Consumption of Nutritionally Enriched Hen Eggs Enhances Endothelium-Dependent Vasodilation via Cyclooxygenase Metabolites in Healthy Young People-A Randomized Study.

Objective: The present study aimed to evaluate the effects of enriched hen egg consumption on endothelium-dependent vasodilation (EDV) and the role of cyclooxygenases in EDV in the microcirculation of young healthy individuals. This study hypothesizes that Nutri4 eggs will improve endothelial function, which will be manifested by changes in microcirculatory flow measured by a laser Doppler flowmeter (LDF) during reactive hyperemia in response to vascular occlusion, in which -3 PUFA plays an important role as well as its degradation pathway by cyclooxygenases.

Materials And Methods: Participants consumed three eggs per day for three weeks: The control group (CTRL, = 14) consumed regular hen eggs (approximately 0.

Brca1 and differentiation.

Breast cancer is one of the most frequent malignancies affecting women. The human breast cancer gene 1 (BRCA1) gene is mutated in a distinct proportion of hereditary breast and ovarian cancers. Tumourigenesis in individuals with germline BRCA1 mutations requires somatic inactivation of the remaining wild-type allelle.

FIP-2, an IkappaB-kinase-gamma-related protein, is associated with the Golgi apparatus and translocates to the marginal band during chicken erythroblast differentiation.

Using an antiserum directed against marginal band associated proteins of chicken erythrocytes we isolated clones encoding the chicken homolog of 14.7K-interacting protein 2 (FIP-2), a protein potentially involved in tumor necrosis factor-alpha/nuclear factor-kappaB signaling, from a chicken erythroblast cDNA library. We found that chicken FIP-2 was expressed in a variety of tissues and cell types, but unlike its human counterpart, alternative splicing does not appear to take place.

Evidence for separable functions of tuberous sclerosis gene products in mammalian cell cycle regulation.

Tuberous sclerosis is an autosomal dominant disease affecting approximately 1 in 6,000 individuals. It is caused by mutations in either TSC1 on chromosome 9q34, which encodes hamartin, or TSC2 on chromosome 16p13.3, which encodes tuberin.

Tuberous sclerosis causing mutants of the TSC2 gene product affect proliferation and p27 expression.

The autosomal dominant disease tuberous sclerosis (TSC) is caused by mutations in either TSC1 on chromosome 9q34, encoding hamartin, or TSC2 on chromosome 16p13.3, encoding tuberin. TSC is characterized by hamartomas that occur in many organs of affected patients and these have been considered to likely result from defects in proliferation control.

Tuberous sclerosis gene products in proliferation control.

Two genes, TSC1 and TSC2, have been shown to be responsible for tuberous sclerosis (TSC). The detection of loss of heterozygosity of TSC1 or TSC2 in hamartomas, the growths characteristically occurring in TSC patients, suggested a tumor suppressor function for their gene products hamartin and tuberin. Studies analyzing ectopically modulated expression of TSC2 in human and rodent cells together with the finding that a homolog of TSC2 regulates the Drosophila cell cycle suggest that TSC is a disease of proliferation/cell cycle control.

The TSC1 gene product, hamartin, negatively regulates cell proliferation.

Tuberous sclerosis is an autosomal dominant hereditary disease caused by mutations in either the TSC1 or the TSC2 tumor suppressor gene. The TSC1 gene on chromosome 9q34 encodes a 130 kDa protein named hamartin, and the TSC2 gene on chromosome 16p13.3 codes for tuberin, a 200 kDa protein.

Cyclin-dependent kinases at the G1-S transition of the mammalian cell cycle.

In the mammalian cell cycle, the transition from the G1 phase to S phase, in which DNA replication occurs, is dependent on tight cell size control and has been shown to be regulated by the cyclin-dependent kinases (Cdks) 2, 3, 4 and 6. Activities of Cdks are controlled by association with cyclins and reversible phosphorylation reactions. An additional level of regulation is provided by inhibitors of Cdks.