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Biomedical subjects

G D Abrams

Publications and source records attributed to G D Abrams.

At least 73 records · Page 4Linked to original sources
PubMed1978

Production of an antibiotic substance by Bacillus licheniformis within the digestive tract of gnotobiotic mice.

In monoxenic mice, vegetative cells and spores of Bacillus licheniformis were enumerated and in vivo antibiotic production was measured at various levels of the digestive tract and in the feces. The apparent independence of vegetative cell and spore populations in the cecum and feces, as well as the marked fluctuations of these two populations in the stomach and small intestine, suggested that sporulation of B. licheniformis and production of antibiotic occur only in the upper levels of the digestive tract. Study of dixenic models wherein B. licheniformis was inoculated after Clostridium perfringens or Lactobacillus sp. or before Lactobacillus sp. revealed the simultaneous disappearance of B. licheniformis from the stomach and antibiotic from the feces. This strain persisted in the cecum, but only in the form of vegetative cells. These models demonstrate that the activity of the microflora in the upper segments can affect the equilibrium of the microflora throughout the digestive tract.

Animals↗
PubMed1977

Pilot studies on recombinant cold-adapted live type A and B influenza virus vaccines.

Recombinant live attenuated type A and B influenza virus vaccines derived from standardized cold-adapted parent strains were given singly and in combination to volunteers. The vaccine viruses were well tolerated, functioned as good antigens, and failed to spread to intimate household contacts. Thirty-nine isolates that were recovered after a single passage in humans appeared genetically stable. The results of histopathologic studies in ferrets encourage development of an animal model for attenuation of the virus.

Animals↗
PubMed1977

Antagonistic effect of extremely oxygen-sensitive clostridia from the microflora of conventional mice and of Escherichia coli against Shigella flexneri in the digestive tract of gnotobiotic mice.

Two extremely oxygen-sensitive strains of Clostridium sp., designated Clostridium E and P, were obtained from digestive microflora of conventional mice and found to constitute a barrier against Shigella flexneri SF-2 when associated in vivo with Escherichia coli K-12. These and other simplified fractions of the conventional microflora were demonstrated to have an effect comparable to that of the total flora. When K-12 and Clostridium E were established in gnotobiotic mice before the introduction of SF-2, the latter was reduced to a level below detection in the digestive tract. Whe SF-2 was established first, the antagonistic effect exerted by Clostridium E and K-12 was variable and, apparently, related to the rate of establishment of Clostridium E. Mutants of SF-2 resistant to the barrier effect of Clostridium E and K-12 appeared at the end of 3 months when SF-2 was established in gnotobiotic mice alone or with K-12, and after only a week when SF-2 was associated only with Clostridium E. These results suggest that the bacterial antagonsim in this model is related to the production in vivo of an antibiotic substance active against SF-2. It appears that the substance may be produced by Clostridium E, stimulated by K-12.

Anaerobiosis↗
PubMed1977

Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog.

Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left anterior descending artery (LAD). Infarct size was determined by dehydrogenase staining after 24 or 96 hours. Heart slices were incubated with nitro-blue tetrazolium and nonstaining infarcted tissue was dissected and weighed. Myocardial depletion of creatine phosphokinase activity (CPK) and lactate dehydrogenase activity (LDH) were determined 24 hours after temporary LCX occlusion. When measured after 24 hours, methylprednisolone sodium succinate treatment did not reduce infarct size or decrease enzyme loss. After temporary LCX occlusion infarct size was 30.4 +/- 3.6% of left ventricular weight in control dogs and 30.0 +/- 2.3% in treated dogs. No significant difference in infarct size was observed in hearts examined 24 or 96 hours after myocardial infarction. After permanent LAD occlusion, infarct size in control dogs was 39.2 +/- 1.6% of left ventricular weight and 33.7 +/- 3.5% in treated dogs. CPK activity in the LCX area decreased by 26.5 +/- 7% in controls and by 28.1% +/- 7% in treated dogs. Treated dogs sustained a significantly greater fall in arterial blood pressure after LCX occlusion than did controls. During LCX occlusion and upon reperfusion, methylprednisolone sodium succinate treated dogs exhibited a significantly greater number of premature ventricular beats. Since infarct size and enzyme depletion were not reduced when measured after 24 hours, methylprednisolone sodium succinate treatment does not appear to have enhanced myocardial cell viability.

Animals↗
PubMed1976

Inhibition of Clostridium perfringens by an antibiotic substance produced by Bacillus licheniformis in the digestive tract of gnotobiotic mice: effect on other bacteria from the digestive tract.

A strain of Bacillus licheniformis, established in the digestive tract of gnotobiotic mice, inhibited the subsequent establishment of a Clostridium perfringens strain ingested by the animals. This inhibitory effect depended on the in vivo production by B. licheniformis of an antibiotic substance having a number of the characteristics of bacitracin. If C. perfringens was the first to become established in the digestive tract of the gnotobiotic mice, B. licheniformis also became established but did not produce any antibiotic. Mutants of C. perfringens resistant to the antibiotic substance were not observed when the antibiotic was produced in situ by B. licheniformis, but were rapidly selected when the Bacillus culture filtrate or bacitracin was administered per os. B. licheniformis was also capable of eliminating from the digestive tract 5 of the 13 additional bacterial strains tested.

Animals↗
PubMed1976

Adhesive properties of Vibrio cholerae: adhesion to isolated rabbit brush border membranes and hemagglutinating activity.

Adhesion of vibrios to the small intestine may occur (i) by association of the bacteria with secreted mucus gel or (ii) by adherence of the bacteria to the surface of epithelial cells. In the present study, vibrios readily adhered to isolated brush border membranes obtained from rabbit intestinal epithelial cells. Adhesion was temperature dependent and required the presence of divalent cations such as calcium. The agglutination of human O erythrocytes by Vibrio cholerae was observed also, and the hemagglutination test appeared to detect the same mechanism that was involved in the adhesion of vibrios to brush borders. When the bacteria were grown in broth they were adhesive and hemagglutinating, but vibrios grown on agar plates or suspended in buffer for 15 min at 37 C lacked these abilities, even though they retained undiminished motility. These two model systems differed, however, in that strontium promoted only adhesion to brush borders. The significance of this difference remains to be determined. Vibrios were observed to penetrate intestinal mucus gel and occasionally to become entrapped in it. However, there was no evidence that vibrios attached to mucus gel.

ABO Blood-Group System↗
PubMed1976

Pathogenetic mechanisms in immune polioencephalomyelitis: induction of disease in immunosuppressed mice.

Immune polioencephalomyelitis (IPE) was induced by the i.p. injection of x-irradiated (10, 000 R) syngeneic line Ib malignant lymphocytes into C58 mice that were 7 or more months old and in young mice immunosuppressed by x-ray or drugs. The occurrence of IPE in young immunosuppressed C58 mice was systematically analyzed. When mice less than 2 weeks old were x-irradiated with 600 R, IPE could not be induced. The incidence in 1-month-old mice was approximately 50% and increased progressively with the age except for a drop in incidence at 3 months. An analysis of the dose effects of x-irradiation on the occurrence of IPE in mice of different ages revealed a marked increase in the incidence in 3- and 5-month-old mice beginning at dose levels of 450 R and 300 R, respectively. Considered together, these data indicated that two subpopulations of immunocytes differing in x-ray sensitivity interacted to protect mice from IPE. It appears that under natural conditions an x-ray sensitive cell population, possibly having suppressor function, decreased with age and made mice susceptible ot induction of IPE. Five-month-old mice were immunosuppressed with an LD10 of cyclophosphamide, prednisolone, or methotrexate to determine whether mice immunosuppressed with drugs also were susceptible to the induction of IPE. The incidence was 89%, 13%, and 5%, respectively. The mouse strain specificity of IPE induction also was studied. In 6- to 8-month-old mice suppressed with 600 R, IPE could not be induced in non-H-2k strains: BALB, C57BL/6, NZB. Of the H-2K strains tested (CBA/J, C3H/He, AKR/J, C58), the disease could be induced only in the C58 and AKR/J strains. Histopathologic studies showed that CNS lesions in immunosuppressed C58 and AKR/J mice did not differ significantly from those in old C58 mice with IPE. Taken together, the results of these studies indicate that IPE can be used as a model for analyzing age-dependent diseases of suspected immunopathologic etiology.

Aging↗
PubMed1976

Ischemic changes in the canine heart as affected by the dimethyl quaternary analog of propranolol, UM-272 (SC-27761).

The effects of the dimethyl quarternary analog of propranolol, UM-272, on myocardial infarct volume were studied in the canine heart. Myocardial infarction was produced by occlusion of the left circumflex coronary artery for 60 minutes followed by reperfusion and quantitation of infarct volume 24 hours later. Groups of dogs were either untreated or pretreated with UM-272 with an initial loading dose of 5.0 mg/kg (group A) or 2.5 mg/kg (group B) 30 minutes before occlusion of the left circumflex coronary artery. Both group A and group B animals received additional doses of 2.5 mg/kg of UM-272 every 90 minutes for a period of 6 hours so that the total respective doses were 15 and 12.5 mg/kg. Control animals received comparable volumes of 0.9% sodium chloride solution. All animals were followed throughout the 6-hour procedure with continuous electrocardiographic recordings which were used to assess the effects of acute myocardial ischemia upon disturbances in cardiac rhythm and the effects of drug treatment. Dogs which survived the procedure were given tetracycline i.v. the next day and sacrificed 1 hour later by an overdose of pentobarbital sodium. The hearts were removed and the left ventricle was sliced and examined first under ultraviolet light to localize the ischemic zone by noting the tetracycline fluorescence. The ventricular slices were next incubated in nitro blue tetrazolium which stains normal myocardial tissue, thus allowing one to quantitate the volume of infarcted myocardium by excising and weighing the nonstained and stained muscle separately. The untreated control group had an infarct volume of 23.8 +/- 3.2 g/100 g of left ventricle. The treated animals in groups A and B had respective infarct volumes of 2.3 +/- 0.8 g/100 g (P less than .001) and 7.0 +/- 3.3 g/100 g (P less than .025) of left ventricle. During the acute phase of ischemia and reperfusion, arrhythmias and alterations in the ST-segment, R-wave amplituted and development of pathologic Q-waves were more prominent in the untreated animals and almost totally absent in the treated animals. UM-272 produced a dose-dependent decrease in heart rate as well as a decrease in developed isometric tension. Pretreatment with UM-272 did not prevent the derangement of function in the ischemic zone nor did it permit a return of function upon reperfusion, even though it reduced the degree of cellular damage resulting from 60 minutes of regional ischemia. A possible mechanism for the protective effect of UM-272 may be through its ability to reduce myocardial contractility and heart rate, both of which would reduce myocardial oxygen consumption and thus produce a more favorable balance between myocardial oxygen supply and myocardial oxygen demand.

Animals↗
PubMed1972

Function of various intestinal bacteria in converting germfree mice to the normal state.

Earlier work had shown that a collection of anaerobic bacteria, in conjunction with facultative anaerobes, may be implanted into germfree mice, thereby rendering the animals "normal" with respect to a variety of parameters tested. The present experiments indicate that a different collection of anaerobic bacteria, isolated from the cecum of normal mice, was necessary to convert germfree mice to the "normal" state when the animals were fed a crude diet, rather than the refined food which had been used in the earlier work. The nature and level of short-chain fatty acids associated with various natural or synthetic "normal" floras in the ceca of mice did not always correlate with the Escherichia coli population present, indicating that fatty acids were not the sole agents inhibiting bacterial populations in the intestine. Experiments are reported which indicate that intestinal anaerobes may under certain circumstances be sufficient to control the populations of other intestinal bacteria such as E. coli. In other instances, such as control of Shigella populations in the mouse intestine, intestinal anaerobes appeared to act synergistically with an E. coli strain, in spite of the fact that the population of the latter was itself suppressed by the anaerobes.

Anaerobiosis↗