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101.
The palpation and enucleation of occult insulinomas (less than 15 mm) can be a difficult surgical problem even with good arteriographic localization. In the authors' limited experience, confirmation of arteriographic findings by pancreatic venous sampling provided little additional localizing information. However, if arteriography is negative or equivocal, venous sampling can indicate the segment of pancreas to be "blindly" resected if the adenoma is not palpable. Venous sampling may be misleading in polyendocrine syndromes because of the frequency of multiple adenomas and variable hormone production. 相似文献
102.
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
103.
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
104.
Distribution of mutations in the PEX gene in families with X-linked hypophosphataemic rickets (HYP) 总被引:8,自引:0,他引:8
Rowe PS; Oudet CL; Francis F; Sinding C; Pannetier S; Econs MJ; Strom TM; Meitinger T; Garabedian M; David A; Macher MA; Questiaux E; Popowska E; Pronicka E; Read AP; Mokrzycki A; Glorieux FH; Drezner MK; Hanauer A; Lehrach H; Goulding JN; O'Riordan JL 《Human molecular genetics》1997,6(4):539-549
Mutations in the PEX gene at Xp22.1 (phosphate-regulating gene with
homologies to endopeptidases, on the X-chromosome), are responsible for
X-linked hypophosphataemic rickets (HYP). Homology of PEX to the M13 family
of Zn2+ metallopeptidases which include neprilysin (NEP) as prototype, has
raised important questions regarding PEX function at the molecular level.
The aim of this study was to analyse 99 HYP families for PEX gene
mutations, and to correlate predicted changes in the protein structure with
Zn2+ metallopeptidase gene function. Primers flanking 22 characterised
exons were used to amplify DNA by PCR, and SSCP was then used to screen for
mutations. Deletions, insertions, nonsense mutations, stop codons and
splice mutations occurred in 83% of families screened for in all 22 exons,
and 51% of a separate set of families screened in 17 PEX gene exons.
Missense mutations in four regions of the gene were informative regarding
function, with one mutation in the Zn2+-binding site predicted to alter
substrate enzyme interaction and catalysis. Computer analysis of the
remaining mutations predicted changes in secondary structure,
N-glycosylation, protein phosphorylation and catalytic site molecular
structure. The wide range of mutations that align with regions required for
protease activity in NEP suggests that PEX also functions as a protease,
and may act by processing factor(s) involved in bone mineral metabolism.
相似文献
105.
Stephania Donayre Pimentel Heather Adams Tamara Ellis Robin Clark Craig Sully Catherine Paré Michael JL. Sullivan 《Journal of traumatic stress》2020,33(5):731-740
Catastrophizing has been discussed as a cognitive precursor to the emergence of posttraumatic stress disorder (PTSD) symptoms following the experience of stressful events. Implicit in cognitive models of PTSD is that treatment-related reductions in catastrophizing should yield reductions in PTSD symptoms. The tenability of this prediction has yet to be tested. The present study investigated the sequential relation between changes in a specific form of catastrophizing—symptom catastrophizing—and changes in PTSD symptom severity in a sample of 73 work-disabled individuals enrolled in a 10-week behavioral activation intervention. Measures of symptom catastrophizing and PTSD symptom severity were completed at pre-, mid-, and posttreatment assessment points. Cross-sectional analyses of pretreatment data revealed that symptom catastrophizing accounted for significant variance in PTSD symptom severity, β = .40, p < .001, sr = .28 (medium effect size), even when controlling for known correlates of symptom catastrophizing, such as pain and depression. Significant reductions in symptom catastrophizing and PTSD symptoms were observed during treatment, with large effect sizes, ds = 1.42 and 0.94, respectively, ps < .001. Cross-lagged analyses revealed that early change in symptom catastrophizing predicted later change in PTSD symptoms; early changes in PTSD symptom severity did not predict later change in symptom catastrophizing. These findings are consistent with the conceptual models that posit a causal relation between catastrophizing and PTSD symptom severity. The clinical implications of the findings are discussed. 相似文献
106.
Conditioned medium (CM) obtained from a human hepatoma cell line, SK- HEP-1, contains colony-stimulating factors (CSFs) active on murine and human bone marrow-derived granulocyte and macrophage colony-forming units (CFU-GM) and a factor capable of inducing granulocyte-macrophage differentiation (GM-DF) of murine myelomonocytic leukemic cells WEHI- 3B(D+) and human promyelocytic leukemic cells HL-60 when assayed in semisolid agar cultures. The human active granulocyte-macrophage colony- stimulating factor (GM-CSF) for day 7 CFU-GM and the GM-DF for WEHI- 3B(D+) and for HL-60 are not separable by acrylamide agarose column chromatography, eluting at an apparent molecular weight between 20,000 and 35,000 daltons, or by isoelectric focusing (isoelectric point, pH 5.4). In addition, SK-HEP-1 CM contains erythroid burst-promoting activity (BPA) and a factor that promotes the growth of human mixed colonies. SK-HEP-1 cells, which grow as an adherent monolayer, appear not to be endothelial or monocytic in origin since by immunofluorescent staining they are negative for Ia (HLA-DR), monocyte antigen 1 and 2, lysozyme, and factor VIII-related antigen. Positive immunofluorescent staining for keratin and fibronectin suggests the possibility that SK- HEP-1 is an epithelial cell line. Constitutive production of GM-DF as well as other hematopoietic activities including GM-CSF, erythroid BPA, and an activity that promotes the growth of human mixed colony progenitors by a human epithelial tumor cell line, SK-HEP-1, suggests that this cell line is a valuable resource for both large-scale production of these factors and the cloning of the gene(s) that code for these regulators. 相似文献
107.
Joseph L Dieleman Alexander S Kaldjian Maitreyi Sahu Carina Chen Angela Liu Abby Chapin Kirstin Woody Scott Aleksandr Aravkin Peng Zheng Ali Mokdad Christopher JL Murray Kevin Schulman Arnold Milstein 《Health services research》2022,57(3):557
ObjectiveTo estimate health care systems'' value in treating major illnesses for each US state and identify system characteristics associated with value.Data sourcesAnnual condition‐specific death and incidence estimates for each US state from the Global Burden Disease 2019 Study and annual health care spending per person for each state from the National Health Expenditure Accounts.Study designUsing non‐linear meta‐stochastic frontier analysis, mortality incidence ratios for 136 major treatable illnesses were regressed separately on per capita health care spending and key covariates such as age, obesity, smoking, and educational attainment. State‐ and year‐specific inefficiency estimates were extracted for each health condition and combined to create a single estimate of health care delivery system value for each US state for each year, 1991–2014. The association between changes in health care value and changes in 23 key health care system characteristics and state policies was measured.Data collection/extraction methodsNot applicable.Principal findingsUS state with relatively high spending per person or relatively poor health‐outcomes were shown to have low health care delivery system value. New Jersey, Maryland, Florida, Arizona, and New York attained the highest value scores in 2014 (81 [95% uncertainty interval 72‐88], 80 [72‐87], 80 [71‐86], 77 [69‐84], and 77 [66‐85], respectively), after controlling for health care spending, age, obesity, smoking, physical activity, race, and educational attainment. Greater market concentration of hospitals and of insurers were associated with worse health care value (p‐value ranging from <0.01 to 0.02). Higher hospital geographic density and use were also associated with worse health care value (p‐value ranging from 0.03 to 0.05). Enrollment in Medicare Advantage HMOs was associated with better value, as was more generous Medicaid income eligibility (p‐value 0.04 and 0.01).ConclusionsSubstantial variation in the value of health care exists across states. Key health system characteristics such as market concentration and provider density were associated with value. 相似文献
108.
T O Stair M A Lippe H Russell J C Feeley 《The American journal of emergency medicine》1989,7(6):563-566
Demographic data and blood samples were collected from 278 patients seen at two District of Columbia emergency departments, and tetanus antitoxin assays by hemagglutination were performed at the Centers for Disease Control. Twenty-seven patients (10%) had antibody levels below the 0.01 U/mL considered protective. Four demographic characteristics were different in the patients with inadequate immunity (in decreasing order of significance): advanced age, fewer years of education, female sex, and non-US origin. Fourteen of the inadequately immunized patients were over 70 years of age. Of the 84 patients who reported their immunization histories, five reported no complete series of tetanus shots but had adequate antibody levels, while three reported a complete series but had inadequate levels. Twenty-two patients with inadequate immunity were not offered immunization in the emergency department because they did not have wounds. Patient recall of immunization history is not a reliable guide to tetanus immunization in the emergency department, but patients in certain demographic groups, such as older women, are more likely to have inadequate immunity. 相似文献
109.
110.