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clinicalkey for nursing数据库的涵盖内容(一)

clinicalkey for nursing数据库的涵盖内容(一)ClinicalKey for Nursing数据库的涵盖内容ClinicalKey for Nursing是一款覆盖广泛的医学数据库，为护理专业人士提供丰富的资源和信息。

下面是该数据库涵盖的内容的概述：1. 护理学科•基础护理学：包括解剖学、生理学、药理学等基础学科的相关内容。

•临床护理学：涵盖各种临床实践和技能的指导，如护理评估、药物管理、病情监测等。

•转化性护理学：介绍护理实践中的创新和改进方法，帮助护士提升护理质量和效果。

2. 疾病与病理学•疾病学：提供各种疾病的定义、病因、临床表现、诊断和治疗等详细信息。

•病理学：介绍各种疾病的病理生理过程，帮助护士理解疾病的发展和影响。

3. 药物管理•药理学：解释药物的作用机制和影响，帮助护士了解不同药物的使用方法和效果。

•药物计算：提供药物剂量计算的指导和实践技巧，帮助护士确保药物的正确使用。

4. 护理研究与实践•护理研究：介绍最新的护理研究成果和方法，帮助护士了解如何开展和评估护理研究。

•证据实践护理：提供基于证据的实践指南和护理方法，帮助护士实践最新的临床指导。

5. 护理领导与管理•护理领导力：介绍护理领导者的角色和职责，帮助护士发展领导才能和管理技巧。

•护理管理：涵盖护理部门管理、人员管理、资源分配等方面的内容，帮助护士提升管理能力。

6. 护理伦理与法律•护理伦理：涉及护理实践中的伦理问题和挑战，帮助护士理解伦理决策和道德原则。

•护理法律：介绍护士在法律框架下的责任和义务，帮助护士遵守法律规定。

通过使用ClinicalKey for Nursing数据库，护理专业人士可以获得全面且实践的信息，提升自己的专业能力和知识水平。

该数据库的涵盖内容广泛，可以满足护理人员在不同领域和层次上的需求。

无论是学习新知识、进行研究，还是提高实践技能和管理能力，都可以在该数据库中找到有价值的资源和支持。

医学英文文献 (1)

Muscle-selective synaptic disassembly and reorganization in MuSK antibody positive MG miceAnna Rostedt Punga ⁎,1,Shuo Lin,Filippo Oliveri,Sarina Meinen,Markus A.RüeggDepartment of Neurobiology/Pharmacology,Biozentrum,University of Basel,Basel,Switzerlanda b s t r a c ta r t i c l e i n f o Article history:Received 23February 2011Revised 15April 2011Accepted 21April 2011Available online 30April 2011Keywords:Myasthenia Gravis MG MuSKNeuromuscular junction MasseterMuscle atrophy DenervationMuSK antibody seropositive (MuSK+)Myasthenia Gravis (MG)patients present a distinct selective fatigue,and sometimes atrophy,of bulbar,facial and neck muscles.Here,we study the mechanism underlying the focal muscle involvement in mice with MuSK+experimental autoimmune MG (EAMG).8week-old female wildtype C57BL6mice and transgenic mice,which express yellow ﬂuorescence protein (YFP)in their motor neurons,were immunized with the extracellular domain of rat MuSK and compared with control mice.The soleus,EDL,sternomastoid,omohyoid,thoracic paraspinal and masseter muscles were examined for pre-and postsynaptic changes with whole mount immunostaining and confocal microscopy.Neuromuscular junction derangement was quanti ﬁed and compared between muscles and correlated with transcript levels of MuSK and other postsynaptic genes.Correlating with the EAMG disease grade,the postsynaptic acetylcholine receptor (AChR)clusters were severely fragmented with a subsequent reduction also of the presynaptic nerve terminal area.Among the muscles analyzed,the thoracic paraspinal,sternomastoid and masseter muscles were more affected than the leg muscles.The masseter muscle was the most affected,leading to denervation and atrophy and this severity correlated with the lowest levels of MuSK mRNA.On the contrary,the soleus with high MuSK mRNA levels had less postsynaptic perturbation and more terminal nerve sprouting.We propose that low muscle-intrinsic MuSK levels render some muscles,such as the masseter,more vulnerable to the postsynaptic perturbation of MuSK antibodies with subsequent denervation and atrophy.These ﬁndings augment our understanding of the sometimes severe,facio-bulbar phenotype of MuSK+MG.©2011Elsevier Inc.All rights reserved.IntroductionAbout 40–70%of acetylcholine receptor (AChR)-antibody seronegative Myasthenia Gravis (MG)patients have antibodies against the muscle tyrosine kinase (MuSK)(Hoch et al.,2001;Sanders et al.,2003).In MuSK-antibody seropositive (MuSK+)MG patients,there is often selective involvement of bulbar-,neck-and facial muscles,as well as muscles that are usually asymptomatic in AChR-antibody seropositive (AChR+)MG,such as the paraspinal muscles (Sanders and Juel,2008).Contrary to conventional AChR+MG patients,the majority of MuSK+patients does not experience symptomatic relief from acetylcholine esterase inhibitors (AChEI)(Evoli et al.,2003)but instead may respond with pronounced nicotinic adverse effects,such as muscle fasciculations and cramps (Punga et al.,2006).Pronounced atrophy of facial muscles has also been described in MuSK+patients,although the concomitant treatment of corticosteroids in most cases has made it dif ﬁcult tojudge whether the MuSK antibodies or the cortisone treatment is the cause of the atrophy (Farrugia et al.,2006).Muscle biopsy studies of the intercostal muscle and biceps brachii muscle from MuSK+patients have shown little AChR loss (Selcen et al.,2004;Shiraishi et al.,2005),however,the neuromuscular junction (NMJ)pathophysiology in the most affected facial or bulbar muscles has not been studied.Nevertheless,MuSK antibodies have been shown to be pathogenic in animals,both after immunization with the extracellular domain of the MuSK protein itself (Jha et al.,2006;Shigemoto et al.,2008;2006;Xu et al.,2006)and after passive transfer of sera from MuSK+MG patients (Cole et al.,2008;ter Beek et al.,2009).MuSK is essential to the process of NMJ formation,maintenance (Wang et al.,2006)and integrity,as perturbations in MuSK protein expression cause pronounced disassembly of the entire NMJ (Hesser et al.,2006;Kong et al.,2004).Other NMJ proteins that are essential for synaptogenesis include Dok-7,a downstream adaptor protein to MuSK (Okada et al.,2006),Lrp4,the co-receptor for neural agrin (Kim et al.,2008;Zhang et al.,2008),rapsyn and the AChR subunits.The effects of MuSK antibodies in-vivo on the gene expression of those synaptic proteins in the facial or bulbar muscles have not yet been established.Here,we hypothesized that low expression levels of MuSK may render some muscles more vulnerable to the effect of MuSK antibodies in the EAMG mouse model.We show that MuSK antibodiesExperimental Neurology 230(2011)207–217⁎Corresponding author at:Institute of Neuroscience,Department of Clinical Neuro-physiology,Uppsala University Hospital,Uppsala,Sweden.Fax:+4618556106.E-mail address:annarostedtpunga@ (A.R.Punga).1Present address:Department of Clinical Neurophysiology,Uppsala University Hospital,Uppsala,Sweden.0014-4886/$–see front matter ©2011Elsevier Inc.All rights reserved.doi:10.1016/j.expneurol.2011.04.018Contents lists available at ScienceDirectExperimental Neurologyj o u r n a l h o me p a g e :w w w.e l s e v i e r.c om /l o c a t e /y e x n rinduce severe fragmentation of the postsynaptic AChR clusters in particular in the masseter and thoracic paraspinal muscles,with less fragmentation in the limb muscles.The severe postsynaptic pertur-bation results in subsequent denervation of muscleﬁbers,not previously described in EAMG or MG.We propose that one underlying mechanism for the severe involvement of the facial masseter muscle, with severely impaired NMJ architecture,atrophy and denervation,is its low intrinsic levels of MuSK.Moreover,muscles respond to the partial denervation caused by MuSK antibodies in two different ways: (1)terminal nerve sprouting in muscles with high intrinsic levels of MuSK(i.e.soleus,sternomastoid)and(2)no nerve sprouting in muscles with low intrinsic MuSK levels(i.e.masseter,omohyoid).MethodsProduction of recombinant rat MuSKpCEP-PU vector containing the His-tagged extracellular domain of recombinant rat MuSK(aa21-491;(Jones et al.,1999))was transfected(Lipofectamine2000;Invitrogen)into HEK293EBNA cells.The overexpressed protein was puriﬁed from the cell superna-tant over a Ni-NTA superﬂow column(Qiagen)and was subsequently dialyzed against PBS.Protein concentration was determined at OD 280nm and purity was ensured by SDS-PAGE.Experimental animalsC57BL6mice and mice expressing yellowﬂuorescence protein (YFP)in their motor neurons under Thy-1promoter(Feng et al., 2000)were originally supplied from Jackson Laboratories(Bar Harbor, Maine,US).For immunization,8week-old female mice were used.All mice were housed in the Animal Facility of Biozentrum,University of Basel,where they had free access to food and water in a room with controlled temperature and a12hour alternating light–dark cycle.All animal procedures complied with Swiss animal experimental regu-lations(ethical application approval no.2352)and EC Directive 86/609/EEC.ImmunizationThe immunization procedure has been described previously(Jha et al.,2006).Brieﬂy,eleven C57BL6and seven Thy1-YFP female mice aged8weeks were anesthetized(Ketamine:111mg/kg and Xylazine: 22mg/kg)and immunized with10μg of MuSK emulsiﬁed in complete Freund's adjuvant(CFA,Difco laboratories,Detroit,Michigan,US) subcutaneously in the hind foot pads,at the base of the tail and dorsolateral on the back.At day28post-injection,immunization was repeated.A3rd immunization was given to mice that did not show any myasthenic weakness after56days.Control mice(8female mice) were immunized with PBS/CFA.Clinical and neurophysiological examinationMuscle weakness was graded every week,as described(Nakayashiki et al.,2000).Brieﬂy,mice were exercised by20consecutive paw grips on a grid and were then placed on an upside-down grid.The time they could hold on to the grid reﬂected the grade of fatigue and muscle weakness.EAMG grades were as follows:grade0,no weakness;grade1, mild muscle fatigue after exercise;grade2,moderate muscle fatigue; and grade3,severe generalized weakness.Evaluation of the response to AChEIs was performed by i.p.injection of a mix of neostigmine bromide (0.0375mg/kg)and atropine sulfate(0.015mg/kg)in mice with EAMG grades2and3(Berman and Patrick,1980).Repetitive stimulation of the sciatic nerve and recording from the gastrocnemius muscle with monopolar needle electrodes was performed under anesthesia,in mice with EAMG grades2(n=2)and3(n=2),using a Saphire1L EMG machine(Medelec).Decrement was calculated as percent amplitude change between the1st and4th compound motor action potentials evoked by a train of10impulses where10%was considered as pathological.ELISASera were obtained from tail vein blood on day0(preimmune sera)and day35post-immunization.ELISA plates(Nunc MaxiSorp, Fisher Thermo Scientiﬁc,Rockford,IL,US)were coated with250ng/ ml of His-labeled rat MuSK(50μl/well),blocked with3%BSA/PBS and then incubated with a sera dilution row(1:3000–1:2,000,000).Pre-immune sera constituted negative and rabbit-anti-MuSK antibody (Scotton et al.,2006)positive controls.After washing,plates were incubated with secondary HRPO-conjugated goat-anti-mouse (1:2000)and goat anti-rabbit antibodies(1:2000;both from Jackson Immuno Research Laboratories,Westgrove,PA,US).HRPO activation by a TMB substrate was terminated with1N HCl after5min. Absorbance was read at450nm.Non-speciﬁc binding,determined by incubation of plates with pre-immune serum,was subtracted.The data were displayed as“half maximum MuSK immunoreactivity”,which represents the immunore-activity at a dilution of1:27,000,where the majority of sera obtained50% of maximum absorbance(in the linear range of the absorption at450nm).Western blotWestern blot of masseter muscles was conducted as described (Bentzinger et al.,2008).10μg of protein was resolved on a4–12%Nu-PAGE Bis–Tris gel(Invitrogen,Eugene,OR,US),transferred to nitrocellulose membrane,probed with rat monoclonal anti-NCAM (CD56;1:100;GeneTex)and rabbit polyclonal anti-pan-actin(1:1000; cell signaling)and then recognized with HRPO-conjugated antibodies (1:5000;Jackson Immuno Research Laboratories,Westgrove,PA,US). Quantitative RT-PCR analysisMouse muscle RNA was extracted and puriﬁed as previously described(Punga et al.,2011).RT-PCR reactions(triplicates)were carried out with Power SYBR Green PCR Master Mix reagent(Applied Biosystems,Warrington,UK).β-actin was used as endogenous control (Punga et al.,2011;Murphy et al.,2003;Yuzbasioglu et al.,2010).The following primer sets were used:MuSK:5′-GCCTTCAGCGGGACTGAG-3′and5′-GAGGCGTGGTGA-CAGG-3′Lrp4:5′-GGATGGCTGTACGCTGCCTA-3′and5′-TTGCCGTTGTCA-CAGTGGA-3′Dok-7:5′-CTCGGCAGTTACAGGAGGTTG-3′and5′-GCAATGC-CACTGTCAGAGGA-3′A C h Rα1:5′-G C C A T T A A C C C G G A A AG T G A C-3′a n d5′-CCCCGCTCTCCATGAAGTT-3′AChRε:5′-CTGTGAACTTTGCTGAG-3′and5′-GGAGATCAG-GAACTTGGTTG-3′AChRγsubunit:5′-AACGAGACTCGGATGTGGTC-3′and5′-GTCGCACCACTGCATCTCTA-3′Rapsyn:5′-AGGTTGGCAATAAGCTGAGCC-3′and5′-TGCTCTCACT-CAGGCAATGC-3′MuRF-1:5′-ACC TGC TGG TGG AAA ACA-3′and5′-AGG AGC AAG TAG GCA CCT CA-3′β-actin:5′-CAGCTTCTTTGCAGCTCCTT-3′and5′-GCAGCGA-TATCGTCATCCA-3′A C h E:5′-G G G C T C C T A C T T T C T G G T T T A C G-3′a n d5′-GGGCCCGGCTGATGAG-3′208 A.R.Punga et al./Experimental Neurology230(2011)207–217NMJ whole mount analysisAlexa Fluor555-conjugatedα-bungarotoxin(1μg/ml;Invitrogen) was injected into soleus,EDL,sternomastoid,omohyoid,masseter and the thoracic paraspinal muscles as described(Bezakova and Lomo, 2001).At least12images of each muscle per mouse(6MuSK-immunized YFP-transgenic mice and4CFA-immunized control mice) were collected with a confocal laser-scanning microscope(Leica TCS SPE).Laser gain and intensity were equal for all images.Quantiﬁcation of pre-and postsynaptic area was performed in ImageJ(http://imagej. /ij/index.html).NMJs containing terminal nerve sprouts(processes with YFP expression)were counted in muscles fromﬁve MuSK+EAMG mice with disease grades1–3.At least275NMJs per muscle were analyzed. The number of postsynapse fragments per NMJ was counted using a ﬂuorescence microscope(Leica DM5000B)in at least50NMJs per muscle deriving fromﬁve MuSK+EAMG grades1–2and from four control mice(Supplemental Fig.1).Fragmentation was classiﬁed as follows:1)normal pretzel-like NMJ;2)slight to moderate fragmen-tation;and3)severe fragmentation or absent postsynapse.The degree of postsynaptic perturbation per muscle was judged based on the percentage of NMJs belonging to each postsynaptic class and was further subdivided into number of postsynapse fragments per NMJ:1–3,4–6,7–9,10–12and more than12.Each NMJ was given the median score for that subgroup.The fragmentation score was obtained by taking the ratio of the score between the EAMG mice and control mice.Statistical analysisIndependent,2-sample t-test was performed for parametric data. For ordinal data(ELISA),the non-parametric test Spearman Rank Correlation was applied.A p-value b0.05was considered signiﬁcant.Fig.1.(A)Development of EAMG after immunization with recombinant rat MuSK.Progress of clinical EAMG grade at the time points week4,5,7and10.*The mice with EAMG grade 3were sacriﬁced after week7(hence no new grade3mice week10)and the remaining mice were sacriﬁced andﬁnally evaluated at week10.(B)One mouse,representative of the most severely affected MuSK+EAMG mice,withﬂaccid paralysis and pronounced kyphosis.(C)Repetitive nerve stimulation performed in the same mouse.Stimulation of the sciatic nerve and recording of the gastrocnemius muscle demonstrated a35%decrement between the1st and4th compound motor action potentials at low frequency3Hz stimulation.(D)Correlation of clinical EAMG grade with MuSK antibody titer.Half of maximum MuSK immunoreactivity(1:27,000dilution)in sera from MuSK immunized mice was assessed by Elisa at450nm.R=0.483(Spearman's Rank Correlation);p b0.05.209A.R.Punga et al./Experimental Neurology230(2011)207–217ResultsMuSK+EAMG presents with prominent kyphosis,paralysis and weight lossOut of the18mice immunized with MuSK,theﬁnal EAMG grade 0was seen in3mice(17%),grade1in8mice(44%),grade2in4mice (22%)and grade3in3mice(17%)(Fig.1A).No difference in disease incidence was found between the groups of C57BL6mice and the YFP-transgenic mice.Based on this,the data were pooled in the current study.The most severe phenotype of EAMG(grade3)includedﬂaccid paralysis,pronounced kyphosis and weight loss(Fig.1B).In-vivo nerve stimulation at3Hz with recording from the gastrocnemius muscle revealed a decrement of10–40%in the MuSK+EAMG mice (Fig.1C),whereas the control mice had normal neuromuscular transmission(data not shown).MuSK immunoreactivity in sera(day 35)correlated with clinical severity(Fig.1D;Spearman Rank Correlation;R=0.483;p b0.05),although some mice developed measurable MuSK antibodies without showing obvious muscle weakness or fatigue.Bulbar symptoms underlying weight loss in MuSK+EAMG The MuSK immunized mice steadily decreased signiﬁcantly in body weight after the2nd immunization(Fig.2A),in contrast to the control mice,and theﬁnal body weight of the MuSK+mice was signiﬁcantly smaller(p b0.001;Fig.2B).This severe weight loss was slowed but not stopped after introduction of wet food(data not shown).Since the timeline of the weight drop also correlated with development of muscle fatigue,the weight loss was assumed to be indicative of chewing and swallowing difﬁculties,some of the cardinal symptoms of MuSK+MG.To determine whether loss of muscle weight signiﬁcantly contributed to the overall lower body weight in the MuSK+EAMG mice,the weight ofﬁve different muscles was assessed.The masseter was the only muscle with a signiﬁcant weight reduction(p b0.01;Fig.2C),implying that this muscle is atrophic and further indicating chewing difﬁculties.Adverse effects of AChEIs in MuSK+EAMGTo elucidate whether AChEIs have any beneﬁcial effect on fatigue or weakness in MuSK+EAMG,a neostigmine test was performed in the mice with EAMG grade3(n=3).No apparent improvement in weakness at rest or exercise-induced fatigue was seen;instead the mice experienced shivering and constant twitching of the tail,trunk and limbs starting after approximately13min(Supplemental Video1).This effect wore off after40min and was interpreted as nicotinic side effects and neuromuscular hyperactivity,usually seen after an overdose of AChEIs.Thus,this intolerance towards AChEIs in MuSK+EAMG indicates an abnormal sensitivity to acetylcholine.Impairment of NMJs in different musclesBecause muscle groups in the bulbar/facial/back region are selectively involved in the MuSK+EAMG model,we next examined the morphological changes of NMJs in the thoracic paraspinal muscles, masseter,omohyoid and sternomastoid and compared them with those in two limb muscles(EDL and soleus).Typical features of postsynaptic impairment were a fainting of AChRﬂuorescence,areas lacking AChRs(holes)and disassembly of AChR clusters.To quantify these impairments,we classiﬁed NMJs into three classes as illustrated in Fig.3A.All muscles from MuSK+EAMG mice displayeddifferentFig.2.Weight loss in MuSK+EAMG.(A)The course of weight loss in two MuSK+mice with EAMG grade3compared to control(Ctrl CFA)mice(n=8).Initial body weight was comparable and weight loss started after the2nd immunization and weight kept dropping even though wet food was provided ad libitum.(B)Mean body weight was dramatically reduced in the MuSK immunized mice(MuSK+;n=18),compared to the control mice.Results shown as mean±SEM(gram);***p b0.001.(C)Muscles were weighed and compared between control mice(n=8)and MuSK+EAMG mice(n=18).Results displayed as mean muscle weight±SEM(mg).The only muscle which was signiﬁcantly lighter in the MuSK+mice was the masseter.**p b0.01.210 A.R.Punga et al./Experimental Neurology230(2011)207–217degrees of NMJ impairment (Fig.3B).Moreover,we also observed that the postsynapses were often fragmented into two to three non-continuous fragments (see illustration in Fig.3A),which is in strong contrast to non-interrupted,pretzel-like shape of AChRs in non-immunized mice.This fragmentation was also quanti ﬁed (Supplemental Fig.1)and expressed as “fragmentation score ”.Because fragmentation differs between muscles,this “fragmentation score ”was normalized to the control.As shown in Fig.3C,the fragmentation score varied between a minimum of 2.0in the soleus muscle and a maximum of 3.3in the masseter muscle.The postsynaptic labeling was markedly reduced in the MuSK+EAMG mice compared to control mice (Fig.4A).In the mild to moderately affected mice,AChR cluster area was reduced signi ﬁcantly by 40–50%in all muscles (p b 0.01),except for the soleus,which had a remaining area of 85%(p b 0.05;Fig.4B).In the most severely affected mice,the postsynaptic area was also lost in the soleus muscle and less than 10%of the α-bungarotoxin staining remained in the masseter,sternomastoid and thoracic paraspinal muscles (p b 0.001).In the soleus,the nerve terminal area was unchanged in the severely affected mice,although in the other muscles the presynaptic area was reduced to about 80%in the mild to moderate cases and to 50%in the most severely affected mice (p b 0.01)(Fig.4C).Thus,both the pre-and postsynaptic data suggest that the masseter is the most affected muscle by MuSK antibodies whereas the soleus is the least affected.mRNA transcript expression of NMJ proteins in different muscles in MuSK+EAMGThe mRNA levels of MuSK differ signi ﬁcantly between muscles,with the highest levels in the soleus muscle and lowest levels in the omohyoid muscle (Punga et al.,2011).Consequently,we additionally analyzed MuSK transcript levels in the masseter and these were even lower,with less than 20%of the mRNA levels detected in the soleus muscle (Supplemental Fig.2;p b 0.01).In the MuSK+EAMG mice,MuSK mRNA levels were signi ﬁcantly reduced to 45%of control in the EDL (p b 0.05)and to 25%in the omohyoid muscle (p b 0.001;Fig.5A).Conversely,MuSK mRNA expression was signi ﬁcantly increased in the masseter muscle (p b 0.01)and remained unchanged in the soleus and sternomastoid muscles.The expression of the AChR αsubunit was unchanged (Fig.5B),whereas the AChR εsubunit transcript was downregulated in the soleus and sternomastoid muscles and conversely a trend towards upregulation was seen in the masseter muscle (Fig.5C).The fetal AChR γsubunit mRNA was upregulated up to 1000-fold in the masseter (p b 0.001)and 5-fold in the soleus (p b 0.05;Fig.5D).The transcript levels of rapsyn,Lrp4and Dok-7were not signi ﬁcantly altered (Fig.5E to G).Finally,the transcript levels of acetylcholine esterase (AChE)were signi ﬁcantly down-regulated only in the sternomastoid and omohyoid muscles (p b 0.05;Fig.5H).Fig.3.Postsynaptic fragmentation of NMJs.(A)Examples from each postsynaptic classi ﬁcation.AChRs stained for alfa-bungarotoxin.(B)At least 275neuromuscular junctions (NMJs)per muscle were assessed in a total of 5MuSK+EAMG mice with moderate to severe disease.The appearance of NMJ postsynapses were divided into 3classes as indicated.Sol:soleus;EDL:extensor digitorum longus;STM:sternomastoid muscle;omo:omohyoid;mass:masseter.(C)Postsynapses were analyzed in at least 50NMJs per muscle in a total of 5MuSK+EAMG mice with slight to moderate disease grade and in 4control mice.Each NMJ in a certain subclass (for details see Supplemental Fig.1)was given the median score for that subclass.The fragmentation score for each muscle is the ratio in score between the EAMG mice and control mice.211A.R.Punga et al./Experimental Neurology 230(2011)207–217In summary,particularly the massive upregulation of MuSK transcripts and AChR γin conjunction with the overall trend for upregulation of mRNA for the other postsynaptic genes in the masseter muscle most likely re ﬂects the severely disturbed neuro-muscular transmission in this muscle as a result of the MuSK antibodyattack.Fig.4.Pronounced reduction of postsynaptic and presynaptic area in different muscles in MuSK+EAMG.(A)Whole mount staining of single ﬁber layer bundles from the paraspinal muscle (ps),sternomastoid (STM),masseter (mass),omohyoid (omo),extensor digitorum longus (EDL)and soleus (sol)muscles from one control mouse immunized with CFA/PBS and one mouse with severe MuSK+EAMG.AChRs are visualized by alexa-555-bungarotoxin (red)and the motor nerve terminals by YFP expression (green).The AChRs are almost completely gone from the paraspinal muscles,STM and masseter.Confocal images of 100×magni ﬁcation,scale bar is 10μm.Quanti ﬁcation of (B)postsynapse (AChR clusters)and (C)presynaptic area in the different muscles;soleus (sol),extensor digitorum longus (EDL),omohyoid (omo),masseter (mass),sternomastoid (STM)and paraspinal muscles (ps).Results are given as %of ctrl area±SEM and at least 12NMJs in each muscle/mouse was measured in mice with EAMG grades 1–2(N =4),in mice with severe grade 3(N =2)and in control mice (N =4).**p b 0.01;#p b 0.001.212 A.R.Punga et al./Experimental Neurology 230(2011)207–217Denervation induced muscle atrophy in MuSK+EAMGThe masseter muscle lost weight and consequently we examined the mRNA levels of the atrophy marker muscle-speci ﬁc RING ﬁnger protein 1(MuRF-1)and assessed signs of denervation.For this analysis we included the same muscles as previously examined,with the addition of thoracic paraspinal muscles due to the pronounced kyphosis of the MuSK+EAMG mice.MuRF-1mRNA levels were signi ﬁcantly upregulated in the masseter muscle (p b 0.05;Fig.6A)and on the contrary MuRF-1transcript levels were strongly reduced in the soleus muscle (p b 0.01)in the MuSK+EAMG mice.Further,the protein levels of neural cell adhesion molecule (NCAM),a marker for denervation,were increased in the masseter muscle as detected by Western blot analysis.This is thus additional evidence of denervation in this particular muscle (Fig.6B).Absence of nerve sprouting may contribute to the severe denervation phenotypePresynaptic nerve terminals were visualized by transgenic YFP expression,allowing observation also of NMJs with absent post-synapses.In the masseter,the nerve terminals were still present although many postsynaptic AChRs were partially or completely lost.Intriguingly,no or little nerve sprouting was observed in these cases (Fig.7).This ﬁnding raised the possibility that postsynaptic perturbation in this muscle did not elicit any nerve sprouting response.To test this hypothesis,we examined ≥450NMJs in each of the muscles for such sprouting response.The quantitative examination of 4MuSK+EAMG mice revealed terminal nerve sprouting in approximately 20%of NMJs in the soleus and in 15%of endplates in the sternomastoid (Fig.7).On the contrary,theFig.5.mRNA levels of postsynaptic proteins in MuSK+EAMG.C:control mice immunized with CFA/PBS.MG:EAMG mice immunized with MuSK.mRNA levels in the control mice are set to 100%and levels in the EAMG mice are relative to the control levels.n=6control mice;n=6MuSK+EAMG mice.Genes of interest are relative to the house keeping gene β-actin.*p b 0.05;***p b 0.001.213A.R.Punga et al./Experimental Neurology 230(2011)207–217omohyoid,EDL,thoracic paraspinal muscles and masseter,showed terminal sprouting at only a few NMJs.In most samples no sprouting was observed,which differed signi ﬁcantly from the soleus (p b 0.001)and the sternomastoid muscle (p b 0.05).Interestingly,the degree of nerve sprouting in each muscle correlates with their endogenous levels of MuSK,suggesting that MuSK levels regulate the nerve sprouting response and consequently reorganization of NMJs (Punga et al.,2011).DiscussionMuSK+MG patients often present with focal weakness of facial,bulbar,neck and respiratory muscles and sometimes also of paraspinal and upper esophageal muscles (Sanders and Juel,2008).The pathopysiological role of MuSK antibodies has been questioned based on the normal levels of MuSK and AChRs at the NMJ in cross-sections of the intercostal muscle and biceps brachii muscle of MuSK+MG patients (Selcen et al.,2004;Shiraishi et al.,2005).Further studies in mice have now shown that MuSK antibodies deplete MuSK from the NMJ,which results in disassembly of the postsynaptic apparatus and a reduced packing of AChRs (Jha et al.,2006;Shigemoto et al.,2006;Cole et al.,2010).Nevertheless,the exact mechanism of how MuSK antibodies affect muscles has so far not been revealed.Here we report that MuSK antibodies cause a severe pre-and postsynaptic disassembly in the facial,bulbar and paraspinal muscles but only a slight disruption in the limb muscles (i.e.soleus and EDL).The most affected muscle was the masseter and intriguingly this muscle expressed less than 20%of MuSK transcripts than the least affected soleus muscle.Considering that fast-twitch muscle ﬁbers require larger depolarization to initiate contraction compared to slow-twitch ﬁbers,we propose that the superfast twitch pattern of the masseter in combination with its critically low MuSK levels makes this muscle extra vulnerable to the synaptic perturbation following the MuSK antibody attack (Laszewski and Ruff,1985).Hence,over-expression of MuSK in vulnerable muscles could potentially alleviate the effects of the antibody-mediated attack against MuSK.Earlier studies of AChR+EAMG rats have been shown to respond to rapsyn-overexpression in the tibialis anterior muscle with no loss of AChRs and almost normal postsynaptic folds,whereas the NMJs of untreated muscles showed typical AChR loss and morphological damage (Losen et al.,2005).Nevertheless,we did not ﬁnd any changes in rapsyn mRNA levels across the examined muscles.Additionally,our ﬁndings underline the importance of examining the clinically affected muscles in MuSK+MG in order to draw the right conclusions regarding NMJ morphology.In the MuSK+EAMG model,the mice exhibited obvious bulbar and thoracospinal muscle weakness,similar to the mouse model of congenital myasthenic syndrome with MuSK mutation (Chevessier et al.,2008).This implies a common clinical phenotype in mice with impaired MuSK function and corresponds well with the phenotype of human MuSK+MG.In contrast,we have noticed in parallel rounds with immunization of C57BL6mice with AChR from Torpedo californica that the AChR-antibody seropositive mice did not develop signi ﬁcant weight loss,neck muscle weakness or kyphosis and also that their ﬂaccid paralysis was reversible with AChEI treatment (Punga et al.,unpublished observations).The adverse effect of AChEIs in MuSK+EAMG resembles the neuromuscular hyperactivity reported in MuSK+MG patients (Punga et al.,2006).We hypothesize that the underlying reason for the hypersensitivity in the muscles to the additional amount of available ACh at the NMJ is a consequence of (1)the denervation of the muscle ﬁbers with extensive AChR fragmentation and (2)the downregulation of AChE in some muscles (e.g.omohyoid and sternomastoid),which may result in AChEI overdose-like phenotype.The downregulation of AChE mRNA is most probably a direct consequence to the loss of MuSK,since MuSK binds collagen Q,an interaction that is thought to be largely responsible for the synaptic localization of AChE-collagen Q complex at the NMJ (Cartaud et al.,2004).The fragmentation and spatial dispersion of AChRs most likely inhibits the response to the increased ACh at the NMJ induced by AChEIs in the most clinically affected muscles.This study also investigated the possibility of MuSK antibodies to initiate a cascade that results in denervation-induced atrophy.MRI studies of newly diagnosed MuSK+patients have con ﬁrmed early muscle atrophy in the temporal,masseter and lingual muscles with fatty replacement (Zouvelou et al.,2009;Farrugia et al.,2006).We observed that,particularly in the masseter and paraspinal muscles,some NMJs were completely depleted of AChRs,and the subsequent loss of synaptic transmission most probably resulted in functional denervation.This explanation is further supported by the fact that pharmacological denervation arises after injection of botulinum toxin A (BotA),which also blocks the cholinergic synaptic transmission,and it is sometimes dif ﬁcult to distinguish this from a surgical denervation due to the similarities in pattern,extent and time course (Drachman and Johnston,1975).Previous studies of passively induced AChR+EAMG in rats have shown an upregulation of the AChR ε,but not the γsubunits;thus suggesting that newly expressed AChRs in the case of antibody mediated AChR loss are of the adult type (Asher et al.,1993).However,our observed massive upregulation of AChR γtranscript in the masseter implies that,except for disturbed neuromuscular transmission,denervation is also ongoing since this usually correlates with the predominant expression of embryonic type receptors and re-expression of the fetal type occurs after experimental denervation (Witzemann et al.,1989).Levels of AChR γmRNA are normally extremely low in all muscles except for the extraocular muscles (Kaminski et al.,1996;MacLennan et al.,1997).Concomitantly with the very prominent increase in transcripts encoding AChR γ,MuSKFig.6.Atrophy-and denervation related markers in MuSK+EAMG mice.(A)mRNA levels of MuRF-1expressed as %of control in relation to β-actin.n=6control mice (C)and n=5MuSK+EAMG mice (MG).*p b 0.05.(B)Western blot of NCAM in the masseter muscle of one MuSK+EAMG mice with disease grade 3(MG)and in one CFA-immunized control mouse (Ctrl).NCAM was detected as 3bands at levels 120,140and 180kD and the loading control β-actin (45kD).An equal amount of protein was loaded.**p b 0.01.214 A.R.Punga et al./Experimental Neurology 230(2011)207–217。

医学文献检索作业：外文数据库检索

•外文数据库检索1.查找Christiane Siemer1992年发表的文献，写出第一篇文献的基本信息；Activation of nonselective cation channels in the basolateral membrane of rat distal colon crypt cells by prostaglandin E2Ion channels in the basolateral membrane of colonic crypts were investigated with the patch-clamp technique during stimulation of secretion. Intact crypts were isolated from rat distal colon and the cell poten...Christiane Siemer, Heinz Gögelein in Pflügers Archiv (1992)•2。

查找题名为"Recruiting and developing female managers for international assignments"的文章,并根据题录填写下列著录信息:•Title: Recruiting and developing female managers for international assignments•Authors : Liehan,Margareg;Walsh,James S•Source: Journal of Management Development•3。

查找药物治疗（drug therapy）心血管疾病（cardiovascular disease）方面的文献。

•检索步骤：•①进入PubMed检索界面•②在输入框内输入“drug therapy AND cardiovascular disease “•③结果：共357798篇•④其中1篇的基本信息是：题名：Expanding Role of Pharmacogenomics in the Management of Cardiovascular Disorders.著者：Pirmohamed M出处:Am J Cardiovasc Drugs. 2013 Apr 12. [Epub ahead of print」（注：素材和资料部分来自网络，供参考。

6.数据库检索外文 Pubmed医学专业研究生必看

3、关键词与主题词检索
Pubmed的关键词检索有何特别？有了Pubmed的特色功能还要主题词检索作什么？
为什么还要强调主题词检索？
2
3 4
只要用主题词检索就足够了吗？
1
(1)为什么还要强调主题词检索？
• 主题词是在关键词的基础上经过规范化处理的，就是在文献存储时，对文献中的同义词、近义词、多义词等进行严格的控制与规范，使得同一主题概论的文献相对集中在一个主题词之下。
• Publisher-Supplied
出版商提供的电子文献题录，每条记录标有:
[PubMed-as supplied by publisher]，分为两类： – MEDLINE 收录，逐步转为In Process, Indexed状态。 – Not MEDLINE：PubMed 收录，MEDLINE不收录，一直标注[PubMed-as supplied by publisher]或 [PubMed]
检索键
只查重点论述的文献
系统自动扩展检索下位词，勾选后不检索下位词
(4)只要用主题词检索就足够了吗
• 不是每个词都有对应的主题词 • 没有主题标引的文献不可以用主题词检索 ----如何识别主题标引的文献策略：根据实际需求选择，最好的是使用主题词与关键词相结合
4、值得推荐的功能与资源
1. 2.
特点
• • • • • • • • 资源免费收录广泛更新迅速数据权威检索方便检索结果精准个性化定制功能丰富外部分析工具功能强大
是目前使用最广泛、影响力最大的生物医学信息资源检索系统。
• MEDLINE Indexed
1966 to prensent的MEDLINE已标引数据，有MeSH字段和摘要，每条记录标有： [PubMed-indexed for MEDLINE]

英文医学数据库检索

Identifier DP：Publication Date
字段标识：字段名称
LA：Language MH：MeSH Terms MAJR：MeSH Major
Topic SH：MeSH Subheadings PT：Publication Type SO：Source TA：Journal Title TI：Title TW：Text Words
Web of Knowledge 索系统
CA化学文摘 (CAPlus)
SciFinder Scholar
5
一、英文数据库概述
• 英文数据库按记录完整性可分为文摘数据库和全文数据库。
• 前面提到的英文专业数据库刚开始都是文摘数据库，但随着信息技术的发展都开始提供全文。
• 新出现的数据库大都提供全文。 • 全文数据库大都需要付费访问。 • 即使是全文数据库，也不是库中的每篇论④ OLDMEDLINE:965年以前的记录17
（2）论文全文
①PubMed Central ②开放存取期刊 ③出版商提供的部分免费期刊 ④链接到出版商网站
（3）题录相关生物信息学数据、图书馆馆藏信息、消费者健康信息和研究工具等资源链接。
18
Pubmed记录来源标识（1）
[PubMed – indexed for Medline]
（一）、Pubmed知识精要
3
常用字段
4
检索途径
5
特色
11
2019-
1. Pubmed沿革
1983-
Pubmed
Medline光盘
19641879-
Medline联机检索
Index Medicus
12
• Medline是美国国立医学图书馆开发的生物医学文献数据库。可获取1950年以来80多个国家和地区5000多种生物医学期刊的文摘。

北京规范化培训课程：如何全面获取国外医学文献(一)答案

1、PubMed数据库的数据来源不包括以下哪项（） *• A.MEDLINE• B.Publisher-SuppliedCitations• C.Genome• D.InProcessCitations2、在PubMed数据库中以下哪项链接可以进行保存检索式，邮件自动文献追踪(automaticemailalerts)的设置（） *• A.Sendto• B.MyNCBI• C.Displaysetting• D.PubMedTools3、在PubMed数据库中要查看某个检索结果的临床试验(ClinicalTrial)方面的文献，应该在哪项过滤功能中查找（） *• A.Searchfields• B.Subjects• C.Species• D.Articletypes4、WebofScience是（） *• A.医学类检索工具• B.多学科检索工具• C.化学类检索工具• D.生物医学类检索工具5、在PubMed数据库中，对检索结果不能进行哪个方面的过滤（） *• A.fund• B.Species• C.Publicationdates• D.Articletypes6、关于PubMed数据库的外部资源链接中错误的说法是（） *• A.外部资源链接功能强大，可链接到各种可获得的WEB在线资源• B.外部链接包括全文、生物学数据库、研究工具等• C.外部资源链接的都是免费资源• D.在PubMed数据库中可点击“Linkout”进入外部资源链接7、在PubMed数据库中要查看某个检索结果的综述(Review)方面的文献，应该在哪项过滤功能中查找（） *• A.Searchfields• B.Subjects• C.Species• D.Articletypes8、在PubMed数据库中检索，以下哪个检索式是错误的（） *• B.child*• C.manORmen• D.hepatitisANDtherapy9、WebofScience被引参考文献检索不包括下列哪个检索字段（） *• A.被引著作• B.被引卷• C.被引期• D.被引主题10、在PubMed数据库中不能对检索结果按以下哪项排序（） *• A.RecentlyAdded• B.FirstAuthor• C.TimeCited• stAuthor11、在WebofScience的高级检索中，以下字段与中文名称对应不正确的是哪项（） *• A.TS=主题词• B.TI=标题• C.AU=作者• D.RID=ResearcherID12、在PubMed的基本检索方式下输入（），系统自动能检索出包含SmithJ的著者撰写的文献 *• A.SmithJ[au]• B.SmithJ[ab]• C.SmithJ[ti]• D.SmithJ[issn]13、PubMedTools不包括以下哪项（） *• A.SingleCitationMatcher• B.ClinicalTrials• C.BatchCitationMatcher• D.ClinicalQueries14、在PubMed数据库中，检索2000年以后作者JoshuaLederberg发表的文献可输入的最佳检索式是（） *• A.LJ• B.JoshuaLederberg• C.Lederberg• D.JL15、在PubMed数据库的检索结果中，文献的导出方式不包括（） *• A.File• B.E-mail• D.Clipboard16、WebofScience数据库所在的检索平台是（） *• A.Entrez• B.Webofknowledge• C.EBSCO• D.OVID17、MeSHMajortopic指的是（） *• A.主题词• B.主要主题词• C.主要关键词• D.关键词18、在PubMed数据库中，可以限定检索结果有免费全文的功能是（） *（A、C不正确，B、D不确定）• A.MyNCBI• B.History• C.Advanced• D.Filter19、对PubMed数据库中的题录进行主题词标引的依据不正确的是哪一个（） *• A.医学主题词表• B.MedicalSubjectHeadings• C.MeSH• D.汉语主题词表20、WebofScience输出记录的功能哪项不正确（） *• A.打印• B.E-mail发送• C.保存到SPSS里• D.存盘（Saveto）21、在PubMed数据库中，检索用西班牙语发表的文献可使用哪个限制条件（） *• A.[la]• B.[ab]• C.[ti]• D.[au]22、PubMed数据库检索结果的显示格式不包括（） *• A.Summary• C.ENDNOTE• D.MEDLINE23、WebofScience数据库对检索结果所作的引文报告不包括以下哪一项（） *• A.被引频次总计• B.施引文献• C.每项平均引用次数• D.h-index24、在PubMed数据库中，检索65岁以上老年人的高血压的治疗，可以用哪种过滤条件来限定（） *• A.Publicationdates• B.Ages• nguages• D.Species25、在PubMed数据库中，以下哪个检索词可以实现自动转换匹配（） *（B、C不正确，A、D不确定）• A.lungcancer• B.lungcancer[ti]• C.”lungcancer“• D.lung-cancer26、PubMed数据库MyNCBI具有的功能包含（） *• A.查主题词• B.查找单篇文献• C.查找多篇文献• D.保存检索式，邮件自动文献追踪27、PubMed数据库中词语自动匹配转换（automatictermmapping）功能不包括以下哪个表（） *• A.MeSHtranslationtable• B.Fullauthortranslationtable• C.Journaltranslationtable• D.Articletypetranslationtable28、下面哪项功能是PubMed数据库不具备的（） *• A.提供部分免费全文的链接• B.对输入的检索词进行词语自动匹配转换功能• C.可以输入化学物质结构式进行检索• D.MyNCBI的定题跟踪功能29、WebofScience不具有以下哪项功能（） *• A.引文跟踪的功能• B.引文检索的功能• C.主题词检索功能• D.对检索结果的分析功能30、有关WebofScience检索结果的分析功能可以帮助回答的问题的说法不正确的是（） *• A.某一专题文献主要集中在什么刊物上• B.某一方面文献的语种分布如何• C.某一专题的研究起始于什么年份或历史上研究的高峰期处什么年代• D.某一专题的研究有关循证医学方面的文献有哪些31、在PubMed数据库中，以下字段与字段缩写对应正确的是（） *• A.PublicationsDate[PD]• B.MeSHTerms[SH]• C.Title[TI]• D.Author[AB]32、在PubMed数据库中不能将检索结果发送到以下哪项中（） *• A.File• B.Clipboard• C.E-mail• D.NoteExpress33、在PubMed数据库中，检索有免费全文的有关甲流的文献，可以用哪种过滤条件来限定（） *• A.Publicationdates• B.Freefulltext• nguages• D.Species34、在PubMed数据库中检索期刊“Cell”上发表的文献可以用哪个检索式（） *• A.Cell• B.Cell[title]• C.Cell[ta]• D.Cell[ISSN]35、有关PubMed数据库以下哪些说法是错误的（） *• A.Pubmed是美国国家生物技术信息中心(NCBI)下属的美国国家医学图书馆(NLM)开发的检索系统• B.免费提供题录和文摘• C.提供与原文的网址链接(部分免费获取）• D.提供检索词自动转换匹配36、PubMed数据库的检索途径不包含（） *• A.基本检索• B.主题词检索• C.高级检索• D.化学物质检索37、WebofScience是（） *• A.全文型数据库• B.事实型数据库• C.多媒体数据库• D.含有引文检索的文摘型数据库38、PubMed数据库支持的逻辑运算符不包括（） *• A.AND• B.OR• C.NOT• D.WITH39、以下哪项不是引文检索中最常见的检索字段?（） *• A.被引作者• B.被引刊名• C.被引文献的页码• D.被引年份40、WebofScience的检索结果不能按以下哪项排序（） *• A.期刊刊名• B.出版日期• C.被引频次• D.第一作者41、在PubMed数据库中，检索研究对象是人类的埃博拉出血热的文献，可以用哪种过滤条件来限定（） *• A.Publicationdates• B.Ages• nguages• D.Species。

外文医学信息资源检索平台及检索技能必备知识(1)

深圳市迈特思创科技有限公司中国研究型医院学会常务理事单位
资源检索平台外文医学信息外文医学信息资源资源检索平台
主讲人：王佳佳
Email：julieapple1416@
深圳市迈特思创科技有限公司
FM RS-外文医学信息资源检索平台 FMR S--外文外文医学医学信息资源检索平台
RS-外文信息资源检索平台 FM FMR S--外文信息资源检索平台
FM RS系统检索功能介绍： FMR � 全中文界面的英文检索系统，支持中、英双语输入检索。 � 丰富的检索功能包括：期刊导航、文本词检索、主题词检索、复合检索功能、检索史和策略检索功能、加载PUBMED功能等 � 多种适合国人使用的功能设置：题名、摘要的机器翻译，主题词翻译，google引文，SCI期刊查收等。
期刊导航检索界面
期刊分类导航
期刊导航检索界面
期刊导航检索界面
策略检索&检索史界面
可删除不需要或错误的检索策略
加载PUBMED检索界面
FMRS特色功能
FMRS特色功能
FMRS特色功能
不同类别临床问题研究方法的证据强度
Type of Question 问题类型 Therapy 治疗 Diagnosis 诊断 Etiology/Harm 病因学/危害 Prognosis 预后 Prevention 预防 Clinical Exam 临床检验 Cost 成本 Suggested best type of Study 最佳研究类型 RCT>cohort > case control > case series 随机对照实验>队列研究>病例对照>病例系列研究 Prospective, blind comparison to a gold standard 与金标准进行预期和盲比 RCT > cohort > case control > case series 随机对照实验>队列研究>病例对照>病例系列研究 Cohort study > case control > case series 队列研究>病例对照>病例系列研究 RCT>cohort study > case control > case series 随机对照实验>队列研究>病例对照>病例系列研究 Prospective, blind comparison to gold standard 与金标准进行预期和盲比 Economic analysis 经济学分析

外文数据库检索之一

三大检索工具之CPCI（原ISTP）
美国《会议录文献引文索引》（Conference Proceedings Citation Index），简称CPCI，原为美国《科技会议录索引》（《 Index to Scientific & Technology Proceedings》，简称《ISTP》）， 1978年创刊，月刊，年报道量约4000个会议、论文约14万篇，有年度累积索引。
我们订购的Web of Science资源：
Science Citation Index Expanded (SCI-EXPANDED) 2004Social Sciences Citation Index (SSCI) 2004Conference Proceedings Citation Index Science （CPCI-S) 2004Conference Proceedings Citation Index – Social Science & Humanities （CPCI-SSH) eedings Citation Index - Social Sciences & Humanities 1990-
14
Thomson将五个引文数据库SCI，SSCI，AHCI，CPCI-S， CPCI-SSH与两个化学数据库整合，，利用互联网的开放环境，创建了网络版的多学科文摘数据库－－Web
3.截词检索
4.名词单复数：
不加双引号，可检索出词的单复数，加双引号后，是精确检索，不能检出单复数变化，需加截词算符，如”power system*”
快速锁定高影响力的论文
排序方式: 被引频次（Times Cited）
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浏览该文章的参考文献

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MESH特性：支持副主题词限定

形式：MeSH词 / Qualifiers 作用：限定；扩大词量
举例：白血病的发病机制研究白血病/病因学 • 副主题词:83个
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MESH特性：扩展检索功能

MESH树状结构体系：主题词概念等级分类体系, 它将MeSH表中的所有主题词, 按照其词义范畴和学科属性,分门别类地归入15个大类,每个大类又逐级划分(主要类目见附录).每个主题词都在这种体系中至少有一个位置, 用来描述这种位置的号码称为树状结构号。

MeSH Database(获取主题词信息并检索)
Single Citation Matcher
(从文献外表特征查找单篇或一组论文)

Batch Citation Matcher Clinical Queries(临床文献查询) Topic-Specific Queries Linkout(外部链接)
34
检索结果
child, preschool [mh] AND asthma/therapy [mh]
35
获取全文1
36
获取全文2
37
日期检索
格式：YYYY/MM/DD [date field]

2009/10/06 [edat]

2008 [dp]
2008:2010 [dp] 2009/01:2010/03 [edat]
30
基本检索：检索方法（规则）
不区分大小写逻辑组配检索

（1） NOT ，AND, OR （2）不输入默认为AND
vitamin c common cold vitamin c AND common cold
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字段检索(教材P.86)
PMID- 14706589 TI - Lymphedema after treatment of breast cancer. AU - Ozaslan C 格式：检索词[字段标识] LA - eng PT - Journal Article Lymphedema[TI] 1832篇 MH - Axilla Ozaslan C[AU] 11篇 MH - Breast Neoplasms/*surgery Axilla[MH] 7073篇 MH - Lymph Node Excision/*adverse effects MH - Lymphedema/*epidemiology SO - Am J Surg 2004 Jan;187(1):69-72.
英文医学数据库检索1
概述

外文文摘数据库检索 Medline与Pubmed, EMBASE, SciFinder Scholar, BioSIS Previews, Engineering Village, Dialog
外文全文数据库检索 OVID Full Text, EBSCOhost, Elsevier SDOS, SpringLink, ProQuest Medical Library, Kluwer Online Journals OCLC FirstSearch
（2002年起可以采用全称）
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Q：如何查询著者Yang发表的论文？
Yang
Yin-Yang[mh] OR Yang[TW]
用：Yang[AU]
47

Q:利用基本检索时，如果要作一些限定，如何实现？（举例：检索“颅脑外伤对
青少年及儿童生长激素的影响”）
48
利用limits
49
limits
时间文献类型研究类别子集文本选项语种性别
MH - Lymphedema/*epidemiology
SO - Am J Surg 2004 Jan;187(1):69-72.
22

《医学主题词表》(医学主题注释词顺表）（Medical Subject Headings)(MESH表）
23
MESH特性（优势）：规范
10例AIDS病人死亡因素分析 1例艾滋病患者的诊断爱滋病患者常见之口腔表征治疗获得性免疫缺陷综合征病人的健康教育主题词：获得性免疫缺陷综合征
web sites
获取全文2
14
PubMed Central (/pmc/)
15
查找的文章提供两种格式
16
可在主页选择其他数据库检索
17
பைடு நூலகம்
1. Pubmed的文献来源

Medline In-process citations Publisher-Supplied Citations
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MESH字段(MEDLINE格式)
TI - Lymphedema after treatment of breast cancer. MH - Axilla MH - Breast Neoplasms/*surgery MH - Lymph Node Excision/*adverse effects
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MESH特性：两种形式
自然语言顺序：心理学试验倒装形式：心理学，临床心理学，比较心理学，教育心理学，实验心理学，医学
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三、检索途径与方法

基本检索高级检索:Advanced Search 其他：Pubmed Tools,Pubmed
Resources
28
主页
29
Q:遇到一个课题时,该选择何种检索方式?
neoplasms"[All Fields] OR ("liver"[All Fields]
AND "cancer"[All Fields]) OR "liver cancer"[All Fields]) AND ("gene therapy"[MeSH Terms] OR ("gene"[All Fields] AND "therapy"[All Fields]) OR "gene therapy"[All Fields])
年龄
字段
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craniocerebral trauma AND growth hormone
选择all child:0-18years
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检索结果
52
高级检索
Search builder
Search history
More resoures
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其他

Journals Database(查询期刊信息并检索)
12
主页
PubMed comprises more than 20 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher 13
38
•词语检索

自动词语匹配功能：输入未加任何限定的检索词时，系统依次进行匹配、转换和检索：MeSH转换表刊名转换表著者索引
39
liver cancer AND gene therapy 2744篇
("liver neoplasms"[MeSH Terms] OR ("liver"[All Fields] AND "neoplasms"[All Fields]) OR "liver
8
联机检索

1964年开发MEDLARS，MEDLINE成为
使用频率最高的数据库
9
光盘检索
1980s至今 SilverPlatter Medline on CD(银盘)

10
光盘
11
二、PubMed概述（P.67）
检索系统:
NCBI
免费：检索:
最强、查全率高
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记录标识（1）
[PubMed - in process]
[ PubMed - as supplied by publisher]
[PubMed – indexed 19 for Medline]
2. PubMed记录的字段

可供检索和显示的字段共60多个 (表4-1-1)
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MEDLINE格式

2
中南大学图书馆（）
3
校园网外文数据库（）
4
Medline与PubMed
一、Medline概述 1.书目数据库: NLM, 最重要 2. 来源： 5200+ 期刊（ 80+ 国家 , (LSTRC), ） 90%英文，涉及医学各领域 3.获取: 印刷、联机、光盘、网络
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精确短语检索

使用引号
“liver cancer” liver cancer
6987篇 146836篇
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截词检索：加*(截取前600个截词)
检索：Immun* Immun[All Fields] OR immun21[All Fields] OR immun68[All Fields] OR immun70[All Fields] OR immuna[All Fields] OR immunabeled[All Fields] OR immunablation[All Fields] OR immunabsorbant[All Fields] OR immunabsorbent[All Fields] OR immunabsorption[All Fields] OR immunabwehr[All Fields] OR immunabwehrreaktionen[All Fields] …… 42