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Background Our study aimed to explore the anxiety levels and possible associated factors in the pediatric medical staff in Jiangsu province during an outbreak of Coronavirus Disease 2019 (COVID-19). Methods Pediatric medical staff (n=534) from nine hospitals in Jiangsu province were enrolled. Their anxiety levels and quality of sleep were assessed using the online SAS and PSQI questionnaires. Results The prevalence of anxiety was 14.0% among the medical staff. In children's hospital staff, anxiety levels in outpatient and emergency departments were significantly higher than those in inpatient departments, except for the intensive care unit. The SAS scores were significantly associated with educational background, professional title, lifestyle, and physical condition. Stepwise multiple linear regression showed that physical condition, lifestyle, attention to the epidemic, professional title, and educational background all had a linear relationship with the individual's anxiety levels. Pearson correlation analysis showed that sleep quality was moderately associated with anxiety levels. Conclusions The prevalence of anxiety was 14.0% in pediatric medical staff in Jiangsu province during an outbreak of COVID-19. Department, professional title, and educational background were associated with anxiety levels in these workers. More attention should be paid to staff who are in poor health, and this anxiety can also be accompanied by poor sleep quality. Peer support can assist with anxiety relief.

To investigate the association of 12 single nucleotide polymorphisms (SNPs) in folate metabolic genes with congenital heart disease (CHD).A total of 160 children with CHD and 188 control children were enrolled. Twelve SNPs related to folate metabolism, including CBS-C699T, DHFR-c594 + 59del19, FOLH1-T1561C, CBS-C699T, DHFR-c594 + 59del19, GSTO1-C428T, MTHFD-G878A and -G1958A, MTHFR-C677T and -A1298C, MTR-A2756G, MTRR-A66G, NFE2L2-ins1 + C11108T, RFC1-G80A, TCN2-C776T and TYMS-1494del6, were genotyped by SNaPShot genotyping technology and confirmed by Sanger sequencing.There were two SNPs including NFE2L2-ins1 + C11108T and GST01-C428T and two compound mutants for (MTHFD-G1958A, MTHFR-C677T and MTR-A2756G) and (MTHFD-G1958A, RFC1-G80A and MTR-A2756G), which might increase the risk of CHD, and DHFR-c594 + 59del19 might decrease the risk of CHD. The CT genotype of NFE2L2-ins1 + C11108T, OR = 2.15 (95% CI = [1.07, 4.32], p 0.05). The CT + TT genotype of NFE2L2-ins1 + C11108T, OR = 1.98 (95% CI = [1.00, 3.93], p 0.05). The TT genotype of GST01-C428T, OR = 3.49, (95CI% = [1.06, 11.5], p 0.05). The GG genotype of DHFR-c594 + 59del19, OR = 0.46 (CI% = [0.24, 0.87], p 0.05). The AG + GG genotype of DHFR-c594 + 59del19, OR = 0.53 (CI% = [0.29, 0.96], p 0.05). The ratios of the two compound mutants for (MTHFD-G1958A, MTHFR-C677T and MTR-A2756G) and (MTHFD-G1958A, RFC1-G80A and MTR-A2756G) in CHD are higher than that in control, p 0.05 (OR = 2.968, 95% CI = [1.022, 8.613]).The CT genotype of NFE2L2-ins1 + C11108T and the TT genotype of GST01-C428T are susceptible factors for CHD. The AG, GG and (AG + GG) genotypes of DHFR-c594 + 59del19 are protective genotypes for CHD. Compound mutants for (MTHFD-G1958A, MTHFR-C677T and MTR-A2756G) and (MTHFD-G1958A, RFC1-G80A and MTR-A2756G) may increase the risk of CHD.

Xiao-yan Yang,1,* Ming-ying Zhang,1,* Qi Zhou,1 Shui-yan Wu,1 Ye Zhao,2 Wei-ying Gu,3 Jian Pan,1 Jian-nong Cen,2 Zi-xing Chen,2 Wen-ge Guo,4 Chien-shing Chen,5 Wen-hua Yan,6 Shao-yan Hu1 1Department of Haematology and Oncology, Children’s Hospital of Soochow University, 2Department of Haematology, The First Affiliated Hospital of Soochow University, Suzhou, 3Department of Haematology, The Third Affiliated Hospital of Soochow University, Changzhou, People’s Republic of China; 4Department of Mathematical Sciences, New Jersey Institute of Technology, Newark, NJ, 5Department of Internal Medicine, Division of Hematology and Medical Oncology and Biospecimen Laboratory, Loma Linda University, Loma Linda, CA, USA; 6Department of Cardiology, Children’s Hospital of Soochow University, Suzhou, People’s Republic ofChina *These authors contributed equally tothis work Abstract: S100A8 has been increasingly recognized as a biomarker in multiple solid tumors and has played pivotal roles in hematological malignancies. S100A8 is potentially an indicator for poor survival in acute myeloid leukemia (AML) in retrospective studies. However, the mechanisms of S100A8 are diverse in cancers. In this study, we investigated the correlation of S100A8 at the transcription level with clinical parameters in 91 de novo AML patients and explored its mechanisms of chemoresistance to etoposide in vitro. The transcription level of S100A8 was significantly lower at initial and relapse stages of AML samples than at complete remission (P

Background Previous studies have identified that mutations in a few genes, including T-BOX5, NKX2-5, EVC and GATA4, are associated with atrial septal defect (ASD). Methods A family of three generations with 4 members who were affected with ASD was investigated. To exclude the presence of any sub-microscopic chromosomal imbalance, high-resolution 1M array-based comparative genomic hybridization (aCGH) was performed. SNaPShot was used to certify the specificity of the finding mutation in the other family members. The coding region of GATA4 and NKX2-5 genes was screened by sequencing in another 30 cases including 10 cases of ventricular septal defect (VSD), 10 cases of atrial septal defect (ASD), 8 cases of VSD combined with ASD and 2 cases of atrioventricular septal defects (AVSD). Results No pathogenic copy number variant was detected by aCGH in the four affected family members with ASD. A novel non-synonymous variant, c.839C>T (T280M) in GATA4, was identified and segregated with all the ASD patients within this Chinese family. Such mutation was absent in other family members or present among sporadic CHD patients. In addition, we identified a non-synonymous variant in the NKX2-5 gene (P257A) associated with one congenital heart disease patient with VSD. Both mutations were not identified among healthy controls. Conclusion T280M mutation of GATA4 is suggested to be associated with ASD in this Chinese family.

Angiotensin II type 1 receptor (AT1R) blockers (ARBs) have been shown to reduce the incidence of type 2 diabetes mellitus; however, the underlying molecular mechanism is unknown. Peroxisome proliferator-activated receptor γ (PPARγ) is the central regulator of insulin and glucose metabolism, which improves insulin sensitivity. Whether candesartan cilexetil, as a prodrug of the AT1R blocker candesartan, has PPARγ-activating properties remains to be elucidated. The aim of the present study was to investigate the effects of oral administration of candesartan cilexetil on glucose tolerance and the actions of PPARγ on liver and adipose tissue in the insulin-resistant obese rat induced by high-fat diet. Animals treated with candesartan cilexetil showed an improved glucose tolerance after oral glucose challenge. Whole-body insulin sensitivity was evaluated using the hyperinsulinemic-euglycemic clamp technique. During high-fat feeding in high-fat diet (HF) rats, the glucose infusion rate (GIR) was 52.3% lower than that in normal chow (NC) rats. However, the GIR was significantly enhanced following candesartan cilexetil treatment. Angiotensin II receptor antagonism also resulted in significant increases in PPARγ protein expression in adipose and liver tissue. These results indicate that PPARγ activation by candesartan cilexetil may provide novel therapeutic options in the treatment of patients with metabolic syndrome.

Background Serum γ-glutamyltransferase (GGT) and uric acid (UA) levels are elevated in patients with diabetes or cardiovascular disease. Prediabetes, characterized by impaired glucose tolerance, is an important risk factor for overt diabetes as well as cardiovascular disease. Therefore, the aim of this study was to explore the relationship between GGT, UA and prediabetes in a Chinese population, and provide a scientific basis for the early prevention and treatment of diabetes. Methods We performed a cross-sectional population-based study in a cohort of 2694 subjects (1211 men and 1483 women, aged 35–86 years). Questionnaires and physical examinations were performed using standardized procedures. Fasting blood was collected to measure glucose and other biochemical parameters. The subjects were divided into two groups with either normal fasting glucose (NFG) or impaired fasting glucose (IFG), according to international diagnostic criteria. Logistic regression analysis was performed to estimate odds ratios (OR) and 95% confidence intervals. Results Compared with the NFG group, the IFG group had significantly higher blood pressure but lower high-density lipoprotein–cholesterol in women. Body mass index, waist circumference, triglyceride, glucose, GGT, and UA levels were significantly higher in males and females in the IFG group than those in the NFG group. Logistic regression analysis revealed that the OR for prediabetes increased with increasing serum GGT quartiles and UA quartiles. GGT and UA were positively associated with prediabetes in men and women, independent of age, ethnicity, smoking, alcohol consumption, blood pressure, physical labor, and other confounders. Conclusions We found that serum GGT and UA levels were positively associated with prediabetes in men and women living in areas inhabited by Chinese ethnic minorities. As elevated GGT and UA levels were associated with significantly increased risk of prediabetes, they may be used as sensitive biological markers of prediabetes.