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21.
Danek Elbaum Ronald L. Nagel Robert M. Bookchin Theodore T. Herskovits 《Proceedings of the National Academy of Sciences of the United States of America》1974,71(12):4718-4722
Alkylureas (methyl-, ethyl-, propyl-, and butyl-) can inhibit both the gelation of deoxyhemoglobin S and red cell sickling without denaturation of the hemoglobin or intrinsic alteration of its oxygen affinity. This effect is directly proportional to the length of the alkyl chain and substantiates the importance of hydrophobic interactions in the polymerization of hemoglobin S. In addition, it opens the possibility that further systematic investigations with these compounds will help quantitate the role of hydrophobic interactions in this system so as to further our understanding of the polymerization of deoxyhemoglobin S. 相似文献
22.
Joanna Drzedon Marta Pawlak Barbara Gawdzik Aleksandra Wypych Karol Kramkowski Pawe Kowalczyk Dagmara Jacewicz 《Materials》2022,15(4)
Polyolefins are used in everyday life, including in the production of many types of plastic. In addition, polyolefins account for over 50% of the polymers produced in the world. After conducting the oligomerization reactions of 2-propen-1-ol, 2-chloro-2-propen-1-ol, and norborene, polyolefins are obtained. In this report, two complexes of oxovanadium(IV) and dioxovanadium(V) with dipicolinate, 2-phenylyridine, and 4,4′-dimethoxy-2,2′-bipyridyl as precatalysts for 2-propen-1-ol, 2-chloro-2-propen-1-ol, and norborene oligomerizations are prepared. We present for the first time the new dipicolinate complex compound of oxovanadium(IV) with 4,4′-dimetoxy-2,2′-bipyridyl. Both complexes were tested for catalytic activity in the oligomerization reactions of 2-propen-1-ol, 2-chloro-2-propen-1-ol, and norbornene. Both synthesized complexes showed high catalytic activity in these oligomerization reactions, except for the oligomerization of norbornene. 相似文献
23.
Coronary artery spatial distribution of chronic total occlusions: Insights from a large US registry
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Santiago Garcia MD M. Chadi Alraies MD Aris Karatasakis MD Demetris Yannopoulos MD Dimitri Karmpaliotis MD Khaldoon Alaswad MD Farouc A. Jaffer MD PhD Robert W. Yeh MD MBA Mitul P. Patel MD John Bahadorani MD Judit Karacsonyi MD Pratik Kalsaria MS Barbara Danek MD Subhash Banerjee MD Emmanouil S. Brilakis MD PhD 《Catheterization and cardiovascular interventions》2017,90(1):23-30
24.
Kevin Peikert Andreas Hermann Adrian Danek 《Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie》2022,49(1):4
BackgroundMcLeod syndrome (MLS) is an X-linked multisystemic progressive disorder caused by loss of function mutations in the XK gene. The rare blood group phenotype of MLS patients with absent Kx antigen requires the support of specialized transfusion institutions because of the risk of transfusion complications. Acanthocytosis of red blood cells occurs in almost all patients. Nonhematological manifestations of MLS are very similar to those of VPS13A disease (chorea-acanthocytosis), an autosomal-recessive condition. Their shared phenotype apart from acanthocytosis includes movement disorders such as chorea and dystonia, epilepsy, peripheral neuropathy, and muscle involvement, typically with creatine kinase (CK) elevation, cardiomyopathy included.SummaryIn this review, we describe the nonhematological manifestations of MLS in comparison with those of VPS13A disease. While there are many similarities, differences such as mode of inheritance, sex distribution, age at manifestation, severity of heart involvement, frequency of feeding dystonia or of involuntary head drops may help to distinguish these disorders in the clinic. Immunohematological demonstration of the McLeod-Kell phenotype or detection of pathogenic mutations of XK (or VPS13A, respectively) is the gold standard for distinction. “Neuroacanthocytosis” was often used as an overarching term, but is potentially misleading, as the term does not refer to a defined disease entity. Its use, if continued, must not prevent clinicians to seek a final diagnosis on the basis of molecular findings. The clinical similarity of MLS and VPS13A disease has long suggested some shared pathophysiology. Evidence for molecular interaction between XK, the McLeod protein, and chorein, the VPS13A gene product, has recently been put forward: XK forms a complex with chorein/VPS13A, a bulk lipid transporter located at various membrane contact sites. The exact role of XK in this complex needs to be further elucidated. Impairment of bulk lipid transport appears as the common denominator of both MLS and VPS13A disease. A variety of further conditions may in time be added to the “bulk lipid transport diseases,” such as the recently recognized disorders caused by mutations in the VPS13B, VPS13C, and VPS13D genes.Key Messages(1) Patients diagnosed with the rare red cell McLeod phenotype (McLeod syndrome, MLS) require interdisciplinary collaboration of transfusion medicine specialists, neurologists, and cardiologists for both their hematological and nonhematological disease manifestations. (2) The phenotypical similarity of MLS and VPS13A disease, often leading to either confusion or insufficient diagnostic depth (under the label of “neuroacanthocytosis”), is based on interaction of the respective proteins, XK and chorein, within the cellular machinery for bulk lipid transport. (3) Overall, the term “bulk lipid transport diseases” seems useful for further research on a group of conditions that may not only share pathophysiology, but may also share treatment approaches. 相似文献
25.
Specialty centers that focus on lucrative services such as cardiology and orthopedics pose a challenge to full-service hospitals in already crowded health care markets. We examine how hospitals in three markets have responded, from aggressively working to keep niche facilities from gaining a foothold to partnering with physicians on their own centers. 相似文献
26.
Scalise D 《Hospitals & health networks / AHA》2002,76(11):42-4, 2
The Institute of Medicine report on medical errors and the resulting attention from the public and health care purchasers pushed patients safety to the forefront of providers' quality initiatives. Now, some health care leaders say the preoccupation with safety is wrongheaded and could detract from broad efforts to improve care. 相似文献
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29.
Danek A 《Der Nervenarzt》2002,73(6):564-569
McLeod syndrome and chorea-acanthocytosis are classified with the so-called neuroacanthocytosis group of syndromes. Both lead to progressive basal ganglia degeneration and were not easily distinguished in the past. With the discovery of their molecular bases, mutations of the X-linked gene XK and autosomal recessive mutations of the gene coding for chorein, respectively, the two phenotypes can now be differentiated and extend the diagnostic spectrum in patients presenting with chorea. The present review compares the two conditions and proposes a practical approach to diagnosis and treatment. Better-defined disease concepts should eventually replace the umbrella term of "neuroacanthocytosis." Animal models are needed to understand the underlying mechanisms. A final common pathway is likely for the pathogenesis of these conditions and is most probably shared with Huntington's disease. 相似文献
30.
The zebrafish (Danio rerio) has become an attractive vertebrate model for studying developmental processes, and is emerging as a model system for studying the mechanisms by which xenobiotic compounds perturb normal development. Embryos treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) shortly after fertilization exhibit a range of adverse effects on the heart: an early reduction in cardiac myocyte number, followed by a change in heart looping and morphology, with an apparent compaction of the ventricle and overall decrease in heart size. These changes are accompanied by impaired cardiac function including a decrease in cardiac output and eventually irreversible ventricular standstill. The mechanisms involved in mediating effects of TCDD on the heart remain unknown. However, it is widely accepted that aryl hydrocarbon receptor (AHR) activation mediates endpoints of TCDD toxicity in vertebrates. In zebrafish, there are multiple forms of AHR and AHR nuclear translocator protein (ARNT) raising the question about whether different endpoints of TCDD toxicity are mediated by different components of the AHR/ARNT pathway. To address this question we used morpholino oligonucleotide technology to specifically block the expression of zfAHR2, zfARNT1, zfARNT2, and zfCYP1A, and assessed the previously described effects of TCDD on heart morphology, size, and function in the developing morphants. We report that blocking zfAHR2 and zfARNT1 expression provided protection against the TCDD-mediated alteration in heart morphology, reduced cardiac myocyte number, decreased cardiac output and ventricular standstill in zebrafish larvae, while the zfarnt2 and zfcyp1a morpholinos did not block the TCDD-induced cardiac toxicity. 相似文献