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21.
目的 研究雌激素受体(ER)a和β在良性肺组织和肺癌组织中的表达及其与临床和病理学特征的关系。方法 采用免疫组织化学方法检测ERa和β在18例肺腺癌和29例肺鳞状细胞癌(共有35例含癌旁肺组织)及12例良性肺病变组织中的表达。切片内阳性细胞数≥20%为ER阳性。结果 ERβ在肺癌组织中的表达主要定位于细胞核,其在肺癌组织中的表达率为44.7%(21/47),而在癌旁肺组织和肺良性病变组织中无明显表达。ERβ在鳞状细胞癌、腺癌中阳性表达率分别为27.6%(8/29)、72.2%(13/18),腺癌组织中ERβ表达率显著高于鳞癌(P<0.05)。ERβ在肺癌、癌旁肺组织和肺良性病变组织中均未见表达。结论 结果提示雌激素受体ERβ与肺癌尤其是肺腺癌的发生可能有关联。  相似文献   
22.
雌孕激素联合补充治疗与脑卒中的预防   总被引:6,自引:0,他引:6  
目的 探讨低剂量雌孕激素联合补充治疗对脑卒中的预防作用。方法 绝经过渡期及绝经后妇女84例随机设激素补充治疗组和对照组 ,采用酶免法测定治疗前后血脂和雌二醇 (E2 )水平。结果 治疗前后 E2、高密度脂蛋白 (HDL)增高 ,低密度脂蛋白 (L DL)、总胆固醇 (TC)降低 ,差异显著 (P<0 .0 5 ) ,甘油三酯 (TG)变化不明显。结论 低剂量雌激素对血脂谱产生有利影响 ,可降低脑卒中的发生  相似文献   
23.
The relationship between the histological grade of dedifferentiation of thyroid cancer and estrogen receptors (ER) was examined immunohistochemically. Thyroid cancers were from postmenopausal females of almost the same mean age (69-73 years old) and within the same period of time (1974–1983). ER immunoreactivity located in the nucleus of the epithelium was found in all 6 well differentiated papillary cancers, and 5 of them (83.3%) showed ER-immunoreactive (ER-IR) cells amounting to 20 or more per visual field (x 100) under a light microscope. Of the 6 cases of poorly differentiated papillary cancer, 5 (83.3%) had 1-19 ER-IR cells per visual field. ER-IR cells were negative in 5 out of 6 cases (83.3%) of anaplastic cancers. Thus, the number of ER-IR cells tended to decrease with the degree of atypism of thyroid cancer (P < 0.001).  相似文献   
24.
Recently we reported that castration of rats eliminates vasopressin immunoreactivity in the lateral septum and other areas that appear to receive vasopressin innervation from the bed nucleus of the stria terminalis. Testosterone treatment counteracts this effect of castration. In the present study, we investigated whether this action of testosterone depends on its androgenic or estrogenic metabolites by treating long-term castrated rats with estradiol (E) and/or 5 alpha-dihydrotestosterone (DHT) or testosterone. The brains were then processed for immunocytochemistry or radioimmunoassay. DHT did not increase vasopressin staining in the lateral septum, although it fully restored the size of the seminal vesicles. E did restore the original fiber density, but individual fibers stained more weakly than in sham-operated males. Only treatment with both E and DHT fully restored the vasopressin innervation. This pattern was also reflected in the radioimmunoassay data. The vasopressin content of the lateral septum decreased about 90% after castration but was fully restored by either testosterone or E + DHT treatment. E alone, however, was only half as effective as E + DHT. The treatments had no effect on the oxytocin content of the septum, or on the vasopressin or oxytocin content of the dorsal vagal complex. The results suggest that E mediates most of the effects of testosterone on the vasopressin innervation of the lateral septum. DHT enhances the response to E but has little effect on its own.  相似文献   
25.
Objective: To investigate the clinical efficacy of estrogen or contraceptives in the treatment of acute bleeding of dysfunctional uterine bleeding (DUB) in adolescent patients and the optimal starting dosage of drugs.Methods: The clinical records of 106 girls who with DUB and moderate or severe anemia from February 1990 to July 2005 were analyzed retrospectively.Results: All 106 patients received hormonal therapy. 56 patients were treated with estradiol benzoate(E2), 30 patients with conjugated equine estrogen(CEE) and 20 patients with combined oral contraceptives (COCs). The rates for rapidly controlling bleeding and for rapidly stopping bleeding in E2 group were higher than those in CEE group ,but similar to those in COCs group. The days for controlling and completely stopping bleeding were not significantly different between the starting dosages (≤8 mg/d and >8 mg/d) of E2 groups, and also there were no statistical difference between the starting dosages (<7.5 mg/d and ≥7.5 mg/d) of CEE groups, but during the treatment the rate of increasing the dosage in <7.5 mg/d group was higher than that of ≥7.5 mg/d group(40% vs. 5%),while there were no statistical difference between the starting dosages (≤3 pills/d and >3 pills/d) of COCs groups. Conclusions: The clinical efficiency of E2 treatment on DUB in adolescent patients is similar to that of COCs. And the efficacies of treatment of DUB with E2, CEE and COCs in the different dosages are similar.  相似文献   
26.
雌激素及其受体对心血管系统保护作用实验研究进展   总被引:8,自引:0,他引:8  
雌激素对心血管系统具有重要的保护作用。雌激素及其受体主要通过调节血管舒张功能、抑制血管平滑肌细胞增殖和迁移以及影响肾素 -血管紧张素等介导这一保护作用。但临床上雌激素替代治疗尚未得到肯定 ,需进一步研究  相似文献   
27.
Shionogi carcinoma 115 (SC115), an androgen-dependent mouse mammary tumor, rapidly loses its androgen responsiveness after androgen withdrawal. The growth of this tumor can also be stimulated by high doses of estrogen or glucocorticoid. In the present study, the maintenance of hormone-responsive growth of SC115 tumors with a high dose of estrogen was examined in castrated male mice using an SCI 15 subline obtained by serial transplantations of SCI 15 tumors in estrogen-treated castrated mice for 3 years (30 generations) (subline E2). Seed tumors from both SC115 and subline E2 could rapidly grow in castrated mice given daily injections of testosterone propionate (TP), 17β-estradiol (E2), or dexamethasone (Dex) (100 μg/mouse/day) but not in those given vehicle alone. Although SCI 15 and subline-E2 tumors grown with TP or Dex showed temporary regression after steroid withdrawal, the tumors grown with E2 did not show such temporary regression. The TP-, E2-, or Dex-induced growth of subline-E2 tumors was almost the same as that of the original SCI 15 tumors. However, responsiveness to androgen, estrogen or glucocorticoid of both tumors disappeared within one passage in steroid-depleted castrated mice. The present findings demonstrate that the loss of responsiveness to androgen as well as to high doses of estrogen or glucocorticoid of SCI 15 tumors can be prevented in castrated mice not only with androgen but also with high doses of estrogen.  相似文献   
28.
L. J. Murphy 《Diabetologia》1988,31(11):842-847
Summary Circulating somatomedin-C/insulin-like growth factor-I levels are low in the diabetic rat and unresponsive to exogenous growth hormone. However, the nature of this defect in growth hormone action remains unclear and there is little data on insulin-like growth factor-I gene expression in response to other stimuli and in non-hepatic tissues where insulin-like growth factor-I may have important paracrine and/or autocrine actions. We have previously shown that 17-beta estradiol stimulates uterine insulin-like growth factor-I expression in the ovariectomised rat. In this report uterine and hepatic insulin-like growth factor-I gene expression have been examined in the streptozotocin-diabetic rat. Serum insulin-like growth factor-I concentrations were significantly reduced in diabetic rats compared to normal rats (0.72±0.08 vs 1.23±0.05U/ml, p<0.0005) and hepatic insulin-like growth factor-I mRNA abundance was similarly reduced in diabetic rats to 49±5% of that seen in non-diabetic intact rats (p<0.005). In contrast, uterine insulin-like growth factor-I mRNA abundance was not significantly reduced in diabetic rats compared to control rats (76±12%, p = NS). Although both diabetic and non-diabetic rats demonstrated a significant increase in uterine wet weight following a single injection of 17-beta estradiol the increase in uterine insulinlike growth factor-I expression was significantly less marked in diabetic rats. Acute administration of insulin together with estradiol had no significant effect on serum insulin-like growth factor-I concentrations or hepatic insulin-like growth factor-I mRNA abundance; however, the uterine insulin-like growth factor-I response was significantly (p<0.01) augmented. The observations reported here demonstrate that hepatic insulin-like growth factor-I gene expression is markedly reduced in the diabetic rat and that the estradiol-induced uterine insulin-like growth factor-I response is significantly diminished, consistent with the hypothesis that there is a defect in insulin-like growth factor-I gene activation in the diabetic rat.  相似文献   
29.

Background

Motherwort has been used as medicinal herb for many years in both China and Europe. In particular, Chinese motherwort has been commonly used to treat disorders of mammary gland in Chinese traditional medicine (TCM). Chinese motherwort aqueous extract (MAE) was previously reported to have anti-cancer activity in breast cancer cells with low potency (IC50s in a range of 8–40 mg/mL). However, treatment of motherwort ethanol extract in vivo markedly suppressed the development of uterine adenomyosis and mammary cancers in mice. Therefore, anti-cancer activity of Chinese motherwort, especially in a form of ethanol extract, needs to be confirmed further at cellular level.

Materials and methods

Aerial part of Chinese motherwort (Leonurus japonicus Houtt) dry powder is extracted with 70% ethanol and the chemical components were characterized with HPLC finger print as well as mass spectrometry. Cytotoxicity of the motherwort aqueous ethanol extract (MAEE) was analyzed with MTT assay on ER negative MDA-MB-231 and ER positive MCF-7 human breast cancer cell lines. Hoechst 33342 staining and flow cytometry were used to verify whether the cell death induced by MAEE is apoptosis in nature. Cell cycle status of MAEE treated cells were analyzed with flow cytometry.

Results

Our results showed that MAEE caused cell death in a dose-dependent and time-dependent fashion in both ER positive and negative breast cancer cells. Morphology, Hoechst 33342 staining and flow cytometry evidence all indicated the cell death is not in an apoptotic nature. Furthermore, low concentrations of MAEE caused cell cycle arrest at G2/M phase.

Conclusions

These data suggest that Chinese motherwort aqueous ethanol extract may effectively inhibit the proliferation of breast cancer cells through mechanisms of both cytotoxicity and cell cycle arrest. The cellular effects of MAEE are non-apoptotic and ER independent on breast cancer cells.  相似文献   
30.
肺血管扩张在肝肺综合征发病机制中作用的研究进展   总被引:3,自引:0,他引:3  
肺血管扩张是肝肺综合征的主要发病机制,然而导致HPS肺血管扩张的机制相当复杂,至今仍不清楚.目前认为肺血管内巨噬细胞聚积和雌激素升高导致的血管活性因子增多和活性增强可能与此有关,近年来这方面的研究很多,本文对此作一综述.  相似文献   
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