Teratogenicity of D-allulose.

The objective of this study was to evaluate whether D-allulose has teratogenic effects on rats. A prenatal developmental toxicity test was conducted in SD rats in compliance with modified OECD guidelines test number 414, prenatal developmental toxicity study. Pregnant female rats received repeated doses of 1250, 2500, or 5000 mg/kg body weight D-allulose, or a vehicle control by gavage on GD 6-15.

90-Day repeated oral toxicity test of D-allulose produced from Microbacterium foliorum.

D-allulose is considered an ideal substitute for sucrose, because it has 70% of the sweetness of sucrose and ultra-low energy. Chemical and biotechnological methods have been developed to produce Dallulose from D-fructose because D-allulose exists in extremely small quantities in nature. In this study, we performed a 90-day repeated oral dose toxicity test on rats using D-allulose produced from Microbacterium foliorum-a non-GMO species isolated from salad ginseng-in dosages of 0, 1250, 2500 and 5000 mg/kg/day.

Association of Acute Myocardial Infarction with ankylosing Spondylitis: A nationwide longitudinal cohort study.

Pertaining to an association between Acute Myocardial Infarction (AMI) and Ankylosing Spondylitis (AS) is sparse. The purpose of this nationwide longitudinal study was to investigate the prevalence of AMI in newly diagnosed AS patients. A total of 12,988 patients were enrolled in the AS group from January 1, 2010 to December 31, 2014 from the Korean National Health Insurance Service (NHIS).

Loss of CDC5 function in Saccharomyces cerevisiae leads to defects in Swe1p regulation and Bfa1p/Bub2p-independent cytokinesis.

In many organisms, polo kinases appear to play multiple roles during M-phase progression. To provide new insights into the function of budding yeast polo kinase Cdc5p, we generated novel temperature-sensitive cdc5 mutants by mutagenizing the C-terminal domain. Here we show that, at a semipermissive temperature, the cdc5-3 mutant exhibited a synergistic bud elongation and growth defect with loss of HSL1, a component important for normal G(2)/M transition.