Idiopathic normal pressure hydrocephalus: survey on current diagnostic and therapeutic procedures in clinical practice in Germany.

Objective: Cerebrospinal fluid (CSF) shunting has become the standard treatment for idiopathic normal pressure hydrocephalus (NPH). Nevertheless, there is still disagreement on diagnostic criteria for selecting patients for surgery and optimal shunt management. The primary aim of the present study was to provide an update on the status of best practice, the use of different diagnostic algorithms and therapeutic management of idiopathic NPH in an European country.

Functions of PMS2 and MLH1 important for regulation of divergent repeat-mediated deletions.

Repeat-mediated deletions (RMDs) are a type of deletion rearrangement that utilizes two repetitive elements to bridge a DNA double-strand break (DSB) that leads to loss of the intervening sequence and one of the repeats. Sequence divergence between repeats causes RMD suppression and indeed this divergence must be resolved in the RMD products. The mismatch repair factor, MLH1, was shown to be critical for both RMD suppression and a polarity of sequence divergence resolution in RMDs.

Case management-based post-stroke care for patients with acute stroke and TIA (SOS-Care): a prospective cohort study.

Background: The high incidence of stroke recurrence necessitates effective post-stroke care. This study investigates the effectiveness of a case management-based post-stroke care program in patients with acute stroke and TIA.

Methods: In this prospective cohort study, patients with TIA, ischemic stroke or intracerebral hemorrhage were enrolled into a 12-month case management-based program (SOS-Care) along with conventional care.

Resolution of sequence divergence for repeat-mediated deletions shows a polarity that is mediated by MLH1.

Repeat-mediated deletions (RMDs) are a type of chromosomal rearrangement between two homologous sequences that causes loss of the sequence between the repeats, along with one of the repeats. Sequence divergence between repeats suppresses RMDs; the mechanisms of such suppression and of resolution of the sequence divergence remains poorly understood. We identified RMD regulators using a set of reporter assays in mouse cells that test two key parameters: repeat sequence divergence and the distances between one repeat and the initiating chromosomal break.