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BackgroundDepression is common among people living with HIV/AIDS; however, studies focusing on the depression of men living with HIV/AIDS are limited. Therefore, we examined the prevalence of depression and its associated factors among men living with HIV/AIDS in China.MethodsA cross-sectional questionnaire survey was conducted in Harbin, China between March and August in 2013. Two-hundred twenty participants completed the Burns Depression Checklist, the Berger HIV Stigma, and the SPIEGEL questionnaire. We also investigated demographics, family support, hostility, and the antiretroviral therapy side effects of men living with HIV/AIDS.ResultsMore than 40% of respondents had depressive symptoms and worry about the health was the major symptom of depression (40.9%). The logistic regression model indicated that bad sleep quality (OR = 3.452), hostility (OR = 1.120), perceived discrimination (OR = 1.110), and antiretroviral therapy side effects (OR = 1.083) were positively associated with depression. Family support (OR = 0.860) was negatively associated with depression for men living with HIV/AIDS. Demographic variables, HIV infection route, disease duration, and CD4+ cell count had no significant associations with depression.ConclusionAlthough China’s work of national HIV prevention and treatment has made much progress during the past several years, the prevalence of depression among men living with patients with HIV/AIDS is still prominent. The strongest factor associated with depression among men living with HIV/AIDS was sleep quality. Future studies should explore the effects of interventions for depression among PLWHA.

Summary The prevalence and prognostic relevance of recurrent gains of CKS1B (cyclin kinase subunit 1B) gene at chromosome 1q21 region was investigated by interphase fluorescence in situ hybridisation in a cohort of 99 multiple myeloma (MM) patients treated with intensive chemotherapy followed by autologous stem cell transplantation. CKS1B amplification (3–8 CKS1B signals) was detected in 31of 99 (31%) patients and was associated with deletions of p53 (P = 0·003) and 13q (P = 0·039) but not with translocation t(11;14) or t(4;14). CKS1B amplification was associated with bone marrow plasmacytosis (P = 0·02), but there was no correlation with patient age, gender, disease stage, lytic bone lesions, albumin, creatinine, C‐reactive protein or beta‐2 microglobulin levels. Patients with CKS1B amplification had a significantly shorter progression‐free survival than those without such amplification (18·5 vs. 25·7 months, P = 0·035). Likewise, a shorter overall survival (44·8 months vs. not reached) was observed; however, the difference did not reach statistical significance (P = 0·20). Seven patients had paired bone marrows obtained at diagnosis and at relapse, the percentage of cells with CKS1B amplification and the level of amplification were significantly increased in the relapse marrows. In this cohort of patients, CKS1B was frequently amplified in MM and may represent genetic instability associated with disease progression.

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