An unusual variant of the gastroepiploic artery: case report.
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Aged↗
Biomedical subjects
D Kaura
Publications and source records attributed to D Kaura.
Wegener's presenting as submandibular swelling.
We describe a patient in whom bilateral swelling of submandibular glands was the initial manifestation of limited Wegener's disease. The diagnosis was based on positive anti-neutrophil cytoplasmic antibody [C-ANCA], dense inflammatory infiltrate predominantly of lymphocytes in submandibular glands, presence of non-caseating ill-formed granulomas in transbronchial biopsy and resolution of symptoms following immuno-suppressive treatment.
Antibodies, Antineutrophil Cytoplasmic↗
Mechanisms of subcellular remodelling in post-infarct heart failure.
Occlusion of a coronary artery results in myocardial ischemia and subsequent myocardial infarction. Whenever the infarct size is more than 30% of the ventricular wall, the remaining myocardium attempts to compensate for the loss of muscle mass by changing the size and shape of cardiocytes in addition to developing cardiac hypertrophy, cardiac dilatation and congestive heart failure. This remodeling of the heart is associated with changes in the extracellular matrix including collagen proteins and is most probably due to the activation of both sympathetic nervous system and renin-angiotensin system as well as increased formation of various growth factors. Alterations in contractile function of the infarcted heart are associated with remodelling of the sarcoplasmic reticulum with respect to Ca(2+)-pump and Ca(2+)-release channels as well as contractile and regulatory proteins of the myofibrils. Myocardial infarction has also been shown to result in remodelling of the sarcolemmal membrane with respect to Ca(2+)-channels, Ca(2+)-transport systems, cardiac receptors and signal transduction mechanisms. Although information regarding remodelling of mitochondria in the infarcted heart is limited, alterations in energy yielding and Ca(2+)-accumulating systems are suspected. Accordingly, it is suggested that changes in cardiac contractile dysfunction due to myocardial infarction are associated with remodeling of both extracellular matrix and subcellular organelles in the heart.
Animals↗
Multiple endocrine neoplasia type-1.
A 38-year-old man with multiple endocrine neoplasia type-1 (Wermer's syndrome) is described. The patient had refractory duodenal ulcers and raised basal acid output (55 mmol/hour) and fasting serum gastrin (1190 pg/ml). Abdominal CT scan revealed mass lesions (gastrinomas) in the head of the pancreas. He also had persistent hypercalcemia, hypophosphatemia, right ureteric calculi, increased urinary calcium and phosphorus and enlarged parathyroids on ultrasound and CT of the neck. Parathormone level was raised, but the pituitary gland was normal on CT scan of the head. The patient was managed initially with histamine H2-blockers, omeprazole and parathyroidectomy; enucleation of the tumor masses in the pancreas was done subsequently.
Adult↗
Alterations in duodenal disaccharidases in chronic smokers.
OBJECTIVE: To assess the effect of smoking on activity of intestinal disaccharidases. METHODS: The study was conducted on patients with non-ulcer dyspepsia who were smokers (n=20) or non-smokers (n=20). Smokers were classified according to smoking index into mild, moderate and heavy smokers. Biopsy specimens were taken from the second part of the duodenum at endoscopy and examined histologically, and for disaccharidase (lactase, sucrase, maltase and trehalase) activities. RESULTS: Mean duration of symptoms was more in smokers than in non-smokers. None of the smokers had endoscopic evidence of duodenal inflammation. Lactase and trehalase levels were significantly decreased in smokers. There was no difference in enzyme levels between mild smokers and non-smokers. Decreased lactase, maltase and trehalase activities were observed in moderate smokers compared to mild smokers. Duration of symptoms had no relation to enzyme activities. CONCLUSIONS: Intestinal disaccharidase levels are diminished by smoking.
Adult↗
Beta-adrenoceptor mediated signal transduction in congestive heart failure in cardiomyopathic (UM-X7.1) hamsters.
In view of the lack of information regarding the status of beta-adrenoceptor mediated signal transduction mechanisms at severe stages of congestive heart failure, the status of beta-adrenoceptors, G-proteins and adenylyl cyclase activities was examined in 220-275 day old cardiomyopathic hamster hearts. Although no changes in the Kd values for beta 1- and beta 2-adrenoceptors were seen, the number of beta 1-adrenoceptors, unlike that of beta 2-adrenoceptors, was markedly decreased in cardiac membranes from failing hearts. The activation of adenylyl cyclase in the failing hearts by different concentrations of isoproterenol was also attenuated in comparison to the control preparations. The basal adenylyl cyclase activity in cardiac membranes from the failing hearts was not altered; however, the stimulated enzyme activities, when measured in the presence of forskolin, NaF or Gpp(NH)p were depressed significantly. The functional activity of Gs-proteins (measured by cholera toxin stimulation of adenylyl cyclase) was depressed whereas that of Gi-proteins (measured by pertussis toxin stimulation of adenylyl cyclase) was increased in the failing hearts. Not only were the Gs- and Gi-protein contents (measured by immunoblotting) increased, the bioactivities of these proteins as determined by ADP-ribosylations in the presence of cholera toxin and pertussis toxin, respectively, were also higher in failing hearts in comparison to the control values. Northern blot analysis revealed that the signals for Gs- and Gi-protein mRNAs were augmented at this stage of heart failure. These results indicate that the loss of adrenergic support at severe stages of congestive heart failure in cardiomyopathic hamsters may involve a reduction in the number of beta 1-adrenoceptors, and an increase in Gi-protein contents as well as bioactivities in addition to an uncoupling of Gs-proteins from the catalytic site of adenylyl cyclase in cardiac membrane.
Adenylate Cyclase Toxin↗