Biomedical subjects
Publications and source records attributed to A Roy.
Depressed gamblers (n = 14) were compared with normal controls (n = 41) for antecedent life events. The depressed gamblers had experienced significantly more life events, and undesirable or exit life events, during the 6 months before the onset of depression.
The authors review the accumulating evidence from preclinical, clinical and postmortem studies suggesting that abnormality in serotonin systems may be associated with both attempts at suicide and aggression towards others and inanimate objects. Although these behaviors are multidetermined they often involve poor impulse control, which may reflect low central serotonin turnover. The need for further studies of possible peripheral biological markers for suicidal and impulsive behavior is discussed.
There are still disagreements concerning the adaptation of cardiac structures in relation to different training stimuli. To eliminate some of the variance due to individual differences in body surface area, we utilized a new approach based on the calculation of the percentages of each individual's normal predicted values (%NPV). We studied 46 strength (S, bodybuilders) and 57 endurance (E, runners) athletes. Left ventricular (LV) mass was 143.8 +/- 21.9 %NPV (mean +/- SD) in E vs. 134.3 +/- 23.4 %NPV in S (P less than 0.05), and LV volume was 131.0 +/- 24.0 %NPV in E vs. 120.0 +/- 25.5 %NPV in S (P less than 0.05). Moreover, the LV wall thickness-to-radius ratio did not differ from normal values in either group. From these data we conclude that 1) cardiac modifications are greater in E than S, 2) the predominant stimulus is a volume overload type in both groups, and 3) concentric LV hypertrophy may not be as prevalent in S as previously suggested.
Explore the source record for details and available documents.
The evidence is reviewed that violent and suicidal behavior is associated with a deficiency of the serotonin system and that individuals with poor impulse control tend to become hypoglycemic during an oral glucose tolerance test, and have low levels of 5-hydroxyindole acetic acid in the cerebrospinal fluid. It is postulated that serotonergic deficits may predispose individuals to poor impulse control, disturbance of glucose metabolism, alcohol abuse, violent behavior and suicide.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Fatty infiltration of the liver may cause a range of focal abnormalities on hepatic sonography which may simulate hepatic nodular lesions. Discrete deposits of fat or islands of normal tissue which are uninvolved by fatty infiltration may stand out as potential space-occupying lesions on the sonograms. Twelve patients with such focally abnormal ultrasound images were referred for liver scintigraphy with 133Xe and 99mTc colloidal SPECT studies to clarify the issue. These examinations helped identify, in nine of 12 patients, the innocent nature of the sonographic abnormalities which were simply related to the fat deposition process. Further, [99mTc]RBC scans defined the additional pathologic process in three patients in whom actual space-occupying lesions were indeed present in the liver. Scintigraphy has an important role to play in the understanding of focal hepatic ultrasound abnormalities particularly in unsuspected hepatic steatosis.
Explore the source record for details and available documents.
In a subline of Reuber H35 rat hepatoma cells that becomes quiescent under serum-deprived conditions, insulin acts as a growth factor. When added to serum-deprived H35 cells, physiologic concentrations of insulin stimulate DNA synthesis, demonstrating that insulin alone is capable of inducing a transition from G0/G1 into S phase. This response, which is induced by nanomolar concentrations of insulin, is mediated directly through the insulin receptor. Here we show that coincident with this growth response, insulin or serum induces dramatic increases in the steady-state levels of c-fos and c-myc mRNAs in serum-deprived H35 cells in a time course similar to that observed in the regenerating liver. Other growth factors, including epidermal growth factor, appear not to affect these cells either in terms of DNA synthesis or c-myc mRNA induction. The phorbol ester phorbol 12-myristate 13-acetate (PMA) also induces c-myc and c-fos mRNAs without inducing DNA synthesis. However, the mechanism of this induction appears to be different from the insulin-induced induction since pretreatment of cells with PMA blocks only the PMA-mediated, not the insulin-mediated, induction of c-myc and c-fos.
The capsular polysaccharide from Klebsiella Serotype K40 contains D-galactose, D-mannose, L-rhamnose, and D-glucuronic acid in the ratios of 4:1:1:1. Methylation analysis of the native and carboxyl-reduced polysaccharide provided information about the glycosidic linkages in the repeating unit. Degradation of the permethylated polymer with base established the identity of the sugar unit preceding the glycosyluronic acid residue. The modes of linkages of different sugar residues were further confirmed by Smith degradation and partial hydrolysis of the K40 polysaccharide. The anomeric configurations of the different sugar residues were determined by oxidation of the peracetylated native and carboxyl-reduced polysaccharide with chromium trioxide. Based on all of these results, the heptasaccharide structure 1 was assigned to the repeating unit of the K40 polysaccharide. (Formula: see text)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We administered verapamil hydrochloride, a calcium channel antagonist, to seven chronically ill schizophrenic patients for five weeks under double-blind, placebo-controlled conditions. No therapeutic effect was noted. Worsening in hostile and uncooperative behaviors and a syndrome of heightened emotional tone was observed during verapamil treatment and during the postverapamil placebo period. Verapamil produced significant increases in cerebrospinal fluid (CSF) and plasma levels of homovanillic acid and in plasma levels of prolactin, as well as significant decreases in plasma levels of 3-methoxy-4-hydroxyphenethyleneglycol. Verapamil and its active metabolite, norverapamil, were partitioned into CSF with CSF/plasma ratios of 0.06 and 0.04, respectively. The lack of therapeutic effects of verapamil in schizophrenic patients differs from earlier reports of its usefulness in treating manic patients. The biochemical and clinical data from our study suggest the possibility that verapamil exerts behaviorally relevant central nervous system activity in schizophrenic patients.
We measured platelet tritiated imipramine binding and serotonin uptake in 51 depressed patients and 43 normal controls. Although there were no significant differences in platelet 3H-imipramine binding or serotonin uptake when the total group of depressed patients was compared with controls, depressed women (n = 32) had a significantly lower maximal density of 3H-imipramine binding sites (beta max) than control women (n = 25). Moreover, among the total group of depressed patients, there were significant negative correlations between the beta max values and plasma cortisol levels at 4 PM (n = 41) and 11 PM (n = 41) following dexamethasone administration. These negative correlations between beta max and cortisol levels were strongest among melancholic patients both at 4 PM before dexamethasone administration (n = 14) and at 11 PM after dexamethasone administration (n = 15). These data suggest that the reported decrease in beta max found among depressed patients may be related to and is perhaps secondary to the hypercortisolemia of depression.
We investigated the possible interactions between corticosteroids and catecholamines in depression by studying the effects of the synthetic glucocorticoid dexamethasone on plasma levels of homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenylglycol (MHPG) in a group of depressed patients and normal controls. In comparison with metabolite levels on a control day, normal controls showed a significant dexamethasone-induced increase in the plasma HVA level and a trend toward a decrease in the plasma MHPG level at 4 PM following dexamethasone administration (1 mg orally at 11 PM). Conversely, depressed patients, particularly those with psychotic features, showed a significant dexamethasone-induced increase in the plasma MHPG level and a blunting of the plasma HVA response relative to the normal controls. Dexamethasone-induced increases in the plasma MHPG level were directly correlated with the severity of depressive symptoms and with postdexamethasone cortisol levels in the depressed patients. These data suggest abnormal corticosteroid-catecholamine interactions in depression and, specifically, in depressed patients with psychotic features.