SUMMARY Carcinoma of the urinary bladder is the most common malignancy in the Middle East and parts of Africa where schistosomiasis is a widespread problem. Much evidence supports the association between schistosomiasis and bladder cancer: this includes the geographical correlation between the two conditions, the distinctive patterns of gender and age at diagnosis, the clinicopathological identity of schistosome-associated bladder cancer, and extensive evidence in experimentally infected animals. Multiple factors have been suggested as causative agents in schistosome-associated bladder carcinogenesis. Of these, N-nitroso compounds appear to be of particular importance since they were found at high levels in the urine of patients with schistosomiasis-associated bladder cancer. Various strains of bacteria that can mediate nitrosation reactions leading to the formation of N-nitrosamines have been identified in the urine of subjects with schistosomiasis at higher intensities of infection than in normal subjects. In experimental schistosomiasis, the activities of carcinogen-metabolizing enzymes are increased soon after infection but are reduced again during the later chronic stages of the disease. Not only could this prolong the period of exposure to activated N-nitrosamines, but also inflammatory cells, sitmulated as a result of the infection, may induce the endogenous synthesis of N-nitrosamines as well as generating oxygen radicals. Higher than normal levels of host cell DNA damage are therefore anticipated, and they have indeed been observed in the case of alkylation damage, together with an inefficiency in the capacity of relevant enzymes to repair this damaged DNA. In experimental schistosomiasis, it was also found that endogenous levels of host cell DNA damage were related to the intensity of infection. All of these factors could contribute to an increased risk of bladder cancer in patients with schistosomiasis, and in particular, the gene changes observed may have potential for use as biomarkers in the early detection of bladder cancer that may assist in alleviating the problem.

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Emotional Intelligence (EI) emerged in the 1990s as an ability based construct analogous to general Intelligence. However, over the past 3 decades two further, conceptually distinct forms of EI have emerged (often termed “trait EI” and “mixed model EI”) along with a large number of psychometric tools designed to measure these forms. Currently more than 30 different widely-used measures of EI have been developed. Although there is some clarity within the EI field regarding the types of EI and their respective measures, those external to the field are faced with a seemingly complex EI literature, overlapping terminology, and multiple published measures. In this paper we seek to provide guidance to researchers and practitioners seeking to utilize EI in their work. We first provide an overview of the different conceptualizations of EI. We then provide a set of recommendations for practitioners and researchers regarding the most appropriate measures of EI for a range of different purposes. We provide guidance both on how to select and use different measures of EI. We conclude with a comprehensive review of the major measures of EI in terms of factor structure, reliability, and validity.

A range of personality traits, attitudes and health beliefs can predict help-seeking behaviour for mental health problems in adolescents. The variable 'Perceived Benefits' is of particular importance as it is: (1) a strong and robust predictor of help-seeking behaviour; and (2) a factor that can theoretically be modified based on health promotion programmes.

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Summary Damage arising from putative environmental sources has been found in the DNA of the gastric and colorectal mucosae of patients presenting with gastrointestinal disorders from the South Manchester area.06-Methylguanine (06-MeG) in the range 0.010->0.300timolesmole-' adenine was heterogeneously distributed both between and within individuals. The pattern of alkylation of tissue DNA appears to differ when comparison is made between gastric and colorectal samples. Most of the gastric tumour DNA samples were alkylated (5/6; 0.087 + 0.097), whereas the DNA of the associated mucosa was alkylated less frequently (2/7) and to a lesser extent; (0.017 ± 0.030; P = 0.07). Conversely, colorectal tumour DNA was alkylated infrequently (1/7) and to a lower extent (0.003 ± 0.007) than the DNA of the adjacent mucosa (8/10 samples alkylated with a mean of 0.083 + 0.106; P = <0.01), or indeed of any other tissue. Although increased levels of DNA damage in tissue associated with malignant disease have been indicated by independent studies of DNA damage at other cancer sites, significant differences were not observed in the present report, neither was there any suggestion of a relationship with smoking or alcohol consumption.The data provided by this report indicate that exposure to putative environmental alkylating agents occurs in the UK at levels comparable to those previously detected in areas of higher cancer risk. Although we cannot determine the extent to which this DNA damage is attributable to normal background exposures, it is evident that the alkylation of tissue DNA occurs and is not uniform. In conjunction with other reports, therefore these differences may begin to provide indications of mechanisms that could be of relevance in the aetiology of gastrointestinal cancers.

The ability of four mutagenic/carcinogenic chemicals administered as single doses to induce a programmed form of cell death (apoptosis) in the BDF1 mouse large bowel was studied and compared with a previous study on the small intestine using the same mice. The number of apoptotic cells was counted following treatment with the direct-acting agents N-nitroso-N-methylurea (NMU) and N-nitroso-N-ethylurea (NEU) and two agents which require metabolic activation 1,2-dimethylhydrazine (DMH) and N-nitrosodimethylamine (NDMA). DMH (80 mg/kg) was the most effective at inducing acute cell death and this was closely followed by NMU (200 mg/kg). The least effective agent in the large bowel was NDMA. The peak yield of apoptosis occurred between 4 h (NEU) and 8 h (DMH) after treatment. An analysis of the changing shapes of the frequency plots of apoptosis at each cell position in the crypt at various times after exposure permits an estimate to be made of the position in the crypt of the primary target cells for the cytotoxic action at time t = 0. For the agents studied, this is in the range of the 5th to the 10th position from the base of the crypt. This distribution for the target cells for apoptotic cell death is not coincident with that for the presumptive stem cells, which is at cell position 1 or 2. Comparisons with results previously obtained in the small intestine (ileum) of the same mice show that the relative cytotoxic effectiveness of the four agents differs. Furthermore, the position of the target cells is at about the 4th position from the bottom of the crypt in the ileum, and here the distribution is coincident with that presumed for the stem cells. Our interpretation of the data is that damaged cells in the stem cell region of the small bowel are removed by the activation of a cell suicide programme, which effectively removes potentially harmful genetic alterations. In contrast, in the large bowel, cell death is not initiated particularly strongly in the stem cell region but tends to occur higher in the crypt. The absence of this selective deletion process may result in the perpetuation of deleterious mutations in the colonic stem cell population and this may explain in part, the higher incidence of cancers observed in the large bowel.