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21.
Moussa Ndong Machiko Kazami Tsukasa Suzuki Mariko Uehara Shin-ichi Katsumata Hirohumi Inoue Ken-Ichi Kobayashi Tadahiro Tadokoro Kazuharu Suzuki Yuji Yamamoto 《Nutrition Research》2009,29(9):640-647
Iron deficiency (ID) is one of the most commonly known forms of nutritional deficiencies. Low body iron is thought to induce neurologic defects but may also play a protective role against cancer development by cell growth arrest. Thus, ID may affect cellular pathways controlling cell growth and proliferation, the mechanism of which is still not fully understood. The serine/threonine protein kinase Akt and its downstream target, the mammalian Target of Rapamycin (mTOR), is known to play a crucial role in the regulation of cell growth and survival. Therefore, we hypothesized that Akt/mTOR pathway could be influenced by ID. Three-week-old male Wistar-strain rats were divided into 3 groups and the 2 groups had free access to a control diet (C group) or an iron-deficient diet (D group). The third group (PF group) were pair-fed the control diet to the mean intake of the D group. After 4 weeks, rats were killed and their brains were sampled. In separate experiments, COS-1 cells were cultured with or without the iron chelator deferoxamine. Western blots of brain samples and COS-1 lysates were used to analyze the expression and phosphorylation state of Akt, TSC2, mTOR, and S6 kinase proteins implicated in the Akt/mTOR pathway. Using 2 different ID models, we show for the first time that iron deficiency depresses Akt activity in rats and in COS-1 cells, leading to a decrease in mTOR activity. 相似文献
22.
M. Mizuguchi H. Yamanouchi T. Ichiyama M. Shiomi 《Acta neurologica Scandinavica》2007,115(S186):45-56
Acute encephalopathy is the most serious complication of pediatric viral infections, such as influenza and exanthem subitum. It occurs worldwide, but is most prevalent in East Asia, and every year several hundreds of Japanese children are affected by influenza-associated encephalopathy. Mortality has recently declined, but is still high. Many survivors are left with motor and intellectual disabilities, and some with epilepsy. This article reviews various syndromes of acute encephalopathy by classifying them into three major categories. The first group caused by metabolic derangement consists of various inherited metabolic disorders and the classical Reye syndrome. Salicylate is a risk factor of the latter condition. The second group, characterized by a systemic cytokine storm and vasogenic brain edema, includes Reye-like syndrome, hemorrhagic shock and encephalopathy syndrome, and acute necrotizing encephalopathy. Non-steroidal anti-inflammatory drugs, such as diclofenac sodium and mephenamic acid, may aggravate these syndromes. Severe cases are complicated by multiple organ failure and disseminated intravascular coagulation. Mortality is high, although methylprednisolone pulse therapy may be beneficial in some cases. The third group, characterized by localized edema of the cerebral cortex, has recently been termed acute encephalopathy with febrile convulsive status epilepticus, and includes hemiconvulsion-hemiplegia syndrome and acute infantile encephalopathy predominantly affecting the frontal lobes. Theophylline is a risk factor of these syndromes. The pathogenesis is yet to be clarified, but an increasing body of evidence points to excitotoxicity and delayed neuronal death. 相似文献
23.
邻近皮瓣修复面部皮肤缺损 总被引:1,自引:0,他引:1
目的 探讨邻近皮瓣修复面部皮肤缺损的应用效果。方法 162例面部病变切除后皮肤缺损患者,其中先天性色素痣63例,基底细胞癌28例,鳞状细胞癌6例,其他皮肤病变65例。均采用邻近皮瓣即时修复,其中菱形皮瓣57例、双叶皮瓣8例,A-T皮瓣23例、V-Y皮瓣13例、Z成形术23例、推进皮瓣27例、鼻状皮瓣11例。结果 162例皮瓣存活良好,手术切口1期愈合,存活后皮瓣颜色与邻近部位无明显差异,术后无眼睑、眉毛、鼻梁及口角牵扯歪钭,术后3个月切口不显露。结论 邻近皮瓣是修复面部较大皮肤缺损的良好方法,手术外观效果好。 相似文献
24.
益气复智颗粒对多发脑梗死性痴呆模型大鼠脑组织细胞凋亡的影响 总被引:1,自引:0,他引:1
目的 观察益气复智颗粒对多发脑梗死性痴呆模型大鼠脑皮质形态学、细胞凋亡的影响。方法 采用颈内动脉注射血栓的方法,复制多发梗死性痴呆大鼠模型,观察益气复智颗粒12.42g/kg分别于手术前、手术前后、手术后灌胃对实验动物脑皮质形态学、细胞凋亡的影响。结果 益气复智颗粒能使脑缺血后脑内神经细胞凋亡数目下降。结论 益气复智颗粒具有较好的保护脑神经元,阻断脑缺血致神经细胞死亡病理过程的作用。 相似文献
25.
Hidero Minami Ryo Matsutani Atsushi Mizokami Mikio Namiki 《International journal of urology》2007,14(4):368-369
Abstract: A 19-year-old woman presented at our hospital with acute urinary retention in September 2005. She had experienced the same chief complaint twice previously. She had used non-steroidal anti-inflammatory drugs before acute urinary retention. The results of physical examinations were unremarkable, and her neurologic signs were not remarkable. The basic laboratory test values were all normal and a psychiatric assessment indicated that her symptoms were not psychogenic. Magnetic resonance imaging was carried out, but revealed only a slight bulging in the L3/L4/L5 disk. Water cystometry showed acontractile detrusor. We made a diagnosis of acute urinary retention as a result of non-steroidal anti-inflammatory drugs because of her use of such drugs before the development of symptoms on multiple occasions. This patient was regularly followed up as an outpatient, and she could void smoothly in February 2006. This is the first report which acute urinary retention associated with non-steroidal anti-inflammatory drugs in Japan. 相似文献
26.
云南省600例0~5岁儿童维生素A缺乏调查 总被引:3,自引:3,他引:0
目的:了解云南省城乡0~5岁儿童维生素A营养状况及影响因素。方法:省、地、县随机整群抽取600例儿童,采用微量荧光光度法检测VitA含量。结果:VitA缺乏发生率16·17%,地、县明显高于省会城市;0岁儿童明显高于其他年龄组;腹泻儿童明显高于正常儿童;VitA缺乏的影响因素:近1周内进食鸡蛋、奶类制品、鱼虾类、肝类、黄绿色蔬菜、鱼肝油等食物有利于维生素A的吸收,急性呼吸道感染、发烧与维生素A缺乏发生率差异不明显。结论:维生素A缺乏发生率城市明显低于农村地、县两级,说明维生素A缺乏防治工作重点在农村,特别是0岁儿童,防治的主要措施是采取合理膳食,均衡营养,控制腹泻流行。 相似文献
27.
通过半年对35名7~12岁轻度碘缺乏病儿童进行补碘,并与同龄、同地的正常儿童和缺碘未补碘儿童进行比较,以观察补碘对儿童脑功能及生长发育的影响。结果发现:①补碘可使儿童碘营养状况恢复正常,尿碘值由(83.2±3.5)μg/L上升到(162.2±1.6)μg/L,血清T4、FT4I和rT3:也与正常儿童一致而与未补碘儿童有显著性差异(P<0.05).②轻度碘缺乏病儿童智商低于正常儿童(P<0.01),补碘在一定程度上改善其智商水平。③轻度碘缺乏病及补碘未能明显影响儿童的生长发育,可能与儿童总营养水平较差有关。 相似文献
28.
C. J. Bowden W. D. Figg N. A. Dawson O. Sartor R. J. Bitton M. S. Weinberger Donna Headlee Eddie Reed C. E. Myers M. R. Cooper 《Cancer chemotherapy and pharmacology》1996,39(1-2):1-8
Introduction: Suramin is a synthetic polysulfonated naphthylurea which has been used for the treatment of African trypanosomiasis and onchocerciasis,
but since the mid-1980s has received attention as a possible antiretroviral and antineoplastic agent. Objective: This clinical trial of suramin was undertaken as a phase I/II study in patients with hormone-refractory prostate cancer,
with the hypothesis that the intensity of therapy with suramin could be increased significantly if measures were undertaken
to maintain the plasma concentrations of the drug under 300 μg/ml. Methods: We report the clinical results of this trial, wherein patients were treated at three different targeted plasma suramin concentrations
(275, 215 and 175 μg/ml) for varying periods of time (2, 4 or 8 weeks), with delivery of the drug by continuous intravenous
infusion. Results: The major toxicity observed in this trial was neurologic, consisting of a motor and sensory peripheral neuropathy that resulted
in both paresis and paralysis of the limbs. Nearly all of this severe (CTEP grade III, IV) neurologic toxicity was observed
in the patients treated at a plasma suramin concentration of 275 μg/ml for 4 or more weeks. A single patient treated at 215 μg/ml
for 8 weeks developed moderate (CTEP grade III) proximal lower extremity weakness, and no patient treated at 175 μg/ml developed
this toxicity. The second most common toxicity observed was infection of the central venous catheter. The overall response
rate for all of the evaluable patients was 17% (13 of 75 patients). In addition, prostate-specific antigen (PSA)-defined responses
were observed in six patients receiving therapy at 175 μg/ml, but these responses were confounded by cessation of therapy
with flutamide during suramin treatment. Conclusions: In summary, although plasma suramin concentrations were maintained below 300 μg/ml, neurologic toxicity nonetheless occurred
with high frequency in patients treated at 275 μg/ml for 4 or more weeks. Therapy at 215 and 175 μg/ml was in general well
tolerated, but central venous catheter-related infection, as well as the inconvenience and expense of continuous infusional
therapy, make this method of drug delivery impractical. Only moderate antitumor activity was observed during this trial, but
it is possible that both continuation of flutamide and flutamide withdrawal during suramin therapy confounded the assessment
of suramin’s activity in hormone-refractory prostate cancer.
Received: 9 June 1995/Accepted: 18 March 1996 相似文献
29.
Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand
PA Crock JD McKenzie AM Nicoll NJ Howard W Cutfield LK Shield G Byrne 《Acta paediatrica (Oslo, Norway : 1992)》1998,87(4):381-386
Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10IUml -1 ), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10–20 IUml -1 ) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors'practice is now to start GH replacement at less than the usual recommended dose of 14IUm-2 week-1 in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilledema does not exclude the diagnosis. 相似文献
30.
Summary Neurofibromatosis is sometimes complicated by impaired renal tubular reabsorption of phosphate, hypophosphatemia, and osteomalacia.
Hyperparathyroidism has also been reported in patients with neurofibromatosis. When hypercalcemia and elevated levels of parathyroid
hormone are found in osteomalacia, however, it may be difficult to determine if the hyperparathyroidism was primary or tertiary.
We describe a patient with neurofibromatosis, hypercalcemic hyperparathyroidism, hypophosphatemic osteomalacia, vitamin D
deficiency, and clear-cell hyperplasia of all four parathyroid glands. Serial biomechanical, bone biopsy, and densitometric
studies confirmed that treatment with ergocalciferol, calcium, and phosphate supplements significantly improved the osteomalacia
but caused increased parathyroid overactivity. After subtotal parathyroidectomy, the parathyroid hormone concentration became
normal and the bone mineral content increased at the spine and hip, but inappropriate phosphaturia persisted. The findings
indicate that hyperparathyroidism, osteomalacia, and vitamin D deficiency adversely affect each other. 相似文献