Effect of pH and type of formulation on the persistence of imidacloprid in water.
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Biomedical subjects
Publications and source records attributed to A Chowdhury.
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(1) The hypothesis that inhalational anesthetics affect G-protein linked alpha2 adrenergic signaling pathway was investigated using human platelets as a model system. (2) Alpha2 receptor stimulation by UK-14304, a potent and selective agonist, inhibits cAMP production induced by prostaglandin I2 (PGI2). (3) Brief stimulation (30 s) with PGI2 raised cAMP levels in platelets by 25-fold; UK-14304 suppressed the PGI2 stimulus by 80%. (4) Halothane at fractional minimum alveolar concentration (MAC) through super physiological levels (16 MAC) had no effect on basal or prostacyclin stimulated levels of cAMP, nor did it have any effect on the inhibition of cAMP production by UK-14304. Moreover, isoflurane, enflurane and sevoflurane had no significant effect on cAMP production at 1.5 or 8 MAC. The results suggest alpha2 and PGI2 signaling pathways are not sensitive to volatile anesthetics including the alpha2 or PGI2 receptor/G-protein complex, G-protein/adenylyl cyclase complex and adenylyl cyclase itself. (5) The possibility that halothane and related anesthetics act more distally in the pathway, on cAMP-dependent protein kinase (PKA), was investigated by measuring the phosphorylation pattern of endogenous platelet proteins by PKA. (6) An increase in the [32P]phosphate incorporation was observed in platelets exposed to either, low doses of PGI2 or isobutylmethylxanthine (IBMX). Halothane, isoflurane, enflurane or sevoflurane further increased the level of [32P]-incorporation. The apparent increase in PKA activity suggests that at least in platelets, volatile anesthetics activate PKA-dependent pathways which should antagonize alpha2 adrenergic signaling.
Toxicokinetic behavior and recoveries of isoproturon from feces, urine, and different tissues of goat were determined after 4, 5, 6, and 7 days following single oral administration at 500 mg/kg. Isoproturon was rapidly absorbed and attained blood concentration within 15 min of administration. The kinetic behavior followed a two-compartment open model. The higher t(1/2)(beta) (9.78 +/- 0.33 h) and V(d)()area (4.49 +/- 0.41 L/kg) associated with lower Cl(B) (0.32 +/- 0.02 L/kg/h) suggested slow elimination from the blood. Approximately 56% of the total administered compound was recovered from feces. The rate of excretion of isoproturon through feces was maximum at 48 h and could not be detected beyond 120 h. The excretion pattern of isoproturon through urine resembled that of feces, and approximately 10-11% was eliminated in urine. A maximum quantity of residue was detected in all tissues of goats slaughtered after 4 days followed by a substantial decline after day 5, and nothing could be detected after day 7. Histopathological study revealed that isoproturon produced moderate cellular changes like fatty degeneration in the liver and kidney and emphysema in the lung after 7 days post administration.
One hundred and six patients suffering from severe dehydrating diarrhoea were studied of whom 36 patients were positive for Vibrio cholerae. Out of 36, 15 were positive for V. cholerae O1, 10 for V. cholerae O139 and 11 for V. cholerae non-O1 non-O139. O1 and O139 were positive for the 301-bp ctxA amplicon and 471-bp tcpA amplicon indicating that the strains possessed toxigenic capability whereas no non-O1 non-O139 strain possessed ctxA or tcpA genes. Post-admission severity of purging and amount of ORS required were less in the V. cholerae non-O1 non-O139 group (P < 0.05) compared to the V. cholerae O1 and O139 groups. It appears from this study that a cholera-like clinical condition can be caused in the absence of CT as exemplified by strains of non-O1 non-O139.
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Endoscopic procedures are difficult in patients with situs inversus owing to left-right reversal of viscera. Conventionally, reversal of the position of the endoscopist in relation to the patient is advocated to overcome the anatomical difficulty. We describe a patient with chronic calcific pancreatitis and pseudocyst of the pancreas who had situs inversus. ERCP was performed with minor modification of maneuvers with the patient in the usual left lateral decubitus and the endoscopist on the left of the table.
This study was carried out to investigate the expression of various growth factors (GFs) involved in mucosal healing and thereby to clarify whether there are potential differences in the expression of GFs between normal colonic mucosa and the uninvolved mucosa of ulcerative colitis (UC). GF mRNA was investigated by reverse transcription polymerase chain reaction in colorectal biopsies from 20 normal controls and 15 UC patients. The positive rates (%) for mRNA expression for normal/UC were: epidermal growth factor (EGF) 65/53, transforming growth factor (TGF)-alpha 100/87, TGF-beta 1 60/33, insulin like growth factor-I 45/33, platelet-derived growth factor-A 55/67, basic fibroblast growth factor 0/0, hepatocyte growth factor (HGF) 50/53, EGF receptor 20/27, erb-B2 75/73, and HGF receptor (c-MET) 55/67. Semiquantitation of mRNA showed significantly lower expression of TGF-beta 1 (P < 0.05) in UC. Differences in expression and mRNA levels were not statistically significant for any other GFs. Our results indicate that mucosa in chronic persistent UC has a low basal expression of TGF-beta 1 mRNA, and, since TGF-beta 1 is a multifunctional GF that plays important roles in regulating repair and regeneration following tissue injury, this low expression may be partially responsible for the intractability of the disease.
Hepatitis B virus (HBV) with X gene mutations has been a putative pathogen of chronic hepatitis without serological markers of known hepatitis viruses. The aim of this study was to reconfirm whether the HBV with the X gene mutation is associated with these serologically "silent" non-B, non-C (NBNC) chronic hepatitis, alcoholic liver disease (ALD) and autoimmune hepatitis (AIH). HBV DNA was amplified from serum and sequenced in 30 patients with NBNC chronic hepatitis in comparison with 20 patients with ALD and 5 patients with AIH. HBV DNA was identified in 21 patients (70%) in NBNC chronic hepatitis by nested polymerase chain reaction while only one patient (5%) in ALD and none in AIH showed HBV DNA. Eighteen (85.7%) of the 21 identified HBV DNAs had an identical 8-nucleotide deletion mutation at the distal part of the X region. This mutation affected the core promoter and the enhancer II sequence of HBV DNA and created a translational stop codon which truncated the X protein by 20 amino acids from the C-terminal end. All the HBV DNAs had a precore mutation at the 83rd nucleotide resulting in disruption of HBe antigen synthesis. These results indicate that HBV mutants are closely associated with the majority of serologically "silent" NBNC chronic hepatitis cases and the population of such mutant HBV DNAs is not uniform.
To investigate the relationship between intrahepatic cytokine expression and interferon (IFN) response in chronic hepatitis C [CH(C)], interleukin (IL)-1 beta, -2, -4, -6, -8, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha and TNF-beta mRNAs were investigated semiquantitatively by reverse transcription polymerase chain reaction using serial liver biopsies taken before and after IFN-alpha treatment from 24 patients with CH(C), including 12 responders and 12 non-responders. Before IFN treatment, IL-2, TNF-beta, IFN-gamma and IL-8 mRNA were associated with severe hepatitis activity whereas IL-4 mRNA was associated with weak hepatitis activity, regardless of IFN response. IL-2, TNF-beta and IFN-gamma mRNAs were significantly greater in IFN non-responders. After IFN treatment a complete response to IFN was significantly associated with the disappearance of these pro-inflammatory cytokines, whereas non-responders retained the expression of cytokine mRNA as before IFN treatment. Our results indicated that IFN-alpha treatment may modulate the intrahepatic cytokine network, and this may be one mechanism of IFN-alpha that reduces hepatitis activity, aside from an anti-viral effect. A difference in cytokine network may be involved in IFN response in CH(C).
A monoclonal antibody, ICT11, specific for the toxin of enterotoxigenic Bacteroides fragilis (ETBF) neutralized the cytotoxic effect of the toxin on human colonic cell line HT-29/C1. In an evaluation using 115 diarrheal stool specimens and culture as the "gold standard," the assay showed a sensitivity of 85% and a specificity of 100%. An ICT11-based sandwich enzyme-linked immunosorbent assay showed a sensitivity of 100% and a specificity of 98% for direct detection of toxin from stool samples compared with those of culture. Thus, ICT11-based assays will be useful for screening for ETBF.
Antibody responses to the lipopolysaccharide (LPS) of shigellae were compared between children with uncomplicated and complicated Shigella dysenteriae 1 infection. One hundred fifteen children between 12 and 60 months of age with S. dysenteriae 1 infection were studied. Of these children, 42 had complications (leukemoid reaction and/or hemolytic-uremic syndrome [complicated shigellosis] and 73 had no complications (uncomplicated shigellosis). Antibodies to the LPS of S. dysenteriae 1 and Shigella flexneri Y were measured in plasma and stools, as were total immunoglobulin A (IgA) and IgG concentrations in plasma and the total IgA concentration in stool, on enrollment and 3 to 5 days later. In the plasma, the concentrations of homologous (IgG) and heterologous (IgA) LPS antibodies on enrollment were higher in children with complicated shigellosis than in those with uncomplicated shigellosis. In stool, the concentrations on enrollment were similar between the two groups of children. There was a rise in antibody concentrations in the plasma (homologous and heterologous) and stool (homologous) between the day of enrollment and 3 to 5 days later in children with uncomplicated shigellosis but not in those with complicated shigellosis. These findings suggest that systemic stimulation is more marked in children with complications, so that a subsequent rise in plasma antibody concentrations does not occur in these children. In contrast, the lack of a rise in stool antibody concentrations in children with complicated shigellosis is suggestive of a lower-level mucosal response. Because the duration of diarrhea before enrollment influenced the homologous antibody concentrations, children were further divided into three subgroups (short [3 to 5 days], medium [6 to 9 days], and long [> 9 days] diarrhea durations before enrollment). Comparisons of homologous antibody concentrations between the two groups of children following such subdivisions showed that in children with complicated shigellosis, antibody concentrations were higher in the plasma of children in the short diarrhea duration subgroup but lower in the stool children in the medium diarrhea duration subgroup. No differences in antibody concentrations were observed in children in the other diarrhea duration subgroups. Thus, complications in shigellosis are associated with an early and strong systemic stimulation without a concomitant stimulation of the mucosal antibody response.
The study was aimed to determine the role of endoscopic retrograde cholangiopancreatography (ERCP) in patients with postcholecystectomy symptoms in respect to interval of presentation following cholecystectomy. 170 patients with postcholecystectomy symptoms and negative upper gastrointestinal endoscopy were evaluated using ERCP. One hundred and seventeen (75%) out of 156 patients with successful ERCP had one or more abnormalities seen at ERCP. Bile duct stones (55 patients), benign strictures of bile duct (27 patients) were the common lesions detected. A significantly higher (p < 0.001) positive diagnosis was possible at ERCP in patients presenting with jaundice (100%) as compared to those without jaundice (61.8%). Spectrum of causes among patients presenting in early post-operative period (< 1 month) was somewhat different from those presenting later. Bile duct ligature and biliary fistula were the predominant causes in the former group, while stones and benign strictures were commoner in the patients presenting late. Endoscopic sphincterotomy and stone removal was performed successfully in 25 out of 30 patients in whom it was attempted. ERCP was found to be a very useful procedure in the management of postcholecystectomy symptoms. Spectrum of underlying disease was different in patients presenting before 1 month following cholecystectomy as compared to those presenting later.
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Hepatitis B virus (HBV) carriers with antibody to hepatitis e antigen comprise asymptomatic carriers (ASCs), who have low replication levels of HBV, and patients with chronic active hepatitis (CAH), who have high levels of viral replication. To investigate whether defects in the X protein might be responsible for this difference in the level of viral replication, nucleotide sequences of X and precore gene regions in serum HBV were analyzed in 19 ASCs and 9 CAH patients. All patients had a point mutation creating a stop codon in the precore region. Seventeen ASCs (87.3%) had identical mutations consisting of 4 noncontiguous 1-bp deletions or an 8-bp deletion, both of which truncate the normal X protein, whereas no CAH patient had an X gene mutation (P < .001). Thus, deletion of the X protein might be responsible for the low levels of viral replication in ASCs.
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Perforin and granzyme A are the major effectors of cytotoxic T cells in cell-mediated cytotoxicity. However, there has been no report on these effectors in chronic viral hepatitis. In the present study, the expression of perforin and granzyme A mRNA was investigated by the reverse transcription polymerase chain reaction method using liver biopsy specimens and peripheral mononuclear cells (PBMC) from 21 patients with chronic hepatitis C and 5 control cases. Perforin mRNA was detected only in the liver of chronic hepatitis patients but not in the control livers. Conversely, perforin mRNA was not expressed in PBMC of the patients with chronic hepatitis (P < 0.01). Granzyme A mRNA was detected both in the liver and PBMC of all the cases including control cases. These results indicated that the perforin is an important effector molecule in the hepatocyte lysis in chronic viral hepatitis C.