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| 1 | Management Recommendations on Sleep Disturbance o Patients with Parkinson's Disease显示文摘INTRODUCTION Sleep disturbance is one of the most common nonmotor symptoms in Parkinson's disease (PD).Sleep disturbance affects 40-98% of PD patients in the world. In China, the prevalence of PD patients with sleep disturbance ranges from 47.66% to 89.10%. Sleep disturbance usually has adverse impact on the quality of life of PD patients. Apossible pathogenesis of PD with sleep disturbance include thalamocortical pathway degeneration and changes of neurotransmitter systems. The etiology of sleep disturbance is multifactorial,involving degeneration of areas regulating sleep,sleep structure affected by drugs,sleep disturbance induced by drug,and sleep fragmentation by multiple factors. | Chun-Feng Liu Tao Wang Shu-Qin Zhan De-Qin Geng Jian Wang Jun Liu Hui-Fang Shang Li-Juan Wang Piu Chan Hai-Bo Chen Sheng-Di Chen Yu-Ping Wang Zhong-Xin Zhao K Ray Chaudhuri | 2018 | Chinese Medical Journal2018，，24： | 26 |
| 2 | The recommendations of Chinese Parkinson’s disease and movement disorder society consensus on therapeutic management of Parkinson’s disease显示文摘Background:Parkinson’s disease(PD)is a chronic,progressive and debilitating disease,which affects over 2.5 million people in China.PD is characterized clinically by resting tremor,muscular rigidity,bradykinesia and postural instability.As the disease progresses,additional complications can arise such as non-motor and neurobehavioral symptoms.Pharmacological treatment and surgical intervention for PD have been implemented in China.Until 10 years ago,there was lack of standardization for the management of PD in different regions and among different physicians,leading to different treatment levels in different regions and different physicians.Since then,the Chinese Parkinson’s Disease and Movement Disorder Society have published three versions of guidelines for the management of PD in China,in 2006,2009 and 2014,respectively.Correspondingly,the overall level of treatment for PD in China improved.Objectives:To update the treatment guidelines based on current foreign and domestic practice guidelines and clinical evidence,and to improve the treatment options available to physicians in the management of PD.Summary:A variety of treatment recommendations in the treatment guidelines have been proposed,including physical activity and disease-modifying medication,which should be initiated at the early-stage of the disease.The principles of dosage titration should be followed to avoid acute adverse reactions to the drugs,to achieve a satisfactory clinical effect with a low dose and to reduce the incidence of long-term motor complications.Moreover,different treatment strategies should be considered at different stages of the disease.Importantly,treatment guidelines and personalized treatments should be valued equally.A set of treatment recommendations has been developed to assist physicians to improve and optimize clinical outcomes for patients with PD in China. | Shengdi Chen Piu Chan Shenggang Sun Haibo Chen Baorong Zhang Weidong Le Chunfeng Liu Guoguang Peng Beisha Tang Lijuan Wang Yan Cheng Ming Shao Zhenguo Liu Zhenfu Wang Xiaochun Chen Mingwei Wang Xinhua Wan Huifang Shang Yiming Liu Pingyi Xu Jian Wang Tao Feng Xianwen Chen Xingyue Hu Anmu Xie Qin Xiao | 2016 | Translational Neurodegeneration2016，5，1： | 23 |
| 3 | Differential stem cell aging kinetics in Hutchinson-Gilford progeria syndrome and Werner syndrome显示文摘Hutchinson-Gilford 早衰症候群(HGPS ) 和沃纳症候群(WS ) 是二最好描绘的人的 progeroid 症候群。HGPS 被一个点变化在 lamin A (LMNA ) 基因引起,导致截断的蛋白质 productprogerin 的生产。WS 被变化在 WRN 基因引起,编码 loss-of-function RecQ DNA helicase。这里,由基因编辑,我们创造了 isogenic 人的胚胎的干细胞(转换字符) 与异质接合(G608G/+) 或同型结合(G608G/G608G ) LMNA 变化和 biallelic WRN 大美人为为 HGPS 和 WS 致病建模,分别地。当转换字符和 endothelial 房间(EC ) 没介绍早熟的老朽的任何特征时, HGPS 间充质、 WS 间充质的干细胞(MSC ) 与不同动力学显示出联系老化的显型。当 HGPS-MSCs 展出了迟了发作的尖锐早衰 characterisitcs 时, WS-MSCs 有早发作的温和早衰显型。一起拿,我们的学习比较并且形成对照不同病理 underpinning 二早衰混乱,并且提供可靠干细胞为病理学、生理的老化识别新治疗学的策略的基于的模型。 | Zeming Wu Weiqi Zhang Moshi Song Wei Wang Gang Wei Wei Li Jinghui Lei Yu Huang Yanmei Sang Piu Chan Chang Chen Jing Qu Keiichiro Suzuki Juan Carlos Izpisua Belmonte Guang-Hui Liu | 2018 | Protein & Cell2018，9，4： | 15 |
| 4 | Chemical screen identifies a geroprotective role of quercetin in premature aging显示文摘Aging increases the risk of various diseases. The main goal of aging research is to find therapies that attenuate aging and alleviate aging-related diseases. In this study, we screened a natural product library for geroprotective compounds using Werner syndrome (WS) human mesenchymal stem cells (hMSCs), a premature aging model that we recently established. Ten candidate compounds were identified and quercetin was investigated in detail due to its leading effects. Mechanistic studies revealed that quercetin alleviated senescence via the enhancement of cell proliferation and restoration of heterochromatin architecture in WS hMSCs. RNA-sequencing analysis revealed the transcriptional commonalities and differences in the geroprotective effects by quercetin and Vitamin C. Besides WS hMSCs, quercetin also attenuated cellular senescence in Hutchinson-Gilford progeria syndrome (HGPS) and physiological-aging hMSCs. Taken together, our study identifies quercetin as a geroprotective agent against accelerated and natural aging in hMSCs, providing a potential therapeutic intervention for treating age-associated disorders. | Lingling Geng Zunpeng Liu Weiqi Zhang Wei Li Zeming Wu Wei Wang Ruotong Ren Yao Su Peichang Wang Liang Sun Zhenyu Ju Piu Chan Moshi Song Jing Qu Guang-Hui Liu | 2019 | Protein & Cell2019，10，6： | 13 |
| 5 | Genetic enhancement in cultured human adult stem cells conferred by a single nucleotide recoding显示文摘 | Jiping Yang Jingyi Li Keiichiro Suzuki Xiaomeng Liu Jun Wu Weiqi Zhang Ruotong Ren Weizhou Zhang Piu Chan Juan Carlos Izpisua Belmonte Jing Qu Fuchou Tang Guang-Hui Liu | 2017 | Cell Research2017，27，9： | 12 |
| 6 | Low-dose quercetin positively regulates mouse healthspan显示文摘Dear Editor,Aging is the leading risk factor for many chronic diseases,accounting for almost 60%of all deaths worldwide.How to achieve healthy aging,alleviate aging-related diseases,and extend healthspan has become a main topic of biomedical research(He et al.,2019).Geroprotective compounds,such as metformin and rapamycin,have been shown to improve both healthspan and lifespan in mice(Martin-Montalvo et al.,2013;Bitto et al.,2016),whereas nicotinamide partially improves healthspan in mice(Mitchell et al.,2018). | Lingling Geng Zunpeng Liu Si Wang Shuhui Sun Shuai Ma Xiaoqian Liu Piu Chan Liang Sun Moshi Song Weiqi Zhang Guang-Hui Liu Jing Qu | 2019 | Protein & Cell2019，10，10： | 12 |
| 7 | Single-cell transcriptomic atlas of primate cardiopulmonary aging显示文摘Aging is a major risk factor for many diseases,especially in highly prevalent cardiopulmonary comorbidities and infectious diseases including Coronavirus Disease 2019(COVID-19).Resolving cellular and molecular mechanisms associated with aging in higher mammals is therefore urgently needed.Here,we created young and old non-human primate single-nucleus/cell transcriptomic atlases of lung,heart and artery,the top tissues targeted by SARS-CoV-2.Analysis of cell type-specific aging-associated transcriptional changes revealed increased systemic inflammation and compromised virus defense as a hallmark of cardiopulmonary aging.With age,expression of the SARS-CoV-2 receptor angiotensin-converting enzyme 2(ACE2)was increased in the pulmonary alveolar epithelial barrier,cardiomyocytes,and vascular endothelial cells.We found that interleukin 7(IL7)accumulated in aged cardiopulmonary tissues and induced ACE2 expression in human vascular endothelial cells in an NF-κB-dependent manner.Furthermore,treatment with vitamin C blocked IL7-induced ACE2 expression.Altogether,our findings depict the first transcriptomic atlas of the aged primate cardiopulmonary system and provide vital insights into age-linked susceptibility to SARS-CoV-2,suggesting that geroprotective strategies may reduce COVID-19 severity in the elderly. | Shuai Ma Shuhui Sun Jiaming Li Yanling Fan Jing Qu Liang Sun Si Wang Yiyuan Zhang Shanshan Yang Zunpeng Liu Zeming Wu Sheng Zhang Qiaoran Wang Aihua Zheng Shuguang Duo Yang Yu Juan Carlos Izpisua Belmonte Piu Chan Qi Zhou Moshi Song Weiqi Zhang Guang-Hui Liu | 2021 | Cell Research2021，31，4： | 10 |
| 8 | Ganoderma lucidum extract ameliorates MPTP-induced parkinsonism and protects dopaminergic neurons from oxidative stress via regulating mitochondrial function, autophagy, and apoptosis显示文摘Neuroprotection targeting mitochondrial dysfunction has been proposed as an important therapeutic strategy for Parkinson's disease. Ganoderma lucidum (GL) has emerged as a novel age nt that protects neurons from oxidative stress. However, the detailed mechanisms underlying GL-induced neuroprotection have not been documented. In this study, we investigated the neuroprotective effects of GL extract (GLE) and the underlying mechanisms in the classic MPTP(1 -methyl-4-phenyl-1,2,3,6- tetrahydropyridine)-induced mouse model of PD. Mice were injected with MPTP to in duce parkins on ism. The n the mice were administered GLE (400 mg kg^-1 d^-1,ig) for 4 weeks. We observed that GLE administration significantly improved locomotor performanee and increased tyrosine hydroxylase expression in the substantia nigra pars compact (SNpc) of MPTP-treated mice. In in vitro study, treatment of neuroblastoma neuro-2a cells with 1 -methyl-4-phenyIpyridinium (MPP^+, 1 mmol/L) caused mitochondrial membrane potential collapse, radical oxygen species accumulation, and ATP depletion. Application of GLE (800 pg/mL) protected n euroblastoma neu ro-2a cells agai nst MPP in suit. Application of GLE also improved mitochondrial movement dysfunction in cultured primary mesencephalic neurons. In addition, GLE counteracted the decline in NIX (also called BNIP3L) expression and increase in the LC3-II/LC3-I ratio evoked by MPP I Moreover, GLE reactivated MPP^+-inhibited AMPK, mTOR, and ULK1. Similarly, GLE was sufficient to counteract MPP1 -induced inhibition of PINK1 and Parkin expression. GLE suppressed MPP^+-induced cytochrome C release and activation of caspase-3 and caspase-9. In summary, our results provide evidence that GLE ameliorates parkinsonism pathology via regulating mitochondrial function, autophagy, and apoptosis, which may involve the activation of both the AMPK/mTOR and PINK1/Parkin signaling pathway. | Zhi-li Ren Chao-dong Wang Tao Wang Hui Ding Ming Zhou Nan Yang Yan-yong Liu Piu Chan | 2019 | Acta Pharmacologica Sinica2019，40，4： | 10 |
| 9 | 镉转化细胞DNA异常甲基化对肿瘤相关基因表达的影响显示文摘目的 对镉转化细胞DNA异常甲基化及其对肿瘤相关基因表达的影响进行研究 ,探讨镉的外遗传致癌机制。方法 从CdCl2 转化BALB/c 3T3细胞中提取基因组DNA ,经甲基化非敏感性酶 (Mse1 )单独消化或Mse1和甲基化敏感性酶 (BstU1 )联合消化 ,消化产物用甲基化敏感性内切酶指纹法 (MSRF)进行分析 ,差异显示出异常甲基化基因片段 ,进一步以异常甲基化DNA为探针进行Southern分子杂交加以证实 ,并进行DNA序列测定 ,与基因文库中的基因进行类比分析。结果 发现镉转化细胞存在异常甲基化DNA ,其中一个甲基化DNA片段为p1 6抑癌基因。结论 DNA高甲基化会导致基因表达抑制 ,因此 ,p1 6基因高甲基化会导致其抑癌功能减弱或丧失 。 | 雷毅雄 吴中亮 Pius Joseph Tong-man Ong | 2003 | 中华劳动卫生职业病杂志2003，21，2： | 9 |
| 10 | Stabilization of heterochromatin by CLOCK promotes stem cell rejuvenation and cartilage regeneration显示文摘Accumulating evidence indicates an association between the circadian clock and the aging process.However,it remains elusive whether the deregulation of circadian clock proteins underlies stem cell aging and whether they are targetable for the alleviation of aging-associated syndromes.Here,we identified a transcription factor-independent role of CLOCK,a core component of the molecular circadian clock machinery,in counteracting human mesenchymal stem cell(hMSC)decay.CLOCK expression was decreased during hMSC aging.In addition,CLOCK deficiency accelerated hMSC senescence,whereas the overexpression of CLOCK,even as a transcriptionally inactive form,rejuvenated physiologically and pathologically aged hMSCs.Mechanistic studies revealed that CLOCK formed complexes with nuclear lamina proteins and KAP1,thus maintaining heterochromatin architecture and stabilizing repetitive genomic sequences.Finally,gene therapy with lentiviral vectors encoding CLOCK promoted cartilage regeneration and attenuated age-related articular degeneration in mice.These findings demonstrate a noncanonical role of CLOCK in stabilizing heterochromatin,promoting tissue regeneration,and mitigating aging-associated chronic diseases. | Chuqian Liang Zunpeng Liu Moshi Song Wei Li Zeming Wu Zehua Wang Qiaoran Wang Si Wang Kaowen Yan Liang Sun Tomoaki Hishida Yanning Cai Juan Carlos lzpisua Belmonte Pedro Guillen Piu Chan Qi Zhou Weiqi Zhang Jing Qu Guang-Hui Liu | 2021 | Cell Research2021，31，2： | 8 |
| 11 | CRISPR/Cas9-mediated gene knockout reveals a guardian role of NF-κB/RelA in maintaining the homeostasis of human vascular cells显示文摘 | Ping Wang Zunpeng Liu Xiaoqian Zhang Jingyi Li Liang Sun Zhenyu Ju Jian Li Piu Chan Guang-Hui Liu Weiqi Zhang Moshi Song Jing Qu | 2018 | Protein & Cell2018，9，11： | 8 |
| 12 | Anti-parkinsonian effects of octacosanol in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine-treated mice显示文摘Our previous research showed that octacosanol exerted its protective effects in 6-hydroxydopamine-induced Parkinsonian rats. The goal of this study was to investigate whether octacosanol would attenuate neurotoxicity in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP)-treated C57BL/6N mice and its potential mechanism. Behavioral tests, tyrosine hydroxylase immunohistochemistry and western blot were used to investigate the effects of octacosanol in a mouse model of Parkinson's disease. Oral administration of octacosanol (100 mg/kg) significantly improved behavioral impairments in mice treated by MPTP and markedly ameliorated morphological appearances of tyrosine hydroxylase-positive neuronal cells in the substantia nigra. Furthermore, octacosanol blocked MPTP-induced phosphorylation of p38MAPK and JNK, but not ERK1/2. These findings implicated that the protective effects afforded by octacosanol might be mediated by blocking the phosphorylation of p38MAPK and JNK on the signal transduction in vivo. Considering its excellent tolerability, octacosanol might be considered as a candidate agent for clinical application in treating Parkinson's disease. | Tao Wang Yanyong Liu Nan Yang Chao Ji Piu Chan Pingping Zuo | 2012 | Neural Regeneration Research2012，7，14： | 7 |
| 13 | Progressive loss of striatal dopamine terminals in MPTP-induced acute parkinsonism in cynomolgus monkeys using vesicular monoamine transporter type 2 PET imaging([^(18)F]AV-133)显示文摘The 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine(MPTP)-induced parkinsonism model, particularly in non-human primates, remains the gold-standard for studying the pathogenesis and assessing novel therapies for Parkinson's disease. However, whether the loss of dopaminergic neurons in this model is progressive remains controversial, mostly due to the lack of objective in vivo assessment of changes in the integrity of these neurons. In the present study, parkinsonism was induced in cynomolgus monkeys by intravenous administration of MPTP(0.2 mg/kg) for 15 days; stable parkinsonism developed over 90 days, when the symptoms were stable. Noninvasive positron emission tomographic neuroimaging of vesicular monoamine transporter 2 with 9-[18F]fluoropropyl-(+)-dihydrotetrabenazine([18F]AV-133) was used before, and 15 and 90 days after the beginning of acute MPTP treatment. The imaging showed evident progressive loss of striatal uptake of [18F]AV-133. The dopaminergic denervation severity had a significant linear correlation with the clinical rating scores and the bradykinesia subscores. Thesefindings demonstrated that [18F]AV-133 PET imaging is a useful tool to noninvasively evaluate the evolution of monoaminergic terminal loss in a monkey model of MPTP-induced parkinsonism. | Yajing Liu Feng Yue Rongping Tang Guoxian Tao Xiaomei Pan Lin Zhu Hank F.Kung Piu Chan | 2014 | Neuroscience Bulletin2014，30，3： | 6 |
| 14 | Single-nucleus transcriptomic landscape of primate hippocampal aging显示文摘The hippocampus plays a crucial role in learning and memory,and its progressive deterioration with age is functionally linked to a variety of human neurodegenerative diseases.Yet a systematic profiling of the aging effects on various hippocampal cell types in primates is still missing.Here,we reported a variety of new aging-associated phenotypic changes of the primate hippocampus.These include,in particular,increased DNA damage and heterochromatin erosion with time,alongside loss of proteostasis and elevated inflammation.To understand their cellular and molecular causes,we established the first single-nucleus transcriptomic atlas of primate hippocampal aging.Among the 12 identified cell types,neural transiently amplifying progenitor cell(TAPC)and microglia were most affected by aging.In-depth dissection of gene-expression dynamics revealed impaired TAPC division and compromised neuronal function along the neurogenesis trajectory;additionally elevated pro-inflammatory responses in the aged microglia and oligodendrocyte,as well as dysregulated coagulation pathways in the aged endothelial cells may contribute to a hostile microenvironment for neurogenesis.This rich resource for understanding primate hippocampal aging may provide potential diagnostic biomarkers and therapeutic interventions against age-related neurodegenerative diseases. | Hui Zhang Jiaming Li Jie Ren Shuhui Sun Shuai Ma Weiqi Zhang Yang Yu Yusheng Cai Kaowen Yan Wei Li Baoyang Hu Piu Chan Guo-Guang Zhao Juan Carlos Izpisua Belmonte Qi Zhou Jing Qu Si Wang Guang-Hui Liu | 2021 | Protein & Cell2021，12，9： | 5 |
| 15 | Deciphering primate retinal aging at single-cell resolution显示文摘Dear Editor, The retina is a light-sensitive highly-organized tissue,which is vulnerable to aging and age-related retinal diseases.Specifically,progressive retinal degeneration leads to visual function deterioration and vision impairment in the elderly(Lin et al.,2016).In diseases such as age-related macular degeneration(AMD),retinitis pigmentosa(RP)and diabetic retinopathy(DR),pathological process lacking effective treatments profoundly and negatively impact on the quality of life in the elderly(Lin et al.,2016;Chen et al.,2019).Thus,an in-depth molecular assessment of the mechanisms driv-ing retinal aging is of urgent scientific and medical importance. | Si Wang Yuxuan Zheng Qingqing Li Xiaojuan He Ruotong Ren Weiqi Zhang Moshi Song Huifang Hu Feifei Liu Guoqiang Sun Shuhui Sun Zunpeng Liu Yang Yu Piu Chan Guo-Guang Zhao Qi Zhou Guang-Hui Liu Fuchou Tang Jing Qu | 2021 | Protein & Cell2021，12，11： | 4 |
| 16 | 镉应答新基因TEF-1δ的生物学功能研究显示文摘目的 探讨镉应答新基因TEF 1δ在细胞转化和致癌过程中的重要作用。方法 应用细胞转染、WesternBlot以及细胞转化等技术与方法 ,对克隆化基因TEF 1δ的生物学功能进行研究。结果 TEF 1δcDNA以pcDNA 3 1 V5 His TOPO为表达载体所转染的CHO细胞和猴肾COS1细胞均可表达相对分子质量为 3 10 0 0的TEF 1δ编码蛋白质 ,而非转染和单纯载体转染的对照细胞则无此蛋白质表达。进一步研究表明 ,TEF 1δcDNA转染NIH3T3细胞可导致TEF 1δ蛋白质超额表达 ,并与细胞转化密切相关。结论 镉的细胞转化和致癌作用至少部分因TEF 1δ基因的高表达所致。TEF 1δ可能是一个新发现的镉应答原癌基因。 | 雷毅雄 Pius Joseph 吴中亮 Tong-man Ong | 2002 | 卫生毒理学杂志2002，16，3： | 3 |
| 17 | A single-cell transcriptomic atlas of primate pancreatic islet aging显示文摘Aging-related degeneration of pancreatic islet cells contributes to impaired glucose tolerance and diabetes.Endocrine cells age heterogeneously,complicating the efforts to unravel the molecular drivers underlying endocrine aging.To overcome these obstacles,we undertook single-cell RNA sequencing of pancreatic islet cells obtained from young and aged non-diabetic cynomolgus monkeys.Despite sex differences and increased transcriptional variations,agedβ-cells showed increased unfolded protein response(UPR)along with the accumulation of protein aggregates.We observed transcriptomic dysregulation of UPR components linked to canonical ATF6 and IRE1 signaling pathways,comprising adaptive UPR during pancreatic aging.Notably,we found aging-relatedβ-cell-specific upregulation of HSP90 B1,an endoplasmic reticulum-located chaperone,impeded high glucose-induced insulin secretion.Our work decodes aging-associated transcriptomic changes that underlie pancreatic islet functional decay at single-cell resolution and indicates that targeting UPR components may prevent loss of proteostasis,suggesting an avenue to delayingβ-cell aging and preventing aging-related diabetes. | Jingyi Li Yuxuan Zheng Pengze Yan Moshi Song Si Wang Liang Sun Zunpeng Liu Shuai Ma Juan Carlos Izpisua Belmonte Piu Chan Qi Zhou Weiqi Zhang Guang-Hui Liu Fuchou Tang Jing Qu | 2021 | National Science Review2021，8，2： | 3 |
| 18 | MPTP Induces Systemic Parkinsonism in Middle-Aged Cynomolgus Monkeys:Clinical Evolution and Outcomes显示文摘In this study,we developed a systemic PD model in middle-aged cynomolgus monkeys using individualized low-dose MPTP,to explore effective indicators for the early prediction of clinical outcomes.MPTP was not stopped until the animals showed typical PD motor symptoms on days 10 to 13 after MPTP administration when the Kurlan score reached 10;this abrogated the differences in individual susceptibility to MPTP.The clinical symptoms persisted,peaking on days 3 to 12 after MPTP withdrawal(rapid progress stage),and then the Kurlan score plateaued.A Kurlan score at the end of the rapid progress stage >15 reflected stable or slowly-progressive PD,while a score <15 indicated spontaneous recovery.The entire clinical evolution and outcome of the systemic PD model was characterized in this study,thus providing options for therapeutic and translational research. | Feng Yue Sien Zeng Rongping Tang Guoxian Tao Piu Chan | 2017 | Neuroscience Bulletin2017，33，1： | 3 |
| 19 | Brain activity in Parkinson's disease patients with mild cognitive impairment显示文摘Mild cognitive impairment(MCI) is common in patients with Parkinson's disease(PD), yet the underlying neural mechanisms of this disease state remain unclear. We investigated alterations in the spontaneous brain activity of PD patients with MCI(PD-MCI) relative to cognitively normal PD patients(PD-CN) and healthy control(HC)subjects. In this work, 13 PD-MCI patients, 16 PD-CN patients, and 16 HC subjects completed resting state functional MRI. Spontaneous brain activity was measured by calculating amplitude of low frequency fluctuation(ALFF) values across the whole brain. Between-group differences and correlations between ALFF values and cognitive test scores were analyzed. ALFF values decreased in the right superior temporal gyrus and increased in the left middle temporal gyrus and left superior frontal gyrus of PD-MCI patients compared with PD-CN patients. In the PD-MCI group, ALFF values in the left middle temporal gyrus were negatively correlated with Montreal Cognitive Assessment and vocabulary test scores,and the ALFF values in the left superior frontal gyrus were negatively correlated with vocabulary test scores. Our study demonstrates that PD-MCI is associated with abnormal spontaneous brain activity in the temporal and frontal lobes. These findings inform the underlying neural mechanism of cognitive impairment in PD. | Linlin Gao Xuemin Wu Jiarong Zhang Piu Chan Tao Wu | 2016 | Science Bulletin2016，61，24： | 3 |
| 20 | Assessment of antidiabetic activity and acute toxicity of leaf extracts from Physalis peruviana L.in guinea-pig显示文摘Objective:To verify the antidiabetic activity of leaf extracts from Physalis peruviana L.popularly used in the Eastern part of the Democratic Republic of the Congo and to point out the possible toxicity.Method:Aqueous decoctions prepared from dried leaves powder were administrated to guinea pigs at the dose range of 100 mg/kg to 3.2 g/kg of body weight.The hypoglycemic activity was evaluated by glucose tolerance test,loading animals with glucose 4 g/kg and measuring blood glucose concentrations at various times.The effect was compared to the control and glibenclamide as antidiabetic reference drug.Acute toxicity was evaluated by recording mortality rate,changes on blood biomarkers and damage caused to vital organs.Results:At a dose of 100 mg/kg,the aqueous extract induced a significant reduction of peak concentration at 30 min after glucose loading as compared with control or reference(P<0.05).At doses greater than 400 mg,some alterations on blood,kidney and liver markers were observed.Upper 800 mg/kg,mortality was observed with LD_(50)estimated at about 1280 mg/kg.At the autopsy,vital organs were in haemorrhage and swelling state.Conclusion:The crude aqueous extracts from the leaves of Physalis peruviana L.present hypoglycemic aclivily in animal model,but at high doses the plant may cause severe intoxication. | Felicien Mushagalusa Kasali Justin Ntokamunda Kadima Pius Tshimankinda Mpiana Koto-te-Nyiwa Ngbolua Damien Sha-Tshibey Tshibangu | 2013 | Asian Pacific Journal of Tropical Biomedicine2013，3，11： | 2 |
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