全文获取类型
收费全文 | 11340篇 |
免费 | 522篇 |
国内免费 | 48篇 |
专业分类
耳鼻咽喉 | 126篇 |
儿科学 | 357篇 |
妇产科学 | 559篇 |
基础医学 | 1996篇 |
口腔科学 | 200篇 |
临床医学 | 916篇 |
内科学 | 1963篇 |
皮肤病学 | 486篇 |
神经病学 | 965篇 |
特种医学 | 519篇 |
外科学 | 1572篇 |
综合类 | 87篇 |
一般理论 | 7篇 |
预防医学 | 466篇 |
眼科学 | 258篇 |
药学 | 661篇 |
中国医学 | 13篇 |
肿瘤学 | 759篇 |
出版年
2023年 | 46篇 |
2022年 | 88篇 |
2021年 | 151篇 |
2020年 | 106篇 |
2019年 | 147篇 |
2018年 | 159篇 |
2017年 | 137篇 |
2016年 | 176篇 |
2015年 | 164篇 |
2014年 | 243篇 |
2013年 | 353篇 |
2012年 | 472篇 |
2011年 | 515篇 |
2010年 | 314篇 |
2009年 | 309篇 |
2008年 | 491篇 |
2007年 | 509篇 |
2006年 | 513篇 |
2005年 | 538篇 |
2004年 | 569篇 |
2003年 | 506篇 |
2002年 | 507篇 |
2001年 | 293篇 |
2000年 | 265篇 |
1999年 | 260篇 |
1998年 | 144篇 |
1997年 | 103篇 |
1996年 | 103篇 |
1995年 | 101篇 |
1994年 | 82篇 |
1993年 | 83篇 |
1992年 | 128篇 |
1991年 | 149篇 |
1990年 | 124篇 |
1989年 | 123篇 |
1988年 | 109篇 |
1987年 | 123篇 |
1986年 | 99篇 |
1985年 | 113篇 |
1984年 | 83篇 |
1983年 | 64篇 |
1981年 | 58篇 |
1979年 | 90篇 |
1978年 | 51篇 |
1977年 | 46篇 |
1975年 | 58篇 |
1974年 | 64篇 |
1931年 | 47篇 |
1928年 | 54篇 |
1913年 | 46篇 |
排序方式: 共有10000条查询结果,搜索用时 15 毫秒
21.
Georgios Amoiridis Ludwig Gutmann Dennis E. Wilkins Raja Sawaya Alain Lagueny Roger Marthan Philippe Schuermans Philippe Le Collen Xavier Ferrer Jean Julien Reha Kuruoglu Shin J. Oh Brian Thompson A. Aggarwal L. Gutmann A. Gutierrez Okifumi Nakazato Russel Johnsen Philip Morling B. A. Kakulas 《Muscle & nerve》1994,17(2):245-253
22.
The metabolism of [1-14C] glutamate to 14CO2 and the glutamate dehydrogenase (GLDH) activity towards alpha-ketoglutarate (alpha-KG) formation were measured in bulk isolated astrocytes derived from control rats and rats with acute hepatic encephalopathy (HE) induced with thioacetamide. In addition, the effects of in vitro treatment of control and HE astrocytes and non-synaptic mitochondria with toxic (3mM) NH4Cl concentration were followed. [1-14C] glutamate oxidation measured as a whole was identical in control and HE astrocytes and was inhibited by ammonia to the same degree in either fraction. In the presence of a glutamate transamination inhibitor--3mM aminooxyacetic acid (AOA), when only the GLDH-mediated part (25% of total) of the glutamate oxidation remained active, the inhibitory effect of ammonia treatment was much more pronounced in HE astrocytes than in control astrocytes. The ability of non-synaptic mitochondria to utilize glutamate to CO2 was not changed in presence of 3mM NH4Cl, whereas a substantial decrease of CO2 production (about 80%) in both the control and HE preparations was observed in the presence of 3mM AOA. GLDH activity was not at all affected by either of the experimental conditions, both in astrocytes and purified non-synaptic mitochondria. Thus, the inhibition of glutamate oxidation in astrocytes by ammonia and the compounded inhibitory effect of HE, ammonia and AOA appeared to be located beyond the glutamate dehydrogenation step within the tricarboxylic acid cycle. 相似文献
23.
J Rakela J D Perkins J B Gross D H Hayes D J Plevak R A Krom J Ludwig 《Mayo Clinic proceedings. Mayo Clinic》1989,64(4):424-428
From 1985 through 1987, we diagnosed acute hepatic failure in 13 patients. Spontaneous recovery occurred in three of these patients. Eight patients underwent liver transplantation, five of whom survived and three of whom died. In addition, two patients died before undergoing transplantation. The survival rate of 62% was better than that among our previous series of similar patients. This improvement seems to be related to the use of orthotopic liver transplantation as a therapeutic alternative among these patients. One of the three patients who died after liver transplantation had normal liver function, but respiratory failure caused by Pneumocystis carinii developed 4 months after the transplantation. The surgical procedure was less difficult in patients with acute fulminant hepatitis than in those with chronic liver disease because fewer problems arose from adhesions, venous collaterals, and ascites. The emerging role of orthotopic liver transplantation in patients with acute hepatic failure is demonstrated by the improvement of survival rates observed by various groups, including ours, when this therapeutic modality is available. 相似文献
24.
Chronic hyperglycemic diabetes in the rat is associated with a selective impairment of cerebral vasodilatory responses 总被引:3,自引:0,他引:3
Diabetes has been reported to impair vasodilatory responses in the peripheral vascular tissue. However, little is known about vasodilatory function in the diabetic brain. We therefore studied, in the N2O-sedated, paralyzed, and artificially ventilated rat, the effects of chronic hyperglycemic diabetes on the cerebral blood flow (CBF) responses to 3 acutely imposed vasodilatory stimuli: hypoglycemia (HG) (plasma glucose = 1.6-1.9 mumol ml-1), hypoxia (HX) (PaO2 = 35-38 mm Hg), or hypercarbia HC) (PaCO2 = 75-78 mm Hg). In addition, we evaluated the somatosensory evoked potential (SSEP) and plasma catecholamine changes in rats exposed to acute glycemic reductions. Diabetes was induced via streptozotocin (STZ, 60 mg kg-1 i.p.). All results in diabetic rats were compared to those obtained in age-matched nondiabetic controls. The animals were studied at 6-8 weeks (HG experiments) or 4-6 months (HG, HX, and HC experiments) post-STZ. Values for CBF were obtained for the cortex (CX), subcortex (SC), brainstem (BS), and cerebellum (CE) employing radiolabeled microspheres. Up to three CBF determinations were made in each animal. In 6-8 week diabetics vs. controls, CBF increased to a lesser value in the CX, SC, and BS (p less than 0.05). Thus, in the diabetics, going from chronic hyperglycemia to acute hypoglycemia, CBF values (in ml 100 g-1 min-1 +/- SD) increased (p less than 0.05) from 89 +/- 22 to 221 +/- 57 in the CX, from 82 +/- 21 to 160 +/- 52 in the SC, and from 79 +/- 34 to 237 +/- 125 in the BS. In controls, going from normoglycemia to acute hypoglycemia, the CBF changes (p less than 0.05) were 128 +/- 27 to 350 +/- 219 (CX), 117 +/- 11 to 358 +/- 206 (SC), and 130 +/- 29 to 452 +/- 254 (BS). CBF changes and absolute values in the CE were similar in the two groups. At 4-6 months post-STZ, a complete loss of the hypoglycemic CBF response was found in the CX, SC, and CE. In the BS, a CBF response to hypoglycemia was seen in the diabetic rats, with the CBF increasing from 114 +/- 28 (hyperglycemia) to 270 +/- 204 ml 100 g-1 min-1 (p less than 0.05), compared to a change from 147 +/- 36 (normoglycemia) to 455 +/- 299 ml 100 g-1 min-1 (p less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS) 相似文献
25.
26.
27.
Oguzkan Sürücü Ulrich Sure Sabine Gaetzner Sonja Stahl Ludwig Benes Helmut Bertalanffy Ute Felbor 《Child's nervous system》2006,22(11):1461-1464
Introduction and background A 3-year-old Bosnian girl with a large symptomatic brainstem and multiple supratentorial cavernous angiomas, who underwent neurosurgical treatment, is presented. As multiple cavernomas are more common in familial cases, genetic analyses and neuroradiological imaging were performed in the patient and her parents to see whether there was any evidence for inheritance. This information is important for genetic counseling and provision of medical care for at-risk relatives. Currently, no recommendation is available on how to manage these cases.Results Genetic analyses demonstrated a novel CCM1 frameshift mutation (c.1683_1684insA; p.V562SfsX6) in the child and the asymptomatic 27-year-old mother. Sensitive gradient-echo magnetic resonance imaging of the mother revealed multiple supratentorial lesions, whereas analogous imaging of the father showed no pathological findings.Conclusion This case exemplifies that seemingly sporadic cases with multiple lesions might well be hereditary and that presymptomatic genetic testing of family members may identify relatives for whom clinical and neuroradiological monitoring is indicated. 相似文献
28.
Summary We have identified cells which secrete human chorionic gonadotropin (HCG) of cultures if first trimester placental villi. As a first step, we identified epithelial cells using a new monoclonal antibody. We then added HCG antibodies to the cultured cells. We found that syncytiotrophoblast (and not cytotrophoblast), Hofbauer cells and some mesenchymal cells stained with HCG antibodies. 相似文献
29.
30.
Different proliferative activity of the glandular and myoepithelial lineages in benign proliferative and early malignant breast diseases. 总被引:3,自引:0,他引:3
Agnes Bánkfalvi Andreas Ludwig Bettina De-Hesselle Horst Buerger Igor B Buchwalow Werner Boecker 《Modern pathology》2004,17(9):1051-1061
The aim of the present study was to explore cell biological characteristics of normal breast, benign proliferative breast diseases and noninvasive breast malignancies based on the recently published adult progenitor cell concept from our group. Here, we investigated the proliferative activity of CK5/14(+), CK8/18/19(+) and alpha-smooth muscle actin(+) cellular phenotypes encountered in normal mammary gland, in a series of usual ductal hyperplasias and early malignant breast diseases, such as atypical ductal and lobular hyperplasias, as well as ductal and lobular in situ carcinomas. Immunohistochemical double labeling was performed on frozen sections from diagnostic breast biopsies by using antibodies to basal cytokeratins (CK5/14), glandular cytokeratins (CK8/18/19), smooth muscle actin and the Ki-67 antigen (MIB1). Normal breast tissues and usual ductal hyperplasias were characterized by a heterogeneous cellular composition of the growth fraction. The proliferative cell compartment consisted of CK8/18/19(+) glandular and, in a variable proportion, CK5/14(+) progenitor phenotypes. In contrast, noninvasive breast malignancies were composed of a monotonous proliferation of CK 8/18/19(+) neoplastic glandular cells. These findings indicate a significant role of progenitor cells in the development of benign proliferative breast diseases and lend support to the view that malignant transformation in the human breast usually occurs in a cell committed to the glandular lineage. Our results provide cell kinetic support to the functional progenitor cell hypothesis, and we propose this concept as an operative model for understanding benign proliferative and malignant breast diseases. 相似文献