全文获取类型
收费全文 | 5222篇 |
免费 | 348篇 |
国内免费 | 16篇 |
专业分类
耳鼻咽喉 | 23篇 |
儿科学 | 235篇 |
妇产科学 | 49篇 |
基础医学 | 555篇 |
口腔科学 | 93篇 |
临床医学 | 666篇 |
内科学 | 1016篇 |
皮肤病学 | 32篇 |
神经病学 | 609篇 |
特种医学 | 493篇 |
外科学 | 508篇 |
综合类 | 70篇 |
一般理论 | 3篇 |
预防医学 | 506篇 |
眼科学 | 259篇 |
药学 | 284篇 |
肿瘤学 | 185篇 |
出版年
2021年 | 64篇 |
2019年 | 54篇 |
2018年 | 75篇 |
2017年 | 49篇 |
2016年 | 75篇 |
2015年 | 59篇 |
2014年 | 79篇 |
2013年 | 120篇 |
2012年 | 176篇 |
2011年 | 181篇 |
2010年 | 137篇 |
2009年 | 106篇 |
2008年 | 195篇 |
2007年 | 196篇 |
2006年 | 192篇 |
2005年 | 176篇 |
2004年 | 199篇 |
2003年 | 171篇 |
2002年 | 174篇 |
2001年 | 162篇 |
2000年 | 174篇 |
1999年 | 128篇 |
1998年 | 73篇 |
1997年 | 72篇 |
1996年 | 75篇 |
1995年 | 54篇 |
1994年 | 50篇 |
1992年 | 115篇 |
1991年 | 114篇 |
1990年 | 127篇 |
1989年 | 137篇 |
1988年 | 130篇 |
1987年 | 132篇 |
1986年 | 156篇 |
1985年 | 132篇 |
1984年 | 85篇 |
1983年 | 100篇 |
1982年 | 65篇 |
1981年 | 55篇 |
1980年 | 57篇 |
1979年 | 95篇 |
1978年 | 78篇 |
1977年 | 69篇 |
1976年 | 53篇 |
1975年 | 49篇 |
1974年 | 55篇 |
1973年 | 53篇 |
1971年 | 41篇 |
1970年 | 43篇 |
1968年 | 42篇 |
排序方式: 共有5586条查询结果,搜索用时 15 毫秒
51.
52.
Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes 总被引:17,自引:8,他引:17
Campuzano V; Montermini L; Lutz Y; Cova L; Hindelang C; Jiralerspong S; Trottier Y; Kish SJ; Faucheux B; Trouillas P; Authier FJ; Durr A; Mandel JL; Vescovi A; Pandolfo M; Koenig M 《Human molecular genetics》1997,6(11):1771-1780
Friedreich ataxia is a progressive neurodegenerative disorder caused by
loss of function mutations in the frataxin gene. In order to unravel
frataxin function we developed monoclonal antibodies raised against
different regions of the protein. These antibodies detect a processed 18
kDa protein in various human and mouse tissues and cell lines that is
severely reduced in Friedreich ataxia patients. By immunocytofluorescence
and immunocytoelectron microscopy we show that frataxin is located in
mitochondria, associated with the mitochondrial membranes and crests.
Analysis of cellular localization of various truncated forms of frataxin
expressed in cultured cells and evidence of removal of an N-terminal
epitope during protein maturation demonstrated that the mitochondrial
targetting sequence is encoded by the first 20 amino acids. Given the
shared clinical features between Friedreich ataxia, vitamin E deficiency
and some mitochondriopathies, our data suggest that a reduction in frataxin
results in oxidative damage.
相似文献
53.
54.
Dithiothreitol prevents age-associated decrease in oocyte/conceptus viability in vitro 总被引:2,自引:0,他引:2
The present study was designed to ascertain whether the negative effects on
reproductive potential of post-ovulatory ageing in vitro of oocytes can be
prevented by antioxidant therapy. Mouse metaphase II (MII) oocytes were
aged in vitro for 12 h prior to insemination in the presence of varying
concentrations of L-ascorbic acid, 6-methoxy-
2,5,7,8-tetramethylchromane-2-carboxylic acid (Trolox), L-cystine
dihydrochloride, ethylenediaminetetraacetic acid (EDTA), beta-
mercaptoethanol and DL-dithiothreitol (DTT). In-vitro ageing of oocytes was
associated with lower fertilization rate, higher proportion of concepti
exhibiting cellular fragmentation at 24 h post-insemination and lower
percentage of concepti reaching the blastocyst stage. Ascorbic acid, Trolox
and EDTA had no effect on cellular fragmentation or potential of oocytes
for development. However, the probability of an oocyte reaching the
blastocyst stage was decreased (P < or = or = 0.05) in oocytes incubated
in the presence of L-cystine (50 and 500 microM) and beta-mercaptoethanol
(5, 50 and 500 microM) when compared to control aged oocytes.
Age-associated cellular fragmentation at 24 h post-insemination was
partially prevented (P < or = 0.05) by incubating oocytes in the
presence of beta-mercaptoethanol (500 microM). DTT (50 and 500 microM)
increased (P < or = 0.05) fertilization rate and number of cells at 81 h
post-insemination to levels similar to those exhibited by control oocytes.
Furthermore, both age-associated fragmentation at 24 h post-insemination (P
< or = 0.05) and decreased potential of oocytes for development to the
blastocyst stage (P < or = 0.05) were prevented, at least in part, by
culturing oocytes in the presence of DTT (50 microM). Although the
mechanism by which DTT exerts its beneficial effects on aged oocytes
remains to be elucidated, it may protect oocytes by preventing oxidation of
free thiol groups and/or altering a redox-independent signalling pathway
that mediates cellular fragmentation and death.
相似文献
55.
56.
Y chromosome microdeletions, in azoospermic or near-azoospermic subjects, are located in the AZFc (DAZ) subregion 总被引:9,自引:2,他引:9
Submicroscopic deletions of the Y chromosome and polymorphisms of the
androgen receptor (AR) gene in the X chromosome have been observed in men
with defective spermatogenesis. To further define the subregions/genes in
the Y chromosome causing male infertility and its relationship to
polymorphisms of the AR polyglutamine tract, we screened the genomic DNA of
202 subfertile males and 101 healthy fertile controls of predominantly
Chinese ethnic origin. Y microdeletions were examined with 16
sequence-tagged site (STS) probes, including the RBM and DAZ genes,
spanning the AZFb and AZFc subregions of Yq11, and related to the size of
trinucleotide repeat encoding the AR polyglutamine tract. Y microdeletions
were detected and confirmed in three out of 44 (6.8%) of azoospermic and
three out of 86 (3.5%) severely oligozoospermic patients. No deletions were
detected in any of the patients with sperm counts of >0.5 x 10(6)/ml,
nor in any of the 101 fertile controls. All six affected patients had
almost contiguous Y microdeletions spanning the entire AZFc region
including the DAZ gene. The AZFb region, containing the RBM1 gene, was
intact in five of the six subjects. Y deletions were not found in those
with long AR polyglutamine tracts. Our study, the first in a Chinese
population, suggest a cause and effect relationship between Y
microdeletions in the AZFc region (possibly DAZ), and azoospermia or
near-azoospermia. Y microdeletions and long AR polyglutamine tracts appear
to be independent contributors to male infertility.
相似文献
57.
Determination of the parent of origin in nine cases of prenatally detected chromosome aberrations found after intracytoplasmic sperm injection 总被引:1,自引:17,他引:1
Van Opstal D; Los FJ; Ramlakhan S; Van Hemel JO; Van Den Ouweland AM; Brandenburg H; Pieters MH; Verhoeff A; Vermeer MC; Dhont M; In't Veld PA 《Human reproduction (Oxford, England)》1997,12(4):682-686
Prenatal cytogenetic analysis of 71 fetuses conceived by intracytoplasmic
sperm injection (ICSI) resulted in the detection of nine (12.7%) chromosome
aberrations including two cases of 47,XXY, four cases involving a 45,X cell
line and three autosomal trisomies. Molecular analysis of the parental
origin of the deleted or supernumerary chromosome was performed by using
polymorphic microsatellite markers. Six cases involving a sex chromosome
abnormality were found to be of paternal origin while the two trisomic
cases that could be analysed were of maternal origin. Two cases involved
the same infertile couple who had two consecutive ICSI pregnancies
terminated because of a chromosome abnormality. The replaced embryos in
both cases originated from a single batch of ICSI fertilized oocytes of
which part was used to initiate the first pregnancy and part was
cryopreserved and used to initiate the second pregnancy.
相似文献
58.
P. H. Wooley J. D. Whalen J. L. Zimmerman T. M. Champion 《Inflammation research》1987,21(3-4):244-246
Type II collagen-induced arthritis (CIA) and mice was used as a model to evaluate the effect of etodolac on the arthritic and immunological parameters of the experimental disease. In a preventative protocol, a significant reduction was observed in the number of joints progressing to ankylosis. At high doses (16 mg/kg/day) a significant delay in the onset of arthritis was also observed. No significant effect was seen on the progression of the disease when etodolac was administered in established CIA. No consistent variations were observed in the anti-type II collagen response or other immunological parameters of the experimental arthritis. 相似文献
59.
A prospective trial of colchicine for primary biliary cirrhosis 总被引:10,自引:0,他引:10
M M Kaplan D W Alling H J Zimmerman H J Wolfe R A Sepersky G S Hirsch G H Elta K A Glick K A Eagen 《The New England journal of medicine》1986,315(23):1448-1454
We entered 60 patients with primary biliary cirrhosis in a double-blind randomized controlled trial to determine whether colchicine is therapeutically effective. Thirty patients had early disease (Stages 1 and 2), and 30 had advanced disease (Stages 3 and 4). Fifteen patients with early disease and 15 with advanced disease received colchicine (0.6 mg twice daily), and the remainder received placebo. Patients were studied about every two months; those remaining in the blind phase at two years underwent repeat liver biopsy and were then placed on open-label colchicine (0.6 mg twice daily). With a few exceptions, the results in patients with early disease were similar to those in patients with advanced disease; hence, data on patients in all stages were combined in the main analysis. During the two-year study period the colchicine-treated patients, as compared with the placebo-treated patients, had improvement in levels of serum albumin, serum bilirubin, alkaline phosphatase, cholesterol, and aminotransferases. However, there was no such improvement in the severity of symptoms or physical findings; moreover, there was no significant difference in the histologic changes noted at liver biopsy in the two treatment groups. At four years after entry, the cumulative mortality from liver disease was 21 percent in patients given colchicine and 47 percent in those given placebo (P = 0.05). The only side effect of colchicine was diarrhea, noted in three patients. The consistent and significant improvement in a number of markers of liver disease and the apparent decreased mortality from liver disease suggest that colchicine may provide some long-term clinical benefit in patients with primary biliary cirrhosis. However, the failure of colchicine to reduce hepatic inflammation and fibrosis leaves uncertain the effect of the drug on the longterm outcome of this disease. 相似文献
60.
Billette J; Janse MJ; van Capelle FJ; Anderson RH; Touboul P; Durrer D 《The American journal of physiology》1976,231(4):1129-1139