Preoperative diagnosis of intraductal papillary mucinous tumors of the pancreas by endoscopic pancreatic biopsy.
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Biomedical subjects
Publications and source records attributed to F Moses.
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Nonsteroidal antiinflammatory drugs can be associated with benign colonic ulcers. The ulcers are easily diagnosed by colonoscopy, and, if uncomplicated, they are best treated by cessation of the nonsteroidal antiinflammatory drugs. Benign colonic ulcers should be included in the differential diagnosis of any patient who presents with gastrointestinal complaints and is taking nonsteroidal antiinflammatory drugs.
As part of a study of the effects of lithium carbonate on neurochemical function in man, platelet and lymphocyte adenylate cyclase activity and lymphocyte beta-adrenergic receptor binding characteristics were determined before and after 2 weeks of lithium treatment in 10 normal volunteers. Lithium had differential effects on platelet and lymphocyte adenylate cyclase activity. In platelets, basal and stimulated (guanyl imidodiphosphate [Gpp[NH]p] or cesium fluoride) adenylate cyclase activity was significantly augmented by lithium treatment. By contrast, in lymphocytes, Gpp(NH)p- and cesium fluoride-stimulated adenylate cyclase activity was unaffected, while basal activity was decreased modestly after lithium. These results are consistent with preclinical studies that suggest that lithium's effects on adenylate cyclase activity are specific with respect to tissue and brain region and that lithium may interfere with guanine nucleotide binding (G) protein function. Lithium treatment significantly increased the ratio of low- to high-affinity dissociation constants for agonist displacement of antagonist binding to lymphocyte beta-adrenergic receptors (thought to reflect coupling between the beta-adrenergic receptor and stimulatory G protein). Lithium had significant effects on measures associated with signal transduction that might be contrasted to its more subtle effects on neuronal function (norepinephrine release) and neuroendocrine systems (responses to serotoninergic challenge) in these same subjects (reported in a companion article). Lithium's primary site of action may be on signal transduction mechanisms. These effects subsequently may be manifested in changes in neurotransmitter function that may be important to lithium's mood-stabilizing actions.
After angioplasty of the superficial femoral artery at Hunter's canal in a 65-year-old woman thrombosis developed and femoropopliteal bypass grafting was necessary. Four weeks later the graft occluded, successful thrombectomy was performed with a Fogarty catheter and the patient heparinised. Three days later a pseudoaneurysm developed on the posterior tibial artery which was excised and the artery which was longitudinally torn repaired with a vein graft giving good functional results. Complications after Fogarty balloon catheter thrombectomy are relatively rare but Pseudoaneurysms can occur after perforation or rupture of smaller vessels.
In primary cultures of cerebellar granule cells of the rat, the accumulation of cyclic GMP was stimulated by glutamate, acting at the N-methyl-D-aspartate recognition site, and by atrial natriuretic factor. The response to glutamate was calcium-dependent, while the response to atrial natriuretic factor was not. Ethanol inhibited the accumulation of cyclic GMP in response to both glutamate and atrial natriuretic factor. However, the response to glutamate was much more sensitive to ethanol, with 30-40% inhibition occurring at 50 mM ethanol. Substantial inhibition of the response to atrial natriuretic factor was observed only at concentrations of ethanol of 200 mM or larger. The data suggest that a major site of action of ethanol in inhibiting the accumulation of cyclic GMP is the coupling of the glutamate receptor to soluble guanylate cyclase. The effect of ethanol on agonist-activated activity of guanylate cyclase may contribute to the pharmacological action of ethanol in vivo.
Measurements of calcium uptake and cyclic GMP production by cerebellar granule cells grown in primary culture demonstrated that ethanol preferentially inhibited N-methyl-D-aspartate (NMDA) receptor-gated cation channel function. Concentrations of ethanol as low as 10 mM inhibited NMDA-stimulated Ca2+ uptake by greater than 30%, and ethanol also inhibited NMDA-stimulated (Ca2+-dependent) cyclic GMP accumulation in a similar, dose-dependent manner. Responses to kainate were significantly less sensitive to ethanol. Studies using various concentrations of NMDA, as well as phencyclidine (PCP) and glycine, suggested that ethanol affected the "coagonist" binding site of the NMDA receptor-channel complex, rather than the PCP recognition site.
Phosphatidylinositol 4,5-bisphosphate (PIP2) breakdown was stimulated by agonists acting at muscarinic cholinergic and alpha 1-adrenergic receptors in mouse brain. Ethanol, in vitro, inhibited basal cerebral cortical PIP2 breakdown with a threshold concentration of 75-100 mM. Basal PIP2 breakdown in hippocampus and striatum was less sensitive to ethanol. A high concentration of ethanol (500 mM) increased the EC50 for carbachol stimulation of PIP2 breakdown in all three brain areas, but had no effect on the EC50 for norepinephrine. Following chronic ingestion of ethanol by mice, the EC50 for carbachol stimulation of PIP2 breakdown in cortex was decreased, and there was no change in striatum. These effects were consistent with previously observed increases in quinuclidinylbenzilate (QNB) binding in cortex, but not striatum, of mice fed ethanol chronically. However, in hippocampus, where chronic ethanol ingestion had also induced an increase in QNB binding, the EC50 for carbachol stimulation of PIP2 breakdown was increased. Binding studies using the specific M1 muscarinic cholinergic receptor antagonist, pirenzepine, revealed that the number of pirenzepine-binding sites was increased in cortex, but not hippocampus (or striatum) of ethanol-fed mice. These results support the hypothesis that high affinity pirenzepine-binding sites are coupled to PIP2 breakdown in mouse cortex. The changes in cerebral cortex represent one of the first demonstrations of a functional correlate of a change in receptor density in ethanol-treated animals. Increased sensitivity to cholinergic agonists in cortex may contribute to particular signs of ethanol withdrawal.
Tranylcypromine produces behavioral excitation while pargyline produces depression. Tranylcypromine increased brain tryptophan which led to an accumulation of tryptamine. The levels of tryptamine after tranylcypromine were found to be 3 times those found after pargyline.
Cessation of chronic ethanol administration, and elimination of ethanol from the body, results in a withdrawal syndrome in mice characterized by behavioural symptoms and hypothermia. During withdrawal, the accumulation rate of [14C] 5-hydroxytryptamine (5-HT) from [14C]tryptophan, was significantly lower in the brainstem of the ethanol-withdrawn animals than in controls. A similar pattern was seen in forebrain. When the rate of 5-HT accumulation was determined using pargyline, no differences occurred between control and ethanol-treated animals. The endogenous concentrations of tryptophan in plasma, and tryptophan, 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) in brain were the same in ethanol-treated and control animals. It is suggested that the changes in accumulation of 14C-5-HT and 14C-5-HIAA in ethanol-withdrawn animals reflected alterations in electrical activity of serotoninergic neurons during withdrawal.
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Episiotomy is a well-established procedure in obstetric care worldwide. This article examines the available research and literature on episiotomy vs perineal tear to determine whether there is any evidence that episiotomy is indeed less traumatic than allowing the perineum to tear.