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1.
There is a diverse range of microbiological challenges facing the food, healthcare and clinical sectors. The increasing and pervasive resistance to broad‐spectrum antibiotics and health‐related concerns with many biocidal agents drives research for novel and complementary antimicrobial approaches. Biofilms display increased mechanical and antimicrobial stability and are the subject of extensive research. Cold plasmas (CP) have rapidly evolved as a technology for microbial decontamination, wound healing and cancer treatment, owing to the chemical and bio‐active radicals generated known collectively as reactive oxygen and nitrogen species. This review outlines the basics of CP technology and discusses the interactions with a range of microbiological targets. Advances in mechanistic insights are presented and applications to food and clinical issues are discussed. The possibility of tailoring CP to control specific microbiological challenges is apparent. This review focuses on microbiological issues in relation to food‐ and healthcare‐associated human infections, the role of CP in their elimination and the current status of plasma mechanisms of action.  相似文献   
2.
Herbivory is a fundamental process that controls primary producer abundance and regulates energy and nutrient flows to higher trophic levels. Despite the recent proliferation of small‐scale studies on herbivore effects on aquatic plants, there remains limited understanding of the factors that control consumer regulation of vascular plants in aquatic ecosystems. Our current knowledge of the regulation of primary producers has hindered efforts to understand the structure and functioning of aquatic ecosystems, and to manage such ecosystems effectively. We conducted a global meta‐analysis of the outcomes of plant–herbivore interactions using a data set comprised of 326 values from 163 studies, in order to test two mechanistic hypotheses: first, that greater negative changes in plant abundance would be associated with higher herbivore biomass densities; second, that the magnitude of changes in plant abundance would vary with herbivore taxonomic identity. We found evidence that plant abundance declined with increased herbivore density, with plants eliminated at high densities. Significant between‐taxa differences in impact were detected, with insects associated with smaller reductions in plant abundance than all other taxa. Similarly, birds caused smaller reductions in plant abundance than echinoderms, fish, or molluscs. Furthermore, larger reductions in plant abundance were detected for fish relative to crustaceans. We found a positive relationship between herbivore species richness and change in plant abundance, with the strongest reductions in plant abundance reported for low herbivore species richness, suggesting that greater herbivore diversity may protect against large reductions in plant abundance. Finally, we found that herbivore–plant nativeness was a key factor affecting the magnitude of herbivore impacts on plant abundance across a wide range of species assemblages. Assemblages comprised of invasive herbivores and native plant assemblages were associated with greater reductions in plant abundance compared with invasive herbivores and invasive plants, native herbivores and invasive plants, native herbivores and mixed‐nativeness plants, and native herbivores and native plants. By contrast, assemblages comprised of native herbivores and invasive plants were associated with lower reductions in plant abundance compared with both mixed‐nativeness herbivores and native plants, and native herbivores and native plants. However, the effects of herbivore–plant nativeness on changes in plant abundance were reduced at high herbivore densities. Our mean reductions in aquatic plant abundance are greater than those reported in the literature for terrestrial plants, but lower than aquatic algae. Our findings highlight the need for a substantial shift in how biologists incorporate plant–herbivore interactions into theories of aquatic ecosystem structure and functioning. Currently, the failure to incorporate top‐down effects continues to hinder our capacity to understand and manage the ecological dynamics of habitats that contain aquatic plants.  相似文献   
3.
目的:采用基因芯片技术,分别构建气虚血瘀证大鼠和红花注射液给药处理后气虚血瘀证大鼠的差异基因表达谱,比较并分析,筛选出红花能够治疗气虚血瘀证的关键基因群,并推测其起治疗作用的基因组调控机制。方法:15只SD大鼠随机分为模型组、给药组、空白对照组。模型组和给药组采用疲劳游泳和饥饿饲养处理。造模一周后,给药组尾静脉注射红花注射液(100mg/kg/d),模型组给予相同体积生理盐水;对照组不做任何处理。造模进行两周后处死大鼠,取血检验血流变指标并评价造模情况;另抽取足够的血分离mRNA并逆转录杂交基因芯片;扫描信号分析确定受红花注射液调控的基因;并通过基因数据库查询相关基因功能,结合相关文献分析初步探讨红花作用的机制。结果:两周后经过检验和观察发现模型组大鼠在不同切率下的全血粘度增加,并且其体征表现出虚弱和瘀血的状态、体重下降,确定造模成功;给药组大鼠则相对于模型组的各项检测指标和状态有所改善,确认药物有疗效。在差异基因的比较中,空白组相对于给药组上调基因252条,下调基因54条;给药组相对于模型组上调基因196条,下调基因32条;两次差异表达基因中有16条相同基因,这些差异基因涉及到炎症损伤、免疫调节反应等方面。结论:红花注射液对于气虚血瘀证有治疗作用,在基因层次上是通过抗炎症损伤机制实现的。  相似文献   
4.
目的:探讨踝肱指数(ABI)与糖尿病周围神经病变及中医证候积分的相关性。方法:选取我院内分泌科收治辩证以气阴两虚 为证型的糖尿病患者66 例,根据踝肱指数实验将患者分为ABI降低组(0.9>ABI>0.5)和ABI 正常组(1.4>ABI>0.9)。记录患者神 经病变症状尼龙丝检查以及中医症候评分,分析ABI与糖尿病周围神经病变及中医证候积分的相关性。结果:ABI降低组的糖尿 病周围神经病变的患病率高于ABI正常组(P<0.05)。ABI 降低组发麻、针刺感症状的发生率高于ABI 正常组,且有统计学差异 (P<0.05)。ABI降低组10 g尼龙丝检查异常者多于ABI正常组,差异显著(P<0.05)。ABI降低组的感觉振动阈值高于ABI正常组 (P<0.05)。ABI数值与中医证候积分呈负向直线相关(P<0.05)。结论:糖尿病患者ABI数值与糖尿病周围神经病变和中医证候积 分具有相关性。  相似文献   
5.
目的:研究心脏康复运动对冠脉支架植入术后患者血脂、血糖、体重指数及生活质量的影响。方法:对实施冠脉支架植入术的 146例患者进行比较分析,根据随机原则分为试验组76 例及对照组70 例。对照组患者给予常规的健康教育及冠心病二级预防指 导,给予定期随访。试验组患者在此基础上给予规律的康复运动指导。经过6 个月随访,比较两组患者血脂、HbA1C、体重指数及 生活质量情况。结果:试验组患者通过为期6 个月的规律的心脏康复运动指导,其血脂、HbA1C等冠心病危险因素控制情况优于 对照组,差异有统计学意义(P<0.05)。同时,6个月后,试验组康复运动六月后sF 量表各项评分与对照组同期比较,差异均有统计 学意义(P<0.05)。结论:规范的心脏康复运动指导能够有效改善冠脉支架植入术后患者血脂、血糖情况,提高患者生活质量。  相似文献   
6.
目的:探讨癌基因Src在体外培养骨肉瘤细胞侵袭伪足形成中的作用。方法:构建Src sh RNA慢病毒表达载体,在HEK293T细胞中包装慢病毒,感染HT-1080骨肉瘤细胞,经嘌呤霉素加压筛选,获得稳定沉默Src基因的骨肉瘤细胞系HT-1080-sh Src;实时定量PCR和Western Blot法检测基因沉默效率;采用原位明胶酶谱法检测侵袭伪足形成;采用侵袭小室实验检测下调Src基因表达对HT-1080细胞侵袭力的影响。结果:成功构建稳定沉默Src基因的骨肉瘤细胞系HT-1080-sh Src及对照细胞系HT-1080-shluc,经实时定量PCR和Western Blot检测,与对照细胞系相比,HT-1080-sh Src细胞中Src基因表达下调3倍以上;下调HT-1080细胞中Src基因表达能显著抑制HT-1080细胞侵袭伪足形成及其对细胞外基质的降解能力;下调Src基因表达能显著抑制骨肉瘤细胞侵袭力。结论:癌基因Src参与调节骨肉瘤细胞HT-1080侵袭伪足形成,促进肿瘤侵袭、转移。  相似文献   
7.
8.
SPHK1 (sphingosine kinase 1), a regulator of sphingolipid metabolites, plays a causal role in the development of hepatocellular carcinoma (HCC) through augmenting HCC invasion and metastasis. However, the mechanism by which SPHK1 signaling promotes invasion and metastasis in HCC remains to be clarified. Here, we reported that SPHK1 induced the epithelial-mesenchymal transition (EMT) by accelerating CDH1/E-cadherin lysosomal degradation and facilitating the invasion and metastasis of HepG2 cells. Initially, we found that SPHK1 promoted cell migration and invasion and induced the EMT process through decreasing the expression of CDH1, which is an epithelial marker. Furthermore, SPHK1 accelerated the lysosomal degradation of CDH1 to induce EMT, which depended on TRAF2 (TNF receptor associated factor 2)-mediated macroautophagy/autophagy activation. In addition, the inhibition of autophagy recovered CDH1 expression and reduced cell migration and invasion through delaying the degradation of CDH1 in SPHK1-overexpressing cells. Moreover, the overexpression of SPHK1 produced intracellular sphingosine-1-phosphate (S1P). In response to S1P stimulation, TRAF2 bound to BECN1/Beclin 1 and catalyzed the lysine 63-linked ubiquitination of BECN1 for triggering autophagy. The deletion of the RING domain of TRAF2 inhibited autophagy and the interaction of BECN1 and TRAF2. Our findings define a novel mechanism responsible for the regulation of the EMT via SPHK1-TRAF2-BECN1-CDH1 signal cascades in HCC cells. Our work indicates that the blockage of SPHK1 activity to attenuate autophagy may be a promising strategy for the prevention and treatment of HCC.  相似文献   
9.
10.
Neoadjuvant chemotherapy, that is, the administration of chemotherapy before surgery, has been commonly used for locally advanced breast cancer to improve the surgical outcomes and increase the opportunity for breast-conserving therapy. Women with breast cancer often receive an anthracycline-based regimen as the neoadjuvant chemotherapy, which is associated with a high risk of emesis. Despite the development of novel antiemetics, chemotherapy-induced nausea and vomiting (CINV) has been commonly reported as a major adverse effect, affecting the quality of life of the patients. However, the factors predicting CINV in women with breast cancer undergoing neoadjuvant chemotherapy remain unclear. In this single-institution, prospective, observational study conducted at an outpatient cancer centre in the Republic of Korea from November 2013 to March 2016, we analysed women with breast cancer who planned to be treated with neoadjuvant chemotherapy before surgery. Candidate factors associated with CINV were assessed before neoadjuvant chemotherapy using the Munich Chronotype Questionnaire, Pittsburgh Sleep Quality Index and Hospital Anxiety and Depression Scale. CINV was assessed after chemotherapy by using the Multinational Association of Supportive Care in Cancer Antiemesis Tool. Of a total of 143 participants, 7 patients were lost to follow-up and 2 patients were excluded due to changes in their treatment plan; thus, 134 patients were finally included in the analyses. Overall, 48.5% of the participants experienced CINV, with delayed CINV prevalence (42.5%) being more common than acute (39.6%). In the univariate analyses, overall CINV was significantly associated with late chronotypes (odds ratio [OR], 3.49; 95% confidence interval [CI], 1.37–8.87; p = 0.009), a history of nausea/vomiting (OR, 2.19; 95% CI, 1.10–4.37; p = 0.026) and anxiety (OR, 2.25; 95% CI, 1.05–4.81; p = 0.036). In the multivariate analyses, late chronotypes (OR, 3.53; 95% CI, 1.27–9.79; p = 0.015) and a history of nausea/vomiting (OR, 2.83; 95% CI, 1.31–6.13; p = 0.008) remained significantly associated with CINV. In conclusion, in women with breast cancer undergoing neoadjuvant chemotherapy before surgery, late chronotypes were found to have an increased risk of CINV; these data suggest that clinicians need to assess and consider the chronotype in the management of CINV.  相似文献   
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