Globe manipulation for consistent good visibility.
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Biomedical subjects
Publications and source records attributed to R Trivedi.
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Cadmium may induce oxidative damage in different tissues by enhancing peroxidation of membrane lipids and altering the antioxidant system of the cells. The peroxidative damage to the cell membrane may cause injury to cellular components due to the interaction of metal ions with the cell organelles. The treatment with Cd (0.4 mg/kg body wt, ip) significantly increased lipid peroxidation (LPO) in heart within 3 h of the Cd injection, while the increase in kidney and liver followed 6 to 12 h after Cd intoxication. The antioxidant enzymes and other antioxidants provide protection to the cells against oxidative damage. The superoxide dismutase (SOD) activity increased in heart, kidney and liver within 24 h of Cd intoxication. The CAT activity increased significantly in heart 9 h after Cd injection; however, no significant change in CAT activity was observed in kidney and liver tissues. The GSH content and the activity of GR decreased in heart, kidney and liver 72 h after Cd administration, which has been suggested to be the cause for increased LPO in the tissues. The hexose monophosphate (HMP) shunt enzymes generate NADPH required for the activity of GR which may affect the GSH content in the tissues. The generalised decrease in glucose 6-phosphate dehydrogenase (G6PDH) and 6 phospho gluconate dehydrogenase (6PGDH) at 9 h followed by an increase in these enzymes in tissues 72 h after Cd intoxication suggest that the production of NADPH by the HMP shunt is required to reduce the oxidative damage. The results show that Cd induced LPO in the tissues and the condition was partially counteracted by the antioxidant system.
Rett syndrome, the commonest condition associated with severe mental retardation in girls, is diagnosed only by its clinical phenotype, because, to date, there is no consistent characteristic alteration in genetic, biochemical, neurotransmitter or morphologic marker. The clinical features at various ages suggest involvement of most parts of the nervous system, however, the brain in Rett syndrome is reduced in weight, without other obvious morphologic alterations. Because of the relative microcephaly, hypotheses regarding failure of development have been suggested. Supporting such hypotheses are the quantitative studies by Jellinger, Seitelberger and Kitt defining a decrease in the amount of melanin in the substantia nigra and by Bauman defining a global decrease in the size of the neurons. In this study the cerebral cortex has been examined using the rapid Golgi technique with the purpose of investigating dendrites of pyramidal neurons in six cortical regions of Rett girls from ages 2.9-35 years. Camera lucida drawings of apical and basal dendrites of two cortical layers and CA1 were prepared. These were submitted to the Sholl analysis. The Sholl analyses were tested for significance using the repeated measures analysis of covariance, with age as a covariate. The studies demonstrate that from our samples there is no evidence that the pyramidal neurons in Rett syndrome degenerate progressively with increasing age but that the basal dendrites of layers three and five pyramidal neurons in the motor and frontal cortex, the apical dendrites of layer five of the motor cortex, and the basal dendrites of layer four of the subiculum are significantly shorter than in non-Rett brains.(ABSTRACT TRUNCATED AT 250 WORDS)
To examine the effect of hypoxia confined to the ventrolateral medulla we microinjected NaCN into the cat medulla (1.0 mm below the ventral surface) unilaterally and investigated cardio-respiratory changes. We studied anesthetized artificially ventilated animals and measured the electrical activity of phrenic and cervical sympathetic nerves and blood pressure. Histotoxic hypoxia depressed phrenic amplitude and elevated sympathetic tone and blood pressure. These responses were obtained predominantly from the region 5.0-8.0 mm caudal to the foramen caecum and 3.0-5.0 mm lateral to the midline (intermediate area). A study with 14C-cyanide showed that total and covalently bound cyanide was confined within a 1 mm diffusion sphere following microinjection. Isolated areas in both rostral and caudal medulla responded to cyanide with elevated sympathetic tone in the absence of phrenic nerve depression, suggesting dissociation of respiratory and vasomotor responses to hypoxia. Thus, the respiratory depression and vasomotor excitation produced by central hypoxia can be reproduced by hypoxia limited to discrete regions of the ventrolateral medulla.
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Brain stem hypoxia caused by vertebral artery injection of sodium cyanide (NaCN) (1-20 micrograms) in artificially ventilated cats depressed phrenic and stimulated sympathetic nerve activity with a simultaneous increase in arterial blood pressure. Larger doses of NaCN caused greater effects. Hypercapnia produced by inhalation of 7% CO2 in O2 tended to reduce NaCN-induced responses on phrenic activity but not on blood pressure or sympathetic activity. Infusion into the vertebral artery with hypoxic saline (3% CO2 in N2) altered blood pressure, also affecting phrenic and sympathetic nerves similarly to NaCN administration. However, washout of CO2 by infusion of 100% O2 bubbled saline at high flow rates (3.6 ml/min) depressed phrenic as well as sympathetic activity and blood pressure. Spinal transection at the first cervical level eliminated sympathetic excitatory response to intravertebral cyanide injection. However, a large dose of NaCN (600 micrograms) given intravenously in spinal animal excited sympathetic activity. We conclude that intravertebral injection of NaCN can be used to study the effects of local hypoxia of the brain stem on cardiorespiratory responses and that hypoxia acts at both these sites (brain stem and spinal cord) to stimulate sympathetic excitation.
In a previous study from our laboratory (Akagi and Townley) we reported that basophils from asthmatic patients off medication show spontaneous histamine release (SHR) significantly higher than asthmatic patients on chronic medication. Both groups of asthmatics showed significantly higher SHR than normal subjects. These findings led us to test the in vitro effect of various therapeutic agents on SHR. Theophylline exerted the most pronounced inhibitory effect on SHR (P less than .005). The effects of isoproterenol and PGE1 were significant (P less than .005) but less than theophylline. These in vitro findings led us to evaluate the effect of a single dose, orally administered bronchodilator on in vitro SHR from asthmatic subjects. The effect of theophylline 250 mg and metaproterenol 20 mg on pulmonary function and SHR was evaluated on separate study days. Four of the eight asthmatic subjects showed greater than 10% SHR. The baseline value of SHR in the same individuals on two different study days showed significant correlation (r = .82). A single dose of metaproterenol or theophylline increased the pulmonary function but failed to influence the SHR. Although SHR occurs in asthmatic subjects, it is not influenced by single dose bronchodilation.
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The clinical presentation and roentgenographic findings of renal cell carcinoma have been consistently variable. These patients can appear with flank pain mimicking ureteral colic, flank tumors, or symptomatic metastasis [1]. Systemic cardiac manifestations including cardiomegaly with congestive heart failure due to arteriovenous fistula formation have been reported [2] Roentgenographic findings may show the tumor to be either vascular or avascular. It may present as a spontaneous perforation of the pelvic ureteral system which is demonstrated by intravenous pyelography (3). In this article, we describe a case of hypernephroma in a cyst wall causing severe spontaneous hemorrhage in the retroperitoneal space resulting in a state of hypovolemic shock.