Continuous positive airway pressure (CPAP) is the standard treatment for obstructive sleep apnea syndrome (OSAS). However, the impact of CPAP on quality of life (QOL) is controversial. The aim of this study was to systematically review and determine whether CPAP improves QOL in patients with OSAS. We performed a comprehensive literature search to identify studies published between 1966 and 2007 comparing values of CPAP with control. Weighted mean difference (WMD) was used to analyze the data. The pooled WMD was calculated by using a fixed or random-effect model. The outcomes for 1,256 patients from 16 studies, of whom 656 patients underwent CPAP and 600 were controls, were included. CPAP led to significant improvements in the Nottingham health profile part 2 (WMD=1.657; 95% CI=3.005, -0.308; p=0.016), but there was no difference in other general QOL scores. Patients undergoing CPAP scored better in physical function (WMD=3.457; 95% CI=0.144, 6.771; p=0.041), body pain (WMD=4.017; 95% CI= -0.008, 8.042; p=0.05), energy vitality (WMD=6.984; 95% CI = 0.557, 13.411; p=0.033) and physical component summary (PCS) (WMD=2.040; 95% CI=0.045, 4.035; p=0.045) using the SF-36 tool. This meta-analysis shows that CPAP does not improve general QOL scores but does improve physical domains and vitality. Study design and QOL questionnaire tools are important to capture and evaluate information efficiently. However, generic QOL instruments may not be adequate in detecting important changes in quality of life in patients with OSAS.

No abstract

sTREM-1 represents a reliable biological marker of bacterial infection, but it may be not a sufficient biological marker for infection of the urinary tract as a result of its low sensitivity. Whether sTREM-1 guidance can reduce antibiotic use as well as the measurement of sTREM-1 in different types of infection will require additional prospective studies.

No abstract

No abstract

No abstract

Dysregulation of circular RNA (circRNA) expression is involved in the progression of cancer. Here, we aimed to study the potential function of hsa_circ_0006401 in colorectal cancer (CRC). CircRNA hsa_circ_0006401 expression levels in CRC and adjacent nontumor tissues were analyzed by real-time quantitative PCR (qRT-PCR) and circRNA in situ hybridization (RNA-ISH). Then, CRC cell proliferation was assessed by cell counting. Wound-healing and transwell assays were utilized to detect the effect of hsa_circ_0006401 on CRC migration. A circRNA-ORF construct was created, and a specific antibody against the splice junction of hsa_circ_0006401 was prepared. Finally, the proteins directly binding to hsa_circ_0006401 peptides were identified by immunoprecipitation combined with mass spectrometry. In our study, we found hsa_circ_0006401 was closely related to CRC metastasis and exhibited upregulated expression in metastatic CRC tissue samples. Proliferation and migration were inhibited in vitro when hsa_circ_0006401 expression was silenced. Downregulation of hsa_circ_0006401 expression decreased CRC proliferation and liver metastasis in vivo. A 198-aa peptide was encoded by sequences of the splice junction absent from col6a3. Hsa_circ_0006401 promoted CRC proliferation and migration by encoding the hsa_circ_0006401 peptide. Hsa_circ_0006401 peptides decreased the mRNA and protein level of the host gene col6a3 by promoting col6a3 mRNA stabilation. In conclusion, our study revealed that circRNAs generated from col6a3 that contain an open-reading frame (ORF) encode a novel 198-aa functional peptide and hsa_circ_0006401 peptides promote stability of the host gene col6a3 mRNA to promote CRC proliferation and metastasis.

Background Helicobacter pylori is an important carcinogenic factor in gastric cancer. Studies have shown that Helicobacter pylori infection is inversely associated with certain diseases such as esophageal cancer and whose infection appears to have a “protective effect.” At present, the relationship between Helicobacter pylori infection and esophageal cancer remains controversial. This study was designed to investigate the relationship between Helicobacter pylori infection and the risk of esophageal cancer in different regions and ethnicities. Methods Systematic search of the articles on the relationship between Helicobacter pylori infection and esophageal cancer from the database with the duration time up to December 2018. This systematic review was performed under the MOOSE guidelines. Results This meta-analysis included 35 studies with 345,886 patients enrolled. There was no significant correlation between Helicobacter pylori infection and esophageal squamous cell carcinoma in the general population (OR: 0.84; 95% CI: 0.64-1.09/OR: 0.74; 95% CI: 0.54-0.97). However, a significant correlation was found in the Middle East (OR: 0.34; 95% CI: 0.22-0.52/95% CI: 0.26-0.44). There was no significant difference in the prevalence of Helicobacter pylori between the case group and the control group in esophageal adenocarcinoma (8.87% vs. 9.67%). The pooled OR was 0.55 (95% CI: 0.43-0.70) or 0.23 (95% CI: 0.15-0.36). When grouped by match or not, the pooled OR of the nonmatching group and the matching group was 0.48/0.21 (95% CI: 0.36-0.65/95% CI: 0.13-0.36) and 0.73/0.71 (95% CI: 0.57-0.92/95% CI: 0.60-0.84), respectively. Conclusion In the general populations, no significant association was found between Helicobacter pylori infection and the risk of esophageal squamous cell carcinoma. However, lower risk was found in the Middle East. Helicobacter pylori infection may reduce the risk of esophageal adenocarcinoma, but such “protection effect” may be overestimated.