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Biomedical subjects

S Cohen

Publications and source records attributed to S Cohen.

At least 991 records · Page 55Linked to original sources
PubMed1979

Localization and chemical characterization of Plasmodium knowlesi schizont antigens.

The identification of malarial antigens that induce protective immunity could provide a rational basis for developing an effective antimalarial vaccine as well as specific serodiagnostic tests indicative of clinical immune status. Since protective immunity is probably induced by stage-dependent rather than stage-independent antigens, the antigenic composition of different stages of Plasmodium knowlesi has been compared, and a limited chemical characterization undertaken. This information should provide some insight into the types of preparative procedure appropriate for the purification of functionally important malarial antigens.

Animals↗
PubMed1979

Suppression of cell-mediated immune reactions by monosaccharides.

Various monosaccharides have been shown capable of inhibiting lymphokine activity in in vitro assay systems. In this study, we demonstrate that L-fucose can inhibit the ability of lymphokine-containing supernatants to induce skin reactions or cause reductions in the macrophage content of peritoneal exudates. Moreover, L-fucose can inhibit the cutaneous delayed hyoersensitivity reaction and the peritoneal macrophage disappearance reaction (MDR) induced by antigen in actively immunized guinea pigs. The effect of L-rhamnose, another sugar with in vitro inhibitory activity, was investigated in the MDR, and was also shown to be inhibitory. L-arabinose, which has no in vitro effects on lymphokines, had no suppressive effect on any of the in vivo systems studied. No monosaccharide inhibition of Arthus reactions or nonspecific inflammation could be found in these studies. The results demonstrate that monosaccharides capable of inhibiting lymphokine activity in vitro are effective in suppressing in vivo manifestations of cellular immunity.

Animals↗
PubMed1979

Resistance transfer factor in E. coli strains isolated from human and water sources.

Conjugation experiments with a recipient E. coli strain F-lac-NaR were performed in order to determine the extent to which transferable drug resistance is prevalent among Gram-negative bacteria isolated from the following sources: healthy infants both treated and untreated with antibiotic drugs; healthy adults previously exposed to antibiotics; water sources; and nosocomial infections. Transferable drug resistance was demonstrated in 56.6% of E. coli isolates from the antibiotic-treated infant group, in 53.2% of isolates from untreated infants, and in 43% of isolates from the adult group. R factor was carried by only 8.3% of the strains isolated from water sources, and by 26.7% of the nosocomial strains. A positive correlation between transferable antibiotic drug resistance and resistance to mercury ions was found in donor and conjugate strains. Acridine and several of its derivatives were found to be active in preventing transfer of R factor.

Acridines↗
PubMed1979

The gastrocolic response: evidence for a neural mechanism.

The aim of this study is to determine the effect of anticholinergic therapy on the gastrocolonic response to a standard meal or its major constituent fat. A rapid increase in rectosigmoidal spike activity occurs after ingesting the standard meal or the fat meal (P less than 0.01). Distal colonic motility returns to fasting levels 50 min after both meals. There is no further increase in spike activity after the 1000-calorie meal, but spike activity increases again 70 min after ingesting the fat (P less than 0.02). The anticholinergic drug, clidinium bromide, inhibits the early increase in spike activity after both meals. However, the anticholinergic has no effect on the delayed peak of activity following the ingestion of fat. This study suggests that (a) the early gastrocolic response to a standard meal and a fat meal is cholinergically mediated and (b) the late increase in rectosigmoidal motility occurs only after fat ingestion and may be controlled by other neural mediators or possibly the gastrointestinal hormones.

Adult↗
PubMed1979

Cell mediated immunity to human myelin basic protein in Vogt-Koyahagi-Harada syndrome.

An immunological basis for neurological involvement in Vogt-Koyanagi-Harada syndrome was sought by means of the migration-inhibition factor technique with human myelin basic protein. The test was carried out in four patients who had recent manifestations of the syndrome, two of whom were evaluated both before and after initiation of steroid treatment; in one patient 4 years after recovery from the syndrome; in three patients having uveitis of other causes, and in 12 healthy controls. The results were positive in all four patients who had recent manifestations, whereas they were negative in all the others. This finding may constitute evidence of a cell-mediated immunity toward components of the nervous system in this disease entity.

Antigens↗
PubMed1978

Angiotensin II mediation of adrenal catecholamine secretion induced by intrarenal isoprenaline infusion.

Isoprenaline infusion into the renal artery of the cat induced an increase in the catecholamine (CA) secretion rate from the adrenal gland. CA release by isoprenaline was preferentially noradrenaline. Intravenous infusion of an angiotensin II (A II) antagonist abolished adrenal CA response to intrarenal isoprenaline injection. It is suggested that intrarenal isoprenaline infusion stimulates renal renin release and A II production which, in turn, stimulates adrenal CA secretion.

Adrenal Glands↗
PubMed1978

A DNA segment within the colicin E1 structural gene on ColE1 affecting immunity to colicin.

Insertion of DNA at the EcoRI site of ColE1 results in increase of immunity to colicin killing in E. coli harboring such recombinant ColE1 plasmid as compared to E. coli (ColE1). This effect is neither due to cis or trans interactions originating from the inserted foreign DNA fragment, nor to changes in plasmid copy number. This defect in the immunity mechanism is not trans complemented for by wild type ColE1. Increase in immunity can also be obtained by deleting a DNA segment from the ColE1 genome. This segment is approximately 120 bp left to the EcoRI site within the colicin structural gene. It is concluded that the structure of DNA per se, around the EcoRI site, within colcin structural gene, is the structure which affects immunity expression.

Colicins↗