Retraction: α-GalCer ameliorates listeriosis by accelerating infiltration of Gr-1 cells into the liver.

Retraction: Emoto, M., Emoto, Y., Yoshizawa, I.

Association of Long-Term Treatment by Botulinum Neurotoxins and Occupational Therapy with Subjective Physical Status in Patients with Post-Stroke Hemiplegia.

The short-term effects of botulinum toxin type A (BoNT-A) treatment in stroke patients with upper limb extremity are well established. This study examined the association between the recovery of motor function of the upper extremity with subjective physical symptoms in outpatients receiving long-term BoNT-A and occupational therapy following stroke. We also investigated the expectations of patients who elected to continue treatment.

GDE5 inhibition accumulates intracellular glycerophosphocholine and suppresses adipogenesis at a mitotic clonal expansion stage.

Mammalian glycerophosphodiesterases (GDEs) were recently shown to be involved in multiple cellular signaling pathways. This study showed that decreased GDE5 expression results in accumulation of intracellular glycerophosphocholine (GPC), showing that GDE5 is actively involved in GPC/choline metabolism in 3T3-L1 adipocytes. Using 3T3-L1 adipocytes, we further studied the biological significance of GPC/choline metabolism during adipocyte differentiation.

Time Course Analysis of Skeletal Muscle Pathology of GDE5 Transgenic Mouse.

Glycerophosphodiesterase 5 (GDE5) selectively hydrolyses glycerophosphocholine to choline and is highly expressed in type II fiber-rich skeletal muscles. We have previously generated that a truncated mutant of GDE5 (GDE5dC471) that lacks phosphodiesterase activity and shown that transgenic mice overexpressing GDE5dC471 in skeletal muscles show less skeletal muscle mass than control mice. However, the molecular mechanism and pathophysiological features underlying decreased skeletal muscle mass in GDE5dC471 mice remain unclear.

A high-throughput screen for inhibitors of the prolyl isomerase, Pin1, identifies a seaweed polyphenol that reduces adipose cell differentiation.

The peptidyl prolyl cis/trans isomerase Pin1 enhances the uptake of triglycerides and the differentiation of fibroblasts into adipose cells in response to insulin stimulation. Pin1 downregulation could be a potential approach to prevent and treat obesity-related disorders. In order to identify an inhibitor of Pin1 that exhibited minimal cytotoxicity, we established a high-throughput screen for Pin1 inhibitors and used this method to identify an inhibitor from 1,056 crude fractions of two natural product libraries.