Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant avian adenovirus CELO bearing sequence RGD in the structure of a HI-loop of long fiber was designed. Experiments in vitro revealed that introduction of RGD-motif into fiber of CELO increased the ability of the virus to be attached to a surface of CAR-negative cells, and raised efficiency of the process of internalization of the virus both in CAR-positive, and in CAR-negative cells.
Mol Gen Mikrobiol Virusol 2008
PMID:[Influence of integrin-binding motif (RGD) on attachment and internalization of avian adenovirus CELO in mammalian cells]. 1848 47

Nitric oxide has been recognized as an important inter- and intra-cellular modulator of testicular steroidogenesis in higher vertebrates with conflicting results. Moreover, its role in regulation of testicular steroidogenesis in ectothermic vertebrates is non-existent. The present study was, therefore, undertaken to examine whether Leydig cells of a freshwater catfish, Clarias batrachus produce nitric oxide (NO), if so, does it regulate its steroidogenic activity? The purified Leydig cells were stained histochemically for NADPH-diaphorase (NADPH-d) activity, and immunocytochemically for neuronal and inducible nitric oxide synthase (nNOS and iNOS) like molecules. Leydig cells were also incubated with NOS inhibitor, N-nitro-l-arginine methyl ester (l-NAME), and NO donor, sodium nitroprusside (SNP). NO and testosterone released in incubation medium were analyzed. A distinct positive NAPDH-d staining was observed in Leydig cells. These cells also exhibited immunoprecipitation of variable intensity with nNOS and iNOS antibodies. Further, l-NAME treatment caused significant suppression in NO production and elevation in testosterone secretion by Leydig cells. On the contrary, exposure of Leydig cells to SNP resulted in increased NO production with concomitant decline in testosterone level. Thus, the present study reports NO production by Leydig cells in fish for the first time, which appears to inhibit its own androgen production.
Gen Comp Endocrinol 2008 Sep 01
PMID:Nitric oxide: An autocrine regulator of Leydig cell steroidogenesis in the Asian catfish, Clarias batrachus. 1866 63

We investigated the mechanism of synaptic suppression by P2Y receptors in mixed hippocampal cultures wherein networked neurons exhibit synchronized Ca(2+) oscillations (SCO) due to spontaneous glutamatergic synaptic transmission. Pharmacological studies suggested that SCO suppression was mediated by P2Y2/P2Y4 receptors. Immunostaining studies and characterization of ATP/UTP-stimulated Ca(2+) responses in solitary neurons and astrocytes revealed that the SCO attenuation was effectuated by astrocytes. We demonstrate that nitric oxide released from activated astrocytes causes synaptic suppression by inhibiting neurotransmitter release. Physiological concentrations of ATP and UTP evoked NO production in astrocytes. SCO suppression was considerably diminished by removal of extracellular NO by membrane-impermeable scavenger c-PTIO or by pretreatment of cells with nitric oxide synthase inhibitor L-NAME. The nitric oxide donor DETA/NO effectively suppressed the SCO. ATP/UTP inhibited KCl-induced exocytosis at presynaptic terminals in an NO-dependent manner. In the absence of exogenously added ATP/UTP, both the NO scavenger and NOS inhibitor enhanced the frequency of SCO, implying that astrocytes release NO during spontaneous synaptic activity and exert a suppressive effect. We report for the first time that under physiological conditions astrocytes use NO as a messenger molecule to modulate the synaptic strength in the networked neurons.
J Gen Physiol 2008 Sep
PMID:Nitric oxide-mediated modulation of synaptic activity by astrocytic P2Y receptors. 1872 29

The present in vitro study for the first time demonstrates the role of extragonadal hormones in regulation of NO production by testicular macrophages in vertebrates and paracrine role of NO in Leydig cell steroidogenesis in fishes. N-nitro L-arginine methyl ester (L-NAME - a NOS inhibitor) treatment substantially reduced NO production by testicular macrophages suggesting that testicular macrophages are one of the sources of testicular NO in the catfish, Clarias batrachus. Significant decline in NO production was also recorded following treatment of macrophages with the gonadotropin (GtH), growth hormone (GH) and insulin indicating that macrophage-produced NO is under endocrine inhibitory control. Treatment of Leydig cells with sodium nitroprusside (SNP) decreased testosterone (T) production. SNP treatment also remarkably suppressed the GtH, GH and insulin-stimulated T production by Leydig cells indicating that Leydig cell steroidogenesis is sensitive to exogenous NO. Further, effect of conditioned medium of testicular macrophages incubated with medium alone (non-treated TMCM) or GtH (GtH-treated TMCM) or GH (GH-treated TMCM) or insulin (insulin-treated TMCM) were also observed on Leydig cell T production. Non-treated TMCM as well as hormone-treated TMCM stimulated T production by Leydig cells; hormone-treated TMCM were more effective in stimulating T production than non-treated TMCM and/or hormones alone. These experiments altogether suggest that testicular macrophage secrete some factors, which influence Leydig cell steroidogenic activity through paracrine mechanism, and these paracrine secretions are under the endocrine control. Decline in NO in hormone-treated TMCM might also be one of the reasons for more stimulation in T production than that of hormones alone.
Gen Comp Endocrinol 2009 Jan 01
PMID:Paracrine role of macrophage produced-nitric oxide (NO) in Leydig cell steroidogenesis in a teleost, Clarias batrachus: Impact of gonadotropin, growth hormone and insulin on NO production by testicular macrophages. 1897 57

Area postrema (AP) is considered to be an important neural center for emesis in carnivores. However, it is also known that AP mediates motor responses induced by apomorphine in rats which do not have an emetic reflex. To shed more light on the possible role of AP in the control of gastric motility in physiological or pathophysiological conditions, we observed the effects of electrical or chemical (apomorphine) stimulation of AP neurons on intragastric pressure (IGP) or intragastric volume (IGV) in rat. We found that electrical stimulation (ES) reduces IGP, and this is sensitive to hexamethonium or L-NAME, and apomorphine also reduces IGP and increases IGV. In slice preparations, apomorphine (10 micromol/l) increased the frequency of spontaneous single unit discharges of AP neurons recorded extracellularly. We also succeeded retrograde labeling of AP neurons by DiI applied into the gastric corpus, for the first time. These observations indicate that rat stomach receives efferent neural input from AP and the excitation of AP neurons relaxes the stomach in rat, suggesting some functional roles of AP neurons in the regulation of gastric motility.
Gen Physiol Biophys 2008 Dec
PMID:Gastric relaxation induced by electrical and chemical stimulation of the area postrema in the rat. 1920 97

The current study was undertaken to investigate the effects of NOx (plasma concentrations of nitrate plus nitrite which are plasma nitric oxide (NO) metabolites) over QT interval and to determine the level of correlation between them in conscious rabbits. For this purpose, twenty-one New Zealand rabbits (5-7 months old) were used and randomly assigned into the following three groups: control (CG; n = 7, 1 ml isotonic NaCl solution per animal/day), L-arginine (ARG-G; n = 7, L-arginine solution 200 mg/kg/day) and L-NAME (NAME-G; n = 7, L-NAME solution 100 mg/kg/day). Injections were performed intraperitoneally at 9:00 a.m. for 9 days. Blood samples were collected 2 h after the injections on day 1, 5 and 9 and the concentration of plasma NOx was determined using a colorimetric method. ECG was also recorded 2 h after the injection on 1st, 5th and 9th days. The heart rate, QT intervals, corrected QT intervals (QTc) and QT dispersion (QTd), QTc dispersion (QTcd) values were calculated from the ECG recordings. Statistically significant differences were observed between HR, QT and QTc values in all groups for all days (p < 0.001). QTd and QTcd values were found statistically significant different in NAME-G compared to CG and ARG-G (p < 0.001). It was also determined that there was a statistically significant correlation between the NOx and HR and QT and QTc in all days. It is concluded from this study that NO is an important molecule for the electrical activation of heart and has effects on the duration of QT/QTc interval, which should be taken into consideration by the physicians. In addition, application of the L-arginine should be further studied.
Gen Physiol Biophys 2009 Mar
PMID:The correlation between the plasma nitric oxide levels and QT/QTc interval in conscious rabbits. 1939 Jan 33

Present study was designed to evaluate effect of perfusion with human platelets reach plasma (PRP) on coronary flow (CF) and oxidative stress markers in coronary vascular bed of the isolated guinea-pig heart. In coronary venous effluent the following oxidative stress markers were estimated: nitrite as a measure of nitric oxide (NO) production, superoxide anion (O2(-)), and index of lipid peroxidation (TBARS). Isolated guinea-pig hearts (n = 6, b.m. 250-300 g) were perfused according to a Langendorff's technique at different (30, 70, and 120 cmH2O) coronary perfusion pressures (CPP). Samples were collected at control conditions and during perfusion with platelets rich plasma (PRP) obtained either from healthy volunteers or from patients with acute myocardial infarction (PRP (AMI)) with/or without previous inhibition of NO synthase (NOS) by Nomega-nitro-L-arginine monomethyl ester (L-NAME, 30 micromol/l). PRP and PRP (AMI) perfusion induced reduction of CF and all evaluated oxidative stress parameters. The reduction of CF was more potentiated in PRP (AMI) as in PRP group, while oxidative stress parameters where significantly decreased only in PRP (AMI). In addition, previous blockade of NOS by L-NAME potentiated these effects only in PRP (AMI) group. It can be concluded that non-activated and activated platelets interact with coronary endothelium in similar way, with more significant influence of activated platelets on CF and oxidative stress markers.
Gen Physiol Biophys 2009
PMID:Human platelets perfusion through isolated guinea-pig heart: the effects on coronary flow and oxidative stress markers. 1989 86

Protamine sulphate (PS) effect on spontaneous and calcium-induced rhythmic contractions of isolated virgin rat uteri was studied. PS caused dose-dependent relaxation of both types of contractions (two-way ANOVA, significant dose effects). Pretreatment with NG-nitro-L-arginine methyl ester (L-NAME; 10(-5) mol/l), methylene blue (MB; 0.9 x 10(-6) mol/l) or propranolol (1.7 x 10(-5) mol/l) enhanced PS-mediated uterine muscle relaxation of spontaneous contractions. Dosedependent relaxation of spontaneous active isolated rat uterus with PS was lower in uteri pretreated with single dose of tetraethylammonium (TEA; 6 x 10(-3) mol/l), glibenclamide (2 x 10(-6) mol/l) and 4-aminopyridine (4-AP; 10(-3) mol/l). Calcium-induced activity of the isolated rat uterus pretreated with the same concentration of L-NAME, MB, or propranolol modified the kinetic of PS-induced relaxation without changes in EC(50) values. Pre-treatment with glibenclamide, TEA and 4-AP significantly reduce PS relaxing effect of calcium-induced activity and according to EC(50) values the order of magnitude was glibenclamide > TEA > 4-AP. PS is mixture of polyamines and may activate different signal-transduction pathways. Our results cleary demonstrate that in uterine smooth muscle PS act dominantly through potassium chanels and marginaly through beta-adrenergic receptos or nitric oxide-dependent pathways.
Gen Physiol Biophys 2009
PMID:Effects of protamine sulphate on spontaneous and calcium-induced contractile activity in the rat uterus are potassium channels-mediated. 1989 92

The goal of the present study was to examine the effectiveness of a non-specific nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) to modulate the toxicity of aluminium chloride (AlCl3). Rats were killed at 3 h and at 30 days after treatments and the striatum was removed. Nitrite, superoxide, superoxide dismutase activity, malondialdehyde and reduced glutathione were determined. AlCl3 exposure promoted oxidative stress in the striatum. The biochemical changes observed in neuronal tissues show that aluminium acts as pro-oxidant, while the NOS inhibitor exerts antioxidant action in AlCl3-treated rats. We conclude that L-NAME can efficiently protect neuronal tissue from AlCl3-induced toxicity.
Gen Physiol Biophys 2009
PMID:The effect of inhibition of nitric oxide synthase on aluminium-induced toxicity in the rat brain. 1989 6

IOxidative stress development in different brain structures and the influence of nitric oxide (NO) overproduction during sepsis was investigated using male Wistar rats. Rats were subjected to cecal ligation and puncture (CLP) or were sham-operated. To evaluate the source of NO production, 30 min before the operation septic and control animals were treated with single intraperitoneal doses of NO synthase (NOS) inhibitors: L-NAME and aminoguanidine (AG) (10, 30 or 90 mg/kg) and 7-nitroindazole (7-NI) (30 mg/kg). The concentration of GSH in the cortex, brain stem, cerebellum, striatum and hippocampus significantly decreased post CLP at both early and late stage sepsis. Lipid peroxidation also occurred in the cortex and cerebellum in late stage sepsis. Pre-treatment with a non-selective NOS inhibitor (L-NAME) and with selective inducible and neuronal NOS inhibitors (AG and 7-NI) revealed benefit effects on the GSH concentrations. Unexpectedly, NOS inhibition resulted in diverse effects on TBARS concentrations, suggesting the importance of specific quantities of NO in specific brain structures during sepsis.
Gen Physiol Biophys 2009
PMID:Nitric oxide synthase inhibitors partially inhibit oxidative stress development in the rat brain during sepsis provoked by cecal ligation and puncture. 1989 7


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