Objective To explore the association of C20orf54 gene rs3746804 position single nucleotide polymorphism and susceptibility to esophageal squamous cell carcinoma (ESCC).Methods Purification of genomic DNA from whole blood was used the Maxwell(R) 16 System.rs3746804 in C20ort54 was detected by direct sequencing in 434 ESCC patients from Changzhi (Shanxi province) and Linzhou (Henan province) and 554 healthy controls from Changzhi,Linzhou and including immigrators from Linzhou to Changzhi.Results For rs3746804,the genotypic frequencies of CT(37.5％ vs 51.0％,37.5％ vs 52.0％),CC (44.2％ vs 34.8％,44.2％ vs 33.0％) in Changzhi ESCC patients showed significant differences with healthy Changzhi controls and the healthy immigrator controls (all P ＜ 0.05),and the frequencies of TT(18.3％ vs 4.1％) and CC (44.2％ vs 54.6％) in Changzhi ESCC patients showed significant differences with Linzhou ESCC patients (all P ＜0.05).The genotypic frequencies of TT (4.1％ vs 15.0％),CT (41.2％ vs 52.0％) and CC(54.6％ vs 33.0％) showed significant differences between Linzhou ESCC patients and the healthy immigrator controls (all P ＜ 0.05),and the frequencies of TT (4.1％ vs 14.1％) and CC (54.6％ vs 34.8％) showed significant differences between Linzhou ESCC patients and Changzhi healthy controls (all P ＜ 0.01).Meanwhile,there were significant differences between ESCC patients (including Changzhi and Linzhou ESCC patients) and healthy controls (including the healthy Changzhi,Linzhou and immigrator controls) in genotypic frequencies of CT(39.2％ vs 48.7％) and CC (48.8％ vs 38.2％) (all P ＜ 0.01).CT and CT + TT genotype could decrease the risk of ESCC compared with the CC genotype (OR =0.630,95％ CI0.481-0.826 ; OR =0.654,95％ CI 0.507-0.844).Conclusion There is a closed relationship between SNP rs3746804 in C20orf54 and susceptibility to ESCC.

ObjectiveTo study the relationship between plasma riboflavin levels and esophageal squamous cell carcinoma.Methods We detected and compared plasma concentrations of riboflavin in patients with esophageal squamous cell carcinoma (ESCC) and immigrants of Linzhou living in Changzhi.Plasma riboflavin levels were quantified in 445 ESCC patients,689 healthy control subjects and 347 immigrants of Linzhou living in Changzhi by using enzyme-linked immunosorbent assay.ResultsThe plasma riboflavin levels in patients with ESCC were significantly lower than those in the healthy controls and immigrants of Linzhou living in Changzhi [ (731.69 ± 330.67 ) μg/L vs ( 1090.43 ± 445.08 ) μg/L,(731.69 ± 330.67) μg/L vs ( 897.58 ± 177.78) μg/L,respectively,all P ＜ 0.05 ],and the plasma riboflavin levels of the healthy controls were higher than those in the immigrants of Linzhou living in Changzhi (P ＜ 0.05).ConclusionPatients with ESCC have decreased plasma riboflavin levels as compared with the healthy controls and immigrants of Linzhou living in Changzhi,there exists a lack of riboflavin in ESCC patients,but the specific mechanism needs further study.

Male infertility is a multifactorial disease, of which the cause of male infertility cannot be determined, which is called idiopathic male infertility, and the incidence rate is gradually rising. Because its cause is unknown, it has become a major problem in the department of reproductive endocrinology. With the in-depth study of epigenetics, the diagnosis and treatment of idiopathic male infertility also has a new direction, especially the important role of DNA methylation in spermatogenesis and embryonic development. More and more gene fragments and loci have been found by scholars, which makes it possible to achieve accurate identification and targeted treatment. This article reviews and summarizes the research progress of DNA methylation related to idiopathic male infertility in recent years, aiming to further elaborate the pathogenesis of idiopathic male infertility and provide new ideas for clinical diagnosis and treatment.

Bacterial endotoxin is considered as one of the critical risk factors in medical devices, especially implanted devices that directly or indirectly contact with blood circulating system. In that case, endotoxin limits for implanted medical devices is important in determine the safety of medical devices. According to GB/T 14233.2-2005, the requirements of endotoxin index for intrathoracic medical devices is 2.15 EU per device. However, the definition of "intrathoracic medical devices" is vague. Specifically, "for cardiovascular system application" instead of "intrathoracic application" is more reasonable. With the deeper understanding of the risk of endotoxin in medical devices and considering the internationally accepted standards, the limits of endotoxin in medical devices for cardiovascular system application is acceptable at 20 EU per device.
Endotoxins

Objective To investigate the effect and mechanism of astragaloside Ⅳ(AS-Ⅳ) activating ROCK/JNK to regulate autophagy in improving isoproterenol (ISO) induced myocardial fibrosis (MF) in mice. Methods The mice were randomly divided into control operation group (Control group), ISO induced myocardial fibrosis group (MF group), AS-Ⅳ treatment group (AS-Ⅳ group) and combination group of astragaloside IV and Y-33075 (ROCK inhibitor) (astragaloside IV+Y-33075 group). After repeated administration for 30 days. The serum levels of LDH, BNP, CTGF in each group were detected. The cardiac function was detected by ultrasound. Myocardial structure and tissue fibrosis degree in each group were detected by Sirius Red and Masson staining. Oxidative stress (ROS) levels in myocardial tissue of each group were detected by DHE staining and the expression of ROCK, JNK, Atg5, Beclin 1, and LC3 Ⅰ/Ⅱ in myocardial tissue were detected by Western blotting. Results Compared with AS-Ⅳ group, the EF value of AS-Ⅳ+Y-33075 group decreased and the degree of myocardial fibrosis increased (P<0.05). The serum level of LDH, BNP, CTGF increased and the level of ROS in myocardial tissue increased while the expression of ROCK, JNK, Atg5, Beclin 1, LC3 Ⅰ/Ⅱ decreased (P<0.05). Y-33075 could block the protective effect of AS-Ⅳ on myocardial injury induced by MF and inhibit the regulation of AS-Ⅳ on ROCK and JNK. Conclusion AS-Ⅳ could attenuate myocardial fibrosis in mice by activating ROCK/JNK signal and promoting autophagy.