Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The trypsin-inhibiting activity of human serum is lowered upon addition of formaldehyde or acetaldehyde thereto. Acetaldehyde reacts with alpha-1-proteinase inhibitor (alpha 1-PI) to decrease its trypsin-inhibiting ability. Acetaldehyde has only a slight effect on the tryptic hydrolysis of benzoyl-DL-arginine-p-nitroanilide. It did not decrease the inhibitory activity of the Kunitz inhibitor (Aprotinin) or soybean trypsin inhibitor. Since aldehydes form covalent products with primary amines, primary amides, arginine, tyrosine, and tryptophan in protein, as well as methylene bridges thereby crosslinking functional groups, it is proposed that one or more such interactions affect alpha 1-PI activity. It is further suggested that chronically high levels of acetaldehyde, as a metabolic produce of ethanol, may be a contributory factor to the generation of pancreatitis in alcoholics by possibly lowering the effective alpha 1-PI level which is a natural protective element from proteolysis by trypsin.
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PMID:Acetaldehyde decreases the antitryptic activity of alpha 1-proteinase inhibitor. 131 22

The ability of two coxsackievirus B3 (CBV3) variants to induce myocarditis in BALB/c mice was studied and plaque-forming assay, polymerase chain reaction (PCR), in situ hybridization, and immunohistochemistry were compared for detecting viruses and viral components in the myocardium. The virological findings were related to histopathologic and ultrastructural changes in the myocardium. CBV3-W induced severe myocarditis characterized by massive myocyte necrosis. Widely distributed myocyte damage clearly preceded modest inflammatory infiltrates in the myocardium. In contrast, CBV3-M1 induced mild myocardial injury. Both variants caused fulminant pancreatitis with nearly complete necrosis of the exocrine pancreas. CBV3 RNA was identified by PCR in the myocardium of CBV3-W-infected mice until the end of the follow-up period of 14 days. Moreover, semiquantitative results were obtained when the PCR/hybridization results were analyzed by a phosphor imaging system. Immunohistochemistry and in situ hybridization from formaldehyde-fixed, paraffin-embedded specimens were highly similar in detecting viral components during the early stages of the myocardial injury. The results indicate that: (i) direct viral damage plays an essential role in acute murine CBV3-induced myocarditis, (ii) PCR appears a useful and sensitive diagnostic method in acute myocarditis, and (iii) immunohistochemistry as a specific and relatively rapid method might be practicable also in studying the early stages of acute myocarditis from archival clinical material.
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PMID:Experimental myocarditis induced by two different coxsackievirus B3 variants: aspects of pathogenesis and comparison of diagnostic methods. 855 Dec 77

Ten hemolytic reactions occurred in our outpatient hemodialysis unit over a 12-month period (December 1989 to December 1990). Eight patients were hospitalized and one died. All patients developed severe abdominal or back pain an average of 2.5 hours into a 4-hour hemodialysis session using a bleach/formaldehyde reprocessed hollow-fiber cupraphan dialyzer (average reuse, three times) with blood flow rates of 375 mL/min. All had visible hemolysis in a spun hematocrit, seven had a significant decrease in hematocrit, and six developed pancreatitis. Hemolysis was further confirmed by a decrease in haptoglobin in all patients and an increase in lactic dehydrogenase in all but the last case. Investigation of each episode failed to find an abnormality in dialysate temperature or tonicity; dialysate or water levels of copper, zinc, nitrates, chloramine, or formaldehyde; or blood pump or venous alarm. Hemolytic reactions continued despite changing to 15-gauge needles, removing bleach from the reuse procedure, or stopping reuse. During the eighth episode, a kink was noted in the arterial blood line. Two subsequent hemolytic reactions occurred, and in each kinks were found in the arterial blood line, either in the excess tubing between the blood pump and drip chamber or in the predialyzer. No further hemolytic reactions occurred after changing to a new arterial blood line without redundant tubing and securing all lines. Hemolytic reactions occurring during hemodialysis have many etiologies, including mechanical trauma, which we report may result from kinking of dialyzer lines. With new blood lines on the market, attention to this aspect of dialysis is mandatory.
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PMID:Hemolytic reactions mechanically induced by kinked hemodialysis lines. 865 3

Coxsackievirus B3 (CVB3), a member of the picornavirus family and enterovirus genus, causes viral myocarditis, aseptic meningitis, and pancreatitis in humans. We genetically engineered a unique molecular marker, "fluorescent timer" protein, within our infectious CVB3 clone and isolated a high-titer recombinant viral stock (Timer-CVB3) following transfection in HeLa cells. "Fluorescent timer" protein undergoes slow conversion of fluorescence from green to red over time, and Timer-CVB3 can be utilized to track virus infection and dissemination in real time. Upon infection with Timer-CVB3, HeLa cells, neural progenitor and stem cells (NPSCs), and C2C12 myoblast cells slowly changed fluorescence from green to red over 72 hours as determined by fluorescence microscopy or flow cytometric analysis. The conversion of "fluorescent timer" protein in HeLa cells infected with Timer-CVB3 could be interrupted by fixation, suggesting that the fluorophore was stabilized by formaldehyde cross-linking reactions. Induction of a type I interferon response or ribavirin treatment reduced the progression of cell-to-cell virus spread in HeLa cells or NPSCs infected with Timer-CVB3. Time lapse photography of partially differentiated NPSCs infected with Timer-CVB3 revealed substantial intracellular membrane remodeling and the assembly of discrete virus replication organelles which changed fluorescence color in an asynchronous fashion within the cell. "Fluorescent timer" protein colocalized closely with viral 3A protein within virus replication organelles. Intriguingly, infection of partially differentiated NPSCs or C2C12 myoblast cells induced the release of abundant extracellular microvesicles (EMVs) containing matured "fluorescent timer" protein and infectious virus representing a novel route of virus dissemination. CVB3 virions were readily observed within purified EMVs by transmission electron microscopy, and infectious virus was identified within low-density isopycnic iodixanol gradient fractions consistent with membrane association. The preferential detection of the lipidated form of LC3 protein (LC3 II) in released EMVs harboring infectious virus suggests that the autophagy pathway plays a crucial role in microvesicle shedding and virus release, similar to a process previously described as autophagosome-mediated exit without lysis (AWOL) observed during poliovirus replication. Through the use of this novel recombinant virus which provides more dynamic information from static fluorescent images, we hope to gain a better understanding of CVB3 tropism, intracellular membrane reorganization, and virus-associated microvesicle dissemination within the host.
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PMID:Coxsackievirus B exits the host cell in shed microvesicles displaying autophagosomal markers. 2472 73