Updating and identifying three novel variants of the CARD14 gene in Chinese Han patients with psoriasis

Psoriasis-2 (PSORS2) is caused by the heterozygous mutation of the caspase recruitment domain 14 (CARD14) gene on chromosome 17q25. To evaluate the contribution of CARD14 variants in psoriasis of the Chinese Han population, we performed deep sequencing of the CARD14 gene in 372 Chinese Han patients with psoriasis. The exonic nucleotide variants were confirmed by Sanger sequencing in the affected individuals and 1114 controls. In 27 patients with psoriasis, we identified 15 variations, including three novel variants: c.381C[G (p.Cys127Trp), c.712A[G (p.Met238Val) and c.2260_2261delinsGG (p.Gln754Gly). These findings could enrich and update the Human Gene Mutation Database of CARD14 variants for psoriasis.

Estimated economic burden of disease of Norovirus gastroenteritis of schools in the Pearl River Delta Region / 中国学校卫生

Objective@#This study aims to estimate the economic burden of disease of outbreak of norovirus gastroenteritis in the Pearl River Delta Region, and provide scientific evidence for the government’s decision-making and control measures.@*Methods@#Using a unified questionnaire, a survey was conducted to the schools and students’ families which had suffered an outbreak of norovirus gastroenteritis in the Pearl River Delta Region from October 2017 to April 2018.@*Results@#The survey found that the mean total economic burden of sick students was 720.41(95%UI=640.45-804.63)RMB. The mean economic burden of sick students who were inpatient, outpatient and self-treatment were 1 712.75(95%UI=328.50-34 00.00), 213.70(95%UI=191.83-236.33) and 58.97(95%UI=43.00-77.69)RMB, respectively. The mean economic burden of transport, extra tutoring and cost of lost labor were 53.63(95%UI=43.98-63.58), 558.49(95%UI=381.40-774.01) and 695.62(95UI=630.25-767.29)RMB. The mean total economic burden of health students was 382.62(95%UI=343.29-424.45)RMB. The mean total economic burden of school was 49 264.53(95%UI=22 363.38-79 976.25)RMB. The total economic burden of disease increases as the level of outbreak increases. The larger the epidemic level, the proportion of sick students’ financial burden gradually decreased, 56.58%,23.27% and 10.93%.@*Conclusion@#The high economic burden of disease of norovirus gastroenteritis in the Pearl River Delta Region, respectively, indicating that relevant departments should strengthen the prevention, control and education in order to mitigate the disease economic burden.

Function of IgD on lymphocyte activation and effect of hIgD-Fc-Ig fusion protein on human PBMC proliferation / 中国药理学与毒理学杂志

OBJECTIVE This study aimed to investigate the influence of IgD on T/B cell activationand construct hIgD-Fc-Ig fusion protein to competitive inhibition IgD binding with IgDR. METHODS T/B cells were sorted by magnetic cell sorting. The differences of mIgD and IgD-R level between different T/B cell subtypes were detected by FCM. Serum IgD level was detected by ELISA. Human IgD-Fc-IgG1- Fc sequence was amplified by cross- PCR and then subcloned into PET28a(+ ) empty vector. After prokaryotic expression through escherichia coli, we obtained the hIgD-Fc-Ig fusion protein by affinity chromatograph. Western blot was used to identify the hIgD- Fc- Ig fusion protein. Human peripheral blood monouclear cells (PBMC) and fibroblast like synoviocytes (FLS) proliferation were detected using a cell counting kit-8 (CCK-8). RESULTS The percentage of CD3+/CD4+, CD3+/IgD+, CD3+/CD4+/IgD+, CD3+/IgD-R+ and CD3+/CD4+/IgD-R+ cells increased significantly in RA patients comparing to healthy people. IgD can stimulate PBMC proliferation. IgD (1, 3, 10, 30 μg·mL-1) stimulate PBMC proliferation significantly after 24 h. We obtained stable and active hIgD-Fc-Ig fusion protein. The hIgD-Fc-Ig fusion protein showed no effect on PBMC proliferation. But it could downregulate human IgD protein promoting proliferation effects in human PBMC. CONCLUSION This result suggests that IgD and IgDR play an important role on T/B cell activation in RA patients and the hIgD-Fc-Ig fusion protein may competitively inhibit IgD's function and may play an therapeutic role in autoimmune diseases.

Effects of immunoglobulin D on expression of IgD receptor and protein tyrosine kinase signaling in human CD4+ T cells / 中国药理学与毒理学杂志

OBJECTIVE To observe whether human CD4 + T cells could be activated by immuno-globulin D (IgD) via IgD receptor(IgDR)-Lck. METHODS Human CD4+ T cells were purified from peripheral blood mononuclear cells (PBMCs) with microbeads. The viability of T cells were detected by CCK-8. The binding affinity and expression of IgDR on T cells were detected by flow cytometry. The protein expression of IgDR, Lck and P-Lck were analyzed by western blot. RESULTS IgD could concentration-dependent bind to IgDR on CD4+ T cells. The expression of IgDR was increased in response to treatment with IgD in a time- dependent and concentration- dependent manner. Stimulating by IgD resulted in enhanced phosphorylation of Lck compared with that in the medium control sample. The expression of Lck was not changed. As inhibitor of PTK, Herbimycin A or A770041, which combined with IgD could significantly inhibit phosphorylation of Lck(Tyr394). The proliferation promoting effect of IgD was blocked by Herbimycin A or A770041. IgD could stimulate CD4+ T cell activation and proliferation through upreg?ulating activating tyrosine residue of Lck (Tyr394) phosphorylation. CONCLUSION These results demon?strate that IgD exaggerates CD4+T cell activities, which may be through promoting Lck phosphorylation.

Correlation and Expression of COX-2 and P53 Protein in Basal Cell Carcinoma of Eyelid / 华中科技大学学报（医学）（英德文版）

.01). Spearman rank correlation analysis demonstrated a positive correlation between the expression of COX-2 and p53 (r=0.113, P=0.421). It was concluded that COX-2 can increase the expression of p53 protein, therefore suppressing apop-tosis.