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Zusammenfassung
Entstehung und Progression von Tumoren werden durch Funktionsst?rungen von spezifischen Genen gesteuert. Obwohl das Prostatakarzinom
zu den h?ufigsten Tumoren geh?rt, ist über die bei diesem Tumor involvierten Gene wenig bekannt. Zytogenetische und molekulare
Untersuchungen haben gezeigt, da? chromosomale Deletionen besonders h?ufig das Y-Chromosom, 7q, 8p, 10q, 13q, 16q und 17p
betreffen. Diese Loci dürften für das Prostatakarzinom relevante Tumorsuppressorgene enthalten. H?ufige DNS-Sequenzvermehrungen
von Chromosom 7, 8q und 11q deuten auf die Lokalisation von m?glichen Onkogenen hin. Bereits heute bestehen Anhaltspunkte
für eine Prognoserelevanz genetischer Ver?nderungen. Der Nachweis von Polysomien in Prim?rtumoren deuten auf eine ungünstige
Prognose hin. Eine Amplifikation des Androgenrezeptors spricht für einen Hormontherapie-resistenten Tumor, welcher m?glicherweise
besonders gut auf eine totale Androgenblockade ansprechen wird. Die Identifikation der alterierten Gene und die Entschlüsselung
ihrer Funktion k?nnte in Zukunft zu deutlich verbesserten Behandlungsstretegien für Patienten mit Prostatakarzinom führten.
相似文献
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Three hundred seven newborns were examined clinically and by ultrasound for congenital dysplasia of the hip (CDH). The purpose of the study was to determine the prevalence of sonographic abnormalities and to discover if sonography could be helpful in detecting cases of CDH that would be missed by clinical diagnosis alone. Eighty-two hips (13.4%) had ultrasound abnormalities despite a normal clinical examination. Of these, three developed definite hip dysplasia. The remaining 79 hips became clinically and sonographically normal within 12 weeks. Ultrasound visualized and recorded the dislocation-reposition maneuver of three other hips that were clinically dislocatable at birth. Dislocation occurred in a craniodorsal direction. 相似文献
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Mary ER O'Brien Janet Hardy Sylvia Tan Jackie Walling Brian Peters Sarah Hatty Eve Wiltshaw 《Cancer chemotherapy and pharmacology》1992,30(3):245-248
Summary A total of 16 patients with recurrent epithelial ovarian cancer were treated with sulofenur (LY 186641), a novel oral sulfonylurea. All subjects had received previous chemotherapy. Anaemia occurred in all 16 patients, 14 of whom required a blood transfusion, and 2/16 patients received methylene blue for breathlessness due to methaemaglobinaemia. Treatment was discontinued in 2/16 cases due to rising liver enzyme values, which reverted to normal on cessation of the drug. There was no nausea or alopecia. Only two minor responses were seen. Plasma drug levels were insufficient to result in antitumour activity as extrapolated from animal data. Further studies that attempt to increase the bioavailability and improve the therapeutic index are warranted. 相似文献
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Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group 总被引:5,自引:0,他引:5
Haines JL; Terwedow HA; Burgess K; Pericak-Vance MA; Rimmler JB; Martin ER; Oksenberg JR; Lincoln R; Zhang DY; Banatao DR; Gatto N; Goodkin DE; Hauser SL 《Human molecular genetics》1998,7(8):1229-1234
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system. While its etiology is not well understood, genetic
factors are clearly involved. Until recently, most genetic studies in MS
have been association studies using the case-control design testing
specific candidate genes and studying only sporadic cases. The only
consistently replicated finding has been an association with the HLA-DR2
allele within the major histocompatibility complex (MHC) on chromosome 6.
Using the genetic linkage design, however, evidence for and against linkage
of the MHC to MS has been found, fostering suggestions that sporadic and
familial MS have different etiologies. Most recently, two of four genomic
screens demonstrated linkage to the MHC, although specific allelic
associations were not tested. Here, a dataset of 98 multiplex families was
studied to test for an association to the HLA-DR2 allele in familial MS and
to determine if genetic linkage to the MHC was due solely to such an
association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta)
in the MHC demonstrated strong genetic linkage (parametric lod scores of
4.60, 2.20 and 1.24, respectively) and a specific association with the
HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results
by HLA-DR2 status showed that the linkage results were limited to families
segregating HLA-DR2 alleles. These results demonstrate that genetic linkage
to the MHC can be explained by the HLA-DR2 allelic association. They also
indicate that sporadic and familial MS share a common genetic
susceptibility. In addition, preliminary calculations suggest that the MHC
explains between 17 and 62% of the genetic etiology of MS. This
heterogeneity is also supported by the minority of families showing no
linkage or association with loci within the MHC.
相似文献
8.
Physical Deletion of the p53 Gene in Bladder Cancer: Detection by Fluorescence in Situ Hybridization 总被引:1,自引:6,他引:1 下载免费PDF全文
Guido Sauter Guoren Deng Holger Moch Russell Kerschmann Kouji Matsumura Sandy De Vries Tracy George Jose Fuentes Peter Carroll Michael J. Mihatsch Frederic M. Waldman 《The American journal of pathology》1994,144(4):756-766
To understand better the role of physical p53 deletion in bladder cancer, 106 formalin-fixed and 45 unfixed bladder tumors were examined using fluorescence in situ hybridization. Probes for centromere 17 and the p53 locus were hybridized simultaneously to interphase tumor cells to analyze p53 and chromosome 17 copy number on a cell by cell basis. 17p deletion was found in four of 43 pTa tumors, 18 of 43 pT1 tumors and 29 of 58 pT2-4 tumors (P = 0.0001). 17p deletion was also highly correlated with grade (P = 0.0001) and with p53 immunostaining (P = 0.0005). Chromosome 17 polysomy was associated with stage, grade, 17p deletions, and p53 immunostaining (P = 0.0001). The strong difference in centromere 17 copy number and 17p deletions between pTa and pT1 tumors supports a relevant biological distinction between pTa and pT1 tumors. 相似文献
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Chromosome 8p deletions are associated with invasive tumor growth in urinary bladder cancer. 总被引:6,自引:2,他引:6 下载免费PDF全文
U. Wagner L. Bubendorf T. C. Gasser H. Moch J. P. Grg J. Richter M. J. Mihatsch F. M. Waldman G. Sauter 《The American journal of pathology》1997,151(3):753-759
Alterations of chromosome 8, including deletions of 8p, occur frequently in many tumors. In this study, fluorescence in situ hybridization was used to study the relationship between 8p deletions, 8q gains, and phenotype in bladder cancer. Cells from 87 tumors were examined by dual-labeling fluorescence in situ hybridization with a centromere 8 probe (pJM12) and P1 probes for 8p22, 8p12, 8q12, and 8q24. Both 8p22 deletions and 8q24 gains were strongly associated with tumor phenotype. There was a marked difference in 8p22 deletions between noninvasive (pTa) tumors (3/33) and minimally invasive (pT1) tumors (8/19; P = 0.005) whereas there was no significant difference between pT1 and muscle-invasive (pT2-4) tumors (19/35; P = 0.3926). Six tumors with 8p22 deletion were examined at 8p12. Three of these tumors showed no 8p12 deletion, narrowing down the site of a putative tumor suppressor gene distal to 8p12. In one other case, there was a marked increase in 8p12 copy number (> 40 per cell; amplification), suggesting the presence of an oncogene involved in bladder cancer at 8p12. The marked difference in 8p22 deletions between noninvasive (pTa) and minimally invasive (pT1) tumors is consistent with a role of a putative tumor suppressor gene on 8p for development of invasive tumor phenotype. 相似文献