Interpersonal and self-reported hostility among combat veterans with and without posttraumatic stress disorder

Despite the low concentrations of heavy metals in the surrounding medium, aquatic organisms take them up and accumulate them in their soft tissues to concentrations several fold higher than those of ambient levels (Bryan 1979; Rainbow et al. 1990). Knowledge of accumulation patterns of a particular trace metal is a prerequisite for understanding the significance of an observed metal concentration in a particular animal, especially from the aspect of biomonitoring. Many marine invertebrates accumulate heavy metals without any regulation and the accumulation necessarily being associated with mechanisms to store the metals in a detoxified form. Two detoxification mechanisms have been described, both of which may occur in one specimen. Heavy metals can either be bound up in insoluble metalliferous 'granules' (Mason and Nott 1981), or are bound to soluble metal-binding ligands, such as metallothioneins (Roesijadi 1992). Some marine decapod crustaceans have an innate ability to regulate the internal concentrations of essential but potentially toxic metals within a constant level, presumably to meet their metabolic demands (Rainbow 1985, 1992). However, at present, there is no such information relating to freshwater decapod crustaceans, especially shrimps which occupy a totally different environment. Macrobrachium malcolmsonii (Milne Edwards), a potential aquaculture species for freshwater is found in abundance in one of the major Indian rivers, the Cauvery. In the present study, an attempt was made to determine whether the freshwater prawn, M. malcolmsonii, is able to regulate the three essential elements, copper, chromium and zinc, over a wide range of dissolved concentrations. These three metals were chosen because the Cauvery River receives pollutants containing these metals (Vijayram et al. 1990).     

Sulphonylureas do not increase insulin secretion by a mechanism other than a rise in cytoplasmic Ca2+ in pancreatic B-cells

The following sequence of events is thought to underlie the stimulation of insulin release by hypoglycaemic sulphonylureas. Interaction of the drugs with a high-affinity binding site (sulphonylurea receptor) in the B-cell membrane leads to closure of ATP-sensitive K+ channels, depolarization, opening of voltage-dependent Ca2+ channels, Ca2+ influx and rise in cytoplasmic [Ca2+]i. Recent experiments using permeabilized islet cells or measuring changes in B-cell membrane capacitance have suggested that sulphonylureas can increase insulin release by a mechanism independent of a change in [Ca2+]i. This provocative hypothesis was tested here with intact mouse islets. When B-cells were strongly depolarized by 60 mM K+, [Ca2+]i was increased and insulin secretion stimulated. Under these conditions, tolbutamide did not further increase [Ca2+]i or insulin release, whether it was applied before or after high K+, and whether the concentration of glucose was 3 or 15 mM. This contrasts with the ability of forskolin and phorbol 12-myristate 13-acetate (PMA) to increase release in the presence of high K+. Tolbutamide also failed to increase insulin release from islets depolarized with barium (substituted for extracellular Ca2+) or with arginine in the presence of high glucose. Glibenclamide and its non-sulphonylurea moiety meglitinide were also without effect on insulin release from already depolarized B-cells. In the absence of extracellular Ca2+, acetylcholine induced monophasic peaks of [Ca2+]i and insulin secretion which were both unaffected by tolbutamide. Insulin release from permeabilized islet cells was stimulated by raising free Ca2+ (between 0.1 and 23 microM). This effect was not affected by tolbutamide and inconsistently increased by glibenclamide. In conclusion, the present study does not support the proposal that hypoglycaemic sulphonylureas can increase insulin release even when they do not also raise [Ca2+]i in B-cells.     

West's syndrome associated with inversion duplication of chromosome 15

We describe a five year old boy with inversion duplication of chromosome 15 (inv dup (15)) who, at the age of six months had started to develop West's syndrome. He later developed cryptogenic myoclonic epilepsy which was resistant to medication. On examination there was dysmorphia, overall hypotonia and diffuse pyramidalism. On starting ACTH the crises of flexion spasms were reduced but these were soon followed by myoclonic crises, both tonic and atonic, which did not respond to the various anticonvulsive treatments given. We comment on the changes in chromosome 15 linked to convulsions, and particularly the phenotypes of the inv dup (15) which depend on the size and genetic composition of the anomaly. This is the third case described in the literature of a patient with West's syndrome associated with supernumerary inversion duplication of chromosome 15. It is suggested that the karyotype be included when studying convulsive encephalopathies and cryptogenic refractory epilepsy, especially in infantile spasms.     

Induction of apoptosis by 2-chlorodeoxyadenosine in B cell chronic lymphocytic leukemia

We investigated whether 2-chlorodexoyadenosine could induce apoptosis in B cell chronic lymphocytic leukemia (B-CLL) cells in vitro using clinically achievable drug doses, measuring apoptosis ratio by flow cytometry. B cells were isolated from previously untreated patients and apoptosis was measured in these cells immediately after isolation and following incubation in vitro, without and with 2-chlorodeoxyadenosine at different concentrations, for 24 and 48 h. Distribution of cellular DNA content and quantitative analysis of apoptosis were determined by standard propidium iodide staining and flow cytometry. Spontaneous apoptosis occurred in B-CLL cells incubated in vitro in the absence of drug, but the level of apoptosis was greater in cells treated with 2-chlorodeoxyadenosine after the second day of culture. The present in vitro study of B-CLL cells from previously untreated patients suggests this chemotherapeutic agent activates a program of cell death by apoptosis using a drug dose equivalent to the physiological concentration used in patients in vivo. These data reveal an interesting possibility in the 2-chlorodeoxyadenosine treatment of untreated patients by neoplastic B cell apoptosis induction.     

Mantle-cell lymphoma: a population-based clinical study

PURPOSE: From a population-based non-Hodgkin's lymphoma (NHL) registry, 41 patients with mantle cell lymphoma (MCL) -- a recently defined distinct B-cell NHL -- were selected and compared with patients with low- or intermediate-grade NHL from the same registry. PATIENTS AND METHODS: The incidence and behavior of MCL in the area of the Comprehensive Cancer Center West (CCCW) from 1981 to 1989 were analyzed. Age, performance, tumor bulk, extranodal localization, stage, response to therapy, and survival were registered. Expression of cyclin D1 protein and Ki-67 were measured in 29 patients. RESULTS: MCL made up 3.7% of NHLs. The median age was 68 years, and the male-to-female ratio was 1.6:1. Seventy-eight percent presented with stage IV, with the majority having bone marrow involvement. The complete response (CR) rate was 32% (13 of 41), with a median duration of 25 months. The median overall survival time was 31.5 months. The International Prognostic Index identified five patients with a low-risk score and a median survival time of 93+ months. In 23 of 29 patients, cyclin D1 overexpression was present, without any relation to overall or disease-free survival. In contrast, a proliferative index less than 10% was significantly related to a better overall survival time (50 v 24 months). CONCLUSION: MCL is a disease of the elderly, who present with widespread disease and with a poor response to therapy. Although it harbors features of an indolent NHL, it behaves clinically as an aggressive NHL with a short overall survival time.