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

Autosomal dominant polycystic kidney disease (ADPKD) is the commonest hereditary nephropathy. We collected 92 cases in VGH. Diagnosis was confirmed by intravenous pyelogram, renal sonogram, or renal CAT scan. The incidence of having positive family history was just only 28.3%. Patients were diagnosed at the mean age of 54 +/- 11 years (26-74 years). The common clinical findings were hypertension (73.9%), abdominal mass, proteinuria, anemia, azotemia, abdominal or back pain and pyuria in orders. Hypertension might present in the early stage with normal renal function (near 40%). Polycystic liver was the major extrarenal lesion (57.6%), but the incidence of abnormal liver function was only 10.1%. Enlarged kidneys were not always palpable, even at end stage of renal function (mean age 56 +/- 9 years, 89.4% kidney palpable). Patient's urine amount was usually nonoliguric, even in uremic stage (82.9%). Sepsis was the first cause of death. Cardiovascular disease and uremia were followed in sequence. Their expired mean age was 61 +/- 7 years (53-74 years).
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PMID:[Autosomal dominant polycystic kidney disease clinical analysis in VGH--Taipei]. 217 45

The myeloperoxidase-hydrogen peroxide-chloride (MPO-H2O2-Cl) system is an antimicrobial system of polymorphonuclear leukocytes. We demonstrated that the MPO-H2O2-Cl system is fungicidal for Trichophyton rubrum. Fungal growth of a synchronous cell culture of T. rubrum germlings was assayed by measuring the uptake of tritiated N-acetyl-D-glucosamine, and the viability of the fungi was assayed by counting colony-forming units. Cytotoxins produced by the interaction of myeloperoxidase with hydrogen peroxide and chloride ion were fungicidal for T. rubrum. Growth inhibition was abolished in the presence of catalase or L-methionine. Polymorphonuclear leukocytes through the MPO-H2O2-Cl system may prevent invasion and sepsis by dermatophytes even in the absence of specific immunity.
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PMID:Inhibition of growth of Trichophyton rubrum by the myeloperoxidase-hydrogen peroxide-chloride system. 253 15

Coculture of endothelial and smooth muscle cells was used to study effects of endotoxin on depolarization-induced Ca2+ transients in fura-2-loaded individual smooth muscle cells. Although endotoxin did not modify the response of cultured smooth muscle cells to depolarization, endotoxin resulted in an attenuation of cytosolic Ca2+ (Cai2+) transients in response to K+ depolarization and failure of KCl-induced contractions in smooth muscle cells when they were cocultured with endothelial cells. The observed endothelial modulation of smooth muscle responses was not accomplished via gap junctions. The possible role of free radical species secreted by endothelial cells in conditioning of smooth muscle responses to depolarization was supported by the results of three sets of experiments: 1) endothelial cells did respond to endotoxin with oxidative burst, 2) pretreatment of cocultured cells with catalase prevented endotoxin-induced downregulation of Ca2+ transients, and 3) in isolated smooth muscle cells, the addition of hydrogen peroxide virtually abolished depolarization-induced Ca2+ transients. Hence vascular endothelium stimulated by endotoxin generates reduced oxygen intermediates, which in turn downregulate depolarization-induced Cai2+ transients in smooth muscle cells. This phenomenon may contribute to the development of hypotension in septicemia.
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PMID:Role of endothelium in endotoxin blockade of voltage-sensitive Ca2+ channels in smooth muscle cells. 255 35

To determine the susceptibility to sepsis in newborn infants deficient in glucose-6-phosphate dehydrogenase (G6PD), we screened 33,943 Saudi Arab infants. Deficiency of G6PD was found in 18%. Sepsis was determined by the presence of clinical signs of sepsis and confirmed by positive blood cultures. Sepsis was documented in 75 infants (2.2/1000). The incidence of sepsis was significantly higher in 6138 G6PD-deficient infants (3.4/1000) than in the 27,805 with normal G6PD activity (1.9/1000; p less than 0.02). The incidence of catalase-positive organism sepsis was higher in G6PD-deficient infants (2.9/1000) compared with those with normal G6PD activity (1/1000; p less than 0.0002), whereas the incidence of catalase-negative organism sepsis did not differ (p less than 0.2). Deficiency of G6PD was more common in infants with late sepsis (46%) than in those with early sepsis (21%) and in all infants screened (18%) (p less than 0.03 and p less than 0.001, respectively). We conclude that neonates with G6PD deficiency are more susceptible to late sepsis and to infection with catalase-positive organisms. The exact mechanism for the increased susceptibility is not clear, but a partial explanation could be lack of leukocyte bactericidal activity associated with G6PD deficiency, and an increased susceptibility to infection caused by hyperferremia resulting from lysis of G6PD-deficient erythrocytes.
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PMID:Incidence and causes of sepsis in glucose-6-phosphate dehydrogenase-deficient newborn infants. 271 88

This study examines the effects of complement activation and of complement-induced oxygen radical production on the principal determinant of hepatic function, i.e., effective hepatic blood flow (EHBF). Female Sprague-Dawley rats received cobra venom factor, 40 units/kg, in two divided doses at 30-minute intervals. At t = 2 hours, thermodilution cardiac output, mean arterial pressure, heart rate, hematocrit, and EHBF by galactose clearance were determined. Complement activation produced a significant depression in EHBF independent of changes in systemic perfusion. To determine whether oxygen radicals participated in the insult, additional animals were pretreated with superoxide dismutase, 6 mg/kg, plus catalase, 15 mg/kg, immediately before complement activation. Concomitant treatment with the oxygen radical scavengers attenuated the degree of complement-induced hepatic ischemia, again independent of effects on systemic perfusion. This study suggests that the reduction in hepatic blood flow that accompanies animal models of trauma and sepsis may result, in part, from the sequelae of complement activation with oxygen radicals as secondary mediators.
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PMID:Contribution of toxic oxygen intermediates to complement-induced reductions in effective hepatic blood flow. 284 55

CDC group DF-2 is the vernacular name given to a slow-growing gram-negative bacterium that causes septicemia and meningitis in humans. Infections frequently (one-third of cases) occur following dog bites or close contact with dogs or occasionally with cats. Splenectomy and alcoholism appear to be strong predisposing factors for DF-2 infection. In addition to 150 DF-2 strains received for identification, we received 9 DF-2-like strains; 6 were isolated from wound or eye infections, 3 of which were associated with dog bites and 1 of which was associated with a cat scratch, and 3 were isolated from dog mouths. The major characteristics of DF-2 include production of acid but no gas from lactose and maltose and usually D-glucose; positive reactions for oxidase, catalase, arginine dihydrolase, gliding motility, and o-nitrophenyl-beta-D-galactopyranoside; growth enhanced by serum and by incubation in a candle jar atmosphere; and negative reactions for sucrose, raffinose, inulin, melibiose, nitrate reduction, indole, and growth on MacConkey agar. DF-2-like strains had the same characteristics, except that acid was formed from sucrose, raffinose, inulin, and melibiose. By the hydroxyapatite method, DNAs from 12 DF-2 strains were 88% related in 60 degrees C reactions and 84% related in 75 degrees C reactions. Related sequences contained 0.5 to 1.5% unpaired bases (divergence). Three DF-2-like strains were 73 to 80% related at 60 degrees C (with 2.0 to 2.5% divergence) and 68 to 75% related at 75 degrees C. The relatedness of DF-2 and DF-2-like strains was 19 to 31% at 60 degrees Celsius and 13 to 19% at 75 degrees Celsius. The relatedness of DF-2 and DF-2-like strains to Capnocytophaga species was 4 to 7%. The DNA relatedness date indicate that eh DF-2 and the DF-2-like strains are separate, previously undescribed species. Both groups are phenotypically and genetically distinct from Capnocytophaga species, although they do share several characteristics with Capnocytophaga species, including cellular morphology, gliding motility, cellular fatty acid composition, enhancement of growth in a candle jar atmosphere, and G+C content. The new species differ from Capnocytophaga species by their positive oxidase and catalase reactions. We chose to avoid creating a new genus and proposed the names Capnocytophaga canimorsus sp. nov. for group DF-2 and C. cynodegmi sp. nov. for the DF-2-like strains.
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PMID:Capnocytophaga canimorsus sp. nov. (formerly CDC group DF-2), a cause of septicemia following dog bite, and C. cynodegmi sp. nov., a cause of localized wound infection following dog bite. 291 17

The physiopathologic similarity between adult respiratory distress syndrome (ARDS) secondary to sepsis and endotoxin-induced pulmonary abnormalities has provided extensive descriptive information confirming bacterial endotoxin as a factor initiating the heterogeneous pulmonary changes in ARDS. The present studies have used an established in vitro model for pulmonary cell injury to examine bacterial endotoxin 1, as a direct cytotoxic agent on the two major alveolar cell types, pulmonary endothelium and epithelium; 2, as a stimulant of neutrophil-mediated pulmonary cell injury, and 3, to examine effector mechanisms of cell-mediated damage by studying the potential effectiveness of antioxidants and antiproteolytic agents in the inhibition of this process. Endotoxin direct toxicity and stimulation of neutrophil-mediated pulmonary cell injury was observed in both pulmonary cell populations in systems free of activated serum complement. Endothelial cells were observed to be more susceptible to both the direct effect of endotoxin and to neutrophil-mediated injury when compared with epithelial cell derived monolayers. The addition of an antiprotease (soybean trypsin inhibitor [STI]) was superior to antioxidants (catalase, superoxide dismutase) in reducing the neutrophil-mediated endothelial toxicity (stimulated 51CR per cent release) observed. A 92 per cent degree of protection was observed with the highest dose of STI (5 milligrams per milliliter) used. Proteases released by activated neutrophils on endotoxin stimulation appear to be the predominant toxic species responsible for endothelial injury in this system.
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PMID:Endotoxin and pulmonary cell injury. 304 36

Free radicals generated during purine catabolism or by activated granulocytes cause tissue injury by peroxidation of lipid membranes. In a canine model of sepsis initiated by intravenous live Escherichia coli, fluorescent products of lipid peroxidation (FP) were measured in serum. Four groups of five dogs infused with 10(9)E. coli/kg were analyzed--I: no further treatment; II: prior depletion of granulocytes with a cytotoxic antibody; III: pre-treatment with superoxide dismutase and catalase; and IV: resuscitation after bacterial infusion to maintain cardiac output greater than 80% of pre-bacteremic levels. In Groups I, II, and III, cardiac output fell to less than 50% of baseline within 1 hr and remained there throughout the study. FP in Groups I and II rose to greater than 200% of baseline (P less than .02 and less than .03). In Groups III and IV, FP did not rise significantly from baseline. The rise in serum FP and the prevention of this rise by-treatment with antioxidants indicate generation of oxygen radicals. Their presence had no effect on hemodynamic parameters. Granulocyte depletion did not alter appearance of FP; however, prevention of low cardiac output blocked FP formation. These data suggest that oxygen free radicals were generated by tissue ischemia, rather than by granulocytes, in this model of septic shock.
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PMID:Oxygen free radical activity during live E. coli septic shock in the dog. 304 73

Neutrophils have been implicated in the pathogenesis of acute lung injury associated with clinical and experimental sepsis. Data from in vitro systems and experimental animals have suggested that neutrophil-derived oxidants, particularly H2O2, may be primarily responsible for endothelial damage, vasoconstriction, and lung edema. With the use of endotoxin infusion as an in vivo model of sepsis we tested the hypothesis that pretreatment with catalase, a peroxide scavenger, would ameliorate the resultant changes in pulmonary vasoconstriction and lung fluid balance. Paired experiments were performed in 16 goats with chronic lung lymph fistulas. One group of animals (n = 7) received endotoxin first alone and then again, several days later, after pretreatment with Ficoll-linked catalase. As a control, identical experiments were performed in a separate group (n = 6) with Ficoll-linked albumin substituted for Ficoll-catalase. A third group (n = 3) was given endotoxin alone and then again during a continuous infusion of catalase. Plasma and lymph levels of catalase were comparable to or exceeded those previously shown to be completely protective in isolated perfused lung preparations and in vitro systems. Endotoxin caused neutropenia, pulmonary arterial hypertension, decreased cardiac output, and increases in lymph flow to approximately three times base line, with a return of all variables toward control values by 6 h. Catalase pretreatment produced no significant differences in any of these variables. These experiments do not support a role for H2O2 as a mediator of acute lung injury due to endotoxemia.
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PMID:Effect of intravenous catalase on the pulmonary vascular response to endotoxemia in goats. 328 99

Over a 50-month period, 2,657 primary laparotomies were performed; 192 patients underwent urgent relaparotomy for complications of primary laparotomy. Forty-seven relaparotomies were performed for Type I intra-abdominal sepsis (IAS-1) with a 12.8 per cent mortality, and 46 for Type 2 IAS with a 82.6 per cent mortality (P less than 0.001). Of the 46 IAS-2 patients, 31 relaparotomies were "directed" by positive peritoneal signs (CAT/ultrasound/PIPIDA examinations) with 94 per cent (29/31) yielding positive findings. Fifteen were "non-directed" in an effort to uncover an occult source of continuing sepsis of MOSF and yielded a 13 per cent (2/15) positive rate (P less than 0.001), and a 93 per cent (14/15) mortality. Relaparotomy for sepsis directed by positive radiologic or clinical findings can be reliably expected to demonstrate a surgical focus whose correction may yield patient survival; non-directed relaparotomy, however, seldom demonstrates a focus and does not contribute to survival.
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PMID:Non-directed relaparotomy for intra-abdominal sepsis. A futile procedure. 371 73


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