全文获取类型
收费全文 | 1704篇 |
免费 | 75篇 |
国内免费 | 38篇 |
专业分类
耳鼻咽喉 | 19篇 |
儿科学 | 51篇 |
妇产科学 | 5篇 |
基础医学 | 255篇 |
口腔科学 | 15篇 |
临床医学 | 278篇 |
内科学 | 281篇 |
皮肤病学 | 1篇 |
神经病学 | 199篇 |
特种医学 | 78篇 |
外科学 | 134篇 |
综合类 | 239篇 |
预防医学 | 62篇 |
眼科学 | 2篇 |
药学 | 152篇 |
中国医学 | 33篇 |
肿瘤学 | 13篇 |
出版年
2023年 | 14篇 |
2022年 | 31篇 |
2021年 | 41篇 |
2020年 | 35篇 |
2019年 | 28篇 |
2018年 | 38篇 |
2017年 | 41篇 |
2016年 | 39篇 |
2015年 | 45篇 |
2014年 | 84篇 |
2013年 | 81篇 |
2012年 | 67篇 |
2011年 | 88篇 |
2010年 | 79篇 |
2009年 | 89篇 |
2008年 | 75篇 |
2007年 | 80篇 |
2006年 | 82篇 |
2005年 | 67篇 |
2004年 | 74篇 |
2003年 | 38篇 |
2002年 | 57篇 |
2001年 | 34篇 |
2000年 | 31篇 |
1999年 | 32篇 |
1998年 | 26篇 |
1997年 | 28篇 |
1996年 | 27篇 |
1995年 | 26篇 |
1994年 | 22篇 |
1993年 | 22篇 |
1992年 | 11篇 |
1991年 | 24篇 |
1990年 | 21篇 |
1989年 | 24篇 |
1988年 | 21篇 |
1987年 | 20篇 |
1986年 | 16篇 |
1985年 | 27篇 |
1984年 | 18篇 |
1983年 | 12篇 |
1982年 | 16篇 |
1981年 | 11篇 |
1980年 | 21篇 |
1979年 | 14篇 |
1978年 | 10篇 |
1976年 | 12篇 |
1975年 | 3篇 |
1971年 | 3篇 |
1969年 | 3篇 |
排序方式: 共有1817条查询结果,搜索用时 15 毫秒
41.
W. Rouslin R.S. Cubicciotti W.D. Edwards M.A. Matlib D.R. Wilson B.B. Hamrell A. Schwartz 《Journal of molecular and cellular cardiology》1979,11(1):91-99
Right ventricular hypertrophy was produced by placing a spiral Monel metal clip around the pulmonary trunks of rabbits causing a sustained 67% occlusion of the vessel. The operation produced a doubling of right ventricular weight, by 13 days post-surgery, which persisted throughout the post-operative period studied (13 to 84 days); only a slight increase in left ventricular free wall weight was observed. Isolated mitochondria exhibited region-specific changes with time in state 3 Qo2. Thirteen days after operation, the state 3 Qo2 of right ventricular mitochondria was depressed to about 85% of controls. Thereafter, respiration increased fairly sharply, peaking at just above control values by 40 days post-operation. Finally, it declined abruptly to about 70% of controls by 84 days. A very different pattern of change was observed when left ventricular mitochondrial respiratory activities were examined. Thirteen days after the operation, state 3 Qo2 was elevated somewhat above controls. Thereafter, it declined linearly and gradually, dropping to about 85% of controls by 84 days. 相似文献
42.
Julio E. González-Aguirre Claudia Paola Rivera-Uribe Erick Joel Rendón-Ramírez Rogelio Cañamar-Lomas Juan Antonio Serna-Rodríguez Roberto Mercado-Longoría 《Archivos de bronconeumología》2019,55(4):195-200
Introduction
Invasive respiratory support is a cornerstone of Critical Care Medicine, however, protocols for withdrawal of mechanical ventilation are still far from perfect. Failure to extubation occurs in up to 20% of patients, despite a successful spontaneous breathing trial (SBT).Methods
We prospectively included ventilated patients admitted to medical and surgical intensive care unit in a university hospital in northern Mexico. At the end of a successful SBT, we measured diaphragmatic shortening fraction (DSF) by the formula: diaphragmatic thickness at the end of inspiration – diaphragmatic thickness at the end of expiration/diaphragmatic thickness at the end of expiration × 100, and the presence of B-lines in five regions of the right and left lung. The primary objective was to determine whether analysis of DSF combined with pulmonary ultrasound improves prediction of extubation failure.Results
Eighty-two patients were included, 24 (29.2%) failed to extubation. At univariate analysis, DSF (Youden's J: >30% [sensibility and specificity 62 and 50%, respectively]) and number of B-lines regions (Youden's J: >1 zone [sensibility and specificity 66 and 92%, respectively]) were significant related to extubation failure (area under the curve 0.66 [0.52–0.80] and 0.81 [0.70–0.93], respectively). At the binomial logistic regression, only the number of B-lines regions remains significantly related to extubation failure (OR 5.91 [2.33–14.98], P < .001).Conclusion
In patients with a successfully SBT, the absence of B-lines significantly decreases the probability of extubation failure. Diaphragmatic shortening fraction analysis does not add predictive power over the use of pulmonary ultrasound. 相似文献43.
Martin Deschênes Sebastian Haidarliu Maxime Demers Jeffrey Moore David Kleinfeld Ehud Ahissar 《Anatomical record (Hoboken, N.J. : 2007)》2015,298(3):546-553
In a number of mammals muscle dilator nasi (naris) has been described as a muscle that reduces nasal airflow resistance by dilating the nostrils. Here we show that in rats the tendon of this muscle inserts into the aponeurosis above the nasal cartilage. Electrical stimulation of this muscle raises the nose and deflects it laterally towards the side of stimulation, but does not change the size of the nares. In alert head‐restrained rats, electromyographic recordings of muscle dilator nasi reveal that it is active during nose motion rather than nares dilation. Together these results suggest an alternative role for the muscle dilator nasi in directing the nares for active odor sampling rather than dilating the nares. We suggest that dilation of the nares results from contraction of muscles of the maxillary division of muscle nasolabialis profundus. This muscle group attaches to the outer wall of the nasal cartilage and to the plate of the mystacial pad. Contraction of these muscles exerts a dual action: it pulls the lateral nasal cartilage outward, thus dilating the naris, and drags the plate of the mystacial pad rostrally to produce a slight retraction of the vibrissae. On the basis of these results, we propose that muscle dilator nasi of the rat should be re‐named muscle deflector nasi, and that the maxillary parts of muscle nasolabialis profundus should be referred to as muscle dilator nasi. Anat Rec, 298:546–553, 2015. © 2014 Wiley Periodicals, Inc. 相似文献
44.
Tammy T. Nguyen Sang S. Oh David Weaver Agnieszka Lewandowska Dane Maxfield Max-Hinderk Schuler Nathan K. Smith Jane Macfarlane Gerald Saunders Cheryl A. Palmer Valentina Debattisti Takumi Koshiba Stefan Pulst Eva L. Feldman Gy?rgy Hajnóczky Janet M. Shaw 《Proceedings of the National Academy of Sciences of the United States of America》2014,111(35):E3631-E3640
Defective mitochondrial distribution in neurons is proposed to cause ATP depletion and calcium-buffering deficiencies that compromise cell function. However, it is unclear whether aberrant mitochondrial motility and distribution alone are sufficient to cause neurological disease. Calcium-binding mitochondrial Rho (Miro) GTPases attach mitochondria to motor proteins for anterograde and retrograde transport in neurons. Using two new KO mouse models, we demonstrate that Miro1 is essential for development of cranial motor nuclei required for respiratory control and maintenance of upper motor neurons required for ambulation. Neuron-specific loss of Miro1 causes depletion of mitochondria from corticospinal tract axons and progressive neurological deficits mirroring human upper motor neuron disease. Although Miro1-deficient neurons exhibit defects in retrograde axonal mitochondrial transport, mitochondrial respiratory function continues. Moreover, Miro1 is not essential for calcium-mediated inhibition of mitochondrial movement or mitochondrial calcium buffering. Our findings indicate that defects in mitochondrial motility and distribution are sufficient to cause neurological disease.Motor neuron diseases (MNDs), including ALS and spastic paraplegia (SP), are characterized by the progressive, length-dependent degeneration of motor neurons, leading to muscle atrophy, paralysis, and, in some cases, premature death. There are both inherited and sporadic forms of MNDs, which can affect upper motor neurons, lower motor neurons, or both. Although the molecular and cellular causes of most MNDs are unknown, many are associated with defects in axonal transport of cellular components required for neuron function and maintenance (1–6).A subset of MNDs is associated with impaired mitochondrial respiration and mitochondrial distribution. This observation has led to the hypothesis that neurodegeneration results from defects in mitochondrial motility and distribution, which, in turn, cause subcellular ATP depletion and interfere with mitochondrial calcium ([Ca2+]m) buffering at sites of high synaptic activity (reviewed in ref. 7). It is not known, however, whether mitochondrial motility defects are a primary cause or a secondary consequence of MND progression. In addition, it has been difficult to isolate the primary effect of mitochondrial motility defects in MNDs because most mutations that impair mitochondrial motility in neurons also affect transport of other organelles and vesicles (1, 8–11).In mammals, the movement of neuronal mitochondria between the cell body and the synapse is controlled by adaptors called trafficking kinesin proteins (Trak1 and Trak2) and molecular motors (kinesin heavy chain and dynein), which transport the organelle in the anterograde or retrograde direction along axonal microtubule tracks (7, 12–24). Mitochondrial Rho (Miro) GTPase proteins are critical for transport because they are the only known surface receptors that attach mitochondria to these adaptors and motors (12–15, 18, 25, 26). Miro proteins are tail-anchored in the outer mitochondrial membrane with two GTPase domains and two predicted calcium-binding embryonic fibroblast (EF) hand motifs facing the cytoplasm (12, 13, 25, 27, 28). A recent Miro structure revealed two additional EF hands that were not predicted from the primary sequence (29). Studies in cultured cells suggest that Miro proteins also function as calcium sensors (via their EF hands) to regulate kinesin-mediated mitochondrial “stopping” in axons (15, 16, 26). Miro-mediated movement appears to be inhibited when cytoplasmic calcium is elevated in active synapses, effectively recruiting mitochondria to regions where calcium buffering and energy are needed. Despite this progress, the physiological relevance of these findings has not yet been tested in a mammalian animal model. In addition, mammals ubiquitously express two Miro orthologs, Miro1 and Miro2, which are 60% identical (12, 13). However, the individual roles of Miro1 and Miro2 in neuronal development, maintenance, and survival have no been evaluated.We describe two new mouse models that establish the importance of Miro1-mediated mitochondrial motility and distribution in mammalian neuronal function and maintenance. We show that Miro1 is essential for development/maintenance of specific cranial neurons, function of postmitotic motor neurons, and retrograde mitochondrial motility in axons. Loss of Miro1-directed retrograde mitochondrial transport is sufficient to cause MND phenotypes in mice without abrogating mitochondrial respiratory function. Furthermore, Miro1 is not essential for calcium-mediated inhibition of mitochondrial movement or [Ca2+]m buffering. These findings have an impact on current models for Miro1 function and introduce a specific and rapidly progressing mouse model for MND. 相似文献
45.
46.
47.
48.
Natalia A. Shevtsova Jeffrey C. Smith Ilya A. Rybak 《The European journal of neuroscience》2013,37(2):212-230
The neural mechanisms generating rhythmic bursting activity in the mammalian brainstem, particularly in the pre‐Bötzinger complex (pre‐BötC), which is involved in respiratory rhythm generation, and in the spinal cord (e.g. locomotor rhythmic activity) that persist after blockade of synaptic inhibition remain poorly understood. Experimental studies in rodent medullary slices containing the pre‐BötC identified two mechanisms that could potentially contribute to the generation of rhythmic bursting: one based on the persistent Na+ current (INaP), and the other involving the voltage‐gated Ca2+ current (ICa) and the Ca2+‐activated nonspecific cation current (ICAN), activated by intracellular Ca2+ accumulated from extracellular and intracellular sources. However, the involvement and relative roles of these mechanisms in rhythmic bursting are still under debate. In this theoretical/modelling study, we investigated Na+‐dependent and Ca2+‐dependent bursting generated in single cells and heterogeneous populations of synaptically interconnected excitatory neurons with INaP and ICa randomly distributed within populations. We analysed the possible roles of network connections, ionotropic and metabotropic synaptic mechanisms, intracellular Ca2+ release, and the Na+/K+ pump in rhythmic bursting generated under different conditions. We show that a heterogeneous population of excitatory neurons can operate in different oscillatory regimes with bursting dependent on INaP and/or ICAN, or independent of both. We demonstrate that the operating bursting mechanism may depend on neuronal excitation, synaptic interactions within the network, and the relative expression of particular ionic currents. The existence of multiple oscillatory regimes and their state dependence demonstrated in our models may explain different rhythmic activities observed in the pre‐BötC and other brainstem/spinal cord circuits under different experimental conditions. 相似文献
49.
Yury M. Morozov Martin H. Dominguez Luis Varela Marya Shanabrough Marco Koch Tamas L. Horvath Pasko Rakic 《The European journal of neuroscience》2013,38(3):2341-2348
Anti‐cannabinoid type 1 receptor (CB1) polyclonal antibodies are widely used to detect the presence of CB1 in a variety of brain cells and their organelles, including neuronal mitochondria. Surprisingly, we found that anti‐CB1 sera, in parallel with CB1, also recognize the mitochondrial protein stomatin‐like protein 2. In addition, we show that the previously reported effect of synthetic cannabinoid WIN 55,212‐2 on mitochondrial complex III respiration is not detectable in purified mitochondrial preparations. Thus, our study indicates that a direct relationship between endocannabinoid signaling and mitochondrial functions in the cerebral cortex seems unlikely, and that caution should be taken interpreting findings obtained using anti‐CB1 antibodies. 相似文献
50.