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| 1 | Autophagy is required for self-renewal and differentiation of adult human stem cells显示文摘 | Souzan Salemi Shida Yousefi Mihai A Constantinescu Martin F Fey Hans-Uwe Simon | 2012 | Cell Research2012，22，2： | 17 |
| 2 | Hepatocellular carcinoma: Review of disease and tumor biomarkers显示文摘Hepatocellular carcinoma(HCC) is a common malignancy and now the second commonest global cause of cancer death. HCC tumorigenesis is relatively silent and patients experience late symptomatic presentation. As the option for curative treatments is limited to early stage cancers, diagnosis in non-symptomatic individuals is crucial. International guidelines advise regular surveillance of high-risk populations but the current tools lack sufficient sensitivity for early stage tumors on the background of a cirrhotic nodular liver. A number of novel biomarkers have now been suggested in the literature, which may reinforce the current surveillance methods. In addition, recent metabonomic and proteomic discoveries have established specific metabolite expressions in HCC, according to Warburg's phenomenon of altered energy metabolism. With clinical validation, a simple and non-invasive test from the serum or urine may be performed to diagnose HCC, particularly benefiting low resource regions where the burden of HCC is highest. | Jin Un Kim Mohamed I F Shariff Mary M E Crossey Maria Gomez-Romero Elaine Holmes I Jane Cox Haddy K S Fye Ramou Njie Simon D Taylor-Robinson | 2016 | World Journal of Hepatology2016，8，10： | 13 |
| 3 | Dementia and osteoporosis in a geriatric population: Is there a common link?显示文摘AIM To determine the existence of a common pathological link between dementia and osteoporosis through reviewing the current evidence base. METHODS This paper reviews the current literature on osteoporosis and dementia in order to ascertain evidence of a common predisposing aetiology. A literature search of Ovid MEDLINE(1950 to June 2016) was conducted. The keywords 'osteoporosis', 'osteoporotic fracture', 'dementia' and 'Alzheimer's disease'(AD) were used to determine the theoretical links with the most significant evidence base behind them. The key links were found to be vitamins D and K, calcium, thyroid disease, statins, alcohol and sex steroids. These subjects were then searched in combination with the previous terms and the resulting papers manually examined. Theoretical, in vitro and in vivo research were all used to inform this review which focuses on the most well developed theoretical common causes for dementia(predominantly Alzheimer's type) and osteoporosis.RESULTS Dementia and osteoporosis are multifaceted disease processes with similar epidemiology and a marked increase in prevalence in elderly populations. The existence of a common link between the two has been suggested despite a lack of clear pathological overlap in our current understanding. Research to date has tended to be fragmented and relatively weak in nature with multiple confounding factors reflecting the difficulties of in vivo experimentation in the population of interest. Despite exploration of various possible mechanisms in search for a link between the two pathologies, this paper found that it is possible that these associations are coincidental due to the nature of the evidence available. One finding in this review is that prior investigation into common aetiologies has found raised amyloid beta peptide levels in osteoporotic bone tissue, with a hypothesis that amyloid beta disorders are systemic disorders resulting in differing tissue manifestations. However, our findings were that the most compelling evidence of a common yet independent aetiology lies in the APOE4 allele, which is a well-established risk for AD but also carries an independent association with fracture risk. The mechanism behind this is thought to be the reduced plasma vitamin K levels in individuals exhibiting the APOE4 allele which may be amplified by the nutritional deficiencies associated with dementia, which are known to include vitamins K and D. The vitamin theory postulates that malnutrition and reduced exposure to sunlight in patients with AD leads to vitamin deficiencies. CONCLUSION Robust evidence remains to be produced regarding potential links and regarding the exact aetiology of these diseases and remains relevant given the burden of dementia and osteoporosis in our ageing population. Future research into amyloid beta, APOE4 and vitamins K and D as the most promising aetiological links should be welcomed. | Candice L Downey Adam Young Emily F Burton Simon M Graham Robert J Macfarlane Eva-Maria Tsapakis Eleftherios Tsiridis | 2017 | World Journal of Orthopedics2017，8，5： | 6 |
| 4 | 血浆游离DNA水平增高可作为预测重型颅脑损伤患者死亡率的独立指标(英文)显示文摘Trauma is the leading cause of death under 45 years worldwide and up to 50% of trauma fatalities are due to brain injury.Prediction of outcome is one of the major problems associated with severe TBI and research efforts have focused on the investigation of biomarkers with prognostic value following TBI. Therefore,our aim was to investigate whether cell-free DNA concentrations correlated to short-term primary outcome( survivor or death) and GCS scores following severe TBI. A total of 188 victims of severe TBI were enrolled in this prospective study,outcome variables comprised: survival and neurological assessment using the GCS at ICU discharge. Control blood samples were obtained from 25 healthy volunteers. Peripheral venous blood was collected at admission in the ICU. Plasma DNA was measured using a real-time quantitative PCR assay for the β-globin gene. There was correlation between higher DNA levels and both fatal outcome and lower hospital admission GCS scores. Plasma DNA concentrations at the chosen cut- off point( ≥171,381 kilogenomesequivalents /L) predicted mortality with a specificity of 90% and a sensitivity of 43%. Logistic regression analysis showed that elevated plasma DNA levels were independently associated with death( P < 0. 001). In conclusion,high cell-free DNA concentration was a predictor of short-term mortality following severe TBI. | Rodrigues Filho EM1 Simon D Ikuta N Klovan C Dannebrock F de Oliveira CO Regner A | 2014 | 中华神经外科疾病研究杂志2014，13，3： | 6 |
| 5 | pRB expression in esophageal mucosa of individuals at high risk for squamous cell carcinoma of the esophagus显示文摘AIM: To investigate the pRb expression in a large group of patients with history of chronic exposure to the main risk factors for development of squamous cell carcinoma of the esophagus. METHODS: One hundred and seventy asymptomatic individuals at high risk for esophageal squamous cell carcinoma (consumption of more than 80 g of ethanol and 10 cigarettes/d for at least 10 years) underwent upper gastrointestinal endoscopy with biopsies of the esophageal mucosa. As a control group, specimens of esophageal mucosa obtained from 20 healthy subjects were also studied. Immunohistochemical assessment of the tissues was performed using a monoclonal antibody anti-pRB protein. RESULTS: Absence of the pRB staining, indicating loss of RB function, was observed in 33 (19.4%) of the individuals at risk for esophageal cancer, but in none of the healthy controls (P < 0.02). Loss of pRb expression increased in a stepwise fashion according to the severity of the histological findings (P < 0.005): normal mucosa (11/97 or 11.3%), chronic esophagitis (17/60 or 28.3%), low-grade dysplasia (3/10 or 30%), high-grade dysplasia 1/2 or 50%) and squamous cell carcinoma (1/1 or 100%). CONCLUSION: Our findings suggest that abnormal expression of the pRB protein may be implicated in the process of esophageal carcinogenesis. Additional studies are warranted to define the role of the pRBprotein as a biomarker for development of esophageal squamous cell carcinoma in individuals at high risk for this malignancy. | Simone S Contu Paulo C Contu Daniel C Damin Renato B Fagundes Fabiano Bevilacqua Aline S Rosa Joo C Prolla Luis F Moreira | 2007 | World Journal of Gastroenterology2007，13，11： | 5 |
| 6 | Mechanisms of autophagy activation in endothelial cell and their targeting during normothermic machine liver perfusion显示文摘Ischaemia-reperfusion injury(IRI) is the leading cause of injury seen in the liver following transplantation. IRI also causes injury following liver surgery and haemodynamic shock. The first cells within the liver to be injured by IRI are the liver sinusoidal endothelial cells(LSEC). Recent evidence suggests that LSEC coordinate and regulates the livers response to a variety of injuries. It is becoming increasingly apparent that the cyto-protective cellular process of autophagy is a key regulator of IRI. In particular LSEC autophagy may be an essential gatekeeper to the development of IRI. The recent availability of liver perfusion devices has allowed for the therapeutic targeting of autophagy to reduce IRI. In particular normothermic machine liver perfusion(NMP-L) allow the delivery of pharmacological agents to donor livers whilst maintaining physiological temperature and hepatic flow rates. In this review we summarise the current understanding of endothelial autophagy and how this may be manipulated during NMP-L to reduce liver IRI. | Yuri L Boteon Richard Laing Hynek Mergental Gary M Reynolds Darius F Mirza Simon C Afford Ricky H Bhogal | 2017 | World Journal of Gastroenterology2017，23，48： | 4 |
| 7 | A family study of endophenotypes for psychosis within an early intervention programme in Hong Kong: Rationale and preliminary findings显示文摘The study of endophenotypes may be a viable strategy to tackle the genetic complexity and phenotypic heterogeneity of psychosis, but this research direction is relatively under-developed in China as compared to Western countries. We have recently initiated one of the first family studies of endophenotypes for psychosis in China. Patients entering an established early psychosis intervention service are recruited into this research project for phenotyping, endophenotyping and genotyping. At the endophenotypic level, four domains (neurological soft signs, neurocognition of prospective memory, social cognition of facial emotion recognition, and affective cognition of anticipatory and consummatory pleasure) are studied in the sample of patients with psychosis and their unaffected siblings. This article illustrates the benefit of a research-oriented clinical programme and its findings based on the data collected as of early 2011. | LUI Simon S Y SHAM Pak CHAN Raymond C K CHEUNG Eric F C | 2011 | Chinese Science Bulletin2011，56，32： | 2 |
| 8 | p38α controls erythroblast enucleation and Rb signaling in stress erythropoiesis显示文摘成红血球细胞的 Enucleation 对哺乳动物在终端区别期间唯一。尽管 erythroid enucleation 广泛地被学习了,包括 retinoblastoma 蛋白质(Rb ) ,仅仅一些基因被识别了调整原子挤出。它由哪个仍然保持大部分未定义发信号的分子,外来的刺激例如 erythropoietin (Epo ) ,是 transduced 导致 enucleation。这里,我们显示出那 p38α,激活 mitogen 的蛋白质 kinase (MAPK ) ,为 erythroid enucleation 被要求。在包含高 Epo 层次并且模仿的一个前 vivo 区别系统强调红血球生成, p38α在 erythroid 区别期间被激活。p38α 的损失;完全堵住主要成红血球细胞的 enucleation。而且, p38α在胎儿、贫血的压力红血球生成期间在 vivo 以一种房间自治的方式调整成红血球细胞 enucleation。显著地, p38α 的损失;导致 p21 目标 Rb 的 p21,和减少的激活的 downregulation,哪个是成红血球细胞 enucleation 的重要管理者。这研究表明那 p38α在压力红血球生成期间是为成红血球细胞 enucleation 的一个关键发信号分子。 | Simon M Schultze Andreas Mairhofer Dan Li Jin Cen Hartmut Beug Erwin F Wagner Lijian Hui | 2012 | Cell Research2012，22，3： | 2 |
| 9 | Oxygen measurements in endometrial and trophoblastic tissues during early pregnancy 显示文摘 | Rodesch F Simon P Donner C | 1992 | Obstet Gynecol1992，80，： | 2 |
| 10 | Ventricular repolarization components on the electrocardiogram显示文摘 | Gan-Xin Yan Ramarao S Lankipalli James F Burke Simone Musco Peter R Kowey | 2003 | Journal of the American College of Cardiology2003，，： | 2 |
| 11 | Dev Cell:科学家阐明人类胚胎原生殖细胞发育的分子机制显示文摘近日,刊登于国际杂志Developmental Cell上的一项研究报道中,来自巴布拉汉研究所(Babraham Insdtute)的研究人员通过研究调查了原生殖细胞发育的早期阶段,同时他们在实验室开发了一种产生类似细胞的策略,这种酷似人类原始生殖细胞的产生对于未来生殖领域的研究,以及分析人类潜在的继代基因调控的遗传机制非常重要。 | Ferdinand von Meyenn Rebecca V. Berrens Simon Andrews Fátima Santos Amanda J. Collier Felix Krueger Rodrigo Osorno Wendy Dean Peter J. Rugg-Gunn Wolf Reik | 2016 | 现代生物医学进展2016，16，35： | 2 |
| 12 | Evaluation and Management of Adult Hypoglycemic Disorders: An Endocrine Society Clinical Practice Guideline显示文摘 | Philip E. Cryer Lloyd Axelrod Ashley B. Grossman Simon R. Heller Victor M. Montori Elizabeth R. Seaquist F John Service | 2009 | The Journal of Clinical Endocrinology & Metabolism2009，，3： | 2 |
| 13 | Longterm multiple color imaging of live cells using quantum dot bioconjugates 显示文摘 | Jaiswal J K Mattoussi H Mauro J M Simon S F | 2003 | Nature Biotechnolgy2003，21，： | 1 |
| 14 | The biological impact of mass-spectrometry-based proteomics 显示文摘 | Cravatt B F Simon G M Yates J R 3rd | 2007 | Nature2007，450，7172： | 1 |
| 15 | Electrode compositions for carbon power supercapacitors显示文摘 | BONNEFOI L SIMON P FAUVARQUE J F | 1999 | J Power Sources1999，80，： | 1 |
| 16 | Metabolic changes in neuronal migration disorders:evaluation by combined MRI and proton MR spectroscopy显示文摘 | Simone IL Federico F Tortorella C | 1999 | Epilepsia1999，40，7： | 1 |
| 17 | Insulin resistance in epileptic girls who gain weight after therapy with valproic acid显示文摘 | Verrotti A Basciani F De Simone M | 2002 | J Child Neurol2002，17，4： | 1 |
| 18 | Early on-treatment prediction of response to peginterferon alfa-2a for HBeAg-negative chronic hepatitisB using HBsAg and HBV DNA levels 显示文摘 | Rijckborst V Hansen BE Cakaloglu Y Ferenci P Tabak F Akdogan M Simon K Akarca US Flisiak R Verhey E Van Vuuren AJ Boucher CA ter Borg MJ Janssen HL | 2010 | Hepatology2010，52，2： | 1 |
| 19 | A new method for the nonlinear transformation of means and covariances in filters and estimators 显示文摘 | SIMON JULIER JEFFREY UHLMANN HUGH F DURRANT-WHYTE | 2000 | IEEE Transactions on Automatic Control2000，45，3： | 1 |
| 20 | 查看详情显示文摘 | Mijatovic T De Nève N Bruyère C Simon G Dewelle J Van Quaquebeke E Van Der A.E Van Vynckt F Lefranc F Kiss R | | 0，，： | 1 |
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