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| 1 | 肿瘤常见症状及中医症状调查量表的设计显示文摘目的:在MDASI(M.D.Anderson Symptom Inventory)症状评估量表的基础上增加中医症状的内容,修订为肿瘤常见症状及中医症状调查表:MDASI-TCM(Traditional Chinese Medicine)症状评估量表,探索中医症状量化评估方法。方法:在MDASI症状评估量表基础上添加一些中医症状条目,修订为MDASI-TCM症状评估量表,对北京、大连等4家医院340例肿瘤患者进行问卷调查,并建立Epidata数据库,在SPSS及Excel软件进行统计学分析。结果:肿瘤常见症状发生频率较高的前5项症状依次为疲乏89.4%、睡眠不安74.4%、口干72.9%、胃口差72.9%和健忘71.2%。患者不适症状对工作、情绪和一般活动的影响分别为89.7%、82.6%和78.6%,严重影响了患者的生活质量。对症状量表进行一致性信度检测:Cron-bach’sα值在MDASI-TCM的23项中为0.9,原MDASI 13项为0.862,新增10项中医症状为0.781。结论:MDASI-TCM肿瘤症状评估量表有较高的信度,可以评估肿瘤的常见症状包括中医方面的症状及严重程度,值得进一步推广,有望成为中医量化评估的工具。 | 赵翌 刘基巍 Xin Shelly Wang 李萍萍 | 2008 | 中华肿瘤防治杂志2008，15，11： | 43 |
| 2 | 地下水铀污染的原位微生物还原与固定:在美国能源部田纳西橡树岭放射物污染现场的试验显示文摘总结了美国斯坦福大学和橡树岭国家实验室等在美国能源部田纳西州橡树岭综合试验基地进行的铀污染原位微生物修复阶段性试验结果.本试验利用微生物以乙醇为电子供体还原地下水和沉积物中的六价铀为不溶解的四价铀,使之原位固定化.随后通过加入溶解氧和硝酸盐来试验微生物还原后的地下水层中还原固定态铀的稳定性.通过预处理和长期间隔注入乙醇溶液,地下水中铀浓度从40~60mg·L-1降至0.03mg·L-1以下,达到了美国环保署饮用水的标准.还原的四价铀主要以U(Ⅳ)-Fe复合物的形态存在.结果表明,固定化后的四价铀只有在厌氧条件下才是稳定的,溶解氧和硝酸盐侵入地下水层后会使固定化的四价铀重新氧化为溶解态的六价铀.在试验过程中,采用多种分子生物学方法检测了微生物种群的变化和与铀氧化还原反应有关的功能微生物.本研究表明,在维持试验系统无氧和无硝酸盐的条件下,通过添加乙醇为电子供体可有效地促进地下水中土著功能微生物的活性,从而实现铀的原位还原固定与稳定. | 吴唯民 Jack Carley David Watson 顾宝华 Scott Brooks Shelly D.Kelly Kenneth Kemner Joy D.van Nostrand 吴力游 许玫英 周集中 罗剑 Erick Cardenas 黄家琪 Matthew W.Fields Terence L.Marsh James M.Tiedje Stefan J.Green Joel E.Kostka Peter K.Kitanidis Philip M.Jardme CraigS.Criddle | 2011 | 环境科学学报2011，31，3： | 28 |
| 3 | Biomarkers and subtypes of deranged lipid metabolism in nonalcoholic fatty liver disease显示文摘Nonalcoholic fatty liver disease(NAFLD)is a heterogeneous and complex disease that is imprecisely diagnosed by liver biopsy.NAFLD covers a spectrum that ranges from simple steatosis,nonalcoholic steatohepatitis(NASH)with varying degrees of fibrosis,to cirrhosis,which is a major risk factor for hepatocellular carcinoma.Lifestyle and eating habit changes during the last century have made NAFLD the most common liver disease linked to obesity,type 2 diabetes mellitus and dyslipidemia,with a global prevalence of 25%.NAFLD arises when the uptake of fatty acids(FA)and triglycerides(TG)from circulation and de novo lipogenesis saturate the rate of FAβ-oxidation and verylow density lipoprotein(VLDL)-TG export.Deranged lipid metabolism is also associated with NAFLD progression from steatosis to NASH,and therefore,alterations in liver and serum lipidomic signatures are good indicators of the disease’s development and progression.This review focuses on the importance of the classification of NAFLD patients into different subtypes,corresponding to the main alteration(s)in the major pathways that regulate FA homeostasis leading,in each case,to the initiation and progression of NASH.This concept also supports the targeted intervention as a key approach to maximize therapeutic efficacy and opens the door to the development of precise NASH treatments. | José M Mato Cristina Alonso Mazen Noureddin Shelly C Lu | 2019 | World Journal of Gastroenterology2019，25，24： | 19 |
| 4 | Thymoma and autoimmunity显示文摘The thymus is a central lymphatic organ that is responsible for many immunological functions,including the production of mature,functional T cells and the induction of self-tolerance.Benign or malignant tumors may originate from the thymus gland,with thymoma being the most common and accounting for 50% of anterior mediastinal tumors.Malignancies linked to thymoma include the loss of self-tolerance and the presence of autoimmunity.In this review,we compiled the current scientific evidence detailing the various interactions between thymoma and autoimmune diseases,including myasthenia gravis,systemic lupus erythematosus,inappropriate antidiuretic hormone secretion,pure red cell aplasia,pernicious anemia,pemphigus and autoimmune thyroid diseases.In recent years,several mechanisms have been proposed to explain these interactions.Most are based on the assumption that the‘sick’thymus,like the‘normal’thymus,can generate mature T cells;however,the T cells generated by the sick thymus are impaired and thus may exert cellular autoreactivity.Here,we present several theories that may shed light on the loss of self-tolerance associated with this epithelial tumor of the thymus. | Shahar Shelly Nancy Agmon-Levin Arie Altman Yehuda Shoenfeld | 2011 | Cellular & Molecular Immunology2011，8，3： | 19 |
| 5 | 乙型肝炎病毒耐药性研究进展显示文摘核苷(酸)类(NA)抗病毒治疗慢性乙型肝炎是近年来的重大进展,但随之而来的病毒变异和耐药性成为令人困扰的问题。为了使广大临床医师能比较充分地了解NA与病毒变异的关系、临床意义和防治,本刊特约请几位国际上著名学者,从病毒学和临床侧面进行介绍。本文作者ShellyXiong为美藉分子病毒学专家,在Gilead公司负责NA抗病毒机制包括耐药性的研究。 | Shelly Xiong | 2006 | 肝脏2006，11，4： | 17 |
| 6 | Dabrafenib,an inhibitor of RIP3 kinase-dependent necroptosis,reduces ischemic brain injury显示文摘Ischemic brain injury triggers neuronal cell death by apoptosis via caspase activation and by necroptosis through activation of the receptor-interacting protein kinases(RIPK) associated with the tumor necrosis factor-alpha(TNF-α)/death receptor. Recent evidence shows RIPK inhibitors are neuroprotective and alleviate ischemic brain injury in a number of animal models, however, most have not yet undergone clinical trials and safety in humans remains in question. Dabrafenib, originally identified as a B-raf inhibitor that is currently used to treat melanoma, was later revealed to be a potent RIPK3 inhibitor at micromolar concentrations. Here, we investigated whether Dabrafenib would show a similar neuroprotective effect in mice subjected to ischemic brain injury by photothrombosis. Dabrafenib administered intraperitoneally at 10 mg/kg one hour after photothrombosis-induced focal ischemic injury significantly reduced infarct lesion size in C57BL6 mice the following day, accompanied by a markedly attenuated upregulation of TNF-α. However, subsequent lower doses(5 mg/kg/day) failed to sustain this neuroprotective effect after 4 days. Dabrafenib bl ocked lipopolysaccharides-induced activation of TNF-α in bone marrow-derived macrophages, suggesting that Dabrafenib may attenuate TNF-α-induced necroptotic pathway after ischemic brain injury. Since Dabrafenib is already in clinical use for the treatment of melanoma, it might be repurposed for stroke therapy. | Shelly A.Cruz Zhaohong Qin Alexandre E R.Stewart Hsiao-Huei Chen | 2018 | Neural Regeneration Research2018，13，2： | 17 |
| 7 | Methionine adenosyltransferases in liver cancer显示文摘Methionine adenosyltransferases(MATs)are essential enzymes for life as they produce S-adenosylmethionine(SAMe),the biological methyl donor required for a plethora of reactions within the cell.Mammalian systems express two genes,MAT1A and MAT2A,which encode for MATα1 and MATα2,the catalytic subunits of the MAT isoenzymes,respectively.A third gene MAT2B,encodes a regulatory subunit known as MATβwhich controls the activity of MATα2.MAT1A,which is mainly expressed in hepatocytes,maintains the differentiated state of these cells,whilst MAT2A and MAT2B are expressed in extrahepatic tissues as well as non-parenchymal cells of the liver(e.g.,hepatic stellate and Kupffer cells).The biosynthesis of SAMe is impaired in patients with chronic liver disease and liver cancer due to decreased expression and inactivation of MATα1.A switch from MAT1A to MAT2A/MAT2B occurs in multiple liver diseases and during liver growth and dedifferentiation,but this change in the expression pattern of MATs results in reduced hepatic SAMe level.Decades of study have utilized the Mat1a-knockout(KO)mouse that spontaneously develops non-alcoholic steatohepatitis(NASH)and hepatocellular carcinoma(HCC)to elucidate a variety of mechanisms by which MAT proteins dysregulation contributes to liver carcinogenesis.An increasing volume of work indicates that MATs have SAMe-independent functions,distinct interactomes and multiple subcellular localizations.Here we aim to provide an overview of MAT biology including genes,isoenzymes and their regulation to provide the context for understanding consequences of their dysregulation.We will highlight recent breakthroughs in the field and underscore the importance of MAT’s in liver tumorigenesis as well as their potential as targets for cancer therapy. | Ben Murray Lucia Barbier-Torres Wei Fan JoséM Mato Shelly C Lu | 2019 | World Journal of Gastroenterology2019，25，31： | 10 |
| 8 | Fatty liver in hepatitis C patients post-sustained virological response with direct-acting antivirals显示文摘AIM To determine steatosis and fibrosis prevalence in hepatitis C patients after a sustained virological response achieved with direct-acting antivirals.METHODS Transient elastography with controlled attenuation parameter(CAP) was used to assess hepatic steatosis post-sustained virological response(SVR);the CAP technology was not available in the United States at study initiation.Liver stiffness/fibrosis was measured before and 47 wk after treatment completion.Patients with genotype 3 and patients with cirrhosis were excluded.RESULTS One hundred and one patients were included in the study.Post-SVR there were decreases from baseline in alanine aminotransferase(ALT)(63.1 to 17.8 U/L),aspartate aminotransferase(51.8 to 21.5 U/L) and fibrosis score(7.4 to 6.1 k Pa)(P < 0.05).Post-SVR,48 patients(47.5%) had steatosis on CAP;of these,6.25% had advanced fibrosis.Patients with steatosis had higher body mass index(29.0 vs 26.1 kg/m2),glucose(107.8 vs 96.6 mg/d L),ALT(20.4 vs 15.3 mg/d L),CAP score(296.3 vs 212.4 d B/m) and fibrosis score(7.0 vs 5.3 k Pa);P < 0.05.Interestingly,compared to baseline,both patients with and without steatosis had change in fibrosis score post-SVR(7.7 k Pa vs 7.0 k Pa and 7.0 k Pa vs 5.3 k Pa);alternatively,(P < 0.05) and therefore patients with steatosis continued to have clinically significant stiffness(≥ 7 k Pa).CONCLUSION Fatty liver is very common in hepatitis C virus(HCV) patients post-SVR.These patients continue to have elevated mean fibrosis score(≥ 7 k Pa) compared to those without fatty liver;some have advanced fibrosis.Long term follow up is needed to assess steatosis and fibrosis in HCV patients post-SVR. | Mazen Noureddin Micaela M Wong Tsuyoshi Todo Shelly C Lu Arun J Sanyal Edward A Mena | 2018 | World Journal of Gastroenterology2018，24，11： | 6 |
| 9 | Methionine adenosyltransferases in liver health and diseases显示文摘Methionine adenosyltransferases(MATs)are essential for cell survival because they catalyze the biosynthesis of the biological methyl donor S-adenosylmethionine(SAMe)from methionine and adenosine triphosphate(ATP).Mammalian cells express two genes,MAT1A and MAT2A,which encode two MAT catalytic subunits,α1 andα2,respectively.Theα1 subunit organizes into dimers(MATIII)or tetramers(MATI).Theα2 subunit is found in the MATII isoform.A third gene MAT2B,encodes a regulatory subunit b,that regulates the activity of MATII by lowering the inhibition constant(Ki)for SAMe and the Michaelis constant(Km)for methionine.MAT1A expressed mainly in hepatocytes maintains the differentiated state of these cells whereas MAT2A and MAT2B are expressed in non-parenchymal cells of the liver(hepatic stellate cells[HSCs]and Kupffer cells)and extrahepatic tissues.A switch from the liverspecific MAT1A to MAT2A has been observed during conditions of active liver growth and dedifferentiation.Liver injury,fibrosis,and cancer are associated with MAT1A silencing and MAT2A/MAT2B induction.Even though both MAT1A and MAT2A are involved in SAMe biosynthesis,they exhibit distinct molecular interactions in liver cells.This review provides an update on MAT genes and their roles in liver pathologies. | Komal Ramani Shelly C.Lu | 2017 | Liver Research2017，1，2： | 5 |
| 10 | Arachidyl amido cholanoic acid improves liver glucose and lipid homeostasis in nonalcoholic steatohepatitis via AMPK and mTOR regulation显示文摘BACKGROUND Arachidyl amido cholanoic acid(Aramchol)is a potent downregulator of hepatic stearoyl-CoA desaturase 1(SCD1)protein expression that reduces liver triglycerides and fibrosis in animal models of steatohepatitis.In a phase IIb clinical trial in patients with nonalcoholic steatohepatitis(NASH),52 wk of treatment with Aramchol reduced blood levels of glycated hemoglobin A1c,an indicator of glycemic control.AIM To assess lipid and glucose metabolism in mouse hepatocytes and in a NASH mouse model[induced with a 0.1%methionine and choline deficient diet(0.1MCD)]after treatment with Aramchol.METHODS Isolated primary mouse hepatocytes were incubated with 20μmol/L Aramchol or vehicle for 48 h.Subsequently,analyses were performed including Western blot,proteomics by mass spectrometry,and fluxomic analysis with 13C-uniformly labeled glucose.For the in vivo part of the study,male C57BL/6J mice were randomly fed a control or 0.1MCD for 4 wk and received 1 or 5 mg/kg/d Aramchol or vehicle by intragastric gavage for the last 2 wk.Liver metabolomics were assessed using ultra-high-performance liquid chromatography-time of flight-MS for the determination of glucose metabolism-related metabolites.RESULTS Combination of proteomics and Western blot analyses showed increased AMPK activity while the activity of nutrient sensor mTORC1 was decreased by Aramchol in hepatocytes.This translated into changes in the content of their downstream targets including proteins involved in fatty acid(FA)synthesis and oxidation[PACCα/β(S79),SCD1,CPT1A/B,HADHA,and HADHB],oxidative phosphorylation(NDUFA9,NDUFB11,NDUFS1,NDUFV1,ETFDH,and UQCRC2),tricarboxylic acid(TCA)cycle(MDH2,SUCLA2,and SUCLG2),and ribosome(P-p70S6K[T389]and P-S6[S235/S236]).Flux experiments with 13Cuniformely labeled glucose showed that TCA cycle cataplerosis was reduced by Aramchol in hepatocytes,as indicated by the increase in the number of rounds that malate remained in the TCA cycle.Finally,liver metabolomic analysis showed that glucose homeostasis was improved by Aramchol in 0.1MCD fed mice in a dose-dependent manner,showing normalization of glucose,G6P,F6P,UDP-glucose,and Rbl5P/Xyl5P.CONCLUSION Aramchol exerts its effect on glucose and lipid metabolism in NASH through activation of AMPK and inhibition of mTORC1,which in turn activate FAβ-oxidation and oxidative phosphorylation. | David Fernández-Ramos Fernando Lopitz-Otsoa Laura Delacruz-Villar Jon Bilbao Martina Pagano Laura Mosca Maider Bizkarguenaga Marina Serrano-Macia Mikel Azkargorta Marta Iruarrizaga-Lejarreta Jesús Sot Darya Tsvirkun Sebastiaan Martijn van Liempd Felix M Goni Cristina Alonso María Luz Martínez-Chantar Felix Elortza Liat Hayardeny Shelly C Lu JoséM Mato | 2020 | World Journal of Gastroenterology2020，26，34： | 5 |
| 11 | 圣安德烈斯断层深部地震复发间隔的周期性、不规则性和倍增特征显示文摘地震的复发历史可能会为未来地震发生的时间提供线索,但大地震之间的时间间隔太长,因而掩盖了所有的复发变化规律。相比之下,小地震频繁发生,而其复发间隔在相对小的时间尺度内也是可以计量的。本研究对一个历时8.5年、包含900多次低频事件的地震序列进行了研究,这些低频地震在加州帕克菲尔德(Parkfield)附近的圣安德烈斯断层下产生了震动。这些地震事件在时间上表现出密集的复发间隔,一般在3~6天之间,但有时这一模式却会突然发生变化。虽然大地震和低频地震的发生环境不同,但是该项研究表明大地震序列可能具有类似的复杂性。 | David R Shelly 赵纪东(译) 左玉玲(校) | 2010 | 国际地震动态2010，，10： | 3 |
| 12 | YAP1对颗粒细胞的重编程可导致具间质谱系和浆液性特征的高级别卵巢癌显示文摘高级别浆液性卵巢癌(HGSC)是临床中最常见、且恶性程度最高的卵巢癌.深入了解高级别浆液性卵巢癌的起源细胞可对该亚型卵巢癌进行有效预防和早期诊断.最近TCGA和AOCS通过分子分型研究发现了一种具有间充质特征的高级别浆液性卵巢癌亚型,并且表明该亚型是所有新发现的亚型中预后最差的一种,而且目前大家对于这种卵巢癌新亚型的起源细胞一无所知.在研究Hippo信号通路在卵巢颗粒细胞生理和病理中的作用时,意外地发现Hippo信号传导途径的主要效应分子YAP1的高度激活可以诱导具有间质谱系和高可塑性的卵巢颗粒细胞的去分化与重编程,最终导致具有浆液性特征的高级别卵巢癌的发生.本文的研究结果揭示了具间质特征的高级别浆液性卵巢癌的一种潜在起源细胞. | 吕向民 何春波 黄聪 滑国华 陈骍程 Barbara K.Timm Victoria M.Maclin Abigail A.Haggerty Shelly K.Aust Denae M.Golden Bhavana J.Dave Yun-An Tseng 陈利 王洪波 陈培超 David L.Klinkebiel Adam R.Karpf Jixin Dong Ronny I.Drapkin Bo R.Rueda John S.Davis 王诚 | 2020 | Science Bulletin2020，65，15： | 2 |
| 13 | 新一代渴望导管: 在肺的栓塞的处理的可行性显示文摘 AIM: To report our preliminary experience with a new generation aspiration catheter in the treatment of symptomatic pulmonary embolism(PE). METHODS: A retrospective database search for pulmonary artery embolectomy since introduction of the Pronto.035' and XL extraction catheter(Vascular Solutions, Minneapolis, MN) at our institution in 10/2009 was performed. Ten consecutive patients were identified in which the Pronto.035' or XL catheter was used between 01/2010 and 03/2013. All patients were referred for catheter based embolectomy due to contraindications to systemic lysis, or for being in such a critical clinical condition that immediate percutaneous treatment deemed warranted. The computed tomography(CT) right to left heart ratio as predictor for the severity of the PE was retrospectively evaluated on standard axial views. The difference between pre- and post-procedure pulmonary pressure measures was taken to assess the procedural effect.RESULTS: Extensive PE was confirmed angiographically in all patients. Measured right- to left ventricle(RV/LV) ratios were elevated beyond one in seven of the eight available CTs. Acute procedural success defined as clinical removal of visible thrombus and improvement in mean pulmonary artery pressure was seen in all recorded patients(n = 8), the mean pulmonary pressures declined from a median(range) of 35.5(19-46) to 23(10-37, P = 0.008) mmHg. Neither death nor other complications occurred intra- or immediately periprocedural, yet short term mortality within 30 d was found in 6 out of 9 patients, one patient was lost in follow up. The cause of death within 30 d in the 6 patients was identified as: Circulatory failure in direct connection with the PE(n = 2), stroke, sepsis, or succumbing to malignancy in a hospice setting(n = 2). CONCLUSION: Success in thrombus removal with improved pulmonary hypertension and systemic hypotension suggests this aspiration technique to be effective. Aspiration catheters should be part of further trials. | Wolf E Heberlein Mollie E Meek Omar Saleh James C Meek Shelly Y Lensing William C Culp | 2013 | World Journal of Radiology2013，5，11： | 2 |
| 14 | Genotoxicity of ferric oxide nanoparticles in Raphanus sativus:Deciphering the role of signaling factors,oxidative stress and cell death显示文摘We have studied the genotoxic and apoptotic potential of ferric oxide nanoparticles(Fe_2O_3-NPs) in Raphanus sativus(radish).Fe_2O_3-NPs retarded the root length and seed germination in radish.Ultrathin sections of treated roots showed subcellular localization of Fe_2O_3-NPs,along with the appearance of damaged mitochondria and excessive vacuolization.Flow cytometric analysis of Fe_2O_3-NPs(1.0 mg/m L) treated groups exhibited 219.5%,161%,120.4% and 161.4% increase in intracellular reactive oxygen species(ROS),mitochondrial membrane potential(ΔΨm),nitric oxide(NO) and Ca2+influx in radish protoplasts.A concentration dependent increase in the antioxidative enzymes glutathione(GSH),catalase(CAT),superoxide dismutase(SOD) and lipid peroxidation(LPO) has been recorded.Comet assay showed a concentration dependent increase in deoxyribonucleic acid(DNA) strand breaks in Fe_2O_3-NPs treated groups.Cell cycle analysis revealed 88.4% of cells in sub-G1 apoptotic phase,suggesting cell death in Fe_2O_3-NPs(2.0 mg/m L) treated group.Taking together,the genotoxicity induced by Fe_2O_3-NPs highlights the importance of environmental risk associated with improper disposal of nanoparticles(NPs) and radish can serve as a good indicator for measuring the phytotoxicity of NPs grown in NP-polluted environment. | Quaiser Saquib Mohammad Faisal Abdulrahman A.Alatar Abdulaziz A.Al-Khedhairy Mukhtar Ahmed Sabiha M.Ansari Hend A.Alwathnani Mohammad K.Okla Sourabh Dwivedi Javed Musarrat Shelly Praveen Shams T.Khan Rizwan Wahab Maqsood A.Siddiqui Javed Ahmad | 2016 | Journal of Environmental Sciences2016，28，9： | 2 |
| 15 | Dysregulation of glutathione synthesis in liver disease显示文摘Glutathione(GSH),a tripeptide that is present in all mammalian tissues,is especially highly concentrated in the liver.GSH synthesis occurs via two adenosine triphosphate(ATP)-requiring enzymatic steps:the first is rate-limiting,catalyzed by glutamate-cysteine ligase,generates g-glutamylcysteine from gluta-mate and cysteine;the second is catalyzed by GSH synthetase,generates GSH from g-glutamylcysteine and glycine.GSH defends against oxidative stress,participates in detoxification of xenobiotics,de-termines the redox status of the cell,and regulates vital processes such as growth and apoptosis.Hepatic GSH plays a central role in the interorgan GSH homeostasis because sinusoidal efflux of hepatic GSH determines plasma GSH level.In liver diseases GSH homeostasis is perturbed by multiple mechanisms.Hepatic GSH biosynthesis is impaired in cholestatic liver injury,endotoxemia,and fibrotic injury largely because the expression of the GSH synthetic enzymes falls.Lower hepatic GSH level further exacerbates and perpetuates ongoing liver injury.However,in hepatocellular carcinoma GSH synthetic enzymes are upregulated and this may play a role in chemoresistance.This review focuses on the current under-standing of hepatic GSH synthesis in health and disease. | Shelly C.Lu | 2020 | Liver Research2020，4，2： | 2 |
| 16 | S-adenosylmethionine显示文摘 | Shelly C Lu | 2000 | Int J Biochem Cell Biol2000，32，： | 2 |
| 17 | Molecular mechanisms of lipopolysaccharide-mediated inhibition of glutathione synthesis in mice显示文摘 | Maria Lauda Tomasi Minjung Ryoo Heping Yang Ainhoa Iglesias Ara Kwang Suk Ko Shelly C. Lu | 2014 | Free Radical Biology and Medicine2014，，： | 2 |
| 18 | Benefits of bilateral cochlear implants and/or hearing aids in children显示文摘 | Ruth Y. Litovsky Patti M. Johnstone Shelly P. Godar | 2006 | International Journal of Audiology2006，，1： | 2 |
| 19 | Neuronal protein-tyrosine phosphatase 1B hinders sensory-motor functional recovery and causes affective disorders in two different focal ischemic stroke models显示文摘Ischemic brain injury causes neuronal death and inflammation.Inflammation activates protein-tyrosine phosphatase 1B(PTP1B).Here,we tested the significance of PTP1B activation in glutamatergic projection neurons on functional recovery in two models of stroke:by photothrombosis,focal ischemic lesions were induced in the sensorimotor cortex(SM stroke)or in the peri-prefrontal cortex(peri-PFC stroke).Elevated PTP1B expression was detected at 4 days and up to 6 weeks after stroke.While ablation of PTP1B in neurons of neuronal knockout(NKO)mice had no effect on the volume or resorption of ischemic lesions,markedly different effects on functional recovery were observed.SM stroke caused severe sensory and motor deficits(adhesive removal test)in wild type and NKO mice at 4 days,but NKO mice showed drastically improved sensory and motor functional recovery at 8 days.In addition,peri-PFC stroke caused anxiety-like behaviors(elevated plus maze and open field tests),and depression-like behaviors(forced swimming and tail suspension tests)in wild type mice 9 and 28 days after stroke,respectively,with minimal effect on sensory and motor function.Peri-PFC stroke-induced affective disorders were associated with fewer active(FosB+)neurons in the PFC and nucleus accumbens but more FosB+neurons in the basolateral amygdala,compared to sham-operated mice.In contrast,mice with neuronal ablation of PTP1B were protected from anxiety-like and depression-like behaviors and showed no change in FosB+neurons after peri-PFC stroke.Taken together,our study identifies neuronal PTP1B as a key component that hinders sensory and motor functional recovery and also contributes to the development of anxiety-like and depression-like behaviors after stroke.Thus,PTP1B may represent a novel therapeutic target to improve stroke recovery.All procedures for animal use were approved by the Animal Care and Use Committee of the University of Ottawa Animal Care and Veterinary Service(protocol 1806)on July 27,2018. | Shelly A.Cruz Zhaohong Qin Konrad M.Ricke Alexandre F.R.Stewart Hsiao-Huei Chen | 2021 | Neural Regeneration Research2021，16，1： | 2 |
| 20 | Catalytic effects of Cu-Co~* on the thermal decomposition of AN and AN/KDN based green oxidizer and propellant samples显示文摘This paper presents the catalytic effects of Cu-Co~* catalyst on the decomposition of AN and AN/KDN based oxidizer and propellant samples. Ozawa-Flynn-Wall(OFW) iso-conversional method was used for the kinetic studies and to compute the activation energy(Ea) values for various decomposition steps of the prepared oxidizer and propellant samples in the temperature range of 50 e500C. TG-DTG experiments were carried out for both oxidizer and propellant samples at the heating rates of 3, 5, and 10C/min. AN/KDN based oxidizer samples were prepared by an evaporative co-crystallization method. Citric acid sol-gel method was used for the synthesis of Cu-Co~* catalyst. The propellant sample contains HTPB as the fuel binder along with other ingredients such as TDI, DOA, and Glycerol. The Cu-Co~* catalyst was used as 2% by weight to the total weight of catalyzed oxidizer and propellant samples. It was observed from the present study that, Cu-Co~* catalyst helps in reducing the Ea values for AN and AN based propellant samples. However, with the percentage increment of KDN in the AN crystals, Ea value increases.Further, it was observed that Cu-Co~* catalyst stabilizes the initial partial decomposition of KDN. | Pratim Kumar Puran Chandra Joshi Rajiv Kumar Shelly Biswas | 2018 | Defence Technology(防务技术)2018，14，3： | 2 |
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