University of Medicine and Dentistry of New Jersey

About: University of Medicine and Dentistry of New Jersey is a based out in . It is known for research contribution in the topics: Population & Poison control. The organization has 14634 authors who have published 19610 publications receiving 1041794 citations.

T cells express a phagocyte-type NADPH oxidase that is activated after T cell receptor stimulation

Abstract: T cell receptor (TCR) stimulation induces rapid generation of reactive oxygen species, although the mechanisms for this are unclear. Here we found that T cells expressed a functional phagocyte-type nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. TCR crosslinking induced oxidase activation through the recruitment of preformed Fas ligand and Fas. TCR stimulation induced three separable events generating reactive oxygen species: rapid hydrogen peroxide production independent of Fas or NADPH oxidase; sustained hydrogen peroxide production dependent on both Fas and NADPH oxidase; and delayed superoxide production that was dependent on Fas ligand and Fas yet independent of NADPH oxidase. NADPH oxidase-deficient T cells showed enhanced activation of the kinase Erk and a relative increase in T helper type 1 cytokine secretion. Thus, mature T cells express a phagocyte-type NADPH oxidase that regulates elements of TCR signaling.

Regulation of Macrophage Polarization and Wound Healing.

Abstract: Background: Macrophages (Mφs) participate in wound healing by coordinating inflammatory and angiogenic processes. Mφs respond to environmental cues by adopting either “classically” activated (M1) proinflammatory or “alternatively” activated (M2a, M2b, M2c, M2d) wound healing phenotypes. The Problem: Mφ polarization is essential for wound healing and aberrations in this process are linked to several pathologies. It is important to elucidate molecular mechanisms underlying Mφ polarization. Basic/Clinical Science Advances: Mφs are categorized as proinflammatory (M1) or anti-inflammatory/wound healing (M2). M1 Mφs are observed in initial tissue damage responses, are induced by exogenous pathogen-associated molecular patterns or endogenous damage-associated molecular patterns, and exhibit increased phagocytosis and pro-inflammatory cytokine production, facilitating innate immunity and wound debridement. M2 Mφs predominate later in repair, express vascular endothelial growth factor, transforming growth factor b...

Ozone's Impact on Public Health: Contributions from Indoor Exposures to Ozone and Products of Ozone-Initiated Chemistry

Abstract: Many studies have reported associations between outdoor ozone concentrations and morbidity and mortality. Hubbell et al. (2005) systematically summarized this literature, including associations between ozone and respiratory-related hospital admissions, lost school days, restricted activity days, asthma-related emergency department visits, and premature mortality. Additionally, ozone has been associated with respiratory symptoms and the use of asthma medication for asthmatic school children using maintenance medication (Gent et al. 2003), and long-term exposure to ozone has been tentatively associated with the development of asthma in adult males (McDonnell et al. 1999). Since the submission of Hubbell et al. (2005), three independent meta-analyses have been published, indicating an increase of 0.87% in mortality per 10-ppb increase in daily ozone (Bell et al. 2005), an increase of 0.39% in mortality per 10-ppb increase in 1-hr daily maximum ozone (Ito et al. 2005), and an increase of 0.41% in mortality per 10-ppb increase in 1-hr daily maximum ozone (Levy et al. 2005); in most of the studies included in the meta analyses, same-day effects were larger than lagged effects. A study of 23 European cities found an increase of 0.66% in mortality per 10 ppb increase in 1-hr maximum ozone during the summer (Gryparis et al. 2004); a study in Genoa, Italy, found an increase of 4.0% in mortality per 25-ppb increase in ozone (Parodi et al. 2005); and a study in Shanghai found an increase of 0.45% in mortality per 5-ppb increase in 2-day average ozone (Zhang et al. 2006). Significantly, even when Bell et al. (2006) used data that included only days with average ozone levels lower than 15 ppb, outdoor ozone was significantly associated with premature mortality. For a more extended review of these and other studies, see the U.S. Environmental Protection Agency ozone criteria document (U.S. EPA 2006). An increase in the concentration of outdoor ozone concomitantly produces an increase in the indoor concentrations of ozone and its reaction products (Weschler 2000). Thus, some of the associations between outdoor ozone and both morbidity and mortality are likely due to outdoor ozone transported into various indoor environments (e.g., residences, workplaces, schools, hospitals, motor vehicles) where subsequent exposures occur. Although indoor ozone concentrations tend to be smaller than corresponding outdoor concentrations, this is somewhat counterbalanced by the much larger fraction of time that most people spend indoors. Moreover, excepting nitrogen dioxide, total concentrations of ozone reaction products are anticipated to be larger indoors than outdoors (see “Products of ozone-initiated indoor chemistry”). My aim in this article is to present evidence supporting the hypothesis that indoor exposures to ozone and its oxidation products contribute to ozone’s overall impact on public health. Apportioning ozone’s health impact among indoor and outdoor ozone, as well as indoor and outdoor oxidation products, is more than an academic exercise. If indoor ozone and the products of its chemistry are adversely affecting the public’s health, relatively simple strategies can mitigate these effects.

Vitamin D-dependent calcium binding proteins: Chemistry, distribution, functional considerations, and molecular biology

Abstract: I. Forward One of the most important contributions to the vitamin D field has been the discovery by Wasserman and Taylor in 1966 (1) of vitamin D-dependent calcium binding protein [calbindin-D (2)]. Early studies using competitive ion exchange methods as well as equilibrium dialysis indicated that administration of vitamin D to rachitic chicks resulted in an increase in the calcium binding activity of crude extracts of intestinal mucosa (1). Further investigations showed that the calcium binding activity was associated with a protein of about 28,000 mol wt (3, 4). Soon after the discovery of avian intestinal calbindin (1), a vitamin D-responsive calcium binding protein was also shown to be present in rat intestine (5, 6). Since the initial discoveries of the avian and rat intestinal calbindins, calbindins have been reported in a variety of species (7–19) and in many other tissues including kidney (20–25), bone (26), and tissues which are not regulators of serum calcium such as pancreas (27–32), placenta (...