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Introduction: The progression of fibrosis in chronic hepatitis C (CHC) is a multifactorial process. The high adverse effects and the cost of standard health care increase the demand to discover new predictors for the progression of fibrosis in CHC patients. Our study aims to establish the relation between the angiogenic marker [vascular endothelial growth factor (VEGF)] and activated hepatic stellate cells (HSCs) represented by the expression of α-smooth muscle actin (α-SMA) and whether these 2 markers can be used as predictors for the progression of fibrosis in patients with CHC., Materials and Methods: Histopathologic and immunohistochemical analyses were used for examining the morphology and the expression of VEGF and α-SMA in 60 CHC biopsies procured from CHC patients. Multivariate analysis was used to correlate the protein expression with staging and grading of liver fibrosis. Cutoff values of α-SMA and VEGF were determined by the receiver operating characteristics curve., Results: There was a positive correlation between VEGF and HSCs expressing α-SMA (ρ=0.287, P=0.026) and both factors were correlated with the stage of fibrosis (P<0.001). Using the receiver operating characteristics curve, both VEGF (area under the curve=0.71, P<0.006) and α-SMA (area under the curve=0.82, P<0.001) were positive predictors for moderate and severe fibrosis., Conclusions: This study demonstrates the relation between VEGF expression and the activated HSCs denoted by the expression of α-SMA in CHC biopsies and together can be used as a predictor for the progression of fibrosis.

Background: Because the occurrence of BK virus (BKV) nephritis is far less frequent than BK viremia or viruria, analysis of risk factors for BKV nephritis as an endpoint could lead to erroneous findings. We undertook a prospective study to evaluate the risk factors for the occurrence of BKV infections using BK viruria and viremia as endpoints., Methods: Two hundred forty renal only transplant recipients were prospectively enrolled into our institutional review board-approved single center study to evaluate various aspects of posttransplant BKV infection. All patients were followed up for a minimum of 6 months posttransplant., Results: Of the 240 subjects, 154 were whites, 61 African Americans, and 25 belonged to other races. A total of 94 developed BKV infection (any degree of BK viruria or viremia) whereas 146 developed no infection. Among these, 33 had BK viruria alone, 61 had BK viremia with viruria and 25 had significant viremia defined as BKV DNA more than 10,000 copies/mL of plasma. Lower proportion of African Americans developed BKV infection, 14 of 61 (23%), as opposed to whites, 67 of 154 (47%). Logistic regression model showed lower risk of any BKV infection in African American recipient race (OR, 0.38; 95% CI, 0.17-0.82; P=0.016) and higher risk of significant BKV infection with occurrence of acute rejection (OR, 3.9; 95% CI, 1.31-11.8; P=0.015). The Kaplan-Meier analysis shows a trend toward greater freedom from BKV infection in African Americans as opposed to other racial groups (P=0.33)., Conclusion: Renal transplant recipients of African American race had a lower risk of posttransplant BKV infection compared with whites, independent of other confounding risk factors.

Our objective was to determine the maximum tolerated doses of tirapazamine and cyclophosphamide given i.v. in combination. Eligible patients had advanced solid tumors refractory to conventional treatment. Tirapazamine (escalated from 80 to 390 mg/m(2)) was given i.v. over 2 h and followed by cyclophosphamide over 1 h. The cyclophosphamide dose was fixed at 1000 mg/m(2) until the tirapazamine dose of 390 mg/m(2) was reached. Once that dose of tirapazamine was reached, the cyclophosphamide dose was escalated to 1250 and 1500 mg/m(2). Twenty-eight patients were enrolled. The dose-limiting toxicity was granulocytopenia. One patient had transient deafness for 2 days. Four other patients had grade 1 ototoxicity. Grade 1 and 2 muscle cramps were observed at all dose levels. Other toxic effects observed included fatigue, nausea, vomiting, headache, diarrhea, drug fever, elevated transaminases and elevated creatine phosphokinase. Three patients had stable disease and the longest time to progression was 5 months. The combination of tirapazamine and cyclophosphamide is feasible, and the dose-limiting toxicity is granulocytopenia. The use of growth factors could possibly allow escalation of tirapazamine doses in future phase II trials. Without growth factor support, the recommended doses of tirapazamine and cyclophosphamide when administered in this schedule are 260 and 1000 mg/m(2), respectively.

A case report is presented of a white woman, gravida 4, para 2, abortus 1, who experienced protrusion of a gravid uterus through the anterior rectus fascia. The uterus subsequently became entrapped and was reduced only after cesarean section at 34 weeks' gestation.