Cooperative action of APJ and α1A-adrenergic receptor in vascular smooth muscle cells induces vasoconstriction.

The apelin receptor (APJ), a receptor for apelin and elabela/apela, induces vasodilation and vasoconstriction in blood vessels. However, the prolonged effects of increased APJ-mediated signalling, involving vasoconstriction, in smooth muscle cells have not been fully characterized. Here, we investigated the vasoactive effects of APJ gain of function under the control of the smooth muscle actin (SMA) gene promoter in mice.

Membranous nephropathy associated with chronic hepatitis B occurring in a short period after acute hepatitis B virus infection.

We herein present a case of membranous nephropathy associated with chronic hepatitis B following acute hepatitis B virus (HBV) infection. A 22-year-old man was admitted to our hospital for evaluation of proteinuria, pitting edema on both legs, and increased body weight in December 2002. At the age of 18, he had suffered from acute hepatitis A and syphilis, and was found to be negative for hepatitis B surface antigen (HBsAg).

[Takotsubo cardiomyopathy thought to be induced by MRSA meningitis and cervical epidural abscess in a maintenance-hemodialysis patient: case report].

A 65-year-old man was admitted to our hospital for high fever and severe left shoulder pain. He was initiated on maintenance hemodialysis for end-stage renal failure caused by diabetic nephropathy 9 years previously. On admission, the serum CRP level was 29.

More stable and reliable pharmacokinetics with preprandial administration of cyclosporine compared with postprandial administration in patients with refractory nephrotic syndrome.

Study Objective: To compare the absorption profile of cyclosporine after preprandial administration with that after postprandial administration, and to determine which administration time resulted in a more stable absorption profile and the timing of the drug concentration that was the most reliable marker for monitoring drug absorption.

Design: Prospective analysis.

Setting: University teaching hospital in Japan.

Hypertension accelerates diabetic nephropathy in Wistar fatty rats, a model of type 2 diabetes mellitus, via mitogen-activated protein kinase cascades and transforming growth factor-beta1.

Although it is known that diabetic nephropathy is accelerated by hypertension, the mechanisms involved in this process are not clear. In this study we aimed to clarify these mechanisms using male Wistar fatty rats (WFR) as a type 2 diabetic model and male Wistar lean rats (WLR) as a control. Each group was fed a normal or high sodium diet from the age of 6 to 14 weeks.