Stress selectively influences center region activity of mice in an open field

Effects of immobilization and footshock stress on locomotor activity in different areas of an open field were examined in mice. Center region activity, peripheral region activity and total activity were used as measurement indices. These results indicate that both immobilization and footshock stress significantly increased total activity across 24 min of behavioral testing. Further analyses revealed that the difference in total activity between the experimental and control groups were mainly attributal to an increase in center region activity. Both stress manipulations markedly augmented peripheral region activity for only the first 6 min. More important, when the proportion of center to peripheral activity was used as an index, both experimental groups manifested an inverted U shape relationship with the maximum effect occurring between 13-18 min of behavioral testing. Similarities of these activity measures in response to different stressors suggests that common neurochemical and/or neurohormonal mechanisms may mediate these behavioral changes.     

Prevention of diabetes in BioBreeding/Worcester rats with monoclonal antibodies that recognize T lymphocytes or natural killer cells

Diabetes-prone BioBreeding/Worcester (BB/Wor) rats received thrice weekly injections of mAb against antigens expressed on the surface of all T cells (OX19), cytotoxic/suppressor, and NK cells (OX8), helper/inducer cells (W3/25, OX35, OX38), and Ia+ cells (OX6, 3JP, OX17). Treatment with OX8 or OX19 achieved stable reductions of splenic and peripheral blood NK cells and helper/inducer T lymphocytes, respectively, and protected against diabetes. OX19 injections also prevented lymphocytic insulitis, thyroiditis, and the synthesis of autoantibodies to thyroid colloid and smooth muscle antigens. OX8 injections reduced splenic NK-mediated YAC-1 cell lysis, but did not prevent insulitis, thyroiditis, or autoantibody synthesis. Injections of mAb specific for antigens on the surface of helper/inducer cells, and for cells expressing IaE antigens provided marginal protection against diabetes without reductions of phenotypic subsets. These findings suggest that pancreatic beta cell destruction in the spontaneously diabetic BB/Wor rat is mediated by the combined action of NK and helper/inducer cells.     

Respiratory symptoms and bronchial reactivity: identification of a syndrome and its relation to asthma

Two postal questionnaire surveys were carried out among the adult population of Southampton aimed at clarifying the diagnostic criteria for asthma (study 1) and at testing the validity of symptoms so identified as diagnostic of bronchial hyper-reactivity (study 2). The questionnaires asked about respiratory symptoms and included three questions thought likely to disclose increased bronchial reactivity. Laboratory measurements on subsamples of respondents included spirometry and bronchial challenge with increasing doses of histamine till a concentration was reached provoking a fall of more than 20% (PC greater than 20) in forced expiratory volume in one second. In the first study no normal subject (that is, one who did not report shortness of breath or wheezing on the questionnaire) had a PC greater than 20 below 0.5 g/l. Of 51 subjects who reported shortness of breath or wheezing, or both, nine had a cluster of abnormalities consisting of one or more symptoms of bronchial irritability, nocturnal dyspnoea, and prolonged morning tightness together with PC greater than 20 values of 0.5 g/l or less. These symptoms in conjunction with a low PC greater than 20 were termed the bronchial irritability syndrome. In the second study bronchial challenge confirmed the close association of these symptoms with bronchial hyper-reactivity, all other subjects being less reactive to histamine. Only 27% of subjects with symptoms of the bronchial irritability syndrome had been diagnosed as asthmatic by their general practitioners. The bronchial irritability syndrome is a definable entity for epidemiological study and patient care.     

Esophageal strictures following nasogastric intubation

Esophageal stricture is not reported to be a common complication of nasogastric intubation. Two patients who had a Levin tube inserted in the stomach for nutrition during a prolonged coma, and finally presented with a severe esophageal stricture were observed and treated. The clinical history of the patients suggests that the pathogenesis of this lesion is probably multifactorial, secondary to induced gastroesophageal reflux, impaired esophageal clearance, high gastric acid output, and use of steroids. Jejunostomy feeding, rather than nasogastric feeding, is probably a better means to provide nutritional support in comatose patients, thus averting the risk of such a serious complication. Esophageal replacement with left colon interposition appears the treatment of choice for these severe esophageal strictures.