Biomedical subjects
Publications and source records attributed to M Singer.
A case report of bleeding from a Meckel's diverticulum diagnosed by Tc99-m pertechnetate scanning is presented. The noninvasive advantage of this method justifies its early use as a diagnostic measure when a Meckel's diverticulum is suspected in the differential diagnosis of lower gastrointestinal bleeding.
Diazepam did not appreciably alter the exocrine pancreatic response to exogenous hormones in nonalcoholic and chronicalcoholic dogs. The use of diazepam during experiments in dogs will therefore not significantly affect measurement of pancreatic secretory capacity.
In five dogs with chronic gastric fistulas (Thomas cannula) and a new type of chronic pancreatic fistula which permits collection of pure nonactivated pancreatic juice after ingestion of a test meal, the following series of experiments were performed: In the first series, a test meal (400 gm. canned dog meat) was given with 200 ml. saline simultaneously infused through the gastric cannula. In response to this stimulus, the 20-minute peak pancreatic flow rate and bicarbonate output were respectively 33% and 34%, of the maximal secretion of the pancreatic gland obtained with secretin in six control dogs provided with gastric and the classical Thomas duodenal fistula. The 20-minute peak protein output represented 84% of the maximal secretory capacity attained with dose-response curves to CCK in the same group of control animals. In the second series either 1.5 or 2.0 gm./kg. ethanol were given instead of saline. Intragastric ethanol induced a dissociation of pancreatic secretion: a significant inhibition of flow rate, of bicarbonate concentration and output and a significant rise of protein concentration; protein output remaining unchanged. It is postulated that ethanol, acting on the stomach and duodenojejunum, evokes, independently of its gastrin-releasing capacity, and unknown humoral or nervous mechanism that counteracts the ethanol-elicited cholinergic-mediated inhibition of pancreatic protein secretion which has been previously described.
Synapse-like structures occurring in regenerating crayfish peripheral nerves are characterized by aggregates of small (250 to 600 A) electron lucent vesicles adjacent to a thickened "presynaptic" membrane. Such synaptoid profiles are seen opposite other axons, glial processes or extracellular fibrous material. Junctions with cellular elements do not show "postsynaptic" specializations. These complexes are compared to axo-glial synapses in the developing spinal cord and to synaptoid configurations observed by others in vertebrate and invertebrate neurosecretory systems.
The loss in protein synthesis which the regenerating forelimb of the newt suffers after denervation can be recovered by infusing into it an extract of newt soluble brain protein. Moreover, the synthesis of basic protein shows a greater response to the active brain principle than does that of acidic protein. The active agent of the nervous tissue is destroyed by heat and trypsin digestion. Extracts of liver and spleen, similarly prepared, do not evoke recovery of lost protein synthesis. Synaptosomal extracts of the frog brain also cause recovery of protein synthesis in the denervated regenerate, demonstrating the likelihood that the active agent is not species-specific within these amphibians, that it is a constituent of the neuronal fraction of nervous tissue, and that it is present in axonal terminals. Additional experiments showed that the nervous agent is likely a basic protein, and that the amount of protein infused is of the order of only 1.0% of the total regenerate protein. The significance of the findings is discussed in relation to the nature of the effect on protein synthesis and the nature of the active principle.
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In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.
247 polyps were removed by electroresection through an endoscope (and 240 recovered) in 160 patients, aged 24-81 years. The histological substrate varied widely. Comparison of histological findings in the biopsy specimen with those of the entire polyp after polypectomy gave differing results in 41 of 87 gastric polyps. Complication rate of endoscopic polypectomy was 1.6%: postoperative bleeding occurred in three, which was treated conservatively, while in one patient ligation of a blood vessel by laparotomy became necessary. There were no perforation or lethal complications. Among three patients with hyperplasiogenic gastric polyps a "borderline lesion" was found in two (early carcinoma type I; adenocarcinoma). In 13 other patients with hyperplasiogenic polyps follow-up examination after one year revealed recurrence in three, absence of polyps in eight. In one patient a small gastric carcinoma (about 1 cm in diameter) was discovered four months later. It is possible that patients with hyperplasiogenic polyps are at a higher risk of cancer. Six-monthly endoscopic observation is, therefore, indicated.
Ruthenium red and horseradish peroxidase were used to compare the uptake of exogenous molecules into crayfish motor axons and their sheaths in severed and intact peripheral nerves. Both tracers penetrated the axonal sheath and were subsequently seen lining small vesicles and tubules in the axoplasm. Tracer appeared to enter the axon via pinocytotic vesicles. There were no perceptible quantitative or qualitative differences in ruthenium red uptake between intact and severed axons. However, counts of tracer-filled vesicles in axons exposed to peroxidase showed that at least three times as much tracer penetrated the severed as opposed to the intact axons.
The interaction of supercoiled, circular SV40 DNA with calf thymus histone fractions has been studied. Five- to ten-fold less f1 histone is required to complex a given amount of DNA compared to the other histones. When the supercoiled DNA is converted to either the relaxed circular form, or full length linear molecules, or gragmented linear or denatured stands, the efficiency of complex formation with f1 histone markedly decreases. We conclude that f1 histone has a special ability to interact with supercoiled DNA. This conclusion is supported by the fact that supercoiled circular Col E1 DNA interacts with f1 as efficiently as does SV40 DNA.
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Wallerian degeneration in the severed newt's (Triturus viridescens) optic nerve is complete between the 10-14th post operative day (p.o.d.). Consequently, the newt optic nerve displays one of the most rapid degenerative responses yet reported for the central nervous system of vertebrates. In most cases it also exhibits the speed of degenerative phenomenon in the vertebrate peripheral nervous system. The degeneration of unmyelinated axons is most rapid and is completed by 2-3 p.o.d., compared to myelinated axons, most of which degenerate between 2-10 p.o.d. Myelin ring formation (vesicular transformation) is the principal form of lamellar breakdown and occurs in a highly organized manner which can be clearly staged. The glial cell response to Wallerian degneration is two-fold: cytoplasmic hypertrophy and myelin-lytic. Glial hypertrophy subsides by the 10-14 p.o.d. with the ingrowth of numerous regenerating nerve fibers. The myelin-lytic response accounts for most of the myelin destruction. Leukocyte-like and microglia-like cells also participate in myelin breakdown but to a lesser degree.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.