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71.
The dural type of spinal arteriovenous malformation (AVM) can be cured by excision or by embolization of the nidus. The common origin of the blood supply to the malformation and to the cord from the same segmental artery would profoundly affect therapeutic choices. This anatomic situation was encountered in two of nine such lesions. The angiographic appearance and the importance of recognizing this common origin is discussed. 相似文献
72.
73.
Pituitary microadenomas: a PET study 总被引:6,自引:0,他引:6
74.
二仙合剂可治疗妇女高血压,在腎型高血压狗也有降压效果。本文用5种高血压大白鼠(神經型、腎型、腎上腺燙伤型、睾丸切除型及卵巢切除型)来比較降压作用,并观察性周期、前庭时值及某些加压物质的升压反应。每天灌胃二仙合剂10克/公斤,共2周,神經型、腎型及睾丸切除型的降压面积%分别为-9,-11及-15%,与同型对照組比較,降压“显著”,腎上腺燙伤型及卵巢切除型的降压“不显著”。每天灌服二仙合剂10克/公斤,共7周,对未成熟大白鼠生长及性腺发育无影响。对神經型、腎型及腎上腺燙伤型雌鼠的性周期紊乱亦无糾正作用。二仙合剂能延长腎型高血压鼠的前庭时值,但在其他型则变化不显著。无明显对抗去甲腎上腺素及垂体后叶素的加压反应的作用。 相似文献
75.
3A1 (CD7) expression precedes T beta gene rearrangements in precursor T (lymphoblastic) neoplasms 总被引:7,自引:0,他引:7
The phenotypes of early stages of T cell maturation are reflected by precursor T (lymphoblastic) neoplasms. In the present study, a series of such neoplasms was analyzed to reveal the developmental association of the expression of stage-related cell surface markers and T cell receptor gene rearrangement. Rearrangements of the T cell receptor beta- chain (T beta) gene were found in most, but not all, cases (88%) of T cell lymphoblastic neoplasms. T beta gene rearrangement preceded surface expression of the T cell receptor-linked molecular complex T3. Of all monoclonal anti-T cell antibodies tested, only antibody 3A1 was capable of reacting with neoplastic cells from all cases irrespective of the occurrence of T cell receptor gene rearrangements. In contrast, markers T1 and T11, normally expressed by mature T cells, were absent from the neoplastic cells in many cases (73% and 60% positive cases, respectively). Thus, antibody 3A1 is a valuable probe for the identification of T lymphoblastic neoplasms since its target antigen is consistently expressed and does not require prior T beta gene rearrangement. Furthermore, expression of 3A1 prior to T beta gene rearrangement suggests that it may be a cell surface protein that participates in the triggering of T cell receptor gene rearrangement and expression. It is concluded that precursor T cell neoplasms display an early T cell development hierarchy that, in sequence, consists of 3A1 expression, T beta gene rearrangements, and surface T3 expression. 相似文献
76.
A novel phenotypic pattern in X-linked inheritance: craniofrontonasal syndrome maps to Xp22 总被引:1,自引:0,他引:1
Feldman GJ; Ward DE; Lajeunie-Renier E; Saavedra D; Robin NH; Proud V; Robb LJ; Der Kaloustian V; Carey JC; Cohen MM Jr; Cormier V; Munnich A; Zackai EH; Wilkie AO; Price RA; Muenke M 《Human molecular genetics》1997,6(11):1937-1941
Craniofrontonasal syndrome (CFNS, OMIM 304110) is a distinctive genetic
disorder whose main clinical manifestations include coronal synostosis,
widely spaced eyes, clefting of the nasal tip and various skeletal
anomalies. CFNS originally was thought to be transmitted as an autosomal
dominant trait, but recent studies suggest that it is X- linked dominant,
whereby all daughters of males are affected, whereas none of their sons are
affected. Here we report data confirming that CFNS is X-linked, mapping to
a 13 cM interval in Xp22 with a maximum two-point lod score of 3.9 (theta =
0) at DXS8022 and a multipoint lod score of 5.08 at DXS1224. Detailed
phenotypic analysis shows that females are more severely affected than
males, a highly unusual characteristic for an X-linked disorder. CFNS
represents the first multiple congenital anomaly syndrome with this unusual
phenotypic pattern of X-linked inheritance.
相似文献
77.
Generalized glycogen storage and cardiomegaly in a knockout mouse model of Pompe disease 总被引:3,自引:2,他引:3
Bijvoet AG; van de Kamp EH; Kroos MA; Ding JH; Yang BZ; Visser P; Bakker CE; Verbeet MP; Oostra BA; Reuser AJ; van der Ploeg AT 《Human molecular genetics》1998,7(1):53-62
Glycogen storage disease type II (GSDII; Pompe disease), caused by
inherited deficiency of acid alpha-glucosidase, is a lysosomal disorder
affecting heart and skeletal muscles. A mouse model of this disease was
obtained by targeted disruption of the murine acid alpha-glucosidase gene
(Gaa) in embryonic stem cells. Homozygous knockout mice (Gaa -/-) lack Gaa
mRNA and have a virtually complete acid alpha-glucosidase deficiency.
Glycogen-containing lysosomes are detected soon after birth in liver, heart
and skeletal muscle cells. By 13 weeks of age, large focal deposits of
glycogen have formed. Vacuolar spaces stain positive for acid phosphatase
as a sign of lysosomal pathology. Both male and female knockout mice are
fertile and can be intercrossed to produce progeny. The first born knockout
mice are at present 9 months old. Overt clinical symptoms are still absent,
but the heart is typically enlarged and the electrocardiogram is abnormal.
The mouse model will help greatly to understand the pathogenic mechanism of
GSDII and is a valuable instrument to explore the efficacy of different
therapeutic interventions.
相似文献
78.
79.
Zouali H; Hani EH; Philippi A; Vionnet N; Beckmann JS; Demenais F; Froguel P 《Human molecular genetics》1997,6(9):1401-1408
Several candidate genes for non-insulin-dependent diabetes mellitus (NIDDM)
map on chromosome 20, including the phosphoenolpyruvate carboxykinase gene
(PCK1) and one of the maturity onset diabetes of the young genes (MODY1).
Thus, we have investigated the entire long arm of chromosome 20. Linkage
analyses were conducted in a total sample of 148 NIDDM families (301 NIDDM
sib pairs) and in a subset of 42 early onset NIDDM families, where genetic
components are likely to play a more important role (55 NIDDM sib pairs
diagnosed at or before 45 years of age), using 10 highly polymorphic
markers with an average map density of 7.5 cM. Using affected sib pair
methods (two-point linkage and multipoint linkage analyses), significant
results were obtained with the 20q13 region, in the vicinity of the PCK1
locus, only in the subset of 55 early onset NIDDM sib pairs (multipoint MLS
= 2.74, P = 0.0004; MLS = 2.34, P = 0.0009 when using a conservative
weighting procedure). Moreover, another region spanning the ribophorin II
(RPNII, phospholipase C (PLC1) and adenosine deaminase (ADA) loci suggested
linkage with NIDDM (multipoint MLS of 1.81 in all NIDDM sib pairs, P =
0.003; MLS = 1.31, P = 0.012 when using a conservative weighting
procedure). Whereas our study suggests the location of a susceptibility
locus for early onset NIDDM in the PCK1 gene region, further investigation
in larger data sets is required to confirm these results and assess the
role of other regions on chromosome 20q in human NIDDM.
相似文献
80.
Factors Contributing to Inappropriate Visits of Frequent Attenders and Their Economic Effects at an Emergency Department in Singapore 下载免费PDF全文