Biomedical subjects
Publications and source records attributed to A Kohn.
Balanorchis anastrophus Fischoeder, 1901, from the reticulum of Bos taurus is reported for the first time in the State of Pará, Brazil. The surface topography as revealed by scanning electron microscopy is presented.
We assessed the effect of long-lasting inhibition of gastric acid secretion on basal and meal-stimulated serum gastrin and gastric acid secretion in 37 patients on long-term maintenance treatment with H2 antagonists for severe relapsing and/or complicated duodenal ulcer disease. After a mean of 142 weeks (range, 28-324 weeks) of continuous treatment, gastric acid secretion, basal plasma gastrin, and gastrin response to a test meal were evaluated. All tests were performed a week after drug discontinuation to exclude rapidly reversible hypergastrinemia. Gastrin levels were above the normal range in seven patients (18.9%). After H2 antagonist were stopped for 6 weeks, basal gastrin returned to normal levels in all cases [from a median of 180 (range, 130-350) pg/ml to 58 (25-90) pg/ml] and peak meal-stimulated gastrin significantly decreased from a median of 500 pg/ml to 245 pg/ml (p = 0.02). In patients with hypergastrinemia, the discontinuation of H2 antagonists for 6 weeks led to a significant decrease of gastric acid secretion. Patients who developed hypergastrinemia spent more weeks on full-dose treatment and had more recurrences during therapy. The results of the present investigation demonstrate that a long-lasting inhibition of gastric acid secretion can induce, in a small percentage of patients, a reversible sustained hypergastrinemia and a consequent increase of acid secretion, which conceivably could lead to more frequent relapses of duodenal ulcer disease.
The action of the ether of artemisinin (artemether) on Schistosoma mansoni in mice and hamsters experimentally infected with the LE strain was studied. In mice, the drug showed high schistosomicidal activity using a single intramuscular dose of 100 mg/kg/day. By the oral route, this dose showed a low activity. Mice treated with a single intramuscular dose of 200 mg/kg/day, and examined 15 days after treatment, presented 100% alteration of the oogram; when examined 45 days after treatment, the oogram was normal. With doses of 100 mg/kg/day, i.m., during 3 or 5 consecutive days, the death rate of mice was very high. Morphologic analysis of the worms collected by perfusion of mice treated with a single dose of 100 mg/kg/day, i.m., detected a marked decrease in the length of male and female worms, degenerative alterations in the parenchyma and in the reproductive system of the females, with the reduction of vitellinic material and in ovary volume; the intestinal contents presented a marked despigmentation. In the male worms significant alteration was not apparent by optical microscopy.
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Mammalian or avian cells were labeled with a fluorescent probe DPH (1,6-diphenyl-1,3,5-hexatriene). Within a few minutes after adsorption of various naked and enveloped viruses, the degree of fluorescence polarization (P) of the DPH embedded in the adsorbing cells as measured at 37 degrees C, was reduced, a finding indicating a decrease in the microviscosity of the lipids in the cell membrane. This change of fluidity was proportional to the concentration of the adsorbing virus and could be abolished or inhibited by homologous specific antiviral sera, but not by heterologous sera. Potential use of fluorescence polarization tests is described for titration of virus concentration, as well as for serological identification of a virus.
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The authors observed the motility of 1067 worms used as a biological parameter indicating the vitality of the parasites, to define the survival time of S. mansoni males and females in 0,85% NaCl and PBS. Among the worms observed in 0,85% NaCl the mean time of survival in minutes was 204 for males and 240 for females and in PBS it was 267 min. for males and 344 min. for females. All the tested differences (media, sex; sex for saline group; sex for PBS group) were significant at a 0.0001 level.
In order to elucidate the nature of the fibrous network present in Schistosoma mansoni tegument, adult worms were studied by light and electron microscopy. It was suggested that this network is formed by bundles of tubular microfibrils 10--12 nm in diameter, similar to oxytalan microfibrils present in higher animals.
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Adsorption of Sendai virus at high multiplicity (500-1,000 HAU/10(6) cells) to HeLa cells grown in monolayers causes immediate changes in the ion barrier of the cell membrane, as well as changes in the morphology of the virus-treated cells. Within minutes of adsorption the cells begin to lose potassium and an extensive influx of ions into the cells occurs. Concomitantly with these changes, the cell membrane becomes depolarized, and the resting potential across its membrane decreases. Twenty to sixty minutes post adsorption the damage to the cell membrane is repaired, and both the potassium uptake and the resting potential return to their pre-exposure values. Scanning electron-micrographs of Sendai infected cells incubated at 37 degrees C show formation of bridging microvilli in a zipper-like fashion within two to five minutes post-adsorption; 30 to 60 minutes thereafter the majority of cells in the monolayer are fused. Biochemical changes induced by virus adsorption and the role of Ca++ ions in the observed effects are discussed.
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Viral infection of cells causes chemical and metabolic changes, which can be detected by gas chromatography (GC) of ether extracts of supernatant fluids and cell homogenates before any significant damage to the cells is observable microscopically. The characteristic and specific GC patterns obtained from BHK-21 and Vero cell cultures infected with encephalomyocarditis, polio, echoviruses, and a togavirus make it possible to distinguish between these infecting viruses. The appearance of 1 or 2 compounds, represented by GC peaks with TR values of 302 and 677 seconds seems to be specific for these viruses. Other peaks found in the supernatant media 1-2 hours after infection probably represent cell constituents leaking into the medium as a result of damage to the cell membrane by the invading virus.
Changes in the dynamic behavior of membrane lipids of mammalian cells induced by adsorption of animal viruses were quantitatively monitored by fluorescence polarization analysis with the aid of the fluorescent probe 1,6-diphenyl 1,3,5-hexatriene embedded in the surface membrane lipid core of intact cells. Adsorption of encephalomyocarditis, West Nile, and polyoma viruses to hamster (baby hamster kidney) and mouse (3T3) cells is accompanied by a rapid and significant increase in the degree of fluidity of membrane lipids of the infected cells. These changes in membrane fluidity, which are virus dose dependent, are inhibited by low temperature and by treatment of the cells before-hand with compounds known to block viral receptors on the cell surface. It is suggested that increase in membrane lipid fluidity, induced by the adsorption of virions, is an early event in the process of cell-virus interactions.