Cisplatin (cis-diamminedichloroplatinum(II)) is an effective chemotherapeutic agent, and is successfully used in the treatment of a wide range of tumors. Despite its effectiveness as an anti-tumor drug, nephrotoxic side effects have significantly restricted its clinical use. Tubular epithelial cell deletion following cisplatin treatment is a major cause of renal injury. Oxidative stress significantly contributes to cisplatin-associated cytotoxicity, and use of antioxidants could counteract such cytotoxic effects of cisplatin. The renal microenvironmental changes following cisplatin treatment is a complex process and could be broadly categorized into three main pathological events, which at times might overlap: initial cytotoxic events, inflammatory events and fibroproliferative events. Stress responses and heat shock proteins generated following cisplatin treatment are actively involved in the initiation and progression of these events. In this article, we will briefly summarize factors involved in various phases of cisplatin-induced renal injuries.

Abstract. there is strong evidence that the angiopoietin family is involved in the regulation of tumour progression. recently, it has been reported that angiopoietin-like 4 (Angptl4) expression in cancer cells promotes the metastatic process by increasing vascular permeability. the present study was conducted to examine Angptl4 expression and its association with clinicopathological factors and prognosis in human colorectal cancers. We examined 144 cases of surgically-resected human colorectal adenocarcinomas by immunohistochemistry, rt-pcr and Western blot analysis. Also, overall survival was investigated. Among 144 cases of adenocarcinoma, 95 cases (66.0%) showed positive staining in the cytoplasm of the carcinoma cells for Angptl4. Histologically, well, moderately, poorly differentiated adenocarcinoma or mucinous carcinoma showed 55.2, 79.3, 61.5 or 44.4% expression of Angptl4, respectively. the expression of Angptl4 was correlated with the depth of tumour invasion (p<0.0005), Vienna classification (category 3-5) (p<0.00005), venous invasion (p<0.0005) and Duke's classification (p<0.005). However, Angptl4 expression was not correlated with overall survival. However, all patients (100%) with distant metastasis showed immunopositivity for Angptl4. the mrnA and the protein expression of Angptl4 were shown in four resected samples and cultured cell lines by rt-pcr or Western blot analysis. These findings suggest that Angptl4 is one of the factors involved in the progression of human colorectal cancer, especially venous invasion and distant metastasis. Introductioncolorectal cancer is one of the most common cancer types in the world today (1). the occurrence and progression of cancer are considered to be a series of genetic events affecting the structure and/or expression of a number of oncogenes, tumour suppressors, and growth factors (2,3). the deep invasive carcinomas, such as colorectal cancer, have higher rates of lymph duct and venous invasions, and lymph node metastasis (3). However, the mechanisms of invasion and metastasis of colorectal cancer are not fully understood.there is strong evidence that the angiopoietin family is involved in the regulation of tumour progression, cellular growth, and differentiation (4-6). Angiopoietin-like 4 (Angptl4) is a member of the family of angiopoietins and is also known as hepatic fibrinogen/angiopoietin-related protein (HeArp) (7), peroxisome proliferator-activated receptor-γ (ppArγ) angiopoietin-related gene (pgAr) (8), or fasting-induced adipose factor (FIAF) (9). Angptl4 is a circulating plasma protein and is expressed in the liver, adipose tissue, placenta, as well as in ischemic tissue (8,9). similar to angiopoietins and other angiopoietin-like proteins, Angptl4 contains an amino-terminal coiled-coil domain and a carboxyl-terminal fibrinogen-like domain (10). Angptl4 induces a strong proangiogenic response, independently of vascular endothelial growth factor (11), and is known to undergo hypoxia-induced gene expression in endothelial cells. this protein is up-regu...

BackgroundThe combination of deworming and improved sanitation or hygiene may result in greater reductions in soil-transmitted helminth (STH) infection than any single intervention on its own. We measured STH prevalence in rural Bangladesh and assessed potential interactions among deworming, hygienic latrines, and household finished floors.MethodologyWe conducted a cross-sectional survey (n = 1,630) in 100 villages in rural Bangladesh to measure three exposures: self-reported deworming consumption in the past 6 months, access to a hygienic latrine, and household flooring material. We collected stool samples from children 1–4 years, 5–12 years, and women 15–49 years. We performed mini-FLOTAC on preserved stool samples to detect Ascaris lumbricoides, Enterobius vermicularis, hookworm, and Trichuris trichiura ova. Approximately one-third (32%) of all individuals and 40% of school-aged children had an STH infection. Less than 2% of the sample had moderate/heavy intensity infections. Deworming was associated with lower Ascaris prevalence (adjusted prevalence ratio (PR) = 0.53; 95% CI 0.40, 0.71), but there was no significant association with hookworm (PR = 0.93, 95% CI 0.60, 1.44) or Trichuris (PR = 0.90, 95% CI 0.74, 1.08). PRs for hygienic latrine access were 0.91 (95% CI 0.67,1.24), 0.73 (95% CI 0.43,1.24), and 1.03 (95% CI 0.84,1.27) for Ascaris, hookworm, and Trichuris, respectively. Finished floors were associated with lower Ascaris prevalence (PR = 0.56, 95% CI 0.32, 0.97) but not associated with hookworm (PR = 0.48 95% CI 0.16,1.45) or Trichuris (PR = 0.98, 95% CI 0.72,1.33). Across helminths and combinations of exposures, adjusted prevalence ratios for joint exposures were consistently more protective than those for individual exposures.ConclusionsWe found moderate STH prevalence in rural Bangladesh among children and women of childbearing age. This study is one of the first to examine independent and combined associations with deworming, sanitation, and hygiene. Our results suggest that coupling deworming with sanitation and flooring interventions may yield more sustained reductions in STH prevalence.

To explore the possible role of heat shock protein (HSP) 47 in the age-related renal changes in Fischer 344 (F 344) rats, the expression of collagen-binding HSP47 with various proteins implicated in phenotypic modulation (alpha-smooth muscle actin, desmin, and vimentin) and fibrosis (type I, type III, and type IV collagens) was examined in young and old F 344 rat kidneys. Male F 344 rats often develop spontaneous nephropathy in old age. Kidneys obtained from 24-month-old F 344 rats showed glomerulosclerosis with marked tubulointerstitial damage including interstitial fibrosis, while no significant histological alteration was found in the kidneys of 6-month-old rats. Immunohistochemical analysis showed an increased accumulation of type I, type III, and type IV collagens in areas of glomerulosclerosis and interstitial fibrosis in old rat kidneys. In kidneys of young rats, collagen-binding HSP47 expression was weak in the glomeruli and occasionally seen in the interstitial cells. In contrast, strong immunostaining for HSP47 was noted in the glomeruli, tubular epithelial cells, and interstitial cells in kidneys of old rats. In addition, phenotypic alterations of mesangial cells and interstitial cells (immunopositive for alpha-smooth muscle actin), glomerular epithelial cells (immunopositive for desmin), and tubular epithelial cells (immunopositive for vimentin) were found in the kidneys of old F 344 rats. Double immunostaining showed that all these phenotypically altered renal cells express HSP47 and that increased expression of HSP47 was always associated with increased expression of collagens in the old rat kidneys. From the above observations, it is concluded that overexpression of HSP47 by phenotypically altered renal cells might play an important role in the excessive assembly of collagens and could thereby contribute to the glomerulosclerosis and interstitial fibrosis found in kidneys of aged F 344 rats.

Background: Role of obesity on renal pathological and structural changes is not