BackgroundCognitive dysfunction has been increasingly recognized in chronic kidney disease (CKD) patients. Senile plaques are important pathophysiological characteristic of cognitive dysfunction. The major component of plaques is the amyloid β (Aβ) peptide released from proteolytic cleavage of amyloid precursor protein (APP). Plasma Aβ has been a focus of the growing literature on blood based biomarkers for cognitive dysfunction. Oxidative stress is prevalent in CKD and it plays an important role in cognitive dysfunction. Increased oxidative stress leads to cause cleavage of APP and Aβ production. The aim of this study is to assess the antioxidant status and Aβ42 levels in plasma of CKD patients with cognitive dysfunction compared to CKD without cognitive dysfunction.MethodsA total of 60 subjects divided into 30 CKD without cognitive dysfunction and 30 CKD with cognitive dysfunction based on neuropsychological assessment tests. To compare antioxidant status and Aβ42 levels in plasma, the following groups such as healthy subjects (n = 30), normocytic normochromic anemia (n = 30) and Alzheimer's disease (AD, n = 10) patients were also maintained. Plasma Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), Reduced glutathione (GSH) and lipid peroxidation (LPO) were determined by spectrophotometrically. Aβ level was determined by immunoblotting method. The parameters were statistically compared with healthy, normocytic normochromic anemia and AD subjects.ResultsLike AD subjects, significantly increased Aβ and LPO level while decreased SOD, CAT, GPx and GSH levels were observed in plasma of CKD patients with cognitive dysfunction when compared to healthy, CKD without cognitive dysfunction and normocytic normochromic anemic subjects.ConclusionResults suggest that elevated plasma oxidative stress and Aβ were seen in CKD patients with cognitive dysfunction may be attributed to pathological changes within the brain.

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Hospital wastewater has the potential to be a threat to the hospital environment as it can contain pathogenic bacteria that may facilitate the resistant nature of organisms within effluent or water treatment plants. The recycling of hospital wastewater should have good quality. This study was carried out to highlight the incidence of antibiotic resistant bacteria in hospital-generated recycled water. This study was conducted in a tertiary care teaching hospital during June 2013-June 2014. One hundred and forty wastewater samples were aseptically collected at different stages in the recycling plant. The samples were processed within 2 hours following standard procedures for identification of bacteria and the pathogenic bacteria were isolated. The mostly identified pathogens were Staphylococcus aureus (11.42%), Pseudomonas aeruginosa (9.28%), Enterococcus faecalis (10%) and Bacillus subtilis (8.57%) which were removed by treatment, but Escherichia coli (16.42%), Klebsiella pneumonia (8.57%), and Proteus mirabilis (11.42%) survived in the final sedimentation tank (lagoon) from where this water will be used for gardening purposes. An antibiogram study showed these pathogens were resistant to first-line antibiotics. Effluent treatment plants in hospitals should be monitored for the fulfillment of the guidelines and quality control of treated water to stop the emergence of multi-drug resistant bacteria in the hospital environment.

Introduction: Chemoprevention may involve perturbation of a variety of steps in tumor initiation, promotion, and progression. Objective: To investigate the antiproliferative and anti-inflammatory potential effects of diindolylmethane (DIM) and lupeol on experimental bladder carcinogenesis. Methods: Sixty healthy male Wistar rats were selected and randomly divided into six groups, with 10 rats in each group. Group I: control; group II: N-butyl- N-(4-hydroxybutyl) nitrosamine (BBN; 150 mg/gavage/twice a week) for 8 weeks, and then they were given 100 ppm concentrations of dimethylarsenic acid (DMA) in the drinking water for 28 weeks; group III: BBN + DMA + DIM (5 mg/kg body weight (b.w.)/day) treatment was started after BBN treatment, and it was orally administered for 28 weeks); group IV: BBN + DMA + lupeol (50 mg/kg b.w./day) treatment was started after BBN treatment, and it was orally administered for 28 weeks); and groups V and VI: DIM and lupeol treatment alone for 36 weeks. Bladder tissues were collected after 36th week study protocol for further analysis. Results: Our results revealed that DIM and lupeol treatment showed inhibition of tumor growth in the bladder by histopathological confirmations as well as significantly ( p < 0.001) increased the expression of phosphotensin (PTEN) and significantly ( p < 0.001) decreased the expression of tumor necrosis factor α, nuclear factor κβ (p65) were quantified using Western blot analysis. DIM and lupeol treatment significantly ( p < 0.001) decreased the levels of Cox-2 in bladder tissue samples and NMP 22 in urine samples were quantified using enzyme-linked immunosorbent assay method. Conclusion: Preventive DIM and lupeol administration act as potent Cox-2 inhibitors, which activates the tumor suppressor protein PTEN against experimental bladder carcinogenesis by antiproliferative and anti-inflammatory properties.