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Biomedical subjects

N Lin

Publications and source records attributed to N Lin.

116 records · Page 7Linked to original sources
PubMed1970

Communication in the physical and the social sciences.

Although composed of similar elements and structured similarly, the communications systems associated with the physical sciences and the social sciences differ markedly with respect to the operation and use of these elements. For both groups of disciplines, as information flows through the system it encounters lags and filtering, and much of a scientist's communication behavior is an effort to compensate for these factors. Because the lags and filtering within each system differ in loci and extent, the members of different disciplines adjust to them differently, and the overall information flow patterns in the physical and in the social sciences differ.

Communication↗
PubMed1967

Role differentiation in copulating cicada killer wasps.

Copulating male and female cicada killer wasps have distinct behavioral roles independent of reproduction. Males terminate copulation, and females initiate the copulatory flight in which the pair in copulation escape potential danger. Separation and escape behavior are mutually exclusive. Separation occurs because the female clings to the substrate and fails to join the male in his frequent attempts at flight; thus he eventually pulls free. Escape occurs when the female begins flight, which the male readily joins. Differences in thresholds for flight probably largely determine both roles. There appears to be an evolutionary balance in escape and separation behavior determined by the behavior of the female, and illustrative of behavioral homeostasis. The female remains still in the presence of mild stimuli, such as attempted male flights, and thereby aids in separation; she initiates escape in the presence of strong stimuli such as potential enemies.

Animals↗
PubMedDate not supplied

Subfornical organ lesions in rats abolish hyperdipsic effects of isoproterenol and serotonin.

Isoproterenol (300 micrograms/ml/kg) and serotonin (2 mg/ml/kg) given SC to rats (n = 27) caused significant drinking (Fisher PLSD, Scheffe F test, Dunnett t) in the 1 and 2 hours after injection. Such drinking was completely prevented in rats later shown to have complete lesions of their subfornical organs (n = 7). In contrast a response not significantly different from the prelesion response was found in rats later given cortical lesions (n = 11) or other lesions which did not damage the subfornical organ (n = 7). We conclude that drinking evoked by SC injection of serotonin and isoproterenol is brought about by peripheral production of angiotensin II. Blood borne angiotensin II in turn stimulates neurons in subfornical organ which initiate the neural organization of a drinking response.

Angiotensin II↗
PubMedDate not supplied

Evidence for genetic influences common and specific to symptoms of generalized anxiety and panic.

BACKGROUND: Generalized anxiety disorder (GAD) and panic disorder (PD) often co-occur and have been shown to be heritable. Researchers have debated the validity of the distinction between GAD and PD. To test for distinction between disorders, we estimated the genetic and environmental contributions which were specific and common to GAD and PD in a cohort of male-male twin pairs. METHODS: Data were obtained from a telephone interview performed in 1992 utilizing the Diagnostic Interview Schedule Version 3-Revised. Interviews were administered to 6724 male-male monozygotic and dizygotic twin pair members of the Vietnam Era Twin Registry. We defined lifetime GAD by the report of six or more DSM-III-R symptoms and lifetime PD by the report of four or more DSM-III-R symptoms. RESULTS: The lifetime co-occurrence of GAD and PD was best explained by a model which did not include family environmental influences. The variance in risk for GAD was due to a 37.9% influence from additive genetic factors with the remainder due to unique environmental influences. The variance in risk for PD was due to a 22.6% additive genetic contribution which was common with GAD and a 21.2% non-additive genetic contribution specific to PD with the remainder of variance in risk for PD due to unique environmental influences. LIMITATIONS: Results may be limited to middle aged males. Model fitting with full diagnostic criteria was not possible due to low prevalences. CONCLUSIONS: Our data suggest a distinction in liability for GAD versus PD. The common genetic influence to GAD and PD may partially account for the risk of the co-occurrence of these disorders in a lifetime.

Age of Onset↗