Cytogenetic studies in non-African Burkitt lymphoma

A particular translocation between chromosomes 8 and 14 has been found repeatedly in cytogenetic studies of Burkitt lymphoma, both of African and non-African origin. We report here our findings in cytogenetic studies of direct tumor preparations from 18 non-African Burkitt lymphoma patients, 9 of whom also had cell lines available for study. A t(8;14) was found in direct tumor material in 10 of the 18 patients. Seven of the 9 cell lines had a t(8;14). A total of 15 patients had either a t(8;14) or a 14q+ present in tumor material and/or cell lines. In addition, 8 patients had a peculiar marker chromosome 1. The t(8;14) was not found in every malignant cell and, where present, it was rarely the sole karyotypic abnormality. The relationship of the t(8;14) to the evolution of the tumor is discussed.     

Expression of superoxide dismutase and xanthine oxidase in myometrium, fetal membranes and placenta during normal human pregnancy and parturition

Superoxide, an agent which attenuates the half-life of nitric oxide, is metabolized and synthesized by superoxide dismutase (SOD) and xanthine oxidase, respectively. Over the last few years much work has focused on the role of nitric oxide in human parturition. The aim of this study was to determine whether the onset of human parturition is associated with a change in the expression of copper/zinc superoxide dismutase (Cu/Zn SOD), manganese superoxide dismutase (Mn SOD) or xanthine oxidase within the uterus. Samples of myometrium, placenta, decidua and fetal membranes were obtained from women before and after the onset of labour at term. Immunocytochemistry was used to localize Cu/Zn SOD, Mn SOD and xanthine oxidase and measure SOD enzyme activity. Cu/Zn and Mn SOD-like immunoreactivity was detected in syncytiotrophoblast cells, villous stromal cells and endothelial cells of blood vessels in the placenta. In the myometrium Cu/Zn and Mn SOD were localized to myocytes and endothelial cells and to some vascular smooth muscle cells. In the fetal membranes we observed staining for Cu/Zn SOD and Mn SOD in the amnion, chorion, extravillous trophoblast and decidua. There was no difference in SOD enzyme activity or staining intensity for SOD between different cell types before and during labour. Xanthine oxidase immunoreactivity was identified in each of the tissues examined and again there was no difference in immunostaining in tissues obtained from women delivered before or after the onset of labour. These results show that the pregnant uterus is capable of both synthesizing and degrading superoxide and suggest that superoxide dismutase and xanthine oxidase may play a role in the maintenance of uterine quiescence during pregnancy, but not in the initiation of parturition.      

Effects of NG-nitro-L-arginine methyl ester, 7-nitro indazole, and agmatine on pentylenetetrazol-induced discriminative stimulus in Long-Evans rats

This study was undertaken to determine any role that nitric oxide (NO) may play in the discriminative stimuli produced by pentylenetetrazol (PTZ). The PTZ-induced discriminative stimulus is pharmacologically similar to anxiety in humans and is used in a behavioral assay of anxiety (the PTZ model of anxiety). In the present study, effects of L-N(G)-nitro arginine methyl ester (L-NAME), 7-nitroindazole (7-NI) and agmatine, NO synthase (NOS) inhibitors, on PTZ-induced discriminative stimulus were investigated in male Long-Evans rats (330-350 g). Rats were trained to discriminate PTZ (16 mg/kg) from saline using a two-lever, food-reinforced choice procedure (FR 10). The rats that met the training criteria were injected with L-NAME (15, 30, and 60 mg/kg), 7-NI (15 and 30 mg/kg), agmatine (20, 40, and 60 mg/kg), and saline or vehicle intraperitoneally before each test. They were tested for the PTZ-discrimination to determine if the NOS inhibitors produce discriminative stimulus similar to PTZ or if they block PTZ-induced discrimination. Treatment with the NOS inhibitory drugs neither substituted for PTZ nor altered the PTZ lever selection in any other way. These findings suggest that PTZ-induced discriminative stimulus may not be related to NO-mediated central mechanisms.     

Effects of venlafaxine on ethanol withdrawal syndrome in rats

The present study was designed to investigate the effects of venlafaxine, a serotonin and noradrenaline reuptake inhibitor (SNRI), on ethanol withdrawal syndrome in rats. Adult male Wistar rats (187-319 g) were used for the study. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair-fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Venlafaxine (5, 10, 20 and 40 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After the 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behaviour and wet dog shakes were recorded or rated. A second series of injections was given at the 6th hour after the first one, and rats were then tested for audiogenic seizures. Venlafaxine produced some inhibitory effects on locomotor hyperactivity, stereotypic behaviours and wet dog shakes. However, a two-way anova of the data did not indicate any significant effect. It reduced the incidence of the audiogenic seizures at the 6th hour of ethanol withdrawal. Venlafaxine (20 mg/kg) also prolonged the latency of the seizures significantly. Our results suggest that acute venlafaxine treatment has limited beneficial effects on ethanol withdrawal syndrome in rats.     

Effects of fluoxetine on ethanol withdrawal syndrome in rats

The present study was designed to investigate the effects of fluoxetine, a selective serotonin reuptake inhibitor, on ethanol withdrawal syndrome in rats. Adult male Wistar rats (218-255 g) were subjects. Ethanol (7.2%, v/v) was given to rats by a liquid diet for 21 days. Control rats were pair fed an isocaloric liquid diet containing sucrose as a caloric substitute to ethanol. Fluoxetine (2.5, 5 and 10 mg/kg) and saline were injected to rats intraperitoneally just before ethanol withdrawal. After 2nd, 4th and 6th hour of ethanol withdrawal, rats were observed for 5 min, and withdrawal signs that included locomotor hyperactivity, agitation, stereotyped behavior, wet dog shakes and tremor were recorded or rated. A second series of injections was given at 6 h after the first one, and subjects were then tested for audiogenic seizures. Fluoxetine produced some dose-dependent and significant inhibitory effects on all the signs of ethanol withdrawal during ethanol withdrawal period. Our results suggest that acute fluoxetine treatment has some beneficial effects on ethanol withdrawal in rats. Thus, this drug may be useful for treatment of ethanol withdrawal syndrome.     

Paraganglioma of the nasal cavity: a case report

We describe the case of a 72-year-old woman presenting with a 1-year history of recurrent epistaxis and unilateral progressive nasal obstruction with associated rhinolalia resulting from the presence of a tumor mass occupying two-thirds of the right nasal cavity. Histopathologically, neoplastic cells or "chief cells" were arranged in well-defined nests, which had the classic alveolar or so-called "zellballen" pattern. Immunohistochemical studies highlighted the presence of S-100 protein-positive sustentacular cells located at the periphery of the clusters of chief cells. The chief cells showed a diffuse and intense positivity for neuron-specific enolase and synaptophysin. A diagnosis of paraganglioma was made. The lesion was excised completely and the patient did not develop recurrences or distant metastases after 8 months of follow-up. Paragangliomas arising in the nasal cavity and paranasal sinuses are extremely rare tumors. We report on the clinical, histopathological and immunohistochemical findings of our case and review the cases previously described in the literature.     

Nitric oxide and substance dependence

The free-radical gas nitric oxide (NO) plays an important role in a diverse range of physiological processes. It is synthesized from the precursor L-arginine by the enzyme NO synthase (NOS), which transforms L-arginine into NO and citrulline. This synthetic pathway exists in the central nervous system (CNS), and NO appears to be a messenger molecule in the CNS, fulfilling most of the criteria of a neurotransmitter. Recent studies indicate that NO may play an important role in dependence on drugs of abuse. The purpose of this review is to address the role of NO in dependence on substances such as opioids, ethanol, psychostimulants and nicotine. Inhibitors of NOS modulate withdrawal from opioids and ethanol, diminishing many signs of withdrawal. In addition, NOS inhibitors suppress signs of withdrawal from nicotine. These data suggest that NO may be involved in the expression of withdrawal signs, and they leave open the possibility that NO may mediate the development of many of these signs. Although preliminary, data to date suggest that glutamate neurotransmission may be related to these beneficial effects of NOS inhibitors on signs of withdrawal. Emerging data further suggest that NO may have a general role in the dependence potential of various classes of drugs of abuse. Thus, modulation of NO systems may be a potential therapeutic target for treatment of substance abuse.     

Nitric oxide synthase inhibition blocks amphetamine-induced locomotor activity in mice.

Effects of N(G)-nitroarginine methyl ester (L-NAME), a nonspecific inhibitor of nitric oxide (NO) synthase, on amphetamine-induced locomotor activity were investigated in Swiss-Webster mice. Locomotor activity was measured for 30 min immediately following amphetamine (1, 2 and 4 mg/kg, i.p.) or saline treatments. L-NAME (15 and 30 mg/kg) and a combination of L-arginine (1000 mg/kg) and L-NAME (30 mg/kg) were injected 30 min before amphetamine (2 mg/kg) to other groups of the mice. L-Arginine was injected 30 min before L-NAME treatment when they were combined. L-NAME (30 mg/kg) and L-arginine (1000 mg/kg) were also tested for ability to depress or stimulate locomotor activity in the absence of amphetamine. Amphetamine caused a dose-dependent increase in locomotor activity of the mice. L-NAME blocked the amphetamine-induced locomotor stimulation dose dependently. L-Arginine pretreatment prevented the inhibitory effects of L-NAME on amphetamine-induced locomotor stimulation. L-NAME and L-arginine did not cause any significant change in locomotor activity in mice not treated with amphetamine. These results suggest that amphetamine-induced locomotor stimulation in mice is modulated by NO.