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1.  Needle Decompression in Appalachia Do Obese Patients Need Longer Needles? 
Introduction:
Needle decompression of a tension pneumothorax can be a lifesaving procedure. It requires an adequate needle length to reach the chest wall to rapidly remove air. With adult obesity exceeding one third of the United States population in 2010, we sought to evaluate the proper catheter length that may result in a successful needle decompression procedure. Advance Trauma Life Support (ATLS) currently recommends a 51 millimeter (mm) needle, while the needles stocked in our emergency department are 46 mm. Given the obesity rates of our patient population, we hypothesize these needles would not have a tolerable success rate of 90%.
Methods:
We retrospectively reviewed 91 patient records that had computed tomography of the chest and measured the chest wall depth at the second intercostal space bilaterally.
Results:
We found that 46 mm needles would only be successful in 52.7% of our patient population, yet the ATLS recommended length of 51 mm has a success rate of 64.8%. Therefore, using a 64 mm needle would be successful in 79% percent of our patient population.
Conclusion:
Use of longer length needles for needle thoracostomy is essential given the extent of the nation’s adult obesity population.
doi:10.5811/westjem.2013.7.15844
PMCID: PMC3876316  PMID: 24381693
2.  Effect of Genetic Variation in LRRTM3 on Risk of Alzheimer Disease 
Archives of neurology  2012;69(7):894-900.
Objective
To explore the role of leucine-rich repeat transmembrane 3 (LRRTM3) in late-onset Alzheimer disease (AD) by independent genetic epidemiologic and functional studies.
Methods
First, we explored associations between LRRTM3 single-nucleotide polymorphisms and AD in the National Institute on Aging Late-Onset Alzheimer’s Disease case-control data set (993 patients and 884 control subjects) and a cohort of Caribbean Hispanics (549 patients and 544 controls) using single-marker and haplo-type analyses. Then we explored the effect of LRRTM3 small-hairpin RNAs on amyloid precursor protein processing.
Results
One single-nucleotide polymorphism in the promoter region (rs16923760; C allele: odds ratio,−0.74, P=.03), and a block of 4 single-nucleotide polymorphisms in intron 2 (rs1925608, C allele: 0.84, P=.04; rs7082306, A allele: 0.75, P=.04; rs1925609, T allele: 1.2, P=.03; and rs10997477, T allele: 0.88, P=.05) were associated with AD in the National Institute on Aging Late-Onset Alzheimer’s Disease data set or the Caribbean His-panic data set. The corresponding haplotypes were also associated with AD risk (.01< P<.05). In addition, LRRTM3 knockdown with small-hairpin RNAs caused a significant decrease in amyloid precursor protein processing (P<.05 to P<.01) compared with the scrambled small-hairpin RNA condition.
Conclusions
These complementary findings support the notions that genetic variation in LRRTM3 is associated with AD risk and that LRRTM3 may modulate γ-secretase processing of amyloid precursor protein. Additional studies are needed to determine whether the specific alleles associated with differential risk for AD indeed confer this risk through an effect of LRRTM3 expression levels that in turn modulates amyloid precursor protein processing.
doi:10.1001/archneurol.2011.2463
PMCID: PMC3391336  PMID: 22393166
3.  Saitohin, which is nested within the tau gene, interacts with tau and Abl and its human-specific allele influences Abl phosphorylation 
Journal of cellular biochemistry  2011;112(11):3482-3488.
Saitohin (STH) is a gene unique to humans and their closest relatives whose function is not yet known. STH contains a single polymorphism (Q7R); the Q allele is human-specific and confers susceptibility to several neurodegenerative diseases. In previous work, we discovered that STH interacts with Peroxiredoxin 6 (Prdx6), a unique member of that family which is bifunctional and whose levels increase in Pick’s disease. In this study, we report that STH also interacts with tau and the non-receptor tyrosine kinase c-Abl (Abl). Furthermore, Abl phosphorylates STH on its single tyrosine residue and STH increases tyrosine phosphorylation by Abl. The effect of Saitohin on Abl-mediated phosphorylation appears to be allele-specific, providing evidence for a new cellular function for STH.
doi:10.1002/jcb.23279
PMCID: PMC3196732  PMID: 21769920
Saitohin interactions; primate-specific gene; human-specific allele; MAP tau; tyrosine kinase Abl; allele-specific effects; neurodegeneration
4.  SORCS1 Alters Amyloid Precursor Protein Processing and Variants May Increase Alzheimer’s Disease Risk 
Annals of neurology  2011;69(1):47-64.
Objective
Sorting mechanisms that cause the amyloid precursor protein (APP) and the β-secretases and γ-secretases to colocalize in the same compartment play an important role in the regulation of Aβ production in Alzheimer’s disease (AD). We and others have reported that genetic variants in the Sortilin-related receptor (SORL1) increased the risk of AD, that SORL1 is involved in trafficking of APP, and that under expression of SORL1 leads to overproduction of Aβ. Here we explored the role of one of its homologs, the sortilin-related VPS10 domain containing receptor 1 (SORCS1), in AD.
Methods
We analyzed the genetic associations between AD and 16 SORCS1–single nucleotide polymorphisms (SNPs) in 6 independent data sets (2,809 cases and 3,482 controls). In addition, we compared SorCS1 expression levels of affected and unaffected brain regions in AD and control brains in microarray gene expression and real-time polymerase chain reaction (RT-PCR) sets, explored the effects of significant SORCS1-SNPs on SorCS1 brain expression levels, and explored the effect of suppression and overexpression of the common SorCS1 isoforms on APP processing and Aβ generation.
Results
Inherited variants in SORCS1 were associated with AD in all datasets (0.001 < p < 0.049). In addition, SorCS1 influenced APP processing. While overexpression of SorCS1 reduced γ-secretase activity and Aβ levels, the suppression of SorCS1 increased γ-secretase processing of APP and the levels of Aβ.
Interpretations
These data suggest that inherited or acquired changes in SORCS1 expression or function may play a role in the pathogenesis of AD.
doi:10.1002/ana.22308
PMCID: PMC3086759  PMID: 21280075

Results 1-4 (4)