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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors evaluated the financial and health implications of treatment choices for three serious classes of infection: hospital-acquired pneumonia, intra-abdominal infection, and sepsis of unknown origin. Data were obtained from a systematic review of clinical literature and published data bases, by written questionnaire from a panel of infectious disease authorities, and from actual costs at a tertiary-care hospital. For pneumonia and sepsis, the third-generation cephalosporin evaluated (ceftizoxime) was found to be less expensive than other regimens, when costs of dose preparation and administration, monitoring, and toxicity were added to drug acquisition costs. The lowest-cost regimen for intra-abdominal infection was metronidazole plus gentamicin. Modest differences in efficacy would easily outweigh differences in toxicity, however, and could justify the use of more expensive regimens (e.g., mezlocillin plus gentamicin for hospital-acquired pneumonia, and cefoxitin plus gentamicin for intra-abdominal infection). If all regimens are assumed to be equally efficacious, then the third-generation cephalosporin was both lowest in cost and, owing to its low toxicity, greatest in net health benefit.
J Gen Intern Med
PMID:Cost-effective choice of antimicrobial therapy for serious infections. 309 40

The role of motility as a virulence factor in Pseudomonas aeruginosa burn wound sepsis was examined using mutants deficient in the Fla or Mot phenotype. Physiological profiles of parental strains and Fla- and Mot- mutants were similar with respect to antibiograms, O antigen types, growth rates, and proteolytic, exotoxin A and phospholipase activities, providing evidence for isogenicity. Lethality studies using a subcutaneous mouse burn model showed that three Fla- mutants and one Mot- mutant were much less virulent (10(2) to 10(5) times) than the parent wild-type. Topical challenges in the flame burn model showed that a Fla- mutant of strain M-2 was approximately tenfold less virulent. A reduction in virulence, although somewhat less than tenfold, was also observed in the scald burn model for M-2 Fla-, and Mot- strains. Tissue colonization experiments revealed a characteristic, rapidly systemic infection in burned mice challenged with wild-type organisms. Nonmotile mutants similarly proliferated in the burn wound, but the characteristic bacteraemia and systemic invasion were markedly absent. The infection remained localized in the skin wound and the mice survived. The pattern of infection by nonmotile mutants in the colonization studies was very similar to that obtained with Fla+ cells in burned animals passively treated with antiflagellar antibody. These results add substantial support to the concept of motility as a P. aeruginosa virulence factor in invasive infections.
J Gen Microbiol 1988 Jan
PMID:Flagella, motility and invasive virulence of Pseudomonas aeruginosa. 314 66

The incidence of nasal carriage of Staphylococcus aureus and the in vitro susceptibility of isolates to fusidic acid, penicillin, erythromycin, methicillin and tetracycline was determined in 204 patients who had been treated previously with a short course of a topical preparation of Fucidin for acute skin sepsis, and in an equal number of control subjects. Staphylococcus aureus was isolated from 36 per cent and 34 per cent of patients in the Fucidin and control groups respectively. Only one of the 144 isolates was resistant to fusidic acid. Short, single courses of topical therapy in general practice are unlikely to be epidemiologically hazardous in the long term. Evidence of possible cross-infection in general practice was obtained.
J R Coll Gen Pract 1984 May
PMID:Nasal carriage and antibiotic susceptibility of Staphylococcus aureus in general practice. 673 60

In conventional usage, "sepsis" denotes a clinical syndrome caused by excessive release of a variety of proinflammatory mediators, including tumor necrosis factor alpha, interleukin-1, and metabolites of arachidonic acid. Because this condition can be precipitated by infectious or noninfectious causes (eg, acute pancreatitis), a recent consensus conference has advocated replacing the term sepsis with the phrase systemic inflammatory response syndrome. Improvements in our understanding of the pathophysiologic basis for systemic inflammatory response syndrome have resulted in the development of a number of novel approaches for treating, preventing, or limiting its deleterious consequences. Although much of this work remains confined to the laboratory, several of these approaches are undergoing (or recently have undergone) clinical evaluation. Among these are the use of monoclonal antibodies against endotoxin, monoclonal antibodies against tumor necrosis factor, recombinant proteins that antagonize the effects of or bind to circulating interleukin-1 or tumor necrosis factor, and drugs that inhibit the enzyme cyclooxygenase, which is responsible for the formation of certain key metabolites of arachidonic acid.
Curr Opin Gen Surg 1993
PMID:Surgical infections: blocking the mediator cascade responsible for sepsis and septic shock. 758 65

Improvements in surgical management and intensive care therapy have enabled many patients to initially survive severe life-threatening trauma or major surgical procedures only to die after delayed bouts of sepsis. This paper reviews literature published within the past year on the effects of nutrient substitution on malnutrition, injury, and the host immune response. Topics discussed include immunodeficiencies in trauma and malnutrition, immunomodulation by nutrition, and parenteral versus enteral nutrition. We also discuss the roles of arginine, glutamine, omega-3 fatty acids, and dietary nucleotides in the host immune response.
Curr Opin Gen Surg 1993
PMID:Malnutrition, injury, and the host immune response: nutrient substitution. 758 22

Survivors of acute respiratory distress syndrome (ARDS) are at risk for long-lasting cognitive decline due to hypoxemia, sepsis and/or psychological sequelae associated with aggressive supportive care in the intensive care unit (ICU). We conducted an exploratory study to assess cognitive performance in long-term survivors of ARDS and to investigate how cognitive functioning is related to employment status and health-related quality of life (HRQOL). At median time of 6.0 years after ICU discharge, forty-six ARDS survivors were tested with SKT, a short cognitive performance test for assessing deficits of memory and attention. A measure of HRQOL (SF-36 Health Status Questionnaire) was also administered, and in a brief psychiatric interview, employment status was rated. 23.9% (n=11) of the patients showed cognitive impairments. However, no extreme and severe cognitive deficits were recorded. They primarily revealed low levels of cognitive function in various tasks assessing attention skills. Disability was found in 41.3% (n=19) of the patients. All ARDS survivors with cognitive deficits were disabled, whereas only 22.9% (n=8) of the cognitively not impaired patients gave evidence of disability. The SF-36 values of the ARDS survivors indicated impaired health status on seven out of eight domains when compared to normative population data. Patients with cognitive deficits described the lowest HRQOL with major limitations in the domains role-physical and social functioning when compared to patients without cognitive impairments. In conclusion, long-term ARDS survivors exhibit impaired health status and the presence of cognitive deficits is associated with disability and considerable impairments in HRQOL. More detailed psychiatric research is required to establish the etiology of these cognitive impairments.
Gen Hosp Psychiatry
PMID:The relationship between cognitive performance and employment and health status in long-term survivors of the acute respiratory distress syndrome: results of an exploratory study. 1131 77

Systemic infection of wheat plants with Soil-borne wheat mosaic virus (SBWMV) requires temperatures below 20 degrees C. Here we examine the cause of the temperature sensitivity by inoculating infectious in vitro transcripts of SBWMV RNA1 and RNA2 to barley mesophyll protoplasts. After RNA inoculation, protoplasts were incubated at temperatures between 15 and 25 degrees C for up to 48 h. Western blot analysis showed that the capsid protein accumulated most abundantly at 17 degrees C but was not detectable at 25 degrees C. Northern blot analysis showed that the wild-type RNA1 and RNA2 and their subgenomic RNAs accumulated most abundantly at 17 degrees C but were barely detectable at 25 degrees C. An RNA1 mutant in which the p152 and p211 replicase genes were placed between the 5'- and 3'-untranslated regions also replicated most efficiently at 17 degrees C but not at 25 degrees C. Thus, the requirement for temperatures lower than 20 degrees C for SBWMV infection is primarily determined by replication of RNA1, which encodes the viral RNA replicase.
J Gen Virol 2003 Apr
PMID:The optimal temperature for RNA replication in cells infected by Soil-borne wheat mosaic virus is 17 degrees C. 1265 2

The complete nucleotide sequences of three human echovirus (EV) 11 strains and one EV19 strain, all of which caused outbreaks of enterovirus uveitis (EU), a new infant disease first identified in 1980 in Siberia, were determined. One EV11 strain which caused an outbreak of sepsis-like disease in Hungary was also sequenced. All four EV11 strains were mosaic recombinants of the prototype EV11 strain Gregory, with their non-structural coding regions and 5' NTRs being more similar to other prototype enteroviruses (EV1, EV9). However, this finding is probably a feature of all circulating enterovirus strains and may not be related to their altered virulence. A full genome sequence comparison of the three subtypes of EU-causing strains excludes the role of recent recombination in their emergence, and points to their independent emergence.
J Gen Virol 2004 Feb
PMID:Recombination in uveitis-causing enterovirus strains. 1476 4

Disseminated intravascular coagulation (DIC) is an acquired coagulation disorder that may occur in a wide variety of clinical conditions. Suspicion of DIC should lead to a differential diagnosis that includes primary fibrinolysis and other bleeding diatheses such as thrombocytopenias of diverse etiology. Confirmation of the diagnosis of DIC should always prompt a search for an underlying medical disorder, including sepsis, severe trauma, solid and hematological malignancies, obstetrical complications, and vascular disorders. Here, we describe an unusual case of acute bleeding and DIC as the presenting manifestation of metastatic prostate cancer in a 60-year-old man. Treatment with a luteinizing hormone-releasing hormone (LHRH) agonist and a short course of an antiandrogen, together with supportive measures (i.e., clotting factors, heparin, and platelets), led to normalization of all coagulation parameters within 1 week, and to clinical improvement and decline in the serum level of prostate-specific antigen (PSA). We discuss the pathogenesis, differential diagnosis, and association of DIC with prostate cancer along with the management of this condition.
J Gen Intern Med 2006 Nov
PMID:Disseminated intravascular coagulation as the presenting sign of metastatic prostate cancer. 1745 72

Tumor necrosis factor-alpha (TNF) is a major mediator of apoptosis as well as immunity and inflammation. Inappropriate production of TNF or sustained activation of TNF signaling has been implicated in the pathogenesis of a wide spectrum of human diseases, including cancer, osteoporosis, sepsis, diabetes, and autoimmune diseases such as multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease. TNF binds to two specific receptors, TNF-receptor type I (TNF-R1, CD120a, p55/60) and TNF-receptor type II (TNF-R2, CD120b, p75/80). Signaling through TNF-R1 is extremely complex, leading to both cell death and survival signals. Many findings suggest an important role of phosphorylation of the TNF-R1 by number of protein kinases. Role of TNF-R2 phosphorylation on its signaling properties is understood less than TNF-R1. Other cellular substrates as TRADD adaptor protein, TRAF protein family and RIP kinases are reviewed in relation to TNF receptor-mediated apoptosis or survival pathways and regulation of their actions by phosphorylation.
Gen Physiol Biophys 2007 Sep
PMID:TNF signaling: early events and phosphorylation. 1806 42


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