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Search Results: 1 - 10 of 6459 matches for " Peizhong Mao "
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Recent progress and concerns in dementia: Distinguishing Alzheimer's disease and dementia with Lewy bodies via biochemical markers in the cerebrospinal fluid  [PDF]
Peizhong Mao
Advances in Biological Chemistry (ABC) , 2012, DOI: 10.4236/abc.2012.22022
Abstract: Dementia is mainly a neurodegenerative disorder involved in several systems, including central nervous system, endocrinology/metabolism system and circulatory system. Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB) are the most common forms of the dementia, accounting for 60% - 80% and 10% - 20% of all cases, respectively. DLB is defined by widespread neocortical, limbic and brainstem Lewy bodies but frequently accompanied by variable levels of AD pathology. This pathological and clinical overlap makes their differential diagnosis complicated. Recent advances in the identification of disease bio-markers now make it possible to detect and distinguish their pathology in the early or preclinical stage of the diseases, even in cognitively normal individuals. In addition to the key biomarkers (amyloid β or Aβ, tau and α-synuclein), neurotrophins such as cocaine- and amphetamine-regulated transcript (CART) have also drawn attention due to their expressions and functions. This article summarizes the progress in the definition, pathology and diagnosis of dementia, with a focus on potential biochemical markers in the cere-brospinal fluid (CSF) in the differential diagnosis of the main forms of dementia. To prediction or early diagnosis of dementia, the role of specific and sensitive CSF biomarkers seems to be crucial in a routine clinical setting. The concerns and challenges in the biomarker field are also discussed.
Potential Antidepressant Role of Neurotransmitter CART: Implications for Mental Disorders
Peizhong Mao
Depression Research and Treatment , 2011, DOI: 10.1155/2011/762139
Abstract: Depression is one of the most prevalent and debilitating public health concerns. Although no single cause of depression has been identified, it appears that interaction among genetic, epigenetic, biochemical, environmental, and psychosocial factors may explain its etiology. Further, only a fraction of depressed patients show full remission while using current antidepressants. Therefore, identifying common pathways of the disorder and using that knowledge to develop more effective pharmacological treatments are two primary targets of research in this field. Brain-enriched neurotransmitter CART (cocaine- and amphetamine-regulated transcript) has multiple functions related to emotions. It is a potential neurotrophic factor and is involved in the regulation of hypothalamic-pituitary-adrenal axis and stress response as well as in energy homeostasis. CART is also highly expressed in limbic system, which is considered to have an important role in regulating mood. Notably, adolescents carrying a missense mutation in the CART gene exhibit increased depression and anxiety. Hence, CART peptide may be a novel promising antidepressant agent. In this paper, we summarize recent progress in depression and CART. In particular, we emphasize a new antidepressant function for CART. 1. Introduction Depression or major depression disorder (MDD) is one of the most prevalent and debilitating public health concerns. MDD affects millions of people each year [1, 2], and the burden of this disease will continue to increase, especially during the extra years of life gained from improved health outcomes in cardiovascular disease, cancer, and other domains [3, 4]. Notably evidence showed that MDD affects more women than men [5]. According to the guidelines developed by the American Psychiatric Association, MDD can be diagnosed when a patient demonstrates at least 2 weeks of depressed mood or loss of interest accompanied by at least four additional symptoms, including constant sadness, irritability, hopelessness, trouble sleeping, low energy or fatigue, feeling worthless or guilty for no reason, significant weight change (gain or loss), difficulty concentrating, and loss of interest in favorite activities [5, 6]. However, the etiology and pathology of this serious biologic disease are still largely unknown. It is likely the result of a complex interaction of genetic, epigenetic, biochemical, environmental, and psychosocial factors. Now, there is compelling evidence that monoaminergic neurotransmission in the brain is disturbed in depressed patients. However, usually it takes between 1
Oxidative Stress and Its Clinical Applications in Dementia
Peizhong Mao
Journal of Neurodegenerative Diseases , 2013, DOI: 10.1155/2013/319898
Abstract: Dementia is a complex disorder that mostly affects the elderly and represents a significant and growing public health burden in the world. Alzheimer’s disease (AD)- associated dementia and dementia with Lewy bodies (DLB) are the most common forms of dementia, in which oxidative stress is significantly involved. Oxidative stress mechanisms may have clinical applications, that is, providing information for potential biomarkers. Thus brain-rich peptides with an antioxidant property, such as CART (cocaine- and amphetamine-regulated transcript), may be promising new markers. This paper summarizes the progress in research regarding oxidative stress in dementia with a focus on potential biomarkers in the cerebrospinal fluid (CSF) in the main forms of dementia. Other central and peripheral biomarkers, especially those considered oxidative stress related, are also discussed. This paper aims to provide information to improve current understanding of the pathogenesis and progression of dementia. It also offers insight into the differential diagnosis of AD and DLB. 1. Introduction Dementia is a multisystem-related neurodegenerative disorder. According to the DSM-IIIR (the Diagnostic and Statistical Manual, 3rd edition, revised) the essential feature of dementia is impairment in short- and long-term memory, associated with impairment in abstract thinking, impaired judgment, other disturbances of higher cortical function, or personality change. The disturbance is severe enough to interfere significantly with work or usual social activities or relationships with others. The diagnosis of dementia is not made if these symptoms occur in delirium. The DSM-IIIR definition of dementia is reliable and is routinely used in clinical guidelines [1, 2]. There are several forms of dementia, including dementia associated with Alzheimer’s disease (AD), dementia with Lewy bodies (DLB), corticobasal degeneration/dementia (CBD), frontotemporal dementias (FTD) (also known as frontotemporal lobar degenerations or FTLD), vascular dementia (VAD), and prion diseases such as Creutzfeldt-Jakob Disease (CJD) [1, 3]. Among all forms of dementia, Alzheimer’s dementia and dementia with Lewy bodies are the most common. AD is accounting for 60–80% of the total number of dementia, characterized by extracellular fibrillar amyloid β (Aβ), especially long form 42 amino acids of Aβ (Aβ42) deposits (amyloid plaques), intracellular neurofibrillary tangles (NFT, phosphate-tau related), and neuronal as well as axonal degeneration in the brain [4–6]. Dementia with Lewy bodies (DLB), accounting for 15–30% of
Recent Advances in Obesity: Genetics and Beyond
Wai W. Cheung,Peizhong Mao
ISRN Endocrinology , 2012, DOI: 10.5402/2012/536905
Abstract: The prevalence of obesity, which is a heritable trait that arises from the interactions of multiple genes and lifestyle factors, continues to increase worldwide, causing serious health problems and imposing a substantial economic burden on societies. For the past several years, various genetic epidemiological approaches have been utilized to identify genetic loci for obesity. Recent evidence suggests that development of obesity involves hormones and neurotransmitters (such as leptin, cocaine- and amphetamine-regulated transcript (CART), and ghrelin) that regulate appetite and energy expenditure. These hormones act on specific centers in the brain that regulate the sensations of satiety. Mutations in these hormones or their receptors can lead to obesity. Aberrant circadian rhythms and biochemical pathways in peripheral organs or tissues have also been implicated in the pathology of obesity. More interestingly, increasing evidence indicates a potential relation between obesity and central nervous system disorders (such as cognitive deficits). This paper discusses recent advances in the field of genetics of obesity with an emphasis on several established loci that influence obesity. These recently identified loci may hold the promise to substantially improve our insights into the pathophysiology of obesity and open up new therapeutic strategies to combat growing obesity epidemic facing the human population today. 1. Introduction Throughout history, science has invested enormous time and effort in the search to understand the physiological basis of obesity. Crucial to this research are the inquiry of how does our body control ingestion, digestion, absorption, and metabolism and how nutrients are distributed among various tissues, organs, and systems [1, 2]. Overweight and obesity, defined as body mass index (BMI, the weight in kilograms divided by the square of the height in meters) >25 and >30, respectively, are associated with premature death through increased risk of many chronic diseases, including type 2 diabetes, cardiovascular disease, and cancer [3–5]. Obesity is a major international public health threat and economic burden. Over the last 3 decades, the prevalence of overweight and obesity has increased rapidly. The latest World Health Organization estimates that 1.6 billion adults (aged 15 years and above) were overweight and 400 million were obese in 2005. These figures are predicted to rise to 2.3 billion overweight and over 700 million obese adults by 2015 [6]. Obesity results when body fat accumulates over time as a result of chronic energy
Neurotransmitter CART as a New Therapeutic Candidate for Parkinson’s Disease
Peizhong Mao,Charles K. Meshul,Philippe Thuillier,P. Hemachandra Reddy
Pharmaceuticals , 2013, DOI: 10.3390/ph6010108
Abstract: Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. To date, there is no effective treatment that halts its progression. Increasing evidence indicates that mitochondria play an important role in the development of PD. Hence mitochondria-targeted approaches or agents may have therapeutic promise for treatment of the disease. Neuropeptide CART (cocaine-amphetamine-regulated transcript), a hypothalamus and midbrain enriched neurotransmitter with an antioxidant property, can be found in mitochondria, which is the main source of reactive oxygen species. Systemic administration of CART has been found to ameliorate dopaminergic neuronal loss and improve motor functions in a mouse model of PD. In this article, we summarize recent progress in studies investigating the relationship between CART, dopamine, and the pathophysiology of PD, with a focus on mitochondria-related topics.
CART Peptide Is a Potential Endogenous Antioxidant and Preferentially Localized in Mitochondria
Peizhong Mao, Charles K. Meshul, Philippe Thuillier, Natalie R. S. Goldberg, P. Hemachandra Reddy
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029343
Abstract: The multifunctional neuropeptide Cocaine and Amphetamine Regulated Transcript (CART) is secreted from hypothalamus, pituitary, adrenal gland and pancreas. It also can be found in circulatory system. This feature suggests a general role for CART in different cells. In the present study, we demonstrate that CART protects mitochondrial DNA (mtDNA), cellular proteins and lipids against the oxidative action of hydrogen peroxide, a widely used oxidant. Using cis-parinaric acid as a sensitive reporting probe for peroxidation in membranes, and a lipid-soluble azo initiator of peroxyl radicals, 2,2′-Azobis(2,4-dimethylvaleronitrile) we found that CART is an antioxidant. Furthermore, we found that CART localized to mitochondria in cultured cells and mouse brain neuronal cells. More importantly, pretreatment with CART by systemic injection protects against a mouse oxidative stress model, which mimics the main features of Parkinson's disease. Given the unique molecular structure and biological features of CART, we conclude that CART is an antioxidant peptide (or antioxidant hormone). We further propose that it may have strong therapeutic properties for human diseases in which oxidative stress is strongly involved such as Parkinson's disease.
Algorithmic criteria for permutation orthogonal systems over finite fields
Peizhong Lu
Chinese Science Bulletin , 1998, DOI: 10.1007/BF02883675
Abstract: Two criteria for orthogonal systems over finite fields are presented. The first one is an algorithm by use of Grobner bases. The second one is a formula of the numbers of adjoint morphisms.
Toxicity of Neurons Treated with Herbicides and Neuroprotection by Mitochondria-Targeted Antioxidant SS31
Tejaswini P. Reddy,Maria Manczak,Marcus J. Calkins,Peizhong Mao,Arubala P. Reddy,Ulziibat Shirendeb,Byung Park,P. Hemachandra Reddy
International Journal of Environmental Research and Public Health , 2011, DOI: 10.3390/ijerph8010203
Abstract: The purpose of this study was to determine the neurotoxicity of two commonly used herbicides: picloram and triclopyr and the neuroprotective effects of the mitochondria-targeted antioxidant, SS31. Using mouse neuroblastoma (N2a) cells and primary neurons from C57BL/6 mice, we investigated the toxicity of these herbicides, and protective effects of SS1 peptide against picloram and triclopyr toxicity. We measured total RNA content, cell viability and mRNA expression of peroxiredoxins, neuroprotective genes, mitochondrial- encoded electron transport chain (ETC) genes in N2a cells treated with herbicides and SS31. Using primary neurons from C57BL/6 mice, neuronal survival was studied in neurons treated with herbicides, in neurons pretreated with SS31 plus treated with herbicides, neurons treated with SS31 alone, and untreated neurons. Significantly decreased total RNA content, and cell viability in N2a cells treated with picloram and triclopyr were found compared to untreated N2a cells. Decreased mRNA expression of neuroprotective genes, and ETC genes in cells treated with herbicides was found compared to untreated cells. Decreased mRNA expression of peroxiredoxins 1–6 in N2a cells treated with picloram was found, suggesting that picloram affects the antioxidant enzymes in N2a cells. Immunofluorescence analysis of primary neurons revealed that decreased neuronal branching and degenerating neurons in neurons treated with picloram and triclopyr. However, neurons pretreated with SS31 prevented degenerative process caused by herbicides. Based on these results, we propose that herbicides—picloram and triclopyr appear to damage neurons, and the SS31 peptide appears to protect neurons from herbicide toxicity.
Synthesis of Ginkgolic Acid Analogues and Evaluation of Their Molluscicidal Activity
Peng Zhang,Jiahu Pan,Wanxing Duan,Xuedong Li,Yao Zhang,Yibiao Zhou,Qingwu Jiang,Zuohua Mao,Peizhong Yu
Molecules , 2011, DOI: 10.3390/molecules16054059
Abstract: Based on the molluscicidal activity of ginkgolic acids (GAs) isolated from Ginkgo biloba L, a series of Z/E isomers of GA analogues were prepared and evaluated for their molluscicidal activities against the host snail Oncomelania hupensis. The results and analysis of the structure-activity relationship revealed that the E-isomers showed better molluscicidal activities than their Z-isomers. Molluscicidal activities decreased with the shortening of the alkenyl chain lengths.
Effects of Light and Monosulfuron on Growth and Photosynthetic Pigments of Anabaena Flos-Aquae Breb  [PDF]
Jianying SHEN, Jing JIANG, Peizhong ZHENG
Journal of Water Resource and Protection (JWARP) , 2009, DOI: 10.4236/jwarp.2009.16049
Abstract: The effects of monosulfuron on growth and photosynthetic pigments of the nitrogen-fixing cyanobacterium Anabaena flos-aquae grown exposed to 2000-, 3000-, and 4000-lux light intensity were studied. Exposed to three light intensities, the seven concentrations of monosulfuron tested can significantly inhibit algal growth in a dose-dependent manner. The cell numbers and growth rate were decreased with the increase in mono-sulfuron concentration, and A. flos-aquae had different degrees of sensitivity to monosulfuron with the most sensitive light intensity being 4000-lux followed by 3000-lux and 2000-lux. The herbicide monosulfuron appeared to have different effects on the synthesis of photosynthetic pigments. The chlorophyll appeared to tackle monosulfuron concentrations. The caroteniod content of algae treated with 0.008 and 0.08 mg/L monosulfuron exposed to 2000-lux had a different stimulatory effect from that of treatments exposed to 3000-lux and 4000-lux, but an inhibitory effect at concentration above 0.8 mg/L. The effect of monosulfuron on biliprotein in cells of A. flos-aquae exposed three light intensities displayed contrary dose dependence.
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