Dietary carbohydrate composition is associated with polycystic ovary syndrome: a case-control study.

BACKGROUND: The present study aimed to investigate the association between dietary carbohydrate components and polycystic ovary syndrome (PCOS) in Iran. METHODS: In this case-control study, the diagnosis of PCOS was made based on the Rotterdam criteria in hospital clinics. Dietary assessments were performed using a validated semi-quantitative food frequency questionnaire. In total, 281 women with incident PCOS and 472 age-matched controls were assessed. Participants were interviewed through the clinics in Tehran, Iran, from February 2012 until March 2014. Average dietary glycaemic index (GI) and glycaemic load (GL) were calculated using GI of Iranian Foods Table and international tables of GI and GL values. We also assessed total dietary carbohydrate, refined grains, whole grains and fibre intakes. RESULTS: Participation rates were 97.5% among cases and 96.3% among controls. Mean (SD) dietary GI values among the controls and cases were 51.8 (4.7) and 59.7 (5.9) (P = 0.02) and GL values were 155.34 (35.2) and 173.6 (39.1) (P < 0.001), respectively. The multivariate adjusted odds ratio (OR) comparing the highest tertile of dietary GI and GL with the lowest tertile were 2.18 [95% confidence interval (CI) = 1.29-3.81; P-test for trend = 0.012] and 2.39 (95% CI = 1.23-3.01; P-test for trend = 0.001), respectively, with a significant trend. Fibre intake was inversely associated with PCOS (OR = 0.73; 95% CI = 0.49-0.91; P-test for trend = 0.013). CONCLUSIONS: The findings of the present study suggest that high dietary GI and GL and low fibre intake are significantly associated with PCOS.

Effects of irradiating adult mdx mice before full-length dystrophin cDNA transfer on host anti-dystrophin immunity.

Duchenne muscular dystrophy is a fatal, genetic disorder in which dystrophin-deficient muscle progressively degenerates, for which dystrophin gene transfer could provide effective treatment. The host immune response to dystrophin, however, is an obstacle to therapeutic gene expression. Understanding the dystrophin-induced host immune response will facilitate the discovery of strategies to prolong expression of recombinant dystrophin in dystrophic muscle. Using whole-body irradiation of the dystrophic mdx mouse before gene transfer, we temporally removed the immune system; a 600 rad dose removed peripheral immune cells, which were restored by self-reconstitution, and a 900 rad dose removed central and peripheral immune cells, which were restored by adoptive transfer of bone marrow from a syngeneic, dystrophin-normal donor. The anti-dystrophin humoral response was delayed and dystrophin expression was partially preserved in irradiated, vector-treated mice. Nonirradiated, vector-treated control mice lost muscle dystrophin expression completely, had an earlier anti-dystrophin humoral response and demonstrated muscle fibers focally surrounded with T cells. We conclude that dystrophin gene transfer induced anti-dystrophin humoral immunity and cell-mediated responses that were significantly diminished and delayed by temporal removal of the host central or peripheral immune cells. Furthermore, manipulation of central immunity altered the pattern of regulatory T cells in muscle.