Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.6 (CAD)
 4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant tumors with poor prognosis, and the interaction between activated pancreatic stellate cells (PSCs) and PDAC cells plays an important role in the development of PDAC. The aim of this study was to identify gene changes in BXPC-3 after cross-talked with PSCs and reveal their potential mechanisms. The gene expression profiling analysis of BXPC-3 was completed after co-cultured with primary PSCs for 48 h. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were performed, and the differentially expressed genes (DEGs) were identified by Agilent GeneSpring GX software. In total, 3657 DEGs were identified in BXPC-3, including 1881 up-regulated genes and 1776 downregulated genes. GO analysis results showed that up-regulated DEGs were significantly enriched in biological processes (BP), including peptide metabolic process, response to stress, and electron transport chain; the down-regulated DEGs were significantly enriched in biological processes, including signaling, multicellular organismal development, and anatomical structure development. KEGG pathway analysis revealed that 19 pathways were upregulated and 32 pathways were downregulated, and that up-regulated DEGs were enriched in protein export and glutathione metabolism, while the down-regulated DEGs were enriched in axon guidance and focal adhesion. The top 10 up-regulated genes, and the top 10 down-regulated genes were identified. By constructing PPI network, we selected out 10 key genes (TP53, SRC, IL6, JUN, ISG15, CAD, STAT1, OAS3, OAS1, VIM) and significant pathways. The associated survival analysis was performed and the SRC, IL-6, ISG15, STAT1, OAS3, OAS1 and VIM were proved to be related to worse overall survival time of PDAC patients. In conclusion, the present study indicated that the identified DEGs promote our understanding of the molecular mechanisms underlying the interaction between pancreatic cancer cells and PSCs and might be used as molecular targets in the future to study the role of tumor microenvironment in the progression of PDAC.
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PMID:Identification of key pathways and genes changes in pancreatic cancer cells (BXPC-3) after cross-talked with primary pancreatic stellate cells using bioinformatics analysis. 3116 32

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant tumors with poor prognosis, and the interaction between activated pancreatic stellate cells (PSCs) and PDAC cells plays an important role in the development of PDAC. The aim of this study was to identify gene changes in BXPC-3 after cross-talk with PSCs and reveal their potential mechanisms. The gene expression profiling analysis of BXPC-3 was completed after co-culture with primary PSCs for 48 h. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) enrichment analyses were performed, and the differentially expressed genes (DEGs) were identified by Agilent GeneSpring GX software. In total, 3657 DEGs were identified in BXPC-3, including 1881 up-regulated genes and 1776 downregulated genes. GO analysis results showed that upregulated DEGs were significantly enriched in biological processes (BP), including peptide metabolic process, response to stress and electron transport chain; the downregulated DEGs were significantly enriched in biological processes, including signaling, multicellular organism development and anatomical structure development. KEGG pathway analysis revealed that 19 pathways were upregulated and 32 pathways were downregulated, and that upregulated DEGs were enriched in protein export and glutathione metabolism, while the downregulated DEGs were enriched in axon guidance and focal adhesion. The top 10 upregulated genes and the top 10 downregulated genes were identified. By constructing PPI network, we selected out 10 key genes (TP53, SRC, IL6, JUN, ISG15, CAD, STAT1, OAS3, OAS1, VIM) and significant pathways. The associated survival analysis was performed and the SRC, IL-6, ISG15, STAT1, OAS3, OAS1 and VIM were proved to be related to worse overall survival time of PDAC patients. In conclusion, the present study indicated that the identified DEGs promote our understanding of the molecular mechanisms underlying the interaction between pancreatic cancer cells and PSCs and might be used as molecular targets in the future to study the role of tumor microenvironment in the progression of PDAC.
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PMID:Identification of key pathways and genes changes in pancreatic cancer cells (BXPC-3) after cross-talk with primary pancreatic stellate cells using bioinformatics analysis. 3116 17

Non-ST-segment elevation myocardial infarction (NSTEMI) is defined as elevated cardiac biomarkers of necrosis in the absence of persistent ST-segment elevation in the setting of anginal symptoms or other acute event. It carries a poorer prognosis than most ST-segment elevation events, owing to the typical comorbidity burden of the older NSTEMI patients as well as diverse etiologies that add complexity to therapeutic decision-making. It may result from an acute atherothrombotic event ('Type 1') or as the result of other causes of mismatch of myocardial oxygen supply and demand ('Type 2'). Regardless of type and other clinical factors, the hospital medicine specialist is increasingly responsible for managing or coordinating the care of these patients. Following published guidelines for risk stratification and basing anti-anginal, anticoagulant, antiplatelet, other pharmacologic therapies, and overall management approach on that individualized patient risk assessment can be expected to result in better short- and long-term clinical outcomes, including near-term readmission and recurrent events. We present here a review of the evidence basis and expert commentary to assist the hospitalist in achieving those improved outcomes in NSTEMI. Given that the Society for Hospital Medicine cites care of patients with acute coronary syndrome as a core competency for hospitalists, it is essential that those specialists stay current on optimal NSTEMI care.Abbreviations: ACC: American college of cardiology; ACCOAST: comparison of prasugrel at the time of diagnosis in patients with non-ST elevation myocardial infarction; ACS: acute coronary syndrome; ADP: adenosine diphosphate; AHA: American heart association; ARB: angiotensin II receptor blocker; ASA: acetylsalicylic acid; CABG: coronary artery bypass graft: CAD: coronary artery disease; CCTA: coronary computed tomography angiography; cTn: cardiac troponin; CRUSADE: can rapid risk stratification of unstable angina patients suppress adverse outcomes with early implementation of the ACC/AHA guidelines; CURE: clopidogrel in unstable angina to prevent recurrent events; CURRENT: OASIS-7 clopidogrel and aspirin optimal dose usage to reduce recurrent events-seventh organization to assess strategies in ischemic syndromes; ECG: electrocardiogram; ED: emergency department; ESRD: endstage renal disease; ESC: European society of cardiology; FDA: food and drug administration; GRACE: global registry of acute coronary events; LVEF: left ventricular ejection fraction; MACE: major adverse cardiac event; MI: myocardial infarction; MVO2: myocardial oxygen demand; NSTEMI: non-ST-segment-elevation myocardial infarction; NTG: Nitroglycerin; PCI: percutaneous coronary intervention; plato: platelet inhibition and patient outcomes; PPI: proton pump inhibitor; PURSUIT: platelet glycoprotein IIb/IIIa in unstable angina: Receptor Suppression Using Integrilin Therapy; RAAS: Renin-Angiotensin-Aldosterone System; SHM: society of hospital medicine; STEMI: ST-segment-elevation myocardial infarction; TIMI: Thrombolysis in Myocardial Infarction; TRITON-TIMI:trial to assess improvement in therapeutic outcomes by optimizing platelet inhibition with prasugrel-thrombolysis in myocardial infarction.
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PMID:Contemporary NSTEMI management: the role of the hospitalist. 3181 70