Digitalizace laboratoří, aplikace big dat a automatizovaná strojová diagnostika ("machine learning") jsou nástroji pro vznik a fungování toho, co se označuje jako precizní medicína. Genomika, její dominantní metody (qPCR, dPCR, ddPCR, NGS), produkující obrovská kvanta dat (big data) a schopnosti počítačových systémů tyto soubory dat využívat v diagnostice a terapii za významného přispění "umělé inteligence" se označují jako strojová automatizovaná diagnostika - machine learning respektive deep learning). Tyto postupy pronikají z průmyslu a výzkumu do rutinní medicíny včetně medicíny laboratorní. Zvládnutí technických a personálních problémů těchto změn bude stát značné úsilí, srovnatelné s před lety realizovanou přeměnou manuální laboratorní práce na automatizovanou činnost a s přeměnou papírové dokumentace výsledků na laboratorní a nemocniční informační systémy. Lze předpokládat nejen zásadní změny metod laboratorní práce, ale i změny požadavků na odbornost personálu laboratoří a rovněž lze předpokládat nevyhnutelnost radikálního ovlivnění činnosti klinických laboratoří. Etický rozměr nastávajících změn bude stejně závažný, jako ten technický a bude možné očekávat nejen významný progres v diagnostice e prognostice chorob, ale i vzestup rizika zdravotní péče v případě chyb a neprofesionality. Automatická strojová aplikace big dat a používání umělé inteligence jsou náročné, je s nimi v medicíně málo zkušeností, ale vyhnout se jim nebude možné.

Digitalization of clinical laboratories, application of big data and methods of machine learning re contemporary tools for precision medicine. Precision medicine is based mainly on the genomic methods, namely of dominant PCR and NGS methods. These methods produces enormous number of dates (big data) and can be explored by means of artificial intelligence in processes called machine learning. Machine learning was primarily used in industry and research and now contemporary penetrates into medicine and also to laboratory medicine. Methods based on the big data and artificial intelligence with exploration of big data is certainly very important factor of future of medicine. It will be needs large requirements not only on high-technology equipment, but also for new type of young laboratory Professional used basically new methods of work and mind. Machine learning, part of precision medicine, necessary namely for oncology and prediction of patients state crettemeans also lot of new types of ethical problems. These ethical questions and problems should be soluted immediately, parallel with introduction of machine learning to laboratory practice.

• MeSH
• Big Data MeSH
• Diagnosis, Computer-Assisted * methods   MeSH
• Precision Medicine MeSH
• Humans MeSH
• Machine Learning MeSH
• Artificial Intelligence MeSH
• Check Tag
• Humans MeSH

Analysis of brown bullhead (Ameiurus nebulosus) bile by ultra performance liquid chromatography high-resolution mass spectrometry (UPLC/HRMS) revealed a series of bile acids similar to those found in humans. Accordingly, we chose this fish as a model organism to examine the metabolism of obeticholic acid, a bile acid used to treat a number of human liver diseases and the one that has the potential to occur as an environmental contaminant. The taurine and glycine conjugates of obeticholic acid and keto-obeticholic acid were identified, as well as the D-cysteinolic acid conjugate of obeticholic acid, likely a metabolite specific to fish. In addition, metabolites of obeticholic acid (sulphate and glucuronide) and several hydroxy-obeticholic acid derivatives were found, representing typical pathways of primary and secondary steroid metabolism. Brown bullhead exposed to obeticholic acid at a dose of 100 mg/kg gave no overt signs of distress or toxicity.

• MeSH
• Water Pollutants, Chemical pharmacokinetics   toxicity   MeSH
• Ecotoxicology methods   MeSH
• Glycine metabolism   MeSH
• Mass Spectrometry MeSH
• Ictaluridae metabolism   MeSH
• Chenodeoxycholic Acid analogs & derivatives   analysis   pharmacokinetics   toxicity   MeSH
• Taurine metabolism   MeSH
• Chromatography, High Pressure Liquid MeSH
• Bile chemistry   MeSH
• Animals MeSH
• Check Tag
• Animals MeSH
• Publication type
• Journal Article MeSH

BACKGROUND: Lipoprotein(a) [Lp(a)] may play a causal role in atherosclerosis. PCSK9 (proprotein convertase subtilisin/kexin 9) inhibitors have been shown to significantly reduce plasma Lp(a) concentration. However, the relationship between Lp(a) levels, PCSK9 inhibition, and cardiovascular risk reduction remains undefined. METHODS: Lp(a) was measured in 25 096 patients in the FOURIER trial (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk), a randomized trial of evolocumab versus placebo in patients with established atherosclerotic cardiovascular disease (median follow-up, 2.2 years). Cox models were used to assess the independent prognostic value of Lp(a) and the efficacy of evolocumab for coronary risk reduction by baseline Lp(a) concentration. RESULTS: The median (interquartile range) baseline Lp(a) concentration was 37 (13-165) nmol/L. In the placebo arm, patients with baseline Lp(a) in the highest quartile had a higher risk of coronary heart disease death, myocardial infarction, or urgent revascularization (adjusted hazard ratio quartile 4: quartile 1, 1.22; 95% CI, 1.01-1.48) independent of low-density lipoprotein cholesterol. At 48 weeks, evolocumab significantly reduced Lp(a) by a median (interquartile range) of 26.9% (6.2%-46.7%). The percent change in Lp(a) and low-density lipoprotein cholesterol at 48 weeks in patients taking evolocumab was moderately positively correlated ( r=0.37; 95% CI, 0.36-0.39; P<0.001). Evolocumab reduced the risk of coronary heart disease death, myocardial infarction, or urgent revascularization by 23% (hazard ratio, 0.77; 95% CI, 0.67-0.88) in patients with a baseline Lp(a) >median, and by 7% (hazard ratio, 0.93; 95% CI, 0.80-1.08; P interaction=0.07) in those ≤median. Coupled with the higher baseline risk, the absolute risk reductions, and number needed to treat over 3 years were 2.49% and 40 versus 0.95% and 105, respectively. CONCLUSIONS: Higher levels of Lp(a) are associated with an increased risk of cardiovascular events in patients with established cardiovascular disease irrespective of low-density lipoprotein cholesterol. Evolocumab significantly reduced Lp(a) levels, and patients with higher baseline Lp(a) levels experienced greater absolute reductions in Lp(a) and tended to derive greater coronary benefit from PCSK9 inhibition. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov . Unique identifier: NCT01764633.

• MeSH
• Anticholesteremic Agents therapeutic use   MeSH
• Atherosclerosis drug therapy   pathology   MeSH
• Adult MeSH
• Double-Blind Method MeSH
• Antibodies, Monoclonal, Humanized therapeutic use   MeSH
• Cholesterol, LDL blood   MeSH
• Middle Aged MeSH
• Humans MeSH
• Lipoprotein(a) blood   MeSH
• Placebo Effect MeSH
• Proportional Hazards Models MeSH
• Proprotein Convertase 9 immunology   metabolism   MeSH
• Risk Factors MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Randomized Controlled Trial MeSH

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine that can trigger apoptosis in many types of human cancer cells via engagement of its two pro-apoptotic receptors TRAIL-R1 (DR4) and TRAIL-R2 (DR5). TRAIL can also activate several other signaling pathways such as activation of stress kinases, canonical NF-κB signaling and necroptosis. Though both receptors are ubiquitously expressed, their relative participation in TRAIL-induced signaling is still largely unknown. To analyze TRAIL receptor-specific signaling, we prepared Strep-tagged, trimerized variants of recombinant human TRAIL with high affinity for either DR4 or DR5 receptor. Using these receptor-specific ligands, we examined the contribution of individual pro-apoptotic receptors to TRAIL-induced signaling pathways. We found that in TRAIL-resistant colorectal HT-29 cells but not in pancreatic PANC-1 cancer cells, DISC formation and initial caspase-8 processing proceeds comparably via both DR4- and DR5-activated signaling. TRAIL-induced apoptosis, enhanced by the inhibitor of the Bcl-2 family ABT-737, or by the translation inhibitor homoharringtonine, proceeded in both cell lines predominantly via the DR5 receptor. ShRNA-mediated downregulation of DR4 or DR5 receptors in HT-29 cells also pointed to a stronger contribution of DR5 in TRAIL-induced apoptosis. In contrast to apoptosis, necroptotic signaling was activated similarly by both DR4- or DR5-specific ligands. Activation of auxiliary signaling pathways involving NF-κB or stress kinases proceeded under apoptotic conditions mainly in a DR5-dependent manner, while these signaling pathways were during necroptosis similarly activated by either of these ligands. Our study provides the first systematic insight into DR4-/DR5-specific signaling in colorectal and pancreatic cancer cells.

• MeSH
• Apoptosis genetics   MeSH
• HT29 Cells MeSH
• Caspase 8 genetics   MeSH
• Colorectal Neoplasms genetics   pathology   MeSH
• Humans MeSH
• RNA, Small Interfering MeSH
• Pancreatic Neoplasms genetics   pathology   MeSH
• Necrosis genetics   pathology   MeSH
• NF-kappa B genetics   MeSH
• Pancreas metabolism   pathology   MeSH
• Cell Proliferation genetics   MeSH
• TNF-Related Apoptosis-Inducing Ligand genetics   MeSH
• Gene Expression Regulation, Neoplastic MeSH
• Signal Transduction genetics   MeSH
• Receptors, TNF-Related Apoptosis-Inducing Ligand genetics   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

BACKGROUND: LDL cholesterol is a well established risk factor for atherosclerotic cardiovascular disease. How much one should or safely can lower this risk factor remains debated. We aimed to explore the relationship between progressively lower LDL-cholesterol concentrations achieved at 4 weeks and clinical efficacy and safety in the FOURIER trial of evolocumab, a monoclonal antibody to proprotein convertase subtilisin-kexin type 9 (PCSK9). METHODS: In this prespecified secondary analysis of 25 982 patients from the randomised FOURIER trial, the relationship between achieved LDL-cholesterol concentration at 4 weeks and subsequent cardiovascular outcomes (primary endpoint was the composite of cardiovascular death, myocardial infarction, stroke, coronary revascularisation, or unstable angina; key secondary endpoint was the composite of cardiovascular death, myocardial infarction, or stroke) and ten prespecified safety events of interest was examined over a median of 2·2 years of follow-up. We used multivariable modelling to adjust for baseline factors associated with achieved LDL cholesterol. This trial is registered with ClinicalTrials.gov, number NCT01764633. FINDINGS: Between Feb 8, 2013, and June 5, 2015, 27 564 patients were randomly assigned a treatment in the FOURIER study. 1025 (4%) patients did not have an LDL cholesterol measured at 4 weeks and 557 (2%) had already had a primary endpoint event or one of the ten prespecified safety events before the week-4 visit. From the remaining 25 982 patients (94% of those randomly assigned) 13 013 were assigned evolocumab and 12 969 were assigned placebo. 2669 (10%) of 25 982 patients achieved LDL-cholesterol concentrations of less than 0·5 mmol/L, 8003 (31%) patients achieved concentrations between 0·5 and less than 1·3 mmol/L, 3444 (13%) patients achieved concentrations between 1·3 and less than 1·8 mmol/L, 7471 (29%) patients achieved concentrations between 1·8 to less than 2·6 mmol/L, and 4395 (17%) patients achieved concentrations of 2·6 mmol/L or higher. There was a highly significant monotonic relationship between low LDL-cholesterol concentrations and lower risk of the primary and secondary efficacy composite endpoints extending to the bottom first percentile (LDL-cholesterol concentrations of less than 0·2 mmol/L; p=0·0012 for the primary endpoint, p=0·0001 for the secondary endpoint). Conversely, no significant association was observed between achieved LDL cholesterol and safety outcomes, either for all serious adverse events or any of the other nine prespecified safety events. INTERPRETATION: There was a monotonic relationship between achieved LDL cholesterol and major cardiovascular outcomes down to LDL-cholesterol concentrations of less than 0·2 mmol/L. Conversely, there were no safety concerns with very low LDL-cholesterol concentrations over a median of 2·2 years. These data support further LDL-cholesterol lowering in patients with cardiovascular disease to well below current recommendations. FUNDING: Amgen.

• MeSH
• Anticholesteremic Agents therapeutic use   MeSH
• Patient Safety MeSH
• Adult MeSH
• Double-Blind Method MeSH
• Risk Assessment MeSH
• Hypercholesterolemia blood   drug therapy   MeSH
• Cholesterol, LDL blood   drug effects   MeSH
• Middle Aged MeSH
• Humans MeSH
• Antibodies, Monoclonal therapeutic use   MeSH
• Follow-Up Studies MeSH
• PCSK9 Inhibitors MeSH
• Proprotein Convertase 9 MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Treatment Outcome MeSH
• Check Tag
• Adult MeSH
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Randomized Controlled Trial MeSH

BACKGROUND & AIMS: Epicardial adipose tissue (EAT) is a source of a number of cytokines which could act in the pathogenesis of coronary artery disease (CAD). The potential relationship between known cardiovascular risk factors, such as smoking, dyslipidaemia or diabetes mellitus and EAT humoral signalling, has not been fully elucidated. Therefore, we designed and conducted a cross-sectional study to determine whether selected cardiovascular risk factors are linked to levels of cytokines in epicardial and subcutaneous adipose tissue (SAT). METHODS: Samples of SAT and EAT were collected from consecutive patients undergoing scheduled cardiac surgery. Tissue concentrations of tumour necrosis factor-ɑ (TNF-α), interleukin-6 (IL-6), adipocyte fatty acid-binding protein, leptin, and adiponectin were determined by ELISA. RESULTS: We enrolled 140 patients. TNF-α and IL-6 concentrations in EAT and SAT were significantly higher in current smokers (CS) than in never smokers (NS) and former smokers (FS). There were no differences between FS and NS. No other clinical variables were associated with cytokine concentrations in a regression analysis. CONCLUSIONS: Smoking was independently associated with higher TNF-α and IL-6 concentrations in EAT and SAT. A novel observation that pro-inflammatory cytokines are elevated in EAT in smokers could contribute to identify potential mechanisms involved in the pathogenesis of adverse effects of tobacco smoking. There were no differences between EAT cytokine production in NS and FS, which support the importance of smoking cessation for cardiovascular risk reduction.

• MeSH
• Interleukin-6 metabolism   MeSH
• Smoking adverse effects   metabolism   MeSH
• Middle Aged MeSH
• Humans MeSH
• Inflammation Mediators metabolism   MeSH
• Smoking Cessation * MeSH
• Pericardium metabolism   MeSH
• Subcutaneous Fat metabolism   MeSH
• Smoking Prevention * MeSH
• Cross-Sectional Studies MeSH
• Aged MeSH
• Tumor Necrosis Factor-alpha metabolism   MeSH
• Up-Regulation MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH

This paper summarises the results of parasitological examinations of the European eel Anguilla anguilla (Linnaeus) in the Czech Republic, carried out at the Institute of Parasitology, Czech Academy of Sciences (previously the Czechoslovak Academy of Sciences) within the period of 50 years (1958-2008). Even though this survey is limited to the Czech Republic, it provides extensive data probably incomparable with any other study anywhere regarding the number of eels examined and parasites found. A total of 723 eels was examined from 42 localities that belong to all of the three main river drainage systems in the country, i.e. the Elbe, Danube and Oder river basins. Of the 31 species of adult and larval macroparasites including Monogenea (4 species), Trematoda (3), Cestoda (3), Nematoda (11), Acanthocephala (5), Hirudinea (1), Bivalvia (1), Copepoda (1), Branchiura (1) and Acariformes (1), most of them (30) were recorded from the Elbe River basin. These parasites can be divided into three main groups regarding their host specificity: parasites specific for eels (26%), non-specific adult parasites occurring also in other fishes (61%) and non-specific larvae (13%). The highest number (19) of parasite species was recorded in the Mácha Lake fishpond system in northern Bohemia. The parasite communities in eels from the individual localities exhibited large differences in their species composition and diversity depending on local ecological conditions. The parasite fauna of A. anguilla in the Czech Republic is compared with that in other European countries. The nematode Cucullanus egyptae Abdel-Ghaffar, Bashtar, Abdel-Gaber, Morsy, Mehlhorn, Al Quraishy et Mohammed, 2014 is designated as a species inquirenda.

• MeSH
• Acanthocephala classification   MeSH
• Anguilla * parasitology   MeSH
• Biodiversity MeSH
• Cestoda classification   MeSH
• Host Specificity MeSH
• Parasites * classification   MeSH
• Rivers parasitology   MeSH
• Statistics as Topic MeSH
• Trematoda classification   MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Geographicals
• Czech Republic MeSH

Recent studies have identified molecular events characteristic of immunogenic cell death (ICD), including surface exposure of calreticulin (CRT), the heat shock proteins HSP70 and HSP90, the release of high-mobility group box protein 1 (HMGB1) and the release of ATP from dying cells. We investigated the potential of high hydrostatic pressure (HHP) to induce ICD in human tumor cells. HHP induced the rapid expression of HSP70, HSP90 and CRT on the cell surface. HHP also induced the release of HMGB1 and ATP. The interaction of dendritic cells (DCs) with HHP-treated tumor cells led to a more rapid rate of DC phagocytosis, upregulation of CD83, CD86 and HLA-DR and the release of interleukin IL-6, IL-12p70 and TNF-α. DCs pulsed with tumor cells killed by HHP induced high numbers of tumor-specific T cells. DCs pulsed with HHP-treated tumor cells also induced the lowest number of regulatory T cells. In addition, we found that the key features of the endoplasmic reticulum stress-mediated apoptotic pathway, such as reactive oxygen species production, phosphorylation of the translation initiation factor eIF2α and activation of caspase-8, were activated by HHP treatment. Therefore, HHP acts as a reliable and potent inducer of ICD in human tumor cells.

• MeSH
• Adenosine Triphosphate secretion   MeSH
• Enzyme Activation immunology   MeSH
• B7-2 Antigen biosynthesis   MeSH
• Apoptosis immunology   MeSH
• Antigens, CD biosynthesis   MeSH
• Dendritic Cells immunology   MeSH
• Eukaryotic Initiation Factor-2 metabolism   MeSH
• Phagocytosis immunology   MeSH
• Phosphorylation MeSH
• HLA-DR Antigens biosynthesis   MeSH
• Hydrostatic Pressure MeSH
• Immunoglobulins biosynthesis   MeSH
• Interleukin-12 secretion   MeSH
• Interleukin-6 secretion   MeSH
• Calreticulin biosynthesis   immunology   MeSH
• Caspase 8 metabolism   MeSH
• Humans MeSH
• Membrane Glycoproteins biosynthesis   MeSH
• Membrane Proteins biosynthesis   MeSH
• Cell Line, Tumor MeSH
• Neoplasms immunology   MeSH
• HMGB1 Protein immunology   secretion   MeSH
• HSP70 Heat-Shock Proteins biosynthesis   immunology   MeSH
• HSP90 Heat-Shock Proteins biosynthesis   immunology   MeSH
• Reactive Oxygen Species metabolism   MeSH
• T-Lymphocytes, Regulatory immunology   MeSH
• Endoplasmic Reticulum Stress immunology   MeSH
• Tumor Necrosis Factor-alpha secretion   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Tumour necrosis factor (TNF) related apoptosis inducing ligand (TRAIL), a membrane-bound ligand from the TNF family, has attracted significant attention due to its rather specific and effective ability to induce apoptotic death in various types of cancer cells via binding to and activating its pro-apoptotic death receptors. However, a significant number of primary cancer cells often develop resistance to TRAIL treatment, and the signalling platform behind this phenomenon is not fully understood. Upon blocking endosomal acidification by the vacuolar ATPase (V-ATPase) inhibitors bafilomycin A1 (BafA1) or concanamycin A, we observed a significantly reduced initial sensitivity of several, mainly colorectal, tumour cell lines to TRAIL-induced apoptosis. In cells pretreated with these inhibitors, the TRAIL-induced processing of caspase-8 and the aggregation and trafficking of the TRAIL receptor complexes were temporarily attenuated. Nuclear factor κB or mitogen activated protein/stress kinase signalling from the activated TRAIL receptors remained unchanged, and neither possible lysosomal permeabilization nor acid sphingomyelinase was involved in this process. The cell surface expression of TRAIL receptors and their TRAIL-induced internalization were not affected by V-ATPase inhibitors. The inhibitory effect of BafA1, however, was blunted by knockdown of the caspase-8 inhibitor cFLIP. Altogether, the data obtained provide the first evidence that endosomal acidification could represent an important regulatory node in the proximal part of TRAIL-induced pro-apoptotic signalling.

• MeSH
• Enzyme Activation MeSH
• Apoptosis MeSH
• Down-Regulation MeSH
• Endosomes metabolism   MeSH
• CASP8 and FADD-Like Apoptosis Regulating Protein metabolism   MeSH
• Caspase 8 metabolism   MeSH
• Hydrogen-Ion Concentration MeSH
• Humans MeSH
• Macrolides pharmacology   MeSH
• Cell Line, Tumor MeSH
• TNF-Related Apoptosis-Inducing Ligand pharmacology   MeSH
• Antineoplastic Agents pharmacology   MeSH
• Sphingolipids physiology   MeSH
• Sphingomyelin Phosphodiesterase metabolism   MeSH
• Death Domain Receptor Signaling Adaptor Proteins metabolism   MeSH
• Signal Transduction drug effects   MeSH
• Receptors, TNF-Related Apoptosis-Inducing Ligand metabolism   MeSH
• Protein Transport MeSH
• Vacuolar Proton-Translocating ATPases antagonists & inhibitors   metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

Death ligands and their tumor necrosis factor receptor (TNFR) family receptors are the best-characterized and most efficient inducers of apoptotic signaling in somatic cells. In this study, we analyzed whether these prototypic activators of apoptosis are also expressed and able to be activated in human pluripotent stem cells. We examined human embryonic stem cells (hESC) and human-induced pluripotent stem cells (hiPSC) and found that both cell types express primarily TNF-related apoptosis-inducing ligand (TRAIL) receptors and TNFR1, but very low levels of Fas/CD95. We also found that although hESC and hiPSC contain all the proteins required for efficient induction and progression of extrinsic apoptotic signaling, they are resistant to TRAIL-induced apoptosis. However, both hESC and hiPSC can be sensitized to TRAIL-induced apoptosis by co-treatment with protein synthesis inhibitors such as the anti-leukemia drug homoharringtonine (HHT). HHT treatment led to suppression of cellular FLICE inhibitory protein (cFLIP) and Mcl-1 expression and, in combination with TRAIL, enhanced processing of caspase-8 and full activation of caspase-3. cFLIP likely represents an important regulatory node, as its shRNA-mediated down-regulation significantly sensitized hESC to TRAIL-induced apoptosis. Thus, we provide the first evidence that, irrespective of their origin, human pluripotent stem cells express canonical components of the extrinsic apoptotic system and on stress can activate death receptor-mediated apoptosis.

• MeSH
• fas Receptor genetics   metabolism   MeSH
• Apoptosis drug effects   MeSH
• Cell Differentiation MeSH
• Embryonic Stem Cells cytology   drug effects   metabolism   MeSH
• CASP8 and FADD-Like Apoptosis Regulating Protein antagonists & inhibitors   genetics   metabolism   MeSH
• Harringtonines pharmacology   MeSH
• Protein Synthesis Inhibitors pharmacology   MeSH
• Caspase 3 genetics   metabolism   MeSH
• Caspase 8 genetics   metabolism   MeSH
• Humans MeSH
• RNA, Small Interfering genetics   metabolism   MeSH
• Pluripotent Stem Cells cytology   drug effects   metabolism   MeSH
• Cell Proliferation MeSH
• Myeloid Cell Leukemia Sequence 1 Protein genetics   metabolism   MeSH
• TNF-Related Apoptosis-Inducing Ligand genetics   metabolism   pharmacology   MeSH
• Receptors, Tumor Necrosis Factor, Type I genetics   metabolism   MeSH
• Gene Expression Regulation MeSH
• Signal Transduction MeSH
• Drug Synergism MeSH
• Receptors, TNF-Related Apoptosis-Inducing Ligand genetics   metabolism   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH