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51.
52.
Senderek J Hermanns B Lehmann U Bergmann C Marx G Kabus C Timmerman V Stoltenburg-Didinger G Schröder JM 《Brain pathology (Zurich, Switzerland)》2000,10(2):235-248
Mutations in the gene for the major protein component of peripheral nerve myelin, myelin protein zero (MPZ, P0), cause hereditary disorders of Schwann cell myelin such as Charcot-Marie-Tooth neuropathy type 1B (CMT1B), Dejerine-Sottas syndrome (DSS), and congenital hypomyelinating neuropathy (CHN). More recently, P0 mutations were identified in the axonal type of CMT neuropathy, CMT2, which is different from the demyelinating variants with respect to electroneurography and nerve pathology. We screened 49 patients with a clinical and histopathological diagnosis of CMT2 for mutations in the P0 gene. Three heterozygous single nucleotide changes were detected: two novel missense mutations, Asp61Gly and Tyr119Cys, and the known Thr124Met substitution, that has already been reported in several CMT patients from different European countries. Haplotype analysis for the P0 locus proved that our patients with the 124Met allele were not related to a cohort of patients with the same mutation, all of Belgian descent and all found to share a common ancestor. Our data suggest that P0 mutations account for a detectable proportion of CMT2 cases with virtually every patient harbouring a different mutation but recurrence of the Thr124Met amino acid substitution. The high frequency of this peculiar genotype in the European CMT population is presumably not only due to a founder effect but Thr124Met might constitute a mutation hotspot in the P0 gene as well. 相似文献
53.
Georg Kb Gerhard Brandl Alexander Marx Hartmut Wekerle Monika Bradl 《European journal of immunology》1996,26(5):981-988
In the Lewis rat, myelin basic protein (MBP)-specific, encephalitogenic T cells preferentially recognize sequence 68–88, and use the Vβ8.2 gene to encode their T cell receptors. To analyze the structural prerequisites for the development of the MBP-specific T cell repertoire, we reconstituted severe-combined immunodeficient (SCID) mice with fetal (embryonic day 15–16) Lewis rat lymphoid tissue, and then isolated MBP-specific T cell lines from the adult chimeras after immunization. Two types of chimera were constructed: SCID mice reconstituted with rat fetal liver cells only, allowing T cell maturation within a chimeric SCID thymus consisting of mouse thymic epithelium and rat interdigitating dendritic cells, and SCID mice reconstituted with rat fetal liver cells and rat fetal thymus grafts, allowing T cell maturation within the chimeric SCID and the intact Lewis rat thymic microenvironment. Without exception, the T cell lines isolated from MBP-immunized SCID chimeras were restricted by MHC class II of the Lewis rat (RT1.B1), and none by I-Ad of the SCID mouse. Most of the T cell lines recognized the immunodominant MBP epitope 68–88. In striking contrast to intact Lewis rats, in SCID mice reconstituted by rat fetal liver only, MBP-specific T cell clones used a seemingly random repertoire of Vβ genes without a bias for Vβ8.2. In chimeras containing fetal Lewis liver plus fetal thymus grafted under the kidney capsule, however, dominant utilization of Vβ8.2 was restored. The migration of liver-derived stem cells through rat thymus grafts was documented by combining fetal tissues from wild-type and transgenic Lewis rats. The results confirm that the recognition of the immunodominant epitope 68–88 by MBP-specific encephalitogenic T cells is a genetically determined feature of the Lewis rat T cell repertoire. They further suggest that the formation of the repertoire requires T cell differentiation in a syngeneic thymic microenvironment. 相似文献
54.
55.
Parathyroid mitogenic activity in plasma from patients with familial multiple endocrine neoplasia type 1 总被引:6,自引:0,他引:6
M L Brandi G D Aurbach L A Fitzpatrick R Quarto A M Spiegel M M Bliziotes J A Norton J L Doppman S J Marx 《The New England journal of medicine》1986,314(20):1287-1293
Hyperplasia of the parathyroid glands is a central feature of familial multiple endocrine neoplasia type 1. We used cultured bovine parathyroid cells to test for mitogenic activity in plasma from patients with this disorder. Normal plasma stimulated [3H]thymidine incorporation, on the average, to the same extent as it was stimulated in a plasma-free control culture. This contrasted with the results of the tests with plasma from patients with familial multiple endocrine neoplasia type 1, in which parathyroid mitogenic activity increased 2400 percent over the control value (P less than 0.001). Plasma from these patients also stimulated the proliferation of bovine parathyroid cells in culture, whereas plasma from normal subjects inhibited it. Parathyroid mitogenic activity in plasma from the patients with familial multiple endocrine neoplasia type 1 was greater than that in plasma from patients with various other disorders, including sporadic primary hyperparathyroidism (with adenoma, hyperplasia, or cancer of the parathyroid), sporadic primary hypergastrinemia, sporadic pituitary tumor, familial hypocalciuric hypercalcemia, and multiple endocrine neoplasia type 2 (P less than 0.05). Parathyroid mitogenic activity in the plasma of patients with familial multiple endocrine neoplasia type 1 persisted for up to four years after total parathyroidectomy. The plasma also had far more mitogenic activity in cultures of parathyroid cells than did optimal concentrations of known growth factors or of any parathyroid secretagogue. This mitogenic activity had an apparent molecular weight of 50,000 to 55,000. We conclude that primary hyperparathyroidism in familial multiple endocrine neoplasia type 1 may have a humoral cause. 相似文献
56.
Continuous production of Rous sarcoma virus free of transformation defective virus in clones of established RSV-transformed quail cells 总被引:3,自引:0,他引:3
Quail embryo fibroblasts were infected with a Schmidt-Ruppin strain RSV × chf recombinant virus. Virus-transformed cells were established as a permanent line and then cloned in methyl cellulose. Out of 140 clones isolated four clones were capable of indefinite growth. These clones were examined for (i) production of sarcoma and td virus particles, (ii) number of integrated virus genome equivalents, and (iii) deletions of the src gene in the provirus. We found that the clones yield about 106 focus-forming units of the sarcoma virus per milliliter of the culture medium. No td virus could be detected by plating of the virus at the endpoint dilution and no 35 S td virus RNA but only 38 S sarcoma virus RNA was found in virions. Hybridization kinetic studies indicated that three different clones contain about 2 virus genome equivalents, and one clone contains about 4 virus genome equivalents per diploid cell. Upon transfection the proviruses of different clones generated sarcoma viruses and no td viruses. Finally digestion with EcoRI restriction endonuclease released in all four clones a 1.9 × 106-dalton fragment characteristic of the complete src gene, while no 0.8 × 106-dalton fragment characteristic of a td provirus could be detected. We concluded that the clones of RSV-transformed quail cells contain only nondefective sarcoma proviruses and produce from these proviruses nondefective focus-forming virions in the absence of any segregant td virions. 相似文献
57.
58.
H. Scheller H. E. Bock M. Knedel R. Marx Linneweh Struppler Schettler F. Strnad 《Journal of molecular medicine (Berlin, Germany)》1958,36(7):334-336
Ohne Zusammenfassung 相似文献
59.
Lymphocyte proliferation in response to acute heavy resistance exercise in women: influence of muscle strength and total work 总被引:3,自引:0,他引:3
Dohi K Mastro AM Miles MP Bush JA Grove DS Leach SK Volek JS Nindl BC Marx JO Gotshalk LA Putukian M Sebastianelli WJ Kraemer WJ 《European journal of applied physiology》2001,85(3-4):367-373
Little is understood about the immune responses to heavy resistance exercise. The purpose of this investigation was to determine
the influence of physical strength and the ability to do more total work on lymphocyte proliferation after an acute bout of
heavy resistance exercise. A group of 50 healthy but non-strength trained women were recruited for the study and tested for
their one repetition maximum (i.e. 1 RM or maximal mass lifted once). From the normal distribution of strength the top and
bottom 8 women [mean age 22.5 (SD 3.1) years] were asked to volunteer to define our two groups (i.e. high strength and low
strength). The two groups were significantly different (P<0.05) in 1 RM squat strength [low strength 39.9 (SD 4.6) kg, 0.65 (SD 0.08) kg·kg body mass–1 and high strength 72.2 (SD 10.7) kg, 1.1 (SD 0.12) kg·kg body mass–1] but were not significantly different in body mass, age, activity levels, and menstrual status (all in same phase). Each
performed a resistance exercise protocol consisting of six sets of 10 RM squats with 2 min rest between the sets. The 10 RM
loads and total work were significantly greater in the high strength group than in the low strength group. Blood samples were
obtained pre-exercise and immediately post-exercise for test for lactate (significant increase with exercise) and cortisol
(no changes) concentrations with no differences noted between groups. Immunological assays on the blood samples determined
the incorporation of tritiated thymidine by lymphocytes in responses to concanavalin A (ConA), phytohemagglutinin (PHA), and
pokeweed mitogen (PWM). Following the squat exercise, there was a significant decrease in lymphocyte responsiveness to PWM
in the high strength but not in the low strength group for both total proliferation and proliferation adjusted per B or T
cell. On the other hand, lymphocytes from the low strength group proliferated to a significantly greater extent (adjusted
per T cell) in response to ConA and PHA. These data indicate that the heavy resistance exercise protocol reduced the lymphocyte
proliferative responses only in the stronger group of subjects. This effect may have been due to the high absolute total work
and the greater exercise stress created by the resistance exercise protocol in the high strength group. Therefore, individuals
performing at the same relative exercise intensity (i.e. 10 RM) in a resistance exercise protocol may have different immune
responses stemming from differences in absolute total work performance.
Electronic Publication 相似文献
60.
Cloning and expression of the gene involved in Sanfilippo B syndrome (mucopolysaccharidosis III B) 总被引:4,自引:1,他引:4
Sanfilippo B syndrome is caused by a deficiency of alpha-N-
acetylglucosaminidase, a lysosomal enzyme involved in the degradation of
heparan sulphate. Accumulation of the substrate in lysosomes results in
degeneration of the central nervous system with progressive dementia often
combined with hyperactivity and aggressive behaviour. In order to clone the
deficient gene, we purified the enzyme from human placenta and obtained
amino acid sequence information. Alignment of one of the CNBr generated
internal peptides to sequence from the database revealed the chromosomal
location of the gene in the 5' upstream flanking region of the gene for
17-beta-hydroxysteroid-dehydrogenase at 17q21.1. The available DNA sequence
was used to clone the cDNA coding for alpha-N- acetylglucosaminidase and
analyse its gene structure. The gene is fully contained in the 5' upstream
flanking region of the gene for 17-beta- hydroxysteroid-dehydrogenase and
interrupted by five introns. The cDNA clone has a length of 2575 bp and
encodes a protein of 743 amino acids. Chinese hamster ovary cells
transfected with the cDNA construct show alpha-N-acetylglucosaminidase
activity about 17-fold over background. This will allow correction studies
with NAG deficient Sanfilippo B cell lines and facilitate the development
of enzyme replacement therapy for these patients.
相似文献