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Kiyoshi Tanikawa Takamichi Enomoto Masahiro Hatano Keiko Motegi Zenjiro Okuno 《Macromolecular chemistry and physics.》1975,176(10):3025-3034
Poly(N-vinylcarbazole), (PNVC), was prepared, fractionated by gel permeation chromatography, and then characterized by viscometry and vapour pressure osmometry. The fractionated PNVC species with relatively narrow molecular weight distributions were successfully used to measure both their electrical dark-conductivity and photoconductivity using a surface type cell in high vacuum (ca. 10?7 mm Hg) at room temperature. A molecular weight dependent photoconductivity was found for the fractionated PNVCs with weight average molecular weights in the range of 1,2·103 to 2,4·105. This observation is in contradiction to Epping's results who has found a molecular weight independent photoconductivity in the molecular weight range of 3·105 to 7·106. Our molecular weight dependence may be well understood in terms of the interrupted overlap of the π-electrons of adjacent carbazolyl groups at the terminal parts of the polymer chains, this effect being all the more stronger the smaller the molecular weight is. 相似文献
74.
A novel insertional mutation at exon VII of the myelin proteolipid protein gene in Pelizaeus -- Merzbacher disease 总被引:1,自引:0,他引:1
Kurosawa Kenjl; Iwakl Akiko; Miyake Sho-ta; Imaizuml Kiyoshi; Kuroki Yoshikazu; Fukumakl Yasuyuki 《Human molecular genetics》1993,2(12):2187-2189
Pelizaeus Merzbacher disease (PMD) is an X-linked neurologicaldisorder characterized by dysmyelination in the central nervoussystem (CNS). Recently mutations of the myelln proteollpid protein(PLP) gene which encodes both PLP and Its Isoform, DM-20 generatedby alternative spllcing, have been demonstrated In PMD patients.We analyzed the seven exons of the PLP gene of a Japanese boyaffected with PMD by direct sequencing and identified an Insertionevent In exon Vll of the PLP gene. This mutation was also presentIn his carrier mother, but was absent In ninety-five X chromosomesof normal Japanese. The frame-shift mutation leads to the productionof truncated PLP with altered carboxyl terminal amlno acid sequences,resulting In conslderable change of the structure of PLP andDM-20 necessary for functional purposes. This is the first reportof a mutation In exon Vll of the PLP gene associated with PMD. 相似文献
75.
Kiyoshi Imaizumi Junko Kimura Mari Matsuo Kenji Kurosawa Mitsuo Masuno Norio Niikawa Yoshikazu Kuroki 《American journal of medical genetics》2002,107(1):58-60
We describe a de novo balanced reciprocal translocation between the long arms of chromosomes 5 and 8 [46,XX,t(5;8)(q35;q24.1)] in a 15-month-old girl with a typical Sotos syndrome phenotype. Involvement of the 5q35 region was previously reported (Maroun et al. [1994: Am J Med Genet 50:291-293]) as one of translocation breakpoints in the present patient. We suggest that the gene responsible for Sotos syndrome is located to a distal long-arm region of chromosome 5. 相似文献
76.
Charcot-Marie-Tooth disease (CMT) is a heterogeneous disorder and is traditionally classified into two major types, CMT type 1 (CMT1) and CMT type 2 (CMT2). Most CMT1 patients are associated with the duplication of 17p11.2-p12 (CMT1A duplication) and small numbers of patients have mutations of the peripheral myelin protein 22 (PMP22), myelin protein zero (MPZ), connexin 32 (Cx32/GJB1), and early growth response 2 (EGR2) genes. Some mutations of MPZ and Cx32 were also associated with the clinical CMT2 phenotype. We constructed denaturing gradient gel electrophoresis (DGGE) analysis as a screening method for PMP22, MPZ, and Cx32 mutations and studied 161 CMT patients without CMT1A duplication. We detected 27 mutations of three genes including 15 novel mutations; six of PMP22, three of MPZ, and six of Cx32. We finally identified 21 causative mutations in 22 unrelated patients and five polymorphic mutations. Eighteen of 22 patients carrying PMP22, MPZ, or Cx32 mutations presented with CMT1 and four of them with MPZ or Cx32 mutations presented with the CMT2 phenotype. DGGE analysis was sensitive for screening for those gene mutations, but causative gene mutation was not identified in many of the Japanese patients with CMT, especially with CMT1. Other candidate genes should be studied to elucidate the genetic basis of Japanese CMT patients. 相似文献
77.
Shin Kobayashi Hiraku Uemura Takashi Kohda Toshiro Nagai Yasutsugu Chinen Kenji Naritomi Ei‐ichi Kinoshita Hirofumi Ohashi Kiyoshi Imaizumi Masato Tsukahara Yoshitsugu Sugio Hidefumi Tonoki Tatsuya Kishino Toshiaki Tanaka Masao Yamada Osamu Tsutsumi Norio Niikawa Tomoko Kaneko‐Ishino Fumitoshi Ishino 《American journal of medical genetics. Part A》2001,104(3):225-231
Silver‐Russell syndrome (SRS) is characterized by prenatal and postnatal growth retardation with morphologic anomalies. Maternal uniparental disomy 7 has been reported in some SRS patients. PEG1/MEST is an imprinted gene on chromosome 7q32 that is expressed only from the paternal allele and is a candidate gene for SRS. To clarify its biological function and role in SRS, we screened PEG1/MEST abnormalities in 15 SRS patients from various standpoints. In the lymphocytes of SRS patients, no aberrant expression patterns of two splice variants (α and β) of PEG1/MEST were detected when they were compared with normal samples. Direct sequence analysis failed to detect any mutations in the PEG1/MEST α coding region, and there were no significant mutations in the 5′‐flanking upstream region containing the predicted promoter and the highly conserved human/mouse genomic region. Differential methylation patterns of the CpG island for PEG1/MEST α were normally maintained and resulted in the same pattern as in the normal control, suggesting that there was no loss of imprinting. These findings suggest that PEG1/MEST can be excluded as a major determinant of SRS. © 2001 Wiley‐Liss, Inc. 相似文献
78.
Analysis of human erythrocyte 5'-nucleotidases in healthy individuals and a patient deficient in pyrimidine 5'-nucleotidase 总被引:2,自引:1,他引:2
Electrophoretic and quantitative analysis of pyrimidine 5'-nucleotidase in human erythrocytes from healthy individuals and a patient deficient in pyrimidine 5'-nucleotidase, using a range of substrates, has shown that the patient has a marked deficiency with UMP, CMP and dCMP as substrates but near normal levels of activity with dUMP and dTMP as substrates. The observations suggest that two separate structural gene loci coding for distinct 5'-nucleotidases with similar electrophoretic mobility exist in man. The genetic determination of these enzymes seems therefore to be homologous with that found in rodents. 相似文献
79.
Requirement of IL-5 for induction of autoimmune hemolytic anemia in anti-red blood cell autoantibody transgenic mice 总被引:2,自引:0,他引:2
Sakiyama Toshio; Ikuta Koichi; Nisitani Sazuku; Takatsu Kiyoshi; Honjo Tasuku 《International immunology》1999,11(6):995-1000
IL-5, IL-10 and lipopolysaccharide (LPS) are known to activateB-1 cells in vivo in normal mice and anti-red blood cell autoantibodytransgenic mice (HL mice). To assess the exact role of IL-5in proliferation and activation of peritoneal B-1 cells, weanalyzed IL-5 receptor chain-deficient HL (IL-5R/x HL) mice generated by the cross between IL-5R/and HL mice. In IL-5R/ x HL mice, Ig-producingB-1 cells in the peritoneal cavity were negligible, althoughthe total number of B-1 cells in the peritoneal cavity wereas many as 30% of that in HL mice. Moreover, LPS- or IL-10-induceddifferentiation of B-1 cells into antibody-producing cells wasseverely impaired in IL-5R/ x HL mice. We alsoused in vivo 5-bromo-2'-deoxyuridine labeling to estimate theproliferation of B-1 cells in IL-5R/ mice. Theabsence of IL-5R did not affect spontaneous proliferation ofperitoneal B-1 cells. However, induced proliferation of peritorealB-1 cells by oral administration of LPS was markedly impairedin IL-5R/ mice. These results suggest that IL-5is required for activation-associated proliferation of B-1 cellsbut not for their spontaneous proliferation and support theidea that IL-5 plays an important role on the induction of autoantibodyproduction from B-1 cells. 相似文献
80.