Functions of HP1 in preventing chromosomal instability.

Chromosomal instability (CIN), caused by errors in the segregation of chromosomes during mitosis, is a hallmark of many types of cancer. The fidelity of chromosome segregation is governed by a sophisticated cellular signaling network, one crucial orchestrator of which is Heterochromatin protein 1 (HP1). HP1 dynamically localizes to distinct sites at various stages of mitosis, where it regulates key mitotic events ranging from chromosome-microtubule attachment to sister chromatid cohesion to cytokinesis. Our evolving comprehension of HP1's multifaceted role has positioned it as a central protein in the orchestration of mitotic processes.

[Postoperative complications of microscopic versus Palomo varicocelectomy for varicocele in army personnel].

OBJECTIVE: To evaluate the postoperative complications of microscopic and conventional Palomo varicocelectomy in the treatment of varicocele in army personnel. METHODS: A total of 260 army personnel with varicocele were randomized to receive microscopic varicocelectomy (group A, n=130) and conventional Palomo varicocelectomy (group B, n=130). The postoperative recurrence and complications (scrotal edema, testicular pain and testicular atrophy) were compared between the two groups. RESULTS: After 1 year of follow-up, the recurrence rates in groups A and B were statistically comparable (5.3% vs 3.8%, P>0.05). The incidences of testicular atrophy and scrotal edema were significantly lower in group A than in group B (0.7% vs 3.1%, P<0.05; 3.1% vs 14.6%, P<0.05), and the rate of testicular pain relief was significantly higher in group A (90.7% vs 67.7%, P<0.05). CONCLUSION: Microscopic varicocelectomy can be a good choice in the treatment of varicocele in army personnel.

DITOP: drug-induced toxicity related protein database.

MOTIVATION: Drug-induced toxicity related proteins (DITRPs) are proteins that mediate adverse drug reactions (ADRs) or toxicities through their binding to drugs or reactive metabolites. Collection of these proteins facilitates better understanding of the molecular mechanisms of drug-induced toxicity and the rational drug discovery. Drug-induced toxicity related protein database (DITOP) is such a database that is intending to provide comprehensive information of DITRPs. Currently, DITOP contains 1501 records, covering 618 distinct literature-reported DITRPs, 529 drugs/ligands and 418 distinct toxicity terms. These proteins were confirmed experimentally to interact with drugs or their reactive metabolites, thus directly or indirectly cause adverse effects or toxicities. Five major types of drug-induced toxicities or ADRs are included in DITOP, which are the idiosyncratic adverse drug reactions, the dose-dependent toxicities, the drug-drug interactions, the immune-mediated adverse drug effects (IMADEs) and the toxicities caused by genetic susceptibility. Molecular mechanisms underlying the toxicity and cross-links to related resources are also provided while available. Moreover, a series of user-friendly interfaces were designed for flexible retrieval of DITRPs-related information. The DITOP can be accessed freely at http://bioinf.xmu.edu.cn/databases/ADR/index.html. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

[Clinical significance of early diagnose and treatment of subclinical renal allograft rejection].

OBJECTIVE: To explore the clinical significance of early diagnose and treatment of subclinical renal allograft rejection. METHODS: Ninety-six renal allograft recipients (54 male and 42 female) with normal renal function aged 17 to 58 years (mean 37.5 years) were included in this study. Early subclinical rejection was diagnosed 3 months after the transplantation by color Doppler examination. RESULTS: Patients with early subclinical rejection were given methylpredisolone followed by adjustment of immunosuppressive regimens, and no difference was observed in 3-year survival rate between these patients and those with normal renal allograft findings. CONCLUSION: Early diagnosis and treatment of subclinical renal allograft rejection is significant to improve renal allograft survival rate.

[Relationship between donor renal graft quality and graft rejection].

OBJECTIVE: To evaluate the correlation between the quality of donor renal grafts and graft rejection. METHODS: The cold ischemia time and the pathological findings by biopsies of the donor grafts in 87 cases were analyzed in conjunction with the occurrence of acute or chronic graft rejection after transplantation. RESULTS: After transplantation, acute rejection occurred in 28 cases, in which 5 (17.8%) had adverse changes in the donor grafts; chronic allograft nephropathy developed in 13 cases, in which 6 (46.1%) had adverse changes in the donor grafts. By binary logistic regression analysis, the cold ischemia time and acute renal tubular injury were identified as the factors affecting acute graft rejection, and cold ischemia time and glomeruloserosis as the risk factors for chronic rejection. CONCLUSION: High-quality donor kidney and minimization of the risk factors help reduce the occurrence of graft rejection after kidney transplantation.

[Expressions of transforming growth factor-beta1 and collagen IV in renal tissues of patients with chronic allograft nephropathy].

OBJECTIVE: To investigate the expressions of transforming growth factor (TGF)-beta1 and collagen IV in the renal tissues of patients with chronic allograft nephropathy (CAN). METHODS: Immunohistochemical method and computer-assisted image analysis system were used to detect the expressions of TGF-beta1 and collagen IV in the renal tissues of patients with CAN, and the association between TGF-beta1 and collagen IV expressions as well as that between their expressions and the pathological grading of CAN were analyzed. RESULTS: The expressions of TGF-beta1 and collagen IV were significantly higher in the renal tissues of the patients than in normal renal tissues (P<0.001), and the expressions tended to increase with the pathological grades of CAN; TGF-beta1 and collagen IV expressions in both the renal glomeruli and the tubulointerstitium were in patients with CAN positively correlated with normal renal tissues (r=0.943, P<0.001; r=0.910, P<0.001). CONCLUSIONS: Abnormal collagen IV deposition is one of the major factors associated with renal fibrosis in CAN, and TGF-beta1 might play an important role in renal fibrosis in CAN through up-regulation of collagen IV in the renal tissues.