Interaction between TP53 and XRCC1 increases susceptibility to cervical cancer development: a case control study.

BACKGROUND: Cervical cancer is the 4th highest cause of female reproductive tract malignancies. Multiple loci have been identified as important determinant factors for tumor susceptibility. In this report, we aimed to explore the roles of gene polymorphisms affecting x-ray repair cross complementing 1 (XRCC1), the tumor protein p53 (TP53), and fibroblast growth factor receptor 3 (FGFR3) in the context of susceptibility to cervical cancer. Additionally, we assessed the impact of single nucleotide polymorphism-single nucleotide polymorphism (SNP-SNP) interaction of these three genes in the context of cervical cancer risk in Chinese women. METHODS: A case-control study consisted of 340 women located in Chongqing. Of these women, 121 were diagnosed with cervical cancer, 118 served as healthy controls, and 101 were specifically recruited elderly patients above the age of 80 who showed no history of cervical cancer. Three SNPs (XRCC1 rs25487, TP53 rs1042522, and FGFR3 rs121913483) were examined using mutation analysis of mismatch amplification PCR (MAMA-PCR) on samples obtained from peripheral blood. RESULTS: Our results indicated that females from southwestern China all exhibited a wild-type phenotype at FGFR3 rs121913483. We also observed that the rs25487 mutation was significantly increased within the cervical cancer population. A 2-locus SNP-SNP interaction pattern (rs25487 and rs1042522) was significantly associated with cervical cancer risk (cases vs. negative controls: OR = 4.63, 95% CI = 1.83-11.75; cases vs. elderly group: OR = 17.61, 95% CI = 4.34-71.50). CONCLUSIONS: This is the first study to identify a novel interaction between the XRCC1 and TP53 genes that is highly associated with susceptibility to cervical cancer risk in a female population in southwestern China.

Demethylation-mediated miR-129-5p up-regulation inhibits malignant phenotype of osteogenic osteosarcoma by targeting Homo sapiens valosin-containing protein (VCP).

Previous studies demonstrated that increased Homo sapiens valosin-containing protein (VCP) may be involved in osteosarcoma (OS) metastasis. However, the underlying mechanism of VCP over-expression in OS remains unknown. In the present study, we found a significantly negative correlation between miR-129-5p and VCP protein expression in OS tissues with pulmonary metastasis (Spearman's rho, rs = -0.948). Bioinformatical prediction, Luciferase reporter assay, Western blot, and RT-PCR assays performed on OS cells indicated that VCP is a target of miR-129-5p. In addition, three CPG islands in the region of miR-129-5p promoter were detected by bioinformatical prediction, and significantly higher expression of miR-129-5p and lower methylation level of miR-129-2 gene in OS cells treated with 5-Aza-2'-deoxycytidine (a potent DNA demethylating agent) than in those untreated cells were observed. Furthermore, lower migratory and invasive ability was found in cells with elevated miR-129-5p than in those with decreased miR-129-5p. These findings indicated that increased miR-129-5p may be mediated by demethylation and inhibit OS cell migration and invasion by targeting VCP in OS, and targeting miR-129-5p/VCP signaling pathway may serve as a therapeutic strategy for OS management, although further studies will be necessary.

[Demand for and the Development of Detection Techniques for Source of Schistosome Infection in China].

Schistosomiasis is a type of zoonotic parasitosis that severely impairs human health. Rapid detection of infection sources is a key to the control of schistosomiasis. With the effective control of schistosomiasis in China, the detection techniques for infection sources have also been developed. The rate and the intensity of infection among humans and livestocks have been significantly decreased in China, as the control program has entered the transmission control stage in most of the endemic areas. Under this situation, the traditional etiological diagnosing techniques and common immunological methods can not afford rapid detection of infection sources of schistosomiasis. Instead, we are calling for detection methods with higher sensitivity, specificity and stability while being less time-consuming, more convenient and less costing. In recent years, many improved or novel detection methods have been applied for the epidemiological surveillance of schistosomiasis, such as the automatic scanning microscopic image acquisition system, PCR-ELISA, immunosensors, loop-mediated isothermal amplification, etc. The development of new monitoring techniques can facilitate rapid detection of schistosome infection sources in endemic areas.

Association of liver X receptor α (LXRα) gene polymorphism and coronary heart disease, serum lipids and glucose levels.

BACKGROUND: To explore the relationship between the liver X receptor α gene (LXRα) rsl2221497 polymorphism and the susceptibility of coronary heart disease (CHD) and serum lipids and glucose levels. METHODS: The single fluorescently labeled probes technique was used to detect the genotype of rsl2221497 in LXRα gene in 240 CHD patients and 250 healthy control subjects. The difference of genotype distribution between the two groups was analyzed using of Chi-square test. The serum lipids and glucose levels between the different genotypes were also compared. RESULTS: The risk of CHD in carriers with (AA + GA) genotype was 1.76 times as that in the GG genotype carriers (OR = 1.76, 95% CI: 1.18-2.87, P <0.05), and the risk of CHD in carriers with A allele increased 0.88 times compared to that in G allele carriers (OR = 1.88, 95% CI:1.21-3.43, P <0.01). Logistic regression analysis showed that after adjusting for other confounding factors, A allele was an independent risk for CHD. However, there were no differences in serum lipids and glucose levels between each genotype. CONCLUSIONS: The rsl2221497 polymorphism in LXRα gene was associated with susceptibility of CHD in Han population.

Global distribution of zoonotic digenetic trematodes: a scoping review.

BACKGROUND: Digenetic trematodes, including blood flukes, intestinal flukes, liver flukes, lung flukes, and pancreatic flukes, are highly diverse and distributed widely. They affect at least 200 million people worldwide, so better understanding of their global distribution and prevalence are crucial for controlling and preventing human trematodiosis. Hence, this scoping review aims to conduct a comprehensive investigation on the spatio-temporal distribution and epidemiology of some important zoonotic digenetic trematodes. METHODS: We conducted a scoping review by searching PubMed, Web of Science, Google Scholar, China National Knowledge Infrastructure, and Wanfang databases for articles, reviews, and case reports of zoonotic digenetic trematodes, without any restrictions on the year of publication. We followed the inclusion and exclusion criteria to identify relevant studies. And relevant information of the identified studies were collected and summarized. RESULTS: We identified a total of 470 articles that met the inclusion criteria and were included in the review finally. Our analysis revealed the prevalence and global distribution of species in Schistosoma, Echinostoma, Isthmiophora, Echinochasmus, Paragonimus, Opisthorchiidae, Fasciolidae, Heterophyidae, and Eurytrema. Although some flukes are distributed worldwide, developing countries in Asia and Africa are still the most prevalent areas. Furthermore, there were some overlaps between the distribution of zoonotic digenetic trematodes from the same genus, and the prevalence of some zoonotic digenetic trematodes was not entirely consistent with their global distribution. The temporal disparities in zoonotic digenetic trematodes may attribute to the environmental changes. The gaps in our knowledge of the epidemiology and control of zoonotic digenetic trematodes indicate the need for large cohort studies in most countries. CONCLUSIONS: This review provides important insights into the prevalence and global distribution of some zoonotic digenetic trematodes, firstly reveals spatio-temporal disparities in these digenetic trematodes. Countries with higher prevalence rate could be potential sources of transmitting diseases to other areas and are threat for possible outbreaks in the future. Therefore, continued global efforts to control and prevent human trematodiosis, and more international collaborations are necessary in the future.

Association study of angiotensin converting enzyme gene polymorphism with elderly diabetic hypertension and lipids levels.

OBJECTIVE: To investigate the relationship between angiotensin converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and diabetic essential hypertension in elderly population. METHODS: Polymerase chain reaction (PCR) technique was used in 260 elderly normal control patients, 205 elderly hypertensive patients and 138 elderly diabetic hypertensive patients to detect the I/D polymorphism in ACE gene. RESULTS: DD genotype frequency (0.352) and D allele frequency (0.543) in elderly hypertensive patients were higher than those in the normal control patients. DD genotype (0.421) and D allele frequency (0.579) in elderly diabetic hypertensive patients were significantly higher than those in the control patients (0.133 and 0.250). The differences of DD genotype and D allele frequency between the elderly hypertensive patients and the elderly diabetic hypertensive patients were not significant (P > 0.05). CONCLUSION: ACE gene deletion is a risk factor for hypertension but is not a risk factor for diabetes in elderly population.

Schistosoma japonicum scFv-IL18 fusion DNA ameliorates hepatic fibrosis in schistosomiasis-infected mice via improving local concentration of IL-18 in liver.

The pathogenesis of chronic schistosomiasis is caused by irritation of the schistosome eggs trapped in liver that induce delayed hypersensitive reactions from the surrounding tissues, leading to the formation of inflammatory granuloma and subsequent fibrosis. A Schistosoma japonicum (S. japonicum) single-chain fragment variable (SjscFv) which specifically binds to the S. japonicum soluble immature egg antigen (SIEA) can be used as a target to deliver specific cytokine towards the site of hepatic fibrosis. To test this hypothesis, a novel recombinant plasmid, pVAX1/SjscFv-IL18, was constructed by fusing SjscFv to IL-18 gene with a 45bp glycine-rich linker. Furthermore, experiments on mice showed that pVAX1/SjscFv-IL18 could effectively express IL-18 in the liver and in serum. Hepatic contents of IL-2 and IFN-γ (Th1-type) in S. japonicum-infected mice vaccinated with pVAX1/SjscFv-IL18 increased significantly but those of their IL-4 and IL-10 (Th2-type) decreased as compared to the analyzed results of 4 cytokines in the liver cells of control mice vccinated with pVAX1/IL18. Consistent with the levels of Th1 and Th2 cytokines, mice vaccinated with pVAX1/SjscFv-IL18 developed much less hepatic fibrosis 20weeks after infection, which was evaluated by average volumn of granuloma and collagen contents. These data suggested that the linkage of IL-18 to the target-specific SjscFv molecule appears to be a potentially promising trial route of therapy, the hepatic fibrosis in S. japonicum-infected mice may be ameliorated through effective expression of IL18 in liver.

Characterization and vaccination of two novel Schistosoma japonicum genes screened from a cercaria cDNA library.

Two novel genes, SJCWL05 and SJCWL06, were harvested from screening of Schistosoma japonicum (S. japonicum) cercaria cDNA library by using pig sera vaccinated (VPS) with S. japonicum immature egg ws-vaccine (S. japonicum iEw). Prokaryotic recombinant plasmids pGEX-4T-1/SJCWL05 and pGEX-4T-1/SJCWL06 were constructed to analyze their immunogenicity, which was confirmed by SDS-PAGE and Western blotting. Two eukaryotic recombinant plasmids, pcDNA3/SJCWL05 and pcDNA3/SJCWL06, were constructed, and their ability to protect mice against challenge of S. japonicum was evaluated. All mice vaccinated with pcDNA3/SJCWL05 or pcDNA3/SJCWL06 developed ELISA-specific anti-S. japonicum SIEA (S. japonicum soluble immature egg antigens) antibody. Immunoprotection experiments showed that worms and liver eggs reduced 34.64% and 39.14% in the pcDNA3/SJCWL05 group and those reduced 27.17% and 27.95% in the pcDNA3/SJCWL06 group, respectively. The reduction rates of intestine and uterine eggs in female worms of both groups reached 39.45% and 38.5% as well as 30.02% and 28.7%, respectively. Results of our study suggest that novel genes, SJCWL05 and SJCWL06, are potential vaccine candidates against schistosomiasis japonica.

TROAP regulates cell cycle and promotes tumor progression through Wnt/ß-Catenin signaling pathway in glioma cells.

AIMS: Experimental evidence demonstrated a crucial role of TROAP (Trophinin-associated protein) in regulating the cell proliferation of multiple tumors, while TROAP expression and function were largely unknown in glioma. We aimed to investigate the oncogenic role of TROAP and its potential mechanisms in gliomagenesis. METHODS: Four gene expression databases (GEO, TCGA, GTEx and CCLE) were enrolled in our study and used for TROAP expression and survival analysis. TROAP expression was quantified by qRT-PCR, western blot and immunohistochemistry assays in glioma tissues and cell lines. TROAP knockdown and overexpression vector were constructed and transfected into glioma cells. CCK-8, colony formation, transwell, and wound healing assays were used to evaluate cell viability, migration and invasion, flow cytometry to determine cell cycle arrest. Gene set enrichment analysis (GSEA) was conducted to screen the pathway involved in TROAP-high phenotype. The expression of cell cycle and Wnt/ß-Catenin signaling proteins were analyzed by immunofluorescence and western blot. RESULTS: Based on the bioinformatic analysis and a series of functional assays, we found the TROAP was enriched in glioma tissues and cell lines, its overexpression was correlated with the clinicopathologic characteristics and poor prognosis. TROAP knockdown inhibited cell proliferation, migration, invasion, and G1/S cell cycle arrest compared with control group in glioma. Mechanism analysis revealed that TROAP activated Wnt/ß-Catenin pathway and upregulated its downstream targets expression, while silencing ß-Catenin or Axin2 could reverse the tumor-promoting effects caused by TROAP, confirming that TROAP-induced malignant phenotype and tumorigenesis via Wnt/ß-Catenin signaling pathway. CONCLUSION: The present study found that TROAP accelerated the progression of gliomagenesis through Wnt/ß-Catenin pathway, and TROAP might be considered as a novel target for glioma therapy.

Microtubule associated protein 9 inhibits liver tumorigenesis by suppressing ERCC3.

BACKGROUND: Chromosomal instability plays an important part in cancer, but its genetic basis in liver tumorigenesis remains largely unclear. We aimed to characterize the mechanistic significance and clinical implication of mitotic regulator microtubule-associated protein 9 (MAP9) in hepatocellular carcinoma (HCC). METHODS: The biological functions of MAP9 were determined by in vitro tumorigenicity assays. Systematic MAP9 knockout mouse (MAP9∆/∆) and hepatocyte-specific MAP9 knockout mouse (MAP9∆/∆hep) were generated to confirm the role of MAP9 in HCC. The clinical impact of MAP9 was assessed in primary HCC tissue samples. FINDINGS: We found that MAP9 was frequently silenced in HCC tissue samples. The transcriptional silence of MAP9 in liver cancer cell lines and tissue samples was mediated by its promoter hypermethylation. MAP9 promoter hypermethylation or downregulation was associated with poor survival and recurrence in patients with HCC. Mechanistically, ectopic expression of MAP9 in LO2 and HepG2 cell lines impaired cell proliferation, colony formation, migration and invasion, and induced cell apoptosis and cycle arrest, whereas knockdown of MAP9 in Miha cell line showed the opposite effects. We found that MAP9∆/∆ mice spontaneously developed a liver hyperplastic nodule and MAP9∆/∆hep accelerated diethylnitrosamine-induced HCC formation. The tumour suppressive effect of MAP9 in HCC was mediated by downregulating excision repair cross-complementation group 3 (ERCC3), a nucleotide excision repair gene. Restoration of ERCC3 expression possessed an oncogenic potency and abrogated the tumour suppressive effects of MAP9. INTERPRETATION: MAP9 is a novel tumour suppressor in HCC by inhibiting ERCC3 expression, and serves as a prognostic factor in HCC patients.

[Detection of tissue protein biomarkers by surface enhanced laser desorption/ionization-time of flight-mass spectrometry in patients with mycosis fungoides].

OBJECTIVE: To search the tissue biomarker in mycosis fungoides (MF) patients by surface enhanced laser desorption/ionization-time of flight-mass spectrometry (SELDI-TOF-MS). METHODS: Skin specimens were collected from 12 MF patients and 15 normal controls to prepare solution of protein. CM10 Proteinchip was used to detect the biomarkers for MF. Differentially expressed protein was identified by immuno capturing. RESULTS: The expression intensity levels of 24 proteins were different between the MF patients and controls. By searching in SWISS-PRO database and literature, the 3498 and 10 837 peaks were found to accord with HNP3 and S100A8 proteins respectively. By immuno capturing, 10 837 could be identified as S100A8 with a special antibody against S100A8. CONCLUSION: A quick, easy, and high throughout proteome analytic method, SELDI-TOF-MS can identify the differential expressed proteins from MF tissue, thus offering a unique platform for biomarker detection of MF.

Valosin-containing protein promotes metastasis of osteosarcoma through autophagy induction and anoikis inhibition via the ERK/NF-κß/beclin-1 signaling pathway.

Valosin-containing protein (VCP) promotes the development of metastasis in osteosarcoma (OS) via the PI3K/Akt signaling pathway. However, inhibition of the PI3K/Akt pathway does not completely reverse VCP-mediated invasion and migration of OS, suggesting that VCP-mediated OS invasion and migration involves additional mechanisms. In the present study, a positive correlation between the expression of VCP and cell autophagy was observed among OS tissues. Inhibiting VCP may decrease the survival of malignant cells; however, an autophagy stimulator may compensate for VCP inhibition and promote malignant cell survival. Altering the level of autophagy did not affect cell invasiveness or migration. ERK, NF-κß and beclin-1 protein expression levels were markedly decreased following VCP inhibition. These findings indicated that VCP may induce autophagy and enhance anoikis resistance without affecting cell invasiveness or migration. Via anoikis resistance, VCP may promote metastasis in OS. Therefore, targeting of the ERK/NF-κß/beclin-1 signaling pathway may be an effective therapeutic strategy for the management of OS.

HELQ reverses the malignant phenotype of osteosarcoma cells via CHK1-RAD51 signaling pathway.

HELQ is a DNA helicase important for repair of DNA lesions and has been linked to several types of cancer. However, little is known about its relationship with osteosarcoma (OS) and its mechanism. In the present study, the expression of HELQ and its downstream mediators in OS cells was assayed by quantitative PCR and western blot analysis. The function of HELQ in OS cells was investigated by Transwell invasion, wound healing, CCK8 assays and Comet assay. The results demonstrated that HELQ gene and protein were expressed in OS cells. OS cell invasion, migration, proliferation and DNA damage repair were enhanced by HELQ knock-down with shRNA-lentivirus and inhibited by HELQ overexpression with lentivirus transfection. Furthermore, the antitumor activities of HELQ may be associated with upregulated expression of the DNA damage-related proteins CHK1 and RAD51. Our findings indicated that HELQ confers an anti-invasive phenotype on OS cells by activating the CHK1-RAD51 signaling pathway and suggested that HELQ could be recognized as a promising therapeutic target for OS and other types of malignant tumors.

Rich1 negatively regulates the epithelial cell cycle, proliferation and adhesion by CDC42/RAC1-PAK1-Erk1/2 pathway.

Rich1, a previously identified Rho GTPase-activating protein (RhoGAP), was found to have close relationship with Rho GTPase family members in multiple cellular processes in nervous cells and platelets. But the exact role of Rich1 in epithelial cells remains obscure. The present investigation demonstrated that up-regulation of Rich1 could cause S-phase arrest, proliferation inhibition and adhesion decline with F-actin amount decrease in epithelial cells. Further exploration in hepatocyte HL7702 revealed that overexpression of Rich1 could greatly elevate the intrinsic GTPase activities on both of CDC42 and RAC1 by stimulating GTP hydrolysis, which consequently attenuated the activities of the Rho proteins and the phosphorylation level of those in PAK1-ERK1/2 signaling cascade. While the GAP domain deleted Rich1 variant or silence of endogenous Rich1 expression could not result in any of the biological effects. It is indicated that Rich1, completely different from in other types of cells, might act as a crucial upstream negative regulator via its GAP domain in control of epithelial cell cycle, proliferation and focal adhesion through CDC42/RAC1-PAK1-ERK1/2 signaling pathway and F-actin dynamics.

[Mechanism of percutaneous myocardial laser revascularization in the treatment of experimental cardiac ischemia].

OBJECTIVE: To evaluate the cardiac angiogenesis after percutaneous myocardial laser revascularization (PMR). METHODS: The left anterior descending coronary arteries of 10 healthy mongrel dogs weighing 14 - 18 kg were ligated partially so as to construct a model of chronic cardiac ischemia. Then the dogs were randomly divided into 2 groups of 5 dogs: PMR and control groups. Cardiogenesis Holmium: YAG laser system was used to make endomyocardial channels (15 +/- 3 channels/dog) in the ischemic ventricular walls in PMR group 2 weeks after the ligation. Sham procedure was conducted on the control group. Myocardial perfusion was examined by single photon emission computed tomography (SPECT) and left ventricle ejection fraction (LVEF) was examined by cardiac ultrasound before the ligation and 1, 4, and 12 weeks after PRM in the PMR group and before and 3, 6, and 14 weeks after the ligation in the control group. In the PRM group one dog was killed after the SPECT and LVEF examination 1 and 4 weeks after the PRM respectively and the remaining 3 dogs were killed after the SPECT and LVEF examination 12 weeks after the PRM. The dogs in the control group were killed after the SPECT and LVEF examination 14 weeks after the ligation. Myocardial pathology and cardiac angiogenesis analysis were conducted in both groups. RESULTS: Three months after PMR or coronary artery ligation, the SPECT scores of the PMR and control groups decreased from 3.2 +/- 0.6 and 3.1 +/- 0.5 to 0.3 +/- 0.2 and 1.2 +/- 0.3 respectively (both P < 0.05), the LVEF of the 2 groups increased from 42.6 +/- 6.5 and 43.2 +/- 8.7 to 55.8 +/- 7.6 and 42.6 +/- 6.5 respectively (both P < 0.05). Microscopy showed that the amount of micrangii was 45.6 +/- 7.4 vessel/field in the PMR region of the PRM group, significantly much more than that in the non-ischemic region of the PRM group (18.2 +/- 4.7), the ischemic region of the control group (21.4 +/- 5.6), and the non-ischemic region of the control group (17.3 +/- 6.9, all P < 0.05). CONCLUSION: PMR promotes angiogenesis in the ischemic myocardial wall, thus improving the blood perfusion of ischemic myocardium and global cardiac systolic function.

Inhibition of Aurora-B suppresses HepG2 cell invasion and migration via the PI3K/Akt/NF-κB signaling pathway in vitro.

In the present study, the effect of Aurora-B inhibition on HepG2 cell invasion and migration in vitro was investigated. A recombinant plasmid targeting the Aurora-B gene (MiR-Aurora-B) was used to inhibit Aurora-B expression in HepG2 cells. Cell migration and invasion were investigated using Transwell migration and invasion assays. The results demonstrated that cell invasion and migration were suppressed by inhibiting Aurora-B. In addition, the effect of Aurora-B inhibition on the activity of the phosphoinositide 3-kinase (PI3K)/Akt/nuclear factor (NF)-κB signaling pathway was investigated by analyzing the protein expression levels of phosphorylated (p)-Akt, Akt, NF-κB p65, matrix metalloproteinase (MMP)-2 and MMP-9 using western blot analysis. The results demonstrated that the protein expression levels of p-Akt, NF-κB p65, MMP-2 and MMP-9 were reduced significantly by inhibiting Aurora-B. Therefore, inhibition of Aurora-B was shown to suppress hepatocellular carcinoma cell migration and invasion by decreasing the activity of the PI3K/Akt/NF-κB signaling pathway in vitro.

Inhibition of Aurora-B suppresses osteosarcoma cell migration and invasion.

Previous studies have suggested that Aurora-B may be involved in cancer metastasis. However, its role has been poorly evaluated in osteosarcoma (OS). The aim of this study was to investigate the correlation between Aurora-B expression and metastasis in human OS. The human OS cell line, U2-OS, and OS biopsy specimens were used in the study. The expression of Aurora-B protein was examined using immunohistochemistry and western blotting in OS tissues and U2-OS cells, respectively. AZD1152-hydroxyquinazoline-pyrazol-anilide, an inhibitor of Aurora-B, was used to inhibit Aurora-B expression in U2-OS cells. The effect of Aurora-B inhibition on U2-OS cell proliferation, invasion and migration was assessed using MTT, colony formation, wound healing and Transwell assays. The results showed that positive expression of the Aurora-B protein was observed in the nucleus, and that Aurora-B expression levels in the cases with pulmonary metastases were significantly higher than in those without metastasis. In vitro, the proliferation, invasion and migration of U2-OS cells were suppressed by the inhibition of Aurora-B. These results suggest that Aurora-B may be involved in OS metastasis, and may be a promising target in the treatment of OS metastasis.

Influence of peritoneal transfer status on fasting blood glucose in non-diabetic nephropathy patients on continuous ambulatory peritoneal dialysis.

BACKGROUND: Extra glucose load in peritoneal dialysis is an important cause of newly-occurred diabetic mellitus, which initiates insulin treatment in some of the dialytic patients. The purpose of this study was to discuss the influence of the peritoneal transfer status on fasting blood glucose in non-diabetic nephropathy patients who are on continuous ambulatory peritoneal dialysis (CAPD). METHODS: One hundred and forty-five patients with total KT/V per week over 2.0 were recruited, including 60 males and 85 females. Fasting blood glucose (FBG), creatinine, blood urea nitrogen (BUN), blood albumin, blood lipid profile and blood C-reactive protein (CRP) were analyzed at the beginning of the peritoneal dialysis and after 12 months. A peritoneal equilibration test (PET) was carried out at the 3rd month of CAPD, and meantime residual renal function, peritoneal solute clearance rate, ultrafiltration volume and urine volume were also evaluated. RESULTS: Twenty-one cases were identified as a low transfer group (L), 32 cases as a low average transfer group (LA), 58 cases as a high average transfer group (HA) and 34 cases as a high transfer group (H). At the end of the 12th month, 83 cases had elevated FBG. Through stepwise multiple regression analysis we found the FBG level in these patients was positively related to glucose load and CRP, and negatively related to glucose absorption in the peritoneum (D/D(0)) and blood albumin (P < 0.05). Kaplan-Meier analysis during a 48-month follow-up found the morbidity of hyperglycemia to be 17/34 cases (50.1%) in the high transfer group, 20/58 cases (34.5%) in the high average transfer group, 11/32 cases (34.3%) in the low average transfer group, and 1/21 cases (5.4%) in the low transfer group. CONCLUSIONS: Patients with high peritoneal transfer capacity might have the highest morbidity from hyperglycemia among patients with these four different peritoneal transfer status. Glucose load, baseline CRP and FBG level before peritoneal dialysis, and D/D0 can efficiently predict hyperglycemia in CAPD patients.