Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.6.1.1 (aspartate aminotransferase)
21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-one patients with severe gram-negative bacterial infections were treated successfully with a combination of cefamandole nafate plus gentamicin or tobramycin. The patients were divided into two treatment groups: group 1 received low-dose therapy (80--100 mg of cefamandole nafate/kg per 24 hr plus 3 mg of either gentamicin or tobramycin/kg per 24 hr), and group 2 patients, who had suspected bacteremia, received high-dose therapy (170 mg of cefamandole nafate/kg per 24 hr plus 5 mg of either gentamicin or tobramycin/kg per 24 hr). All of the patients were clinically and bacteriologically cured of their primary infections. All four episodes of bacteremia were cleared within 24 hr after therapy was initiated. There was a uniform decrease in the rate of creatinine clearance which was slightly greater in group 2 patients; however, all creatinine clearance values were within the normal range and actually improved during therapy. There was no difference between the clearance values of the tobramycin-treated patients and gentamicin-treated patients. A few transient abnormalities in results of liver function tests occurred during the study. In one patient whose serum was positive for hepatitis-associated antigen, the alkaline phosphatase, aspartate aminotransferase, and bilirubin values were elevated on admisssion of the patient to the hospital, increased fivefold during therapy, and decreased to the base-line admission values six days after therapy; however, it is difficult to establish that this reaction was antibiotic-induced hepatic toxicity.
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PMID:Efficacy and safety of cefamandole plus either gentamicin or tobramycin in therapy of severe gram-negative bacterial infections. 34 93

Ceforanide, a new cephalosporin antibiotic with a long half-life (3 h), can be administered twice daily. We evaluated its antimicrobial activity, pharmacology, and clinical efficacy. Twenty-seven patients with infections due to susceptible organisms received ceforanide, 0.5, 1, or 2 g, intramuscularly or intravenously every 12 h for 6 to 28 days. In vitro studies with the clinical isolates from 27 patients treated plus 263 additional isolates showed that ceforanide was active against cephalothin-susceptible gram-positive and gram-negative microorganisms. In addition, ceforanide inhibited 65% of cephalothin-resistant Escherichia coli and 65% of Enterobacter spp. at </=12.5 mug/ml. After a single 1-g intramuscular dose, the mean peak plasma concentration at 1 h was 48.9 mug/ml and that at 12 h was 4.7 mug/ml. Plasma accumulation occurred in some patients. The infections included 10 pneumonias, 3 with bacteremia and 1 with empyema; 11 soft tissue infections, 4 with abscesses and 3 with sepsis; and 3 urinary tract infections. One case each of endocarditis, osteomyelitis, and septic thrombophlebitis, all due to Staphylococcus aureus, were treated. Clinical response was satisfactory in all patients; bacteriological response was satisfactory in 26 of 27 patients. Ceforanide was well tolerated. Three patients developed mild increases in liver enzymes, and one developed slight eosinophilia. In another case, the antibiotic was discontinued because of a fivefold rise in serum glutamic-oxalacetic transaminase (aspartate aminotransferase) and serum glutamic-pyruvic transaminase (alanine aminotransferase) and a twofold rise in lactic acid dehydrogenase and alkaline phosphatase.
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PMID:Ceforanide: in vitro and clinical evaluation. 50 95

This study was designed to ascertain if certain characteristics of febrile patients could help to identify infectious or bacteremic conditions. Patients with axillary temperature higher than 37,4 degrees C visiting the emergency room and requiring hospitalization were included in the study. The sample included 345 patients. Infections made up 89% of the causes of fever. The most frequent site of infection was the respiratory system (39%). 13% of hemocultures were positive. Gram negative germs were the most frequent agents. Infectious FS was related with the presence of predisposing factors, duration of fever, erythrocyte sedimentation rate and hemoglobin. Bacteremia was associated to treatment prior hospitalization, average temperature, hemoglobin, AST and urinary sediment. We may conclude that infections are the most frequent cause of FS. We could not found any clinical or analytical parameters that, used together, could help us to identify infectious or bacteremic FS.
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PMID:[Febrile syndrome in hospitalized patients]. 139 57

One hundred consecutive patients with blood cultures positive for microbial growth were prospectively surveyed for the presence of hepatic abnormalities and clinical evidence of infection. Complete data for 82 patients were available for analysis. Fifty-four percent had elevated bilirubin levels, and 34% had total bilirubin values of greater than or equal to 2.0 mg/dl. The levels of total bilirubin were disproportionately elevated compared with those of aspartate aminotransferase, alkaline phosphatase, and cholesterol. Nine of the 23 patients with elevated bilirubin levels had an increase in serum bilirubin one to nine days before their initial positive blood culture. Disproportionate elevations of direct and total serum bilirubin values compared with values for other liver-function tests appear to be associated with bacteremia in adults more frequently than previously recognized and may have some predictive value in such patients.
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PMID:Frequency and characteristics of hyperbilirubinemia associated with bacteremia. 398 23

Mammary glands of 6 lactating Holstein cows were inoculated with Haemophilus somnus strain 43826. Three cows developed chronic mastitis and shed bacteria for up to 1 year. Three cows developed acute gangrenous mastitis, with evidence of bacteremia and endotoxemia. Cows with gangrenous mastitis had lower somatic cell counts early after inoculation in affected quarter secretions compared with those in cows that developed chronic mastitis. Cows with gangrenous mastitis developed hypocalcemia, hypoalbuminemia, azotemia, hyperbilirubinemia, mildly increased serum aspartate aminotransferase and creatine kinase activity, and a marked neutropenia with a degenerative left shift. Histopathologic examination of gangrenous quarters revealed edema, necrosis, and vascular thrombosis with few inflammatory cells. A limited survey failed to recover H somnus from dairy cows with clinical mastitis or from mammary secretions from 41 beef cattle at an abattoir.
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PMID:Haemophilus somnus: investigations of its potential role in bovine mastitis. 407 31

Hepatic cytokine gene expression is independently stimulated by circulating microbial products and reductions in the cellular O2 supply. Although these stimuli occur sequentially after gram-negative bacteremia, it is unknown whether their interplay augments production of interleukin (IL)-1 by the liver. We studied the effects of intraportal Escherichia coli (EC) bacteremia and secondary constant-flow hypoxia (Po2, approximately 46 Torr for 30 min) on IL-1 alpha and IL-1 beta gene expression in ex situ buffer-perfused rat livers over 180 min (n = 67). At t = 0, normoxic EC and normal saline (NS) controls received 10(9) live EC serotype 055:B5 and 0.9% NaCl, respectively; in livers subjected to EC+hypoxia-reoxygenation (H/R) and NS+H/R, hypoxia began 0.5 h after EC or NS and was followed by 120 min of reoxygenation. Portal and hepatic venous perfusates were serially analyzed for bacterial colony-forming units, O2 uptake, and aspartate aminotransferase. At 60 min (peak hypoxia) and 180 min, cDNAs for IL-1 alpha and IL-1 beta were hybridized to whole liver RNA, and IL-1 beta protein levels in venous perfusates were assessed. Intrahepatic levels of reduced glutathione (GSH) were measured as an index of oxidative stress. Compared with normoxic EC, IL-1 alpha transcripts decreased at 180 min in EC+H/R livers (P < 0.0001) as did IL-1 beta mRNA (P < 0.05), despite similar EC clearance, GSH levels, posthypoxic O2 uptake, and aspartate aminotransferase release. Hepatic secretion of IL-1 beta likewise fell in EC+H/R vs. EC controls (P < 0.005). Prostaglandin H synthase-2 (COX-2) message accumulation was not enhanced by H/R, and indomethacin did not reverse H/R-mediated suppression of IL-1 production. In contrast, H/R-related falls in EC-induced IL-1S expression were reversed by allopurinol or catalase. Thus brief hypoxic stress of the liver causing neither GSH depletion nor functional impairment downregulates postbacteremic IL-1 expression by a mechanism involving O2 radicals but not cyclooxygenase metabolites.
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PMID:Brief hypoxic stress downregulates E. coli-induced IL-1 alpha and IL-1 beta gene expression in perfused liver. 894 69

Up-regulation of the leukocyte beta 2 integrin, CD18, is a key event in neutrophil-endothelial adhesion and neutrophil-mediated organ injury. Inhibition of CD18 with monoclonal antibodies reduces lung and liver neutrophil sequestration in animal models of Gram-negative bacteremia or endotoxemia. However, with a persistent septic challenge, interference with host leukocyte phagocytic defense could adversely affect outcome. To assess the effects of inhibiting CD18 on organ neutrophil responses, bacteremia, and organ injury after fecal peritonitis, mice underwent cecal ligation and puncture (CLP). At the time of CLP and 12 h later, mice received intravenous anti-CD18 antibody or control IgG. At 3, 6, and 18 h after CLP, lung and liver tissue neutrophil content were measured by myeloperoxidase (MPO) assay, peritoneal cells and blood leukocytes were differentially counted, blood was cultured, and serum aspartate aminotransferase was measured. There was a significant reduction in peritoneal neutrophil migration and an increase in blood neutrophils after anti-CD18 treatment compared with results from treatment with the control antibody. In the anti-CD18-treated group, liver MPO was increased fivefold at 6 and 18 h, while lung MPO was increased two-fold at 18 h when compared with the control antibody-treated group. The anti-CD18-treated group also had an increase in bacteria cultured from the blood at 6 and 18 h and an increase in serum aminotransferase at 18 h. Our data demonstrate that peritoneal neutrophil migration in response to an endogenous fecal challenge is CD18-dependent, and that this mechanism forms a vital part of host defense. Inhibition of CD18 increased neutrophil sequestration in the liver and lung and increased liver injury. This study demonstrates a paradoxical increase in organ neutrophil sequestration using a leukocyte anti-adhesion therapy during sepsis and suggests that anti-adhesion therapies targeted towards neutrophil may worsen outcome if given during an ongoing, localized infection.
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PMID:Inhibition of neutrophil migration at the site of infection increases remote organ neutrophil sequestration and injury. 937 66

Previous studies show that isogenic mutants deficient in streptococcal pyrogenic exotoxin B (SPE B) cause less mortality and skin tissue damage than wild-type strains of Streptococcus pyogenes when inoculated into mice via an air pouch. In this study, the growth and dissemination of bacteria, pathologic changes in various organs, and their correlation with SPE B production were examined. Bacterial numbers in the air pouch from wild-type strain NZ131-infected mice increased at 48 h, while those from speB mutant SW510-infected mice continuously reduced. Mice infected with NZ131 developed bacteremia and greater dissemination in the kidney, liver, and spleen; those infected with SW510 showed either no or slight bacteremia and dissemination. Co-inoculation of SW510 with recombinant SPE B showed a higher bacterial count in the air pouch, bacteremia, and organ dissemination compared to co-inoculation with a C192S mutant lacking protease activity. The histopathologic changes examined showed lesions in kidney and liver in the NZ131-infected but not in SW510-infected mice. The elevation in sera of BUN, AST, and ALT correlated positively with renal and liver impairment. Taken together, SPE B produced during S. pyogenes infection plays a pathogenic role. A direct effect of SPE B on vessel permeability change was also demonstrated.
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PMID:Histopathologic changes in kidney and liver correlate with streptococcal pyrogenic exotoxin B production in the mouse model of group A streptococcal infection. 1504 62

Intragastric inoculation of Klebsiella pneumoniae can cause invasive diseases, including necrosis of liver tissues and bacteremia. The effect of concanavalin A (ConA) on K. pneumoniae was tested. Pretreatment with ConA was able to protect mice from K. pneumoniae infection in an intragastric model. K. pneumoniae-induced mouse death and liver injury such as liver necrosis, as well as blood levels of aspartate aminotransferase and alanine aminotransferase, were inhibited in a dose-dependent manner by ConA. ConA administered intravenously as late as 24 h after K. pneumoniae inoculation was still protective. In an in vitro assay, ConA was able to bind K. pneumoniae cells directly and further agglutinate them but had no effect on their in vitro growth. Surveys of bacterial counts of ConA-treated mice revealed that the bacteria were eliminated effectively in both blood and liver tissues. Furthermore, the bactericidal activity of macrophages against K. pneumoniae was also enhanced in a dose-dependent manner by ConA in an in vitro culture. These data suggest that ConA is a potentially therapeutic agent for K. pneumoniae-induced liver infection.
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PMID:Concanavalin A protects mice from a lethal inoculation of intragastric Klebsiella pneumoniae and reduces the induced liver damage. 1760 78

Bacterial infections are a serious complication of end-stage liver disease (ESLD) that occurs in 20% to 60% of patients. We retrospectively reviewed medical records of patients with ESLD who were identified by our microbiology laboratory as having Streptococcus salivarius bacteremia. Of 592 patients listed for transplantation between January 1998 and January 2006, 9 (1.5%) had 10 episodes of S salivarius bacteremia. Of 2 patients already receiving quinolone prophylaxis for spontaneous bacterial peritonitis (SBP), 1 later presented with a second episode. The male-to-female ratio was 1:1.2. Medians for age, Model for End-Stage Liver Disease score, and Child-Turcotte-Pugh score were 50 years, 17, and 10, respectively. Presenting symptoms and signs in 10 episodes of infection were ascites (in 8 episodes), elevated temperature (6), abdominal pain (5), and encephalopathy (4). Median laboratory values included: white blood cell count, 15.1 x 10(9)/L; creatinine, 0.9 mg/dL; albumin, 3.1 gm/dL; aspartate aminotransferase, 64 U/L; alanine aminotransferase, 52.5 U/L; ammonia, 67 mug/dL; and prothrombin time, 17.3 seconds. Ascitic fluid in patients with peritonitis showed a median white blood cell count of 466 cells/mm(3) (range, 250-12,822 cells/mm(3)), with 66% polymorphs, protein of 0.9 gm/dL, and albumin of 0.4 gm/dL. S salivarius may cause primary bacteremia and SBP in liver transplantation candidates despite quinolone prophylaxis.
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PMID:Streptococcus salivarius bacteremia and spontaneous bacterial peritonitis in liver transplantation candidates. 1843 54


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