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排序方式: 共有253条查询结果,搜索用时 15 毫秒
31.
Detection of reactive oxygen species (ROS) and apoptosis in human fragmented embryos 总被引:8,自引:2,他引:8
Yang HW; Hwang KJ; Kwon HC; Kim HS; Choi KW; Oh KS 《Human reproduction (Oxford, England)》1998,13(4):998-1002
In human in-vitro fertilization (IVF)-embryo transfer, the in-vitro culture
environment differs from in-vivo conditions in that the oxygen
concentration is higher, and in such conditions the mouse embryos show a
higher concentration of reactive oxygen species (ROS) in simple culture
media. ROS are believed to cause damage to cell membranes and DNA
fragmentation in somatic cells. This study was conducted to ascertain the
level of H2O2 concentration within embryos and the morphological features
of cell damage induced by H2O2. A total of 62 human oocytes and embryos (31
fragmented, 15 non-fragmented embryos, 16 unfertilized oocytes) was
obtained from the IVF-embryo transfer programme. The relative intensity of
H2O2 concentrations within embryos was measured using
2',7'-dichlorodihydrofluorescein diacetate by Quanti cell 500 fluorescence
imaging and DNA fragmentation was observed with transmission electron
microscopy and an in-situ apoptosis detection kit. The H2O2 concentrations
were significantly higher in fragmented embryos (72.21 +/- 9.62, mean +/-
SEM) compared to non-fragmented embryos (31.30 +/- 3.50, P < 0.05) and
unfertilized oocytes (30.75 +/- 2.67, P < 0.05). Apoptosis was observed
only in fragmented embryos, and was absent in non-fragmented embryos.
Electron microscopic findings confirmed apoptotic bodies and cytoplasmic
condensation in the fragmented blastomeres. We conclude that there is a
direct relationship between increased H2O2 concentration and apoptosis, and
that further studies should be undertaken to confirm these findings.
相似文献
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骨骼肌缺血再灌注损伤的机制 总被引:1,自引:0,他引:1
目的:对近年来骨骼肌缺血再灌注损伤的发病机制进行综述。资料来源:应用计算机检索MEDLINE、CBM、CNKI数据库及手工检索1998-01/2006-11期间的相关文献。中文检索词包括"骨骼肌,缺血再灌注损伤,发病机制";英文检索词有"Skeletal muscle","ischemia and reperfusion injury","oxygen freeradical","calcium overload"和"neutrophil"。资料选择:共收集到相关文献300篇,阅读全部文章的文题和大部分文章的摘要。选择文献所述内容与骨骼肌缺血再灌注损伤机制相关的文献。排除重复性研究。资料提炼:共得到符合纳入条件的文献55篇,排除145篇。选择其中30篇进行分析,英文24篇,中文6篇。资料综合:骨骼肌缺血再灌注损伤的机制由于有许多因素的介入而变的十分复杂,目前主要以氧自由基学说,钙超载学说和中性粒细胞学说为主,同时也注意到了一氧化氮和细胞凋亡以及微循环的无复流现象在其中的作用。结论:氧自由基学说,钙超载学说,中性粒细胞学说,一氧化氮,细胞凋亡以及微循环的无复流现象在骨骼肌缺血再灌注损伤中起着重要作用。 相似文献
34.
Liu JM; Chen YM; Chao Y; Liu SM; Tiu CM; Wu HW; Chiou TC; Hsieh RK; Chen LT; Whang-Peng J 《Japanese journal of clinical oncology》1998,28(7):431-435
BACKGROUND: To evaluate the efficacy and toxicity of cisplatin/etoposide
continuous infusion chemotherapy for cancer of unknown primary site in
Taiwan, a region with a high prevalence of endemic viral infections.
METHOD: Between April 1994 and February 1996, 20 patients with a diagnosis
of CUPS were treated, including 15 males and five females, of average age
63.3 years (range 41-83 years). Continuous intravenous infusion of
etoposide 80 mg/m2 and cisplatin 25 mg/m2 was given for 3 days every 3
weeks. Pretreatment tumor marker and viral serology studies were performed
for baseline evaluation. Nearly two-thirds of the patients had poorly
differentiated carcinoma. The average number of metastatic sites was 2.65
(range 1-4), with liver and lymph node involvement predominating. RESULTS:
The overall response rate was 25% (95% CI 17.7-32.3%); 30.7% for poorly
differentiated cancers and 25% for well differentiated cancers. Median
survival was 4 months (range 1-12 months), 4.8 months for patients
attaining partial response. Toxicity was moderate, grade 3 and 4
neutropenia occurred in 55% and grade 3 and 4 thrombocytopenia in 40%;
other toxicities were mild. CA125 and CA199 were elevated in more than 50%
of patients. Viral serology studies were not significantly different from
those of the indigenous population. CONCLUSION: Etoposide and cisplatin
combination chemotherapy has modest activity in patients with extensive
CUPS and, at the schedule and dosage given, it is associated with moderate
toxicity.
相似文献
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从头序木(AraliadasyphylaMiq)叶中分离到6个三萜化合物,用化学方法和波谱(UV,IR,MS,1HNMR,13CNMR,13CDEPT,HMQC,HMBC)分析,确定其中4种化合物的结构,分别为齐墩果酸(I),16β羟基18βH齐墩果酸(I),齐墩果酸28OβD吡喃葡萄糖甙(II)和16β羟基18βH齐墩果酸28OβD吡喃葡萄糖甙(IV)。用NOESY谱确定化合物I的立体构型。以上4个化合物均为首次从该植物中分离到,化合物IV为新化合物。 相似文献
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40.
Evaluation of inflammatory bowel disease with 99mTc-DTPA 总被引:1,自引:0,他引:1