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

The authors have compared 11 laboratory tests for diagnosis f neonatal sepsis: WBC cont, neutr. count, band count (> 8%), immature/mature neutrophil ratio (I:M > 0.2), throm. count, C reactive protein, alpha 1-antitrypsin, alpha 2-macroglobulin, IgM, GIC, C3 fraction of the complement. We determine higher sensitivity and specificity of CRP (80.1%; 80%), C3 fraction of the complement (82.4%; 86.5%) and I:M ratio (96.9%). We conclude that this tests are useful indicators of early diagnostic of neonatal infection.
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PMID:[A comparison between 11 clinico-laboratory indices for the early diagnosis of neonatal sepsis]. 865 18

A wide range of immunomodulating agents are now available which may be of benefit in reducing inflammatory cell activation in meningococcal sepsis. In order to facilitate selection of candidate anti-inflammatory agents for clinical trials, we have used an in vitro whole blood model to evaluate the effects on meningococcal induced neutrophil and monocyte activation, of dexamethasone, prostacyclin, pentoxifylline and a human IgM anti-lipid A monoclonal antibody (HA-1A). Known concentrations of heat and penicillin killed meningococci were added to whole blood and the time course of cellular activation was determined. Using elastase alpha 1-antitrypsin (elastase-alpha 1-AT) and TNF alpha production as markers of neutrophil and monocyte activation respectively, plasma levels of elastase-alpha 1-AT and TNF alpha were found to increase in a dose-dependent manner. Elastase-alpha 1-AT was detected early, with most release occurring between 15-30 min whereas TNF alpha was detected later, between 120-180 min. Dexamethasone, prostacyclin and pentoxifylline caused a dose-dependent inhibition of TNF alpha release but had no effect on elastase release. HA-1A had no effect on either TNF alpha or elastase release. This model may be useful in determining the sequence of inflammatory cell activation and in selecting candidate anti-inflammatory agents for evaluation in clinical trials.
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PMID:Assessment of the effect of candidate anti-inflammatory treatments on the interaction between meningococci and inflammatory cells in vitro in a whole blood model. 901 41

The objective of our study was to examine the changes in coagulation parameters and inflammatory reaction over the course of 15 days in patients with severe sepsis. We tried to identify mechanisms by which sepsis-induced pathophysiological changes may influence the effectiveness of subcutaneously (SC) administered enoxaparin 40 mg once daily. A total of 16 patients (8 men, 8 women; age 35-83 years) meeting the inclusion criteria of severe sepsis were enrolled in this study. The follow-up was performed on days 1, 2, 3, 6, 9, 12, and 15 of hospitalization at the intensive care unit (ICU). Blood coagulation (activated partial thromboplastin time [aPTT], prothrombin time [PT], fibrinogen, antithrombin (AT), protein C [PC], D-dimer, fragment 1.2 [F1.2], factor Xa [FXa] inhibition) and inflammatory reactants (interleukin 6 [IL-6], C-reactive protein [CRP], orosomucoid, alpha-1-antitrypsin) were tested. The mean FXa inhibition was 0.17 (+ or - 0.17) IU/mL. The arbitrarily established range of FXa inhibition for prophylaxis, 0.2 to 0.4 IU/mL, was reached in 22 cases (20%), while in 74 cases (68%), it was below and in 13 cases (12%) above the aforementioned range. Factor Xa inhibition positively correlated with AT (r = .42; P < .001) and PC (r = .45; P < .001) activities. A negative correlation was found between the FXa inhibition and alpha-1-antitrypsin concentrations (r = -.33; P = .01) but only in the subgroup with alpha-1-antitrypsin concentrations > or = 2.2 g/L. We confirmed that in most patients with sepsis, the prophylaxis with enoxaparin did not lead to the required FXa inhibition. The inhibition of FXa by enoxaparin depends mainly on the AT and PC activities.
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PMID:FXa inhibition and coagulation changes during DVT prophylaxis by enoxaparin over the course of a 15-day follow-up in septic patients. 1985 May 87

Platelet dysfunction and thrombocytopenia are common responses to sepsis, but how sepsis changes platelet function is not completely understood. This is due, in part, to our lack of understanding of how sepsis alters platelet protein patterns. The aim of the present study, accordingly, was to investigate the response of the platelet proteome to sepsis. We applied proteomic technology to analyze platelet samples of rats with sepsis. Rats were divided into two groups: 1) sham surgery and 2) sepsis induced by cecal ligation and puncture (CLP) surgery. Platelet samples were collected from surviving rats 12 and 24h after surgery, and platelet proteins were separated by two-dimensional electrophoresis (2-DE). Differentially expressed proteins were identified by mass spectrometry (MS). In the CLP group, there were 20 spots that were statistically significantly different at 12h. Of these spots, 16 spots were increased and four spots were decreased. At 24h, there were six spots increased in the CLP group. Of the 26 spots, 12 proteins associated with platelet activation, acute phase proteins, cytoskeleton structure, and energy production were identified. Of interest, alpha-1-antitrypsin precursor (AAT) and ATP synthase beta subunit (ATPB) were both increased at 12 and 24h of sepsis by 2-DE and immunoblotting. By providing the platelet profiles, our results demonstrate that this proteomic approach brings us closer to understanding how platelet dysfunction develops after sepsis.
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PMID:Altered proteomic pattern in platelets of rats with sepsis. 2201

Plasma protein therapies (PPTs) are a group of essential medicines extracted from human plasma through processes of industrial scale fractionation. They are used primarily to treat a number of rare, chronic disorders ensuing from inherited or acquired deficiencies of a number of physiologically essential proteins. These disorders include hemophilia A and B, different immunodeficiencies and alpha 1-antitrypsin deficiency. In addition, acute blood loss, burns and sepsis are treated by PPTs. Hence, a population of vulnerable and very sick individuals is dependent on these products. In addition, the continued well-being of large sections of the community, including pregnant women and their children, travelers and workers exposed to infectious risk is also subject to the availability of these therapies. Their manufacture to adequate amounts requires large volumes of human plasma as the starting material of a complex purification process. Mainstream blood transfusion services run primarily by the not-for-profit sector have attempted to provide this plasma through the separation of blood donations, but have failed to provide sufficient amounts to meet the clinical demand. The collection of plasma from donors willing to commit to the process of plasmapheresis, which is not only time consuming but requires a long term, continuing commitment, generates much higher amounts of plasma and has been an activity historically separate from the blood transfusion sector and run by commercial companies. These companies now supply two-thirds of the growing global need for these therapies, while the mainstream government-run blood sector continues to supply a shrinking proportion. The private sector plasmapheresis activity which provides the bulk of treatment products has been compensating the donors in order to recognize the time and effort required. Recent activities have reignited the debate regarding the ethical and medical aspects of such compensation. In this work, we review the landscape; assess the contributions made by the compensated and non-compensated sectors and synthesize the outcomes on the relevant patient communities of perturbing the current paradigm of compensated plasma donation. We conclude that the current era of "Patient Centeredness" in health care demands the continuation and extension of paid plasma donation.
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PMID:The Ethics of Paid Plasma Donation: A Plea for Patient Centeredness. 2523 54

Sepsis is defined as the systemic inflammatory response to infection and is one of the leading causes of mortality in critically ill patients. The goal of the present study is to elucidate the molecular mechanism of sepsis. Transcription profile data (GSE12624) were downloaded that had a total of 70 samples (36 sepsis samples and 34 non-sepsis samples) from the Gene Expression Omnibus database. Protein-protein interaction network analysis was conducted in order to comprehensively understand the interactions of genes in all samples. Hierarchical clustering and analysis of covariance (ANCOVA) global test were performed to identify the differentially expressed clusters in the networks, followed by function and pathway enrichment analyses. Finally, a support vector machine (SVM) was performed to classify the clusters, and 10-fold cross-validation method was performed to evaluate the classification results. A total of 7,672 genes were obtained after preprocessing of the mRNA expression profile data. The PPI network of genes under sepsis and non-sepsis status collected 1,996/2,147 genes and 2,645/2,783 interactions. Moreover, following the ANCOVA global test (P<0.05), 24 differentially expressed clusters with 12 clusters in septic and 12 clusters in non-septic samples were identified. Finally, 207 biomarker genes, including CDC42, CSF3R, GCA, HMGB2, RHOG, SERPINB1, TYROBP SERPINA1, FCER1 G and S100P in the top six clusters, were collected using the SVM method. The SERPINA1, FCER1 G and S100P genes are thought to be potential biomarkers. Furthermore, Gene oncology terms, including the intracellular signaling cascade, regulation of programmed cell death, regulation of cell death, regulation of apoptosis and leukocyte activation may participate in sepsis.
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PMID:Identification of potential biomarkers of sepsis using bioinformatics analysis. 2856 54


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