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排序方式: 共有226条查询结果,搜索用时 15 毫秒
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Kenneth V. Honn Dean G. Tang Xiang Gao Igor A. Butovich Bin Liu Jozsef Timar Wolfgang Hagmann 《Cancer metastasis reviews》1994,13(3-4):365-396
Arachidonic acid metabolites have been implicated in multiple steps of carcinogenesis. Their role in tumor cell metastasis, the ultimate challenge for the treatment of cancer patients, are however not well-documented. Arachidonic acid is primarily metabolized through three pathways, i.e., cyclooxygenase, lipoxygenase, and P450-dependent monooxygenase. In this review we focus our attention on one specific lipoxygenase, i.e., 12-lipoxygenase, and its potential role in modulating the metastatic process. In mammalian cells there exist three types of 12-lipoxygenases which differ in tissue distribution, preferential substrates, and profile of their metabolites. Most of these 12-lipoxygenases have been cloned and sequenced, and the molecular and biochemical determinants responsible for catalysis of specific substrates characterized. Solid tumor cells express 12-lipoxygenase mRNA, possess 12-lipoxygenase protein, and biosynthesize 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid], as revealed by numerous experimental approaches. The ability of tumor cells to generate 12(S)-HETE is positively correlated to their metastatic potential. A large collection of experimental data suggest that 12(S)-HETE is a crucial intracellular signaling molecule that activates protein kinase C and mediates the biological functions of many growth factors and cytokines such as bFGF, PDGF, EGF, and AMF. 12(S)-HETE plays a pivotal role in multiple steps of the metastatic cascade encompassing tumor cell-vasculature interactions, tumor cell motility, proteolysis, invasion, and angiogenesis. The fact that 12-lipoxygenase is expressed in a wide diversity of tumor cell lines and 12(S)-HETE is a key modulatory molecule in metastasis provides the rationale for targeting these molecules in anti-cancer and anti-metastasis therapeutic protocols. 相似文献
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Honn KV Aref A Chen YQ Cher ML Crissman JD Forman JD Gao X Grignon D Hussain M Porter AT Pontes JE Powell I Redman B Sakr W Severson R Tang DG Wood DP 《Pathology oncology research : POR》1996,2(1-2):98-109
Rates of prostate cancer (PCa) have increased so dramatically over the last decade that the age adjusted incidence rate for PCa is now greater than that any other cancer among men in the United States. This review, published as a three part series, provides a state-of-art assessment of the PCa problem in its divergent aspects.Part 1 covers epidemiology, incidence and progression. Several epidemiological studies have demostrated that first degree male relatives of men with PCa are at increased risk of developing the disease. Familial and genetic factors as well as medical, anthropometric, dietary, hormonal and occupational factors involved in PCa are discussed. Postmortem examination of the prostate in men without evidence of PCa documented a high frequency of adenocarcinoma. Latent disease occurred as early as the second decade of life. Although there is no significant difference in incidence between Caucasian and African-American males, high grade prostatic intraepithelial neoplasia (HGPIN) is higher in the latter group. While dietary fat, androgens and certain environmental factors may be determinants for PCa, the exact mechanism of tumorigenesis is still relatively unknown. The current thinking of the role of genomic instability, chromosomal alterations, tumor suppressor genes and the androgen receptor are explored. 相似文献
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Michelle Brusatori Michael H. Wood Stephanie C. Tucker Krishna Rao Maddipati S. Kiran Koya Gregory W. Auner Kenneth V. Honn Berhane Seyoum 《Journal of Diabetes》2022,14(4):271
BackgroundThis study profiles ceramides extracted from visceral and subcutaneous adipose tissue of human subjects by liquid chromatography‐mass spectrometry to determine a correlation with status of diabetes and gender.MethodsSamples of visceral and abdominal wall subcutaneous adipose tissue (n = 36 and n = 31, respectively) were taken during laparoscopic surgery from 36 patients (14 nondiabetic, 22 diabetic and prediabetic) undergoing bariatric surgery with a body mass index (BMI) >35 kg/m2 with ≥1 existing comorbidity or BMI ≥40 kg/m2. Sphingolipids were extracted and analyzed using liquid chromatography‐mass spectrometry.ResultsAfter logarithm 2 conversion, paired analysis of visceral to subcutaneous tissue showed differential accumulation of Cer(d18:1/16:0), Cer(d18:1/18:0), and Cer(d18:1/24:1) in visceral tissue of prediabetic/diabetic female subjects, but not in males. Within‐tissue analysis showed higher mean levels of ceramide species linked to insulin resistance, such as Cer(d18:1/18:0) and Cer(d18:1/16:0), in visceral tissue of prediabetic/diabetic patients compared with nondiabetic subjects and higher content of Cer(d18:1/14:0) in subcutaneous tissue of insulin‐resistant female patients compared with prediabetic/diabetic males. Statistically significant differences in mean levels of ceramide species between insulin‐resistant African American and insulin‐resistant Caucasian patients were not evident in visceral or subcutaneous tissue.ConclusionsAnalysis of ceramides is important for developing a better understanding of biological processes underlying type 2 diabetes, metabolic syndrome, and obesity. Knowledge of the accumulated ceramides/dihydroceramides may reflect on the prelipolytic state that leads the lipotoxic phase of insulin resistance and may shed light on the predisposition to insulin resistance by gender. 相似文献
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Although exposure of LLC-PK1 epithelial cell sheets to phorbol esters (TPA)
causes a near immediate and total decrease of transepithelial electrical
resistance (TER), continuation of exposure for 3 to 4 days results in a
tachyphylactic response as TER begins to return to control levels. Recovery
of TER is maximal by 5 to 6 days, but reaches only 70 to 80% of control
level. A reciprocal change in the transepithelial flux of D-mannitol
indicates that the TER decrease is indicative of an increase in tight
junction permeability. Exposure of cell sheets to TPA for several days also
results in the appearance of multilayered polyp- like foci (PLFs) across
the otherwise one cell layer thick cell sheets. The pattern of penetration
of the electron dense dye, ruthenium red, from the apical surface, across
the tight junction and into the lateral intercellular space indicates that
the tight junctions of the cell sheet become uniformly leaky after acute
exposure to TPA. However, when exposure is continued for several days, only
the junctions of cells in the PLFs manifest leakiness. The decrease in TER
following acute TPA exposure correlates with the translocation of protein
kinase C-alpha (PKC alpha) into a membrane-associated compartment. With
exposure of several days, only a trace of PKC alpha is visible by Western
immunoblot, and this is in the membrane-associated compartment.
Immunofluorescent microscopy indicates that the trace of PKC alpha seen in
the Western immunoblots is ascribable distinctly to cells of the PLFs.
Monolayer areas between PLFs show no discernible immunofluorescent signal.
The data therefore indicate that tight junction barrier function may be
restored in certain areas by the down regulation of PKC alpha from the
membrane-associated compartment. Failure to down regulate may result in the
paracellular leakiness and abnormal cell architecture of the PLFs. Possible
implications of this model for in vivo epithelial tumor promotion are
discussed.
相似文献
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The cathepsin B-like cysteine proteinase activity which has been implicated in tumor malignancy has been attributed to several cellular sources, including viable tumor cells, necrotic tumor cells, and host-inflammatory cells. We have isolated subpopulations of cells from eight rodent tumors of five histological types, using centrifugal elutriation, and verified the cellular composition of the subpopulations cytologically. Ninety-two % or greater of the cathepsin B-like activity was associated with the isolated fractions containing greater than or equal to 95% tumor cells of 86 +/- 2% (SE) viability (beta fractions). The isolated fractions consisting of necrotic tumor cells and inflammatory cells (alpha fraction) apparently contain a cysteine proteinase inhibitor, since both cathepsin B-like and cathepsin H activities in the beta fraction of B16 amelanotic melanomas could be inhibited by addition of the alpha fraction. 相似文献
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Tumor angiogenesis, the formation of new capillary blood vessels in tumors from pre-existing vasculature, is required for tumor growth and progression. Eicosanoids, the bioactive lipids derived from arachidonic acid, possess potent and diverse biological activities. In response to stimuli, arachidonic acid is mobilized from phospholipid pools and metabolized by cyclooxygenases (COX), lipoxygenases (LOX), and p450 epoxygenases (EOX) to form a variety of eicosanoids. The involvement of eicosanoids in tumor angiogenesis and progression is implicated by the observations that nonsteroidal anti-inflammation drugs (NSAIDs) reduce tumor growth and angiogenesis. Subsequently, it is found that the levels of COX-2 and/or 12-LOX are frequently increased in various cancers. Further studies using molecular and pharmacological approaches have found that COX-2 and 12-LOX, when overexpressed in carcinoma cells, enhance their angiogenic potential and stimulate tumor growth. In this article, we discuss how COX and LOX in cancer cells modulate tumor angiogenesis and present the possibility of using NSAIDs and LOX inhibitors as antiangiogenesis agents. 相似文献