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Biomedical subjects

J Aronoff

Publications and source records attributed to J Aronoff.

10 recordsLinked to original sources
PubMed2000

Are cultic environments psychologically harmful?

This article is the first critical review of research that addresses the question of whether cult membership is psychologically harmful. The available evidence warrants three conclusions: (a) persons entering cults do not necessarily exhibit psychopathology; (b) current cult members appear psychologically well-adjusted generally, and demonstrate few conspicuous symptoms of psychopathology. However, pathology may be masked by conformity pressures and demand characteristics associated with the cultic environment; (c) a small but growing body of research indicates that at least a substantial minority of former cult members experience significant adjustment difficulties. There also are indications that these difficulties cannot be ascribed to demand characteristics. Although the review highlights definitional and methodological issues and problems that temper conclusions that can be drawn from the literature, no evidence indicates that cults improve adjustment after members leave the cultic environment.

Humans↗
PubMed1996

Recall of childhood neglect and physical abuse as differential predictors of current psychological functioning.

The differential effects of neglect and physical abuse on psychological functioning are not well understood. The present study examined the relationship between reported neglect and physical abuse and symptomatology and attachment styles in a sample of 236 male and 276 female undergraduates. In contrast to physical abuse, which must involve some parental involvement in a child's life, neglect is characterized by a lack of parent-child interaction. As such, it was hypothesized that childhood neglect would be more predictive of symptomatology and dysfunctional attachment styles than would physical abuse. Results confirmed the expected relationship between neglect and more severe psychological problems and anxious attachment styles. Implications of these results point to the need to focus both empirically and theoretically on neglect and physical abuse as potentially separate moderators of psychosocial functioning.

Adult↗
PubMed1988

The recognition of threatening facial stimuli.

Two studies examined the information that defines a threatening facial display. The first study identified those facial characteristics that distinguish between representations of threatening and nonthreatening facial displays. Masks that presented either threatening or nonthreatening facial displays were obtained from a number of non-Western cultures and scored for the presence of those facial features that discriminated between such displays in the drawings of two American samples. Threatening masks contained a significantly higher number of these characteristics across all cultures examined. The second study determined whether the information provided by the facial display might be more primary nonrepresentational visual patterns than facial features with obvious denotative meaning (e.g., diagonal lines rather than downturned eyebrows). The subjective response to sets of diagonal, angular, and curvilinear visual stimuli revealed that the nonrepresentational features of angularity and diagonality in the visual stimulus appeared to have the ability to evoke the subjective responses that convey the meaning of threat.

Aggression↗
PubMed1983

The suppression of myogenic functions in heterokaryons formed by fusing chick myocytes to diploid rat fibroblasts.

Heterokaryons were formed by fusing differentiated chick skeletal myocytes to fibroblasts derived from skin, lung or heart cultures. The heterokaryons were analyzed for the synthesis of skeletal myosin light chains, acetylcholine receptor, total CPK activity and the ability to spontaneously fuse to form myotubes. Whereas all of the above myogenic functions were expressed in control heterokaryons formed between myocytes and myoblasts, all were extinguished in the crosses between myocytes and fibroblasts. These results confirm that the suppression of myogenic functions previously observed in cell hybrids involving fibroblastoid tumor cells also occurs in heterokaryons isolated using biochemical inhibitors between diploid fibroblasts and chick skeletal myocytes.

Animals↗
PubMed1983

Vitamin K-dependent proteins and anticonvulsant medication.

Certain anticonvulsant drugs, especially phenytoin and phenobarbital, interfere with vitamin K metabolism as indicated by a raised serum osteocalcin level. This finding may be of importance in the pathogenesis of side effects of these medications.

Adolescent↗
PubMed1983

Regulation of rat myosin light-chain synthesis in heterokaryons between 5-bromodeoxyuridine-blocked rat myoblasts and differentiated chick myocytes.

Terminal cell differentiation in a variety of model systems is inhibited by the thymidine analogue 5-bromodeoxyuridine (BUdR). We investigated the mode of action of BUdR by forming heterokaryons between undifferentiated BUdR-blocked rat myoblasts and differentiated chick skeletal myocytes. We analyzed newly synthesized proteins on two-dimensional polyacrylamide gels. The induction of rat skeletal myosin light-chain synthesis was reduced fivefold, as compared with controls, when chick myocytes were fused to BUdR-blocked rat myoblasts. This indicates that plasma membrane effects cannot be the proximate cause for the inhibition of myogenesis by BUdR, since BUdR is able to block the effect of chick inducing factors even when a differentiated chick myocyte is in direct cytoplasmic continuity with the BUdR-blocked rat nucleus. The observation that chick cells required an 80% substitution of BUdR for thymidine to block myogenesis, whereas L6 rat myoblasts required only a 20% substitution led to a hypothesis involving a DNA-mediated action of BUdR. This model yielded three testable predictions: (a) putative chick inducing molecules should be present in limiting quantities, (b) exploiting gene-dosage effects to increase the quantity of putative chick inducing factors might overcome the inhibition produced in the rat myoblasts by a 35% BUdR for thymidine substitution, and (c) these gene-dosage effects should be abolished by increasing the level of BUdR substitution in the rat myoblast to 60-80%. All three of these predictions have been verified, providing strong indirect evidence that the inhibition of myogenesis produced by BUdR is a direct result of its incorporation into cellular DNA.

Animals↗