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. On GD 20, one day prior to the expected day of delivery, pregnant rats were weighed and anesthetized, and laparotomized to remove the uterine and its content were weighed. Fetuses were examined macroscopically for any soft tissue and skeletal changes. The evaluation indicators included general sign observation, body weight, food consumption, animal death, corpora lutea, numbers of embryonic or fetal deaths, and viable fetuses including live birth rate, fetal resorption rate, and stillbirth rate, as well as sex, body weights, and skeletal and soft tissue alterations of fetuses. No treatment-related abnormalities were observed in prenatal developmental toxicity and fetal malformation parameters, indicating that D-allulose had no teratogenic effects on pregnant rats and fetuses. From the findings of this prenatal developmental toxicity study, the NOAEL of D-allulose was estimated to be 5000 mg/kg/day in pregnant SD rats.

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). The control group consisted of 64,940 subjects according to 1:5 age-sex stratified matching. The AMI incidence rates in AS and control group were compared using the Kaplan-Meier method. The hazard ratio of AMI and the control group was estimated by Cox proportional hazards regression analyses. During a 6 year follow up, 62 patients (0.48%) in the AS group and 157 persons (0.24%) in the control group developed AMI. The hazard ratio of AMI in the AS group was 1.99 (95% confidence interval [95% CI], 1.48-2.67) after adjusting for sex and age. The hazard ratio of AMI in the AS group was 1.81 (95% CI, 1.34-2.43) after adjusting for demographics and comorbid medical disorders. The incidence rate of AMI increases in newly diagnosed AS patients.

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. Loss of SWE1, which phosphorylates and inactivates the budding yeast Cdk1 homolog Cdc28p, suppressed the cdc5-3 hsl1Delta defect, suggesting that Cdc5p functions at a point upstream of Swe1p. In addition, the cdc5-4 and cdc5-7 mutants exhibited chained cell morphologies with shared cytoplasms between the connected cell bodies, indicating a cytokinetic defect. Close examination of these mutants revealed delayed septin assembly at the incipient bud site and loosely organized septin rings at the mother-bud neck. Components in the mitotic exit network (MEN) play important roles in normal cytokinesis. However, loss of BFA1 or BUB2, negative regulators of the MEN, failed to remedy the cytokinetic defect of these mutants, indicating that Cdc5p promotes cytokinesis independently of Bfa1p and Bub2p. Thus, Cdc5p contributes to the activation of the Swe1p-dependent Cdc28p/Clb pathway, normal septin function, and cytokinesis.