Disease relevance of Release

• Rat glomerular mesangial cells synthesize basic fibroblast growth factor. Release, upregulated synthesis, and mitogenicity in mesangial proliferative glomerulonephritis [1].
• Co-cultivation of PAEC and HEK293 led to productive infection of the human cells and expression of PERV types A and B. INTERPRETATION: Release of infectious virus from PAEC occurred without mitogenic stimulation, suggesting a serious risk of retrovirus transfer after xenotransplantation [2].
• Role of the sigma subunit of Escherichia coli RNA polymerase in initiation. II. Release of sigma from ternary complexes [3].
• TLR4-Dependent NF-{kappa}B Activation and Mitogen- and Stress-Activated Protein Kinase 1-Triggered Phosphorylation Events Are Central to Helicobacter pylori Peptidyl Prolyl cis-, trans-Isomerase (HP0175)-Mediated Induction of IL-6 Release from Macrophages [4].
• Proceedings: Release of RNA virus from human rheumatoid synovial fibroblast-mouse fibroblast hybrids [5].

Psychiatry related information on Release

• METHODS: Cardiovascular risk and risk reduction were analyzed in five subgroups defined by quintiles (Q) of pretreatment resting HR in the Metoprolol Controlled Release/Extended Release Randomized Intervention Trial in Chronic Heart Failure (MERIT-HF) [6].
• Despite shorter Release reaction times (RTs) for gender decisions than semantic ones, Release and Hold ERPs diverged 84 ms earlier in the semantic context than in the gender context, indicating faster onset for the processing of meaning [7].
• Fourteen patients enrolled in rehabilitation and 12 controls were administered the Release from Proactive Inhibition paradigm involving trials of recalling words from the same category followed by a shift to a new category or continued presentation of identical material [8].
• No precise etiologic basis is yet clearly identifiable; however, this report offers support for a central mechanism explained by the "Release Theory." Additionally, it appears that such hallucinations might be managed safely with psychotropic medications other than antipsychotics [9].
• All patients were assessed using CAMCOG (Cambridge Cognitive Examination), tests examining frontal lobe function (Behavioural Dyscontrol Scale [BDYS], Trail-Making Tests A and B, Controlled Word Association Test) and a scale for primitive reflexes (Frontal Release Signs Scale) [10].

High impact information on Release

• Role for the PP2A/B56delta Phosphatase in Regulating 14-3-3 Release from Cdc25 to Control Mitosis [11].
• The Putative RNA Helicase Dbp4p Is Required for Release of the U14 snoRNA from Preribosomes in Saccharomyces cerevisiae [12].
• The TRPM7 Ion Channel Functions in Cholinergic Synaptic Vesicles and Affects Transmitter Release [13].
• Functional Maturation of CA1 Synapses Involves Activity-Dependent Loss of Tonic Kainate Receptor-Mediated Inhibition of Glutamate Release [14].
• Leukocyte-platelet interaction. Release of hydrogen peroxide by granulocytes as a modulator of platelet reactions [15].

Chemical compound and disease context of Release

• ATP-Sensitive K+ Channels Regulate the Release of GABA in the Ventromedial Hypothalamus During Hypoglycemia [16].
• Francisella tularensis-Infected Macrophages Release Prostaglandin E2 that Blocks T Cell Proliferation and Promotes a Th2-Like Response [17].
• Facilitated diffusion properties of melibiose permease in Escherichia coli membrane vesicles. Release of co-substrates is rate limiting for permease cycling [18].
• Induction of Vascular Leakage and Blood Pressure Lowering through Kinin Release by a Serine Proteinase from Aeromonas sobria [19].
• The substrate requirements for the catalytic activity of the mouse Cdc25 homolog Guanine nucleotide Release Factor, GRF, were determined using the catalytic domain of GRF expressed in insect cells and E. coli expressed H-Ras mutants [20].

Biological context of Release

• Biogenesis of microsomal membrane glycoproteins in rat liver. III. Release of glycoproteins from the Golgi fraction and their transfer to microsomal membranes [21].
• Arabidopsis Separase AESP Is Essential for Embryo Development and the Release of Cohesin during Meiosis [22].
• Cx36-Mediated Coupling Reduces {beta}-Cell Heterogeneity, Confines the Stimulating Glucose Concentration Range, and Affects Insulin Release Kinetics [23].
• Execution of Macrophage Apoptosis by PE_PGRS33 of Mycobacterium tuberculosis Is Mediated by Toll-like Receptor 2-dependent Release of Tumor Necrosis Factor-{alpha} [24].
• The active site of antithrombin. Release of the same proteolytically cleaved form of the inhibitor from complexes with factor IXa, factor Xa, and thrombin [25].

Anatomical context of Release

• SAD: A Presynaptic Kinase Associated with Synaptic Vesicles and the Active Zone Cytomatrix that Regulates Neurotransmitter Release [26].
• CONCLUSIONS: Release of ETs in the intestinal mucosa increased in sensitized animals after EA challenge [27].
• Clearance of gut-derived endotoxins by the liver. Release and modification of 3H, 14C-lipopolysaccharide by isolated rat Kupffer cells [28].
• By contrast, only 2 patients and 1 patient, respectively, without side-branch occlusion had slight rises in CKMB and troponin T. Release of the contractile protein troponin T reflects more severe damage to myocytes than simple leakage of CKMB [29].
• BACKGROUND & AIMS: Release of 5-hydroxytryptamine (5-HT) from mucosal enterochromaffin cells and activation of 5-HT(3) receptors (5-HT(3)Rs) on neurons in the gut wall is important in the response of the gut to the luminal environment [30].

Associations of Release with other chemical compounds

• Tryptophan acts by inhibiting Release Factor 2-mediated cleavage of this peptidyl-tRNA at the tnaC stop codon [31].
• There was a linear correlation between the percentage of histamine secretion and tryptase release (r = 0.79, P < 0.001) induced by cross-linking of Fc epsilon RI [32].
• Sustained Activity of Calcium Release-activated Calcium Channels Requires Translocation of Mitochondria to the Plasma Membrane [33].
• Regulation of renin angiotensins by gonadotropic hormones in cultured murine Leydig tumor cells. Release of angiotensin but not renin [34].
• Eosinophil chemotactic factor (ECF). I. Release from polymorphonuclear leukocytes by the calcium ionophore A23187 [35].

Gene context of Release

• TLR3-Mediated Synthesis and Release of Eotaxin-1/CCL11 from Human Bronchial Smooth Muscle Cells Stimulated with Double-Stranded RNA [36].
• Linear regression analysis of data from all 18 subjects revealed that the fasting IGF-I concentration negatively predicted fold-autoinhibition of GHRH-stimulated peak GH release (r = -0.847, P = 0.006) and positively forecast fold-autoinhibition of basal GH release (r = +0.869, P < 0.001) [37].
• AsialoGM1-Mediated IL-8 Release by Human Corneal Epithelial Cells Requires Coexpression of TLR5 [38].
• Effects of interleukins on Crouzon fibroblast phenotype in vitro. Release of cytokines and IL-6 mRNA expression [39].
• Fibrinolysis during cardiac surgery. Release of tissue plasminogen activator in arterial and coronary sinus blood [40].

Analytical, diagnostic and therapeutic context of Release

• Studies on the mechanism of natural killer (NK) cell-mediated cytotoxicity (CMC). I. Release of cytotoxic factors specific for NK-sensitive target cells (NKCF) during co-culture of NK effector cells with NK target cells [41].
• BACKGROUND: Release of endogenous proinflammatory cytokines such as tumor necrosis factor (TNF)-alpha in response to endotoxin is responsible for the production of large amounts of nitric oxide (NO), which may exert detrimental effects on the myocardium in animal models, isolated hearts, and isolated cardiac myocytes [42].
• Oxygen radical generation induced by postischemic reperfusion can overwhelm endogenous radical scavenging systems, resulting in "oxidative stress." Release of oxidized glutathione (GSSG) upon reflow has been taken as evidence for the occurrence of oxidative stress in postischemic hearts [43].
• In patients with inferior infarction, neither enzyme release (r = 0.30 to 0.40) nor ejection fraction (r = 0.22 to 0.31) correlated well with the ECG indices of infarct size [44].
• 3. Release of catecholamines by the ionophore was dependent on the calcium concentration of the perfusion medium [45].

References