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| 1 | Genomics identifies medulloblastoma subgroups that are enriched for specific genetic alterations显示文摘 | Thompson MC Fuller C Hogg TL Dalton J Finkelstein D Lau CC Chintagumpala M Adesina A Ashley DM KeUie SJ Taylor MD Curran T Gajjar A Gilbertson RJ | 2006 | 中国神经肿瘤杂志2006，4，1： | 17 |
| 2 | XRCC1 and DNA polymerase β in cellular protection against cytotoxic DNA single-strand breaks显示文摘 | Julie K Horton Mary Watson Donna F Stefanick Daniel T Shaughnessy Jack A Taylor Samuel H Wilson | 2008 | Cell Research2008，18，1： | 17 |
| 3 | Calcium signaling and T-type calcium channels in cancer cell cycling显示文摘Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca2+ channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca2+ channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel isminimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca2+ channels are not expressed in epithelial cells, selective T-type Ca2+ channel blockers may be useful in the treatment of certain types of cancers. | James T Taylor Xiang-Bin Zeng Jonathan E Pottle Kevin Lee Alun R Wang Stephenie G Yi lennifer A S Scruggs Suresh S Sikka Ming Li | 2008 | World Journal of Gastroenterology2008，14，32： | 12 |
| 4 | Smoking in schizophrenic patients:A critique of the selfmedication hypothesis显示文摘A common remark among laypeople, and notably also among mental health workers, is that individuals with mental illnesses use drugs as self-medication to allay clinical symptoms and the side effects of drug treatments. Roots of the self-medication concept in psychiatry date back at least to the 1980 s. Observations that rates of smokers in schizophrenic patients are multiple times the rates for regular smoking in the general population, as well as those with other disorders, proved particularly tempting for a self-medication explanation. Additional evidence came from experiments with animal models exposed to nicotine and the identification of neurobiological mechanisms suggesting self-medication with smoking is a plausible idea. More recently, results from studies comparing smoking and non-smoking schizophrenic patients have led to the questioning of the self-medication hypothesis. Closer examination of the literature points to the possibility that smoking is less beneficial on schizophrenic symptomology than generally assumed while clearly increasing the risk of cancer and other smoking-related diseases responsible for early mortality. It is a good time to examine the evidence for the self-medication concept as it relates to smoking. Our approach is to focus on data addressing direct or implied predictions of the hypothesis in schizophrenic smokers. | Francesca Manzella Susan E Maloney George T Taylor | 2015 | World Journal of Psychiatry2015，5，1： | 4 |
| 5 | Integrating insulin-like growth factor 1 and sex hormones into neuroprotection:Implications for diabetes显示文摘Brain integrity and cognitive aptitude are often impaired in patients with diabetes mellitus, presumably a result of the metabolic complications inherent to the disease. However, an increasing body of evidence has demonstrated the central role of insulin-like growth factor 1(IGF1) and its relation to sex hormones in many neuroprotective processes. Both male and female patients with diabetes display abnormal IGF1 and sexhormone levels but the comparison of these fluctuations is seldom a topic of interest. It is interesting to note that both IGF1 and sex hormones have the ability to regulate phosphoinositide 3-kinase-Akt and mitogen-activated protein kinases-extracellular signal-related kinasesignaling cascades in animal and cell culture models of neuroprotection. Additionally, there is considerable evidence demonstrating the neuroprotective coupling of IGF1 and estrogen. Androgens have also been implicated in many neuroprotective processes that operate on similar signaling cascades as the estrogen-IGF1 relation. Yet, androgens have not been directly linked to the brain IGF1 system and neuroprotection. Despite the sex-specific variations in brain integrity and hormone levels observed in diabetic patients, the IGF1-sex hormone relation in neuroprotection has yet to be fully substantiated in experimental models of diabetes. Taken together, there is a clear need for the comprehensive analysis of sex differences on brain integrity of diabetic patients and the relationship between IGF1 and sex hormones that may influence brain-health outcomes. As such, this review will briefly outline the basic relation of diabetes and IGF1 and its role in neuroprotection. We will also consider the findings on sex hormones and diabetes as a basis for separately analyzing males and females to identify possible hormone-induced brain abnormalities. Finally, we will introduce the neuroprotective interplay of IGF1 and estrogen and how androgen-derived neuroprotection operates through similar signaling cascades. Future research on both neuroprotection and diabetes should include androgens into the interplay of IGF1 and sex hormones. | Jacob Huffman Christina Hoffmann George T Taylor | 2017 | World Journal of Diabetes2017，8，2： | 4 |
| 6 | Auditor brand name reputations and industry specializations显示文摘 | Allen T Craswell Jere R Francis Stephen L Taylor | 1995 | Journal of Accounting and Economics1995，，3： | 4 |
| 7 | 青少年甘油磷酸胆碱代谢和心血管病的危险因素:一项队列研究显示文摘甘油磷酸胆碱(glycerophosphocholine,GPC)代谢物可调节动脉粥样硬化,从而导致心血管病风险。临床前期心血管病可能从青春期就开始。研究人员应用靶向血清脂质组学鉴定一组新的GPC,并测试在青春期时这些GPC中的任何一种是否与心血管病传统危险因子,如过量内脏脂肪、升高的血压、胰岛素抵抗和致动脉粥样硬化血脂异常相关。 | Syme C Czajkowski S Shin J Abrahamowicz M Leonard G Perron M Richer L Veillette S Gaudet D Strug L Wang Y Xu H Taylor G Paus T Bennett S Pausova Z 刘莉 叶鹏 | 2016 | 中华高血压杂志2016，24，10： | 3 |
| 8 | Frequent amplification of a chr19q13.41 microRNA polycistron in aggressive primitive neuroectodermal brain tumors显示文摘 | Li M Lee KF Lu Y Clarke I Shih D Eberhart C Collins VP Van Meter T Picard D Zhou L Boutros PC Modena P Liang ML Scherer SW Bouffet E Rutka JT Pomeroy SL Lau CC Taylor MD Gajjar A Dirks PB Hawkins CE Huang A. | 2009 | 中国神经肿瘤杂志2009，7，4： | 3 |
| 9 | Towards a standard diet-induced and biopsy-confirmed mouse model of non-alcoholic steatohepatitis: Impact of dietary fat source显示文摘BACKGROUND The trans-fat containing AMLN(amylin liver non-alcoholic steatohepatitis,NASH)diet has been extensively validated in C57BL/6J mice with or without the Lep^ob/Lep^ob(ob/ob)mutation in the leptin gene for reliably inducing metabolic and liver histopathological changes recapitulating hallmarks of NASH.Due to a recent ban on trans-fats as food additive,there is a marked need for developing a new diet capable of promoting a compatible level of disease in ob/ob and C57BL/6J mice.AIM To develop a biopsy-confirmed mouse model of NASH based on an obesogenic diet with trans-fat substituted by saturated fat.METHODS Male ob/ob mice were fed AMLN diet or a modified AMLN diet with trans-fat(Primex shortening)substituted by equivalent amounts of palm oil[Gubra amylin NASH,(GAN)diet]for 8,12 and 16 wk.C57BL/6J mice were fed the same diets for 28 wk.AMLN and GAN diets had similar caloric content(40%fat kcal),fructose(22%)and cholesterol(2%)level.RESULTS The GAN diet was more obesogenic compared to the AMLN diet and impaired glucose tolerance.Biopsy-confirmed steatosis,lobular inflammation,hepatocyte ballooning,fibrotic liver lesions and hepatic transcriptome changes were similar in ob/ob mice fed the GAN or AMLN diet.C57BL/6J mice developed a mild to moderate fibrotic NASH phenotype when fed the same diets.CONCLUSION Substitution of Primex with palm oil promotes a similar phenotype of biopsyconfirmed NASH in ob/ob and C57BL/6J mice,making GAN diet-induced obese mouse models suitable for characterizing novel NASH treatments. | Michelle L Boland Denise Oro Kirstine S T■lb■l Sebastian T Thrane Jens Christian Nielsen Taylor S Cohen David E Tabor Fiona Fernandes Andrey Tovchigrechko Sanne S Veidal Paul Warrener Bret R Sellman Jacob Jelsing Michael Feigh Niels Vrang James L Trevaskis Henrik H Hansen | 2019 | World Journal of Gastroenterology2019，25，33： | 3 |
| 10 | Supercritical fluid chromatography of Ginkgolide A,B,C and J and bilobalide显示文摘 | Strode T B Taylor L T Van Beek T A | 1996 | J Chromatogr A1996，738，： | 2 |
| 11 | Kinetics of the OH + CH3CF2Cl Reaction over an Extended Temperature Range 显示文摘 | Fang T D Taylor P H Delinger B | 1997 | J Phys Chem A1997，101，： | 2 |
| 12 | 卒中介入治疗培训指南:国际多学会共识文件显示文摘1背景
缺血性卒中是全球人口死亡和残疾的首要原因。很多急性大血管闭塞(emergent large vesselocclusion,ELVO)患者都会遗留长期残疾。事实上,这些颅内大动脉闭塞经常会导致大面积脑损伤,进而造成患者死亡或严重致残。 | Lavine SD Cockroft K Hoh B Bambakidis N Khalessi AA Woo H Riina H Siddiqui A Hirsch JA Chong W Rice H Wenderoth J Mitchell P Coulthard A Signh TJ Phatorous C Khangure M Klurfan P ter Brugge K Iancu D Gunnarsson T Pongpech S Rodesch G Soderman M Taylor A Krings T Orbach D Picard L Suh DC Zheng HQ Jansen O Muto M Szikora I Pierot L Brouwer P Gralla J Renowden S Andersson T Fiehler J Turjman F White P Januel AC Spelle L Kulcsar Z Chapot R Biondi A Dima S Taschner C Szajner M Krajina A Sakai N Matsumaru Y Yoshknura S Ezura M Fujinaka T Iihara K Ishii A Higashi T Hirohata M Hyodo A Ito Y Kawanishi M Kiyosue H Kobayashi E Kobayashi S Kuwayama N Matsumoto Y Miyachi S Murayama Y Nagata I Nakahara I Nemoto S Niimi Y Oishi H Satomi J Satow T Sugiu K Tanaka M Terada T Yamagami H Diaz O Lylyk P Jayaraman MV Patsalides A Gandhi CD Lee SK Abruzzo T Albani B Ansari SA Arthur AS Baxter BW Bulsara KR Chen M Almandoz JE Fraser JF Heck DV Hetts SW Hussain MS Klucznik RP Leslie-Mawzi TM Mack WJ McTaggart RA Meyers PM Mocco J Prestigiacomo CA Pride GL Rasmussen PA Starke RM Sunenshine PJ Tarr RW Frei DF Pabo M Nogueira RG Zaidat OO Jovin T Linfante I Yavagal D Liebeskind D Novakovic R Pongpech S 许岩 孙瑞 郭芮兵 | 2017 | 国际脑血管病杂志2017，25，5： | 2 |
| 13 | Implementation of heuristic search strategies for distribution feeder reconfiguration显示文摘 | Taylor T Lubkeman D | 1990 | IEEE Trans on Power Delivery1990，5，1： | 2 |
| 14 | Cuticular features and epidermal patterns in genus Araucaria de Jussieu 显示文摘 | Stockey R A Taylor T N | 1978 | Bot Gaz1978，139，： | 1 |
| 15 | Selective blockade of T-type Ca^2+ channels suppresses human breast cancer cell proliferation 显示文摘 | TAYLOR J T HUANG L POTTLE J E | 2008 | Cancer Lett2008，267，1： | 1 |
| 16 | Bottom-line Compliance with the IASC : A Comparative Analysis 显示文摘 | Evans T G M E Taylor | 1982 | International Journal of Accounting1982，18，1： | 1 |
| 17 | S100A4 (p9Ka) protein in colon carcinoma and liver metastases: association with earcinoma cells and T-lymphocytes 显示文摘 | TAYLOR T HERRINGTON S PRIME W | 2002 | Br J Cancer2002，86，3： | 1 |
| 18 | The Epidemiology of Peste des Petits Ruminants in the Sultanate of Oman显示文摘 | TAYLOR W P ALBUSAIDY S BARRETT T | 1990 | Vet Microbiol1990，22，4： | 1 |
| 19 | 显示文摘 | Rancourt J D Taylor L T | 1998 | JMS-Pure Appl Chem1998，35，4： | 1 |
| 20 | An Advanced High-current Low-emittance DC Microwave Proton Source显示文摘 | Mouris J | 1993 | Nucl Instrum Methods1993，336，： | 1 |
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