Racial/Ethnic Differences in Influenza and Pneumococcal Vaccination Rates Among Older Adults in New York City and Los Angeles and Orange Counties.

Introduction: Disparities in vaccination rates exist among racial/ethnic minority adults. This study examined factors associated with influenza (flu) and pneumococcal vaccination rates among non-Hispanic black, Hispanic, and Asian American adults aged 50 or older living in New York City or Los Angeles and Orange counties in California.

Methods: We used data collected by the REACH US Risk Factor Survey 2009-2012 in New York City and California.

Chromosomal instability during neurogenesis in Huntington's disease.

Huntington's disease (HD) is a fatal neurodegenerative disease caused by expansion of CAG repeats in the Huntingtin gene (). Neither its pathogenic mechanisms nor the normal functions of HTT are well understood. To model HD in humans, we engineered a genetic allelic series of isogenic human embryonic stem cell (hESC) lines with graded increases in CAG repeat length.

Predictors of intracranial hemorrhage volume and distribution in brain arteriovenous malformation.

Background and purpose Despite evidence regarding risk factors for brain arteriovenous malformation (bAVM)-associated spontaneous intracranial hemorrhage (ICH), few data exist describing the spectrum of clinical outcomes that bAVM-associated ICH may manifest. This study aimed to identify the demographical, clinical, and bAVM anatomical variables associated with ICH volume and the presence of intraventricular hemorrhage (IVH) of ruptured bAVMs, two indicators of worse clinical outcome, to help better predict outcome for unruptured bAVMs. Methods Computed tomography images ( n = 169) of patients with ruptured bAVM in a prospectively maintained institutional database were retrospectively reviewed to calculate ICH volume and the presence or absence of IVH.

Observation of improved adherence with frequent urine drug testing in patients with pain.

Objective: To determine the relationship between urine drug testing (UDT) frequency and patient adherence for prescribed buprenorphine, carisoprodol, fentanyl, hydrocodone, methadone, morphine, and oxycodone.

Setting: Patients with pain routinely seen by private practitioners.

Design: A retrospective analysis was conducted on urinary excretion data analyzed by Millennium Laboratories between March 2008 and May 2011.

Factors affecting carisoprodol metabolism in pain patients using urinary excretion data.

Carisoprodol is a skeletal muscle relaxant prescribed to treat pain. Carisoprodol is metabolized to meprobamate, an active metabolite with anxiolytic effects, by the genetically polymorphic CYP2C19 enzyme. Concomitant use of CYP2C19 substrates or inhibitors may alter carisoprodol metabolism, with therapeutic and/or toxic implications for effectively treating patients with pain.

Evaluating the relationship between carisoprodol concentrations and meprobamate formation and inter-subject and intra-subject variability in urinary excretion data of pain patients.

Using urinary carisoprodol data from pain patients, our objectives were to determine the relationship between carisoprodol concentration and its conversion to meprobamate, and quantify the intra-subject and inter-subject variability in carisoprodol metabolism. Liquid chromatography-tandem mass spectrometry was used to quantitate carisoprodol and meprobamate concentrations in urine specimens. The log creatinine-corrected carisoprodol versus log creatinine-corrected meprobamate showed a marginal positive relationship (R(2) = 0.

Heterozygous mutation of Drosophila Opa1 causes the development of multiple organ abnormalities in an age-dependent and organ-specific manner.

Optic Atrophy 1 (OPA1) is a ubiquitously expressed dynamin-like GTPase in the inner mitochondrial membrane. It plays important roles in mitochondrial fusion, apoptosis, reactive oxygen species (ROS) and ATP production. Mutations of OPA1 result in autosomal dominant optic atrophy (DOA).

Heterozygous mutation of Opa1 in Drosophila shortens lifespan mediated through increased reactive oxygen species production.

Optic atrophy 1 (OPA1) is a dynamin-like GTPase located in the inner mitochondrial membrane and mutations in OPA1 are associated with autosomal dominant optic atrophy (DOA). OPA1 plays important roles in mitochondrial fusion, cristae remodeling and apoptosis. Our previous study showed that dOpa1 mutation caused elevated reactive oxygen species (ROS) production and resulted in damage and death of the cone and pigment cells in Drosophila eyes.

The molecular mechanisms of OPA1-mediated optic atrophy in Drosophila model and prospects for antioxidant treatment.

Mutations in optic atrophy 1 (OPA1), a nuclear gene encoding a mitochondrial protein, is the most common cause for autosomal dominant optic atrophy (DOA). The condition is characterized by gradual loss of vision, color vision defects, and temporal optic pallor. To understand the molecular mechanism by which OPA1 mutations cause optic atrophy and to facilitate the development of an effective therapeutic agent for optic atrophies, we analyzed phenotypes in the developing and adult Drosophila eyes produced by mutant dOpa1 (CG8479), a Drosophila ortholog of human OPA1.

Studies on the mechanism of interaction of a bioresponsive endosomolytic polyamidoamine with interfaces. 1. Micelles as model surfaces.

Polymers are appealing as pH-responsive elements of multicomponent systems designed to promote cytosolic delivery of macromolecular drugs (including proteins and genes), but so far the delivery efficiency achieved has been relatively modest. Therefore, the aim of this study was to apply several physicochemical techniques that are well established in the colloid field (surface tension measurements, small-angle neutron scattering (SANS), and electron paramagnetic resonance (EPR)) to probe the mechanism of endosomolytic polymer-surface interaction over the pH range 7.4 to 5.