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11.
为了研究β-1,4-半乳糖基转移酶 和 (β-1,4-Gal T- and )蛋白表达的亚细胞结构定位 ,本实验构建了β-1,4-Gal T- 和 融合绿色荧光蛋白 (GFP)表达质粒 ,分别将构建的质粒转染到 PC12细胞和肝癌 772 1细胞中 ,在荧光显微镜下观察β-1,4-Gal T- 和 在其中表达的亚细胞结构定位。发现 ,β-1,4-Gal T- 和 主要表达在这两种细胞的细胞核旁的 Golgi复合体 ,说明它们主要分布在 Golgi复合体上。提示它们可能是在 Golgi复合体参与蛋白质的糖链修饰 相似文献
12.
No mutations or polymorphisms have previously been reported in pp32r1 (ANP32C; GenBank: AF008216.1). pp32r1 is part of the highly conserved ANP32 family, some of whose members are associated with control of histone acetylation, mRNA stability, and specialized forms of apoptosis. Although 87.6% identical at the protein level, pp32r1 is functionally distinct from pp32 (ANP32A) in its failure to suppress oncogenesis in in vitro transformation systems and its tumorigenicity in in vivo assays. The present study found that pp32r1 expression levels vary among human tumor cell lines, with the highest levels found in prostatic adenocarcinoma cell lines. pp32r1 also appears to be polymorphic at nucleotide g.4520 and nucleotide g.4664 in human tobacco-associated oral mucosal lesions, human fibroblast cell lines, and several carcinoma cell lines. PC-3 human prostatic adenocarcinoma cells likewise appear to be polymorphic at these loci, but additionally contain a g.4870T>C transversion mutation. The mutation results in a p.Tyr140His substitution, which lies in a functionally important region of the molecule. In the PC-3 prostate cancer line, the mutation is either homozygous, or hemizygous accompanied by loss of heterozygosity. ACHN cells stably transfected with pp32r1 containing this mutation showed a markedly increased rate of growth. The pp32r1 mutation could thus be causally associated with the neoplastic growth properties of PC-3, and be of potential clinical significance. 相似文献
13.
目的探讨应用NT-PC治疗髌骨骨折的方法及治疗结果。方法根据NT-PC结构及固定原理对30例髌骨骨折的治疗。结果30例髌骨骨折髌关节面均达到解剖复位,患者能下地行走,扶栏杆或徒手上下一层楼、屈膝平均达到90°的时间是1.5~3.5周。患膝关节伸、屈活动范围达到健侧水平的时间是2~10周。结论根据NT-PC的特点治疗髌骨骨折,尤其是粉碎性骨折,不但在术中容易得到髌关节面的解剖复位,而且术后能有效地将其维持,固定于解剖位直至骨质愈合。术后可早期活动,无需石膏固定,无膝关节功能障碍。 相似文献
14.
Safarova ER Shram SI Zolotarev YA Myasoedov NF 《Bulletin of experimental biology and medicine》2003,135(3):268-271
We studied the effects of Semax (antiinsulin peptide with neuroprotective effect) on the survival of cultured rat pheochromocytoma cell after oxidative stress induced by short-term incubation with hydrogen peroxide. Studies with fluorescent dyes propidium iodide and Hoechst 33258 showed that cell incubation with hydrogen peroxide led to the formation of damaged cells with characteristic signs of necrosis. Semax dose-dependently reduced the number of cells damaged by oxidative stress. The efficiency of Semax depended on the time of its addition to the culture medium. The results suggest that the neuroprotective effect of Semax in ischemic stroke can be due to its capacity to protect neurons from damage caused by oxidative stress. 相似文献
15.
A Microsoft Windows-based front-end, NM-Win, has been written to provide a more user-friendly environment to do nonlinear mixed effect modeling with the NONMEM program. NM-Win utilizes an object-oriented interface design which allows users to view and edit control, PRED, and/or data files using Windows Notepad. In addition, calls made to the Microsoft FORTRAN compiler and linker which generate the final NONMEN executable are performed simply by clicking the Run NONMEN button. During the executive step, iterations can be viewed in a window to check the progress of the run. Errors encountered while NONMEN or NM-TRAN is running are brought to a window for ease in debugging. Advanced options allow the user the flexibility of compiling user-written PRED files and creating linker response files. While the PC platform is not optimal for large data set or complex models, it does permit easier debugging and offers multitasking while Windows is running. 相似文献
16.
Dr. Frank E. Block Jr MD Kris Minic Reynolds CFI John S. McDonald MD 《Journal of clinical monitoring and computing》1995,11(3):207-211
Automated anesthesia recordkeepers have been used to monitor patients during surgery in up to 90% of cases at The Ohio State University. The record-keeping devices are complex and can be difficult to troubleshoot. The 1st-CLASS Fusion Program, an expert system shell-program, has been programmed to allow the resident or nurse anesthetist to solve the two most common types of problems associated with the recordkeeper: printer problems and patient monitor problems. Use of this program allows the resident or nurse anesthetist to troubleshoot the recordkeeper quickly and accurately and promotes in the user a sense of competence and control over the technology. 相似文献
17.
Ultrastructural confirmation of neuronal protection by melatonin against the neurotoxin 6-hydroxydopamine cell damage 总被引:9,自引:0,他引:9
6-Hydroxydopamine (6-OHDA) is a neurotoxin used in the induction of experimental Parkinson's disease in both animals and cultured neuronal cells. Biochemical and molecular approaches showed previously that low doses of 6-OHDA induced apoptosis in PC12 cells, while high doses of this neurotoxin induced necrosis. Melatonin has been shown to protect against the neuronal programmed cell death induced by 6-OHDA, although it was not able to prevent the massive necrotic cellular death occurring after the addition of high doses of the neurotoxin. In the present work, we demonstrate by ultrastructural analysis that although low doses of 6-OHDA induced apoptosis in PC12 cells, it also damaged the non-apoptotic cells, morphologically corresponding this damage to incipient and reversible necrotic lesions. When the doses of the neurotoxin increase, there are still apoptotic cells, although most of the cells show necrotic irreversible lesions. We also found that melatonin partially prevents the incipient necrotic lesions caused by low doses of 6-OHDA. The fact that melatonin was shown in previous work to prevent apoptosis caused by low doses of 6-OHDA, but not necrosis induced by high doses of the neurotoxin, seemed to indicate that this agent is only able to protect against apoptosis. However, our present results, melatonin preventing also the incipient necrotic neuronal lesions, suggest that this hormone may provide a general protection against cell death, suggesting that higher doses should be tried in order to prevent the necrotic cell death induced by high doses of the neurotoxin. 相似文献
18.
目的:测定血能达片的急性毒性和验证其抗栓疗效及选药提供依据。方法:小白鼠一次Ig血能达26g/kg;五组动物分别给血能达(XND)3g/kg,溶栓胶种(RSC)1.25g/kg,复方丹参(CDDP)1.25g/kg,消栓通络(XSTL)2.5g/kg和NS Ig,qd 1次,连续7d。第7日药后1h,IV Collagen-Adr诱发血栓[1],观察死亡数;用毛细血管法测凝血时间,扭体法测痛。结果:小白鼠口服最大耐受量为26g/kg,临床用量的866.7倍;4种药物除消栓通络外,均有明显的抗栓作用(P<0.05-0.01);还证中、高剂量血能达尚有延长凝血时间和镇痛作用(P<0.05-0.01),其余3种药则没有。结论:血能达毒性小,具有溶栓胶囊,复方丹参等效的抗栓疗效,还能抗凝和镇痛。 相似文献
19.
环维黄杨星D对实验性脑缺血的保护作用 总被引:11,自引:0,他引:11
目的:探讨环维黄杨星D(Cycloirobuxiure D,CVB-D)对大鼠局灶性脑缺血再灌注损伤及PC12细胞缺氧性损伤的保护作用。方法:采用线栓法制成局灶性脑缺血再灌注大鼠模型和连二亚硫酸钠(Na2S2O4)引起的PC12细胞缺氧损伤模型,探讨CVB-D对模型大鼠神经行为、脑梗塞范围、脑含水量、脑指数的影响,以及其对PC12细胞缺氧样损伤的保护作用。结果:CVB-D能降低模型大鼠神经行为学评分、脑梗塞率、脑指数、脑含水量,抑制Na2S2O4造成的PC12细胞缺氧样损伤,降低LDH的漏出,增加细胞存活率。结论:CVB-D对实验性脑缺血有保护作用。 相似文献
20.
James A. Fyfe Lilia M. Beauchamp Anthony O. Caggiano Raymond D. Price Takayuki Yamaji Nobuya Matsuoka Thomas A. Krenitsky 《Drug development research》2004,62(1):49-59
The ability of endogenous neurotrophins, including nerve growth factor (NGF), to promote the survival and development of neurons provides convincing evidence for their therapeutic potential, despite significant barriers to their successful clinical use. Many of these barriers might be surmountable, however, by strategies that enhance endogenous neurotrophin signaling. We evaluated a series of substituted pyrimidines for their ability to enhance the effects of NGF. KP544 [2‐amino‐5‐(4‐chlorophenylethynyl)‐4‐(4‐trans‐hydroxycyclohexylamino) pyrimidine] amplified NGF‐induced neurite outgrowth of PC12 cells approximately 2‐fold at 2 µM. KP544 also enhanced choline acetyltransferase activity, a marker of differentiation induced by either NGF or by cyclic AMP, by 3‐ to 8‐fold, with a 2‐fold amplification at 0.12–0.3 µM. This amplification occurred at all concentrations of NGF used including those that maximally stimulated the cells. KP544 did not increase the levels of phosphorylated mitogen‐activated protein kinases (MAPK) above that seen with NGF alone. These studies suggested that KP544 functions within the cell at a site that is downstream from or independent of MAPK signaling. NGF‐induced neurite outgrowth in a human cell line (SH‐SY5Y neuroblastoma cells) was also enhanced with KP544 treatment. Primary embryonic rat cortical cultures were used to extend the observations beyond the studies with the immortalized cell lines. In addition to effects on neurite outgrowth, KP544 protected these cells from glutamate‐induced death. Overall, the data suggest that KP544 can selectively interact in the differentiation pathway downstream of MAPK in a manner that amplifies nerve growth factor and cyclic AMP effects and is also neuroprotective. Drug Dev. Res. 62:49–59, 2004. © 2004 Wiley‐Liss, Inc. 相似文献