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991.
100对615系种鼠,常规饲养繁殖,观察33个月(终生),其乳腺癌发病率为5.5%(11例全部发生于经产雌鼠),低于肺腺癌(11%,22例,雌雄各半)而居第二位,故615系小鼠仍属低乳癌品系。对615系小鼠的46例自发乳腺癌进行了病理形态学检查分析:瘤细胞可分为小、中、大三类。组织分型属A型者18例,多由小细胞及少量中细胞构成;属B型者28例,除小细胞外往往可见较多的中细胞甚或主要由大细胞与中细胞构成。B型乳腺癌的分化程度似较A型者为低。转移主要发生于肺部。7例经镜检证实属乳腺癌的肺转移瘤,其原代瘤属A型者1例,属B型者6例。肺转移瘤的组织像与原发瘤基本相同者4例;而细胞变大,呈实心排列,显示分化程度低于原发瘤者3例。 相似文献
992.
本文对6例乳腺导管扩张症进行了临床病理报道,6例术前皆被误诊乳腺其他疾病,根据此种情况作了如何正确诊断的阐述.提出了常见误诊病例如何鉴别。 相似文献
993.
本文用显微分光光度计对39例手术切除的不同组织学类型的人体肺癌标本癌细胞核的DNA含量进行了测量。其中高、中、低分化的鳞癌分别为3、6和5例;高、中、低分化的腺癌分别为3、5和5例;未分化癌大细胞型和小细胞型各为3例和6例。结果发现各类型肺癌的DNA含量均有统计学上的差异(P<0.01)。各DNA含量直方图的峰值部位及分布范围亦不同。从而提示了根据DNA含量的不同,可能有助于肺癌组织学类型及其分化程度的判别:而DNA含量直方图对肺癌类型的判别亦可能是有益的。 相似文献
994.
个性化护理干预对妇科恶性肿瘤手术后生活质量的影响 总被引:2,自引:0,他引:2
[目的]探讨个性化护理干预对妇科恶性肿瘤手术后生活质量的影响。[方法]将46例在我科因妇科恶性肿瘤手术的患者随机分为实验组和对照组,通过实施个性化护理干预,对两组患者进行SF-36量表和Olson婚姻质量问卷进行测评。[结果]对妇科恶性肿瘤手术后患者进行个性化护理干预后其生活质量明显提高,差异有显著性意义(P〈0.01)。[结论]个性化护理干预能提高妇科恶性肿瘤手术后生活质量。 相似文献
995.
Background Gene therapy by adenovirus-mediated wild-type p53 gene transfer has been shown to inhibit lung cancer growth in vitro, in animal models, and in human clinical trials. The antitumor effect of selective cyclooxygenase (COX)-2 inhibitors has been demonstrated in preclinical studies. However, no information is available on the effects of p53 gene therapy combined with selective COX-2 inhibitor on COX-2 gene expression and growth inhibition of human lung cancer cells. Methods We evaluated the effects of recombinant adenovirus-p53 (Adp53) gene therapy combined with selective CADX-2 inhibitor on the proliferation, apoptosis, cell cycle arrest of human lung adenocarcinoma A549 cell line, and the effects of tumor suppressor exogenous wild type p53 on COX-2 gene expression. Results Ad-p53 gene therapy combined with selective COX-2 inhibitor celecoxib shows significant synergistic inhibition effects on the growth of human lung adenocarcinoma A549 cell line. Exogenous p53 gene can suppress COX-2 gene expression. Conclusions Significant synergistic inhibition effects of A549 cell line by the combined Ad-p53 and selective COX-2 inhibitor celecoxib may be achieved by enhancement of growth inhibition, apoptosis induction and suppression of COX-2 gene expression. This study provides first evidence that the administration of p53 gene therapy in combination with COX-2 inhibitors might be a new clinical strategy for the treatment or prevention of NSCLC. 相似文献
996.
997.
目的比较基底节脑出血开颅手术治疗与钻颅抽吸治疗的有效性与安全性。方法回顾性分析我院近5年来基底节出血行外科开颅治疗和钻颅抽吸治疗的所有病例,应用统计学方法进行疗效比较。结果共136例基底节出血病例,其中30例行外科开颅清除血肿治疗,106例行钻颅抽吸治疗。两组病例在年龄、出血量、意识状态等预后影响因素方面差异无统计学意义(P〉0.05)。基底节出血开颅手术治疗有效性与安全性与钻颅抽吸治疗相比差异无统计学意义(P〉0.05)。结论基底节出血外科开颅治疗有效性与安全性并不优于钻颅抽吸治疗。 相似文献
998.
Evidence from both experimental carcinogenesis and studies in human cirrhotic liver suggest that defective repair of the
promutagenic DNA base lesion, O
6-methylguanine, is a factor in the multistep process of hepatocellular carcinogenesis. Ubiquitous environmental alkylating
agents such as N-nitroso compounds can produce O
6-methylguanine in cellular DNA. Unrepaired, O
6-methylguanine can lead to the formation of G ? A transition mutations, a known mechanism of human oncogene activation and
tumour suppressor gene inactivation. Combined treatment of rodents with an agent producing O
6-methylguanine in DNA, and an agent promoting cell proliferation, leads to development of hepatic nodules and hepatocellular
carcinoma (HCC), cell division, hence DNA replication, being required for the propagation of tumorigenic mutation(s) in hepatocyte
DNA. The paramount importance of O
6-methylguanine in hepatocellular carcinogenesis is indicated by the observation that transgenic mice engineered to have increased
hepatic levels of repair enzyme O
6-methylguanine-DNA methyltransferase (MGMT) are significantly less prone to hepatocellular carcinogenesis following alkylating
agent treatment. Cirrhosis is a universal risk factor for development of human HCC, and a condition that is characterized
by increased hepatocyte proliferation as a result of tissue regeneration. Levels of the human repairing enzyme for O
6-methylguanine were found to be significantly lower in cirrhotic liver than in normal tissue. In accord with findings from
animal models, this suggested a mechanism in which persistence of O
6-methylguanine due to defective DNA repair by MGMT, together with increased hepatocyte proliferation, might lead to specific
gene mutation(s) and hepatocellular carcinogenesis. Screening for the presence and persistence of O
6-methylguanine in human DNA presently involves formidable technical difficulty. Indications are that such limitations might
be overcome by the use of an ultrasensitive method such as immuno-polymerase chain reaction (PCR). This approach should allow
parallel measurement of DNA adduct and repair enzyme in routine liver biopsy samples. It might also enable investigation of
O
6-methylguanine in human genes specifically associated with hepatocellular carcinogenesis. Given the wide variation in human
MGMT levels observed between individuals, tissues, and cells, this technology should be adapted to permit the ultrasensitive
localisation and measurement of adducts and repairing enzyme in liver biopsy tissue sections. Ability to ultrasensitively
measure O
6-methylguanine, and its repair enzyme, should prove valuable in the risk assessment of cirrhotic patients for developing hepatocellular
carcinoma.
Received for publication on July 6, 1998; accepted on Aug. 12, 1998 相似文献
999.
1000.
3例前列腺癌施行双侧睾丸节除术后2-12周的患,每天肌注苯甲酸雌二醇1mg,d。治疗前后分别每10min采血一次,作7h LH脉冲分析。结果表明,3例患平均血清LH水平分别由177.58±3.20,138.30±5.83和145.88±3.82IU/LGHBTGC 174.90±7.60,132.02±5.77和142.80±3.65IU/L(P均<0.01),但LH脉冲幅度和频率无明显变化( 相似文献