全文获取类型
收费全文 | 1954篇 |
免费 | 187篇 |
国内免费 | 15篇 |
专业分类
耳鼻咽喉 | 14篇 |
儿科学 | 46篇 |
妇产科学 | 42篇 |
基础医学 | 321篇 |
口腔科学 | 21篇 |
临床医学 | 189篇 |
内科学 | 498篇 |
皮肤病学 | 97篇 |
神经病学 | 114篇 |
特种医学 | 53篇 |
外科学 | 391篇 |
综合类 | 8篇 |
一般理论 | 1篇 |
预防医学 | 57篇 |
眼科学 | 14篇 |
药学 | 121篇 |
中国医学 | 10篇 |
肿瘤学 | 159篇 |
出版年
2023年 | 10篇 |
2022年 | 67篇 |
2021年 | 131篇 |
2020年 | 56篇 |
2019年 | 71篇 |
2018年 | 93篇 |
2017年 | 66篇 |
2016年 | 86篇 |
2015年 | 69篇 |
2014年 | 104篇 |
2013年 | 91篇 |
2012年 | 126篇 |
2011年 | 147篇 |
2010年 | 77篇 |
2009年 | 66篇 |
2008年 | 113篇 |
2007年 | 124篇 |
2006年 | 112篇 |
2005年 | 116篇 |
2004年 | 85篇 |
2003年 | 67篇 |
2002年 | 60篇 |
2001年 | 17篇 |
2000年 | 9篇 |
1999年 | 13篇 |
1998年 | 12篇 |
1997年 | 10篇 |
1996年 | 4篇 |
1995年 | 8篇 |
1994年 | 3篇 |
1991年 | 15篇 |
1990年 | 8篇 |
1989年 | 9篇 |
1988年 | 4篇 |
1987年 | 15篇 |
1986年 | 8篇 |
1985年 | 8篇 |
1984年 | 8篇 |
1983年 | 5篇 |
1981年 | 3篇 |
1977年 | 4篇 |
1976年 | 3篇 |
1973年 | 3篇 |
1971年 | 4篇 |
1970年 | 5篇 |
1969年 | 4篇 |
1968年 | 7篇 |
1967年 | 7篇 |
1934年 | 2篇 |
1933年 | 2篇 |
排序方式: 共有2156条查询结果,搜索用时 31 毫秒
991.
992.
993.
Dmitry A. Bolotin Ilgar Z. Mamedov Olga V. Britanova Ivan V. Zvyagin Dmitriy Shagin Svetlana V. Ustyugova Maria A. Turchaninova Sergey Lukyanov Yury B. Lebedev Dmitriy M. Chudakov 《European journal of immunology》2012,42(11):3073-3083
The TCR repertoire is a mirror of the human immune system that reflects processes caused by infections, cancer, autoimmunity, and aging. Next generation sequencing (NGS) is becoming a powerful tool for deep TCR profiling; yet, questions abound regarding the methodological approaches for sample preparation and correct data interpretation. Accumulated PCR and sequencing errors along with library preparation bottlenecks and uneven PCR efficiencies lead to information loss, biased quantification, and generation of huge artificial TCR diversity. Here, we compare Illumina, 454, and Ion Torrent platforms for individual TCR profiling, evaluate the rate and character of errors, and propose advanced platform‐specific algorithms to correct massive sequencing data. These developments are applicable to a wide variety of next generation sequencing applications. We demonstrate that advanced correction allows the removal of the majority of artificial TCR diversity with concomitant rescue of most of the sequencing information. Thus, this correction enhances the accuracy of clonotype identification and quantification as well as overall TCR diversity measurements. 相似文献
994.
We analyzed the clinicopathologic features of 10 cases of vulvovaginal myofibroblastoma to widen its morphological and immunohistochemical spectrum. Most tumors (8/10 cases) were located in the vagina. The patients' age ranged from 44 to 77 years, and tumor size ranged from 0.4 to 3 cm. Histologically, 5 tumors had the characteristics of vulvovaginal myofibroblastoma. In addition, we identified 3 cases composed of spindle-shaped cells arranged in short fascicles with intervening thick collagen bands, closely reminiscent of mammary myofibroblastoma. Notably, 1 case resembled Sertoli cell tumor, sclerosing type, because of its predominant cord-like arrangement. In another case, there were highly cellular areas composed of uniform-packed, rounded cells that, at low magnification, looked like a malignant "small round blue cell tumor." A variably thick band of native connective tissue separated tumors from the overlying squamous epithelium even if, in 3 cases, tumor cells extended up to the epithelium. In 7 cases, a variable number of vessels showed perivascular hyalinization. Only rare mitotic figures were identified. All tumors were diffusely positive for vimentin, desmin, and CD99. A variable staining intensity was observed for CD34, Bcl-2, B-cell lymphoma 2 (Bcl-2) CD10, estrogen receptor, and progesterone receptor in most cases, but none expressed α-smooth muscle actin. We emphasize that vulvovaginal myofibroblastoma encompasses a morphological spectrum wider than previously described. The overlapping morphological and immunohistochemical features of vulvovaginal and mammary myofibroblastomas led us to speculate that these are related entities with morphological variations on a common basic theme likely dependent on anatomical location. 相似文献
995.
Kacerovska D Requena L Michal M Grossmann P Treskova I Roucka P Kazakov DV 《The American Journal of dermatopathology》2012,34(7):729-736
ABSTRACT:: Two unusual Carney complex patients are described. In one of them, several cutaneous biopsies revealed myxoid lesions that were rather more close to authentic adnexal neoplasms with myxoid stroma than to a "myxoma with an epithelial component." These included lesions resembling trichofolliculoma, infundibular cyst, and trichodiscoma. Additionally, 1 soft tissue myxoma was unique in the sense that it greatly resembled a cardiac myxoma, begging the question whether this could represent an embolus from the patient's cardiac myxoma. Given the large size and complexity and heterogeneity of the cutaneous lesions, the authors suggest that these may represent authentic cutaneous neoplasms accompanied by myxoid stroma and not adnexal elements induced by the stroma. However, the latter mechanism is well recognized and demonstrated by our second patient in whom adnexal-type elements in the cutaneous lesion were clearly induced by the myxoid stroma but were unusually complex by manifesting panfollicular and also sebaceous differentiation. 相似文献
996.
ABSTRACT:: The authors report on a case of panfolliculoma with sebaceous differentiation occurring on the scalp of a 53-year-old white man and discuss the pertinent literature. 相似文献
997.
Androgen deprivation induces human prostate epithelial neuroendocrine differentiation of androgen-sensitive LNCaP cells 总被引:3,自引:0,他引:3
Yuan TC Veeramani S Lin FF Kondrikou D Zelivianski S Igawa T Karan D Batra SK Lin MF 《Endocrine-related cancer》2006,13(1):151-167
Neuroendocrine (NE) cells are the minor cell populations in normal prostate epithelial compartments. During prostate carcinogenesis, the number of NE cells in malignant lesions increases, correlating with its tumorigenicity and hormone-refractory growth. It is thus proposed that cancerous NE cells promote prostate cancer (PCa) cell progression and its androgen-independent proliferation, although the origin of the cancerous NE cells is not clear. To investigate the role of cancerous NE cells in prostate carcinogenesis, we characterized three NE subclone cell lines-NE-1.3, NE-1.8 and NE-1.9, which were transdifferentiated from androgen-sensitive human PCa LNCaP cells by culturing in an androgen-depleted environment, resembling clinical androgen-ablation therapy. These subclone cells acquire many features of NE cells seen in clinical prostate carcinomas, for example exhibiting a neuronal morphology and expressing multiple NE markers, including neuron-specific enolase, chromogranin B, neurotensin, parathyroid hormone-related peptide, and to a lesser degree for chromogranin A, while lacking androgen receptor (AR) or prostate specific antigen (PSA) expression. These cells represent terminally differentiated stable cells because after 3 months of re-culturing in a medium containing androgenic activity, they still retained the NE phenotype and expressed NE markers. Despite these NE cells having a slow growth rate, they readily developed xenograft tumors. Furthermore, media conditioned by these NE cells exhibited a stimulatory effect on proliferation and PSA secretion by LNCaP cells in androgen-deprived conditions. Additionally, we found that receptor protein tyrosine phosphatase alpha plays a role in upregulating multiple NE markers and acquiring the NE phenotype. These NE cells thus represent cancerous NE cells and could serve as a useful cell model system for investigating the role of cancerous NE cells in hormone-refractory proliferation of PCa cells. 相似文献
998.
Gabrilovich DI 《Expert opinion on biological therapy》2006,6(8):823-832
Mutations in the p53 gene are the most frequent genetic alterations in human tumours, occurring in approximately 50% of all cancers. The p53 protein is pivotal in maintaining genetic integrity after DNA damage, and alterations in the p53 pathway, including mutations in the p53 gene, greatly increase the probability of tumour formation. Gene therapy using adenoviral p53 has emerged as a novel treatment option, with the potential to be safe and effective in a wide range of cancer types. INGN 201 (Ad5CMV-p53, Advexin), a replication-impaired adenoviral vector that carries the p53 gene, has been evaluated in both preclinical and clinical trials. Results show that Advexin is a well-tolerated and efficacious treatment for numerous cancers, both as monotherapy and in combination with radiation and/or chemotherapy agents. In addition, there is now data to support the use of Advexin in cancer immunotherapy. 相似文献
999.
Veprintsev DB Freund SM Andreeva A Rutledge SE Tidow H Cañadillas JM Blair CM Fersht AR 《Proceedings of the National Academy of Sciences of the United States of America》2006,103(7):2115-2119
The tumor suppressor p53 consists of four 393-residue chains, each of which has two natively unfolded (N- and C-terminal) and two folded (core and tetramerization) domains. Their structural organization is poorly characterized as the protein tends to aggregate, has defied crystallization, and is at the limits of NMR studies. We first stabilized the protein by mutation to make it more suitable for extended study and then acquired NMR spectra on full-length protein and various combinations of shorter domain constructs. The NMR spectrum (15N,1H transverse relaxation optimized spectroscopy) of full-length p53 was close to that expected from the sum of the spectra of isolated individual domains. However, patterns of changes in chemical shifts revealed unexpected interactions between the core domains. We used the NMR data as constraints in docking algorithms and found a previously uncharacterized self-complementary surface for the association of core domains into dimers within the tetrameric complex. Binding to DNA requires about a 70 degrees rotation to break those subunit interactions and form the known protein:protein interface in the p53-DNA complex. We verified the interactions by the effects of mutation on DNA binding. Spectroscopic, biophysical, and mutational data conspired to give a picture of the p53 tetramer as a dimer of loosely tethered core dimers of appropriate symmetry to be poised to bind target DNA. 相似文献
1000.