Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To further understand the development of fatty liver during gram-negative sepsis, we measured fatty acid uptake in addition to esterification and secretion of lipids by freshly isolated hepatocytes from fasted and fed control and Escherichia coli-treated rats. Rats were made septic by intravenous (IV) injection of 8 x 10(7) live E coli colonies per 100 g body weight. For the fasted groups, food was removed after E coli injection. Fed rats received a nutritionally adequate diet intragastrically for 5 days before and 24 hours after inducing sepsis. Twenty-four hours after E coli injection, the esterification of newly synthesized fatty acids, as measured by 3H2O incorporation, and the esterification of exogenous fatty acids, measured from 14C-palmitate incorporation, into triglyceride (TG), total cholesterol, and total phospholipid phosphorus were significantly greater in hepatocytes from fasted septic rats compared with their control rats. In fed septic rats, esterification of 14C-palmitate into TG was fourfold greater than in the fed control rats. The increased rates of esterification in hepatocytes from fasted and fed septic rats were not accompanied by an increase in the labeled TG in the medium. This inability to secrete the additional TG that the hepatocytes produce resulted in a higher concentration of cellular TG in fasted and fed septic rats than in their controls. The enzymes glycerol-3-phosphate acyltransferase (GPAT) and phosphatidate phosphohydrolase (PPH) do not appear to be factors contributing to the increased TG synthesis, since the increase in enzyme activity was not accompanied by a similar increase in TG synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulatory factors in the development of fatty infiltration of the liver during gram-negative sepsis. 820 57

Most staghorn calculi are infection stones composed of struvite and/or carbonate apatite. Sometimes, cystine, uric acid, whewellite and brushite stones also assume a staghorn configuration when located in the kidney. It is very important in stone crushing to know the composition and architecture of the stones. Struvite stones show a concentric laminal structure and are fragile because of wide interstices of crystals and rich organic matrix. These stones usually contain many bacterial colonies in the interstices of crystals and bacteria break out of the stones when they are crushed. Therefore, perioperative administration of antibiotics is necessary for prevention of bacteremia and sepsis. Whewellite stones and uric acid stones have a smooth surface and reveal compact radial and laminal structure especially in the peripheral layer. They are very hard and are refractory to crushing, and the fragments are large. Cystine stones show a compact radial monomineral texture and are very hard. The fragments made by crushing are large. Therefore, combination therapy of stone crushing and irrigation of alkali solution may be useful for treatment of cystine stones as well as uric acid stones. Calcium phosphate stones, hydroxyapatite or brushite stones, are rare and are formed in hyperparathyroidism, Cushing syndrome and renal tubular acidosis. Hydroxyapatite stones are rich in matrix and fragile. Brushite stones reveal radiate structure and are hard. There is no general method of treatment for staghorn calculi but we should select the most reasonable method including open surgery for each case taking into consideration the stone composition, predisposing factors and possibility of stone residue and recurrence.
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PMID:[Treatment of staghorn calculi on the basis of composition and structure]. 826 80

Calciphylaxis, a syndrome of disseminated calcification found in chronic renal failure patients with secondary hyperparathyroidism, results in soft tissue calcification and vascular medial calcinosis leading to subsequent ischemic tissue necrosis. It is a rarely occurring condition in which patients present with painful, violaceous, mottled lesions of the extremities and/or trunk that progress to skin and subcutaneous tissue necrosis, non-healing ulcers, and gangrene. We reviewed the clinical course of seven patients (aged 24-69) with calciphylaxis treated at our institution over a 4-year period (October 1988-June 1992). All seven patients underwent parathyroidectomy, with a mean time of 8 weeks (range 3-20 weeks) between the onset of calciphylactic symptoms and parathyroidectomy. Four patients died, three secondary to wound-related sepsis. Of the three survivors, two healed soft tissue lesions primarily. The other required extremity amputation and wound excision before healing. Neither anatomical location of the soft tissue lesions nor post-parathyroidectomy serum calcium and phosphorus levels had any bearing on wound healing or mortality. Lesion severity at the time of parathyroidectomy appeared to best correlate with clinical course. Although treatment with phosphate-binding antacids, total or subtotal parathyroidectomy, and avoidance of challengers such as Vitamin D or local tissue trauma remain the mainstays of therapy, the uniform cure for calciphylaxis remains elusive. Prognosis for patients with calciphylaxis is dismal, even following late surgical intervention. Earlier recognition of the signs and symptoms of calciphylaxis should lead to timely parathyroidectomy in the hopes of ameliorating the symptoms and preventing or retarding its progressive sequelae.
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PMID:Calciphylaxis: early recognition and management. 830 50

After a near total small bowel resection for an acute thrombosis of the mesenterial artery, a 61 year-old man was treated with total parenteral nutrition at home for five years. The treatment was complicated by episodes of sepsis, anaemia and uremia. After four years he developed pain in long bones and the back and grave hypercalcuria. Roentgenogram showed demineralisation. There was no hyperparathyroidism and serum phosphate and serum calcium were normal. His chronic metabolic acidosis was treated continuously with enteral acetate. He received basal amounts of vitamin D and amino acids. By administering calcitonin we were able to cure his progressive bone pains and normalize his calcium urinary output. No side effects were observed. Therefore, calcitonin may contribute to the treatment of bone disease associated with total parenteral nutrition.
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PMID:[Calcitonin treatment of metabolic bone disease induced by parenteral nutrition]. 832 48

We showed previously that a mutant strain of group B Streptococcus (GBS) defective in capsule production was avirulent. This study describes the derivation of an unencapsulated mutant from a highly encapsulated wild-type strain of type III GBS, COH1, by transposon mutagenesis with Tn916 delta E. The mutant, COH1-13, was sensitive to phagocytic killing by human leukocytes in vitro and was relatively avirulent in a neonatal rat sepsis model compared with the wild-type strain. No capsular polysaccharide was evident in the cytoplasm or on the cell surface of the mutant strain. The Tn916 delta E insertion site in COH1-13 was mapped to the same chromosomal location as the Tn916 insertion site in the unencapsulated type III mutant COH31-15 reported previously. Nucleotide sequencing of DNA flanking the insertion site in COH1-13 revealed an open reading frame, designated cpsD, with significant homology to the rfbP gene of Salmonella typhimurium. RfbP encodes a galactosyl transferase enzyme that catalyses the transfer of galactose to undecaprenol phosphate, the initial step in O-polysaccharide synthesis. A particulate fraction of a lysate of wild-type strain GBS COH1 mediated the transfer of galactose from UDP-galactose to an endogenous acceptor. The galactose-acceptor complex partitioned into organic solvents, suggesting it is lipid in nature or membrane-associated. Galactosyl transferase activity was significantly reduced in the unencapsulated mutant strain COH1-13. These results, together with the similarity in deduced amino acid sequence between cpsD and rfbP suggest that cpsD encodes a galactosyl transferase essential for assembly of the GBS type III capsular polysaccharide.
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PMID:Identification of cpsD, a gene essential for type III capsule expression in group B streptococci. 835 11

During the last decade, episodes of sepsis have increased and Escherichia coli has remained the most frequent clinical isolate. Lipopolysaccharides (LPS; endotoxin) are the major toxic and antigenic components of gram-negative bacteria and qualify as targets for therapeutic interventions. Molecules that neutralize the toxic effects of LPS are actively investigated. In this paper, we describe a murine monoclonal antibody (MAb; WN1 222-5), broadly cross-reactive and cross-protective for smooth (S)-form and rough (R)-form LPS. As shown in enzyme-linked immunosorbent assay and the passive hemolysis assay, WN1 222-5 binds to the five known E. coli core chemotypes, to Salmonella core, and to S-form LPS having these core structures. In immunoblots, it is shown to react with both the nonsubstituted core LPS and with LPS carrying O-side chains, indicating the exposure of the epitope in both S-form and R-form LPS. This MAb of the immunoglobulin G2a class is not lipid A reactive but binds to E. coli J5, an RcP+ mutant which carries an inner core structure common to many members of the family Enterobacteriaceae. Phosphate groups present in the inner core contribute to the epitope but are not essential for the binding of WN1 222-5 to complete core LPS. Cross-reactivity for clinical bacterial isolates is broad. WN1 222-5 binds to all E. coli clinical isolates tested so far (79 blood isolates, 80 urinary isolates, and 21 fecal isolates) and to some Citrobacter, Enterobacter, and Klebsiella isolates. This pattern of reactivity indicates that its binding epitope is widespread among members of the Enterobacteriaceae. WN1 222-5 exhibits biologically relevant activities. In vitro, it inhibits the Limulus amoebocyte lysate assay activity of S-form and R-form LPS in a dose-dependent manner and it neutralizes the LPS-induced release of clinically relevant monokines (interleukin 6 and tumor necrosis factor). In vivo, WN1 222-5 blocks endotoxin-induced pyrogenicity in rabbits and lethality in galactosamine-sensitized mice. The discovery of WN1 222-5 settles the long-lasting controversy over the existence of anti-core LPS MAbs with both cross-reactive and cross-protective activity, opening new possibilities for the immunotherapy of sepsis caused by gram-negative bacteria.
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PMID:A broadly cross-protective monoclonal antibody binding to Escherichia coli and Salmonella lipopolysaccharides. 835 7

Neuropathic complications of the burn patient are frequently undiagnosed. A retrospective study was performed looking at neuropathies in patients admitted to a tertiary care burns centre from 1984 to 1991. Nineteen out of a total of 800 patients had signs and symptoms of neuropathy, confirmed on neurophysiological testing. Most patients were severely burned with 11 patients (69%) having a total burn surface area of > 20%. Twenty-eight percent were full thickness burns. Mononeuritis multiplex was the most common finding in these patients, occurring in 11 (69%). This has not been reported before. Three patients (19%) had an isolated mononeuropathy, one (6%) had a radiculopathy and one had a generalized axonal polyneuropathy. Of the patients with mononeuropathy, nine had lesions only in burned areas and four had lesions in burned and unburned areas. Eleven patients had complications of sepsis with five also having renal failure. Age, sex, serum albumin, magnesium, phosphate, creatinine, the presence of sepsis and the number or type of drug did not correlate with the number of affected nerves nor the extent of recovery. The length of hospitalization and severity of the burns were the only two factors which correlated with the number of affected nerves. Vascular occlusion of the vasa nervorum, direct thermal injury or a disseminated neurotoxin are postulated as possible aetiological mechanisms.
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PMID:Neuropathy in burn patients. 838 17

Catheter-related sepsis is a common complication associated with the use of central venous catheters (CVC). In an attempt to overcome this problem benzalkonium chloride was incorporated into a CVC polymer. The effect of the presence of benzalkonium chloride on microbial colonization of the CVC was then assessed in vitro. MICs and MBCs of benzalkonium chloride for a range of organisms were performed and good activity against Gram-positive organisms was confirmed. In order to assess the antimicrobial activity of the benzalkonium-chloride-impregnated catheter, 2 cm lengths were placed on to nutrient agar plates inoculated with various micro-organisms. Zones of inhibition against five strains of Staphylococcus epidermidis and two strains of Staphylococcus aureus were demonstrated. Smaller zones of inhibition was also produced with Gram-negative species and Candida albicans. The zone sizes correlated with the MICs. Bacterial adherence to the benzalkonium-chloride-impregnated catheters was determined in both static and dynamic models and was significantly reduced compared with control catheters, containing no antimicrobial agent (P < 0.01). Inhibition of microbial adherence to benzalkonium-chloride-impregnated catheters placed in 25% human blood in phosphate-buffered saline (PBS), for up to seven days or PBS alone for 14 days was detected. The findings indicate that benzalkonium-chloride-impregnated catheters exhibit reduced microbial colonization by a range of organisms in vitro. The incorporation of benzalkonium chloride into a CVC may thus offer an effective method for the prevention of catheter related sepsis.
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PMID:A novel antimicrobial central venous catheter impregnated with benzalkonium chloride. 814 34

This study was designed to test the hypothesis that tissue factor pathway inhibitor (TFPI) plays a significant role in vivo in regulating coagulation that results from exposure of blood to tissue factor after vascular injury as in the case of gram negative sepsis. Highly purified recombinant TFPI (6 mg/kg) was administered either 30 min or 4 h after the start of a lethal intravenous Escherichia coli infusion in baboons. Early posttreatment of TFPI resulted in (a) permanent seven-day survivors (5/5) with significant improvement in quality of life, while the mean survival time for the controls (5/5) was 39.9 h (no survivors); and (b) significant attenuations of the coagulation response and various measures of cell injury, with significant reductions in pathology observed in E. coli sepsis target organs, including kidneys, adrenals, and lungs. TFPI administration did not affect the reduction in mean systemic arterial pressure, the increases in respiration and heart rate, or temperature changes associated with the bacterial infusion. TFPI treated E. coli infected baboons had significantly lower IL-6 levels than their phosphate buffered saline-treated controls, however tumor necrosis factor levels were similarly elevated in both groups. In contrast to the earlier 30-min treatment, the administration of TFPI at 4 h, i.e., 240 min, after the start of bacterial infusion resulted in prolongation of survival time, with 40% survival rate (2/5) and some attenuation of the coagulopathic response, especially in animals in which fibrinogen levels were above 10% of normal at the time of TFPI administration. Results provide evidence for the significance of tissue factor and tissue factor pathway inhibitor in bacterial sepsis, and suggest a role for blood coagulation in the regulation of the inflammatory response.
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PMID:Tissue factor pathway inhibitor reduces mortality from Escherichia coli septic shock. 851 93

It is unknown whether continuous renal replacement techniques result in diminished morbidity and mortality when compared to conventional dialytic techniques. To investigate this issue a previously described, retrospectively studied group of critically ill patients with severe acute renal failure treated by conventional dialysis (CD) was compared to a prospectively studied group of similar patients treated by acute continuous hemodiafiltration (ACHD). A combined retrospective and prospective clinical and laboratory investigation was carried out for 234 consecutive critically ill patients with severe acute renal failure in the intensive care unit of a tertiary institution. Biochemical, clinical and outcome data in all patients treated by conventional dialytic techniques (intermittent hemodialysis and/or peritoneal dialysis) during a 5-year period were retrospectively analyzed, and a prospective analysis of the same biochemical, clinical and outcome data in all patients treated by acute continuous hemodiafiltration was done over a similar time span, with statistical comparison of findings. One hundred and fifty patients were treated by ACHD and 84 by CD. ACHD patients were more severely ill (mean APACHE II score: 28.2 vs. 25.8; p < 0.01) and older (mean age: 59.9 vs. 55.5 years; p < 0.01). There were no significant differences in the incidence of sepsis, bacteremia and need for mechanical ventilation. ACHD resulted in better control of uremia (mean steady-state plasma urea level: 20.1 vs. 31.7 mmol/l; p < 0.001) and hyperphosphatemia (mean serum phosphate: 1.26 vs. 1.95 mmol/l) after 24 h of initiation of therapy. It also allowed the administration of full nutritional support in a significantly greater percentage of patients (91.3 vs. 64.8%; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Severe acute renal failure: a comparison of acute continuous hemodiafiltration and conventional dialytic therapy. 853 50


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