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Correlation of neuroendocrine and anti-edema activities of alanine-corticotropin-releasing factor analogs.
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Thirty-three ovine corticotropin-releasing factor (CRF) analogs, systematically substituted with alanine (Ala) residues, were tested for inhibitory activity on edema induced in the pentobarbital-anesthetized rat paw by heat (immersion in 58 degrees C water for 1 min). The activity of each analog,
Type II hereditary angioneurotic edema that may result from a single nucleotide change in the codon for alanine-436 in the C1 inhibitor gene.
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Identical single-base changes in the C1 inhibitor gene that may result in dysfunctional inhibitor proteins are described in two different families with type II hereditary angioneurotic edema. Initially, a restriction fragment length polymorphism was defined that resulted from loss of a Pst I site
Are alanine, cysteine, glycine and valine amino acids the cause of non-immune hydrops fetalis?
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Our objective was to measure amniotic fluid amino acid concentrations in pregnant women diagnosed as having fetuses with non immune hydrops fetalis in the second trimester of pregnancy. Twenty-three pregnant women who had fetuses with non immune hydrops fetalis detected by ultrasonography (non
Patterns of serum aspartic and alanine aminotransferase as well as aldolase activity in attacks of bronchial asthma, paroxysmal tachycardia and pulmonary edema.
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[Behavior of the activity of aspartate aminotransferase and alanine aminotransferase in attacks of bronchial asthma, pulmonary edema and paroxysmal tachycardia].
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[Pattern of activity of aspartic aminotransferase, alanine aminotransferase and aldolase in attacks of bronchial asthma, paroxysmal tachycardia and pulmonary edema].
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Diminished but Not Abolished Effect of Two His351 Mutants of Anthrax Edema Factor in a Murine Model.
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Edema toxin (ET), which is composed of a potent adenylate cyclase (AC), edema factor (EF), and protective antigen (PA), is one of the major toxicity factors of Bacillus anthracis. In this study, we introduced mutations in full-length EF to generate alanine EF(H351A) and arginine EF(H351R) variants.
Differences in regional myocardial perfusion, metabolism, MVO2, and edema after coronary sinus machine perfusion preservation of canine hearts.
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Machine perfusion improves solid organ preservation for transplantation. We have demonstrated that antegrade perfusion preservation of hearts is superior to cold storage but may be limited by aortic valve incompetence. We hypothesized that retrograde perfusion (RP) through the coronary sinus may
Structure of anthrax edema factor-calmodulin-adenosine 5'-(alpha,beta-methylene)-triphosphate complex reveals an alternative mode of ATP binding to the catalytic site.
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Anthrax edema factor (EF) is a key virulence factor secreted by Bacillus anthracis. Here, we report a structure, at 3.0 A resolution, of the catalytic domain of EF (EF3) in complex with calmodulin (CaM) and adenosine 5'-(alpha,beta-methylene)-triphosphate (AMPCPP). Although the binding of the
Effect of Hydroxyethyl Starch Priming on the Systemic Inflammatory Response and Lung Edema after Cardiopulmonary Bypass in a Rat Model.
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Cardiopulmonary bypass (CPB) preserves patients' lives during open heart surgery by providing sufficient oxygen delivery and blood supply to vital organs. However, previous studies have suggested that the interaction of hemodilution and vascular hyperpermeability induces tissue edema and an
Association of nonimmune hydrops fetalis with familial hemophagocytic lymphohistiocytosis in identical twin neonates with perforin His222Arg (c665A>G) mutation.
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BACKGROUND
This is the first study demonstrating that nonimmune hydrops fetalis (NIHF) in identical twin neonates is associated with biallelic gene defect causing familial hemophagocytic lymphohistiocytosis.
METHODS
Preterm male twins (31(4/7) wk) with NIHF and hepatosplenomegaly gradually developed
MD simulations of anthrax edema factor: calmodulin complexes with mutations in the edema factor "switch a" region and docking of 3'-deoxy ATP into the adenylyl cyclase active site of wild-type and mutant edema factor variants.
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Bacillus anthracis, a spore-forming infectious bacterium, produces an exotoxin, called the edema factor (EF), that functions in part by disrupting internal signalling pathways. When complexed with human host cell calmodulin (CaM), EF becomes an active adenylyl cyclase, producing the internal signal
Rifaximin, but not growth factor 1, reduces brain edema in cirrhotic rats.
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OBJECTIVE
To compare rifaximin and insulin-like growth factor (IGF)-1 treatment of hyperammonemia and brain edema in cirrhotic rats with portal occlusion.
METHODS
Rats with CCl₄-induced cirrhosis with ascites plus portal vein occlusion and controls were randomized into six groups: Cirrhosis;
Anti-inflammatory effects of anthocyanins-rich extract from bilberry (Vaccinium myrtillus L.) on croton oil-induced ear edema and Propionibacterium acnes plus LPS-induced liver damage in mice.
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Bilberry (Vaccinium myrtillus L.) has been known to play a protective role in human health due to its high anthocyanin content. This study investigated the anti-inflammatory effects of bilberry extract (BE, containing 42.04% anthocyanin) on Propionibacterium acnes (P. acnes) plus lipopolysaccharide
[Sequential observations of brain edema with proton magnetic resonance imaging and spectroscopy].
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The purpose of this study was to assess the relationship between morphological and metabolic changes in brain edema using proton magnetic resonance systems. The serial changes during the first 24 hours in the cold-injury trauma rat brain model were investigated by proton magnetic resonance imaging
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