ObjectiveTo investigate the pregnancy outcomes for patients with stage 3–4 chronic kidney disease (CKD) and the effects of pregnancy on kidney function.MethodsClinical data of pregnant women with CKD in the Peking University First Hospital between January 1st 2005 and October 1st 2016 were retrospectively analysed. The pregnancy outcomes of patients with different stages of CKD were compared. Patients with stage 3–4 CKD were followed up by telephone interview, and non-pregnant patients with stage 3–4 CKD were selected using the propensity score method to analyse the effects of pregnancy on kidney function.ResultsA total of 293 women with 300 pregnancies met the study criteria. There were 30 cases of stage 3–4 CKD. The incidence of adverse pregnancy outcomes of patients with stage 3–4 CKD was significantly higher than that with stage 1 CKD. The mean postpartum follow-up time of pregnant patients with CKD was 49.0 ± 33.1 months. A total of 26 cases of stage 3–4 CKD were followed up. During the follow-up period, 8 patients progressed to ESRD. A total of 28 non-pregnant patients with stage 3–4 CKD were selected as the control group. The results of multivariate analysis revealed that pregnancy did not increase the risk of deterioration of kidney function.ConclusionPatients with stage 3–4 CKD in early pregnancy had a significantly increased risk of adverse pregnancy outcomes. Pregnancy itself did not seem to accelerate kidney disease progression in patients with stage 3–4 CKD.

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This study was undertaken to determine if prolonged daily subcutaneous administration of ultra low dose IL-2 could influence the constitutive endogenous production of a type 1 (IFN-gamma) cytokine in patients with AIDS or AIDS-associated malignancies. Using a quantitative reverse transcription PCR assay, we demonstrate that daily administration of one type 1 cytokine, IL-2, for 3 mo increases significantly the constitutive endogenous gene expression of another type 1 cytokine, IFN-gamma, in vivo. The predominant source of IFN-gamma appears to be IL-2-expanded natural killer cells and CD8(+) T cells. Moreover, PBMC obtained from these patients during IL-2 therapy showed normalization of a profound deficit in IFN-gamma protein production after stimulation with extracts from infectious agents in vitro. Our data suggest that prolonged exogenous administration of a type 1 cytokine in a nontoxic fashion to patients with AIDS and AIDS-associated malignancies can enhance significantly the endogenous type 1 cytokine profile in vivo. Consequently, ultra low dose IL-2 therapy has the potential to improve the immunodeficient hosts' immune response to infectious pathogens that require IFN-gamma for clearance.

Human liver cancer is the cancer commonly seen clinically. The transcription of ribosomal DNA (rDNA) is a critical step for cells, and epigenetic marks such as post-translational histone modifications have been involved in the regulation of rDNA transcription. But less is known about the pathogenesis of the liver cancers concerning the rDNA transcription regulation. Here we aligned the ChIP-seq data of histone modification markers and CTCF to the human genome assembly which contains a single rDNA repeat in human liver cancer cell and validated their distribution with ChIP-QPCR. Human liver cancer cell possesses a higher enrichment of H3K4me1 and H3K27me3 at ~28 kb within the intergenic spacer (IGS) of rDNA and a higher enrichment of H3K4me3 and H3K27ac upstream of TSS. Furtherly, we studied whether UBF could affect histone modification markers and CTCF at rDNA in human liver cancer cell. UBF depletion leads to a decrease of gene activation mark H3K4me3 across the rDNA promoter. And other histone modification marks and CTCF were not altered after UBF depletion. Taken together, our data showed a high resolution map of histone modification marks at rDNA in human liver cancer cell and provide novel evidence to decipher chromatin-mediated regulation of rDNA in liver cancer.