Gy, zinc and phytate content of the national food supply, and

Gy, zinc and phytate content of the national food supply, and percent of dietary zinc obtained from animal source foods (ASF) for countries with a .5 absolute increase in the prevalence of inadequate zinc intake between 1990 and 2005. (DOCX)AcknowledgmentsWe thank Janet Peerson (University of California, Davis) for assistance with the statistical analyses. We also acknowledge Majid Ezzati (Imperial College of London), as well as Abigail Donner and Gitanjali Singh (Harvard School of Public Health) for assistance with project ML-281 biological activity coordination and cleaning of the data from the national food balance sheets.Author 1531364 ContributionsConceived and designed the experiments: KRW KHB. Performed the experiments: KRW. Analyzed the data: KRW KHB. Wrote the paper: KRW KHB.
Age-related macular degeneration (AMD) is the major cause of legal blindness in industrialized nations [1,2,3,4]. It is a multifactorial disease leading to the loss of central vision at the final stage. Both genetic and environmental factors may play a fundamental role in the disease development and progression [5,6]. Cigarette smoke is the single most important environmental risk factor for AMD [7,8,9]. Recent studies have detected a two- to threefold increased risk for AMD in smokers compared to nonsmokers [8,10]. One reason for these adverse effects could be attributed to the various potent oxidants, which are contained in cigarette smoke [11,12]. Therefore, it is assumed that cigarette smoke mediates its toxic effects via increased production of reactive oxygen species (ROS) and thus oxidative stress [10]. Oxidative stress plays the key role in the process of ageing and age-related diseases. In age-related diseases, it induces a number of biological events such as cell death, advanced senescence, and extracellular matrix (ECM) production [13]. These characteristic findings can also be found in ocular age-related diseases such as AMD. In the setting of massive deposition of extracellular debris, the loss of retinal pigment epithelial (RPE) cells is the key event of the atrophic form of AMD leading to the loss of central vision [14]. In early AMD, advanced cellular senescence of the RPE may represent an initial step in the pathogenesis of AMD [15]. Cellular senescence can be identified by increased senescence-associated alactosidase (SA-?Gal) activity and elevated expression of senescence-associated biomarkers such as apolipoprotein J (ApoJ), connective tissue growth factor (CTGF), and fibronectin [16,17,18]. ApoJ, also called clusterin, is abundant in drusen [19]. CTGF and fibronectin accumulate in the Bruch’s membrane, in drusen and in basal linear deposits of AMD eyes [20,21,22]. Fibronectin and also the basement membrane component Madrasin site laminin have been shown to be secreted by senescent 24786787 human RPE cells [23]. In AMD donor eyes, increased ECM accumulation can lead to a diffuse thickening of the Bruch’s membrane beneath the RPE, and thus an impaired diffusion of oxygen towards the retina [23,24]. In this study, we hypothesized that cigarette smoke is responsible for these cellular changes in the RPE of AMD patients. In our experiments, we used cigarette smoke extract (CSE) as a well-established in vitro model of cigarette smoke exposure [25,26,27]. We first examined at which concentration CSE could induce cell death in primary cultured human RPE cells. Furthermore, we wanted to known whether or not CSE could increase lipid peroxidation in human RPE cells. In addition, we investigated the eff.Gy, zinc and phytate content of the national food supply, and percent of dietary zinc obtained from animal source foods (ASF) for countries with a .5 absolute increase in the prevalence of inadequate zinc intake between 1990 and 2005. (DOCX)AcknowledgmentsWe thank Janet Peerson (University of California, Davis) for assistance with the statistical analyses. We also acknowledge Majid Ezzati (Imperial College of London), as well as Abigail Donner and Gitanjali Singh (Harvard School of Public Health) for assistance with project coordination and cleaning of the data from the national food balance sheets.Author 1531364 ContributionsConceived and designed the experiments: KRW KHB. Performed the experiments: KRW. Analyzed the data: KRW KHB. Wrote the paper: KRW KHB.
Age-related macular degeneration (AMD) is the major cause of legal blindness in industrialized nations [1,2,3,4]. It is a multifactorial disease leading to the loss of central vision at the final stage. Both genetic and environmental factors may play a fundamental role in the disease development and progression [5,6]. Cigarette smoke is the single most important environmental risk factor for AMD [7,8,9]. Recent studies have detected a two- to threefold increased risk for AMD in smokers compared to nonsmokers [8,10]. One reason for these adverse effects could be attributed to the various potent oxidants, which are contained in cigarette smoke [11,12]. Therefore, it is assumed that cigarette smoke mediates its toxic effects via increased production of reactive oxygen species (ROS) and thus oxidative stress [10]. Oxidative stress plays the key role in the process of ageing and age-related diseases. In age-related diseases, it induces a number of biological events such as cell death, advanced senescence, and extracellular matrix (ECM) production [13]. These characteristic findings can also be found in ocular age-related diseases such as AMD. In the setting of massive deposition of extracellular debris, the loss of retinal pigment epithelial (RPE) cells is the key event of the atrophic form of AMD leading to the loss of central vision [14]. In early AMD, advanced cellular senescence of the RPE may represent an initial step in the pathogenesis of AMD [15]. Cellular senescence can be identified by increased senescence-associated alactosidase (SA-?Gal) activity and elevated expression of senescence-associated biomarkers such as apolipoprotein J (ApoJ), connective tissue growth factor (CTGF), and fibronectin [16,17,18]. ApoJ, also called clusterin, is abundant in drusen [19]. CTGF and fibronectin accumulate in the Bruch’s membrane, in drusen and in basal linear deposits of AMD eyes [20,21,22]. Fibronectin and also the basement membrane component laminin have been shown to be secreted by senescent 24786787 human RPE cells [23]. In AMD donor eyes, increased ECM accumulation can lead to a diffuse thickening of the Bruch’s membrane beneath the RPE, and thus an impaired diffusion of oxygen towards the retina [23,24]. In this study, we hypothesized that cigarette smoke is responsible for these cellular changes in the RPE of AMD patients. In our experiments, we used cigarette smoke extract (CSE) as a well-established in vitro model of cigarette smoke exposure [25,26,27]. We first examined at which concentration CSE could induce cell death in primary cultured human RPE cells. Furthermore, we wanted to known whether or not CSE could increase lipid peroxidation in human RPE cells. In addition, we investigated the eff.

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