Biomedical subjects

J Nandi

Publications and source records attributed to J Nandi.

At least 19 recordsLinked to original sources

PubMed2006

Hyperbaric oxygenation ameliorates indomethacin-induced enteropathy in rats by modulating TNF-alpha and IL-1beta production.

The effect of hyperbaric oxygenation (HBO2) was investigated in a rat model of indomethacin-induced enteropathy. Enteropathy was induced by two subcutaneous injections of indomethacin (7.5 mg/kg) 24 hr apart. Six groups of rats (n=8) were treated with and without HBO2 (100% oxygen at 2.3 atm absolute) for 1 hr once or twice a day for 2 or 5 days. Disease activity index (DAI) and total ulcer length were measured. Other rats were randomized into two groups (n=16) with and without HBO2 (1 hr once a day) and four rats were killed in each group at 12, 24, 48, and 72 hr after the final injection of indomethacin. Serum and intestinal mucosal TNF-alpha, IL-1beta, myeloperoxidase (MPO), and iNOS expression was measured. HBO2 treatment significantly attenuated indomethacin -induced intestinal ulceration and improved DAI. Indomethacin increased MPO activity and iNOS expression, and these were reduced by HBO2 treatment, with a concomitant reduction in TNF-alpha and IL-1beta. Our data suggest that HBO2 treatment has a beneficial effect on indomethacin-induced enteropathy and this effect is possibly mediated by decreased production of TNF-alpha and IL-1beta.

Animals↗

PubMed2005

Inhibition of TNF-alpha improves indomethacin-induced enteropathy in rats by modulating iNOS expression.

TNF-alpha, including other proinflammatory cytokines alone or in combination, induces iNOS expression and upregulates inflammatory responses. We evaluated the relationship between TNF-alpha and iNOS expression in indomethacin-induced jejunoileitis in male Sprague-Dawley rats. Rats were fed a daily dose of a phosphodiesterase inhibitor-either theophylline or pentoxifylline-for 2 days. Jejunoileitis was induced with two subcutaneous injections of indomethacin (7.5 mg/kg) 24 hr apart and theophylline or pentoxifylline continued for 12 hr or 4 days. Other rats received a single intraperitoneal injection of anti-TNF-alpha monoclonal antibody (TNF-Ab) 30-min before indomethacin. At 4 days TNF-Ab, theophylline, or pentoxifylline treatment significantly decreased indomethacin-induced ulceration, myeloperoxidase activity, and disease activity index. Although indomethacin significantly increased serum TNF-alpha and nitrate/nitrite levels over the control value as early as 12 hr, iNOS expression was detected only after 4 days. Serum IL-1beta level did not change at 12 hr but increased fourfold at 4 days. Treatment with TNF-Ab, theophylline, or pentoxifylline significantly reduced serum/tissue TNF-alpha, IL-1beta, nitrate/nitrite, and iNOS expression. The downregulation of nitrate/nitrite by these inhibitors suggests that TNF-alpha modulates iNOS expression.

Animals↗

PubMed2001

Nitric oxide inhibitors ameliorate indomethacin-induced enteropathy in rats.

The role of nitric oxide (NO) synthase inhibitors in indomethacin (INDO) -induced enteropathy was investigated in male Sprague-Dawley rats. Rats were subcutaneously administered 5% sodium bicarbonate (controls), two doses of INDO 7.5 mg/kg, and three different inducible NO synthase (iNOS) inhibitors at various concentrations 24 hr, apart; aminoguanidine (AG), guanidinoethyldisulfide (GED), and n-(3-aminomethyl)benzylacetamidine (1400W). Rats were killed four days after the initial injection and small intestinal mucosa was assayed for myeloperoxidase (MPO) activity and iNOS expression by western blot analysis. Serum nitrite/nitrate (NOx) concentration was measured colorimetrically. INDO produced acute ulcers along the mesenteric border from the ileum to proximal jejunum. Rats treated with AG (25 and 50 mg/kg), GED (2.5 mg/kg), and 1400W (0.1 mg/kg) showed decreased total ulcer length and MPO activity by 51, 72, 53, and 61% and by 58, 88, 68, and 70%, respectively, compared to INDO alone. All inhibitors similarly reduced INDO-enhanced serum NOx concentrations to its basal levels. Significant iNOS expression was detected in INDO-treated rats, but the inhibitors did not alter iNOS expression. Our data suggest that NO derived from iNOS may be a key factor in the pathogenesis of acute INDO-induced enteropathy in rats.

Amidines↗

PubMed2001

Role of nitric oxide in acidosis-induced intestinal injury in anesthetized rats.

We investigated the pathogenic mechanism(s) of small intestinal injury during acidosis in relation to circulating nitric oxide (NO) in an experimental rat model. Rats were anesthetized, paralyzed, and mechanically ventilated with room air. Hydrochloric acid (0.16 mmol bolus followed by 0.132 mmol/kg/h) was infused through the jugular vein for 5 hours. Control rats received a saline infusion. Arterial blood gases, blood pressure, and blood pH were measured every 30 minutes. The involvement of NO in this acidosis model was assessed by measuring plasma concentration of nitrite/nitrate (NOx) and by evaluating inducible NO synthase (iNOS) expression in small intestinal mucosa. Intestinal injury was assessed by measuring myeloperoxidase (MPO) activity, thiobarbituric acid reactants (TBARS), and histologic scores. HCl infusion was associated with hypotension, decreased blood pH, increased plasma concentration of NOx, augmented intestinal mucosal iNOS expression, MPO activity, TBARS, and histopathologic injury scores. Pretreatment with an iNOS inhibitor, aminoguanidine (AG, 50 mg/kg), reversed HCl-induced hypotension without a change in blood pH. HCl-induced lesions, MPO activity, TBARS, and plasma NOx production were decreased by AG. Our data show that the pathogenic mechanisms of acidosis-induced small intestinal lesions involve up-regulation of NO production by increased expression of iNOS and augmentation of superoxide radicals and MPO activity.

Acidosis↗

PubMed2000

Efficacy of chloroquine in febrile Plasmodium falciparum infected children in Mewat region of Haryana.

During 1996, Mewat region of Gurgaon district in Haryana experienced high incidence of Plasmodium falciparum malaria, assuming epidemic proportion in large number of villages affected by floods. Mortality due to fever was also high. In vivo 7 days study amongst 32 febrile P. falciparum infected children of 1 to 14 years age group in flood affected villages of Ferozpur Jhirka Community Health Centre of Mewat region was carried out. All the 32 cases showed good response to chloroquine suggesting that drug was effective and useful as first line of treatment, reducing severity of P. falciparum infection and resolving fever due to infection of the species. The study also indicated that chloroquine was an effective drug in controlling epidemic situation and mortality in areas of high incidence of P. falciparum. Pyrogenic stimulus was variable among different developmental stages of P. falciparum and suggestive of the need of earliest possible initiation of anti-malaria treatment, community based fever survey and blood smear examination. Increase in incidence of fever in an endemic community, particularly in children, should be considered as an indicator of impending outbreak of P. falciparum malaria. Effectiveness of diagnostic and control measures taken can be evaluated on the basis of incidence of malaria particularly due to P. falciparum infection and also incidence of fever in an endemic community.

Adolescent↗

PubMed2000

Anthropophily of Anophelines in Duars of West Bengal and other regions of India.

Attempts have been made to identify the source of blood meals of twenty three anopheline species from various areas of high malaria endemicity in India. Anopheles minimus, Anopheles fluviatilis and Anopheles dirus showed a high propensity for human blood in North-Eastern parts of the country while Anopheles sundicus was found to be anthropophilic in Andaman & Nicobar Islands. Anopheles culicifacies, Anopheles maculatus and Anopheles philippinensis were found primarily zoophilic in north-eastern areas. High anthropophily has been closely related to sporozoite infection in anophelines specially in Anopheles minimus and is of great epidemiological significance.

Animals↗

PubMed1999

Dietary nucleotides augment dextran sulfate sodium-induced distal colitis in rats.

We have previously shown that enteral and parenteral supplementation of nucleotides (NT) accelerates healing of small-bowel ulcers in rats with indomethacin-induced ileitis. The purpose of this study was to evaluate whether dietary NT supplementation would similarly affect ulcer healing in dextran sulfate sodium (DSS)-induced colitis in rats. Male Sprague-Dawley rats were randomly assigned to receive either nucleotide-free (NF) or NT-supplemented diets. After 2 d of prefeeding, colitis was induced by including 40 g/L of DSS in drinking water for 3 d, followed thereafter by tap water. Rats from each group were killed at 7 and 12 d after induction of colitis. Additional rats were also used for both the groups as controls (untreated groups). The length of colon was measured and evaluated by histological score. Colonic myeloperoxidase (MPO) activity was assessed. In a separate series of experiments, rats were studied at 0, 4, 7, and 12 d for interleukin-1beta (IL-1beta) in rectal dialysate and plasma. Ulceration predominated in the distal colon in DSS-treated rats. There was no significant difference between the histological scores of the NF and NT-supplemented groups either at 7 or 12 d. MPO activity at 7 and 12 d was significantly higher in the NT-supplemented compared to NF group (7 d: 1013 +/- 172 vs. 409.9 +/- 103.2; 12 d: 471.9 +/- 112.4 vs. 223.6 +/- 21.6 units. min-1. g colon-1). IL-1beta concentration in rectal dialysate was significantly higher at 7 d in both groups compared to 0 and 4 d. At 12 d it continued to be significantly elevated in the NT-supplemented group and was greater than in the NT-free group. Our data on the proinflammatory cytokine, in conjunction with MPO activity, strongly suggest that NT supplementation aggravates the severity of DSS-induced colitis in rats.

Animals↗

PubMed1999

Acidosis stimulates nitric oxide production and lung damage in rats.

Systemic hypotension during sepsis is thought to be due to nitric oxide (NO) overproduction, but it may also be due to acidosis. We evaluated in healthy rats the consequences of acid infusion on NO and blood pressure. Sprague-Dawley rats were anesthetized, and ventilated with room air. The animals were randomized into four groups. Group 1 (C, n = 10) received only normal saline at rates comparable to the other groups. Group 2 (A1, n = 10) received hydrochloric acid at 0.162 mmol in the first 15 to 30 min, followed by a continuous infusion of 0.058 mmol/h for 5 h. Group 3 (AG+A1, n = 6) was pretreated with aminoguanidine (AG, 50 mg/kg), and HCl was infused as above. Group 4 (A2, n = 7) received HCl at twice the rate used in A1. Nitric oxide concentration in the exhaled gas (ENO), blood gases, and mean arterial pressure were measured every 30 min. Acid infusion in A1 caused the pH to fall gradually from 7.43 +/- 0. 01 to 7.13 +/- 0.05. This moderate decrease in pH was associated with a marked increase in ENO (1.6 +/- 0.3 to 114.2 +/- 22.3 ppb), an increase in plasma nitrite/nitrate (17.3 +/- 3.7 to 35.2 +/- 4.3 microM), and a significant decrease in blood pressure (110.5 +/- 6.3 to 63.3 +/- 15.0 mm Hg). Furthermore, acidosis caused lung inflammation, as suggested by the increase in lung myeloperoxidase activity (282.2 +/- 24.7 to 679.3 +/- 57.3 U/min/g) and lung injury score (1.7 +/- 0.2 to 3.5 +/- 0.6). Acidosis after AG pretreatment was associated with a similar change in pH, but the increase in ENO, nitrite/nitrate, and systemic hypotension were prevented. Furthermore, lung injury was attenuated by AG, as suggested by a lower myeloperoxidase activity, though lung injury score was not altered. In this model, moderate acidosis causes increases in NO, hypotension, and lung inflammation. Lung inflammation and injury are due in part to acidosis and NO production. This is the first report to show a direct effect of chronic acidosis on NO production and lung injury. These results have profound implications on the role of acidosis on NO production and lung injury during sepsis.

Acidosis↗

PubMed1999

Expression and characterization of protein kinase C in isolated rabbit parietal cells.

We investigated the expression, characterization and distribution of protein kinase C (PKC) isozymes in isolated rabbit parietal cells (PC). Cellular extracts of PC were analyzed by Western blot using isozyme-specific antibodies. The Ca2+-independent PKC-epsilon was detected in cytosolic, membrane and cytoskeletal fractions of basal and histamine-stimulated PC, whereas the Ca2+-dependent PKC-alpha was confined to the cytosolic and membrane fractions. Cytosolic and membrane fractions were partially purified by DEAE cellulose column chromatography with elution of increasing NaCl concentration. Eluates of 0.15 M and 0.3 M NaCl PC fractions were identified as PKC-alpha and -epsilon isoforms, respectively. Phorbol 12-myristate 13-acetate (TPA) treatment of PC for 15, 30 and 60 sec decreased significantly cytosolic PKC-alpha and increased membrane-associated PKC-alpha. In contrast to the distribution of PKC-alpha, TPA did not alter membrane or cytosolic level of PKC-epsilon. Comparison of the dose-response curves between TPA-induced hydrogen (H+) secretion, as measured by aminopyrine (AP) uptake, and the membrane-associated PKC-alpha suggests that translocation of PKC-alpha is not involved in the H+ secretory process in PC. Furthermore, a PKC inhibitor, staurosporine, produced a concentration-dependent enhancement of histamine-stimulated H+ secretion. These findings suggest that PKC-alpha plays a negative modulatory role, rather than an obligatory role, in H+ secretion. The localization and distribution of PKC-epsilon into the cytoskeletal fraction of PC also suggests that this isozyme may be involved in the cellular regulation of reversible morphological transformation during stimulation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1998

Induction of an ATPase inhibitor protein by propylthiouracil and protection against paracetamol (acetaminophen) hepatotoxicity in the rat.

1. The purpose of the present study was to test the following hypothesis: propylthiouracil (PTU) treatments of rats induces an increase in the concentration and activity of the mitochondrial ATPase (m-ATPase) inhibitor protein (IF1). The PTU-induced elevated baseline levels of this inhibitor protein inactivated m-ATPase, and prevented hepatotoxicity by a toxic dose of acetaminophen (AAP) (paracetamol), by maintaining hepatic adenosine 5'-triphosphate (ATP) levels. 2. Male Wistar rats were either gavaged with a toxic dose of AAP alone, or after pretreatment with PTU for periods of 3 and 12 days. 3. Twenty four hours after acetaminophen treatment alone, toxicity was manifested by: an approximately 10 fold increase in serum transaminase levels (serum glutamic oxaloacetic transaminase and serum glutamic pyruvic transaminase); depletion of hepatic reduced glutathione (GSH) and ATP levels; loss of inhibitor protein activity, and extensive pericentral necrosis of the hepatocytes. Propylthiouracil pretreatment for 12 days enhanced the concentration of the following metabolites in the liver: ATP (1.5 fold), ATPase inhibitor protein (IF1) (4.5 fold), and reduced glutathione (1.3 fold), while the activity of the inhibitor protein increased 2 fold. When the PTU treated rats were challenged with AAP, transaminases were not elevated, and only sporadic areas of necrosis were detected by histological examination of the liver tissue. In contrast to the 12 day treatment with PTU the 3 day treatment had no protection against AAP. No histological evidence of protection was manifested and the transaminases were not different from AAP treated controls. Most of the protective metabolites were depleted. 4. Our findings suggest that PTU-induced increased concentration of inhibitor protein and GSH, are contributing factors in the prevention of hepatotoxicity by maintaining hepatic m-ATP levels and reducing the harmful effect of the toxic metabolite of AAP.

Acetaminophen↗

PubMed1997

Dietary supplementation of nucleotides and arginine promotes healing of small bowel ulcers in experimental ulcerative ileitis.

We previously showed that intravenous total parenteral nutrition supplemented with nucleosides and nucleotides (NS/NT) promoted ulcer healing in rats with indomethacin-induced ileitis. The present study evaluated whether dietary NT supplementation would similarly affect ulcer healing in this model. Female Lewis rats were randomized into either control or experimental groups receiving yeast RNA containing NT or arginine, glutamine, fish oil, guar gum, or a combination of yeast RNA+arginine diets. Ileitis was induced by two doses of indomethacin (7.5 mg/kg) administered subcutaneously 24 hr apart. Ulcer number and length were determined at 4, 8, and 14 days after induction of ileitis. Ileal villous and crypt length, crypt-villous ratio, and bromodeoxyuridine (BrdU) labeling were studied in the control and yeast RNA-supplemented diet groups. Ileal ulceration was present in all groups at 4 and 8 days and was almost healed by 14 days. Rats receiving yeast RNA, arginine, and yeast RNA + arginine diets showed a significant decrease in ulcer number (56%, 28%, and 34%, respectively) and length (67%, 41%, and 48%, respectively) compared to controls at 8 but not at 4 days. Glutamine, fish oil, and guar gum had no effect on ulcer healing at 4, 8, or 14 days. Among the histological parameters, a significant decrease in crypt length in the yeast RNA-supplemented group at 8 days suggested an acceleration of the healing process and restoration to a near-normal crypt-villous architecture. We conclude that the yeast RNA, arginine, and yeast RNA + arginine diets accelerated ulcer healing, as indicated by decreased ulcer number and length. We postulate that the underlying mechanism(s) contributing to ulcer healing may be related, in part, to increased cell proliferation.

Animal Feed↗

PubMed1996

Mode of food intake reduction in Lewis rats with indomethacin-induced ulcerative ileitis.

The mechanism of anorexia in inflammatory bowel disease is poorly understood. To gain insight into possible pathophysiologic mechanisms, the feeding indices and food intake were studied in an animal model of Crohn's disease. The anorexia of indomethacin-induced ulcerative ileitis was compared with that of the well-known anorexia of total parenteral nutrition (TPN). Forty-five female Lewis rats were randomized to four groups: Control, Indomethacin, Indomethacin + TPN, and TPN. Feeding indices and food intake were continuously measured using the Automated Computerized Rat Eater Meter. Interleukin-1 alpha (IL-1 alpha), tumor necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) were assayed in plasma, mononuclear cell culture, or ileum to determine their role in mediating anorexia. In the TPN group, spontaneous food intake (SFI) decreased (52%; p < 0.05), primarily via reduction in meal number (MN, 54%; p < 0.05) and, to a lesser extent, meal size (MZ, 35%; p < 0.05). In comparison, in the Indomethacin group SFI decreased (74%; p < 0.05) primarily via reduction in MZ (67%, p < 0.05); MN also decreased but to a lesser extent (27%; p < 0.05). In the Indomethacin + TPN group, SFI decreased (55%; p > 0.05) primarily via reduction in MN (79%; p < 0.05), whereas MZ decreased slightly (19%; p < 0.05). Only in the Indomethacin group were IL-1 alpha and TNF-alpha detected in the mononuclear cell culture and plasma, respectively. In the Indomethacin group, an inverse correlation existed between MZ and TNF-alpha (p < 0.05). In the Indomethacin group, IL-1 alpha, PGE2, and LTB4 concentrations did not correlate with feeding indices. SFI reduction in this model was mediated primarily via a decrease in MZ. TNF-alpha is proposed to mediate this effect and TPN was shown to overcome the effect on MZ.

Animals↗

PubMed1996

Effects of a phorbol ester and isoquinoline sulfonamides on rabbit parietal cell function.

The role of protein kinase C (PKC) on gastric H+ secretion, as measured by aminopyrine (AP) uptake and other intracellular signal transduction products, was investigated in isolated rabbit parietal cells using the PKC activator 12-0-tetradecanoyl phorbol 13-acetate (TPA) and several PKC inhibitors, including isoquinoline sulfonamides (H-7, H-8, H-89 and HA-1004) and calphostin-C. TPA dose-dependently inhibited histamine (10(-4) M)- and carbachol (10(-4) M)-stimulated AP uptake without affecting the response to dibutyryl cyclic AMP (10(-3) M). H-7 and calphostin-C dose-dependently augmented secretagogue-stimulated AP uptake, whereas H-8 and H-89 inhibited the response to secretagogues, and HA-1004 had no effect. H-7 and calphostin-C-induced augmentation of AP uptake was blocked by a calcium (Ca++) antagonist, lanthanum chloride, which suggests that the enhanced AP response was regulated by extracellular Ca++. Moreover, H-7 treatment partially reversed the TPA (10(-7) M)-induced inhibition of secretagogue-stimulated AP uptake. TPA reduced histamine- and carbachol-stimulated cAMP and inositol 1,4,5-triphosphate production by 50% and 96%, respectively, with a concomitant reduction of adenylate cyclase and intracellular free Ca++ by 44% and 78%. TPA increased the distribution of membrane-associated PKC by 20% and decreased histamine-stimulated PKA by 30%. In contrast, H-7 inhibited both PKC and protein tyrosine kinase activity in vitro but had no effect on these parameters in vivo. The results indicate that TPA-induced inhibition of secretagogue-stimulated AP uptake in PC is presumably mediated by activation of PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1996

Ecological observations on the anopheline mosquitoes of Jalpaiguri Duars, West Bengal.

A nine month entomological study was conducted from August 1989 to April 1990 in Jalpaiguri duars of West Bengal where malaria has been persistent problem. Amongst the anopheline fauna three vector species were recorded; An. minimus was the principal vector supported by A. dirus during the rainy months and An. fluviatilis in dry months. All the three vectors were found in close association with human orbit and An. minimums was found to be primarily a domestic vector. The primary role of An. minimus in the transmission of malaria in the region has been highlighted. Observations on seasonal variation, biting preferences, and biting time and vector infection rates were recorded.

Animals↗

PubMed1995

Effects of nonsteroidal antiinflammatory drugs on ulcerogenesis and gastric secretion in pylorus-ligated rat.

The effects of nonsteroidal antiinflammatory drugs on ulcerogenesis and gastric secretion were evaluated in a pylorus-ligated rat model. Oral administration of salicylate (50 mg/kg), aspirin (50 mg/kg), and indomethacin (3.5 mg/kg) significantly increased ulcerogenesis over the basal value by six- to sevenfold, but ibuprofen's (10 mg/kg) fourfold increase was not significant. Aspirin in conjunction with histamine (0.5 mg/kg subcutaneously) significantly increased ulcerogenesis by 2.7-fold compared to histamine alone. Basal acid secretion was increased significantly by 156% after indomethacin, but not by other nonsteroidal antiinflammatory drugs. In contrast, all nonsteroidal antiinflammatory drugs, except indomethacin, significantly decreased histamine-stimulated acid secretion. Non-steroidal antiinflammatory drugs had no effect on pepsinogen secretion. Ranitidine pretreatment (25 mg/kg intraperitoneally) significantly decreased basal acid and pepsinogen secretion in all treatment groups by > 85% and > 40%, respectively, and ulcerations induced by salicylate, aspirin, and indomethacin were also inhibited by 90%, 60%, and 60%, respectively. The observed inhibition of prostaglandin E2 generation by nonsteroidal antiinflammatory drugs under basal secretory conditions appeared to correlate with the extent of ulcerogenesis. Our data support the concept that acid, in addition to inhibition of prostaglandin E2 synthesis, plays an important role in the pathogenesis of nonsteroidal antiinflammatory drug-induced gastropathy.

Animals↗

PubMed1995

Tyrosine phosphorylation as a possible regulatory mechanism in the expression of human immunodeficiency virus genes.

Phosphorylation of proteins on serine, threonine and tyrosine is one of the significant regulatory mechanisms in gene expression and post-translational modifications in both eukaryotes and prokaryotes. Protein tyrosine phosphorylation in particular is implicated in cell proliferation, differentiation and certain pathological modifications including transformation. The overall protein tyrosine phosphorylation is modulated by protein tyrosine kinases (PTK) and protein tyrosine phosphatases (PTP). There are several viruses known to contain PTK and PTPs. A computer-based protein sequence search using the FAST P programme was used to investigate whether, theoretically, a sequence for a putative protein tyrosine phosphatase is present in the genomic sequence of the human immunodeficiency virus (HIV). A conserved motif GXGXXG characteristic of both PTK and PTP was found at the 5' LTR region of the HIV genome. Interesting sequence similarities with regulatory proteins of other retroviruses, viz. VPx of HIV-2 and X-protein of HTLV-1, and some transforming proteins were also observed. The implication of the possible phosphorylation event in association with the HIV regulatory proteins tat, rev and nef in AIDS-related malignancies is discussed.

Amino Acid Sequence↗

PubMed1995

Performance evaluation of a particle agglutination test for antibody to human immunodeficiency virus 1: comparison with enzyme immunoassay.

A performance evaluation of a particle agglutination test (PAT), manufactured by Fujirebio Inc., Japan (Serodia-HIV), for antibody to human immunodeficiency virus type-1 (anti-HIV-1) was carried out and compared with a currently available enzyme immunoassay (EIA), manufactured by Genetic Systems Corp., USA, (HIV-1/HIV-2 EIA). Testing 2,878 Indian donor and patient samples, both tests showed 100% sensitivity and comparable specificity (PAT: 99.8%; EIA: 99.7% among donor samples). We conclude that PAT is a specific and sensitive test for anti-HIV-1; it is simple to perform and does not require sophisticated equipment. Hence it is suitable for mass screening of blood donors in a developing country like India, especially in rural areas where presently no HIV-testing facilities are available.

Agglutination Tests↗

PubMed1995

Effects of cyclic adenosine monophosphate-dependent protein kinase and calcium-dependent protein kinase modulators on stimulated gastric acid secretion in the perfused rat stomach.

The effects of cyclic adenosine monophosphate-dependent protein kinase (PKA) and calcium-dependent protein kinase (PKC) modulators on secretagogue-stimulated gastric acid secretion were studied in the continuously perfused stomach of the anesthetized rat. Intravenous histamine (0.25 mg/kg/h) and pentagastrin (2 micrograms/kg/h) increased secretion above baseline by three- and fourfold, respectively. Parenteral administration of a PKC activator, 12-o-tetradecanoylphorbol-13-acetate (TPA; 0.1 nmol/h), decreased histamine- and pentagastrin-stimulated secretion by 64 and 40%, respectively. Administration of PKC inhibitors, calphostin C and 1-(5-isoquinolinyl sulfonyl)-2 methylpiperazine (H-7; 10 nmol/h, each), increased histamine- and pentagastrin-stimulated secretion by 115 and 74% and 42 and 79%, respectively, while equimolar concentrations (10 nmol/h) of three other isoquinoline sulfonamides (HA-1004, H-8, and H-89) had no effect, except for H-89 (100 nmol/h) which inhibited the histamine- and penta-gastrin-stimulated acid secretion by 44%. Basal secretion was not significantly altered by the aforementioned drugs. The TPA-induced inhibition of pentagastrin-stimulated secretion was partially reversed by treatment with H-7. These findings support a role of PKA and PKC in the modulation of stimulated gastric acid secretion in vivo.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗