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排序方式: 共有3310条查询结果,搜索用时 15 毫秒
1.
Setsuyo Morimoto Keiko Hirano Keiko Tabata Haruka Asaumi Yuko Morikawa Yuki Matsumi Shuhei Naka Michiyo Matsumoto-Nakano 《Pediatric Dental Journal》2019,29(3):138-145
Early onset periodontitis is rarely seen in infants, though often leads to an acute and serious clinical course when encountered in such patients. Autoimmune neutropenia presents systemic and dental symptoms, as depressed resistance to bacterial infection is caused by a disorder that reduces the number of neutrophils. This disease can result in not only gingival inflammation but also destruction of periodontal tissues, such as attachment loss, alveolar bone absorption, and early tooth loss in primary as well as mixed dentition. Here, we report treatment of a child with marginal periodontitis from the age of 3 years–7 years 9 months. No systemic manifestations were noted until 3 years of age, thus the patient had never received a detailed examination or medication related to the disease. Following examinations at our department, we referred the patient to a pediatrician at our university hospital for possible systemic disease, who made a diagnosis of autoimmune neutropenia. Although administration of antibiotics and professional dental care were continued, neutrophil count was not increased and progressive periodontal destruction was observed. Extraction of teeth with poor prognosis was performed and a prosthetic strategy for the missing teeth developed. It is important to recognize that periodontitis along with autoimmune neutropenia can appear in infants, even though the incidence is quite low. Early detection and early treatment of this disease is necessary for delaying progression of periodontitis and optimal occlusal induction of permanent teeth. 相似文献
2.
Taichi Goto Gojiro Nakagami Takeo Minematsu Sanai Tomida Masamichi Shinoda Koichi Iwata Hiromi Sanada 《Experimental dermatology》2019,28(9):1010-1016
Cutaneous wound pain causes physical and psychological stress for patients with wounds. Previous studies reported that stress induces hyperalgesia and deteriorates wound healing. However, the effect of the stress response such as in hypothalamic‐pituitary‐adrenal (HPA) axis on local wound area is unclear. We aimed to investigate the effects of a stress response on the mechanical withdrawal threshold in the local wound area and describe the identification of a wound pain exacerbation. We topically injected adrenocorticotropic hormone (ACTH) into the granulation tissue of full‐thickness cutaneous wound model rats on the fifth day postwounding and measured the mechanical withdrawal thresholds, cytochrome P450 2Bs levels and concentration of 5,6‐epoxyeicosatrienoic acid in wound exudate. We found that ACTH induced mechanical hypersensitivity at 4 and 6 hours after injection (P = .004 and .021, respectively), and increased gene expression of cytochrome P450 2B12 expression (P = .046). Concentration of 5,6‐EET in the wound exudate was moderately correlated with the mechanical withdrawal threshold (r = ?.630). Finally, the mechanical withdrawal threshold in the 5,6‐EET group was significantly lower than that in the control group at 2 hours after the injection (P = .015). We propose that 5,6‐EET is one of the most promising contributors to the wound pain exacerbation. These findings could guide clinical wound and pain management. 相似文献
3.
Yoshiki Imamura Takahiro Shinozaki Akiko Okada‐Ogawa Noboru Noma Masahiro Shinoda Koichi Iwata Akihiko Wada Osamu Abe Kelun Wang Peter Svensson 《Journal of oral rehabilitation》2019,46(6):574-587
Burning mouth syndrome (BMS) is a chronic oro‐facial pain disorder of unknown cause. It is more common in peri‐ and post‐menopausal women, and sex hormone dysregulation is believed to be an important causative factor. Psychosocial events often trigger or exacerbate symptoms, and persons with BMS appear to be predisposed towards anxiety and depression. Atrophy of small nerve fibres in the tongue epithelium has been reported, and potential neuropathic mechanisms for BMS are now widely investigated. Historically, BMS was thought to comprise endocrinological, psychosocial and neuropathic components. Neuroprotective steroids and glial cell line–derived neurotrophic factor family ligands may have pivotal roles in the peripheral mechanisms associated with atrophy of small nerve fibres. Denervation of chorda tympani nerve fibres that innervate fungiform buds leads to alternative trigeminal innervation, which results in dysgeusia and burning pain when eating hot foods. With regard to the central mechanism of BMS, depletion of neuroprotective steroids alters the brain network–related mood and pain modulation. Peripheral mechanistic studies support the use of topical clonazepam and capsaicin for the management of BMS, and some evidence supports the use of cognitive behavioural therapy. Hormone replacement therapy may address the causes of BMS, although adverse effects prevent its use as a first‐line treatment. Selective serotonin reuptake inhibitors (SSRIs) and serotonin and noradrenaline reuptake inhibitors (SNRIs) may have important benefits, and well‐designed controlled studies are expected. Other treatment options to be investigated include brain stimulation and TSPO (translocator protein 18 kDa) ligands. 相似文献
4.
Photopheresis and leukocytapheresis: cytapheresis treatment against immune-mediated diseases. 总被引:1,自引:0,他引:1
Toshio Shinoda 《Therapeutic apheresis》2002,6(4):245-246
5.
S. Horita T. Shinoda H. Yoshimoto M. Masuo Y. Miura 《Clinical and experimental nephrology》2002,6(1):71-74
We report a case of infectious endocarditis in a 77-year-old woman who was undergoing maintenance hemodialysis therapy, and
who was also having a prosthetic aortic valve replacement. The disease resulted from a local skin infection at the needle
puncture site of the arteriovenous fistula. Ampicillin-resistant Staphylococcus aureus was the causal organism. Surgical treatment could not be performed because of associated intracranial hemorrhage due to septic
embolism. In spite of intensive treatment with several antibiotics, a ventricular septal abscess just beneath the prosthetic
aortic valve progressed to form a ventricular septal fistula. The resultant intracardiac left-to-right shunt led to refractory
congestive heart failure. The patient finally died of heart failure. The formation of a ventricular septal fistula is considered
to be a rare and extraordinary complication of infectious endocarditis in a hemodialysis patient with aortic valve replacement.
Received: July 25, 2001 / Accepted: November 3, 2001 相似文献
6.
The authors studied the clinical features and outcome at 6 months in 191 patients with subarachnoid hemorrhage (SAH) from ruptured aneurysms. Aneurysm repair (AR) was undertaken in 123 cases (64.4%). In the non-AR group (n = 68), 48.5% of the patients were 70 years of age or older, compared with 12.2% in the AR group. The duration from onset to admission was less than 3 hours in 48 non-AR cases (70.6%) and in 42 AR cases (34.1%). Among non-AR patients, 63.2% were Hunt and Hess grade IV or V, whereas the figure for AR patients was only 14.7%. By 6 months after SAH, 94.1% of non-AR patients had died, and the remainder were vegetative or severely disabled. In contrast, only 15.4% in the AR group died, and over 50% showed good recovery. The large majority of non-AR patients were treated conservatively because they were judged to be poor surgical risks and, among these patients, nearly one half were elderly. In the 10 elderly patients considered good surgical candidates, vasospasm was the most common reason (70%) for not performing AR. 相似文献
7.
Yuki Izawa Masanori Yoshizumi Keisuke Ishizawa Yoshiko Fujita Shuji Kondo Shoji Kagami Kazuyoshi Kawazoe Koichiro Tsuchiya Shuhei Tomita Toshiaki Tamaki 《Hypertension research》2007,30(11):1107-1117
Big mitogen-activated protein kinase 1 (BMK1), also known as extracellular signal-regulated kinase 5 (ERK5), is a newly identified member of the mitogen-activated protein (MAP) kinase family. Recently, several studies have suggested that BMK1 plays an important role in the pathogenesis of cardiovascular disease. To clarify the pathophysiological significance of BMK1 in the process of vascular remodeling, we explored the molecular mechanisms of BMK1 activation in vascular smooth muscle cells (VSMCs). From the results of co-immunoprecipitation and immunoblotting analyses, it was found that platelet-derived growth factor (PDGF), a known potent mitogen, activated BMK1 and triggered the Gab1-SHP-2 interaction in rat aortic smooth muscle cells (RASMCs). The abrogation of SHP-2 phosphatase activity by transfection of the SHP-2-C/S mutant suppressed PDGF-stimulated BMK1 activation. Infection with an adenoviral vector expressing dominant-negative MEK5alpha, which can suppress PDGF-stimulated BMK1 activation to the control level, inhibited PDGF-induced RASMC migration. Moreover, we observed an increase of BMK1 activation in injured mouse femoral arteries. From these findings, it is suggested that BMK1 activation leads to VSMC migration induced by PDGF via Gab1-SHP-2 interaction, and that BMK1-mediated VSMC migration may play a role in the pathogenesis of vascular remodeling. 相似文献
8.
9.
Abstract: A prospective study was performed to determine whether low-density lipoprotein (LDL) apheresis, when performed only immediately before and after percutaneous transluminal coronary angioplasty (PTCA), is effective in preventing restenosis of coronary artery lesions following PTCA. Thirty-six patients with coronary heart disease (CHD) and hypercholesterolemia were divided into 2 groups. The 9 patients in the LDL group underwent LDL-apheresis 1 day before and 5 days after PTCA while the 27 patients of the control group underwent PTCA but did not undergo LDL-apheresis. Follow-up coronary angiography (CAG) was performed 4 months after PTCA. The rate of restenosis of coronary artery lesions was significantly lower in the LDL group (0%) than in the control group (30%). These findings suggest that LDL-apheresis, when performed before and after PTCA, is effective in preventing restenosis of coronary artery lesions in patients with CHD and hypercholesterolemia. 相似文献
10.
Abstract: This study was investigated to clarify the role of intracellular Ca2+ following endotoxin treatment (1 mg/kg, intraperitoneally) to D-galactosamine-sensitized mice (400 mg/kg, intraperitoneally), and to observe lipid peroxide levels, an index of hepatotoxicity, in endotoxin/galactosamine (Ga1N)-challenged mice under activation of macrophages, especially Kupffer cells, by zymosan. The liver lipid peroxide level and serum glutamic pyruvic transminase activity in mice 18 hr after administration of endotoxin/Ga1N were markedly higher than those in mice treated only with endotoxin. In spite of an increase in lipid peroxide formation, there was little or no effect of Ga1N administration on xanthine oxidase and superoxide dismutase activities in mice given endotoxin. However, the injection of verapamil (10 mg/kg, subcutaneously) markedly decreased lipid peroxide levels in liver of endotoxin/Ga1N-injected mice. In the mice given a Ca2+-deficient diet, lipid peroxide level in liver after endotoxin/Ga1N injection was markedly decreased compared to that in mice fed a normal diet. Administration of dexamethasone (200 μg/kg, intraperitoneally) in mice 1 hr before treatment with endotoxin/Ga1N did not induce lipid peroxide formation. Administration of endotoxin to Ga1N-treated mice resulted in a higher level of liver cytosolic free Ca2+ ([Ca2+]i) than that in endotoxin-treated mice. On the other hand, Ca2+-ATPase activity in liver plasma membrane in the endotoxin/Ga1N-treated mice was markedly decreased as compared with endotoxin alone. On the contrary, the Ca2+-ATPase activity in liver mitochondria was higher in endotoxaemic mice treated with Ga1N than in mice given endotoxin alone. State 3 respiration and respiratory control index, which are parameters of mitochondrial function, were decreased more in the liver of mice treated with endotoxin/Ga1N than in the endotoxin-treated group. These findings suggest that [Ca2+]i may participate in the lipid peroxide formation which results from endotoxin/Ga1N-induced hepatotoxicity under conditions of zymosan-activated macrophages, and that the increases of endotoxin-sensitivity caused by Ga1N challenge may greatly contribute to Ca2+-mobilization in the hepatocyte. 相似文献