Objective To investigate the correlation between helicobacter pylori (H.pylori) infection with gastric muco?sa pathologic changes in chronic gastritis. Methods A total of 250 patients with chronic gastritis who came to Tianjin Union Medicine Center from November 2011 to March 2013 were collected in this study. Electronic gastroscope examina?tions, pathology and Urea-14C breath tests were performed in patients. There were 153 cases with chronic atrophic gastritis (CAG group), and 97 cases without chronic atrophic gastritis (non-CAG group). The positive rate of H.pylori was compared between two groups. At the same time the positive rate of H.pylori was compared between different parts of CAG patients. The positive rates of H.pylori were compared between different pathologic features of chronic gastritis (active degree, the de?gree of inflammation, atrophy and intestinal classification). Results The positive rate of H.pylori was higher in CAG pa?tients than that of non-CAG patients (70.6%vs 35%,χ2=30.552). The positive rate of H.pylori was higher in antral and cor?pus atrophy of CAG group than that of antral atrophy (82.6%vs 65.4%,χ2=4.578). With the aggravating activity of gastritis, the inflammation, chronic gastritis, atrophy and intestinal classification, the positive rate of H.pylori was increased (χ2=200.643, 206.715, 73.286, 218.432). Conclusion H.pylori infection is related with chronic gastritis, chronic atrophic gas?tritis. And antral and corpus atrophy CAG is closely related with H.pylori infection.

Objective: To retrospectively analyze the potential correlation between cardiac magnetic resonance (CMR) imaging and clinical features and idiopathic arrhythmia in patients with straight back syndrome (SBS). Methods: Patients receiving CMR imaging examination from April 2015 to March 2016 at our department (n=1 432) were screened, 76 patients met the diagnosis criteria of flat chest (anteroposterior diameter/transthoracic diameter (APD/TTD) ratio<0.37 at the T8 vertebra). After excluding 33 patients with structural heart disease, 43 SBS patients were divided into two groups: SBS without obvious morphological change in the heart (group A, n=19) and SBS with morphological change of the heart (group B, n=24). CMR images were analyzed, focusing the heart morphological changes induced by SBS. The clinical data were collected to comprehensively analyze the medical history, electrocardiogram and electrophysiological examination in order to observe the relationship between SBS induced heart morphological change and the arrhythmia type and origin. Results: There were 21 male patients in this cohort, mean age was (28.5±11.5) years (13-58 years). APD/TTD ratio was similar between the two groups (0.30±0.03 vs. 0.29±0.04, P>0.05). LVEF tended to be lower in group B than in group A ((47.48±12.77)%vs. (59.31±9.04)%, P>0.05) . In group B, there were 15 patients with left ventricular enlargement, 2 with left ventricular wall thickening, 5 with uncoordinated ventricular wall motion, 5 with tricuspid regurgitation, 3 with mitral regurgitation, 2 with myocardial fibrosis, 5 with increased trabecular and 16 with decreased left ventricular function. Direct compression sign of right ventricle (disappeared precordial fat tissue space, secondary right atria enlargement and tricuspid regurgitation) and left atria (with or without secondary left ventricular enlargement and mitral regurgitation) were evidenced in patients of group B. CMR revealed that the arrhythmia origin corresponded the compression site of the heart in 8 cases (42.1%) in group A and 13 cases (54.2%) in group B, not corresponded to the compression site in 6 patients (31.6%) in group A and in 7 patients (29.2%) in group B, not attributable in 5 patients (26.3%) in group A and 4 patients (16.7%) in group B. The percent of arrhythmia origin corresponded the compression site of the heart tended to be higher in group B as compared to group A (P>0.05). Conclusion SBS can induce changes of cardiac morphology and cardiac function. SBS induced cardiac compression is linked with the development of arrhythmias and might be one of the reasons of arrhythmias in these patients.

Objective:To analyze the relationship between maternal mutations in basal core promoter region of hepatitis B virus (HBV) genotype C and intrauterine transmission.Methods:We collected information on general demographic characteristics and process of delivery among 399 pairs of consecutive HBsAg-positive mothers and their neonates, from the Third People’s Hospital of Taiyuan in Shanxi province, China. Fluorescence quantitative polymerase chain reaction (FQ-PCR) and Electro-chemiluminescence immuno-assay (ECLIA) kits were used to detect both maternal and neonatal HBV DNA and serological markers in the peripheral blood. From 113 mothers with HBV DNA load ≥10 6 IU/ml, we selected 22 mothers whose neonates were with intrauterine transmission and randomly selected the same number of mothers whose neonates were without intrauterine transmission, as controls. The whole-length HBV DNA were extracted, amplified, cloned, sequenced and genotyped. Finally, a total of 39 mothers with genotype C of HBV were selected for mutation analysis. Results:Thirty-nine cases of genotype C (88.63 %) were finally included in the study, with 19 cases in the intrauterine transmission group and 20 cases as controls. Rates of A1762T/G1764A double mutations were significantly different between the intrauterine transmission group and the control group (7.53 % vs. 27.72 %, P<0.001). Results from the multivariate analysis showed that the A1762T/G1764A double mutations had reduced the risk of intrauterine transmission (a OR=0.065, 95 %CI: 0.006-0.746, P=0.028). Maternal A1762T/G1764A double mutations appeared to be possibly associated with neonatal HBeAg ( P=0.050). Conclusion:A1762T/G1764A double mutations of HBV DNA from the genotype C of those HBsAg-positive mothers could reduced the risk of HBV intrauterine transmission during pregnancy.

Objective:To analyze the virus genome mutation of mothers with C genotype HBV and explore its relationship with HBV intrauterine transmission.Methods:A total of 399 mothers carrying HBV and their newborns hospitalized in the obstetrics department of the Third People's Hospital of Taiyuan from 2011 to 2013 were selected. Necessary information about mothers and children was obtained through a questionnaire survey and medical records. HBV DNA and HBV serological markers were detected by quantitative fluorescence PCR and electrochemiluminescence. Within 24 hours after birth and before active/passive immunization, those with positive HBsAg and/or HBV DNA in femoral venous blood were determined as HBV intrauterine transmission. According to the requirements of cloning and sequencing, mothers' HBV DNA load should be ≥10 6 IU/ml. Among 54 cases of HBV intrauterine transmission, 22 pairs of mothers and their newborns meeting the requirements of cloning and sequencing were used as the intrauterine transmission group. The same number of mothers and their newborns without intrauterine transmission was selected as the random seed method's control group. After PCR amplification of HBV DNA, gene cloning, and sequencing, the gene mutation analysis of mothers with C genotype HBV was performed. Results:Among the 44 samples, 39 (88.63%, 39/44) were genotype C, 2 were genotype B, and 3 were mixed genotype B, and C. A total of 406 clone beads from 42 mothers with C genotype HBV were analyzed for gene mutation, including 204 in the intrauterine transmission group and 202 in the control group. The base substitution mutation rate of PreS1, S, C, and P regions in the HBV intrauterine transmission group were significantly lower than those in the control group ( χ 2 ranged from 8.67 to 40.73, P<0.05). The mutation rate of base deletion in PreC and X regions in the HBV intrauterine transmission group was lower than that in the control group ( χ 2 values were 17.82 and 34.78, P<0.001). Two clones in the X region had 31 bp insertion mutations between nt1644 and nt1645, and two clones had 27 bp insertion mutations between nt1649 and nt1650, all of which took place in the control group. Conclusions:The base substitution mutations in the PreS1, S, C, and P segments of the HBV genome in mothers with C genotype HBV were associated with the occurrence of intrauterine transmission of HBV. Deletion mutations in the PreC region, insertion and deletion mutations in the X region may reduce intrauterine transmission risk.

Objective:To explore the effects of neonatal stimulator of interferon genes (STING) innate immune signaling pathway of HBsAg-positive mothers on non/hypo-response to hepatitis B vaccine (HepB) in their infants.Methods:From November 2019 to June 2022, HBsAg-positive mothers and their infants in the Third People's Hospital of Taiyuan were recruited as the study subjects. The epidemiological and clinical data were collected by questionnaire survey and medical records review. The key molecular proteins of STING innate immune signaling pathway (STING, pIRF3) and immune cells associated with vaccine response (DC, T and B and plasma cells) in neonatal cord blood were detected by flow cytometry. Follow up was conducted for infants for 1-2 months after the full vaccination of HepB. Serum hepatitis B surface antibody (anti-HBs) was detected by chemiluminescence microparticle immunoassay. Unconditional logistic regression model, nomogram and Bayesian network model were used to evaluate the effect of STING innate immune signaling pathway on non/hypo-response to HepB and related factors in infants, and the relationship between various factors.Results:A total of 195 pairs of HBsAg-positive mothers and infants were recruited, the rate of non/hypo-response to HepB in the infants was 12.31% (24/195). High maternal HBV DNA load, low expression of neonatal STING, low expression of pIRF3 and low percentage of plasma cells were risk factors for non/hypo-response to HepB in the infants ( OR=4.70, 3.46, 3.18 and 2.20, all P<0.05). The nomogram constructed by these factors had good predictive efficacy (area under curve=0.81, 95% CI: 0.63-0.83). The results of Bayesian network model showed that the infants with a high maternal HBV DNA load had a higher conditional probability of low STING expression (62.50%) and a higher conditional probability of low pIRF3 expression (58.54%). The conditional probabilities of low expression of DC, T, B and plasma cells were 53.16%, 60.20%, 68.42% and 57.14%, respectively. Conclusion:Maternal HBV DNA might inhibit STING innate immune signaling pathways in infants and immune cells associated with HepB response, resulting in non/hypo-response to HepB in infants of HBsAg-positive mothers.

Coronavirus disease 2019(COVID-19),which is caused by SARS-CoV-2,varies with regard to symptoms and mortality rates among populations.Humoral immunity plays critical roles in SARS-CoV-2 infection and recovery from COVID-19.However,differences in immune responses and clinical features among COVID-19 patients remain largely unknown.Here,we report a database for COVID-19-specific IgG/IgM immune responses and clinical parameters(named COVID-ONE-hi).COVID-ONE-hi is based on the data that contain the IgG/IgM responses to 24 full-length/truncated proteins corresponding to 20 of 28 known SARS-CoV-2 proteins and 199 spike protein peptides against 2360 serum samples collected from 783 COVID-19 patients.In addition,96 clinical parameters for the 2360 serum samples and basic information for the 783 patients are integrated into the database.Furthermore,COVID-ONE-hi provides a dashboard for defining samples and a one-click analysis pipeline for a single group or paired groups.A set of samples of interest is easily defined by adjusting the scale bars of a variety of parameters.After the"START"button is clicked,one can readily obtain a comprehensive analysis report for further interpretation.COVID-ONE-hi is freely available at www.COVID-ONE.cn.