Baseline characteristics and prevalence of cardiovascular disease in newly visiting or referred chronic kidney disease patients to nephrology centers in Japan: a prospective cohort study.

Background: About 39,000 patients were newly prescribed renal replacement therapy in Japan in 2011, resulting in a total of more than 300,000 patients being treated with dialysis. This high prevalence of treated end stage kidney disease (ESKD) patients is an emergent problem that requires immediate attention. We launched a prospective cohort study to evaluate population specific characteristics of the progression of chronic kidney disease (CKD).

Intracellular ClC-3 chloride channels promote bone resorption in vitro through organelle acidification in mouse osteoclasts.

ClC-7 Cl(-) channels expressed in osteoclasts are important for bone resorption since it has been shown that disruption of the ClCN7 gene in mice leads to severe osteopetrosis. We have previously reported that Cl(-) currents recorded from mouse osteoclasts resemble those of ClC-3 Cl(-) channels. The aim of the present study was to determine the expression of ClC-3 channels in mouse osteoclasts and their functional role during bone resorption.

Study of the oral microbial flora in patients with renal disease.

Aim: The aim of this study is to bacteriologically investigate the oral environment in patients with renal disease and thereby reveal their influence on both caries and periodontal diseases.

Methods: The authors compared oral microbial flora between patients with renal disease (non-haemodialysis: n = 40, haemodialysis: n = 41) and healthy people (n = 62), and also between haemodialysis patients and non-haemodialysis patients in the disease group. Cariogenic bacteria were identified according to Dentocult System, whereas periodontal bacteria were identified using the polymerase chain reaction method.

CLC-3 deficiency leads to phenotypes similar to human neuronal ceroid lipofuscinosis.

Background: CLC-3 is a member of the CLC chloride channel family and is widely expressed in mammalian tissues. To determine the physiological role of CLC-3, we generated CLC-3-deficient mice (Clcn3-/- ) by targeted gene disruption.

Results: Together with developmental retardation and higher mortality, the Clcn3-/- mice showed neurological manifestations such as blindness, motor coordination deficit, and spontaneous hyperlocomotion.