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The Impact of Material Hardship on Children`s Physical Health Trajectories
Joan P. Yoo(유조안),Kristen S. Slack,Jane L. Holl 한국아동복지학회 2012 한국아동복지학 Vol.- No.37
본 연구는 미국에서 복지수급을 받고 있는 가정에서 자라나는 아이들의 빈곤 경험이 이들의 건강궤적에 미치는 영향에 대해 탐색적으로 분석하는 데 그 목적 이 있다. 최근 건강불평등에 대한 연구를 통해 빈곤이 개인의 건강에 장?단기적 으로 미치는 영향에 대한 관심이 증대되고 있으나, 아동기의 빈곤이 건강궤적에 미치는 영향에 대한 연구는 아직까지 탐색적인 수준에 머무르고 있다. 따라서 본 연구는 물질적 빈곤 경험이 저소득층 아동의 건강 궤적에 미치는 영향을 분석함 으로써 아동 건강불평등의 영향요인에 대한 이해를 증진시키고자 한다. 본 연구 에서는 1998년에 복지수급을 받고 있던 저소득층 가구들을 표본으로 2001년부터 2004년까지 총 4차년도의 패널데이터를 수집한 일리노이 가족 연구(Illinois Families Study)와 이 연구의 아동부가조사(Illinois Families Study-Child Well-being Supplement) 데이터를 활용하였다. 질병으로 인한 아동의 의료이용 횟수와 앓아누운 날 수를 주요 종속 변수로 활용하였으며, 데이터의 분석은 패널데이터의 특성을 고려하여 다층성장모형 분석방법을 이용하였다. 독립변수들을 투입하지 않은 무조건모형에 서는 의료이용 횟수와 앓아누운 날 수는 아이의 연령이 증가함에 따라 감소하는 것으로 나타났으며, 이는 전반적으로 아동의 건강상태가 계속 좋아지는 것으로 해석될 수 있다. 반면에 물질적 빈곤과 건강궤적의 관계에서는 물질적 빈곤을 많 이 경험할수록 저소득층 아동의 건강궤적에 부정적인 영향을 미치는 것으로 나 타났으며, 물질적 빈곤의 개별적인 종류가 저소득층 아동의 신체적 건강에 미치는 영향은 측정 지표에 따라 다르게 나타났다. 구체적으로 불안정한 주거와 아동 의 미충족 의료수준은 아동의 질병으로 인한 의료 이용궤적의 초기값과 유의미한 관계를 갖는 것으로 조사되었으며, 식품 미보장은 아동이 앓아누운 날 수로 측정된 건강궤적의 변화율과 통계적으로 유의미한 관계를 갖는 것으로 나타났다. 이러한 미국의 연구 결과는 한국에서 아동 건강 불평등에 대한 연구의 활성화 및 이를 극복하기 위한 정책적?실천적 방안 모색의 필요성에 대한 함의를 지닌다. The aim of this study is to understand the relationship between indicators of material hardship and the health trajectories of low-income children, and to explore how material hardship explains individual differences in low-income children`s health trajectories. The analyses for this paper are conducted using data from the Illinois Families Study (IFS) and the Illinois Families Study-Child Well-being Supplement (IFS-CWB). IFS is a five-year panel study that examined the well- being and adaptation of former and current welfare recipients and their families. Multilevel growth curve analysis is employed to examine the association. While the analytic findings suggest that the associations between material hardship variables vary by health outcomes, results show that generally children who experience economic hardships are more likely to show trajectories of health that led to worse health than their counterparts. Particularly, children`s unmet medical needs and housing insecurity were found to be associated with number of sick visits to health professional trajectory, while food hardship was found to be associated with number of days a child was sick in bed trajectory. Implications for the study findings are discussed.
Mount, Matthew P.,Zhang, Yi,Amini, Mandana,Callaghan, Steve,Kulczycki, Jerzy,Mao, Zixu,Slack, Ruth S.,Anisman, Hymie,Park, David S. American Society for Biochemistry and Molecular Bi 2013 The Journal of biological chemistry Vol.288 No.20
<P>We have earlier reported the critical nature of calpain-CDK5-MEF2 signaling in governing dopaminergic neuronal loss <I>in vivo</I>. CDK5 mediates phosphorylation of the neuronal survival factor myocyte enhancer factor 2 (MEF2) leading to its inactivation and loss. However, the downstream factors that mediate MEF2-regulated survival are unknown. Presently, we define <I>Nur77</I> as one such critical downstream survival effector. Following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment <I>in vivo</I>, <I>Nur77</I> expression in the nigrostriatal region is dramatically reduced. This loss is attenuated by expression of MEF2. Importantly, MEF2 constitutively binds to the <I>Nur77</I> promoter in neurons under basal conditions. This binding is lost following 1-methyl-4-phenylpyridinium treatment. <I>Nur77</I> deficiency results in significant sensitization to dopaminergic loss following 1-methyl-4-phenylpyridinium/MPTP treatment, <I>in vitro</I> and <I>in vivo</I>. Furthermore, <I>Nur77</I>-deficient MPTP-treated mice displayed significantly reduced levels of dopamine and 3,4-Dihydroxyphenylacetic acid in the striatum as well as elevated post synaptic FosB activity, indicative of increased nigrostriatal damage when compared with WT MPTP-treated controls. Importantly, this sensitization in <I>Nur77</I>-deficient mice was rescued with ectopic <I>Nur77</I> expression in the nigrostriatal system. These results indicate that the inactivation of <I>Nur77</I>, induced by loss of MEF2 activity, plays a critical role in nigrostriatal degeneration <I>in vivo</I>.</P>
The role of Cdk5-mediated apurinic/apyrimidinic endonuclease 1 phosphorylation in neuronal death
Huang, En,Qu, Dianbo,Zhang, Yi,Venderova, Katerina,Haque, M. Emdadul,Rousseaux, Maxime W.C.,Slack, Ruth S.,Woulfe, John M.,Park, David S. Nature Publishing Group 2010 NATURE CELL BIOLOGY Vol.12 No.6
Accumulating evidence suggests that deregulated cyclin-dependent kinase 5 (Cdk5) plays a critical part in neuronal death. However, the pathogenic targets of Cdk5 are not fully defined. Here we demonstrate that the Cdk5 activator p35 interacts directly with apurinic/apyrimidinic endonuclease 1 (Ape1), a protein crucial for base excision repair (BER) following DNA damage. Cdk5 complexes phosphorylate Ape1 at Thr 232 and thereby reduces its apurinic/apyrimidinic (AP) endonuclease activity. Ape1 phosphorylation is dependent on Cdk5 in in vitro and in vivo. The reduced endonuclease activity of phosphorylated Ape1 results in accumulation of DNA damage and contributes to neuronal death. Overexpression of Ape1<SUP>WT</SUP> and Ape1<SUP>T232A</SUP>, but not the phosphorylation mimic Ape1<SUP>T232E</SUP>, protects neurons against MPP<SUP>+</SUP>/MPTP. Loss of Ape1 sensitizes neurons to death. Importantly, increased phosphorylated Ape1 was also observed in post-mortem brain tissue from patients with Parkinson's and Alzheimer's diseases, suggesting a potential link between Ape1 phosphorylation and the pathogenesis of neurodegenerative diseases.
Prevalence and Incidence of Epilepsy in an Elderly and Low-Income Population in the United States
Derek H. Tang,Daniel C. Malone,Terri L. Warholak,Jenny Chong,Edward P. Armstrong,Marion K. Slack,Chiu-Hsieh Hsu,David M. Labiner 대한신경과학회 2015 Journal of Clinical Neurology Vol.11 No.3
Background and Purpose Te purpose of this study was to estimate the incidence and prevalence of epilepsy among an elderly and poor population in the United States. Methods Arizona Medicaid claims data from January 1, 2008 to December 31, 2010 were used for this analysis. Subjects who were aged ≥65 years and were continuously enrolled in any Arizona Medicaid health plans (eligible to patients with low income) for ≥12 months between January 1, 2008 and December 31, 2009 were considered eligible for inclusion in the study cohort. In addition to meeting the aforementioned criteria, incident and prevalent cases must have had epilepsy-related healthcare claims. Furthermore, incident cases were required to have a 1-year “clean” period immediately preceding the index date. Negative binomial and logistic regression models were used to assess the factors associated with epilepsy incidence and prevalence. Results Te estimated epilepsy incidence and prevalence for this population in 2009 were 7.9 and 19.3 per 1,000 person-years, respectively. Te incidence and prevalence rates were signifcantly higher for patients with comorbid conditions that were potential risk factors for epilepsy and were of younger age than for their non-comorbid and older counterparts (p<0.05). Te prevalence rates were signifcantly higher for non-Hispanic Blacks and male benefciaries than for non-Hispanic Whites and female benefciaries, respectively (p<0.05). Conclusions Tis patient population had higher epilepsy incidence and prevalence compared with the general US population. Tese diferences may be at least in part attributable to their low socioeconomic status.
Amini, Mandana,Ma, Chun-lei,Farazifard, Rasoul,Zhu, Guoqi,Zhang, Yi,Vanderluit, Jacqueline,Zoltewicz, Joanna Susie,Hage, Fadi,Savitt, Joseph M.,Lagace, Diane C.,Slack, Ruth S.,Beique, Jean-Claude,Baud Society for Neuroscience 2013 The Journal of neuroscience Vol.33 No.13
<P>Ubiquitous classical (typical) calpains, calpain-1 and calpain-2, are Ca<SUP>+2</SUP>-dependent cysteine proteases, which have been associated with numerous physiological and pathological cellular functions. However, a clear understanding of the role of calpains in the CNS has been hampered by the lack of appropriate deletion paradigms in the brain. In this study, we describe a unique model of conditional deletion of both calpain-1 and calpain-2 activities in mouse brain, which more definitively assesses the role of these ubiquitous proteases in brain development/function and pathology. Surprisingly, we show that these calpains are not critical for gross CNS development. However, calpain-1/calpain-2 loss leads to reduced dendritic branching complexity and spine density deficits associated with major deterioration in hippocampal long-term potentiation and spatial memory. Moreover, calpain-1/calpain-2-deficient neurons were significantly resistant to injury induced by excitotoxic stress or mitochondrial toxicity. Examination of downstream target showed that the conversion of the Cdk5 activator, p35, to pathogenic p25 form, occurred only in the presence of calpain and that it played a major role in calpain-mediated neuronal death. These findings unequivocally establish two central roles of calpain-1/calpain-2 in CNS function in plasticity and neuronal death.</P>