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目的研究大黄附子汤对重症急性胰腺炎(SAP)小鼠肠道微皱褶细胞(M细胞)变化的影响,为大黄附子汤临床防治SAP提供理论基础。 方法选取40只健康SPF级C57BL/6J雄性小鼠,随机分为4组(每组10只):空白对照组、大黄附子汤对照组、SAP组、大黄附子汤治疗组,其中SAP组和大黄附子汤治疗组分别以3.5 g/kg剂量腹腔注射20% L-精氨酸,空白对照组和大黄附子汤对照组注射等剂量的等渗盐水;于造模后12、24、36 h,空白对照组和SAP组给予等渗盐水0.2 mL,大黄附子汤对照组和治疗组给予大黄附子汤0.2 mL灌肠,均于造模完成48 h后处死取材,使用ELISA检测血清淀粉酶、内毒素、IL-1β及TNF-α含量,取回肠及胰腺组织行HE染色、评分,免疫组化染色检测M细胞特异性蛋白GP2并评分。 结果(1)一般情况:对照组腹腔注射后小鼠一般情况好,精神状态良好,能正常进水,四肢活动自如,行动未受影响;SAP组小鼠腹腔注射后一般情况差,精神萎靡,反应迟钝,行动迟缓,呼吸急促,拱背收腹,饮水减少。(2)SAP组淀粉酶、内毒素、IL-1β及TNF-α水平较对照组明显升高(P<0.05);与SAP组进行对比,大黄附子汤治疗组血清淀粉酶、内毒素、IL-1β及TNF-α水平出现显著下降(P<0.05)。(3)HE染色:SAP组胰腺及回肠组织坏死严重,可见大量白细胞浸润。大黄附子汤治疗组胰腺及回肠组织轻度坏死,可见少量中性粒细胞等白细胞浸润。(4)免疫组化染色:SAP组与对照组相比GP2表达降低(P<0.05);相较于SAP组,大黄附子汤治疗组GP2的表达水平升高(P<0.05)。 结论大黄附子汤治疗可改善作为肠道免疫应答起始的M细胞数量与功能,增强肠道免疫应答,减轻肠免疫屏障损伤,减少内毒素入血,改善SAP症状。 相似文献
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We describe two cases of acute‐onset erythema, peeling, and pruritus or tenderness isolated to the palmar surface of the hands. A detailed exposure history revealed significant periods of contact with homemade slime; given the clinical findings and timing of exposure, acute contact dermatitis of the hands was suspected. Symptoms and clinical findings resolved after avoidance of the suspected causative contactants. There are few if any reported cases of contact dermatitis to homemade slime in the literature; this serves to highlight the importance of a thorough exposure history in the evaluation of hand dermatitis. 相似文献
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胃癌患者在手术应激状况下,内脏血流减少,肠黏膜处于低灌注状态,易发生肠黏膜损伤。此外,手术刺激可导致肠黏膜充血、水肿、糜烂,加重肠黏膜损伤。近年来,肠内营养被作为保护肠黏膜屏障功能的有效手段。早期肠内营养在肠黏膜屏障功能保护中的作用机制已被证实,然而不同研究结果有一定差异。本研究综述了国内外有关胃癌术后患者行早期肠内营养支持的相关研究,整理、分析既往研究的结论和争议,为早期肠内营养支持的推广应用提供参考。 相似文献
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Rebecca Whear Rebecca A. Abbott Alison Bethel David A. Richards Ruth Garside Emma Cockcroft Heather Iles-Smith Pip A. Logan Ann Marie Rafferty Maggie Shepherd Holly V. R. Sugg Anne Marie Russell Susanne Cruickshank Susannah Tooze GJ Melendez-Torres Jo Thompson Coon 《Journal of advanced nursing》2022,78(1):78-108
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Li-Bin Zhu Yu-Chen Zhang Han-Hui Huang Jing Lin 《World Journal of Clinical Pediatrics》2021,10(5):84-92
As the major source of energy for colonic mucosal cells and as an important regulator of gene expression, inflammation, differentiation, and apoptosis in host cells, microbiota-derived butyrate can enhance the intestinal mucosal immune barrier, modulate systemic immune response, and prevent infections. Maintaining a certain level of butyrate production in the gut can help balance intestinal microbiota, regulate host immune response, and promote the development and maintenance of the intestinal mucosal barrier. Butyrate-producing bacteria act as probiotics and play important roles in a variety of normal biological functions. Bacteriotherapeutic supplementation by using fecal microbiota transplantation to restore butyrate-producing commensal bacteria in the gut has been very suc cessful in the treatment of recurrent and refractory Clostridium difficile (C. difficile) infection or C. difficile-negative nosocomial diarrhea. Administration of probiotics that include butyrate-producing bacteria may have a role in the treatment of inflammatory bowel diseases and in the prevention of necrotizing enterocolitis and late-onset sepsis in premature infants. Furthermore, modulating gut micro biota with dietary approaches may improve intestinal dysbiosis commonly seen in patients with obesity-associated metabolic disorders. Supplementation with a butyrate-producing bacterial stain might be used to increase energy expenditure, improve insulin sensitivity, and to help control obesity and metabolic syndrome. 相似文献
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Shunsuke Iriyama Haruyo Yamanishi Naomi Kunizawa Tetsuji Hirao Satoshi Amano 《Experimental dermatology》2019,28(3):247-253
Daily exposure to sunlight is known to affect the structure and function of the epidermal basement membrane (BM), as well as epidermal differentiation and epidermal barrier function. The aim of this study is to clarify whether the inhibition of BM‐degrading enzymes such as heparanase and matrix metalloproteinase 9 (MMP‐9) can improve the epidermal barrier function of facial skin, which is exposed to the sun on a daily basis. 1‐(2‐hydroxyethyl)‐2‐imidazolidinone (HEI) was synthesized as an inhibitor of both heparanase and MMP‐9. HEI inhibited not only the BM damage at the DEJ but also epidermal proliferation, differentiation, water contents and transepidermal water loss abnormalities resulting from ultraviolet B (UVB). This was determined in this study by the use of UVB‐induced human cultured skins as compared with the control without HEI. Moreover, topical application of HEI improved epidermal barrier function by increasing water content and decreasing transepidermal water loss in daily sun‐exposed facial skin as compared with non‐treated skins. These results suggest that the inhibition of both heparanase and MMP‐9 is an effective way to care for regularly sun‐exposed facial skin by protecting the BM from damage. 相似文献
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