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Multiplexed sequencing relies on specific sample labels, the barcodes, to tag DNA fragments belonging to different samples and to separate the output of the sequencers. However, the barcodes are often corrupted by insertion, deletion and substitution errors introduced during sequencing, which may lead to sample misassignment. In this paper, we propose a barcode construction method, which combines a block error-correction code with a predetermined pseudorandom sequence to generate a base sequence for labeling different samples. Furthermore, to identify the corrupted barcodes for assigning reads to their respective samples, we present a soft decision identification method that consists of inner decoding and outer decoding. The inner decoder establishes the hidden Markov model (HMM) for base insertion/deletion estimation with the pseudorandom sequence, and adapts the forward-backward (FB) algorithm to output the soft information of each bit in the block code. The outer decoder performs soft decision decoding using the soft information to effectively correct multiple errors in the barcodes. Simulation results show that the proposed methods are highly robust to high error rates of insertions, deletions and substitutions in the barcodes. In addition, compared with the inner decoding algorithm of the barcodes based on watermarks, the proposed inner decoding algorithm can greatly reduce the decoding complexity.

Tungsten disulfide monolayers have attracted extensive attention in nanoelectronics and optoelectronics applications due to their remarkable electronic and optical properties. High-quality WS2 monolayers with a scalable size and uniform thickness can be synthesized by a chemical vapor deposition method (CVD). However, they commonly contain intrinsic structural defects and different populations of charge carriers, which are responsible for different contributions of excitons, trions, and biexcitons to their photoluminescence (PL) emission. Here, we adopt sodium sulphide (Na2S) solution to chemically treat CVD-grown WS2 monolayers by a simple immersing method. The results show that WS2 monolayers have a significantly enhanced PL emission by a factor of 25-fold and an obvious red-shift of the PL wavelength, resulting from the different excitonic states induced by effective n-type doping after Na2S treatment. This work provides a simple but promising chemical doping route to significantly improve the optical properties of WS2 monolayers and paves the way for the realization of practical WS2 monolayer based optoelectronic applications.

Growing evidence has indicated that single-stranded DNA-binding proteins 1 ( SSBP1 ) is involved in tumor initiation and progression. However, effects of single nucleotide polymorphisms (SNPs) in SSBP1 gene on gastric cancer (GC) prognosis are still unknown. In present study, two functional SNPs from SSBP1 were selected and genotyped in a large cohorts of 1030 resected GC patients (326 in the training set, 704 in the validation set) to explore the association of SNPs with patients' survival. The rs6976500 G allele (CG/GG) genotypes were found significantly associated with both worse overall survival (OS) and recurrence-free survival (RFS) in the training and the independent validation set when compared to C allele genotype, which reaching a more robust statistical significance in the pooled analysis. Furthermore, integration of rs6976500 genotypes and TNM stage significantly improved the prognosis prediction models based on TNM stage alone. In addition, only carriers with at least one G allele of rs6976500 gained significant survival benefit from FOLFOX-based ACT. Mechanistically, SNP rs6976500 G allele genotype could significantly decrease promoter transcriptional activity and markedly reduce expression level of SSBP1 compared with the C allele genotype in GC cells. This was further substantiated by immunohistochemical assay in 70 GC tissue samples. Our study presents the first evidence that SNP rs6976500 G allele genotypes might contribute to GC prognosis by attenuating SSBP1 promoter activity and gene expression, and provides the guidance in refining therapeutic decisions of GC patients. Further exploration on its function is needed to clarify the exact biological mechanism behind., Competing Interests: CONFLICTS OF INTEREST The authors have no conflicts of interest to declose.

Objective: To evaluate effect of telephone follow-up combined with written instruction on compliance and Helicobacter pylori (H. pylori) eradication in patients with H. pylori infection.
 Methods: A total of 160 H. pylori positive patients were randomly divided into an experimental group and a control group (n=80 in each group). All the patients got the guide instruction named "the guidance of clinical medication for H. pylori infection patients" before the treatment. The patients in the experimental group were added individualized follow-up with telephone. The compliance, eradication of H. pylori, adverse events, and satisfaction were compared between the 2 groups.
 Results: The eradication rate of H. pylori in the perprotocol analysis for the experimental group and control group were 64.4% (47/73) and 56.5%(35/62), respectively (P=0.380), while in the intention-to-treat analysis, the rates were 58.8% (47/80) and 43.8% (35/80, P=0.082), respectively. The compliance rate in the experimental group was significantly higher than that in the control group (91.3% vs 77.5%, P<0.05). There was significant difference in patients' satisfaction in good ones (75.3% vs 51.6%) and poor ones (5.5% vs 21.0%) between the 2 groups (P<0.05). There were 11 patients in the experimental group and 36 patients in the control group, who appeared adverse reactions such as nausea, bad breath, abdominal distention, poor appetite, and defecation habit change during the process of eradicating H. pylori, but the occurrence rate in the experimental group was obviously lower than that in the control group (15.1% vs 58.1%, P<0.05).
 Conclusion: The telephone follow-up cannot increase the H. pylori eradication rate, but it can improve compliance and satisfaction for the patients and relieve adverse effects.

Background: This research is dedicated to investigating the effects and potential mechanism of action of the aryl hydrocarbon receptor on the intestinal mucosal immune system in dextran sulfate sodium (DSS)-induced colitis., Methods: Colitis was induced by the administration of 3% DSS to wild-type C57BL/6J mice for 7days. 6-formylindolo(3, 2-b)carbazole (FICZ), an endogenous agonist of the aryl hydrocarbon receptor (AhR), was given intraperitoneally on a daily basis beginning 2days after the start of DSS administration. The mice were weighed and assessed, and colon tissues were measured. Intraepithelial lymphocytes (IELs) were isolated from the colon and examined by flow cytometry and quantitative real-time PCR., Results: FICZ ameliorated DSS-induced colitis, resulting in a reduced disease activity index and improvement in the histology and length of the colon. Colitis reduced the percentage and number of CD8αα + TCRαβ + IELs. FICZ prevented the reduction in the numbers of CD8αα + TCRαβ + IELs by upregulating the expression of the IL-15 receptor and the aryl hydrocarbon receptor (AhR), and attenuating the apoptotic rate of CD8αα + TCRαβ + IELs. Finally, IL-10 was increased and IFN-γ was decreased in CD8αα + TCRαβ + IELs by FICZ administration in DSS-induced colitis., Conclusions: The results suggest that AhR activation ameliorated DSS-induced acute colitis, in a manner that is associated with the local expansion and functions of CD8αα + TCRαβ + IELs in acute colitis. The findings indicate that AhR-related ligands might be targeted as novel drug targets for IBD., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Objective: To investigate the role of the PI3K/Akt signaling pathway in hydrogen sulfide-induced alterations in expression of collagen I and collagen III in hepatic stellate cells., Methods: In vitro cultured rat hepatic stellate cells (HSC-T6) were treated with hydrogen sulfide, or left untreated for use as controls, and divided into groups for treatment with different inhibitors for the various factors involved in the PI3K/Akt signaling pathway. Reverse transcription-PCR was used to measure Collagen I and collagen III mRNA expression. Western blotting was used to detect the protein expression of PI3K and p-Akt, which are upstream proteins of the PI3K/Akt pathway., Results: Compared with the untreated control cells, the hydrogen sulfide treated cells showed elevated expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F =14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt (F =23.522, P less than 0.05). Compared to the cells treated with hydrogen sulfide alone, the cells treated with the various inhibitors showed lower expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F=14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt protein (F =23.522, P less than 0.05)., Conclusion: Hydrogen sulfide can activate the PI3K/Akt pathway and elevate the expression of collagen I and collagen III in rat hepatic stellate cells.

Background: Esophageal squamous cell carcinoma (ESCC) incidence is high in Kazak Autonomous Prefecture, Xinjiang, China. Roasting food has been reported to be related with the risk of various cancers and is very popular in the area, and may be related with the risk of ESCC. The promoter methylation inactivation of p16 gene can increase the risk of ESCC. Thus, we want to know whether long-term roasting food is related with the risk of ESCC by effecting the promoter methylation of p16 gene., Materials and Methods: Ninety ESCC patients and 60 healthy subjects were recruited from Kazak Autonomous Prefecture. MassARRAY was used to detect p16 promoter methylation in ESCC tissues, as well as in normal esophageal tissues. The association between the p16 promoter methylation and daily roasting meat intake was examined., Results: Daily roasting meat intake was related with the risk of ESCC (p<0.01) and the mean CpG methylation rates of p16 promoter (p<0.01). In ESCC patients, the mean methylation rates of CpG 11-12 and CpG 33-34-35 were 29.4% and 37.4%, respectively, which was significantly higher than the rates in normal esophageal tissues (16.7% and 12.4%, respectively; p<0.01). The methylation of p16 promoter is also related with daily roasting meat intake (p<0.01) in Kazakh Chinese with ESCC. For the CpG methylation of the p16 promoter in the well, moderately and poorly differentiated ESCC, there are significant differences (p<0.05) for the 19 CpG units in the ESCC and controls., Conclusion: Roasting meat intake was associated with the risk of ESCC via effects on the methylation of p16 promoter. These results suggest roasting food intake should be limited in the diet.