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1The Open Quantum Materials Database (OQMD): assessing the accuracy of DFT formation energies显示文摘The Open Quantum Materials Database(OQMD)is a high-throughput database currently consisting of nearly 300,000 density functional theory(DFT)total energy calculations of compounds from the Inorganic Crystal Structure Database(ICSD)and decorations of commonly occurring crystal structures.To maximise the impact of these data,the entire database is being made available,without restrictions,at www.oqmd.org/download.In this paper,we outline the structure and contents of the database,and then use it to evaluate the accuracy of the calculations therein by comparing DFT predictions with experimental measurements for the stability of all elemental ground-state structures and 1,670 experimental formation energies of compounds.This represents the largest comparison between DFT and experimental formation energies to date.The apparent mean absolute error between experimental measurements and our calculations is 0.096 eV/atom.In order to estimate how much error to attribute to the DFT calculations,we also examine deviation between different experimental measurements themselves where multiple sources are available,and find a surprisingly large mean absolute error of 0.082 eV/atom.Hence,we suggest that a significant fraction of the error between DFT and experimental formation energies may be attributed to experimental uncertainties.Finally,we evaluate the stability of compounds in the OQMD(including compounds obtained from the ICSD as well as hypothetical structures),which allows us to predict the existence of~3,200 new compounds that have not been experimentally characterised and uncover trends in material discovery,based on historical data available within the ICSD.Scott Kirklin James E Saal Bryce Meredig Alex Thompson Jeff W Doak Muratahan Aykol Stephan Rühl Chris Wolverton 2015npj Computational Materials2015,,1:62
2帕博利珠单抗单用或与放疗联用治疗转移性非小细胞肺癌:两个随机试验的汇总分析显示文摘背景放疗可以提高整个机体对免疫治疗的应答。在Ⅱ期PEMBRO-RT研究和Ⅰ/Ⅱ期MDACC研究中,患有转移性非小细胞肺癌(NSCLC)的患者被随机分配入组,接受免疫治疗(帕博利珠单抗)+放疗联合疗法,或免疫治疗单一疗法。当上述2个研究单独分析时,联合疗法组显示出潜在获益。由于每个研究的样本量较小,缓解率和结局并未显示出统计学意义,然而却有显著的临床获益。因此,本研究进行汇总分析,来判断放疗是否会改善转移性NSCLC患者的免疫治疗应答。方法PEMBRO-RT和MDACC研究纳入标准:患者年龄≥18岁,患有转移性NSCLC,且有≥1处未经放疗照射的病灶,以便进行射野外应答监测。PEMBRO-RT研究纳入曾接受过化疗患者,MDACC研究纳入曾接受过治疗或新诊断患者。2个研究中的患者均未接受过免疫治疗。在PEMBRO-RT研究中患者被等比例随机分配入组,并根据吸烟状态进行分层(分为<10年组和≥10年组)。MDACC研究的患者根据放疗计划可行性被等比例随机分配入2个受试组。由于联合治疗组的干预本质,每个研究中的放疗均不适用盲法。在2个研究中,不论是否进行放疗,均静脉滴入帕博利珠单抗(每3周200 mg)。在PEMBRO-RT研究中,在放疗(24 Gy 3次分割照射)结束后1周给予第1剂帕博利珠单抗。在MDACC研究中,在第1次放疗(50 Gy 4次分割照射或45 Gy 15次分割照射)同时给予帕博利珠单抗。仅检测未经照射病灶的应答。本研究的终点为最佳射野外(远隔)应答率(ARR)、最佳射野外疾病控制率(ACR)、12周时ARR、12周时ACR、无进展生存期(PFS)和总生存期(OS)。2个研究的意向治疗(ITT)人群均纳入分析。PEMBRO-RT研究(NCT02492568)和MDACC研究(NCT02444741)均在ClinicalTrials.gov上注册。发现纳入148例患者,76例接受帕博利珠单抗治疗,72例接受帕博利珠单抗+放疗治疗。所有患者随访时间中位数为33个月[四分位距(IQR):32.4~33.6]。148例患者中124例(84%)组织学特征为非鳞癌,111例(75%)患者曾经接受过化疗。组间没有基线特征差异,包括PD-L1表达状态和转移灶体积。最常见的照射部位为肺转移灶(39%,28/72)、胸腔内淋巴结(21%,15/72)和非原发灶(17%,12/72)。帕博利珠单抗组和联合治疗组的最佳ARR分别为19.7%(15/76)和41.7%(30/72),OR=2.96,95%CI:1.42~6.20,P=0.0039;最佳ACR分别为43.4%(33/76)和65.3%(47/72),OR=2.51,95%CI:1.28~4.91,P=0.0071;PFS中位数分别为4.4(IQR:2.9~5.9)和9.0个月(IQR:6.8~11.2),HR=0.67,95%CI:0.45~0.99,P=0.045;OS中位数分别为8.7(IQR:6.4~11.0)和19.2个月(IQR:14.6~23.8),OR=0.67,95%CI:0.54~0.84,P=0.0004。在汇总分析中没有发现新的安全问题。解读帕博利珠单抗免疫疗法+放疗显著提高转移性NSCLC患者的应答和改善治疗结局。这些结果需要在三期临床试验中进行验证。陈大卫(翻译) 于金明(校对) Willemijn S M E Theelen Vivek Verma Brian P Hobbs Heike M U Peulen Joachim G J V Aerts Idris Bahce Anna Larissa N Niemeijer Joe Y Chang Patricia M de Groot Quynh-Nhu Nguyen Nathan I Comeaux George R Simon Ferdinandos Skoulidis Steven H Lin Kewen He Roshal Patel John Heymach Paul Baas James W Welsh 2021中华肿瘤防治杂志2021,28,24:49
3Phylogenetic reconstruction of Chirita and allies (Gesneriaceae) with taxonomic treatments显示文摘Chirita D. Don, a large genus in the subfamily Cyrtandroideae of Gesneriaceae, has been the subject of much debate whether it is a natural group or not. In addition, the highly heterogeneous Chirita has also been very problematic with regard to delimitation and subdivision. Here we used the nrDNA internal transcribed spacer and cpDNA trnL-F for molecular phylogenetic analaysis, combined with morphological data. Our results suggest that Chirita is an artificial, polyphyletic genus. The most important character that defines Chirita, the dorso-ventrally oblique and bilamellar stigma, has evolved convergently in different clades of diandrous Cyrtandroideae. Chirita sensu stricto only includes the species of Chirita sect. Chirita, whereas Chirita sect. Microchirita is an independent clade located at the basal node of the phylogenetic tree. Chirita sect. Liebigia is closely related to Didymocarpus with an entire stigma unlike other species of Chirita. The species of Chirita sect. Gibbosaccus, Chiritopsis, Primulina, and Wentsaiboea form a monophyletic group that is sister to a strongly supported clade comprising four monotypic genera Paralagarosolen, Calcareoboea, Petrocodon, and Tengia. We further analyzed the morphological evolution of Chirita and identified a series of morphological synapomorphies for the monophyletic groups revealed herein, and thereby provide a taxonomic treatment in this study.Yin-Zheng WANG Ru-Bing MAO Yan LIU Jia-Mei LI Yang DONG Zhen-Yu LI James E SMITH 2011Journal of Systematics and Evolution2011,49,1:30
4Molecular overview of progressive familial intrahepatic cholestasis显示文摘Cholestasis is a clinical condition resulting from the imapairment of bile flow.This condition could be caused by defects of the hepatocytes,which are responsible for the complex process of bile formation and secretion,and/or caused by defects in the secretory machinery of cholangiocytes.Several mutations and pathways that lead to cholestasis have been described.Progressive familial intrahepatic cholestasis(PFIC)is a group of rare diseases caused by autosomal recessive mutations in the genes that encode proteins expressed mainly in the apical membrane of the hepatocytes.PFIC 1,also known as Byler’s disease,is caused by mutations of the ATP8B1 gene,which encodes the familial intrahepatic cholestasis 1 protein.PFIC 2 is characterized by the downregulation or absence of functional bile salt export pump(BSEP)expression via variations in the ABCB11 gene.Mutations of the ABCB4 gene result in lower expression of the multidrug resistance class 3 glycoprotein,leading to the third type of PFIC.Newer variations of this disease have been described.Loss of function of the tight junction protein 2 protein results in PFIC 4,while mutations of the NR1H4 gene,which encodes farnesoid X receptor,an important transcription factor for bile formation,cause PFIC 5.A recently described type of PFIC is associated with a mutation in the MYO5B gene,important for the trafficking of BSEP and hepatocyte membrane polarization.In this review,we provide a brief overview of the molecular mechanisms and clinical features associated with each type of PFIC based on peer reviewed journals published between 1993 and 2020.Sriram Amirneni Nils Haep Mohammad A Gad Alejandro Soto-Gutierrez James E Squires Rodrigo MFlorentino 2020World Journal of Gastroenterology2020,26,47:17
5Expanding etiology of progressive familial intrahepatic cholestasis显示文摘BACKGROUND Progressive familial intrahepatic cholestasis(PFIC)refers to a disparate group of autosomal recessive disorders that are linked by the inability to appropriately form and excrete bile from hepatocytes,resulting in a hepatocellular form of cholestasis.While the diagnosis of such disorders had historically been based on pattern recognition of unremitting cholestasis without other identified molecular or anatomic cause,recent scientific advancements have uncovered multiple specific responsible proteins.The variety of identified defects has resulted in an ever-broadening phenotypic spectrum,ranging from traditional benign recurrent jaundice to progressive cholestasis and end-stage liver disease.AIM To review current data on defects in bile acid homeostasis,explore the expanding knowledge base of genetic based diseases in this field,and report disease characteristics and management.METHODS We conducted a systemic review according to PRISMA guidelines.We performed a Medline/PubMed search in February-March 2019 for relevant articles relating to the understanding,diagnosis,and management of bile acid homeostasis with a focus on the family of diseases collectively known as PFIC.English only articles were accessed in full.The manual search included references of retrieved articles.We extracted data on disease characteristics,associations with other diseases,and treatment.Data was summarized and presented in text,figure,and table format.RESULTS Genetic-based liver disease resulting in the inability to properly form and secrete bile constitute an important cause of morbidity and mortality in children and increasingly in adults.A growing number of PFIC have been described based on an expanded understanding of biliary transport mechanism defects and the development of a common phenotype.CONCLUSION We present a summary of current advances made in a number of areas relevant to both the classically described FIC1(ATP8B1),BSEP(ABCB11),and MDR3(ABCB4)transporter deficiencies,as well as more recently described gene mutations--TJP2(TJP2),FXR(NR1H4),MYO5B(MYO5B),and others which expand the etiology and understanding of PFIC-related cholestatic diseases and bile transport.Sarah AF Henkel Judy H Squires Mary Ayers Armando Ganoza Patrick Mckiernan James E Squires 2019World Journal of Hepatology2019,11,5:13
6Consequences of bullying victimization in childhood and adolescence:A systematic review and meta-analysis显示文摘AIM To identify health and psychosocial problems associated with bullying victimization and conduct a meta-analysis summarizing the causal evidence.METHODS A systematic review was conducted using Pub Med, EMBASE, ERIC and Psyc INFO electronic databases up to 28 February 2015. The study included published longitudinal and cross-sectional articles that examined health and psychosocial consequences of bullying victimization. All meta-analyses were based on qualityeffects models. Evidence for causality was assessed using Bradford Hill criteria and the grading system developed by the World Cancer Research Fund.RESULTS Out of 317 articles assessed for eligibility, 165 satisfied the predetermined inclusion criteria for meta-analysis.Statistically significant associations were observed between bullying victimization and a wide range of adverse health and psychosocial problems. The evidence was strongest for causal associations between bullying victimization and mental health problems such as depression, anxiety, poor general health and suicidal ideation and behaviours. Probable causal associations existed between bullying victimization and tobacco and illicit drug use. CONCLUSION Strong evidence exists for a causal relationship between bullying victimization, mental health problems and substance use. Evidence also exists for associations between bullying victimization and other adverse health and psychosocial problems, however, there is insufficient evidence to conclude causality. The strong evidence that bullying victimization is causative of mental illness highlights the need for schools to implement effective interventions to address bullying behaviours.Sophie E Moore Rosana E Norman Shuichi Suetani Hannah J Thomas Peter D Sly James G Scott 2017World Journal of Psychiatry2017,7,1:12
7Calcium 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 2008World Journal of Gastroenterology2008,14,32:12
8Clarifying sub-genomic positions of QTLs for flowering habit and fruit quality in U.S. strawberry (Fragaria×ananassa) breeding populations using pedigree-based QTL analysis显示文摘The cultivated strawberry(Fragaria×ananassa)is consumed worldwide for its flavor and nutritional benefits.Genetic analysis of commercially important traits in strawberry are important for the development of breeding methods and tools for this species.Although several quantitative trait loci(QTL)have been previously detected for fruit quality and flowering traits using low-density genetic maps,clarity on the sub-genomic locations of these QTLs was missing.Recent discoveries in allo-octoploid strawberry genomics led to the development of the IStraw90 single-nucleotide polymorphism(SNP)array,enabling high-density genetic maps and finer resolution QTL analysis.In this study,breeder-specified traits were evaluated in the Eastern(Michigan)and Western(Oregon)United States for a common set of breeding populations during 2 years.Several QTLs were validated for soluble solids content(SSC),fruit weight(FWT),pH and titratable acidity(TA)using a pedigree-based QTL analysis approach.For fruit quality,a QTL for SSC on linkage group(LG)6A,a QTL for FWT on LG 2BII,a QTL for pH on LG 4CII and two QTLs for TA on LGs 2A and 5B were detected.In addition,a large-effect QTL for flowering was detected at the distal end of LG 4A,coinciding with the FaPFRU locus.Marker haplotype analysis in the FaPFRU region indicated that the homozygous recessive genotype was highly predictive of seasonal flowering.SNP probes in the FaPFRU region may help facilitate marker-assisted selection for this trait.Sujeet Verma Jason D Zurn Natalia Salinas Megan M Mathey Beatrice Denoyes James F Hancock Chad E Finn Nahla V Bassil Vance M Whitaker 2017Horticulture Research2017,4,1:10
9Effect of vildagliptin as add-on therapy to a low-dose metformin显示文摘AIM:To evaluate the efficacy and safety of the addition of vildagliptin to low-dose metformin and compare it to an uptitration of metformin in type 2 diabetes mellitus(T2DM) patients who have inadequate control with metformin monotherapy.METHODS:Eligible patients were randomized to receive vildagliptin 100 mg qd or metformin(500 mg qd for 2 wk and then 500 mg bid) added to open label me tformin 500 mg bid for the 24 wk.The primary endpoi nt was baseline to endpoint hemoglobin A1c(HbA1c) change.RESULTS:The adjusted mean change from baseline in HbA1c at the 24th wk was-0.51% in the vildagliptin/metformin group(mean baseline HbA1c:7.4%) and-0.37% in the metformin monothera py group(mean baseline HbA1c:7.3%).The mean diffe rence was-0.14% with 95% Confidence Interval(-0.24%,-0.05%).As non-inf e riority(margin of 0.4%) was achieved,a test for superiority was performed.This test showed statistically significant superiority of the combination over monotherapy group(P = 0.002).Gastrointestinal(GI) adverse events were signif icantly more frequent in the metformin group than the combin ation group(21.0% vs 15.4%,P = 0.032).CONCLUSION:In patients with T2DM inadequately controlled with metformin up to 1000 mg daily,the addition of vildagliptin 100 mg daily achieved larger HbA1c reduction with fewer GI events than with increa sing the metformin dose.Claudia Filozof Sherwyn Schwartz James E Foley 2010World Journal of Diabetes2010,1,1:8
10评估清晨或夜晚服用降压药对24h动态血压的影响:清晨或夜间服用降压药的希腊英国联合研究显示文摘观察数据显示,临床血压水平与随后的主要不良心血管事件之间存在强烈的线性关系。然而,动态血压监测显示,夜间血压水平比24h或白天血压水平更能预测主要的不良心血管事件。此外,夜间与白天的血压比值和杓型状态也是心血管结局的重要独立预测因素。这些发现可能对抗高血压药物的最佳给药时间有影响,一些研究表明,夜晚服用降压药可能较白天服药减少心血管事件。Poulter NR Savopoulos C Anjum A Apostolopoulou M Chapman N Cross M Falaschetti E Fotiadis S James RM Kanellos I Szigeti M Thom S Sever P Thompson D Hatzitolios AI 赵狄 练桂丽 2018中华高血压杂志2018,26,10:7
11Tight junction disruption: Helicobacter pylori and dysregulation of the gastric mucosal barrier显示文摘Long-term chronic infection with Helicobacter pylori(H. pylori) is a risk factor for gastric cancer development. In the multi-step process that leads to gastric cancer,tight junction dysfunction is thought to occur and serve as a risk factor by permitting the permeation of luminal contents across an otherwise tight mucosa. Mechanisms that regulate tight junction function and structure in the normal stomach,or dysfunction in the infected stomach,however,are largely unknown. Although conventional tight junction components are expressed in gastric epithelial cells,claudins regulate paracellular permeability and are likely the target of inflammation or H. pylori itself. There are 27 different claudin molecules,each with unique properties that render the mucosa an intact barrier that is permselective in a way that is consistent with cell physiology. Understanding the architecture of tight junctions in the normal stomach and then changes that occur during infection is important but challenging,because most of the reports that catalog claudin expression in gastric cancer pathogenesis are contradictory. Furthermore,the role of H. pylori virulence factors,such as cytotoxin-associated gene A and vacoulating cytotoxin,in regulating tight junction dysfunction during infection is inconsistent in different gastric cell lines and in vivo,likely because non-gastric epithelial cell cultures were initially used to unravel the details of their effects on the stomach. Hampering further study,as well,is the relative lack of cultured cell models that have tight junction claudins that are consistent with native tissues. This summary will review the current state of knowledge about gastric tight junctions,normally and in H. pylori infection,and make predictions about the consequences of claudin reorganization during H. pylori infection.Tyler J Caron Kathleen E Scott James G Fox Susan J Hagen 2015World Journal of Gastroenterology2015,21,40:7
12Prolonged high-fat-diet feeding promotes non-alcoholic fatty liver disease and alters gut microbiota in mice显示文摘BACKGROUND Non-alcoholic fatty liver disease (NAFLD) has become an epidemic largely due to the worldwide increase in obesity. While lifestyle modifications and pharmacotherapies have been used to alleviate NAFLD, successful treatment options are limited. One of the main barriers to finding safe and effective drugs for long-term use in NAFLD is the fast initiation and progression of disease in the available preclinical models. Therefore, we are in need of preclinical models that (1) mimic the human manifestation of NAFLD and (2) have a longer progression time to allow for the design of superior treatments. AIM To characterize a model of prolonged high-fat diet (HFD) feeding for investigation of the long-term progression of NAFLD. METHODS In this study, we utilized prolonged HFD feeding to examine NAFLD features in C57BL/6 male mice. We fed mice with a HFD (60% fat, 20% protein, and 20% carbohydrate) for 80 wk to promote obesity (Old-HFD group, n = 18). A low-fat diet (LFD)(14% fat, 32% protein, and 54% carbohydrate) was administered for the same duration to age-matched mice (Old-LFD group, n = 15). An additional group of mice was maintained on the LFD (Young-LFD, n = 20) for a shorter duration (6 wk) to distinguish between age-dependent and age-independent effects. Liver, colon, adipose tissue, and feces were collected for histological and molecular assessments.RESULTS Prolonged HFD feeding led to obesity and insulin resistance. Histological analysis in the liver of HFD mice demonstrated steatosis, cell injury, portal and lobular inflammation and fibrosis. In addition, molecular analysis for markers of endoplasmic reticulum stress established that the liver tissue of HFD mice have increased phosphorylated Jnk and CHOP. Lastly, we evaluated the gut microbial composition of Old-LFD and Old-HFD. We observed that prolonged HFD feeding in mice increased the relative abundance of the Firmicutes phylum. At the genus level, we observed a significant increase in the abundance of Adercreutzia, Coprococcus, Dorea, and Ruminococcus and decreased relative abundance of Turicibacter and Anaeroplasma in HFD mice. CONCLUSION Overall, these data suggest that chronic HFD consumption in mice can mimic pathophysiological and some microbial events observed in NAFLD patients.Kandy T Velázquez Reilly T Enos Jackie E Bader Alexander T Sougiannis Meredith S Carson Ioulia Chatzistamou James A Carson Prakash S Nagarkatti Mitzi Nagarkatti E Angela Murphy 2019World Journal of Hepatology2019,11,8:6
13Recent trends in liver transplantation for alcoholic liver disease in the United States显示文摘AIM To examine temporal changes in the indications for liver transplantation(LT) and characteristics of patients transplanted for alcoholic liver disease(ALD).METHODS We performed a retrospective cohort analysis of trends in the indication for LT using the United Network for Organ Sharing(UNOS) database between 2002 and 2015. Patients were grouped by etiology of the liver disease and characteristics were compared using χ~2 and t-tests. Time series analysis was used identifying any year with a significant change in the number of transplants per year for ALD, and before and after eras were modeled using a general linear model. Subgroup analysis of recipients with ALD was performed by age group, gender, UNOS region and etiology(alcoholic cirrhosis, alcoholic hepatitis and hepatitis C-alcoholic cirrhosis dual listing).RESULTS Of 74216 liver transplant recipients, ALD(n = 9400, 12.7%) was the third leading indication for transplant after hepatitis C and hepatocellular carcinoma. Transplants for ALD, increased from 12.8%(553) in 2002 to 16.5%(1020) in 2015. Time series analysis indicated a significant increase in the number of transplants per year for ALD in 2013(P = 0.03). There were a stable number of transplants per year between 2002 and 2012(linear coefficient 3, 95%CI:-4.6, 11.2) an increase of 177 per year between 2013 and 2015(95%CI: 119, 234). This increase was significant for all age groups except those 71-83 years old, was observed for both genders, and was incompletely explained by a decrease in transplants for hepatitis C and ALD dual listing. All UNOS regions except region 9 saw an increase in the mean number of transplants per year when comparing eras, and this increase was significant in regions 2, 3, 4, 5, 6, 8, 10 and 11.CONCLUSION There has been a dramatic increase in the number of transplants for ALD starting in 2013.Catherine E Kling James D Perkins Robert L Carithers Dennis M Donovan Lena Sibulesky 2017World Journal of Hepatology2017,9,36:6
14Dynamic chromatin states in human ES cells reveal potential regulatory sequences and genes involved in pluripotency显示文摘Pluripotency,一个细胞的能力区分并且产生所有胚胎的系,定义象胚胎的茎(ES ) 那样的哺乳动物的细胞类型的一个小数字细胞。当它通常被保持了时,那 pluripotency 是 transcriptional 的产品激活并且维持关键干细胞基因的表达式的规章的网络,积累的证据在建立并且保卫 ES 房间的 pluripotency 为 epigenetic 进程正在指向一个关键角色,象维持区分的房间类型的身份一样。以便更好在 pluripotency 理解 epigenetic 机制的角色,我们检验了在经历区别进一个 mesendodermal 系的人的 ES 房间(hESCs ) 染色体宽的染色质修正的动力学。我们发现在倡导者的染色质修正在区别期间仍然保持大部分不变,除了在在在 H3K27 的 acetylation 和 methylation 之间的一个动态开关标记在基因表示的激活和 silencing 之间的转变的倡导者的一个小数字,建议在在大多数差别上的房间命运承诺的一个层次表示了基因。我们也在 50 000 潜在的 enhancers 上印射,并且在染色质修正,特别 H3K4me1 和 H3K27ac 观察了大得多的动力学,它与他们的潜在的目标基因的表示相关。这些 enhancers 的进一步的分析揭示了 pluripotency 和可以在 hESCs 授与发展胜任的一个平衡状态的一口染色质签名陈述语气的潜在地关键的 transcriptional 管理者。我们的结果提供在定义 enhancers 和 pluripotency 支持染色质修正的角色的新证据。R David Hawkins Gary C Hon Chuhu Yang Jessica E Antosiewicz-Bourget Leonard K Lee Que-Minh Ngo Sarit Klugman Keith A Ching Lee E Edsall Zhen Ye Samantha Kuan Pengzhi Yu Hui Liu Xinmin Zhang Roland D Green Victor V Lobanenkov Ron Stewart James A Thomson Bing Ren 2011Cell Research2011,21,10:6
15急性冠状动脉综合征发生1个月后的生长分化因子15水平与主要出血风险增加相关显示文摘用双重抗血小板治疗的急性冠状动脉综合征(acutecoronarysyndromes,ACS)患者在初次就诊测量的生长分化因子15(growthdifferentiationfactor-15,GDF-15)与大出血相关。Lindholm D Hagstrm E James SK Becker RC Cannon CP Himmelmann A Katus HA Maurer G López-Sendón JL Steg PG Storey RF Siegbahn A Wallentin L 刘莉 叶鹏 2017中华高血压杂志2017,25,5:5
16Characterization and target identification of a DNA aptamer that labels pluripotent stem cells显示文摘Zhonggang Hou Susanne Meyer Nicholas E Propson jeff Nie Peng Jiang Ron Stewart James A Thomson 2015Cell Research2015,25,3:5
17A post-classical theory of enamel biomineralization… and why we need one显示文摘Enamel crystals are unique in shape,orientation and organization.They are hundreds of thousands times longer than they are wide,run parallel to each other,are oriented with respect to the ameloblast membrane at the mineralization front and are organized into rod or interrod enamel.The classical theory of amelogenesis postulates that extracellular matrix proteins shape crystallites by specifically inhibiting ion deposition on the crystal sides,orient them by binding multiple crystallites and establish higher levels of crystal organization.Elements of the classical theory are supported in principle by in vitro studies;however,the classical theory does not explain how enamel forms in vivo.In this review,we describe how amelogenesis is highly integrated with ameloblast cell activities and how the shape,orientation and organization of enamel mineral ribbons are established by a mineralization front apparatus along the secretory surface of the ameloblast cell membrane.James P Simmer Amelia S Richardson Yuan-Yuan Hu Charles E Smith Jan Ching-Chun Hu 2012International Journal of Oral Science2012,4,3:4
18Identification of pathologic features associated with “ulcerative colitis-like” Crohn's disease显示文摘AIM: To identify pathologic features associated with this 'ulcerative colitis(UC)-like' subgroup of Crohn's disease(CD).METHODS: Seventeen subjects diagnosed as having UC who underwent proctocolectomy(RPC) from 2003-2007 and subsequently developed CD of the ileal pouch were identified. UC was diagnosed based on preoperative clinical, endoscopic, and pathologic studies. Eighteen patients who underwent RPC for UC within the same time period without subsequently developing CD were randomly selected and used as controls. Pathology reports and histological slides were reviewed for a wide range of gross and microscopic pathological features, as well as extent of disease. The demographics, gross description and histopathology of the resection specimens were reviewed and compared between the two groups. RESULTS: Patients with 'UC-like' CD were on average 13 years younger than those with 'true' UC(P < 0.01). More severe disease in the proximal involved region and active ileitis with/without architectural distortion were observed in 6 of 17(35%) and 7 of 17(41%) 'UC-like' CD cases, respectively, but in none of the 'true' UC cases(P < 0.05). Active appendicitis occurred in 8 of 16(50%) 'UC-like' CD cases but in only two(11%) 'true' UC cases(P < 0.05). Conspicuous lamina propria neutrophils were more specific for 'UClike' CD(76% vs 22%, P < 0.05). In addition, prominent lymphoid aggregates tended to be more common in 'UC-like' CD(P = 0.07). The 'true' UC group contained a greater number of cases with severe activity(78% vs 47%). Therefore, the features more commonly seen in 'UC-like' CD were not due to a more severe disease process. Crohn's granulomas and transmural inflammation in non-ulcerated areas were absent in both groups.CONCLUSION: More severe disease in the proximal involved region, terminal ileum involvement, active appendicitis, and prominent lamina propria neutrophils may be morphological factors associated with 'UC-like' CD.Samuel D James Paul E Wise Tania Zuluaga-Toro David A Schwartz M Kay Washington Chanjuan Shi 2014World Journal of Gastroenterology2014,20,36:4
19Understanding development and ripening of fruit crops in an‘omics’ era显示文摘Next generation sequencing has revolutionized plant biology.Not only has our understanding of plant metabolism advanced using model systems and modern chromatography,but application of‘omics’-based technology has been widely extended to non-model systems as costs have plummeted and efficiency increased.As a result,important fundamental questions relating to important horticultural crops are being answered,and novel approaches with application to industry are in progress.Here we review recent research advances on development and ripening of fruit crops,how next generation sequencing approaches are driving this advance and the emerging future landscape.Nigel E Gapper James J Giovannoni Christopher B Watkins 2014Horticulture Research2014,1,1:4
20Heterogeneity in mouse spasmolytic polypeptide-expressing metaplasia lineages identifies markers of metaplastic progression显示文摘Victoria G Weis Josane F Sousa Bonnie J LaFleur Ki Taek Nam Jared A Weis Paul E Finke Nadia A Ameen James G Fox James R Goldenring 2013Gut2013,,9:3
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