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排序方式: 共有8140条查询结果,搜索用时 15 毫秒
41.
Shigemitsu Iwai MD Kei Torikai MD Chris M. Coppin MD Yoshiki Sawa MD 《Journal of artificial organs》2007,10(1):29-35
Currently used bioprosthetic valves have several limitations such as calcification and functional deterioration, and revitalization
through cellular ingrowth is impossible. To overcome these obstacles, we have developed a minimally immunogenic tissue-engineered
valve that consists of an unfixed, decellularized porcine valve scaffold capable of being spontaneously revitalized in vivo
after implantation. Porcine aortic root tissue was decellularized using detergents such as sodium lauryl sulfate and Triton
X-100. The porcine valve was treated very gently and plenty of time was allowed for constituents to diffuse in and out of
the matrix. In a preliminary study, a piece of decellularized porcine valve tissue was implanted into the rat subdermal space
for 14 and 60 days and the structural integrity and calcification were evaluated. As an in vivo valve replacement model, the
decellularized porcine valve was implanted in the pulmonary valve position in dogs and functional and histological evaluation
was performed after 1, 2, and 6 months. Histological examination showed that the newly developed detergent treatment effectively
removed cellular debris from the porcine aortic tissue. Decellularized porcine valve tissue implanted subdermally in rats
showed minimal inflammatory cell infiltration and calcification. In the valve replacement model, spontaneous reendothelialization
and repopulation of the medial cells were observed within 2 months, and good valve function without regurgitation was observed
by echocardiography up to 6 months. The minimally immunogenic decellularized porcine valve proved effective in mitigating
postimplant calcification and provided a suitable matrix for revitalizing prostheses through in situ recellularization, cellular
ingrowth, and tissue remodeling. 相似文献
42.
An increase in number of T-cell receptor gamma/delta-bearing T cells in athymic nude mice treated with complete Freund's adjuvants. 总被引:3,自引:0,他引:3 下载免费PDF全文
It has been reported previously that environmental antigens such as intestinal microflora play an important role in an age-associated increase in number of T-cell receptor gamma/delta-bearing T cells. To extend the scope of this finding, this study examined the influences of local inflammation on the accumulation and/or proliferation of gamma/delta T cells in athymic nude mice injected subcutaneously with complete Freund's adjuvants (CFA). The inguinal lymph nodes (ILN) in nude mice injected with CFA in their hind footpads 7 days previously contained an increased number of CD3+CD4-CD8- cells. Increased levels of proliferative responses against syngeneic stimulator cells were noted in the LN cells of CFA-injected nude mice in association with increases in expression of gamma- and delta-chain gene messages. Furthermore, the LN cells showed an early proliferative response to purified protein derivative (PPD) from Mycobacterium bovis. These results suggest that local inflammation by CFA may induce functional gamma/delta T cells in nude mice, which may proliferate rapidly at the inflamed sites and represent a first line of defence in such animals against the invasion of various pathogens. 相似文献
43.
Masaki Iwai Yasutaka Ishu Yoshihiro Kitagawa Kazunobu Tada Motomu Kashiwadani Takeshi Okanoue Kei Kashima 《Medical molecular morphology》1993,26(3-4):207-210
The immunoreactivity of albumin (ALB) was observed in the hepatocytes of fetal rats on day 18 of gestation, and was especially observable in immature rough endoplasmic reticulum (rER) and Golgi apparatus (GA); by then, a small amount of silver grains of ALB mRNA could already be detected. Just after birth, immunoreactivity of ALB could be observed in fine granules or diffusely in all hepatocytes, and was present in rER and GA. One week after birth immunoreactivity of ALB was observed in all hepatocytes and was visible in developed rER and GA; the grains of ALB mRNA were present in all hepatocytes. 相似文献
44.
Takagi A Matsuzaki T Sato M Nomoto K Morotomi M Yokokura T 《Medical microbiology and immunology》1999,188(3):111-116
The present study was designed to determine whether tumor induction by 3-methylcholanthrene (MC), a carcinogenic hydrocarbon,
can be inhibited by oral administration of Lactobacillus casei strain Shirota (LC). C3H/HeN mice were divided into four groups and assigned to the following treatments: treated with MC
and given control or LC-containing diet; treated with vehicle only and given control or LC-containing diet. MC (1 mg) was
injected intradermally at 7 weeks of age and the tumor incidence was monitored; LC was mixed into a diet at a concentration
of 0.05% (w/w) and the diet was fed from the day of MC injection throughout the study. Spleen cells were analyzed for the
immune parameters at 12 and 16 weeks after the MC injection. Oral feeding of mice with LC reduced tumor incidence (P < 0.05). MC treatment lowered the in vitro response to concanavalin A (Con A) of spleen cells, the secretion of interleukin-2
in spleen cell culture after stimulation of the cells with Con A and the proportions of CD3+, CD4+ and CD8+ splenic cells. However, the analysis of the spleen cells obtained from the mice treated with MC and given the LC-containing
diet revealed that these disrupted host immune parameters were maintained at the level of normal controls. These results suggest
that oral feeding of mice with LC inhibits MC-induced tumorigenesis by modulating the disrupted host immune responses during
MC carcinogenesis.
Received: 14 April 1999 相似文献
45.
Clinicopathological significant and prognostic influence of cadherin-17 expression in gastric cancer 总被引:5,自引:0,他引:5
Ito R Oue N Yoshida K Kunimitsu K Nakayama H Nakachi K Yasui W 《Virchows Archiv : an international journal of pathology》2005,447(4):717-722
Cadherin-17 (CDH17), also called liver–intestine cadherin, is a structurally unique member of the cadherin superfamily. Our
serial analysis of gene expression demonstrated that CDH17 was one of the most up-regulated genes in advanced gastric carcinomas.
CDH17 expression is known to be regulated by Cdx2. In the present study, we examined the expression of CDH17 in primary gastric
carcinoma tissues by immunohistochemistry, and analyzed the correlation of CDH17 expression with clinicopathological characteristics
and patients prognosis. CDH17 expression was detected in 63/94 (67%) of gastric adenocarcinomas in addition to intestinal
metaplasia. The expression of CDH17 tended to be associated with intestinal type carcinoma, and carcinomas with CDH17 expression
was significantly more frequent in advanced stage cases (80%) than in early stage (53%). The prognosis of patients with positive
CDH17 expression was significantly poorer than that of the negative cases (P=0.0314). However, multivariate analysis revealed that CDH17 was not an independent prognostic factor. Six of seven cases
that showed positive expression of Cdx2 simultaneously expressed CDH17 protein. These results suggested that the expression
of CDH17 was characteristic of the advanced gastric carcinoma that is associated with poor prognosis. 相似文献
46.
ABC proteins: key molecules for lipid homeostasis 总被引:2,自引:0,他引:2
Takahashi K Kimura Y Nagata K Yamamoto A Matsuo M Ueda K 《Medical molecular morphology》2005,38(1):2-12
Forty-nine ABC protein genes exist on human chromosomes. Eukaryotic ABC proteins were originally recognized as drug efflux pumps involved in the multidrug resistance of cancer cells. However, it is now realized that one of their major physiological roles is cellular lipid transport and homeostasis, and their dysfunction is often associated with human diseases. ABCA1 and ABCA7 mediate the apolipoprotein-dependent formation of a high-density lipoprotein–cholesterol complex. ABCA3 is indispensable for pulmonary surfactant secretion. ABCG5 and ABCG8 are involved in the secretion of plant sterols and cholesterol into bile. However, the primary substrates and mechanism of action of these ABC proteins have not been precisely defined. In this review article, we first describe the general structure and functions of eukaryotic ABC proteins. The current model of ABCA1 functionality is then explained based on studies on a topological model, subcellular localization, apoA-I dependence of HDL formation, functional defects of Tangier disease mutants, and ATP hydrolysis of purified ABCA1. ABCA1 is supposed to function as a transporter of lipids as well as a receptor for apoA-I. ABCA3 is likely involved in accumulating phospholipids and cholesterol in lamellar bodies and in generating multivesicular structures. 相似文献
47.
Autoimmunity and inflammation due to a gain-of-function mutation in phospholipase C gamma 2 that specifically increases external Ca2+ entry 总被引:3,自引:0,他引:3
Yu P Constien R Dear N Katan M Hanke P Bunney TD Kunder S Quintanilla-Martinez L Huffstadt U Schröder A Jones NP Peters T Fuchs H de Angelis MH Nehls M Grosse J Wabnitz P Meyer TP Yasuda K Schiemann M Schneider-Fresenius C Jagla W Russ A Popp A Josephs M Marquardt A Laufs J Schmittwolf C Wagner H Pfeffer K Mudde GC 《Immunity》2005,22(4):451-465
The identification of specific genetic loci that contribute to inflammatory and autoimmune diseases has proved difficult due to the contribution of multiple interacting genes, the inherent genetic heterogeneity present in human populations, and a lack of new mouse mutants. By using N-ethyl-N-nitrosourea (ENU) mutagenesis to discover new immune regulators, we identified a point mutation in the murine phospholipase Cg2 (Plcg2) gene that leads to severe spontaneous inflammation and autoimmunity. The disease is composed of an autoimmune component mediated by autoantibody immune complexes and B and T cell independent inflammation. The underlying mechanism is a gain-of-function mutation in Plcg2, which leads to hyperreactive external calcium entry in B cells and expansion of innate inflammatory cells. This mutant identifies Plcg2 as a key regulator in an autoimmune and inflammatory disease mediated by B cells and non-B, non-T haematopoietic cells and emphasizes that by distinct genetic modulation, a single point mutation can lead to a complex immunological phenotype. 相似文献
48.
Frequent importation of enterovirus 71 from surrounding countries into the local community of Yamagata, Japan, between 1998 and 2003 下载免费PDF全文
Mizuta K Abiko C Murata T Matsuzaki Y Itagaki T Sanjoh K Sakamoto M Hongo S Murayama S Hayasaka K 《Journal of clinical microbiology》2005,43(12):6171-6175
Phylogenetic analysis of 45 enterovirus 71 (EV71) isolates for 6 years in Yamagata, Japan, clarified that the annual outbreak of hand-foot-and-mouth disease was due to four genetically distinct subgenogroups, including a novel "B5." Our results suggest that the importation of EV71 from surrounding countries has had a major epidemiological impact on the local community used in our study. 相似文献
49.
ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats 总被引:28,自引:1,他引:28
Nishitoh H Matsuzawa A Tobiume K Saegusa K Takeda K Inoue K Hori S Kakizuka A Ichijo H 《Genes & development》2002,16(11):1345-1355
Expansion of CAG trinucleotide repeats that encode polyglutamine is the underlying cause of at least nine inherited human neurodegenerative disorders, including Huntington's disease and spinocerebellar ataxias. PolyQ fragments accumulate as aggregates in the cytoplasm and/or in the nucleus, and induce neuronal cell death. However, the molecular mechanism of polyQ-induced cell death is controversial. Here, we show the following: (1) polyQ with pathogenic repeat length triggers ER stress through proteasomal dysfunction; (2) ER stress activates ASK 1 through formation of an IRE1-TRAF2-ASK1 complex; and (3) ASK1(-/-) primary neurons are defective in polyQ-, proteasome inhibitor-, and ER stress-induced JNK activation and cell death. These findings suggest that ASK1 is a key element in ER stress-induced cell death that plays an important role in the neuropathological alterations in polyQ diseases. 相似文献
50.