which are the largest family of membrane receptors in the human genome. GPCRs have seven transmembrane domains and signal by interacting with G proteins. They regulate many important physiological processes and are involved in many diseases. The document outlines the structure and function of GPCRs and G proteins, including how GPCRs activate G proteins, the different classes of GPCRs, mechanisms of GPCR regulation like phosphorylation and desensitization, and the roles of GTPases in general.
Cell signalling 1
Cell signaling involves communication between cells through extracellular signaling molecules that bind to receptor proteins on the cell surface or inside the cell. These receptors activate intracellular signaling pathways that lead to changes in target proteins and cell behavior. The major types of cellular signaling pathways are those using membrane receptors, including ion channel-linked receptors, enzyme-linked receptors, and G protein-coupled receptors, which activate intracellular signaling proteins upon ligand binding.
Cell Signalling
Cell signaling involves the transmission and reception of information between cells through signal molecules. Signal molecules can act through direct cell contact, over long distances via neurons, locally through paracrine signaling, or systemically through endocrine signaling. Signal molecules bind to membrane receptors on target cells and initiate intracellular responses through ion channels, enzymes, or G-proteins. This allows for complex and specific cell communication critical to multicellular organism function.
Cell signaling
Cells communicate through signaling molecules that are detected by receptors on other cells. Signals are transmitted across the cell membrane by signal transduction pathways and cause changes in cell function. Signals may target nearby (paracrine), distant (endocrine), or adjacent (juxtacrine) cells. Ion channels in the cell membrane are important for signal transduction and are classified by their method of gating, such as ligand-gated channels that open in response to neurotransmitters.
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Poster Filippa Pettersson ICDT 2010
This study investigated the mechanisms by which the HDAC inhibitor vorinostat induces apoptosis in acute myeloid leukemia (AML) cells. The results showed that vorinostat causes early DNA damage and activation of p38 MAPK in AML cell lines. Activation of p38 was required for vorinostat-induced G2/M cell cycle arrest and apoptosis. However, the role of p38 activation varied among different HDAC inhibitors, being pro-apoptotic for vorinostat but not necessary for apoptosis induced by other inhibitors. This highlights the importance of understanding specific mechanisms of individual HDAC inhibitors.
Inhibition of glutathione by buthionine sulfoximine enhanced the anti-cancer ...
Multiple myeloma (MM) is an incurable blood cancer. Melphalan is an alkylating agent given prior to stem cell transplantation to MM patients. Increased glutathione confers resistance to melphalan. This study investigate the effect of inhibition of glutathione by BSO in preclinical models of MM. Pretreatment with BSO enhanced the anti-cancer effect of melphalan in cell lines and animal models. BSO and melphalan combination was well tolerated by animals and enhanced the survival as compared to controls, BSO and melphalan alone. BSO enhanced depth and duration of responses induced by melphalan. In the combination group, majority of treated animals achieved complete response (CR) and more than 20% had maintained CR. Also, the survival of animals was doubled after combination treatment as compared to BSO or melphalan alone. Mechanistic investigation demonstrated that BSO enhanced melphalan induced DNA damage, caspase cleavage and apoptosis. The combination also achieved multi-logs of cells kills in nine human multiple myeloma cell lines and primary MM cells isolated from blood and bone marrows. Interestingly, the effect of BSO and melphalan combination was abolished when cells were treated with N-acetyl cysteine and sodium thiosulfate but not with vitamin C and vitamin E. This observation suggests that effect of BSO is primarily driven by its ability to deplete glutathione and therefore preventing melphalan detoxification. Together, this study provides framework for testing the combination in a Phase I trial.
sclabas2003
This document discusses a study that investigated how inhibiting the epidermal growth factor receptor (EGFR) signaling pathway with the anti-EGFR monoclonal antibody IMC-C225 affects nuclear factor-kappa B (NF-κB) activation and regulation of apoptosis genes in human pancreatic cancer cells. The study found that IMC-C225 treatment blocked EGFR activation in pancreatic cancer cells, leading to decreased NF-κB DNA binding activity. This downregulation of NF-κB by IMC-C225 resulted in decreased expression of the anti-apoptotic genes bcl-xl and bfl-1. Therefore, targeting the NF-κB pathway with an anti-EGFR antibody may help restore apoptosis in pancreatic cancer cells and
sclabas2005
1) Aspirin inhibited constitutive NF-κB activity and Cox-2 expression in human pancreatic carcinoma cell lines in a dose-dependent manner.
2) Aspirin did not significantly inhibit the in vitro growth of pancreatic carcinoma cell lines.
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miR-138-5p Promotes Proliferation of Human Melanoma Cells by Inhibiting hTERT...
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This study examined the role of miR-138-5p in regulating human melanoma cell proliferation. The study found that miR-138-5p expression was significantly higher in melanoma tissues compared to controls. Overexpression of miR-138-5p promoted proliferation of Me45 melanoma cells, while inhibition of miR-138-5p suppressed proliferation. Bioinformatics analysis predicted that miR-138-5p targets the 3'-UTR of hTERT, and luciferase assays confirmed this. Knockdown of hTERT reversed the promotive effects of miR-138-5p on cell proliferation, indicating miR-138-5p regulates proliferation by directly targeting hTERT. Therefore, this study demonstrates that miR-138-5Effects of Ginsenoside Rh2 on STAT3 Signaling Pathway in Human Gastric Cancer...
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This study investigated the effects of Ginsenoside Rh2 on the STAT3 signaling pathway in human gastric cancer NCI-N87 cells. The results showed that Ginsenoside Rh2 treatment decreased phosphorylation of STAT3 and Jak2 proteins in NCI-N87 cells and inhibited IL-induced phosphorylation of these proteins. Ginsenoside Rh2 selectively inhibited phosphorylation of Tyr705 in the STAT3 molecule by downregulating phosphorylation of Jak2 protein specifically. Transfection of a CA-STAT3 plasmid reversed the G0/G1 phase arrest and apoptosis caused by Ginsenoside Rh2, indicating it acts by inhibiting the STAT3 pathway.Research Poster
This study investigated the effects of high-dose ascorbic acid (ASC) alone and in combination with the drug sorafenib (SF) on liver (HepG2), brain (SKNSH), and kidney (HEK) cell lines. ASC at 5mM caused more cell death than other compounds in SKNSH and HepG2 cells. ASC combined with lower doses of SF produced greater cytotoxic effects than other combinations in SKNSH cells. While ASC and SF individually killed cancer cells in a dose-dependent manner, very high doses of ASC up to 100mM did not kill non-cancerous HEK kidney cells. The results suggest that high-dose ASC alone or with lower doses of SF
Prodigiosin and breast cancer cells
1) Prodigiosin, a bacterial metabolite, induces apoptosis in human breast cancer cells. Gene expression profiling found that prodigiosin strongly increased expression of the NAG-1 gene.
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Cancer Research 2
This study found that oncogenic Ras sensitizes normal human cells to TRAIL-induced apoptosis by enhancing caspase 8 recruitment and activation at the DISC. Specifically:
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This document describes an experiment examining the effect of the PI3K/AKT pathway on HOXA1 expression in prostate cancer stem-like cells induced by diepoxybutane (DEB). DU145 prostate cancer cells were treated with DEB to generate cancer stem cells. RNA and protein were extracted from treated and untreated cells. PCR and gel electrophoresis showed expression of HOXA1, p38, cMYC, and JNK-2 genes in DEB-treated cells. Western blot and immunofluorescence were used to analyze protein expression and localization of HOXA1, p53, and pro-caspase 9. Results indicate DEB activates the PI3K/AKT pathway, leading to changes in
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This document discusses a study examining the expression of cancer testis antigen (CTA) genes in glioma stem cells. The key findings are:
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cancerres
This study found that transforming growth factor beta 1 (TGF-β1) induces desmoplasia, the proliferation of fibrotic tissue, in experimental models of human pancreatic carcinoma. The researchers transfected pancreatic tumor cells (PANC-1) that do not normally induce desmoplasia or express TGF-β1 with the TGF-β1 gene. They found that the TGF-β1-transfected cells gained the ability to induce fibroblast growth in culture and in vivo in nude mice. This effect was due both to the direct effects of TGF-β1 and its upregulation of other growth factors and matrix proteins. Therefore, TGF-β1 plays an important role in the desm
Olaparib Upregulates miR-630 Expression to Enhance the Chemotherapeutic Sensi...
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This study explored the role of miR-630 in enhancing the chemotherapeutic sensitivity of BRCA1 mutant triple-negative breast cancer (TNBC) cell lines. The researchers found that combining carboplatin and gemcitabine chemotherapy with the PARP inhibitor olaparib upregulated miR-630 expression in BRCA1 mutant MDA-MB-436 and HCC1937 TNBC cell lines. Overexpression of miR-630 suppressed cell proliferation, migration, and invasion, whereas inhibition of miR-630 increased these effects. Therefore, miR-630 plays an important tumor suppressor role in increasing the chemotherapeutic sensitivity of PARP inhibitors for BRCA1 mutant TNBC, which may be one mechanism of how PARjf9020625-2
This document summarizes research examining the effects of taurine supplementation on cardiac abnormalities in NZB/W F1 mice fed a high-cholesterol diet. The study found that mice fed a cholesterol/taurine diet had less abnormal cardiac histology, fewer apoptotic cardiac cells, and decreased levels of proteins involved in apoptosis compared to mice fed a cholesterol-only diet or control diet. This suggests taurine has protective effects against cardiac abnormalities induced by a high-cholesterol diet in this mouse model of systemic lupus erythematosus.
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The document summarizes a study that examined gene expression profiling in MCF-7 breast cancer cells infected with Newcastle disease virus (NDV). The study found that NDV infection changed the expression levels of many genes involved in tumor progression, cell cycle regulation, apoptosis, and other cellular processes. Specifically, the study used a gene expression kit to measure changes in 21 genes related to these processes in MCF-7 cells infected with NDV. It found that NDV infection altered the expression of genes like PUMA, Bcl-2, ESR1, and MYBL2. The results provide insight into the gene regulation mechanisms by which NDV selectively kills cancer cells.Gene expression profiling in apoptotic mcf 7 cells infected with newcastle di...
Gene expression profiling in apoptotic mcf 7 cells infected with newcastle di...Mohamed Khalid Ali Xundhur
1) The document analyzes gene expression profiling in MCF-7 breast cancer cells infected with Newcastle disease virus (NDV). It finds that NDV infection changes the expression level of many genes involved in tumor progression, cell cycle regulation, apoptosis, and other processes.
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This document summarizes a study examining the effect of doxycycline pretreatment on nuclear factor kappa B (NFκB) activation and chemoresistance in pancreatic cancer cells. The study found that doxycycline induced sustained NFκB activation in pancreatic cancer cells, followed by desensitization to further NFκB activation by tumor necrosis factor alpha (TNF-α) or paclitaxel. This desensitization was accompanied by decreased expression of TNF receptors and epidermal growth factor receptor. Doxycycline pretreatment augmented the cytotoxic and apoptotic effects of TNF-α and paclitaxel. The results suggest that desensitization of NFκB using doxycycline pretreatment may help overcome
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ABSTRACT: A prima vista, un mattoncino Lego e la backdoor XZ potrebbero avere in comune il fatto di essere entrambi blocchi di costruzione, o dipendenze di progetti creativi e software. La realtà è che un mattoncino Lego e il caso della backdoor XZ hanno molto di più di tutto ciò in comune.
Partecipate alla presentazione per immergervi in una storia di interoperabilità, standard e formati aperti, per poi discutere del ruolo importante che i contributori hanno in una comunità open source sostenibile.
BIO: Sostenitrice del software libero e dei formati standard e aperti. È stata un membro attivo dei progetti Fedora e openSUSE e ha co-fondato l'Associazione LibreItalia dove è stata coinvolta in diversi eventi, migrazioni e formazione relativi a LibreOffice. In precedenza ha lavorato a migrazioni e corsi di formazione su LibreOffice per diverse amministrazioni pubbliche e privati. Da gennaio 2020 lavora in SUSE come Software Release Engineer per Uyuni e SUSE Manager e quando non segue la sua passione per i computer e per Geeko coltiva la sua curiosità per l'astronomia (da cui deriva il suo nickname deneb_alpha).
Artificial Intelligence for XMLDevelopment
In the rapidly evolving landscape of technologies, XML continues to play a vital role in structuring, storing, and transporting data across diverse systems. The recent advancements in artificial intelligence (AI) present new methodologies for enhancing XML development workflows, introducing efficiency, automation, and intelligent capabilities. This presentation will outline the scope and perspective of utilizing AI in XML development. The potential benefits and the possible pitfalls will be highlighted, providing a balanced view of the subject.
We will explore the capabilities of AI in understanding XML markup languages and autonomously creating structured XML content. Additionally, we will examine the capacity of AI to enrich plain text with appropriate XML markup. Practical examples and methodological guidelines will be provided to elucidate how AI can be effectively prompted to interpret and generate accurate XML markup.
Further emphasis will be placed on the role of AI in developing XSLT, or schemas such as XSD and Schematron. We will address the techniques and strategies adopted to create prompts for generating code, explaining code, or refactoring the code, and the results achieved.
The discussion will extend to how AI can be used to transform XML content. In particular, the focus will be on the use of AI XPath extension functions in XSLT, Schematron, Schematron Quick Fixes, or for XML content refactoring.
The presentation aims to deliver a comprehensive overview of AI usage in XML development, providing attendees with the necessary knowledge to make informed decisions. Whether you’re at the early stages of adopting AI or considering integrating it in advanced XML development, this presentation will cover all levels of expertise.
By highlighting the potential advantages and challenges of integrating AI with XML development tools and languages, the presentation seeks to inspire thoughtful conversation around the future of XML development. We’ll not only delve into the technical aspects of AI-powered XML development but also discuss practical implications and possible future directions.
Climate Impact of Software Testing at Nordic Testing Days
My slides at Nordic Testing Days 6.6.2024
Climate impact / sustainability of software testing discussed on the talk. ICT and testing must carry their part of global responsibility to help with the climat warming. We can minimize the carbon footprint but we can also have a carbon handprint, a positive impact on the climate. Quality characteristics can be added with sustainability, and then measured continuously. Test environments can be used less, and in smaller scale and on demand. Test techniques can be used in optimizing or minimizing number of tests. Test automation can be used to speed up testing.
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