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1.
《Gaceta sanitaria / S.E.S.P.A.S》2016,30(6):421-425
ObjectiveThe loss of chance in healthcare has been forcibly introduced in the adjudications pronounced in recent years. Our objective was to analyse the verdicts of guilt resulting from the loss of chance ordered by the Contentious-Administrative Court (i.e., in the public healthcare system), in which both the origin of the disease to be treated and the sequelae were oncological processes.MethodWe analysed 137 cancer-related court judgments from the Contentious-Administrative Court, which referred to the concept of loss of chance, issued in Spain up to May 2014.ResultsOf the 137 sentences, 119 (86.9%), were pronounced due to diagnostic error and 14 (10.2%) due to inadequate treatment. Since 2010, 100 sentences have been passed (73.0%), representing an increase of more than 170% with respect to the 37 (27.0%) ordered in the first six years of the study (from 2004 to 2009). Most of the patients (68.6%) died, predominantly from breast cancer and gynaecological cancer (24.1%), and gastrointestinal cancers (21.1%). These malignancies were the ones most often involved in the sentences.ConclusionsThe litigant activity due to loss of chance in oncological processes in the public health care has significantly increased in the last years. The judgments were mainly given because of diagnostic error or inadequate treatment. 相似文献
2.
目的 探讨男孩8岁时父亲去世对其带来的创伤影响。方法 运用质的研究方法,对一名在8岁时经历父亲去世的男大学生进行深入访谈,采用主要概念或主题突出分类的方法进行编码分析。结果 父亲去世使个体产生了强烈的不安全感,严重的自卑感和神经症性的防御机制。结论 父亲去世后,家庭氛围是影响孩子心理健康的重要因素。 相似文献
3.
庆大霉素中毒性耳聋 总被引:1,自引:0,他引:1
庆大霉素目前仍是主要的致聋抗生素,庆大霉素中毒性耳聋的发病机制包括自由基损伤学说、内耳微循环障碍学说、毛细胞线粒体功能失常学说、细胞凋亡等,并发现一些与耳聋相关的基因。聚DL-天冬氨酸(PAA)、表皮生长因子(EGF)表皮生长因子(EGF)、碱性成纤维细胞生长因子(bFGF)、神经营养凼子3(NT3)、高压氧等对庆大霉素的耳毒性有一定的拈抗作用。中医药丹参、天鼓冲剂、复聪片、耳聋左慈丸等也可减轻庆大霉素的耳毒性。庆大霉素中毒性耳聋基因治疗具有良好的前景。制造一种由病毒DNA序列和非病毒载体结构共同组成的复合型载体,也许是未来基因治疗载体得到完善、基因治疗得到突破性进展的着手点之一。 相似文献
4.
5.
沈阳市961名老年干部牙健康状况调查 总被引:4,自引:0,他引:4
目的了解并分析沈阳市老年干部牙健康状况。方法按第二次全国口腔健康流行病学抽样调查标准,对沈阳市961名60岁以上的老年干部进行口腔健康调查,结果用SPSS软件处理。结果患龋率为67.12%,患龋者的龋均随着年龄的增长而逐渐增高(P<0.05),龋齿全部充填率为33.18%。缺牙率为80.65%,人均失牙7.38颗,人均保留牙的数目与年龄呈负相关(P<0.01)。无牙牙合率为10.20%,无牙牙合与牙列缺损的修复率分别为98.98%和36.04%。牙周健康状况与年龄呈负相关(P<0.01)。结论牙列缺失及缺损是老年人常见的口腔疾患,龋病和牙周病是其主要原因。加强老年人的口腔保健意识,是提高口腔疾病治疗成功率的重要环节,进而增进老年人的全身健康。 相似文献
6.
染色体1pter-p36.21杂合性缺失与瘢痕疙瘩的关系 总被引:5,自引:0,他引:5
目的寻找瘢痕疙瘩1pter-36.21中可能存在的肿瘤抑制基因的杂合性丢失(LOH)区域,为发现和定位瘢痕抑制基因提供线索和依据。方法采用聚合酶链反应(PCR)-变性聚丙烯酰胺凝胶电泳技术,对25例瘢痕疙瘩组织和外周静脉血标本进行微卫星分析。结果瘢痕疙瘩组织在所选的位点上的LOH发生率为60%(15/25),明显高于正常对照组织的4%(1/25,P<0.05),在所选的位点上均未发现微卫星不稳定性(MSI)。D1S243位点、D1S468位点、D1S507位点、D1S199位点的LOH发生率分别为28%(7/25)、40%(10/25)、52%(13/25)、12%(3/25),其中D1S243、D1S468、D1S507的LOH发生率比较具有统计学意义(P<0.05)。结论发生在D1S243-D1S468-D1S507位点的LOH存在与瘢痕疙瘩有关的潜在瘢痕抑制基因(SSG),而1pter-36.21上LOH微卫星不稳定性与瘢痕疙瘩发生的关系不大。 相似文献
7.
We have established a rat model that reflects the course of development of alcohol and opiate addiction. The present study
with d-amphetamine aimed to define general principles in the development of an addiction. Male rats had a continuous free choice
between d-amphetamine solutions (100, 200 and 400 mg/l) and water for 47 weeks. An initial intake of high doses of d-amphetamine during the first weeks of drug choice was followed by an individually stable pattern of drug consumption of moderate
drug doses. During this period of controlled consumption (from week 10 to week 40), the voluntary intake of d-amphetamine depended on individual factors (dominant rats: 0.37 ± 0.02 mg/kg per day, subordinate rats: 0.57 ± 0.05 mg/kg
per day) and environmental variables (group housing: 0.21 ± 0.02 mg/kg per day, single housing: 0.41 ± 0.03 mg/kg per day).
Beginning with week 41, voluntary d-amphetamine consumption progressively increased (1.9 ± 0.2 mg/kg per day in week 47), although the experimental conditions
remained unchanged. Drug intake during a retest (free choice as before) after 6 months of drug deprivation revealed that the
rats had persistently lost their control over drug intake and were no longer able to adjust drug taking to internal and external
conditions. These addicted rats took very high drug doses, even when all d-amphetamine solutions but not water were adulterated with bitter tasting quinine (6.6 ± 0.6 mg/kg per day; age-matched controls:
0.37 ± 0.04 mg/kg per day). Forced intake of d-amphetamine for 47 weeks (7.1 ± 0.3 mg/kg per day) via the drinking fluid caused physical dependence (hyperreactivity during
withdrawal) but did not lead to drug addiction (voluntary intake in the retest with adulteration: 0.42 ± 0.04 mg/kg per day).
Both the temporal development and the prerequisites of psychostimulant addiction were in principle the same as for alcohol
and opiates.
Received: 3 April 1998/Final version: 26 August 1998 相似文献
8.
Loss of heterozygosity on chromosomes 3p,8p,9p and 17p in the progression of squamous cell carcinoma of the larynx 总被引:4,自引:0,他引:4
Yoo WJ Cho SH Lee YS Park GS Kim MS Kim BK Park WS Lee JY Kang CS 《Journal of Korean medical science》2004,19(3):345-351
Previous molecular genetic studies of laryngeal squamous cell carcinoma (SCC)have shown certain chromosomal regions with recurring alterations. But studies of sequential molecular alterations and genetic progression model of laryngeal SCC have not been clearly defined. To identify the chromosomal alterations associated with the carcinogenesis of laryngeal SCC, we analyzed genomic DNA from microdissected squamous metaplasia, squamous dysplasia, invasive SCC, and metastatic carcinoma samples from 22 laryngeal SCC patients for loss of heterozygosity (LOH) at microsatellite loci. Ten microsatellite markers on chromosome 3p, 8p, 9p, and 17p were used. LOH at 9p21 was observed in the all stages including squamous metaplasia, squamous dysplasia, invasive SCC and metastatic carcinoma. LOH at 17p13.1, 3p25 and 3p14.2 was observed from the squamous dysplasia, invasive SCC and metastatic carcinoma. LOH at 8p21.3-p22 was observed mainly from the invasive SCC and metastatic carcinoma. The results suggest that 9p21 in the early event, 17p13.1, 3p25 and 3p14.2 in the intermediate event and 8p21.3- p22 in the late event may be involved in the laryngeal carcinogenesis. 相似文献
9.
Kazuhiko Orikasa Shin-ichi Fukushige Senji Hoshi Seiichi Orikasa Keiichi Kondo Yasuhide Miyoshi Yoshinobu Kubota A. Horii 《Journal of human genetics》1998,43(4):228-230
Prostate cancer is a major cause of cancer death among elderly men in America, Europe, and Japan. However, the molecular
mechanism of carcinogenesis is not yet well characterized. Frequent loss of heterozygosity (LOH) on chromosome 10q was reported
in prostate cancer, and a candidate tumor suppressor gene, PTEN, was isolated on chromosome band 10q23.3. To investigate the genetic alterations of PTEN, we examined 45 primary prostate cancer specimens. LOH at the PTEN locus was observed in two (11.1%) of 18 tumors. However, no mutations were observed in any of the primary prostate cancers.
These data suggest that mutation of the PTEN gene does not play a major role in prostate carcinogenesis of Japanese patients.
Received: February 6, 1998 / Accepted: July, 3, 1998 相似文献
10.
Mutation analysis of the TSC1 and TSC2 genes in Japanese patients with pulmonary lymphangioleiomyomatosis 总被引:2,自引:0,他引:2
Sato T Seyama K Fujii H Maruyama H Setoguchi Y Iwakami S Fukuchi Y Hino O 《Journal of human genetics》2002,47(1):20-28
Pulmonary lymphangioleiomyomatosis (LAM) is a destructive lung disease characterized by a diffuse hamartomatous proliferation
of smooth muscle cells (LAM cells) in the lungs. Pulmonary LAM can occur as an isolated form (sporadic LAM) or in association
with tuberous sclerosis complex (TSC) (TSC-LAM), a genetic disorder with autosomal dominant inheritance with various expressivity
resulting from mutations of either the TSC1 or TSC2 gene. We examined mutations of both TSC genes in 6 Japanese patients with TSC-LAM and 22 patients with sporadic LAM and identified six unique and novel mutations.
TSC2 germline mutations were detected in 2 (33.3%) of 6 patients with TSC-LAM and TSC1 germline mutation in 1 (4.5%) of 22 sporadic LAM patients. In accordance with the tumor-suppressor model, loss of heterozygosity
(LOH) was detected in LAM cells from 3 of 4 patients with TSC-LAM and from 4 of 8 patients with sporadic LAM. Furthermore,
an identical LOH or two identical somatic mutations were demonstrated in LAM cells microdissected from several tissues, suggesting
LAM cells can spread from one lesion to another. Our results from Japanese patients with LAM confirmed the current concept
of pathogenesis of LAM: TSC-LAM has a germline mutation but sporadic LAM does not; sporadic LAM is a TSC2 disease with two somatic mutations; and a variety of TSC mutations causes LAM. However, our study indicates that a fraction of sporadic LAM can be a TSC1 disease; therefore, both TSC genes should be examined, even for patients with sporadic LAM.
Received: August 30, 2001 / Accepted: November 2, 2001 相似文献