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Biomedical subjects

S Levine

Publications and source records attributed to S Levine.

At least 433 records · Page 24Linked to original sources
PubMed1980

Thymolysis induced by EN3638 and other drugs and its relation to immunosuppression.

The effect on the thymus of EN3638, an oxime derivative of salicylic acid, was investigated because the drug has immunosuppressive properties. It caused a moderate reduction in thymic weight of normal adult and weanling rats and it retarded the regeneration of the thymus that follows acute corticosteroid-induced involution. These effects of EN3638 were not mediated by the adrenal nor due to the salicylate part of the molecule. At high dose levels, the drug also reduced slightly the weight of spleen and lymph nodes and the rate of body growth. Thymolytic doses of EN3638 were also immunosuppressive for experimental allergic encephalomyelitis (EAE). At doses that caused equivalent degrees of thymolysis. EN3638 was somewhat more potent for suppression of EAE than cyclophophosphamide or hydrocortisone.

Animals↗
PubMed1980

ACTH4--10 affects behavior but not plasma corticosterone levels in a conditioned taste aversion situation.

Rats injected with LiCl after they consumed a sweetened milk solution subsequently avoided the milk. ACTH4--10 injection prior to a retention test for the aversion augmented the behavioral measure of the aversion. Rats consuming milk paired earlier with LiCl showed elevated plasma levels of corticosterone. The augmented avoidance response in ACTH4--10 injected rats was not paralleled by an augmented pituitary-adrenal response.

Adrenocorticotropic Hormone↗
PubMed1980

Flavor preexposures in a conditioned taste aversion situation: a dissociation of behavioral and endocrine effects in rats.

A series of experiments examined the effects of flavor preexposures on pituitary-adrenal/behavior relations in a conditioned taste aversion paradigm. It was found that reexposure to a novel milk solution paired earlier with lithium chloride (LiCl) elicited conditioned activation of the pituitary-adrenal system (Experiment 1). The unconditioned response to LiCl (measured by changes in plasma levels of corticosterone) did not vary as a function of prior (2 and 5 vs. 10) exposures to the milk solution (Experiment 2). Increased familiarity with the substance (resulting from 10 prior exposures) rendered the conditioning of a taste aversion to this substance less effective. Further, reexposure to this familiar substance after its pairing with LiCl was not accompanied by the characteristic conditioned pituitary-adrenal activation (Experiment 3). By titrating the number of conditioned stimulus (CS) preexposures (Experiment 4) it was found that within the range of preexposures manipulated (5-10), subjects exhibited (a) a coupling of behavioral and pituitary-adrenocortical responses when the conditioned taste aversion to the milk solution was paralleled by elevated plasma corticosterone (5-6 preexposures), (b) a coupling of these two response systems when flavor consumption was accompanied by suppressed plasma titers of corticoids (9-10 preexposures), or (c) a dissociation of the two system when the conditioned taste aversion was not accompanied by conditioned adrenocortical activity (7-8 preexposures). These data are discussed in terms of a dissociation in the effects of CS preexposures on conditioned adrenocortical and behavioral response systems.

Adrenocorticotropic Hormone↗
PubMed1980

Effect of essential fatty acid deficiency on experimental allergic encephalomyelitis in rats.

Previous claims that experimental allergic encephalomyelitis (EAE) was enhanced by essential fatty acid (EFA) deficiency were reinvestigated. Deficiency was induced in Lewis rats by feeding a fat-free diet starting in late gestation, at weaning or in adult life with or without a previous period of starvation. Retardation of growth, the typical dermatitis, increased water consumption and testicular atrophy gave evidence of EFA deficiency. Control rats were fed a complete diet or a fat-free diet supplemented with corn oil. EAE was induced in EFA-deficient and control rats by conventional active sensitization with neural antigen and adjuvants or by passive transfer of living lymphoid cells from sensitized nutritionally normal donors. Contrary to previous reports, EFA deficiency did not enhance EAE in any of seven experiments, and these results were supported by histological examinations. In fact, we found inhibition of clinical signs, but not histological lesions, when EFA deficiency was moderately advanced. This was accompanied by (and probably related to) thymic atrophy, possibly due to nonspecific stress. Also we found that EFA deficiency had no effect on a non-immunological model of brain inflammation that resembles EAE in the occurrence of lymphocytic infiltrates.

Aging↗
PubMed1980

Lesions of amygdala, pyriform cortex and other brain structures due to dipiperidinoethane intoxication.

Single doses of dipiperidinoethane (DPE) produced symmetrical necrosis in pyriform cortex, amygdala and other areas of gray matter in rats, mice and gerbils. The necrosis was detectable in 10 hours and fully developed in 24 hours. Its distribution and severity were not influenced by carotid artery ligation. DPE was not a cumulative poison. There was a high degree of chemical specificity: neurotoxic activity was present in DPE derivatives modified by methylation of the two piperidine rings, but neurotoxicity was absent in derivatives with different ring systems or different connecting chains.

Amygdala↗
PubMed1980

Metabolic requirements for the maturation of respiratory syncytial virus.

The metabolic processes required for maturation of respiratory syncytial (RS) virus was determined by testing with metabolic inhibitors in HeLa cells that had been trypsinized 18 h p.i. Although > 90% of the virus synthesized by that time remained cell-associated, treatment with trypsin inactivated at least 90% of the cell-associated virus. The trypsinized cells, when re-plated in virus growth medium, immediately resumed virus synthesis and this continued exponentially for at least 10 h, during which as little as 1 to 2 p.f.u./cell of new infectious virus could be detected. Treatment of these cells with 6-azauridine revealed that no further synthesis of virus RNA is required for a full yield of infectious virus. Treatment with cycloheximide, 2-deoxy-D-glucose and cytochalasin B suggested that neither protein synthesis nor glycosylation is required for the first 1 to 2 h following the resumption of virus production, but both processes are required for a full yield. These results suggest that with RS virus, the maturation process itself does not require RNA or protein synthesis or glycosylation. Trypsin, in addition to inactivating accumulated virus, released non-infectious particular material. The polypeptides of this material were similar to those of the RS virion except for a deficiency in glycoproteins. The trypsin apparently cleaved the virus glycoproteins on cell surfaces, which resulted in the inactivation of cell-associated virus and the release of a glycoprotein-deficient particle from cell surfaces. The pool of virus glycoproteins is evidently the limiting factor in infectious virus production by cells trypsinized 18 h p.i. The non-glycosylated polypeptides of cell-associated virus are the same as those of free virus.

Cytochalasin B↗
PubMed1980

Altered plasma corticosterone responses during lactation in mice of two inbred strains.

Plasma corticosterone levels during lactation were examined in inbred A/J (A) and C57BL/6J (C) mice. Following shock, lactating A females showed a diminished corticosterone response relative to nonlactating controls on day 5 of lactation, but not on day 12. In contrast, plasma corticosterone levels of lactating C females 5 and 15 min following shock were lower than those of controls on day 12, but not on day 5. Consistent with these findings, lactating A females had significantly lower plasma levels of corticosterone 15 min following nonnociceptive treatments (involving distrubance, exposure to novelty, and pup manipulation) when tested on day 5 then they did when tested on day 12, whereas lactating C females had lower levels on day 12 than on day 5. Lactating females of each strain showed the same response to shock on day 12 if they reared A pups as they did if they reared C pups. This indicates that the difference found between the strains on day 12 was due to a difference in some property of A and C mothers, rather than to a difference in a characteristic, such as suckling patterns, of the pups of the two strains. It was also found that at long intervals following shock (45 and 90 min) 5-day lactating C females had higher levels of plasma corticosterone than did controls. There was no effect of lactation on resting adrenocorticoid levels in A or C females at either 5 or 12 days. The results indicate that laboratory mice show changes in hypothalamo-pituitary-adrenal activity during lactation which both vary with strain of the mother, and differ in several respects from those previously reported for rats.

Animals↗
PubMed1980

Enhancement of allergic encephalomyelitis by particulate adjuvants inoculated long before antigen.

Carbonyl iron and several other particulate materials have been reported to enhance the development of experimental allergic encephalomyelitis when injected with neural antigen. In the present work, silicon and silica powders have been added to the list of particulate adjuvants. In addition, several particulate materials, but not carbonyl iron, were effective adjuvants when inoculated four weeks or even six months before the neural antigen. It was necessary for adjuvant and antigen to be injected in the same region, but both intraperitoneal and subcutaneous routes were effective. The long-lasting adjuvanticity of certain particulates in the tissues is probably related to their bland and unabsorbable nature. The reasons for restrictions in the range of adjuvants and antigens that are effective in this system and the possibility of a similar occurrence in nature remain to be investigated.

Adjuvants, Immunologic↗