Mast Cells And Ethanol Consumption: Interactions In The Prostate, Epididymis And Testis Of Uchb Rats.

Alcoholism has reached alarming proportions while fertility rates slowing in populations. The assessment of inflammatory effects with emphasis on the variation of the mast cells comparing ethanol chronic ingestion on reproductive organs deserves attention. The mast cells were investigated with light microscopy using toluidine blue to locate and count total mast cells and immunohistochemistry to identify the connective tissue mast cells (CTMC). The increase in total mast cells in the prostate, total and degranulated mast cells in epididymis of UChB rats was accompanied by a greater proportion of mucosal mast cells (MMC) in these organs. In addition, a lower incidence of degranulated mast cells was observed in epididymis of control rats. Ethanol increases the number of total and degranulated mast cells in the prostate and epididymis, as well as associated with increasing MMC, and therefore, it could be leading to inflammation in these organs. © 2011 John Wiley & Sons A/S.66317017

The annexin 1-/- mouse: phenotypic studies

We investigated the phenotype of Anx-A1-/- mice and studied the appearance of the gene expression during embryonic and postnatal development. Anx-A1-/- mice are fertile and there were no apparent differences in litter sizes or other breeding statistics when compared to litter mate Anx-A1+/+ controls. The null mice grew at the same rate as the Anx-A1+/+ controls and appeared normal at all ages. Plasma sodium, potassium and possibly calcium were slightly elevated in an apparently genotype-dependent fashion, although all these differences were probably still within the normal range. The liver enzyme ALT was significantly elevated in the Anx-A1-/- mice but most other aspects of blood chemistry were no different. In terms of post mortem pathology, there were few exceptional findings although genotype related changes were seen in the weight of the liver, heart, thymus, pancreas, pituitary gland and kidney at necroscopy. Examination by western blotting of the tissue concentrations of other members of the annexin family revealed that Anx-A1 gene deletion lead, in some organs (e.g. lung and thymus), to changes in the tissue concentration of other annexins as well as the pro-inflammatory enzymes COX-2, cPLA2 and iNOS. There was some evidence of a sexual dimorphism in this effect. Anx-A1 gene expression was first detected at embryonic day 10.5 in the corneal epithelium. Thereafter, the skin, bone and respiratory tract were among several sites that displayed strong gene expression during embryonic development whereas the brain and the heart exhibited little gene expression at any developmental stage. These findings are discussed in relation to several proposed roles for the protein

BRCA2 Polymorphic Stop Codon K3326X and the Risk of Breast, Prostate, and Ovarian Cancers

Surgical oncolog

BRCA2 Polymorphic Stop Codon K3326X and the Risk of Breast, Prostate, and Ovarian Cancers

Background: The K3326X variant in BRCA2 (BRCA2∗c.9976A>T p.Lys3326∗rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormonerelated cancers. Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76637 cancer case patients and 83796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided. Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9×10-6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8×10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor-negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4×10-5 and ORw = 1.50, 95% CI = 1.28 t