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Aldo‐keto reductase family 1 member B10 (AKR1B10) is a secretory protein overexpressed in hepatocellular carcinoma (HCC). We aimed to evaluate AKR1B10 as a serum marker for detection of HCC. Herein, we conducted a cohort study that consecutively enrolled 1,244 participants from three independent hospitals, including HCC, healthy controls (HCs), benign liver tumors (BLTs), chronic hepatitis B (CHB), and liver cirrhosis (LC). Serum AKR1B10 was tested by time‐resolved fluorescent assays. Data were plotted for receiver operating characteristic (ROC) curve analyses. Alpha‐fetoprotein (AFP) was analyzed for comparison. An exploratory discovery cohort demonstrated that serum AKR1B10 increased in patients with HCC (1,567.3 ± 292.6 pg/mL; n = 69) compared with HCs (85.7 ± 10.9 pg/mL; n = 66; P < 0.0001). A training cohort of 519 participants yielded an optimal diagnostic cutoff of serum AKR1B10 at 267.9 pg/mL. When ROC curve was plotted for HCC versus all controls (HC + BLT + CHB + LC), serum AKR1B10 had diagnostic parameters of the area under the curve (AUC) 0.896, sensitivity 72.7%, and specificity 95.7%, which were better than AFP with AUC 0.816, sensitivity 65.1%, and specificity 88.9%. Impressively, AKR1B10 showed promising diagnostic potential in early‐stage HCC and AFP‐negative HCC. Combination of AKR1B10 with AFP increased diagnostic accuracy for HCC compared with AKR1B10 or AFP alone. A validation cohort of 522 participants confirmed these findings. An independent cohort of 68 patients with HCC who were followed up showed that serum AKR1B10 dramatically decreased 1 day after operation and was nearly back to normal 3 days after operation. Conclusion: AKR1B10 is a potent serum marker for detection of HCC and early‐stage HCC, with better diagnostic performance than AFP.

Background: It is well-known that altered hypothalamus-pituitary-adrenal (HPA) axis process has an important role in the neurodegenerative process in schizophrenia (SZ). However, this neurodegenerative mechanism has not been clarified in SZ. Therefore, the main purpose of this study was to determine HPA axis damage in the first-episode, unmedicated schizophrenia (FES) patients and chronic schizophrenia (CSZ) patients in comparison with healthy controls (HC) by means of quantitative analysis of the peripheral blood mRNA expression of glucocorticoid receptor (GR), GR transcripts containing exons 1B (GR-1B) and neuron specific enolase (NSE) genes and serum cortisol and NSE, a specific serum marker for neuronal damage. Methods: In the present study, 43 FES patients, 39 CSZ and 47 HC were included. The peripheral blood mRNA expressions for GR, GR 1B and NSE genes were determined by real-time quantitative polymerase chain reaction (RT-qPCR). Serum cortisol and NSE were analyzed by electrochemiluminescence immunoassay technique. Results: Levels of GR mRNA were significantly lower in FES and CSZ than that in HC. The expression of GR-1B mRNA was significantly decreased in CSZ when compared with that in HC. Levels of NSE mRNA were significantly lower in CSZ than that in FES patients or HC patients. CSZ patients showed significantly lower cortisol concentrations than FES and HC patients. FES patients showed significantly higher NSE concentrations than CSZ and HS. Conclusion: Our findings support that there is disrupted HPA axis system in the SZ, and suggest that CSZ patients suffer a greater HPA axis damage than FES patients. Meanwhile, our research implicated underlying GR mRNA dysregulation in SZ and the potential importance of the functional GR-1B transcription in CSZ.

Background Six Sigma methodology with a zero‐defect goal has long been applied in commercial settings and was utilized in this study to assure/improve the quality of various analytes. Methods Daily internal quality control (QC) and external quality assessment data were collected and analyzed by calculating the sigma (σ) values for 19 analytes based on the coefficient of variation, bias, and total error allowable. Standardized QC sigma charts were established with these parameters. Quality goal index (QGI) analysis and root cause analysis (RCA) were used to discover potential problems for the analytes. Results Five analytes with σ ≥ 6 achieved world‐class performance, and only the Westgard rule (13s) with one control measurement at two QC material levels (N2) per QC event and a run size of 1000 patient samples between QC events (R1000) was needed for QC. In contrast, more control rules (22s/R4s/41s) along with high N values and low R values were needed for quality assurance for five analytes with 4 ≤ σ

Schizophrenia (SZ) is a debilitating and heterogeneous disease. We hypothesized that the oxytocin (OXT) system, inflammation and one-carbon metabolism would have a link with SZ. In this study, serum OXT, OXT receptor (OXTR), interleukin-6 (IL-6), high sensitivity CRP (hsCRP) and homocysteine (Hcy) levels were measured in 52 first-episode schizophrenia (FES) patients and 41 healthy controls (HC) from the Second Xiangya Hospital of Central South University. Meanwhile, the mRNA expressions of OXT and OXTR genes were determined by real-time quantitative PCR. Serum OXT and OXTR levels were significantly lower in FES patients (518.96 ± 22.22 and 174.60 ± 17.11 pg/ml) than the HC group (711.58 ± 40.57 and 252.15 ± 20.62 pg/ml). Serum IL-6 and hsCRP levels showed no difference between the two groups (1.82 ± 0.30 vs. 1.69 ± 0.36 pg/ml, 0.66 (0.22, 1.07) vs. 0.31 (0.13, 0.91) mg/L), but serum Hcy levels were significantly higher in FES patients (20.18 ± 1.83 vs. 15.24 ± 0.82 μmol/ml). The FES patients (0.27 ± 0.02 and 0.20 ± 0.02) have relatively higher mRNA expressions of OXT and OXTR genes than the HC group (0.16 ± 0.01 and 0.14 ± 0.01). In summary, our results suggested the possible function of the OXT system and Hcy in the pathogenesis of SZ.

Systemic inflammatory response syndrome (SIRS) was considered to play an important role in the progress of acute pancreatitis, but its specific relation with infected pancreatic necrosis remains largely unclear. We aimed to investigate the correlation between SIRS duration and infected pancreatic necrosis, and its application in prediction of infected pancreatic necrosis. A prospective observational cohort study of 2130 patients with acute pancreatitis from 2012 to 2017. The SIRS duration at the first week was registered daily, and demographic, radiology, and all clinical laboratory data were prospectively collected and retrospectively reviewed. A significant upward tendency of infected pancreatic necrosis incidence was observed with increased SIRS duration. In multivariate logistic regression, SIRS duration (odds ratio, 1.305; 95% CI, 1.161–1.468) was independently associated with infected pancreatic necrosis. ROC analysis demonstrated that the areas under curves of SIRS duration for predicting persistent multi-organ failure, pancreatic infection, and mortality were 0.97 (95% CI, 0.96–0.98), 0.92 (95% CI, 0.91–0.94), and 0.86 (95% CI, 0.83–0.90), respectively, which were comparable to, or even greater than, the area under curves of APACHE II and CT severity index scores. Early SIRS duration was strongly associated with infected pancreatic necrosis and could serve as an easy bedside indicator to predict pancreatic infection.