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  1. Article ; Online: Environmental pollution, Health Expenditure and Economic Growth in Southeast Asian Countries

    Mojtaba Abbasian / Hossein Ebrahimzadeh Asmin / Mehrdad Alirezaei Shahraki / Arezoo Barahoei

    محیط زیست و مهندسی آب, Vol 7, Iss 4, Pp 590-

    ARDL Panel Approach

    2021  Volume 600

    Abstract: Economic growth contributes to better health and better health to economic growth, Considering the effects of environmental pollution on the health of people in the community and its costs, it is expected that by improving the quality of the environment, ...

    Abstract Economic growth contributes to better health and better health to economic growth, Considering the effects of environmental pollution on the health of people in the community and its costs, it is expected that by improving the quality of the environment, on the one hand, the costs saved in the health sector will be used for investment and production growth, On the other hand, by improving the level of health in society, productivity will increase, which can be a stimulus for more production. Therefore, in this study, the relationship between environmental pollution, health expenditure (HE) and economic growth (Y) in Southeast Asian countries from 1990 to 2019 using long-term and short-term analytical method of combined group average estimator or PMG has been investigated. The panel unit root test and determine the degree of co-integration model variables 1 and the panel co-integration test and concluded that a long-term relationship between the co-integration model variables there, Model estimation showed that only economic growth with a coefficient of 1.336 has a positive and long-term effect on HE, which means that a unit of change in economic growth increases and changes health costs by 1.336 in the same direction. According to the principles, the quality of the environment had an inverse and significant relationship with health costs, Coefficient of 0.848 indicates the impact of health costs on this variable.
    Keywords economic growth ; environmental pollution ; health expenditure ; panel ardl ; Environmental sciences ; GE1-350 ; Water supply for domestic and industrial purposes ; TD201-500
    Subject code 339
    Language Persian
    Publishing date 2021-12-01T00:00:00Z
    Publisher Iranian Rainwater Catchment Systems Association
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Biphasic and cardiomyocyte-specific IFIT activity protects cardiomyocytes from enteroviral infection.

    Taishi Kimura / Claudia T Flynn / Mehrdad Alirezaei / Ganes C Sen / J Lindsay Whitton

    PLoS Pathogens, Vol 15, Iss 4, p e

    2019  Volume 1007674

    Abstract: Viral myocarditis is a serious disease, commonly caused by type B coxsackieviruses (CVB). Here we show that innate immune protection against CVB3 myocarditis requires the IFIT (IFN-induced with tetratricopeptide) locus, which acts in a biphasic manner. ... ...

    Abstract Viral myocarditis is a serious disease, commonly caused by type B coxsackieviruses (CVB). Here we show that innate immune protection against CVB3 myocarditis requires the IFIT (IFN-induced with tetratricopeptide) locus, which acts in a biphasic manner. Using IFIT locus knockout (IFITKO) cardiomyocytes we show that, in the absence of the IFIT locus, viral replication is dramatically increased, indicating that constitutive IFIT expression suppresses CVB replication in this cell type. IFNβ pre-treatment strongly suppresses CVB3 replication in wild type (wt) cardiomyocytes, but not in IFITKO cardiomyocytes, indicating that other interferon-stimulated genes (ISGs) cannot compensate for the loss of IFITs in this cell type. Thus, in isolated wt cardiomyocytes, the anti-CVB3 activity of IFITs is biphasic, being required for protection both before and after T1IFN signaling. These in vitro findings are replicated in vivo. Using novel IFITKO mice we demonstrate accelerated CVB3 replication in pancreas, liver and heart in the hours following infection. This early increase in virus load in IFITKO animals accelerates the induction of other ISGs in several tissues, enhancing virus clearance from some tissues, indicating that-in contrast to cardiomyocytes-other ISGs can offset the loss of IFITs from those cell types. In contrast, CVB3 persists in IFITKO hearts, and myocarditis occurs. Thus, cardiomyocytes have a specific, biphasic, and near-absolute requirement for IFITs to control CVB infection.
    Keywords Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2019-04-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Disruption of neuronal autophagy by infected microglia results in neurodegeneration.

    Mehrdad Alirezaei / William B Kiosses / Claudia T Flynn / Nathan R Brady / Howard S Fox

    PLoS ONE, Vol 3, Iss 8, p e

    2008  Volume 2906

    Abstract: There is compelling evidence to support the idea that autophagy has a protective function in neurons and its disruption results in neurodegenerative disorders. Neuronal damage is well-documented in the brains of HIV-infected individuals, and evidence of ... ...

    Abstract There is compelling evidence to support the idea that autophagy has a protective function in neurons and its disruption results in neurodegenerative disorders. Neuronal damage is well-documented in the brains of HIV-infected individuals, and evidence of inflammation, oxidative stress, damage to synaptic and dendritic structures, and neuronal loss are present in the brains of those with HIV-associated dementia. We investigated the role of autophagy in microglia-induced neurotoxicity in primary rodent neurons, primate and human models. We demonstrate here that products of simian immunodeficiency virus (SIV)-infected microglia inhibit neuronal autophagy, resulting in decreased neuronal survival. Quantitative analysis of autophagy vacuole numbers in rat primary neurons revealed a striking loss from the processes. Assessment of multiple biochemical markers of autophagic activity confirmed the inhibition of autophagy in neurons. Importantly, autophagy could be induced in neurons through rapamycin treatment, and such treatment conferred significant protection to neurons. Two major mediators of HIV-induced neurotoxicity, tumor necrosis factor-alpha and glutamate, had similar effects on reducing autophagy in neurons. The mRNA level of p62 was increased in the brain in SIV encephalitis and as well as in brains from individuals with HIV dementia, and abnormal neuronal p62 dot structures immunoreactivity was present and had a similar pattern with abnormal ubiquitinylated proteins. Taken together, these results identify that induction of deficits in autophagy is a significant mechanism for neurodegenerative processes that arise from glial, as opposed to neuronal, sources, and that the maintenance of autophagy may have a pivotal role in neuroprotection in the setting of HIV infection.
    Keywords Medicine ; R ; Science ; Q
    Subject code 590 ; 571
    Language English
    Publishing date 2008-08-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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