Increased urine catecholamines and cortisol in women with irritable bowel syndrome

OBJECTIVES: There are few data on the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis in individuals with chronic GI symptoms. The current study was designed to describe and compare urine catecholamine (norepinephrine, epinephrine) and cortisol levels in women diagnosed with irritable bowel syndrome (IBS-patients), women who report similar symptom levels but had not sought health care services (IBS-nonpatients; IBS-NP), and asymptomatic (control) women. METHODS: Seventy-three women (24 IBS; 24 IBS-NP; 25 controls) were interviewed for demographic, GI, gynecological, and psychological data and then followed for two menstrual cycles with a daily health diary. Urine samples were obtained in the evening and morning at specific phases across two menstrual cycles. RESULTS: Women in the IBS group had significantly higher PM and AM urine norepinephrine levels. Urine epinephrine and cortisol levels were also generally higher in women with IBS. Differences in neuroendocrine indicators of arousal were not accounted for by differences in demographic variables, lifestyle characteristics, menstrual distress, or average daily measures of anxiety or depression. CONCLUSIONS: Increases in indicators of sympathetic nervous system activation in women seeking health care for IBS may reflect greater symptom distress or may contribute to increased symptom distress.     

Interlaboratory comparison of the assessment of P450 activities in human hepatic microsomal samples

The present study had 3 goals: (a) to provide a preliminary investigation of the dimensions involved in the capacity for intimacy toward the best friend and the sexual partner during adolescence; (b) to determine whether the specific areas of the capacity for intimacy toward the best friend are the same as toward the sexual partner; and (c) to consider the usefulness of conceiving the capacity for intimacy as a multidimensional concept. Canadian high school students (N = 465; 257 girls, 208 boys) completed a questionnaire on the capacity for intimacy, best friend version; 232 of them completed the partner version of the questionnaire. Factorial analysis on the best friend version of the questionnaire identified 3 factors: Social Intimacy, Positive Intimacy, and Negative Intimacy. Factorial analysis on the partner version of the questionnaire identified 4 factors: Social Intimacy, Positive Intimacy, Negative Intimacy, and Sexual Intimacy.     

Neurone-glia interactions in the hypothalamus and pituitary

Research in the hypothalamus and pituitary has provided compelling evidence that neurone-glia interactions are important in regulating the activity of both neurones and glia. These interactions involve receptor-mediated signalling, intracellular Ca2+ signalling, growth factor-steroid actions and activity-dependent modifications in neurone-glia anatomical relationships. This review focuses on neuroendocrine systems, such as the intermediate lobe of the pituitary and the hypothalamo-neurohypophysial system, which exemplify some of these activities. Although their functional significance has not been fully elucidated, the synaptic responses, release of bioactive factors and changing morphology of certain glia highlight their integral role in hypothalamic function.     

Reduction of S-T segment elevation with infusion of nitroprusside in patients with acute myocardial infarction

It is pointed out that the arrival or fixation probability of a mutant gene can be easily inferred analytically. The mean first arrival time for a single overdominant mutation to reach frequency y attains its maximum when x is close to but still slightly less than y/2, where x is the equilibrium frequency of the mutant gene in an infinitely large population. For an advantageous mutation, the mean first arrival time decreases with an increasing degree of dominance if selection is strong, but it first increases, after reaching a maximum, then decreases as the degree of dominance increases, if selection is weak. Contrary to our intuition, the mean age of an advantageous mutant gene increases with increasing degree of dominance, except when selection is very strong. A simple explanation is given in terms of the sojourn time at a particular gene frequency.     

Glucocorticoid therapy for immune-mediated diseases: basic and clinical correlates

Glucocorticoids are pleiotropic hormones that at pharmacologic doses prevent or suppress inflammation and other immunologically mediated processes. At the molecular level, glucocorticoids form complexes with specific receptors that migrate to the nucleus where they interact with selective regulatory sites within DNA; this results in positive and negative modulation of several genes involved in inflammatory and immune responses. At the cellular level, glucocorticoids inhibit the access of leukocytes to inflammatory sites; interfere with the functions of leukocytes, endothelial cells, and fibroblasts; and suppress the production and the effects of humoral factors involved in the inflammatory response. Clinically, several modes of glucocorticoid administration are used, depending on the disease process, the organ involved, and the extent of involvement. High doses of daily glucocorticoids are usually required in patients with severe diseases involving major organs, whereas alternate-day regimens may be used in patients with less aggressive diseases. Intravenous glucocorticoids (pulse therapy) are frequently used to initiate therapy in patients with rapidly progressive, immunologically mediated diseases. The benefits of glucocorticoid therapy can easily be offset by severe side effects; even with the greatest care, side effects may occur. Moreover, for certain complications (for example, infection diathesis, peptic ulcer, osteoporosis, avascular necrosis, and atherosclerosis), other drug toxicities and pathogenic factors overlap with glucocorticoid effects. Minimizing the incidence and severity of glucocorticoid-related side effects requires carefully decreasing the dose; using adjunctive disease-modifying immunosuppressive and anti-inflammatory agents; and taking general preventive measures.     

Novel autocrine feedback control of catecholamine release. A discrete chromogranin a fragment is a noncompetitive nicotinic cholinergic antagonist

Catecholamine secretory vesicle core proteins (chromogranins) contain an activity that inhibits catecholamine release, but the identity of the responsible peptide has been elusive. Size-fractionated chromogranins antagonized nicotinic cholinergic-stimulated catecholamine secretion; the inhibitor was enriched in processed chromogranin fragments, and was liberated from purified chromogranin A. Of 15 synthetic peptides spanning approximately 80% of chromogranin A, one (bovine chromogranin A344-364 [RSMRLSFRARGYGFRGPGLQL], or catestatin) was a potent, dose-dependent (IC50 approximately 200 nM), reversible secretory inhibitor on pheochromocytoma and adrenal chromaffin cells, as well as noradrenergic neurites. An antibody directed against this peptide blocked the inhibitory effect of chromogranin A proteolytic fragments on nicotinic-stimulated catecholamine secretion. This region of chromogranin A is extensively processed within chromaffin vesicles in vivo. The inhibitory effect was specific for nicotinic cholinergic stimulation of catecholamine release, and was shared by this chromogranin A region from several species. Nicotinic cationic (Na+, Ca2+) signal transduction was specifically disrupted by catestatin. Even high-dose nicotine failed to overcome the inhibition, suggesting noncompetitive nicotinic antagonism. This small domain within chromogranin A may contribute to a novel, autocrine, homeostatic (negative-feedback) mechanism controlling catecholamine release from chromaffin cells and neurons.     

The functional anatomy of a hysterical paralysis

The concept of a conversion disorder (such as hysterical paralysis) has always been controversial (Ron, M.A. (1996). Somatization and conversion disorders. In: B.S. Fogel, R.B. Schiffer & S.M. Rao (Eds.), Neuropsychiatry. Williams and Wilkins, Baltimore, MD). Although the diagnosis is recognised by current psychiatric taxonomies, many physicians still regard such disorders either as feigned or as failure to find the responsible organic cause for the patient's symptoms. We report a woman with left sided paralysis (and without somatosensory loss) in whom no organic disease or structural lesion could be found. By contrast, psychological trauma was associated with the onset and recurrent exacerbation of her hemiparalysis. We recorded brain activity when the patient prepared to move and tried to move her paralysed (left) leg and when she prepared to move and did move her good (right) leg. Preparing to move or moving her good leg, and also preparing to move her paralysed leg, activated motor and/or premotor areas previously described with movement preparation and execution. The attempt to move the paralysed leg failed to activate right primary motor cortex. Instead, the right orbito-frontal and right anterior cingulate cortex were significantly activated. We suggest that these two areas inhibit prefrontal (willed) effects on the right primary motor cortex when the patient tries to move her left leg.