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B. Leveugle B. A. Faucheux C. Bouras N. Nillesse G. Spik E. C. Hirsch Y. Agid P. R. Hof 《Acta neuropathologica》1996,91(6):566-572
Changes in the distribution of the iron-binding protein lactotransferrin have recently been described in the central nervous
system during a variety of neurodegenerative disorders. To investigate whether lactotransferrin is associated with the neuropathological
changes that characterize Parkinson’s disease, we analyzed the distribution of this protein in the mesencephalon of neurologically
normal individuals and patients affected with Parkinson’s disease using quantitative immunohistochemical methods. High levels
of lactotransferrin were observed in a large population of neurons in the substantia nigra of control cases. Lactotransferrin-positive
neurons were severely affected by the neurodegenerative process that occurs in Parkinson’s disease as indicated by a severe
decrease in the number of immunolabeled neurons in all of these cases. Quantitative analysis also demonstrated higher immunolabeling
levels of lactotransferrin in the surviving neurons in the substantia nigra and ventral tegmental area of Parkinson’s disease
cases compared to control cases. These results suggest that lactotransferrin may participate actively in the mechanism of
neuronal degeneration in Parkinson’s disease.
Received: 16 October 1995 / Revised, accepted: 1 December 1995 相似文献
4.
Absence of the amyloid precursor protein gene mutation (APP717: Val->Ile) in 85 cases of early onset Alzheimer''s disease.
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5.
Comparison of positive allergy skin tests among asthmatic children from rural and urban areas living within small geographic area. 总被引:1,自引:0,他引:1
Haim Bibi David Shoseyov David Feigenbaum Pnina Nir Rosa Shiachi Shimon Scharff Ronit Peled 《Annals of allergy, asthma & immunology》2002,88(4):416-420
BACKGROUND: Evidence of increased asthma and allergic response among urban versus rural residents has been reported. OBJECTIVE: To evaluate the prevalence of allergic response among asthmatic children from urban and rural areas living within close proximity. METHODS: In all, 448 asthmatic children from urban (363) and rural (85) areas were studied. The study group consisted of 234 9-year-olds and 214 12-year-olds. A health questionnaire was completed on each child who subsequently underwent allergic skin prick tests (SPTs). RESULTS: There was significantly more positive SPT response to house-dust mite, mold, cat, and cypress among asthmatic children from urban areas compared with children living in rural areas: 58.3% versus 37.6%, 46.1% versus 31.8%, 17.45 versus 5.9%, and 26.2% versus 15.3%, respectively. Positive SPT for indoor allergens were significantly greater among asthmatic urban residents than asthmatic rural residents: 63.3% versus 45.5%, respectively (P < 0.02). Positive SPT response to all the allergens checked was higher among the 12-year-old age group when compared with the 9-year-olds, 34.6% versus 22.7%, respectively (P = 0.05). CONCLUSIONS: Allergic response measured by SPT is significantly more common among asthmatic children from urban areas as opposed to rural, even though both areas are within small distance of one another. Further, asthmatic children living in urban areas demonstrated more allergic response to both indoor and outdoor allergens. The allergic response tends to increase with increased age in both urban and rural asthmatic children. 相似文献
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BACKGROUND: Omeprazole is an inhibitor of the parietal cell enzyme H+/K+ adenosine triphosphatase. Immediate-type hypersensitivity reactions, such as urticaria, angioedema, and hypotension, induced by omeprazole and other proton pump inhibitors are rare. OBJECTIVES: To confirm the immediate-type mechanism of recurrent anaphylactic reactions to the repeated administration of omeprazole using skin testing and to enable safe administration of the drug after successful oral desensitization. METHODS: Intradermal skin tests were performed with omeprazole (0.04 and 0.4 mg/mL) prepared from the oral and intravenous commercial preparations and with pantoprazole (0.02 and 0.2 mg/mL) prepared from the oral commercial preparation. Skin tests were repeated after completion of the desensitization. Oral desensitization was applied at a starting dose of 0.001 mg of omeprazole, and a full dose of 16 mg was achieved after 5.6 hours (cumulative dose of 32.6 mg). RESULTS: Intradermal skin test results were positive to omeprazole and pantoprazole at all tested concentrations. After successful desensitization, omeprazole was administered in the full dose uneventfully. The wheal size of the intradermal skin tests performed after completion of the desensitization was significantly reduced. CONCLUSION: When indicated, this newly designed desensitization protocol may be used in patients with omeprazole-induced anaphylaxis. 相似文献
8.
S. Hunot V. Bernard B. Faucheux F. Boissière E. Leguern C. Brana P. P. Gautris J. Guérin B. Bloch Y. Agid E. C. Hirsch 《Journal of neural transmission (Vienna, Austria : 1996)》1996,103(8-9):1043-1052
Summary Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopaminergic neurons. Since dopaminergic neurons degenerate in Parkinson's disease, this factor is a potential therapeutical tool that may save dopaminergic neurons during the pathological process. Moreover, a reduced GDNF expression may be involved in the pathophysiology of the disease. In this study, we tested whether altered GDNF production may participate in the mechanism of cell death in this disease. GDNF gene expression was analyzed by in situ hybridization using riboprobes corresponding to a sequence of the exon 2 human GDNF gene. Experiments were performed on tissue sections of the mesencephalon and the striatum from 8 patients with Parkinson's disease and 6 control subjects matched for age at death and for post mortem delay. No labelling was observed in either group of patients. This absence of detectable expression could not be attributed to methodological problems as a positive staining was observed using the same probes for sections of astroglioma biopsies from human adults and for sections of a newborn infant brain obtained at post-mortem. These data suggest that GDNF is probably expressed at a very low level in the adult human brain and its involvement in the pathophysiology of Parkinson's disease remains to be demonstrated. GDNF may represent a powerful new therapeutic agent for Parkinson's disease, however. 相似文献
9.
Spinocerebellar ataxia type 7 (SCA7): a neurodegenerative disorder with neuronal intranuclear inclusions 总被引:8,自引:13,他引:8
Holmberg M; Duyckaerts C; Durr A; Cancel G; Gourfinkel-An I; Damier P; Faucheux B; Trottier Y; Hirsch EC; Agid Y; Brice A 《Human molecular genetics》1998,7(5):913-918
Autosomal dominant cerebellar ataxia with progressive macular degeneration
is caused by a CAG/glutamine repeat expansion in the SCA7 gene/protein.
Neuronal intranuclear inclusions were detected in the brain of an early
onset SCA7 case with the 1C2 antibody directed against an expanded
polyglutamine domain. Nuclear inclusions were most frequent in the inferior
olivary complex, a site of severe neuronal loss in SCA7. They were also
observed in other brain regions, including the cerebral cortex, not
considered to be affected in the disease. Using confocal microscopy we
showed that some inclusions were ubiquitinated, but to varying degrees,
ranging from <1% in the cerebral cortex to 60% in the inferior olive. In
addition, we also observed cytoplasmic staining using the 1C2 antibody,
particularly in the supramarginal gyrus, the hippocampus, the thalamus, the
lateral geniculate body and the pontine nuclei. These data confirm that the
presence of intranuclear inclusions in neurons is a common characteristic
of disorders caused by CAG/polyglutamine expansions, but unlike what has
been reported for Huntington's disease, SCA1 and SCA3/MJD, in SCA7 the
inclusions were not restricted to the sites of severe neuronal loss.
相似文献
10.
Screening for proteins with polyglutamine expansions in autosomal dominant cerebellar ataxias 总被引:2,自引:8,他引:2
Stevanin G; Trottier Y; Cancel G; Durr A; David G; Didierjean O; Burk K; Imbert G; Saudou F; Abada-Bendib M; Gourfinkel-An I; Benomar A; Abbas N; Klockgether T; Grid D; Agid Y; Mandel JL; Brice A 《Human molecular genetics》1996,5(12):1887-1892
Expansion of trinucleotide CAG repeats coding for polyglutamine has been
implicated in five neurodegenerative disorders, including spinocerebellar
ataxia (SCA) 1 and SCA3 or Machado-Joseph disease (SCA3/MJD), two forms of
type I autosomal dominant cerebellar ataxias (ADCA). Using the 1C2 antibody
which specifically recognizes large polyglutamine tracts, particularly
those that are expanded, we recently reported the detection of proteins
with pathological glutamine expansions in lymphoblasts from another form of
ADCA type I, SCA2, as well as from patients presenting with the distinct
phenotype of ADCA type II. We now have screened a large series of patients
with ADCA or isolated cases with cerebellar ataxia, for the presence of
proteins with polyglutamine expansions. A 150 kDa SCA2 protein was detected
in 16 out of 40 families with ADCA type I. This corresponds to 24% of all
ADCA type I families, which is much more frequent than SCA1 in this series
of patients (13%). The signal intensity of the SCA2 protein was negatively
correlated to age at onset, as expected for an expanded and unstable
trinucleotide repeat mutation. The disease segregated with markers closely
linked to the SCA2 locus in all identified SCA2 families. In addition, a
specific 130 kDa protein, which segregated with the disease, was detected
in lymphoblasts of patients from nine families with ADCA type II. It was
also visualized in the cerebral cortex of one of the patients,
demonstrating its translation in the nervous system. Finally, no new
disease-related proteins containing expanded polyglutamine tracts could be
detected in lymphoblasts from the remaining patients with ADCA or isolated
cases with cerebellar ataxia.
相似文献