Implications of Serum 25-Hydroxyvitamin D on the Prevalence of Neoplastic Polyps: A Cross-Sectional Study.

BACKGROUND: Vitamin D is believed to help in the suppression of malignant cells. Epidemiologic studies suggest that there is an association between vitamin D deficiency and an increased risk of colorectal cancer. The primary aim of this study is to determine if the prevalence of neoplastic polyps is inversely related to serum 25-hydroxyvitamin D levels 25(OH)D. METHODS: A prevalence study conducted between April 2009 and October 2009 evaluated 651 patients undergoing colonoscopy in order to determine if an association existed between low 25(OH)D levels and the prevalence of neoplastic colon polyps. Multivariate logistic and linear regression analyses were used to establish an association between 25(OH)D levels and histology of colon polyp with gender, race, age and BMI. RESULTS: The presence of tubular adenoma, villous adenoma, tubulo-villous adenoma, or malignancies did not differ (P = 0.5) among the stratified 25(OH)D groups (10 ng, 10.1 - 30 ng, > 30 ng). In addition, despite having more African-Americans than Caucasians in the lowest 25(OH)D category (22.7% versus 7.7%), the presence of neoplastic polyps did not differ significantly (P = 0.8) between the categorized racial groups (Caucasian and African-Americans). CONCLUSIONS: Low plasma 25(OH)D levels are not associated with an increased prevalence of neoplastic polyps.

Chondrogenic derivatives of embryonic stem cells seeded into 3D polycaprolactone scaffolds generated cartilage tissue in vivo.

In spite of recent scientific advances, treatment and repair of cartilage using tissue engineering techniques remains challenging. The major constraint is the limited proliferative capacity of mature autologous chondrocytes used in the tissue engineering approach. This problem can be addressed by using stem cells, which can self-renew with greater proliferative potential. Cartilage tissue engineering using adult mesenchymal stem cells derived from bone marrows has met with limited success. In this study we explored cartilage tissue generation from embryonic stem cells (ESCs). ESCs were induced to differentiate into chondroprogenitors, capable of proliferating and subsequently differentiating into cartilage-producing cells. The chondrogenic cells expressed chondrocyte-specific markers and deposited extracellular matrix proteins, proteoglycans. ESC-derived chondrogenic cells and polycaprolactone scaffolds seeded with these cells implanted in mice (129 SvImJ) generated cartilage tissue in vivo. Postimplant analysis of the retrieved tissues demonstrated cartilage-like tissue formation in 3-4 weeks. The cells of retrieved tissues also expressed the chondrocyte-specific marker collagen II. These findings suggest that ESCs can be used for tissue engineering and cultivation of cartilage tissues.

Paternal alcohol exposure affects sperm cytosine methyltransferase messenger RNA levels.

BACKGROUND: Although paternal alcohol exposure has been shown to affect the growth and behavior of offspring, the mechanisms underlying these effects still remain to be elucidated. This study examines one possible mechanism, namely, altered genomic imprinting as reflected by changes in sperm cytosine methyltransferase messenger RNA (mRNA) levels. METHODS: Male rats were treated with alcohol for 9 weeks before breeding. Resulting fetuses were counted and weighed, and paternal sperm was examined for changes in cytosine methyltransferase mRNA levels. RESULTS: Alcohol did not affect mating, fecundity, or litter size, but it did result in significantly decreased mean fetal weight, increased fetal runt incidence in offspring, and decreased cytosine methyltransferase mRNA levels in paternal sperm, compared with pair-fed and ad libitum controls. CONCLUSIONS: Alcohol-induced reductions in cytosine methyltransferase mRNA levels may reflect altered genomic imprinting caused by reduced DNA methylation, which, in turn, may lead to the expression of normally silent paternal alleles and may be a mechanism for paternal alcohol effects.