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21.
G. N. Kryzhanovskii V. K. Reshetnyak M. L. Kukushkin M. P. Gorizontova V. S. Smirnova 《Bulletin of experimental biology and medicine》1992,114(3):1217-1220
Laboratory of Pathophysiology of Pain and Laboratory of General Pathology of the Microcirculation, Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 9, pp. 229–231, September, 1992. 相似文献
22.
Vladimir Mironov Martin A. Hritz Joseph C. LaManna Antal G. Hudetz Sami I. Harik 《Brain research》1994,660(1)
We performed 3-dimensional studies of vascular casts of the microvasculature of the cerebral cortex of rats that were exposed to three weeks of hypobaric hypoxia and of control rats. Scanning electron microscopy of the casts gave the qualitative impression of increased vascularity of the cerebral cortex, particularly the deeper layers, in hypoxic rats. Quantitative analysis of capillary segment lengths revealed a significant shift in the frequency distribution to longer lengths (from 77 ± 8 to 90 ± 14 μm) in the deep, but not in the superficial, layers of the cerebral cortex of hypoxic rats. These findings agree with previous results reporting increased capillary density in the brain after exposure to prolonged hypobaric hypoxia and suggest that capillary segment elongation plays a role in the increased capillary density in the deeper layers of the cerebral cortex. 相似文献
23.
Irwin M. Braverman 《Microcirculation (New York, N.Y. : 1994)》1997,4(3):329-340
The cutaneous microcirculation is organized as two horizontal plexuses. One is situated 1–1.5 mm below the skin surface, and the other is at the dermal-subcutaneous junction. Ascending arterioles and descending venules are paired as they connect the two plexuses. From the upper layer, arterial capillaries arise to form the dermal papillary loops that represent the nutritive component of the skin circulation. There are sphincter-like smooth muscle cells at the point where the ascending arterioles divide to form the arteriolar component of the upper horizontal plexus. At the dermal subcutaneous junction, there are collecting veins with 2-cusped valves that are oriented to prevent the retrograde flow of blood. Laser Doppler flowmetry (LDF) has demonstrated vasomotion of red cell flux localized to the sites of ascending arterioles. The simultaneous recording by LDF of red cell flux and the concentration of moving red blood cells from individual sites allows one to construct by computer topographic maps of these two valves. The two maps, based on initial studies using correlative skin biopsy specimens, can define 1-mm3 volumes of skin that are predominantly arteriolar in composition, predominantly venular in composition, or essentially devoid of all microvascular elements. The electron and light microscopic features that define the microvascular segments, when coupled with the ability of LDF to define the predominant microvascular segments under the probe, will allow one to study both the mechanisms of normal physiological states and the pathogenetic mechanisms underlying pathological skin disorders in which the microvasculature plays a predominant role. 相似文献
24.
Objective : To measure the functional diameter of alveolar septal microvessels under conditions in which the pulmonary arterial pressure and the lung inflation pressure are equal, at 25 cm H2O (zone I-II border), and to compare these results with those obtained when inflation pressure exceeded arterial pressure by 5 or 10 cm H2O (zone I). Methods : We perfused isolated rat lungs (PA 25, PPA 25, PLA 0 cm H2O) with fluorescent latex particles of specific diameters (0.49, 1.05, 2.0, 4.0, or 10 μm) and then prepared samples for histology. Using a confocal, laser-scanning fluorescence microscope, we measured latex particle densities within the septal plane of individual alveoli. We compared these particle densities with those in arterioles supplying the septa and calculated the density ratio. We fit curves produced by the Verniory equation to these ratios to estimate the septal microvessel functional diameter. Results : Particle densities in septa ranged from 0.06 ± 0.02 particles per μm2 ‘for 0.49-μm-diameter particles to 0.007 ± 0.004 particles per μm2 for 4.0-μm-diameter particles. The 10-μm particles did not enter septa. Calculations based on these data suggest a septal microvessel functional diameter of 6–8 μm. Conclusions : In a previous study, conducted at the same value of Pinflat, but with PPA set at 15 or 20 (5 or 10 cm H2O into zone I), we estimated the capillary diameter to be 1.7 μm. Thus, the septal capillary diameter seems to increase by three- to fourfold as PPA is raised to equal Pinflat. 相似文献
25.
对甲状腺机能亢进症(甲亢)患者进行了临床辨证分型,同步观察甲皱微循环及检测TT_3 TT_4 FT_4I、吸~(131)碘率,探讨它们之间的关系。结果表明甲亢患者微循环积分明显高于对照组(P<0.01),但不同类型甲亢的血淤情况亦不相同。心肝火旺型的微循环积分低于气滞痰凝型和血瘀型,但TT_3、TT_4、FT_4I明显增高;气滞痰凝型居中;血淤型的微循环积分明显增高,但TT_3、TT_4、FT_4I低于其他两型。吸~(131)碘率三型间无差异(P>0.05)。 相似文献
26.
Focal reduction of villous blood flow in early indomethacin
enteropathy: a dynamic vascular study in the rat 总被引:3,自引:0,他引:3
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Background—Oral indomethacin causes villousshortening, microvascular damage, and distortion, which might inducemucosal ischaemia and necrosis.
Aims—In order to determine the early events inindomethacin induced jejunal injury we examined the temporal relationsbetween morphological damage and changes in villous blood flowfollowing indomethacin.
Methods—In anaesthetised rats, mid jejunal villiwere exteriorised in a chamber and observed by fluorescence microscopy.Blood flow in surface capillaries was calculated from velocities and diameters. Indomethacin was applied by both luminal and intravenous routes for 90 minutes, after which the animal was perfusion fixed andthe villi were processed for histological examination. Control animalsreceived intravenous or luminal bicarbonate (1.25%).
Results—Blood flow slowed in individual villi at20 minutes, and progressed to complete stasis (in another group) by 45 minutes. Histological examination at 20 minutes revealed microvascular distortion, but no villous shortening: crypt depth:villous height ratios were 0.356 (0.02) in test and 0.386 (0.01) in surrounding villi(p>0.5). At stasis, the villi under study showed epithelial clumpingand were shortened: crypt depth:villous height ratios were 0.92 (0.2)in test and 0.42 (0.06) in surrounding villi (p<0.02). Vehicle alonehad no effect on either blood flow or histology.
Conclusions—Focal slowing of villous blood flowand microvascular distortion precede villus shortening and epithelialdisruption, and indicate that damage to surface microvasculature is anearly event in indomethacin induced mucosal injury in this model.
Aims—In order to determine the early events inindomethacin induced jejunal injury we examined the temporal relationsbetween morphological damage and changes in villous blood flowfollowing indomethacin.
Methods—In anaesthetised rats, mid jejunal villiwere exteriorised in a chamber and observed by fluorescence microscopy.Blood flow in surface capillaries was calculated from velocities and diameters. Indomethacin was applied by both luminal and intravenous routes for 90 minutes, after which the animal was perfusion fixed andthe villi were processed for histological examination. Control animalsreceived intravenous or luminal bicarbonate (1.25%).
Results—Blood flow slowed in individual villi at20 minutes, and progressed to complete stasis (in another group) by 45 minutes. Histological examination at 20 minutes revealed microvascular distortion, but no villous shortening: crypt depth:villous height ratios were 0.356 (0.02) in test and 0.386 (0.01) in surrounding villi(p>0.5). At stasis, the villi under study showed epithelial clumpingand were shortened: crypt depth:villous height ratios were 0.92 (0.2)in test and 0.42 (0.06) in surrounding villi (p<0.02). Vehicle alonehad no effect on either blood flow or histology.
Conclusions—Focal slowing of villous blood flowand microvascular distortion precede villus shortening and epithelialdisruption, and indicate that damage to surface microvasculature is anearly event in indomethacin induced mucosal injury in this model.
Keywords:indomethacin; jejunum; villi; microcirculation; endothelium; microthrombi
相似文献27.
IL-8 mRNA in human gingival epithelial cells (HGECs) is up-regulated by Fusobacterium nucleatum, and up-/down-regulated by Porphyromonas gingivalis in a complex interaction in the early stages (< or = 4 h) after infection. The mechanisms involved in this regulation in response to F. nucleatum and/or P. gingivalis infection, and identification of co-regulated cytokine genes, are the focus of this investigation. Heat, formalin or protease treatment of F. nucleatum cells attenuated the IL-8 mRNA up-regulation. NF-kappaB, mitogen-activated protein kinase (MAPK) p38 and MAPK kinase/extracellular signal-regulated kinase (MEK/ERK) pathways were involved in IL-8 mRNA induction by F. nucleatum. Pretreatment of P. gingivalis with heat, formalin or protease enhanced IL-8 mRNA induction. NF-kappaB, MARK p38, and MEK/ERK pathways were also involved in this induction. In contrast, down-regulation of IL-8 mRNA by P. gingivalis involved MEK/ERK, but not NF-kappaB or MAPK p38 pathways. cDNA arrays analysis revealed that mRNA down-regulation by P. gingivalis is a specific reaction that only a number of genes, e.g. IL-1beta, IL-8, macrophage inflammatory protein-2alpha, and migration inhibitory factor-related protein-14, are affected based on examination of 278 cytokine/receptor genes. These data indicate that F. nucleatum and P. gingivalis trigger specific and differential gene regulation pathways in HGECs. 相似文献
28.
29.
高压氧对人重症牙周炎牙龈血流量、血流速度和血浓度作用及机理研究 总被引:4,自引:2,他引:4
目的 :探讨高压氧 (HBO)对人重症牙周炎牙龈血流量 (GBF)、血流速度 (BCV)和血浓度 (BC)的作用及HBO治疗牙周炎的机理。方法 :选自口腔中心门诊的 3 0例重症牙周炎患者 ,随机分为二组 ,即治疗组和对照组 ,治疗组用HBO治疗 ,对照组用漱口液漱口。用激光多普勒血流仪测定二组治疗前后的GBF、BCV和BC。结果 :HBO能使牙周炎患者GBF增加 2 .1倍 ,BCV增加 6.7倍 ,BC降低为治疗前的 5 8.2 % ,与对照组比均有非常显著性差异 (P <0 .0 1)。结论 :HBO能使牙周炎患者GBF和BCV增加 ,BC减少 ,能改善牙龈微循环 ,对治疗牙周炎有积极意义 相似文献
30.
E. D. Klimenko O. M. Pozdnyakov 《Bulletin of experimental biology and medicine》1992,114(4):1557-1559
Laboratory of Experimental Pathomorphology, Research Institute of General Pathology and Pathological Physiology, Russian Academy of Medical Sciences, Moscow. (Presented by Academician of the Russian Academy of Medical Sciences D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 114, No. 10, pp. 437–439, October, 1992. 相似文献