Associated factors in modulating aflatoxin B1-albumin adduct level in three Chinese populations.

To elucidate the potential factors modulating exposure to aflatoxin B1 (AFB1) in three Chinese populations, an epidemiologic study was conducted in Fusui County and Nanning City of Guangxi Province and Chengdu City of Sichuan Province. The incidence rates of hepatocelluar carcinoma (HCC) for males in these three regions were 92-97 per 100,000, 32-47 per 100,000, and 21 per 100,000, respectively. Eighty-nine residents from Fusui, 196 residents from Nanning, and 118 residents from Chengdu were screened for AFB1-albumin adduct (AAA) levels and hepatitis virus (HBV, HCV, HDV, HEV, and HGV) infections, as well as liver biochemistry (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], y-glutamyl transpeptidase [GGT], 5'-nucleotidase, globulin [GLO], direct bilirubin, indirect bilirubin, and bile acid levels). At least one marker of hepatitis virus (HV) infection was present in 47.2% (42/89) of subjects from Fusui, while in Nanning and Chengdu the values were 15.8% (31/196) and 22.0% (26/118), respectively. In contrast to females, a higher level of AAA was observed in males; the difference was statistically significant in both the Nanning (P = 0.023) and the Chengdu (P = 0.026) subjects. In the Chengdu group, there was a significantly higher level of AAA in cases with HV infection (P = 0.041). There was a close association between AAA level and BMI in the adults without HV infection (r = 0.148, P = 0.044). Also, AAA was closely associated with DBIL and GGT in non-HV-infected minors (P < 0.05), closely associated with ALB, GLO, and GGT in HV-infected minors (P < 0.05), and closely associated with IBIL, GLO, TBA, and AST in non-HV-infected adults (P < 0.01). The co-effect of HV infection and AFB1 exposure may be responsible for the high risk of HCC in the Fusui region, whereas age, gender, BMI, and HV infection may modify individual aflatoxin levels. The relationship between AAA level and liver biochemistry indicates injury induced by aflatoxin to both hepatic parenchyma and biliary tract. But the associations vary with age and HV infection status.

Transfection with virus interleukin-10 to prolong murine heart allograft / 中华外科杂志

<p><b>OBJECTIVE</b>To prolong murine heart allograft by modifying hematopoietic stem cells with virus interleukin-10 (vIL-10).</p><p><b>METHODS</b>The recombinant of murine stem cell virus (MSCVneo) vIL-10 was composed of MSCVneo and vIL-10 cDNA and transduced hematopoietic stem cells from CBA (H-2(K)) mice's bone marrow in vitro. The transduced hematopoietic stem cells were transplanted into a syngenic CBA (H-2(K)) mouse with lethal irradiation (900 rad) in the same day through penis vein. The mouse's heterotopic heart transplantation was conducted using CBA (H-2(K)) mice as recipients, which vIL-10 in serum were positive by enzyme-linked immunosorbent assay, and donors hearts from C57BL/6 (H-2b) mice. Five animals in each group were sacrificed to test histopathology changes, the expression of interleukin (IL)-2, IL-4, IL-6, mIL-10, interferon (IFN)-gamma, inducible nitric oxide synthase (iNOS), B7-1, B7-2 and CD(4)(+) and CD(8)(+) T cells subset infiltration in heart transplants with reverse transcriptase polymerase chain reaction, immunohistochemistry and regular pathology.</p><p><b>RESULTS</b>Survival time of mice's allografts experimental group was (80.0 +/- 33.3) days. And survival time of control groups were (10.4 +/- 1.0) days, (11.6 +/- 1.1) days and (11.2 +/- 1.7) days, respectively (P < 0.01). Heart transplants from experimental group were characterized by sparse lymphocytes infiltration, mild endocarditis and vasculitis and preserved myocardial architecture, which had acute rejection of grade I. Cardiac allografts from other control groups developed severe cellular rejection with severe infiltrating lymphocytes, myocyte injury and necrosis, interstitial edema and hemorrhage, which had acute rejection of grade III. The expression of IL-2, INF-gamma, B7-1, B7-2 and iNOS mRNA in allografts in experimental group markedly down-regulated, whereas that in allografts in control groups markedly upregulated (P < 0.05). CD(4)(+) and CD(8)(+) T cell subsets infiltration in heart transplants from experimental group decreased, and that in control groups increased (P < 0.05).</p><p><b>CONCLUSION</b>Engineering Hematopoietic stem cells with vIL-10 can protect cardiac allografts from acute rejection and prolong cardiac allografts survival.</p>