Restless legs syndrome in patients with type 2 diabetes: effectiveness of pramipexole therapy.

Objective: We investigated the prevalence of restless legs syndrome (RLS) in Japanese patients with type 2 diabetes and assessed the efficacy of pramipexole therapy.

Design: One hundred patients with type 2 diabetes without secondary causes of RLS were sequentially screened for the 12-week, prospective, single arm study. RLS was screened by essential diagnostic criteria developed by the International Restless Legs Study Group.

Endogenous Wnt/beta-catenin signaling is required for cardiac differentiation in human embryonic stem cells.

Background: Wnt/beta-catenin signaling is an important regulator of differentiation and morphogenesis that can also control stem cell fates. Our group has developed an efficient protocol to generate cardiomyocytes from human embryonic stem (ES) cells via induction with activin A and BMP4.

Methodology/principal Findings: We tested the hypothesis that Wnt/beta-catenin signals control both early mesoderm induction and later cardiac differentiation in this system.

A1C but not serum glycated albumin is elevated because of iron deficiency in late pregnancy in diabetic women.

OBJECTIVE We have already reported that A1C is elevated because of iron deficiency in late pregnancy among nondiabetic pregnant women. This report examined whether the same phenomenon is observed in pregnant women with diabetes. RESEARCH DESIGN AND METHODS This longitudinal study was conducted in 17 pregnant women with diabetes (20-35 weeks of pregnancy).

Biphasic role for Wnt/beta-catenin signaling in cardiac specification in zebrafish and embryonic stem cells.

Understanding pathways controlling cardiac development may offer insights that are useful for stem cell-based cardiac repair. Developmental studies indicate that the Wnt/beta-catenin pathway negatively regulates cardiac differentiation, whereas studies with pluripotent embryonal carcinoma cells suggest that this pathway promotes cardiogenesis. This apparent contradiction led us to hypothesize that Wnt/beta-catenin signaling acts biphasically, either promoting or inhibiting cardiogenesis depending on timing.

The Polycomb-group gene Rae28 sustains Nkx2.5/Csx expression and is essential for cardiac morphogenesis.

The Polycomb-group (PcG) gene Rae28 is a mammalian homologue of the Drosophila gene polyhomeotic. PcG genes are known to maintain transcription states, once initiated, probably by regulating chromatin structure. Since homozygous Rae28-deficient (Rae28(-/-)) mice displayed cardiac anomalies similar to congenital heart diseases in humans, we examined the role of Rae28 in cardiac morphogenesis at the molecular level.

A case of hypereosinophilic syndrome presenting mid-ventricular obstruction.

A 59-year-old man with hypereosinophilic syndrome (HES) who had been maintained with low-dose prednisolone for 5 years developed the characteristic features of hypertrophic cardiomyopathy. Left ventricular endomyocardial biopsy revealed no eosinophilic infiltration but extensive myocardial fibrosis. Cardiac involvement in HES presents as endocardial fibrosis, resulting in a clinical presentation of restrictive cardiomyopathy.

Overexpression of Polycomb-group gene rae28 in cardiomyocytes does not complement abnormal cardiac morphogenesis in mice lacking rae28 but causes dilated cardiomyopathy.

The Polycomb-group genes (PcG) are widely conserved from Drosophila to mammals and are required for maintaining positional information during development. The rae28 gene (rae28) is a member of the mouse PcG. Mice deficient in rae28 (rae28(-/-)) demonstrated that rae28 has a role not only in anteroposterior patterning but also in cardiac morphogenesis.

Bcl-xl reduces doxorubicin-induced myocardial damage but fails to control cardiac gene downregulation.

Objective: We recently reported that doxorubicin (Dox), an effective anti-cancer drug, induces apoptosis in cardiac myocytes in association with reduction of Bcl-xl expression. In the present study, we further examined whether overexpression of Bcl-xl ameliorates Dox-induced cardiac myocyte damage.

Methods And Results: Overexpression of the Bcl-xl gene by adenovirus vector resulted in an 11-fold increase in Bcl-xl protein in neonatal rat cardiac myocytes (BCL) compared to that in cells with beta-galactosidase gene transfection (CTL).

Cardiac-specific activation of signal transducer and activator of transcription 3 promotes vascular formation in the heart.

Signal transducer and activator of transcription 3 (STAT3) functions in cell proliferation, differentiation, and cell survival. Previously, we have demonstrated that the activation of STAT3 is required for glycoprotein 130-mediated induction of VEGF in cardiac myocytes, but the functional importance of STAT3 as an angiogenic mediator remains to be determined. To address this issue, we first generated the adenoviral vector expressing constitutively active STAT3 (caSTAT3).