UMLS:C0036690 - FACTA Search

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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neonatal group B streptococcal (GBS) sepsis and pneumonia cause lung endothelial cell injury. GBS invasion of the lung endothelium may be a mechanism for injury and the release of vasoactive eicosanoids. Pulmonary artery endothelial cells (PAEC) and lung microvascular endothelial cells (LMvEC) were isolated from neonatal piglets and were characterized as endothelial on the basis of morphology, uptake of acyl low-density lipoprotein, factor VIII staining, and formation of tube-like structures on Matrigel. PAEC and LMvEC monolayers were infected with COH-1 (parent GBS strain), isogenic mutants of COH-1 devoid of capsular sialic acid or all capsular polysaccharide, or a noninvasive Escherichia coli strain, DH5 alpha. Intracellular GBS were assayed by plate counting of colony-forming units resistant to incubation with extracellular antibiotics. All GBS strains invaded LMvEC significantly more than PAEC, showing that the site of lung endothelial cell origin influences invasion. DH5 alpha was not invasive in either cell type. Both isogenic mutants invaded PAEC and LMvEC more than COH-1 did, showing that GBS capsular polysaccharide attenuates invasion. Live GBS caused both LMvEC and PAEC injury as assessed by lactate dehydrogenase release; heat-killed GBS and DH5 alpha caused no significant injury. Supernatants from PAEC and LMvEC were assayed by radioimmunoassay for prostaglandin E2 (PGE2), the stable metabolite of prostacyclin (6-keto-PGF1 alpha), and the thromboxane metabolite thromoxane B2. At 4 h, live COH-1 caused no significant increases in eicosanoids from both PAEC and LMvEC. At 16 h, live COH-1, but not heat-killed COH-1, caused a significant increase in 6-keto-PGF1 alpha greater than PGE2 from LMvEC, but not PAEC. We conclude that live GBS injure and invade the lung microvascular endothelium and induce release of prostacyclin and PGE2. We postulate that GBS invasion and injury of the lung microvasculature contribute to the pathogenesis of GBS disease.
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PMID:Group B streptococci (GBS) injure lung endothelium in vitro: GBS invasion and GBS-induced eicosanoid production is greater with microvascular than with pulmonary artery cells. 780 66

Adult respiratory distress syndrome (ARDS) can develop as a complication of various disorders, including sepsis, but it has not been possible to identify which of the patients at risk will develop this serious disorder. We have investigated the ability of six markers, measured sequentially in blood, to predict development of ARDS in 26 patients with sepsis. At the initial diagnosis of sepsis (6-24 h before the development of ARDS), serum manganese superoxide dismutase concentration and catalase activity were higher in the 6 patients who subsequently developed ARDS than in 20 patients who did not develop ARDS. These changes in antioxidant enzymes predicted the development of ARDS in septic patients with the same sensitivity, specificity, and efficiency as simultaneous assessments of serum lactate dehydrogenase activity and factor VIII concentration. By contrast, serum glutathione peroxidase activity and alpha 1Pi-elastase complex concentration did not differ at the initial diagnosis of sepsis between patients who did and did not subsequently develop ARDS, and were not as effective in predicting the development of ARDS. Measurement of manganese superoxide dismutase and catalase, in addition to the other markers, should facilitate identification of patients at highest risk of ARDS and allow prospective treatment.
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PMID:Serum antioxidants as predictors of adult respiratory distress syndrome in patients with sepsis. 809 98

We investigated whether the multiple pathophysiological signals generated in a peritonitis septic model alter the mRNA levels of glycolytic and gluconeogenic enzymes, and whether these alterations are associated with glucose dyshomeostasis. Rats were sham-operated in the control group, and peritonitis sepsis was produced by a 1 cm cecal incision in the septic group. At 2, 4, and 6 hr post-surgery, total cellular RNAs were isolated from livers, and Northern blots performed to measure mRNA levels of aldolase B (ADL), lactate dehydrogenase (LDH), pyruvate kinase (PK), phosphoenolpyruvate carboxykinase (PEPCK), and glucokinase (GK). Hepatic PEPCK enzymatic activity was measured by condensing 14CO2 with phosphoenolpyruvate (PEP) to form malate. Serum glucose concentrations were also measured. We found the following: At 2 hr of peritonitis sepsis, serum glucose concentrations, mRNA levels of all enzymes, and PEPCK enzymatic activity increased over control levels. At 4 hr of peritonitis sepsis, serum glucose concentrations and mRNA levels of GK and PK continued to increase; mRNA levels of all other enzymes, as well as PEPCK enzymatic activity decreased to or below control levels. At 6 hr of peritonitis sepsis, serum glucose concentrations, mRNA levels of all enzymes, and PEPCK enzymatic activity decreased to or below control levels. We concluded that sepsis affects mRNA levels of glycolytic and gluconeogenic enzymes at the transcriptional level, and that these alterations are associated with glucose dyshomeostasis.
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PMID:Altered levels of mRNA encoding enzymes of hepatic glucose metabolism in septic rats. 840 44

Group B streptococci (GBS) are the most common cause of neonatal sepsis and pneumonia. The pathogenesis of GBS disease is not completely defined. GBS-induced endothelial cell injury is suggested by histological findings at autopsy and in animal studies. We hypothesized that (i) type III GBS (COH-1) invade and injure human umbilical vein endothelial (HUVE) cells and (ii) isogenic mutations in GBS capsule synthesis would influence HUVE invasion. Confluent HUVE monolayers were infected for 0.5, 2, or 6 h. Media with penicillin plus gentamicin were added and incubated for 2 h to kill extracellular bacteria. Cells were washed and lysed, and the number of live intracellular bacteria was determined by plate counting. COH-1 invaded HUVE cells in a time-dependent manner at levels 1,000-fold higher than those of the noninvasive Escherichia coli strain but significantly lower than those of Staphylococcus aureus. There was no evidence for net intracellular replication of GBS within HUVE cells. COH-1 infection of HUVE cells caused the release of lactate dehydrogenase activity. GBS invasion was inhibited by cytochalasin D in a dose-dependent manner; GBS-induced lactate dehydrogenase release was attenuated by cytochalasin D. The isogenic strains COH 1-11, devoid of capsular sialic acid, and COH 1-13, devoid of all type III capsule, invaded HUVE cells three- to fivefold more than the parent COH-1 strain. The type III capsular polysaccharide and particularly the capsular sialic acid attenuate GBS invasion of HUVE cells. Electron micrographs of lung tissue from a GBS-infected newborn Macaca nemestrina also showed GBS within capillary endothelial cells. We conclude that endothelial cell invasion and injury are potential mechanisms in the pathogenesis of GBS disease.
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PMID:Group B streptococci invade endothelial cells: type III capsular polysaccharide attenuates invasion. 842 76

The Nippon-Zeon (NZ) ventricular assist device is a sac type, air driven, heterotopic, external pump. Its performance has been evaluated in Japan as a bridge to myocardial recovery. Few data are available on the device as a bridge to heart transplantation. Since 1991, 10 patients (9 men) were bridged to heart transplantation with NZ, all in biventricular support. The mean age was 39 +/- 13 years (range, 21-60 years), mean body weight was 75 +/- 13 kg (range, 51-95 kg). Five patients had a dilated cardiopathy, and five were ischemic (three acute myocardial infarctions). Despite maximal inotropic support, including enoximone in seven, epinephrine in three, and intraaortic balloon pumping in one, eight patients were anuric, three were in acute hepatic failure, and three were intubated. Preoperative hemodynamic and biologic values were: cardiac index, 1.57 +/- 0.4 l/min/m2; pulmonary capillary wedge pressure, 34 +/- 5 mmHg; creatinine, 200 +/- 80 mumol/l; blood urea nitrogen, 17.5 +/- 8 mmol/l; total bilirubin 36 +/- 6 mumol/l; aspartate aminotransferase, 1,000 +/- 2,000 IU/l. In all patients, a biventricular assist device was implanted without the use of cardiopulmonary bypass. Improvement occurred immediately in all but one. Mean left ventricular flow was 4.5 +/- 0.8 l/min. Anticoagulation was maintained with intravenous heparin. Recently for bleeding was required in one case (10%), and two patients had positive blood cultures that were successfully treated. There was no mechanical failure. Hemolysis was not significant (lactate dehydrogenase, 378 +/- 50 IU/l; plasma-free hemoglobin below 10 mg/dl). Each device was free of thrombi and deposits at time of explantation. One patient died while on assist. Nine patients (90%) were transplanted after 11 +/- 8 days (range, 1-32 days). Three died early after transplantation, one of graft failure, two of sepsis. Six patients (66%) could be discharged. The follow-up ranges from 7 to 28 months. NZ is a simple, reliable, pneumatic device driven by a light, silent console; it can be rapidly implanted without cardiopulmonary bypass in patients in desperate condition who are awaiting cardiac transplantation. The difficulty of patient rehabilitation while using this device should limit the duration of support to weeks to allow the patient to be in optimal condition for heart transplantation.
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PMID:Use of the Nippon-Zeon pneumatic ventricular assist device as a bridge to cardiac transplantation. 855 33

Cytokines are thought to play an important role in the hepatocellular dysfunction that occurs during sepsis. Some cytokines have been shown to increase lipogenesis and to induce toxicity in isolated hepatocytes. Oxygen free radicals have been implicated as mediators of some cytokine effects. In this study we investigate a possible protection action of S-adenosyl-L-methionine against the toxic effects of cytokines on isolated hepatocytes. Isolated rat hepatocytes were precultured for 24 hr and then cultured for 1, 2, 3, 6, 12, or 24 hr in the presence or absence of S-adenosyl-L-methionine (12 micromol/l0) and/or either tumor necrosis factor (100, 200, or 500 ng/ml) or interleukin-1 (30, 60, or 120 IU/ml). Lactate dehydrogenase (media), and malondialdehyde, reduced glutathione, and the incorporation of D-[U- 14 C] glucose into different lipid fractions (cells) were determined. Both cytokines significantly increased hepatocyte malondialdehyde content, lactate dehydrogenase release, and triacylglycerol synthesis. None of these effects were observed in the presence of S-adenosyl--L-methionine. In addition, S-adenosyl-L-methionine was able to attenuate the decrease in phosphatidylcholine labeling also induced by both cytokines, and to prevent the increase in free fatty acid synthesis induced by tumor necrosis factor. Incubation in the presence of S-adenosyl-L-methionine also increased hepatocyte glutathione content (7.1 +/- 0.7, after 24 hr, vs 3.6 +/- 0.3 nmole/mg protein, P < 0.01), and prevented the decrease in glutathione induced by tumor necrosis factor (5.4 +/- 0.2 vs 2.1 +/- 0.1 nmole/mg protein, 100 ng/ml TNF alpha at 24 hr, P < 0.01). Our results show that S-adenosyl-L-methionine has a protective effect on hepatocytes against the in vitro effect of cytokines.
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PMID:S-adenosylmethionine protects hepatocytes against the effects of cytokines. 860 15

Prior attempts to create an animal model of empyema by direct inoculation of bacteria alone into the pleural space have been unsuccessful. The animals either died of overwhelming sepsis or cleared the infection from the pleural space without development of an empyema. We hypothesized that injection of bacteria with a nutrient agar into the pleural space would allow the bacteria to remain in the pleural space for an extended time period, permitting an empyema to develop. The bacterium Pasteurella multocida in brain heart infusion (BHI) agar was injected into the right hemithorax of 12 New Zealand white male rabbits. Our preliminary studies showed that the animals died in less than 7 days if they were not given parenteral antibiotics. For this reason, the rabbits were given penicillin, 200,000 U, IM, every 24 h starting 24 h after bacterial injection. Pleural fluid was sampled by thoracentesis at 12, 24, 48, 72, and 96 h after bacterial injection. Pleural fluid pH, glucose, lactate dehydrogenase (LDH), leukocyte count, and Gram's stain and culture (in one half of the animals) were obtained at each time point. Pleural biopsy specimens were obtained at autopsy after 96 h. The mean pleural fluid pH reached a nadir of 7.01 at 24 h and remained less than 7.1 throughout the experiment. The mean pleural fluid glucose level reached a nadir of 10 mg/dL at 24 h. The mean pleural fluid LDH peaked at 21,000 IU/L at 24 h and the mean pleural fluid leukocyte count peaked at 12 h with a value of 67,000 cells per cubic millimeter. Gram's stains revealed organisms and cultures were positive for growth in all animals at 12 and 24 h. Some animals had positive Gram's stains and growth on cultures up to 72 h after bacterial injection. At autopsy, all rabbits injected with bacteria had gross pus in the right pleural space and had developed a thick pleural peel. Microscopic specimens of the pleura revealed large numbers of leukocytes (primarily polymorphonuclear lymphocytes) with invasion of the adjacent lung and chest wall. In conclusion, this model more closely mimics the empyema that occurs in humans, relative to previous animal models. This model appears appropriate for additional randomized studies in which different methods for the treatment of empyema can be evaluated.
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PMID:Serial pleural fluid analysis in a new experimental model of empyema. 863 29

We report the cases of six patients with AIDS in whom reactive hemophagocytic syndrome (RHPS) secondary to disseminated histoplasmosis was diagnosed. RHPS was diagnosed by established criteria, including fever (duration of > or = 7 days, with peak temperatures of > 38.5 degrees C), unexplained thrombocytopenia with anemia and/or neutropenia, and bone marrow biopsy findings of hemophagocytic histiocytosis. Disseminated Histoplasma capsulatum infection was diagnosed on the basis of the results of cultures of the bone marrow sample. The serum lactate dehydrogenase (LDH) level was elevated (> 1,000 IU/L) in all patients, and five of six patients had hyperferritinemia (range of ferritin level, 15,848-425,984 ng/mL). Five patients had features resembling severe sepsis with multiorgan dysfunction. Three patients recovered, and the findings of RHPS resolved following therapy with amphotericin B. In patients with AIDS, the combination of fever, cytopenia, elevated serum LDH level (> 1,000 IU/L), and/or hyperferritinemia (ferritin level of > 10,000 ng/mL) is a clue to the diagnosis of RHPS and disseminated histoplasmosis; bone marrow biopsy is valuable in establishing the diagnosis.
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PMID:Reactive hemophagocytic syndrome: a new presentation of disseminated histoplasmosis in patients with AIDS. 874 33

From 1984 through 1992, staff at The Marine Mammal Center (TMMC, Sausalito, California, USA) examined 207 northern elephant seals (Mirounga angustirostris) with a condition of unknown etiology called northern elephant seal skin disease (NESSD). The skin lesions were characterized by patchy to extensive alopecia and hyperpigmentation, punctate or coalescing epidermal ulceration, and occasionally, massive skin necrosis. Microscopic lesions included ulcerative dermatitis with hyperkeratosis, squamous metaplasia and atrophy of sebaceous glands. All diseased seals were less than 2 years of age and suffered from emaciation, depression, and dehydration. Mortality from septicemia increased significantly with severity of skin ulceration. Compared to 14 apparently unaffected seals, diseased seals had depressed levels of circulating thyroxine, triiodothyronine, retinol, serum iron, albumin, calcium, and cholesterol. Levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, gamma glutamyl transpeptidase, blood urea nitrogen, and uric acid were elevated. Morphometrically, diseased animals were approximately 15% smaller than normal seals of the same sage. Serum and blubber concentrations of 36 polychlorinated biphenyl congeners (sigma PCB) and dichloro-diphenyl-dichloroethylene (p,p'-DDE) were negatively correlated with body mass. Mean concentrations of sigma PCB and p,p'-DDE in serum in diseased seals were elevated as compared to apparently normal seals. Etiology of this syndrome remains unknown, but the possibility of PCB toxicosis cannot be ruled out.
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PMID:Clinical and pathological characterization of northern elephant seal skin disease. 924 88

Nitric oxide (NO) is a multifunctional messenger in many vertebrates. In the liver, NO was found to play an important but controversial role in injury produced by toxins or sepsis. The purpose of the present investigation was to further characterize the role of NO in hepatocyte oxidative injury. A cellular system formed of immobilized and perfused rat hepatocytes was used to test the ability of the latter to produce endogenous NO after lipopolysaccharide administration in vivo (LPS, 20 mg/kg i.p.) and how hepatocyte functionality competence is modified according to NO level. This cellular system also was used to delineate a relationship between exogenously delivered NO to the perfusion medium as produced by the NO donor, sodium nitroprusside (2.0 and 0.2 mM), and any alteration in the degree of injury as evoked by anoxia/reoxygenation or cumene hydroperoxide (1.0 mM and 0.2 mM). Rat hepatocytes were immobilized in low-gelling agarose and perfused with Williams E medium. Endogenous or exogenous NO was evaluated by measuring the end products of NO (NO2- + NO3-) in the perfusion medium. Functional integrity of hepatocytes was evaluated from lactate dehydrogenase (LD) leakage, urea synthesis in the perfusion medium and lipid peroxides (LP) formation. Normal, anoxia/reoxygenation or cumene hydroperoxide injured hepatocytes did not exhibit measurable NO while LPS-treated hepatocytes produced NO. Apparently, within the present experimental conditions, it seems that there was an inverse relation between the rate of NO produced after LPS administration and the rate of lipid peroxides formed in the hepatocytes. Low concentration of sodium nitroprusside (as NO donor) significantly decreased LD leakage, increased the rate of urea synthesis and increased trypan blue exclusion by hepatocytes in anoxia/reoxygenation or cumene hydroperoxide injured (0.2 mM) cells. Lipid peroxides were decreased by NO in cumene hydroperoxide injured hepatocytes. The present data suggest that NO endogenously produced, or exogenously delivered, has an ameliorative role in mild oxidative liver injury models, but not in severe cases and that inside hepatocytes, there is a very delicate balance between the rate of NO production and its consumption. The disturbance in this balance may be responsible for injury due to the formation of more toxic oxygen species.
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PMID:Possible dual role of nitric oxide in oxidative stress injury: a study in perfused hepatocytes. 963 60

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