Background Exposure to pesticides is associated with an increase in the incidence of cancer. We aimed to investigate the association of serum organochlorine pesticides (OCPs) and organophosphorus pesticides (OPs) levels and GSTM1/GSTT1 gene polymorphism with bladder cancer (BC). Methods This study was performed on 57 patients with BC and 30 controls (C). Acetylcholinesterase (AChE) activity, arylesterase activity of paraoxonase‐1 (ARE), total antioxidant capacity (TAC), and malondialdehyde (MDA) levels were determined in serums of all participants. Genomic DNA was extracted using the salting out method and GSTM1/GSTT1 gene polymorphisms were examined by multiplex polymerase chain reaction assay. Measurement of OCPs (α‐hexachlorocyclohexane [α‐HCH], β‐HCH, γ‐HCH, 2,4‐dichlorodiphenyltrichloroethane [2,4‐DDT], 4,4‐DDT, 2,4‐ dichlorodiphenyldichloroethylene [2,4‐DDE], and 4,4‐DDE) in serum was carried out using an FID‐equipped gas‐chromatography system. Results AChE activity was significantly lower, ARE activity and TAC were declined but it was not statistically significant, however, α‐HCH, γ‐HCH, 4,4‐DDE, 2,4‐DDT, and 4,4‐DDT pesticides, and MDA were significantly higher in BC patients compared with the control subjects. Also, a positive correlation was found between the number of smoked cigarettes and the years of smoking with BC development. There was no association between GSTM1/GSTT1 gene polymorphisms and OCPs in BC patients. Conclusion Due to the higher levels of some OCPs in the BC patients, along with the reduction in AChE activity and increased MDA levels, it may be concluded that OCPs and OPs play an important role in the induction of BC in southeastern Iran.

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Background:To improve patient survival after a renal transplant, it is important to detect which variables affect it.Objectives:This study aimed to assess the effect of renal allograft failure on patient survival.Patients and Methods:This retrospective cohort study included 405 renal transplant patients from Kerman University of Medical Sciences hospital, Kerman, Iran from 2004 to 2010. Kaplan-Meier method was used to estimate survival rates of patients, and time-dependent Cox regression was used to examine the effect of allograft failure on patient survival.Results:During 4.06 years (median) of follow-up 28 (6.9%) patients died and 20 (71.4%) of dead patients had allograft failure. Survival rate of patients with allograft failure at 1-, 3-, 5-, and 7-year were 0.98, 0.8, 0.53, and 0.53, respectively; in patients with allograft function these values were 0.99, 0.98, 0.97, and 0.96, respectively. The unadjusted death rate was 0.5 per 100 patient years for the maintained allograft function, which increased to 9 per 100 patient years for patients following allograft failure. In fully adjusted model the risk of death increased in patients with allograft failure (HR = 2.09; 95% CI: 1.56-2.81), pretransplant diabetes (HR = 2.81; 95% CI: 1.2-6.7), patients with BMI ≥ 25 (vs. 18.5 ≤ BMI < 25) (HR = 3.56; 95% CI: 1.09-11.6). With an increase in recipient age this risk increased (HR = 1.04 per year increase; 95% CI: 1.01-6.7). Receiving a living kidney transplant decreased this risk (HR = 0.52; 95% CI: 0.39-0.69).Conclusions:An increase in recipient age and BMI, affliction with diabetes, allograft failure, and receiving deceased kidney transplant increased the risk of death.