The alternative complement component factor B regulates UV-induced oedema, systemic suppression of contact and delayed hypersensitivity, and mast cell infiltration into the skin.

Ultraviolet (UV) wavelengths in sunlight are the prime cause of skin cancer in humans with both the UVA and UVB wavebands making a contribution to photocarcinogenesis. UV has many different biological effects on the skin that contribute to carcinogenesis, including suppression of adaptive immunity, sunburn and altering the migration of mast cells into and away from irradiated skin. Many molecular mechanisms have been identified as contributing to skin responses to UV.

Pharmacologically antagonizing the CXCR4-CXCL12 chemokine pathway with AMD3100 inhibits sunlight-induced skin cancer.

One way sunlight causes skin cancer is by suppressing anti-tumor immunity. A major mechanism involves altering mast cell migration via the C-X-C motif chemokine receptor 4-C-X-C motif chemokine ligand 12 (CXCR4-CXCL12) chemokine pathway. We have discovered that pharmacologically blocking this pathway with the CXCR4 antagonist AMD3100 prevents both UV radiation-induced immune suppression and skin cancer.

The immune-modulating cytokine and endogenous Alarmin interleukin-33 is upregulated in skin exposed to inflammatory UVB radiation.

The cellular and molecular mechanisms by which UV radiation modulates inflammation and immunity while simultaneously maintaining skin homeostasis is complex and not completely understood. Similar to the effects of UV, IL-33 has potent immune-modulating properties that are mediated by the downstream induction of cytokines and chemokines. We have discovered that exposure of mice in vivo or human skin samples ex vivo to inflammatory doses of UVB induced IL-33 expression within the epidermal and dermal skin layers.

Helicobacter species in the human colon.

Objective: To determine the prevalence, frequency and colonization patterns of Helicobacter species throughout the colon.

Method: Patients having initial colonoscopy for nonspecific gastrointestinal disturbance had colonic biopsies taken from up to four sites during colonoscopy and examined for evidence of the Helicobacteraceae family using a group-specific PCR. Serum was also collected and examined for IgG reactivity to Helicobacter pylori.

Ovine small intestinal adenocarcinomas are not associated with infection by herpesviruses, Helicobacter species or Mycobacterium avium subspecies paratuberculosis.

Sheep in New Zealand more frequently develop small intestinal adenocarcinoma (SIA) than sheep in other countries. The reasons for this high rate of intestinal neoplasia are not known. In man, differences between countries in the incidence of neoplasia are often due to differences in the rate of infection by carcinogenic viruses or bacteria.

Alterations in Helicobacter pylori outer membrane and outer membrane vesicle-associated lipopolysaccharides under iron-limiting growth conditions.

Outer membrane vesicles (OMVs) shed from the gastroduodenal pathogen Helicobacter pylori have measurable effects on epithelial cell responses. The aim of this study was to determine the effect of iron availability, and its basis, on the extent and nature of lipopolysaccharide (LPS) produced on H. pylori OMVs and their parental bacterial cells.

E-cadherin expression and bromodeoxyuridine incorporation during development of ovarian inclusion cysts in age-matched breeder and incessantly ovulated CD-1 mice.

Background: Female CD-1/Swiss Webster mice subjected to incessant ovulation for 8 months and 12-month breeder mice both developed ovarian inclusion cysts similar to serous cystadenomas. The majority of cysts appeared to be dilated rete ovarii tubules, but high ovulation number resulted in more cortical inclusion cysts. We hypothesized that comparison of inclusion cyst pathology in animals of the same age, but with differences in total lifetime ovulation number, might allow us to determine distinguishing characteristics of the two types of cyst.

Incessant ovulation, inflammation and epithelial ovarian carcinogenesis: revisiting old hypotheses.

Epithelial ovarian cancer (EOC) is often a lethal disease because in many cases early symptoms go undetected. Although research proceeds apace, as yet there are few reliable and specific biomarkers for the early stages of the disease. EOC is an umbrella label for a highly heterogeneous collection of cancers, which includes tumours of low malignant potential, serous cystadenomas, mucinous and clear cell carcinomas, all of which are likely to arise from a number of epithelial cell types and a variety of progenitor lesions.