The impact factors on the cost and length of stay among acute ischemic stroke.

Background: Understanding hospital costs and length of stay (LOS) can optimize the in-hospital management of acute stroke. We investigated cost and LOS in first-ever and recurrent stroke patients in Taiwan.

Methods: Data were examined in patients at Chang Gung Memorial Hospital in Chiayi County of Taiwan from April 1, 2008, to March 31, 2010 [corrected].

APOE and AβPP gene variation in cortical and cerebrovascular amyloid-β pathology and Alzheimer's disease: a population-based analysis.

Cortical and cerebrovascular amyloid-β (Aβ) deposition is a hallmark of Alzheimer's disease (AD), but also occurs in elderly people not affected by dementia. The apolipoprotein E (APOE) ε4 is a major genetic modulator of Aβ deposition and AD risk. Variants of the amyloid-β protein precursor (AβPP) gene have been reported to contribute to AD and cerebral amyloid angiopathy (CAA).

A de novo missense mutation of the FUS gene in a "true" sporadic ALS case.

Mutations in the Cu/Zn superoxide dismutase (SOD1), transactive response (TAR)-DNA binding protein (TARDBP) and fused in sarcoma (FUS) genes account for approximately 1 third of familial amyotrophic lateral sclerosis (ALS) cases. Mutations in these genes have been found in 1% to 2% of apparently sporadic cases. We present the first case of an ALS patient carrying a de novo missense mutation of the FUS gene (c.

Kinesin-associated protein 3 (KIFAP3) has no effect on survival in a population-based cohort of ALS patients.

It was recently reported that rs1541160 on chromosome 1q24.2 has a marked effect on survival of amyotrophic lateral sclerosis (ALS) patients by influencing KIFAP3 expression. The cohorts used in that study were collected from ALS specialty clinics.

Abundant quantitative trait loci exist for DNA methylation and gene expression in human brain.

A fundamental challenge in the post-genome era is to understand and annotate the consequences of genetic variation, particularly within the context of human tissues. We present a set of integrated experiments that investigate the effects of common genetic variability on DNA methylation and mRNA expression in four human brain regions each from 150 individuals (600 samples total). We find an abundance of genetic cis regulation of mRNA expression and show for the first time abundant quantitative trait loci for DNA CpG methylation across the genome.

FUS mutations in sporadic amyotrophic lateral sclerosis.

Mutations in the FUS gene have recently been described as a cause of familial amyotrophic lateral sclerosis (ALS), but their role in the pathogenesis of sporadic ALS is unclear. We undertook mutational screening of all coding exons of FUS in 228 sporadic ALS cases, and, as previous reports suggest that exon 15 represents a mutational hotspot, we sequenced this exon in an additional 1295 sporadic cases. Six variants in six different cases were found, indicating that FUS mutations can underlie apparently sporadic ALS, but account for less than 1% of this form of disease.

A two-stage genome-wide association study of sporadic amyotrophic lateral sclerosis.

The cause of sporadic amyotrophic lateral sclerosis (ALS) is largely unknown, but genetic factors are thought to play a significant role in determining susceptibility to motor neuron degeneration. To identify genetic variants altering risk of ALS, we undertook a two-stage genome-wide association study (GWAS): we followed our initial GWAS of 545 066 SNPs in 553 individuals with ALS and 2338 controls by testing the 7600 most associated SNPs from the first stage in three independent cohorts consisting of 2160 cases and 3008 controls. None of the SNPs selected for replication exceeded the Bonferroni threshold for significance.

Risk factors and subtype analysis of acute ischemic stroke.

Background And Purpose: Stroke risk factors and subtypes were examined for associations with mortality and recurrence rate in Taiwanese patients with first-ever and recurrent stroke.

Methods: This study examined patients with initial and recurrent stroke from 2003 to 2005 for risk factors, demographic data, Bamford subtypes and transient ischemic attack.

Results: One thousand and twenty-one patients with 1,085 stroke episodes were recruited.

Spontaneous intrapetrous internal carotid artery dissection: a case report and literature review.

Although hemodynamic change has been identified as the main mechanism of infarcts in intracranial internal carotid artery dissection, no report has utilized computed tomography perfusion study to evaluate the cerebral flow change in such cases. This report presents a rare case of intrapetrous internal carotid artery dissection with watershed infarction. Additionally, a literature review addresses the clinical profiles and related neuroimaging findings of such patients.

Avascular necroses inducing limb-girdle syndrome.

Disuse myopathy can be caused by many disorders. However, disuse myopathy with symmetrical weakness of the proximal muscles in the four limbs is rare. Here we report a 45-year-old man who presented with the appearance of myopathy similar to the clinical picture of limb-girdle syndrome with symmetrical weakness of proximal muscles in four limbs.

Bilateral common carotid artery occlusion--a case report and literature review.

Although unilateral common carotid artery (CCA) occlusion and bilateral internal carotid artery (ICA) occlusion have been reported in the past, bilateral CCA occlusion is rare. The management and mechanism of unilateral CCA occlusion and bilateral ICA occlusion are debatable, but those of bilateral CCA occlusion are largely unknown. Herein, we present a case of bilateral CCA occlusion that had an acceptable outcome with medical treatment.

Deleted 4977-bp mitochondrial DNA mutation is associated with sporadic amyotrophic lateral sclerosis: a hospital-based case-control study.

We investigated the relationship between the most common 4977-bp deleted mitochondrial DNA (mtDNA) mutations and the occurrence of sporadic amyotrophic lateral sclerosis (ALS). Primer-shift and quantitative polymerase chain reaction (PCR) were used to determine the 4977-bp deleted mtDNA in the muscle specimens from 36 patients with sporadic ALS and 69 age-matched controls with other neuromuscular disorders. We found that the 4977-bp deleted mtDNA mutations were significantly higher in the ALS patients than controls in both frequency (50.