The immune system may either have a protective role against sunburn and skin cancer or, conversely, promote solar damage. The skin is poised to react to infections and injury, such as sunburn, with rapidly acting mechanisms (innate immunity) that precede the development of acquired immunity and serve as an immediate defense system. Some of these mechanisms, including activation of defensins and complement, modify subsequent acquired immunity. An array of induced immune-regulatory and pro-inflammatory mediators is evident, at the gene expression level, from the microarray analysis of both intrinsically aged and photoaged skin. Thus, inflammatory mechanisms may accentuate the effect of UV radiation to amplify direct damaging effects on molecules and cells, including DNA, proteins, and lipids, which cause immunosuppression, cancer, and photoaging. A greater understanding of the cutaneous immune system's response to photo-skin interactions is essential to comprehensively protect the skin from adverse solar effects. Sunscreen product protection measured only as reduction in redness (current "sun" protection factor) may no longer be sufficient, as it is becoming clear that protection against UV-induced immune changes is of equal if not of greater importance. Greater knowledge of these processes will also enable the development of improved strategies to repair photodamaged skin.

Objectives This study examined the main and interactive effects of MDD and lifetime nonsuicidal self-injury (NSSI) on current suicide risk and past suicide attempts. We predicted that individuals with a history of NSSI and current MDD would be at greater suicide risk than those with either risk factor alone. An interaction between lifetime MDD and NSSI was hypothesized for past suicide attempts. Methods 204 substance dependent inpatients completed self-report measures and a diagnostic interview. Results Patients with both a history of NSSI and current MDD, relative to all other groups, had the greatest suicide risk. No support was found for the lifetime MDD by NSSI interaction. Conclusion Findings suggest the relevance of both NSSI and MDD in suicide risk.

Experimental evidence on the anticancer properties of dietary prebiotics such as chicory inulin and oligofructose and dietary probiotics has accumulated in recent years. Various experimental models ranging from chemoprevention studies, tumour implantation models to genetically modified mice models, etc. have systematically shown the protective effects of these food ingredients. In some studies it appeared that synbiotics (combination of pre-and probiotics) exerted synergistic activity against processes of carcinogenesis. The logical next step in research was to find out if these observations also would be valid for human volunteers. This was the principal goal of the EU-sponsored SYNCAN project (QLK1-1999-346) which involved the integration of an in vitro study to select the most suitable synbiotic preparation, the application of this synbiotic in an in vivo rat model of chemically induced colon cancer, and, as the heart of the project, the investigation of the synbiotic effects in a human intervention study. The in vitro tests consisted of fermentation studies where the interaction of pre-and probiotics was studied. Cell-free supernatants were generated from various synbiotic combinations fermented by faecal slurry, which were then used to optimise a series of bioassays. In the rat study the anticarcinogenic effect of prebiotics and synbiotics but not of probiotics was demonstrated. Using tissue samples generated in this model, attempts were made to gain a better insight into the mechanisms underlying cancer development. The human intervention study consisted of two groups of volunteers. One group was composed of people at high risk (polypectomised subjects) for colon cancer and the other of volunteers (colon cancer subjects) who had previously undergone 'curative resection' for colon cancer but were not currently receiving treatment. The present paper describes the experimental design of the SYNCAN study, and demonstrates a functional effect of the synbiotic preparation (probiotic survival during gastrointestinal transit and modification of the intestinal flora).

Background-Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa. Aims-To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC. Patients-Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls. Methods-Crypt cell proliferation was measured at five sites in the colon using two diVerent techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed. Results-There were no significant diVerences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant diVerences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers. Conclusion-Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC. (Gut 1998;43:85-92)