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2014, Vol.5  No.6
Our aim was to contribute to a better understanding of the pathophysiology of anemia in elderly, by studying how aging affects renal function, iron metabolism, erythropoiesis and the inflammatory response, using an experimental animal model. The study was performed in male Wistar, a group of young rats with 2 months age and an old one with 18 months age. Old rats presented a significant higher urea, creatinine, interferon (INF)-gamma, ferritin and soluble transferrin receptor serum levels, as well as increased counts of reticulocytes and RDW. In addition, these rats showed significant lower erythropoietin (EPO) and iron serum levels. Concerning gene expression of iron regulatory proteins, old rats presented significantly higher mRNA levels of hepcidin (Hamp), transferrin (TF), transferrin receptor 2 (TfR2) and hemojuvelin (HJV); divalent [Detail] ...

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  • Table of Content
      21 November 2014, Volume 5 Issue 6 Previous Issue    Next Issue
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    Original Article
    Aging is Associated with Impaired Renal Function, INF-gamma Induced Inflammation and with Alterations in Iron Regulatory Proteins Gene Expression
    Costa Elísio,Fernandes João,Ribeiro Sandra,Sereno José,Garrido Patrícia,Rocha-Pereira Petronila,Coimbra Susana,Catarino Cristina,Belo Luís,Bronze-da-Rocha Elsa,Vala Helena,Alves Rui,Reis Flávio,Santos-Silva Alice
    Aging and Disease. 2014, 5 (6): 356-365.   DOI: 10.14366/AD.2014.0500356
    Abstract   HTML   PDF (0KB) ( 1017 )

    Our aim was to contribute to a better understanding of the pathophysiology of anemia in elderly, by studying how aging affects renal function, iron metabolism, erythropoiesis and the inflammatory response, using an experimental animal model. The study was performed in male Wistar, a group of young rats with 2 months age and an old one with 18 months age. Old rats presented a significant higher urea, creatinine, interferon (INF)-gamma, ferritin and soluble transferrin receptor serum levels, as well as increased counts of reticulocytes and RDW. In addition, these rats showed significant lower erythropoietin (EPO) and iron serum levels. Concerning gene expression of iron regulatory proteins, old rats presented significantly higher mRNA levels of hepcidin (Hamp), transferrin (TF), transferrin receptor 2 (TfR2) and hemojuvelin (HJV); divalent metal transporter 1 (DMT1) mRNA levels were significantly higher in duodenal tissue; EPO gene expression was significantly higher in liver and lower in kidney, and the expression of the EPOR was significantly higher in both liver and kidney. Our results showed that aging is associated with impaired renal function, which could be in turn related with the inflammatory process and with a decline in EPO renal production. Moreover, we also propose that aging may be associated with INF-gamma-induced inflammation and with alterations upon iron regulatory proteins gene expression.

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    Reduced Apoptosis by Ethanol and Its Association with PKC-δ and Akt Signaling in Ischemic Stroke
    Hafeez Adam,Elmadhoun Omar,Peng Changya,Y. Ding Jamie,Geng Xiaokun,Guthikonda Murali,Ding Yuchuan
    Aging and Disease. 2014, 5 (6): 366-372.   DOI: 10.14336/AD.2014.0500366
    Abstract   HTML   PDF (0KB) ( 872 )

    Along with thrombolytic therapy, which has a number of limitations, stroke outcome may be improved with neuroprotective therapies that disrupt ischemic cell death. Recent research has shown a neuroprotective role of ethanol administration during ischemic stroke, such as its ability to reduce infarct volume and neurologic deficit. In order to investigate this further, we assessed the hypothesis that ethanol’s neuroprotective effect is through reduction of apoptosis and the modulation of the important apoptotic PKC-δ and Akt signaling pathway. Ethanol (1.5 g/kg) was given by intraperitoneal injections to 54 Sprague-Dawley rats after 2 hours of middle cerebral artery (MCA) occlusion, followed by 3 or 24 hours of reperfusion. We measured apoptotic cell death, PKC-δ, and Akt mRNA and protein expressions in each of ischemic groups with or without ethanol treatment using ELISA, real-time PCR and Western blot analysis. Our results showed that cell death was significantly increased in rats following 2 hour MCA occlusion and 24 hour reperfusion. Subsequently, cell death was significantly reduced by an administration of ethanol. We further found that ethanol administration, prior to either 3 or 24 hours of reperfusion, significantly decreased the expression of PKC-δ while simultaneously increasing the expression Akt at both mRNA and protein levels at the two points. In conclusion, our study suggests that ethanol administration following ischemic stroke modulates the gene and protein profile in such a way that it increased expression of anti-apoptotic Akt and decreased the pro-apoptotic PKC-δ. This ultimately results in a decrease in neuronal apoptosis, thus conferring neuroprotection.

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    Review Article
    Use of Anthropometry for the Prediction of Regional Body Tissue Distribution in Adults: Benefits and Limitations in Clinical Practice
    Scafoglieri Aldo,Pieter Clarys Jan,Cattrysse Erik,Bautmans Ivan
    Aging and Disease. 2014, 5 (6): 374-393.   DOI: 10.14366/AD.2014.05003743
    Abstract   HTML   PDF (0KB) ( 1183 )

    Regional body composition changes with aging. Some of the changes in composition are considered major risk factors for developing obesity related chronic diseases which in turn may lead to increased mortality in adults. The role of anthropometry is well recognized in the screening, diagnosis and follow-up of adults for risk classification, regardless of age. Regional body composition is influenced by a number of intrinsic and extrinsic factors. Therapeutic measures recommended to lower cardiovascular disease risk include lifestyle changes. The aim of this review is to systematically summarize studies that assessed the relationships between anthropometry and regional body composition. The potential benefits and limitations of anthropometry for use in clinical practice are presented and suggestions for future research given.

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    Regulation and Role of TGFβ Signaling Pathway in Aging and Osteoarthritis Joints
    Baugé Catherine,Girard Nicolas,Lhuissier Eva,Bazille Celine,Boumediene Karim
    Aging and Disease. 2014, 5 (6): 394-405.   DOI: 10.14336/AD.2014.0500394
    Abstract   HTML   PDF (0KB) ( 1125 )

    Transforming growth factor beta (TGFβ) is a major signalling pathway in joints. This superfamilly is involved in numerous cellular processes in cartilage. Usually, they are considered to favor chondrocyte differentiation and cartilage repair. However, other studies show also deleterious effects of TGFβ which may induce hypertrophy. This may be explained at least in part by alteration of TGFβ signaling pathways in aging chondrocytes. This review focuses on the functions of TGFβ in joints and the regulation of its signaling mediators (receptors, Smads) during aging and osteoarthritis.

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    The Circadian Timing System: A Recent Addition in the Physiological Mechanisms Underlying Pathological and Aging Processes
    Arellanes-Licea Elvira,Caldelas Ivette,De Ita-Pérez Dalia,Díaz-Muñoz* Mauricio
    Aging and Disease. 2014, 5 (6): 406-418.   DOI: 10.14336/AD.2014.0500406
    Abstract   HTML   PDF (0KB) ( 1110 )

    Experimental findings and clinical observations have strengthened the association between physio-pathologic aspects of several diseases, as well as aging process, with the occurrence and control of circadian rhythms. The circadian system is composed by a principal pacemaker in the suprachiasmatic nucleus (SNC) which is in coordination with a number of peripheral circadian oscillators. Many pathological entities such as metabolic syndrome, cancer and cardiovascular events are strongly connected with a disruptive condition of the circadian cycle. Inadequate circadian physiology can be elicited by genetic defects (mutations in clock genes or circadian control genes) or physiological deficiencies (desynchronization between SCN and peripheral oscillators). In this review, we focus on the most recent experimental findings regarding molecular defects in the molecular circadian clock and the altered coordination in the circadian system that are related with clinical conditions such as metabolic diseases, cancer predisposition and physiological deficiencies associated to jet-lag and shiftwork schedules. Implications in the aging process will be also reviewed.

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    Early-life Exposure to Endocrine Disrupting Chemicals and Later-life Health Outcomes: An Epigenetic Bridge?
    Vaiserman* Alexander
    Aging and Disease. 2014, 5 (6): 419-429.   DOI: 10.14336/AD.2014.0500419
    Abstract   HTML   PDF (0KB) ( 1827 )

    A growing body of evidence demonstrates that adverse events early in development, and particularly during intrauterine life, may program risks for diseases in adult life. Increasing evidence has been accumulated indicating the important role of epigenetic regulation including DNA methylation, histone modifications and miRNAs in developmental programming. Among the environmental factors which play an important role in programming of chronic pathologies, the endocrine-disrupting chemicals (EDCs) that have estrogenic, anti-estrogenic, and anti-androgenic activity are of specific concern because the developing organism is extremely sensitive to perturbation by substances with hormone-like activity. Among EDCs, there are many substances that are constantly present in the modern human environment or are in widespread use, including dioxin and dioxin-like compounds, phthalates, agricultural pesticides, polychlorinated biphenyls, industrial solvents, pharmaceuticals, and heavy metals. Apart from their common endocrine active properties, several EDCs have been shown to disrupt developmental epigenomic programming. The purpose of this review is to provide a summary of recent research findings which indicate that exposure to EDCs during in-utero and/or neonatal development can cause long-term health outcomes via mechanisms of epigenetic memory.

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    The Role of NMDA Receptors in the Development of Brain Resistance through Pre- and Postconditioning
    Celso Constantino Leandra,Inês Tasca Carla,Rodrigues Boeck Carina
    Aging and Disease. 2014, 5 (6): 430-441.   DOI: 10.14336/AD.2014.0500430
    Abstract   HTML   PDF (0KB) ( 1275 )

    Brain tolerance or resistance can be achieved by interventions before and after injury through potential toxic agents used in low stimulus or dose. For brain diseases, the neuroprotection paradigm desires an attenuation of the resulting motor, cognitive, emotional, or memory deficits following the insult. Preconditioning is a well-established experimental and clinical translational strategy with great beneficial effects, but limited applications. NMDA receptors have been reported as protagonists in the adjacent cellular mechanisms contributing to the development of brain tolerance. Postconditioning has recently emerged as a new neuroprotective strategy, which has shown interesting results when applied immediately, i.e. several hours to days, after a stroke event. Investigations using chemical postconditioning are still incipient, but nevertheless represent an interesting and promising clinical strategy. In the present review pre- and postconditioning are discussed as neuroprotective paradigms and the focus of our attention lies on the participation of NMDA receptors proteins in the processes related to neuroprotection.

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  Editors-in-Chief  
Kunlin Jin, M.D., Ph.D., Professor
Ashok K. Shetty, Ph.D., Professor
David A. Greenberg, M.D., Ph.D., Professor
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