Implementation of secondary stroke prevention protocol for ischaemic stroke patients in primary care

published_or_final_versio

Glycogen Synthase Kinase 3 Beta (GSK3β) Phosphorylates the RNAase III Enzyme Drosha at S300 and S302

The canonical microRNA (miRNA) pathway commences with the enzymatic cleavage of the primary gene transcript (pri-miRNA) by the RNAase III enzyme Drosha in the nucleus into shorter pre-miRNA species that are subsequently exported to the cytoplasm for further processing into shorter, mature miRNA molecules. Using a series of reporter constructs, we have previously demonstrated that phosphorylation of Drosha at Ser 300 and 302 was required for its nuclear localization. Here, we identify GSK3β as the culprit kinase. We demonstrate that Drosha is unable to selectively localize to the nucleus in cells deficient in GSK3β. These findings expand the substrate base of GSK3β to include a central component of the miRNA biogenesis pathway

Measurement of the Branching Fraction of J/psi --> pi+ pi- pi0

Using 58 million J/psi and 14 million psi' decays obtained by the BESII experiment, the branching fraction of J/psi --> pi+ pi- pi0 is determined. The result is (2.10+/-0.12)X10^{-2}, which is significantly higher than previous measurements.Comment: 9 pages, 8 figures, RevTex

First observation of psi(2S)-->K_S K_L

The decay psi(2S)-->K_S K_L is observed for the first time using psi(2S) data collected with the Beijing Spectrometer (BESII) at the Beijing Electron Positron Collider (BEPC); the branching ratio is determined to be B(psi(2S)-->K_S K_L) = (5.24\pm 0.47 \pm 0.48)\times 10^{-5}. Compared with J/psi-->K_S K_L, the psi(2S) branching ratio is enhanced relative to the prediction of the perturbative QCD ``12%'' rule. The result, together with the branching ratios of psi(2S) decays to other pseudoscalar meson pairs (\pi^+\pi^- and K^+K^-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.Comment: 5 pages, 4 figures, 2 tables, submitted to Phys. Rev. Let

Sh3pxd2b Mice Are a Model for Craniofacial Dysmorphology and Otitis Media

Craniofacial defects that occur through gene mutation during development increase vulnerability to eustachian tube dysfunction. These defects can lead to an increased incidence of otitis media. We examined the effects of a mutation in the Sh3pxd2b gene (Sh3pxd2bnee) on the progression of otitis media and hearing impairment at various developmental stages. We found that all mice that had the Sh3pxd2bnee mutation went on to develop craniofacial dysmorphologies and subsequently otitis media, by as early as 11 days of age. We found noteworthy changes in cilia and goblet cells of the middle ear mucosa in Sh3pxd2bnee mutant mice using scanning electronic microscopy. By measuring craniofacial dimensions, we determined for the first time in an animal model that this mouse has altered eustachian tube morphology consistent with a more horizontal position of the eustachian tube. All mutants were found to have hearing impairment. Expression of TNF-α and TLR2, which correlates with inflammation in otitis media, was up-regulated in the ears of mutant mice when examined by immunohistochemistry and semi-quantitative RT-PCR. The mouse model with a mutation in the Sh3pxd2b gene (Sh3pxd2bnee) mirrors craniofacial dysmorphology and otitis media in humans

Rapid Spread of Severe Fever with Thrombocytopenia Syndrome Virus by Parthenogenetic Asian Longhorned Ticks

Publishe

Factors affecting the outcome of surgically treated non-iatrogenic traumatic cervical esophageal perforation: 28 years experience at a single center

<p>Abstract</p> <p>Background</p> <p>We reviewed our experience with non-iatrogenic traumatic cervical esophageal perforations, paying particular attention to factors affecting the outcome of such cases.</p> <p>Methods</p> <p>In total, 30 patients treated surgically between 1980 and 2008 for non-iatrogenic traumatic cervical esophageal perforation in our clinic were reviewed.</p> <p>Results</p> <p>There were 25 male and 5 female patients with a median age of 27.5 years. The type of injury was external trauma in 21 (70%) patients and endoluminal injury in the remaining 9 (30%) patients. The mechanism of injury was gunshot in 16 patients, stabbing in 4, falling in 1 (extraluminal injury), and foreign body in 9 (endoluminal injuries). The overall mortality rate was 16.6% (5/30). The mortality rate for extraluminal injuries was 19%, and for endoluminal injuries was 11.1%. Mortality in patients treated within 24 h of sustaining injury was substantially less than in those for whom diagnosis and treatment were delayed (12.5 and 21.4%, respectively). The mortality rate was 33.3% (3/9) for patients with tracheal injuries and 9.5% (2/21) for those without tracheal injuries.</p> <p>Conclusions</p> <p>A treatment delay greater than 24 h, the presence of tracheal injury, or extraluminal perforation significantly affected the outcome of surgically treated non iatrogenic traumatic cervical esophageal perforation.</p