Yu-Jing Zhang

Prevalence and correlates of suicidal ideation in SLE inpatients: Chinese experience

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Because of double damages of body and mind, SLE patients are in a potential risk of suicide. Many factors may contribute to the occurrence of suicide in SLE: socioeconomic factors, medical factors, mental health, family support and coping style. This study aims to investigate the prevalence and correlates of suicidal ideation in SLE inpatients in China in order to determine whether they had risk of suicide, and if so, what factors should be paid more attention to prevent suicide in wards. A total of 285 SLE patients were interviewed with questionnaires on suicidal ideation and socio-demographic characteristics, Beck Depression Inventory (BDI), Family APGAR and Trait Coping Style Questionnaire (TCSQ). Disease activity was assessed with SLE Disease Activity Index. The other medical information was collected from the patients’ medical records. In total, 34.4% of SLE patients had current suicidal ideation. Significant individual risk factors for current suicidal ideation in SLE patients included having religious belief, heavy self-reported financial burdens, long duration of SLE, low level of family functioning and negative coping style. And in the presence of these risk factors, being separated, divorced or widowed, having premorbid suicidal ideation and depression were independent predictors of suicidal ideation. In summary, the rate of suicidal ideation in SLE patients in China is higher than that in other countries. Factors that contribute to risk of suicidal ideation include social and cultural domains and physical and psychological health. Although the association of suicidal ideation to religions and medical factors is still to be investigated, these findings may give some references to suicide prevention efforts for SLE patients in China.

IL-33 in rheumatoid arthritis: Potential role in pathogenesis and therapy

Rheumatoid arthritis (RA) is characterized by chronic inflammatory disease, including synovial proliferation and excessive pro-inflammatory cytokines production, leading to cartilage and bone destruction. Cytokine-mediated immunity plays an important role in the pathogenesis of various autoimmune diseases such as RA. Recently, the IL-1 family member IL-33, was recognized to perform as an inflammatory cytokine, exerted profound effects in human RA and experimental inflammatory arthritis. Furthermore, inhibition of IL-33 signaling proposed a potential therapeutic approach. In this review, we summarize recent advances on the pathological roles of IL-33 in RA and discuss the therapeutic significance of these new findings.

Association of PTPN22 C1858T Polymorphism and Type 1 Diabetes: A Meta-analysis

Recently, protein tyrosine phosphatase nonreceptor 22 (PTPN22) C1858T polymorphism has been identified as a susceptibile gene for type 1 diabetes (T1D), but studies are inconsistence, In order to assess the association between PTPN22C1858T polymorphism and T1D based on different ethnicities, a meta-analysis was performed, including 26 studies, total of 16,240 patients and 17,997 controls. Meta-analysis was performed on T versus C, T/T+T/C versus C/C (dominant model) and T/T versus T/C+C/C (recessive model) in a fixed/random effects model. The results indicated an association between the PTPN22 C1858T polymorphism and T1D in all subjects. The overall odds ratio (OR) of T versus C using the fixed effects model was 1.948 (95% CI = 1.859∼2.041, P < 0.001). After stratification by ethnicity, analysis revealed that the PTPN22 C1858T polymorphism T allele was significantly associated with T1D in Europeans, Americans (OR = 1.946, 95% CI = 1.852∼2.045, P < 0.001; OR = 1.946, 95% CI = 1.690∼2.242, P < 0.001, respectively). Meta-analysis of the T/T+T/C genotype and the T/T genotypes showed the same results as that shown by the PTPN22 C1858T polymorphism T allele. This meta-analysis suggests a possible association between the PTPN22 C1858T polymorphism and T1D, especially in European and American populations.

IRF7, a functional factor associates with systemic lupus erythematosus

Systemic lupus erythematosus is an autoimmune disease attributing to a combination of genetic and environmental factors. Abnormal expression/function of type I interferons has been demonstrated with the pathogenesis of SLE, especially IFN-α, which can be regulated by IFN regulatory factor 7 (IRF7). Single nucleotide polymorphisms (SNPs) near/in IRF7 have been substantiated related to onset of SLE, moreover, regulation of IRF7 expression/function has been found important in SLE. Therefore, we will discuss the association of IRF7 and SLE based on recent understandings to render more information about the mechanisms of IRF7 might perform in.

Association between leptin and systemic lupus erythematosus

Leptin, the product of ob gene, is a 16-kDa nonglycosylated peptide hormone produced by adipocytes that regulates appetite and energy expenditure at the hypothalamic level. As is known to be a satiety factor that can regulate body weight by inhibiting food intake and stimulating energy expenditure, leptin is a pleiotropic hormone whose multiple effects include regulation of endocrine function, reproduction and immunity. Since leptin has been considered to be a pro-inflammatory cytokine, investigations of leptin in the pathogenesis of autoimmune diseases have been detected, such as systemic lupus erythematosus, rheumatoid arthritis and osteoarthritis. Recently, the role of leptin in the modulation of immune response and inflammation has been discussed in the autoimmune diseases increasingly but less in systemic lupus erythematosus (SLE). Therefore, this article will focus on the current understanding of the role of leptin with such similar pathogenic mechanism in SLE in order to provide insights which may assist in the development of leptin-based approaches for the treatment of SLE.

HIV/AIDS stigma among older PLWHA in south rural China

Stigma is a common problem among people living with HIV/AIDS (PLWHA). However, little is known about HIV/AIDS-related stigma in older PLWHA over the age of 50. This study described the stigma of HIV/AIDS and its factors based on 120 PLWHA aged 50 or older in an area of high HIV prevalence in south rural China. Each participant completed a face-to-face questionnaire that collected information on demographic characteristics, AIDS-related events and experience of HIV/AIDS-related stigma. Finally, only 18.1% reported experiencing external stigma compared with 64.3% feeling internal stigma. Regression analysis indicated that social support and health status were the two variables that were significantly predictive of both external and internal stigma. Whatever, the more support were received from family members by PLWHA, the less external stigma was perceived. Negative marital situation was also related to external stigma. Reducing HIV/AIDS stigma requires a supportive environment, positive attitude and correct knowledge of AIDS. Health workers and policy makers should take practical approaches to reduce prejudice.

HIV, other sexually transmitted infections, and risk behaviors among female sex workers in Liuzhou, China

To determine the prevalence of infections with HIV and hepatitis C virus (HCV), and of syphilis among female sex workers (FSWs) in Liuzhou, China, along with levels of HIV‐related knowledge and frequencies of risk behaviors.

Role of CREM in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a complex autoimmune disease. Immune complex, autoantibodies and autoreactive lymphocytes are involved in manifestations of SLE. Recently, investigations have indicated that expression of the transcription factor cAMP responsive element modulator (CREM) is abnormal in T cells and might play an important role in the pathogenesis of SLE. CREM has much influence on the promoters, such as IL-2, c-fos, TCR ζ, and SYK. Moreover, activity of CREM itself has been demonstrated, particularly with an auto-regulatory feedback mechanism. Therefore, we will discuss the association of CREM and SLE based on current knowledge to unravel the mechanism of CREM performance.

Reduced expression of CD55 and CD59 on peripheral blood cells from Systemic lupus erythematosus: Profitable to diagnose some complications?

Recently, I’ve found several articles about decreased expression of CD55 and CD59 in systemic lupus erythematosus (SLE), most of which accompanied with autoimmune hemolytic anemia (AIHA) and lymphopenia. SLE is a prototypic, systemic, autoimmune disease, characterized by a diverse array of autoantibody production, complement activation and immune-complex deposition, which causes tissue and organ damage. The etiology and pathogenetic mechanisms of SLE have not been clearly elucidated and there’re a few reports about CD55 and CD59 on peripheral blood cells in SLE. At this time, I make such a hypothesis: Reduced expression of CD55 and CD59 on peripheral blood cells from systemic lupus erythematosus might be profitable to diagnose some complications. CD55 and CD59 are glycosylphosphatidylinositol-anchored proteins with complement inhibitory properties, expressed on hematopoietic and non-hematopoietic cells. CD55, also named decay accelerating factor (DAF), one molecule on the cell surface where it accelerates the decay of C3 and C5 convertases from the classic and alternative pathway of complement to prevent their amplification and self-damaging effect on cells [1]. While CD59 blocks the interaction of the C5b-8 complex with C9, thereby preventing the formation of the lytic membrane attack complex (MAC) [2]. Valladares, et al. [3] showed that significantly decreased expression of CD55 and CD59 on T lympholeukocyte in 30 SLE patients with lymphopenia compared to controls and excessive expression of those molecules in 10 SLE cases without lymphopenia. Another study indicated diminished expression of CD55 on RBC in one SLE patient [4]. Patin, et al. [5] analyzed CD55 and CD59 on RBC in 11 SLE patients with AIHA and found MFI (mean fluorescence intensity) of CD55 and CD59 were diminished in 6 cases, and reduced CD59 was found in another 4 cases. Alegretti, et al. [6] assayed the expression of CD55 and CD59 on RBC, lymphocyte, granulocyte in 23 SLE patients and 23 controls. They reported that the MFI of CD55 on RBC in six SLE patients plus AIHA significantly reduced compared to controls. And decreased expression of CD55+ and CD59+ on lymphocyte were found in 11 SLE patients accompanied by lymphocytopenia compared with controls although the expression of CD55 and CD59 in SLE showed no association with SLEDAI (SLE disease activity index). When granulocyte assayed, SLE patients had decreased expression of CD59+ and CD55 than controls, but no correlations was found between the expression of CD59+ and SLEDAI.