Informant sex/gender moderates associations between reported functioning and memory performance in Mexican American adults.

In neuropsychological evaluations, assessing cognitive functioning is often achieved using objective neuropsychological measures, whereas subjective informant reports are typically obtained to determine manifest daily functioning. Informant reports of participant functioning and their associations with objective participant performance on neuropsychological testing have been shown to vary based on informant characteristics. However, associations among informant characteristics, reported functioning, and neuropsychological performance have not been adequately examined with Mexican American or other Hispanic/Latino samples, despite these populations' disproportionately higher rates of dementia due to Alzheimer's disease and related disorders.

Preparation of Extracellular Matrices Produced by Cultured and Primary Fibroblasts.

Fibroblasts secrete and organize extracellular matrix (ECM), which provides structural support for their adhesion, migration, and tissue organization, besides regulating cellular functions such as growth and survival. Cell-to-matrix interactions are vital for vertebrate development. Disorders in these processes have been associated with fibrosis, developmental malformations, cancer, and other diseases.

TRPC6 channel translocation into phagosomal membrane augments phagosomal function.

Defects in the innate immune system in the lung with attendant bacterial infections contribute to lung tissue damage, respiratory insufficiency, and ultimately death in the pathogenesis of cystic fibrosis (CF). Professional phagocytes, including alveolar macrophages (AMs), have specialized pathways that ensure efficient killing of pathogens in phagosomes. Phagosomal acidification facilitates the optimal functioning of degradative enzymes, ultimately contributing to bacterial killing.

Cell-based potassium ion channel screening using the FluxOR assay.

FluxOR technology is a cell-based assay used for high-throughput screening measurements of potassium channel activity. Using thallium influx as a surrogate indicator of potassium ion channel activity, the FluxOR Potassium Ion Channel Assay is based on the activation of a novel fluorescent dye. This indicator reports channel activity with a large fluorogenic response and is proportional to the number of open potassium channels on the cell, making it extremely useful for studying K(+) channel targets.

Disease-causing mutations in the cystic fibrosis transmembrane conductance regulator determine the functional responses of alveolar macrophages.

Alveolar macrophages (AMs) play a major role in host defense against microbial infections in the lung. To perform this function, these cells must ingest and destroy pathogens, generally in phagosomes, as well as secrete a number of products that signal other immune cells to respond. Recently, we demonstrated that murine alveolar macrophages employ the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel as a determinant in lysosomal acidification (Di, A.

Surfactant-enhanced rapid spreading of drops on solid surfaces.

We study the surfactant-enhanced spreading of drops on the surfaces of solid substrates. This work is performed in connection with the unique ability of aqueous trisiloxane solutions to wet highly hydrophobic substrates effectively, which has been studied for nearly two decades. We couple a lubrication model to advection-diffusion equations for surfactant transport.

A new homogeneous high-throughput screening assay for profiling compound activity on the human ether-a-go-go-related gene channel.

Long QT syndrome, either inherited or acquired from drug treatments, can result in ventricular arrhythmia (torsade de pointes) and sudden death. Human ether-a-go-go-related gene (hERG) channel inhibition by drugs is now recognized as a common reason for the acquired form of long QT syndrome. It has been reported that more than 100 known drugs inhibit the activity of the hERG channel.

Functional properties and differential neuromodulation of Na(v)1.6 channels.

The voltage-gated sodium channel Na(v)1.6 plays unique roles in the nervous system, but its functional properties and neuromodulation are not as well established as for Na(V)1.2 channels.

Preparation of extracellular matrices produced by cultured and primary fibroblasts.

Fibroblasts secrete and organize extracellular matrix (ECM), which provides structural support for their adhesion, migration, and tissue organization, besides regulating cellular functions such as growth and survival. Cell-to-matrix interactions are vital for vertebrate development. Disorders in these processes have been associated with fibrosis, developmental malformations, cancer, and other diseases.

Sites and molecular mechanisms of modulation of Na(v)1.2 channels by Fyn tyrosine kinase.

Voltage-gated sodium channels are important targets for modulation of electrical excitability by neurotransmitters and neurotrophins acting through protein phosphorylation. Fast inactivation of Na(V)1.2 channels is regulated via tyrosine phosphorylation by Fyn kinase and dephosphorylation by receptor phosphoprotein tyrosine phosphatase-beta, which are associated in a signaling complex.

Regulation of Na(v)1.2 channels by brain-derived neurotrophic factor, TrkB, and associated Fyn kinase.

Voltage-gated sodium channels are responsible for action potential initiation and propagation in neurons, and modulation of their function has an important impact on neuronal excitability. Sodium channels are regulated by a Src-family tyrosine kinase pathway, and this modulation can be reversed by specifically bound receptor phosphoprotein tyrosine phosphatase-beta. However, the specific tyrosine kinase and signaling pathway are unknown.

Stromagenesis: the changing face of fibroblastic microenvironments during tumor progression.

During tumorigenesis, reciprocal changes in stromal fibroblasts and tumor cells induce changes to the neoplastic microenvironmental landscape. In stromagenesis, both the complex network of bi-directional stromal fibroblastic signaling pathways and the stromal extracellular matrix are modified. The presence of a 'primed' stroma during the early, reversible stage of tumorigenesis is optimal for stromal-directed therapeutic intervention.

The functional expression of mu opioid receptors on sensory neurons is developmentally regulated; morphine analgesia is less selective in the neonate.

Opioid requirements in neonatal patients are reported to be lower than older infants and this may be a reflection of the developmental regulation of opioid receptors. In this study we have investigated the postnatal regulation of Mu opioid receptor (MOR) function in both rat lumbar dorsal root ganglion (DRG) cultures and behavioural mechanical and thermal reflex tests in rat pups. Immunostaining with MOR and selective neurofilament (NF200) antibodies was combined with calcium imaging of MOR function in cultured neonatal and adult rat dorsal root ganglion cells.

Cold-sensitive, menthol-insensitive neurons in the murine sympathetic nervous system.

Several mechanisms have been implicated in underlying the perception of cold, most notably the activation of TRPM8 and TRPA1. We have used ratiometric calcium imaging to reveal a population of neurons in the superior cervical ganglion (SCG) of the mouse that respond to cooling but are insensitive to menthol. Furthermore we show that the expression of the mRNA transcripts encoding the recently identified noxious cold-sensitive channel TRPA1 but not TRPM8 are expressed in the SCG.

Quantitative single-cell differences in mu-opioid receptor mRNA distinguish myelinated and unmyelinated nociceptors.

A remarkable feature of opioids is that they inhibit pain that persists from previous injuries without eliminating either the initial pain of a new injury or the protective reflexes triggered by it. Here we ask whether selective expression of the mu-opioid receptor (MOR) gene in primary nociceptors (pain-sensing neurons) might contribute to this aspect of opioid specificity. We quantified single-cell levels of MOR mRNA and measured opioid inhibition of Ca channels on identified nociceptors and low-threshold mechanosensors (non-nociceptors) isolated from rats.

Extracellular signal-regulated kinase (ERK) activation is required for GP Ibalpha-dependent endothelial cell migration.

The GP Ib complex can participate in endothelial cell (EC) migration on von Willebrand factor (vWF) or the mixed matrix of vWF and type I collagen (vWF/collagen). In this study, viper venom proteins alboaggregin (albo) A or B blocked GP Ibalpha, and echistatin inhibited alphavbeta3 binding. Albo A, B and echistatin inhibited EC migration on vWF and vWF/collagen.

Evaluation of endothelial cell migration with a novel in vitro assay system.

In this study we introduce a novel in vitro 'oil-drop' assay system for the measurement of endothelial cell (EC) migration, based on the original concept of the Teflon fence assay (Pratt et al., 1984; Am. J.

Isolation and characterization of EMS16, a C-lectin type protein from Echis multisquamatus venom, a potent and selective inhibitor of the alpha2beta1 integrin.

We have isolated and characterized EMS16, a potent and selective inhibitor of the alpha2beta1 integrin, from Echis multisquamatus venom. It belongs to the family of C-lectin type of proteins (CLPs), and its amino acid sequence is homologous with other members of this protein family occurring in snake venoms. EMS16 (M(r) approximately 33K) is a heterodimer composed of two distinct subunits linked by S-S bonds.

Arterial shear stress stimulates surface expression of the endothelial glycoprotein Ib complex.

Exposure to shear stress has been shown to alter the expression of a number of surface components of cultured endothelial cells (EC). However, relatively few studies have examined the status of human EC surface proteins after prolonged flow, more closely corresponding to the steady state in vivo. Since the promoter region of glycoprotein (Gp) Ib alpha contains several copies of a putative shear stress response element, 5'-GAGACC-3', we investigated the response of cultured human umbilical vein EC (HUVEC) GpIb alpha to shear stress over a 72 h time period.

Glycoprotein Ibalpha can mediate endothelial cell migration on von Willebrand factor-containing substrata.

We have previously shown that, in addition to the vitronectin receptor (VNR, alpha(v)beta(3)), the GP Ib complex can participate in endothelial cell (EC) attachment to von Willebrand Factor (vWF) (D. A. Beacham, M.

Mu and delta opioids but not kappa opioid inhibit voltage-activated Ba2+ currents in neuronal F-11 cell.

Whole-cell patch-clamp recordings were used to study Ba2+ currents through voltage-dependent Ca2+ channels in dorsal root ganglion x mouse neuroblastoma hybrid (F-11) cells. Opioid agonists selective for either mu (Tyr-D-Ala-Gly-Mephe-Gly-ol; DAMGO) or delta (Tyr-D-Pen-Gly-Phe-D-Pen-OH; DPDPE) receptors inhibited high-threshold Ba2+ currents. The inhibition was reversible, naloxone-sensitive, and dose-dependent.

Cytokine treatment of endothelial cells increases glycoprotein Ib alpha-dependent adhesion to von Willebrand factor.

Endothelial cells (EC) possess at least two membrane receptors for von Willebrand factor (vWF), the vitronectin receptor (VNR, alpha(v)beta3), which recognizes an Arg-Gly-Asp (RGD) sequence in the C-terminus of vWF, and glycoprotein Ib alpha (GP Ib alpha), which interacts with a region in the N-terminal A1 domain of vWF. In the absence of added cytokines, EC attachment to a vWF substratum is mediated largely through the alpha(v)beta3, with a smaller contribution by GP Ib alpha. In the present study, we have examined the effect of cytokines on the receptor specificity of EC attachment to wild-type vWF (WT-vWF) and to vWF, which had been mutated in the C-terminal RGDS sequence (RADS-vWF).