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)

An unexplained increase in the frequency of pyogenic liver abscesses of unknown etiology has, fourtunately, been paralleled by significant advances in diagnostic and therapeutic methods. This report reviews experience with 14 patients operated upon at NYU Medical Center since 1971. Eight cases (57%) were cryptogenic. Other abscesses were associated with biliary disease (3); abdominal sepsis (2); and trauma (1). Abscesses were present on hospitalization in 12 patients. Clinical findings included fever (101-108 F); 100%; leucocytosis, 71%; anorexia and vomiting, 50%; localized tenderness and hepatomegaly, 50%; hypoalbuminemia, 86%; hypocholesterolemia, 78%; elevated SGOT, 71%; and elevated aikaline phosphatase, 43%. Technetium hepatic scintiscans showed focal defects in 10 of 12 patients (83%), but did not detect multiple abscesses in 2 of these. Hepatic arteriography performed in 10 patients was highly accurate, outlining single abscesses in 6 and multiple abscesses in 4. Furthermore, in one patient a false positive scintiscan was demonstrated by negative arteriography, confirmed by autopsy. In 4 patients, arteriography indicated an abscess in the posterior-superior area of the right hepatic lobe. With precise anatomical localization, a trans-thoracic approach permitted uncomplicated drainage in each case. This approach provides excellent exposure and direct drainage for abscesses in this area. An additional therapeutic adjunct in two patients, with 4 and 11 abscesses each, was postoperative intraportal infusion of antibiotics through the umbilical vein. Thirteen patients (83%) recovered, one dying from pulmonary embolism. Primary hepatic abscesses occur with increasing frequency. Primary hepatic abscesses occur with increasing frequency. Primary hepatic abscesses occur with increasing frequency. The methods described allow more precise preoperative diagnosis and direct surgical drainage.
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PMID:New diagnostic and therapeutic techniques in the management of pyogenic liver abscesses. 113 Aug 69

All cases of neonatal bacteremia occurring at Neonatal Department of Pediatric Clinic, Catholic University of Rome, from January 1976 to December 1983 were examined retrospectively. Twenty-seven (30%) newborn infants with positive blood cultures for coagulase-negative staphylococcus were identified. Seven (25.9%) of the 27 infants were born at term, 4 AGA and 3 SGA; mean birth weight was 2,804 gm (range 2,280-3,670). All of these neonates had clinical evidence and laboratory signs of sepsis, and one had the cerebrospinal-fluid culture positive for coagulase-negative staphylococcus. In the remaining 20 infants (74.1%) the mean birth weight was 1,445 gm (range 810 - 2,400) and mean gestational age was 32 weeks (range 27 - 36). In 15 of the 20 preterm infants clinical signs of septicemia were associated with positive blood culture, and sixty percent of these had received an umbilical artery catheter. An half of coagulase-negative staphylococci isolated from our neonatal sepsis were DNAse-positive and/or phosphatase-positive and/or mannitol-positive. Two full-term infants, one with Down syndrome and one with cardiac malformation, died at 9 days and at 2 weeks of age, respectively. Three of 15 preterm infants with coagulas-negative staphylococcal septicemia died; deaths were among infants of very low birth weights and immature gestations who had severe respiratory syndrome. These data show that coagulase-negative staphylococcus can be important cause of septicemia in patients with compromised host defenses as newborn infants, and especially in the premature babies receiving invasive procedures.
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PMID:[Neonatal sepsis caused by coagulase-negative staphylococci]. 408 16

In the present study, rat cardiac sarcoplasmic reticulum (SR) phospholamban (PLB) phosphatase was partially purified by chromatography on DEAE-Sephacel. This PLB phosphatase was indentical to phosphatase-1. It was shown on electrophoresis of SDS-PAGE autoradiography that the PLB phosphatase in rats during early sepsis (ES) depressed dephosphorylation of substrates (32P-phosphorylase a and 32P-SR). However, dephosphorylation of the substrates by the partially purified phosphatase during late sepsis (LS) was same as that in control rats. The partially purified PLB phosphatase activity in ES rats was significantly decreased, but showed no change in LS rats. The results above were confirmed by a studing of the substrate concentration (enzyme concentration, time)--enzyme reaction velocity curve in showing that both affinity and maximum initial velocity (Vmax) of the phosphatase in the ES rats were decreased, but had no change in those in the LS rats.
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PMID:[Alteration of phospholamban phosphatase activity associated with cardiac sarcoplasmic reticulum during sepsis in rats]. 748 77

Ninety minutes after i.v. injection of Escherichia coli lipopolysaccharide (LPS) (1 mg/kg) into rats, phorbol 12-myristate 13-acetate (PMA)-stimulated superoxide anion (O2-) secretion was enhanced in suspensions of in vivo LPS-treated alveolar macrophages (AM phi) when compared with saline (SAL)-treated AM phi. The purpose of this investigation was to dissect the in vitro mechanism of PMA-stimulated O2- generation in both LPS and SAL-treated rat AM phi, with a panel of inhibitors of protein kinase C (PKC), protein serine-threonine phosphatase(s) (PSP), protein tyrosine kinase(s) (PTK) and phosphatase(s) (PTP), phospholipase A2 (PLA2), cyclooxygenase (CO) and 5-lipoxygenase (5-LO). The following agents blocked PMA-stimulated O2- generation in both LPS- and SAL-treated AM phi (expressed as percentage of control): 1) PKC inhibitors: staurosporine: 100 nM, 7.0% (LPS) and 5.6% (SAL); sphingosine: 10 microM, 21% (LPS) and 10.5% (SAL); 2) PTK inhibitor: genistein: 100 microM, 44% (LPS) and 31% (SAL); 3) PTP inhibitors: phenylarsine oxide, 10 microM, 12.1% (LPS) and 18% (SAL); diamide, 1000 microM, 10.1% (LPS) and 10.5% (SAL); and 4) PLA2 inhibitors: manoalide: 1 microM, 29.3% (LPS) and 5.2% (SAL); scalaradial: 1 microM, 7.7% (LPS) and 7.1% (SAL); and WAY 125,984: 10 microM, 17.1% (LPS) and 14.5% (SAL). In addition, it was observed that exogenously added arachidonic acid (AA)-stimulated O2- generation in a time- and dose-dependent manner in both LPS and SAL-treated AM phi. The following inhibitors enhanced or did not affect PMA-stimulated O2- generation in LPS- and SAL-treated AM phi (expressed as percentage of of control): 1) PSP inhibitors: okadaic acid: 0.5 microM, 117% (LPS) and 153% (SAL); calyculin A: 1 microM, 112% (LPS) and 101% (SAL); 2) CO and 5-LO inhibitors: indomethacin: 10 microM, 107% (LPS) and 90% (SAL); WY 50, 295: 1 microM, 99% (LPS) and 103% (SAL); and 3) the PTP inhibitor orthovanadate upon prolonged preincubation. In both in vivo LPS- or SAL-primed AM phi, PMA-stimulated O2- generation appears to be modulated by PKC, PLA2, AA, PTK, PTP and PSP. No modulatory role was evident for either CO or 5-LO metabolites. These findings might bear on the design of therapeutic approaches for the modulation of O2- release by AM phi in the early stages of sepsis and adult respiratory distress syndrome.
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PMID:Modulation of superoxide generation in in vivo lipopolysaccharide-primed rat alveolar macrophages by arachidonic acid and inhibitors of protein kinase C, phospholipase A2, protein serine-threonine phosphatase(s), protein tyrosine kinase(s) and phosphatase(s). 761 27

Gut fuel utilisation has several unique features. Arterial and luminal fuels provide nutrition for the enterocyte, the former being of more importance. This factor, and the heterogeneity of cell types within the gut makes it difficult to define its fuel utilisation. Metabolic control logic suggests that modulation of the maximal activity of any pathway resides in those enzymes that operate in vivo at rates far below their maximal capacity and that catalyse non-equilibrium reactions. On this basis, although enterocyte hexokinase activity is much higher than in other 'glycolytic' cells (for example, brain), potentially high rates of glucose utilisation are modulated by substrate cycling of glucose 6-phosphate back to glucose through glucose 6-phosphatase. Glutamine metabolism proceeds by glutaminase to produce glutamate, which may then be transaminated (aspartate-aminotransferase and alanine-amino transferase) to produce alpha-ketoglutarate, alanine, and aspartate. The end products of glutamine metabolism by incubated gut preparations in vitro (mainly alanine), suggests that enterocytes, not immune cells, are responsible for most gut glutamine metabolism. High flux rates of glucose and glutamine metabolism in the enterocyte may result from the need for de novo synthesis of purines and pyrimidines and ribose sugars for nucleic acid synthesis. Sepsis reduces rates of glucose and glutamine metabolism, perhaps to preserve the increased consumption of these fuels by activated lymphocytes and macrophages in the gut wall.
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PMID:Quantitative aspects of glucose and glutamine metabolism by intestinal cells. 812 83

Twenty isolates of Pasteurella (Moraxella) anatipestifer from ducks with serositis and septicemia in Thailand between 1988 and 1989 were characterized by various tests. Eighteen isolates fermented glucose and maltose, 3 fructose and 1 each mannose, arabinose, trehalose or sorbitol. All isolates produced gelatinase but not urease, while 2, 3, 5 and 6 produced indole, were CAMP positive, and were proteolytic for milk and coagulated serum respectively. Seven enzymes, phosphatase alkaline, esterase (C4), esterase lipase (C8), leucine arylamidase, valine arylamidase, phosphatase acid and phosphoamidase were detected from all the isolates. The isolates were highly susceptible to ampicillin, erythromycin, penicillin G and tylosin. Gel-diffusion precipitin tests demonstrated that serotype 1 was most prevalent (60%) and serotype 6 followed (5%). Seven isolates (35%) were untypable. These results indicated that P. anatipestifer of serotype 1 played an important role in recent outbreaks of the disease in Thailand.
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PMID:Physiological characteristics, antimicrobial susceptibility and serotypes of Pasteurella anatipestifer isolated from ducks in Thailand. 820 23

The pyruvate dehydrogenase (PDH) complex undergoes reversible phosphorylation catalyzed by a PDH kinase (inactivating) and a PDH phosphatase (activating). In skeletal muscle, a decreased proportion of PDH complex in the active, nonphosphorylated form (PDHa) limits glucose oxidation and promotes the conversion of pyruvate to lactate. Increased lactate formation with the accompanying hyperlactatemia is a frequent metabolic complication of sepsis. The time course for inactivation of the PDH complex in skeletal muscle during sepsis was contrasted with changes in PDHa during sterile inflammation 3,7, or 14 days following the implantation of the foreign body nidus. Total PDH complex activity was not altered in any of the conditions examined. Sepsis, but not sterile inflammation, caused a reduction in the muscle PDHa measured 3 or 7 days following induction of sepsis. The inhibition of the muscle PDHa during sepsis was associated with a sustained hyperlactatemia. PDH kinase activity measured in extracts of mitochondria was enhanced twofold during this period. Fourteen days after induction of sepsis, there were no differences in the PDHa or plasma lactate concentrations in septic rats compared with either control or sterile inflammation. Furthermore, the PDH kinase activity was decreased to values observed in control values. The results are consistent with the hypothesis that a reduced PDHa in skeletal muscle during sepsis is responsible, in part, for the hyperlactatemia characteristic of septic hypermetabolism. Furthermore, the results provide evidence that the decrease in PDHa results from a stable stimulation of PDH kinase activity.
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PMID:Sepsis-induced alterations in pyruvate dehydrogenase complex activity in rat skeletal muscle: effects on plasma lactate. 885 41

Peripheral stem cells were mobilized and collected in 20 children with stage 4 neuroblastoma. A total of 37 leukaphereses were performed in the 20 patients. The mean number of collected cells was 5.6 +/- 2.4 x 10(8)/kg (range 1.9-10.5), and the number of collected CD34+ progenitors was 6.1 +/- 6.3 x 10(6)/kg (range 0.75-21.7). CD34-positive selection was performed using the CellPro method. Of the adsorbed cells, 42 +/- 20% (range 4.3-76.6) stained positively for CD34, and the number of positively selected CD34+ cells was 2.0 +/- 1.9 x 10(6)/kg (range 0.09-7.1). The mean recovery of CD34+ cells was 36 +/- 20% (range 6-67). For detection of contaminating neuroblastoma cells before and after CD34-positive selection, a murine antidisialoganglioside GD2 antibody (14.G2a) was used, followed by the alkaline phosphatase antialkaline phosphatase (APAAP) method. Before the positive selection, various numbers of contaminating neuroblastoma cells were found in the leukaphereses of 7 patients. After positive selection, neuroblastoma cells were still detectable in all 7 patients, with a mean log depletion of tumor cells of 1.41 +/- 0.45 (range 0.69-2.13). In 1 patient, contaminating neuroblastoma cells were found only after CD34-positive selection. In 15 of the 20 patients, high-dose chemotherapy was performed, and positively selected CD34+ cells were reinfused in 12 patients. In 10 of these, the mean time to reach > 0.5 x 10(9)/L granulocytes was 12.3 +/- 1.7 days (range 10-16). One patient died at day 7 due to sepsis, and in 1 patient the backup was given at day 15. Because of the low number of collected CD34+ cells, 3 patients were grafted with a combination of unmanipulated PBSC and CD34+ progenitors. In summary, we have shown that positive selection of peripheral CD34+ progenitors is feasible in pediatric patients. However, strategies to improve the recovery of the CD34+ cells and the purging efficacy of this method (i.e., higher enrichment of CD34+ cells, combination of positive and negative selection methods) should be evaluated further.
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PMID:Positive selection and transplantation of peripheral CD34+ progenitor cells: feasibility and purging efficacy in pediatric patients with neuroblastoma. 923 78

Streptococcus pneumoniae, the pneumococcus, is the most common cause of sepsis and meningitis. Multiple-antibiotic-resistant strains are widespread, and vancomycin is the antibiotic of last resort. Emergence of vancomycin resistance in this community-acquired bacterium would be catastrophic. Antibiotic tolerance, the ability of bacteria to survive but not grow in the presence of antibiotics, is a precursor phenotype to resistance. Here we show that loss of function of the VncS histidine kinase of a two-component sensor-regulator system in S. pneumoniae produced tolerance to vancomycin and other classes of antibiotic. Bacterial two-component systems monitor environmental parameters through a sensor histidine-kinase/phosphatase, which phosphorylates/dephosphorylates a response regulator that in turn mediates changes in gene expression. These results indicate that signal transduction is critical for the bactericidal activity of antibiotics. Experimental meningitis caused by the vncS mutant failed to respond to vancomycin. Clinical isolates tolerant to vancomycin were identified and DNA sequencing revealed nucleotide alterations in vncS. We conclude that broad antibiotic tolerance of S. pneumoniae has emerged in the community by a molecular mechanism that eliminates sensitivity to the current cornerstone of therapy, vancomycin.
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PMID:Emergence of vancomycin tolerance in Streptococcus pneumoniae. 1037 90

During Gram-negative sepsis bacterial LPS induces endothelial cell contraction, actin reorganization, and loss of endothelial integrity by an unknown signal mechanism. In this study, we provide evidence that LPS-stimulation of endothelial cells (HUVEC) decreases myosin light chain (MLC) phosphatase, resulting in an increase in MLC phosphorylation followed by cell contraction. All of these LPS effects could be blocked by the Rho-GTPase inhibitor C3 transferase from Clostridium botulinum or the Rho kinase inhibitor Y-27632. These data suggest that LPS induces MLC phosphorylation via Rho/Rho kinase-mediated inhibition of MLC phosphatase in HUVEC. Furthermore, we observed that cAMP-elevating drugs, known to exert a vasoprotective function, mimicked the effects of C3 transferase and Y-27632, i.e., inhibited LPS-induced MLC phosphatase inactivation and MLC phosphorylation. cAMP elevation did not inhibit myosin phosphorylation induced by constitutively active V14Rho or the MLC phosphatase inhibitor calyculin and did not induce phosphorylation of RhoA in HUVEC, indicating inhibition of an upstream regulator of Rho/Rho kinase. Taken together, Rho/Rho kinase appears to be a central target for inflammatory mediators causing endothelial cell contraction such as bacterial toxins, but also for vasoprotective molecules elevating intracellular cAMP.
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PMID:Cyclic AMP blocks bacterial lipopolysaccharide-induced myosin light chain phosphorylation in endothelial cells through inhibition of Rho/Rho kinase signaling. 1084 13


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