Presepsin did not outperform traditional sepsis biomarkers in diagnosing sepsis from SIRS and in prognostication of mortality in critically ill patients. Presepsin may have a limited adjunct value for both diagnosis and an early risk stratification, performing independently of clinical illness severity.
The polydactylous rat strain (PD/Cub) is a highly inbred (F Ͼ 90) genetic model of metabolic syndrome. The aim of this study was to analyze the genetic architecture of the metabolic derangements found in the PD/Cub strain and to assess its dynamics in time and in response to diet and medication. We derived a PD/Cub ϫ BN/Cub (Brown Norway) F2 intercross population of 149 male rats and performed metabolic profiling and genotyping and multiple levels of genetic linkage and statistical analyses at five different stages of ontogenesis and after high-sucrose diet feeding and dexamethasone administration challenges. The interval mapping analysis of 83 metabolic and morphometric traits revealed over 50 regions genomewide with significant or suggestive linkage to one or more of the traits in the segregating PD/Cub ϫ BN/Cub population. The multiple interval mapping showed that, in addition to "single" quantitative train loci, there are more than 30 pairs of loci across the whole genome significantly influencing the variation of particular traits in an epistatic fashion. This study represents the first whole genome analysis of metabolic syndrome in the PD/Cub model and reveals several new loci previously not connected to the genetics of insulin resistance and dyslipidemia. In addition, it attempts to present the concept of "dynamic genetic architecture" of metabolic syndrome attributes, evidenced by shifts in the genetic determination of syndrome features during ontogenesis and during adaptation to the dietary and pharmacological influences.quantitative trait loci; pharmacogenetics; nutrigenetics; triglyceride; insulin resistance; obesity METABOLIC SYNDROME is a complex condition arising from an intricate network of interacting genetic and environmental factors. The dynamics of the increase in its worldwide prevalence qualify the syndrome as a major healthcare issue for years to come. The syndrome comprises several clinical features, each representing a complex trait of its kind, i.e., hypertriglyceridemia, hyperinsulinemia, insulin resistance, obesity, and hypertension (11,36). It is therefore self evident that detailed analysis of the genetic determinants underlying such metabolic clustering is rather complicated in the general human population and only somewhat more feasible in particular circumstances, e.g., in population isolates (32). Although some progress has been made and several studies succeeded in identification of genes potentially involved in the pathogenesis of metabolic syndrome (13,17,35,51), its genetic determination is far from being fully understood.As in other complex diseases, defined animal models of metabolic syndrome are proving to be important tools for deciphering the causative genes and gene-gene and geneenvironment interactions (8). There are numerous rodent strains expressing all or a subset of metabolic syndrome attributes found in humans [e.g., Otsuka Long-Evans Tokushima Fatty rat (16), Goto-Kakizaki rat (10), hereditary hypertriglyceridemic rat (53, 54), and spontaneously hypertensive rat ...
Background/Aims: The determination of neuron-specific enolase (NSE) is relatively frequently requested in the differential diagnosis of small-cell lung carcinoma and non-small-cell lung carcinoma. The individual results of different immunoassays are often not comparable, which has been confirmed by long-term external quality assessments. In this study, we assessed the possible sources of these differences. Methods: More than 3,000 NSE analyses were performed using seven different immunoassays: DELFIA (PerkinElmer), Elecsys 2010 or Modular Analytics E 170 (Roche), Kryptor (B.R.A.H.M.S.), the enzyme-linked immunosorbent assay DRG and three assays based on immunoradiometric assays (DiaSorin, Immunotech and Schering-CIS). The following parameters were evaluated: precision profile of the individual methods, linearity on dilution and modified recovery, comparability and discrimination of immunoassays, sensitivity, and specificity. Results: There were differences in the correlation of values of certain low-concentration specimens. Some assays correlate well while others do not (up to fivefold difference), especially in the case of controls prepared synthetically. Therefore, the current non-standardized preparation of controls is questionable in our opinion. In the cutoff range, the difference in the results of native samples did not exceed its double value. The variation in values >100 µg/l obtained with different assays is <40%. Conclusion: Our results confirmed expected matrix interferences especially in the range of normal and cutoff NSE concentrations. Another source of discrepancies can be attributed to different antibody affinity to αγ- and γγ-enolase isoenzymes. Finally, improper settings of cutoff values also contribute to the different discrimination of the methods.
Our findings suggest a more complex relationship among advanced glycation, oxidative stress and metabolism of ethanol and their link to nutrition and nutrition-associated parameters. AGE as a result of oxidative stress might be similarly linked to increased cardiovascular risk of heavy alcohol drinkers, as are malnutrition and inflammation; however, further studies are needed to confirm this hypothesis.
We have previously shown that interferon-gamma (IFN-gamma) inhibits expression of the metastasis-promoting protein S100A4. In the present study, we further explore the mechanism behind the IFN-gamma-mediated effects on the human S100A4 promoter and demonstrate that IFN-gamma represses S100A4 promoter activity through induction of the class II transactivator (CIITA). The acidic domain in the N-terminal part of CIITA was crucial for the observed IFN-gamma-induced inhibition of S100A4 promoter activity, probably by binding the histone acetyltransferase CBP/p300. Importantly, overexpression of CIITA significantly reduced the expression of endogenous S100A4. Our data suggest a model where CIITA represses S100A4 transcription through sequestering of CBP/p300, thereby reducing the level of CBP/p300 at the S100A4 promoter, which in turn leads to inhibition of S100A4 transcription.
Background & Aims: Severity of portal hypertension is usually quantified by measuring the hepatic venous pressure gradient (HVPG). However, due to its invasiveness, alternative markers are being sought. Bile acids (BA), being synthesized, metabolized, and transported by the liver, seem to have the potential to serve as endogenous markers. The aim of the present study was to determine whether serum BA reflect the severity of portal hypertension. Methods:We correlated serum concentrations of individual BA with portal pressure (as HVPG) in an exploratory cohort of 21 cirrhotic patients with portal hypertension.The predictive potential of selected candidates was then confirmed in an independent validation cohort (n = 214). Additionally, nine previously published noninvasive markers were added to the stepwise logistic regression model to identify the most relevant ones, which were eventually used to create a prognostic index of portal hypertension.Results: Serum levels of taurochenodeoxycholic acid (TCDCA) significantly correlated with HVPG and showed a high potential to predict clinically significant portal hypertension (HVPG ≥ 10 mm Hg: AUROC = 0.97 ± 0.06). This was confirmed in the validation cohort (AUROC = 0.96 ± 0.01). The predictive index (constructed based on AST/ ALT, spleen diameter, and TCDCA concentration) was able to distinguish clinically significant portal hypertension with 95% sensitivity and 76% specificity.Conclusions: TCDCA seems to be a promising noninvasive marker of clinically significant portal hypertension. Its predictive potential may be further enhanced when it is combined with both the AST/ALT ratio and spleen diameter.
Introduction: The aim of the study is to assess the degree of adherence of medical laboratories to Kidney Disease Improving Global Outcomes (KDIGO) 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease (CKD) in laboratory practice in Czechia and Slovakia. Materials and methods: An electronic questionnaire on adherence to KDIGO 2012 guideline was designed by an external quality assessment (EQA) provider SEKK spol. s.r.o. The questionnaire was placed and distributed through website to all medical biochemistry laboratories in Czechia and Slovakia (N = 396). Results: A total of 212 out of 396 laboratories responded to the questions, though some laboratories only answered some questions, those applicable to their practice. A total of 48 out of 212 laboratories adopted the KDIGO 2012 guideline in full extent. The metrological traceability of creatinine measurement to standard reference material of SRM 967 was declared by 180 out of 210 laboratories (two of the responding laboratories did not measure creatinine). Thirty laboratories are not well educated on traceability of creatinine measurement and seven laboratories do not calculate estimated glomerular filtration rate (eGFR). Both urinary albumin concentration and albumin to creatinine ratio are reported by 144 out of 175 laboratories (37 of the responding laboratories did not measure urinary albumin). Conclusion: Majority of laboratories in Czechia and Slovakia adopted some parts of the KDIGO 2012 guideline in their practice, but only 23% of the laboratories apply them completely. Thus, further education and action should be conducted to improve its implementation.
Elevated maternal serum concentration of sCD14-ST could be an independent and relevant risk factor for preterm delivery.
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