Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Between November 1984 and December 1989, 318 non-cemented Porous Coated Anatomic (PCA; How-medica, Rutherford, New Jersey) total hip replacements were performed by the authors. A follow-up of 1 to 6 years was allowed. The average age was 53.1 years (from 17 to 71 years). The distribution of right-to-left was approximately equal. There were 192 hip replacements for primary and post-traumatic osteo-arthritis, 42 for rheumatoid arthritis, 40 for avascular necrosis, 29 for congenital dislocation or hip dysplasia with secondary osteo-arthritis, 6 for Perthes disease, 5 for previous sepsis, 2 of whom had had a Girdlestone procedure, 2 for revision of a painful cup arthroplasty, and 1 for conversion of a previously fused hip. All patients were evaluated on a one hundred point Harrington Arthritis Research Centre Scale. Points were awarded for pain (0-35), function (0-35), motion (0-10), deformity (0-10) and gait (0-10). Pre-operative total scores averaged 45.5 (9-71) and postoperative scores averaged 83.9 (55-98). The overall results were excellent 20.5% (90-100), good 59.8% (80-90), fair 16.4% (70-80), and poor 3.3%. Postoperative radiographs were evaluated using zonal analysis. There was no deterioration on the radiographs after two years.
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PMID:Porous coated anatomic non-cemented total hip arthroplasty. 173 38

In 1987, Yeager et al. reported that intraoperative epidural anesthesia with local anesthetics and postoperative epidural analgesia with opiates diminished postoperative morbidity. In our first clinical trial on this topic, the better postoperative analgesia with epidural bupivacaine-fentanyl failed to improve the outcome after major abdominal operations over that obtained with parenteral piritramide. This randomized controlled investigation was designed to assess whether intraoperative epidural anesthesia with bupivacaine plus light general anesthesia and postoperative epidural analgesia with morphine would diminish the overall rate of postoperative complications after major abdominal operations compared with general anesthesia (without epidural) followed by patient controlled analgesia with morphine, and with intraoperative epidural anesthesia with bupivacaine and light general anesthesia followed by postoperative bupivacaine-morphine analgesia. METHODS. A total of 292 patients undergoing infrarenal aortic bypass operation, gastric resection, gastrectomy, duodenum-preserving pancreatic resection, Whipple's operation or cystectomy and neobladder formation were randomly divided into three groups: 1. PCA group (patient controlled analgesia, n = 107): patients were operated on under general anesthesia (midazolam, fentanyl, N2O/O2, if necessary with addition of halothane, enflurane or isoflurane; muscle relaxation with pancuronium bromide). Postoperative management consisted in patient-controlled analgesia with morphine (Prominject), bolus 2 mg, lock-out 5 min (recovery room, intensive care unit) or 15 min (surgical ward). 2. EBM group (epidural bupivacaine+morphine, n = 95): operation under light general anesthesia (midazolam, low-dose fentanyl, N2O/O2, pancuronium bromide). In addition, a mixture of bupivacaine (0.25%) and morphine (60 micrograms/ml) was infused (approximately 0.1 ml/kg.h) via an epidural catheter during and after the operation (approximately 72 h). 3. EM group (epidural morphine, n = 90): operation under the same kind of general-epidural anesthesia as in the EBM group. Postoperatively, epidural injection of morphine (0.05 mg/kg in 10 ml of saline) on request up to the 3rd postoperative day. Quality of analgesia (at rest and when patients coughed vigorously), strength of cough, and rate-pressure product were recorded at 8:00 h, 12:00 noon, 16:00 h and 20:00 h on the 1st, 2nd and 3rd postoperative days. Incidence and intensity of all postoperative complications (cardiovascular, pulmonary, renal and other organ failure, reoperations, major infection, sepsis, thromboembolism, metabolic and mental disturbances) were assessed from the day of operation until discharge or death (n = 10), respectively. RESULTS AND DISCUSSION. In the PCA and EM groups analgesia was equal but of slightly inferior quality compared with the EBM group. The ability to cough was best in the EBM group and significantly worse in the PCA and EM groups, with no difference between the last two. (ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Patient-controlled analgesia versus epidural analgesia using bupivacaine or morphine following major abdominal surgery. No difference in postoperative morbidity]. 175 32

Systemic infection of mice with a Candida albicans strain (PCA-2) incapable of yeast-mycelial conversion is known to activate host macrophages and confer protection against subsequent challenge with highly pathogenic cells of the same species or by other micro-organisms. In an attempt to define the relative contributions of different immune components to the protection mediated by PCA-2, we evaluated the effect of manipulations known to selectively deplete immune functions. By means of cytostatic drug or silica induced toxicity, it was possible to demonstrate that no crucial role in protection is played by cytotoxic T lymphocytes or B cells, nor by PCA-2 induced granulocytosis alone. The cells responsible for this effect were dacarbazine-resistant silica-sensitive macrophages whose activity in vivo paralleled the in vitro expression of splenic candidacidal activity. Macrophage activation by PCA-2 and increased anti-Candida resistance did not result from an immunological response mediated by T-dependent effectors, as these effects could be reproduced in athymic mice.
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PMID:Immunomodulation by a low-virulence, agerminative variant of Candida albicans. Further evidence for macrophage activation as one of the effector mechanisms of nonspecific anti-infectious protection. 285 17

A comparative experimental study was carried out of antigenic staphylococcal preparations developed in the USSR and Czechoslovakia for the immune therapy of chronic staphylococcal infection. The efficiency of the preparations was unequivocally confirmed using the rabbit staphylococcal sepsis model. The immunogenicity of tested strains was shown not to always correlate with their virulence. Preparations obtained by means of aqueous extraction from mildly virulent immunogenic strains exhibited greater protective activity than those prepared from highly virulent strains. The PCA phenomenon did not differ significantly provided the tested preparations were administered at doses which ensured equal protective action.
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PMID:Experimental investigation of preparations for the immunotherapy of staphylococcal infections. 342 56

Systemic infection of mice with a Candida albicans strain (PCA-2) incapable of yeast-mycelial conversion conferred protection against a subsequent intravenous challenge with the pathogenic strain of the parent organism, strain CA-6. Protection was nonspecific since it was also detected upon challenge of mice with Staphylococcus aureus. Moreover, the PCA-2 organisms had to be viable, their effects being most evident when they were given intravenously at a dose of 10(6) cells 7 to 14 days prior to microbial challenge. Thus, all mice pretreated with PCA-2 and challenged 14 days later with viable CA-6 cells lived through a 60-day observation period, whereas all control mice not treated with PCA-2 died within 3 days. In an attempt to correlate the immunostimulatory effects observed in vivo with possible modifications in in vitro functions, it was found that administration of PCA-2 was accompanied by an increase in the number of peripheral blood polymorphonuclear cells and by the activation in the spleen of cells with highly candidacidal activity in vitro. Moreover, the adoptive transfer of plastic-adherent cells from PCA-2-infected mice into histocompatible recipients conferred considerable protection against subsequent CA-6 challenge.
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PMID:Evidence for macrophage-mediated protection against lethal Candida albicans infection. 394 7

Disseminated intravascular coagulation (DIC) is a common occurrence during clinical sepsis and can be induced in the experimental host by LPS. Fibrin deposition in the hepatic microcirculation has been observed within 30 min of i.v. injection of LPS. Because mononuclear phagocytes have been shown to produce a PCA after exposure to LPS, we have examined the ability of a homogeneous population of explanted hepatic macrophages to express PCA. Addition of as little as 10 ng/ml of LPS stimulated a 15- to 20-fold increase in PCA over control culture levels within 7 1/2 hr post-treatment. The PCA was found to be membrane-associated, with approximately 90 to 95% of the total PCA present in the cellular lysates, and more than 85% was inhibited by pretreatment of the cells with the diazonium salt of sulfanilic acid, an inhibitor of ecto-enzymes. In contrast to tissue thromboplastin produced by other M phi populations, the H-M phi PCA was found to be markedly sensitive both to heat inactivation at 56 degrees C and to inhibition by 1 mM DFP. Additionally, assays involving both a 1-stage coagulation test as well as an enzyme assay with a Factor Xa-specific substrate (using normal and deficient human plasmas) demonstrated that the H-M phi PCA appears to activate Factor X directly. Unlike tissue thromboplastin, the H-M phi PCA is non-dependent of Factor VII activation. These studies: 1) demonstrate the LPS induces a unique PCA in the H-M phi, and 2) support a role for the H-M phi in the initiation of DIC in endotoxemic shock.
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PMID:The induction of a unique procoagulant activity in rabbit hepatic macrophages by bacterial lipopolysaccharides. 702 10

The efficacy, safety and usefulness of murine anti-endotoxin monoclonal IgM antibody "E5, an intravenous dose of 2 mg/kg" were evaluated in 88 patients with suspected Gram-negative sepsis from 37 institutes in Japan. Out of these, 74 patients were evaluable for the efficacy, 85 for safety and 75 for clinical usefulness. In assessing the efficacy, the patients were divided into 3 groups based on the plasma endotoxin levels (Endospecy with new PCA treatment of plasma): H group with a level of above 9.8 pg/ml and M group with a level of 3.0-9.8 pg/ml and L group with a level of below 3.0 pg/ml. 1. The efficacy rates as assessed following administration of E5 were 73.1% in the H group, 70.4% in the M group and 38.1% in the L group being higher in the groups with significantly high plasma endotoxin levels. 2. In both the H and M groups in whom plasma endotoxin levels were significantly high, the majority of the patients showed rapid reduction of the levels after administration of E5. 3. In all groups, improvement in body temperature, pulse rate, blood TNF-alpha and blood IL-6 was observed after treatment with E5. In the H and M groups with an endotoxin level of > or = 3.0 pg/ml, improvement in platelet count as well as in CRP was noted. The H group showed also improvement in WBC. 4. Improvement in the shock score was noted in all the groups but was more outstanding in the H and M groups in the early stage of treatment. 5. Side effects were seen in 5 (5.9%) of 85 patients and all thought to be allergic in symptoms such as rash, itching, fever and flare. 6. The reaction to the prick test performed before administration of E5 was negative in all these 5 patients. For 3 of the 5 patients, anti-E5 IgE antibody was measured. In all of them, the IgE levels were higher than those of healthy controls. Also, in 47.6% of patients, an elevation of anti-E5 IgG antibody was noted two weeks after the administration. 7. Clinical laboratory abnormalities were observed in 3 (3.5%) of 85 patients. They were an elevation of S-GOT.S-GPT and lowering of BUN, increased Al-p and decreased CH50, increased neutrophilia (%) and were all slight in the degree of the changes. 8. The clinical usefulness of E5 was evaluated for 75 patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Phase II study of edobacomab (E5) in the treatment of gram-negative sepsis]. 813 82

Induction of tissue factor (TF) expression on monocytes and endothelial cells is central to the development of septic coagulopathy. Serum concentrations of endotoxin in septic patients who develop disseminated intravascular coagulation (DIC) do not, however, reach the levels that would directly stimulate TF expression on either monocytes or endothelium. We show, using an in vitro coculture system, that the interaction of monocytes with endothelium induces the expression of significant levels of TF. Unstimulated cocultures of monocytes (2 x 10(4)/well) and endothelial cells (2 x 10(4)/well) produced 35.3 +/- 8.5 mU of PCA/well, representing a 5-fold increase over the combined PCA of each cell type cultured alone (7.1 +/- 1.5 mU, n = 6, P < 0.001). Significant enhancement was also found in the presence of low concentrations of LPS. Induction of TF protein was confirmed by Western blotting. Fixation of monocytes with paraformaldehyde completely abolished TF induction in cocultures, whereas fixation of endothelium had no effect, suggesting that TF induction occurred in monocytes rather than endothelial cells. Induction of TF in cocultures could be further augmented by preincubating the endothelial cells with IFN-gamma. When endothelium was prestimulated with 500 U/ml IFN-gamma there was 142 +/- 11% increase over unstimulated cocultures (n = 5, P < 0.01). TF induction was inhibited by 32 +/- 6% in the presence of anti-ICAM-1 mAb (n = 5, P < 0.01). Our results suggest that monocyte interactions with vascular endothelium, regulated by inflammatory cytokines, and mediated by adhesive ligand binding, leads to the induction of functional monocyte TF protein, which may be responsible for the initiation of DIC in sepsis.
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PMID:Induction of tissue factor expression in human monocyte/endothelium cocultures. 854 49

Plasma endotoxin contents of the patients with sepsis or typhoid fever were measured by two sophisticated chromogenic limulus tests; Endospecy and Toxicolor tests. Endospecy test is the endotoxin-specific test and Toxicolor is responsible for both endotoxin and (1,3)-beta-D-glucan. Plasma was pretreated by our new PCA method which resolved the problem as to the detection of a lesser amount of plasma endotoxin when pretreated by the conventional PCA method. Although Toxicolor values have been reported to exceed more than the Endospecy value, under complicated pathophysiological situations, almost all specimens of these patients had a similar value, except in one expired septic shock case. In 18 typhoid fever cases, Salmonella typhi was isolated only from the bile in 5 cases, however endotoxemia occurred in 11 cases (61.1%). Within the first 4 days, the incidence of endotoxemia was higher (10/14, 71.4%). These results suggest that endotoxin assay seemed to be a useful tool for the diagnosis of typhoid fever.
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PMID:Plasma endotoxin in typhoid fever. 892 38

Sepsis is a systemic inflammatory response that results from the inability of the immune system to limit bacterial spread during an ongoing infection. Recently, we have documented an impaired neutrophil migration toward the infectious focus in severe sepsis. This impairment seems to be mediated by circulating cytokines, chemokines, and NO. Platelet-activating factor (PAF) plays an important role in the orchestration of different inflammatory reactions, including the release of cytokines, chemokines, and free radicals. Using a PAFR antagonist, PCA-4248, and PAFR-deficient mice, we investigated whether signaling via PAFR was relevant for the failure of neutrophils to migrate to the site of infection after lethal sepsis caused by cecum ligation and puncture in mice. In PAFR-deficient mice or mice pretreated with PCA-4248 (5 mg/kg) and subjected to lethal sepsis, neutrophil migration failure was prevented, and bacterial clearance was more efficient. There was also reduced systemic inflammation (low serum cytokine levels), lower nitrate levels in plasma, and higher survival rate. Altogether, the results firmly establish a role for PAFR in mediating the early impairment of neutrophil migration toward the infectious focus. Blockade of PAFR may prevent the establishment of severe sepsis.
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PMID:Signaling via platelet-activating factor receptors accounts for the impairment of neutrophil migration in polymicrobial sepsis. 1681 86


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