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991.
Kazuyuki Furuta Mayuko Natsuhara Hirotsugu Takano Soken Tsuchiya Yasushi Okuno Hiroshi Ohtsu Masahiro Nishibori Robin L. Thurmond Noriyasu Hirasawa Kazuhisa Nakayama Atsushi Ichikawa Yukihiko Sugimoto Satoshi Tanaka 《European journal of immunology》2014,44(1):204-214
Mast cells are the major sources of histamine, which is released in response to immunological stimulations. The synthesis of histamine is catalyzed by histidine decarboxylase (HDC). Previous studies have shown that Hdc?/? mast cells exhibit aberrant granule morphology with severely decreased granule content. Here, we investigated whether the histamine synthesized in mast cells regulates the granule maturation of murine mast cells. Several genes, including those encoding granule proteases and enzymes involved in heparin biosynthesis, were downregulated in Hdc?/? peritoneal mast cells. Impaired granule maturation was also found in Hdc?/? BM‐derived cultured mast cells when they were cocultured with fibroblasts in the presence of c‐kit ligand. Exogenous application of histamine and several H4 receptor agonists restored the granule maturation of Hdc?/? cultured mast cells. However, the maturation of granules was largely normal in Hrh4?/? peritoneal mast cells. Depletion of cellular histamine with tetrabenazine, an inhibitor of vesicular monoamine transporter‐2, did not affect granule maturation. In vivo experiments with mast cell deficient KitW/KitW‐v mice indicated that the expression of the Hdc gene in mast cells is required for granule maturation. These results suggest that histamine promotes granule maturation in mast cells and acts as an proinflammatory mediator. 相似文献
992.
Atsushi Tashiro Tomoyuki Masuda Ikuo Segawa 《Virchows Archiv : an international journal of pathology》1990,416(6):473-478
Summary We performed an ultrastructural, morphometric comparison of mitochondria and myofibrils of cardiomyocytes using endomyocardial biopsy specimens in hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM). Biopsies came from the right ventricular side of the interventricular septum in nine patients with HCM, nine with DCM, and nine controls with arrhythmia and/or ST depression. Morphometric analysis was carried out using electron microscopic photographs and an image analyser. Mitochondria were significantly greater in number and smaller in size in HCM than in the control group. In DCM, the size of mitochondria was also significantly smaller than in the control group, although their number was similar to that of the control group. No statistically significant difference was found regarding the size of mitochondria between HCM and DCM. The percentages of both mitochondrial and myofibrillar areas in cytoplasm were smaller in the DCM than the HCM and control groups, though no difference was seen between the latter two. The ratio of mitochondrial area to myofibrillar area was almost the same in each group. These results suggest increased mitochondrial function to match hypertrophic cardiomyocytes in HCM, and decreased mitochondrial function and cardiomyocytic contractility in DCM. 相似文献
993.
Acceleration of bone formation with BMP2 in frame-reinforced carbonate apatite–collagen sponge scaffolds 总被引:2,自引:0,他引:2
Isao Hirata Yuji Nomura Manabu Ito Atsushi Shimazu Masayuki Okazaki 《Journal of artificial organs》2007,10(4):212-217
The development is expected of scaffold biomaterials that feature a shape-maintaining property in addition to high porosity
and large pores that cells can easily invade. To develop a new biodegradable scaffold biomaterial reinforced with a frame,
synthesized carbonate apatite (CO3Ap) was mixed with neutralized collagen gel, and the CO3Ap–collagen mixtures were lyophilized into sponges in a porous hydroxyapatite (HAp) frame ring. X-ray diffraction and Fourier
transform infrared spectroscopy (FT-IR) analyses together with chemical analysis indicated that the synthesized CO3Ap had a crystalline nature and a chemical composition similar to that of bone. Scanning electron microscope (SEM) observation
showed that the CO3Ap–collagen sponge had a sui pore size for cell invasion. In proliferation and differentiation experiments with osteoblasts,
alkaline phosphatase and osteopontin activity were clearly detected. When these sponge–frame complexes with bone morphogenic
protein (rh-BMP2) were implanted beneath the periosteum cranii of rats, significant new bone was created at the surface of
the periosteum cranii after 4 weeks of implantation. These reinforced CO3Ap–collagen sponges with rh-BMP2 are expected to be used as hard tissue scaffold biomaterials for the therapeutic purpose
of the rapid cure of bone defects. 相似文献
994.
Asuka Iwanaga Tokiharu Sato Kazushi Sugihara Atsushi Hirao Nobuyuki Takakura Hiroshi Okamoto Masahide Asano Katsuji Yoshioka 《Neuroscience letters》2007
We previously identified c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase-associated protein 1 (JSAP1, also known as JNK-interacting protein 3) as a scaffolding factor for JNK intracellular signaling pathways. Targeted gene-disruption studies have shown that JSAP1-null mice are unable to breathe and die shortly after birth. Although neural defects might be responsible for their death, there has been no convincing evidence for this. Here we first generated genetically engineered mice carrying a loxP-flanked (floxed) jsap1 gene. To evaluate the validity of this deletion as a jsap1 conditional knockout (KO), we created mice in which the same exon was deleted in all cell lineages, and compared their phenotypes with those of the jsap1 conventional KO mice reported previously. The two KO lines showed indistinguishable phenotypes, i.e., neonatal death and morphological defects in the telencephalon, indicating that the conditional deletion was a true null mutation. We then introduced the floxed jsap1 deletion mutant specifically into the neural lineage, and found that the jsap1 conditional KO mice showed essentially the same phenotypes as the JSAP1-null mice. These results strongly suggest that the neonatal death of jsap1-deficient mice is caused by defects in the nervous system. 相似文献
995.
996.
Vascular flow patterns of hepatic tumors in contrast-enhanced 3-dimensional fusion ultrasonography using plane shift and opacity control modes. 总被引:4,自引:0,他引:4
Masao Ohto Hirotoshi Kato Hirohiko Tsujii Hitoshi Maruyama Shoichi Matsutani Hitoshi Yamagata 《Journal of ultrasound in medicine》2005,24(1):49-57
OBJECTIVE: This study was conducted to determine whether contrast-enhanced 3-dimensional (3D) fusion ultrasonography with combined use of the plane shift and opacity control modes can serve as a useful tool for identifying the vascular characteristics of hepatic tumors in 3D perspective. METHODS: Contrast-enhanced 3D fusion ultrasonography was performed in 31 patients with hepatic tumors after the intravenous injection of contrast media. The shapes, courses, and distributions of tumor vessels, displayed in 3D perspective, were examined to identify the characteristic vascular flow patterns of various tumors. Images before and after contrast media administration were compared for evaluation of the effectiveness of contrast enhancement with regard to tumor diameter for various types of tumors. The images were interpreted in a blinded manner by 3 physicians specializing in abdominal ultrasonography, and vascular flow patterns were determined on the basis of consensus. RESULTS: The characteristic vascular flow patterns observed in hepatocellular carcinomas are reticular flow within the tumor and flow showing a ringlike distribution surrounding the tumor. Metastatic tumors show a vascular flow pattern running between adjacent tumor nodules, and hemangiomas show localized nodular flow at the tumor margins. Contrast enhancement was found to be useful for showing the vascular flow patterns in small hepatocellular carcinomas and hemangiomas. CONCLUSIONS: Contrast-enhanced 3D fusion ultrasonography makes it possible to display images combining the plane shift and opacity control modes to show tumor vessels, including minute vascular flow within hepatic tumors, in 3D perspective and to identify tumor-specific vascular flow patterns. 相似文献
997.
Lipopolysaccharide interaction with cell surface Toll-like receptor 4-MD-2: higher affinity than that with MD-2 or CD14 总被引:20,自引:0,他引:20
Akashi S Saitoh S Wakabayashi Y Kikuchi T Takamura N Nagai Y Kusumoto Y Fukase K Kusumoto S Adachi Y Kosugi A Miyake K 《The Journal of experimental medicine》2003,198(7):1035-1042
Toll-like receptors (TLRs) are innate recognition molecules for microbial products, but their direct interactions with corresponding ligands remain unclarified. LPS, a membrane constituent of gram-negative bacteria, is the best-studied TLR ligand and is recognized by TLR4 and MD-2, a molecule associated with the extracellular domain of TLR4. Although TLR4-MD-2 recognizes LPS, little is known about the physical interaction between LPS and TLR4-MD-2. Here, we demonstrate cell surface LPS-TLR4-MD-2 complexes. CD14 greatly enhances the formation of LPS-TLR4-MD-2 complexes, but is not coprecipitated with LPS-TLR4-MD-2 complexes, suggesting a role for CD14 in LPS loading onto TLR4-MD-2 but not in the interaction itself between LPS and TLR4-MD-2. A tentative dissociation constant (Kd) for LPS-TLR4-MD-2 complexes was approximately 3 nM, which is approximately 10-20 times lower than the reported Kd for LPS-MD-2 or LPS-CD14. The presence of detergent disrupts LPS interaction with CD14 but not with TLR4-MD-2. E5531, a lipid A antagonist developed for therapeutic intervention of endotoxin shock, blocks LPS interaction with TLR4-MD-2 at a concentration 100 times lower than that required for blocking LPS interaction with CD14. These results reveal direct LPS interaction with cell surface TLR4-MD-2 that is distinct from that with MD-2 or CD14. 相似文献
998.
Temporal changes in cholinergic functions following transient cerebral ischemia (10 min) were studied in the hippocampus of awake unrestrained gerbils using in vivo microdialysis. These data were compared with the results for temporal change in the area of each CA1 cell soma, measured with a microcomputer imaging device. KCl-induced release of acetylcholine (ACh) tended to be lower within 1 day after recirculation, and was significantly lower on the 4th, 7th and 14th days. Atropine-induced release of ACh gradually decreased over the test period. In histological estimation, no differences were observed within the 1st day, but a significant decrease of the area of CA1 cell soma was observed from the 4th to 14th days. Moreover, ischemia over 2 min decreased KCl- and atropine-induced ACh release on the 14th day without significant changes of hippocampal CA1 pyramidal cell. From these results, it is clear that ischemia produced dysfunction of hippocampal cholinergic neurons, and that dysfunction of the hippocampal cholinergic system following transient ischemia precedes pyramidal cell damage in the hippocampal CA1 subfield. 相似文献
999.
1000.
Impact of left atrial size on isolation area in the acute phase of pulmonary vein isolation using 28 mm cryoballoon 下载免费PDF全文
Akio Chikata MD PhD Takeshi Kato MD PhD Kazuo Usuda MD PhD Shuhei Fujita MD PhD Michiro Maruyama MD PhD Yoshiki Nagata MD PhD Satoru Sakagami MD PhD Naomi Kanamori MD Takanori Yaegashi MD PhD Takahiro Saeki MD PhD Takashi Kusayama MD PhD Soichiro Usui MD PhD Hiroshi Furusho MD PhD Shuichi Kaneko MD PhD Masayuki Takamura MD PhD 《Pacing and clinical electrophysiology : PACE》2018,41(7):700-706