None of the 12 normal- and disease-control muscle biopsies contained conformational or PHF-1 immunoreactive tau. This first demonstration of conformational tau in s-IBM, because of its abundance in non-atrophic muscle fibers, suggests that it might play an early role in s-IBM PHFs formation and thus be pathogenically important. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Objective: The Levitronix CentriMag (Levitronix LLC, Waltham, Mass) ventricular assist system
is designed for temporary left, right, or biventricular support. Advantages include ease of use, excellent reliability, and low thrombosis risk,. which may allow wider application of short-term support and improved outcomes in patients with Romidepsin in vivo cardiogenic shock. This multi-institutional study evaluated
safety, effectiveness, and outcomes of the CentriMag in patients with cardiogenic shock.
Methods: Thirty-eight patients were supported at 7 centers. Patients included 12 after cardiotomy, 14 after myocardial infarction, and 12 with right ventricular failure after implantable left ventricular assist device placement. Devices were implanted in left (n = 8), right (n = 12), or biventricular (n = 18) configuration. Support was continued until recovery, transplantation, or implantation U0126 ic50 of long-term ventricular assist device.
Results: Mean support duration for the entire cohort (n = 38) was 13 days (1-60 days), with 47% of patients (18/38) surviving 30 days after device removal. Mean CentriMag biventricular support (n = 18) duration was 15 days (1-60 days), with 44% (8/18) surviving at 30 days. Mean CentriMag right ventricular support with a commercially available
left ventricular assist device (n = 12) duration was 14 days (1-29 days), with 58%(7/12) surviving at 30 days. Complications included bleeding (21%), infection (5%), respiratory failure (3%), hemolysis (5%), and for neurologic dysfunction (11%). There were no CentriMag or pump failures.
Conclusions: In this preliminary study, the CentriMag provided short-term support for patients with cardiogenic shock with a low incidence of device-related complications and no device failures. (J Thorac Cardiovasc Surg 2011;141:932-9)”
“Huntington disease (HD) is caused by the expansion of polyglutamine (polyQ) repeats in the amino-terminal of hungtintin (htt). PolyQ-expanded htt forms intracellular ubiquitinated aggregates in neurons and causes neuronal cell death. Here, utilizing a HD cellular model, we report that Tollip, an ubiquitin binding protein that participates in intracellular transport via endosomes, co-localizes with and stimulates aggregation of polyQ-expanded amino-terminal htt. Furthermore, we demonstrate that Tollip protects cells against the toxicity of polyQ-expanded htt.