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排序方式: 共有640条查询结果,搜索用时 31 毫秒
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Parsa CF Silva ED Sundin OH Goldberg MF De Jong MR Sunness JS Zeimer R Hunter DG 《Ophthalmology》2001,108(4):738-749
PURPOSE: To report ocular and renal findings specific to the inheritable entity called papillorenal (also known as renal-coloboma) syndrome and relate these to a common cause. DESIGN: Observational case series and genetic study. PARTICIPANTS: Two unrelated probands presenting with absent central retinal vessels and 11 available family members. TESTING: Doppler ultrasonographic imaging of the optic nerves and kidneys, fluorescein angiography, and genetic testing for PAX2 mutations were performed. In selected cases, indocyanine green angiography, scanning laser ophthalmoscope perimetry, Retinal Thickness Analyzer measurements, visual evoked potentials, and magnetic resonance imaging were also performed. MAIN OUTCOME MEASURES: Better defined characteristics of the papillorenal syndrome. RESULTS: Numerous cilioretinal vessels were present with rudimentary or absent central retinal vessels. Superonasal visual field defects, typical for papillorenal syndrome, corresponded to inferotemporal areas of anomalous retinal and choroidal perfusion and hypoplastic retina. Renal hypoplasia was discovered in two affected members of one family (with previously unsuspected renal failure in one case), and recurrent pyelonephritis was discovered in four affected members of the other family. No PAX2 mutations were detected. CONCLUSIONS: In the papillorenal syndrome, the hereditary absence of central retinal vessels may be missed, leading to confusion with isolated coloboma, low-tension glaucoma, and morning glory anomaly. Greater awareness of this syndrome will avoid unneeded glaucoma therapy, allow earlier recognition of renal diseases, and allow genetic counseling. We propose that the papillorenal syndrome is a primary dysgenesis that causes vascular abnormalities predominantly affecting the eye, kidney, and urinary tract, leading to hypoplasia of these structures. The absence of defects in the PAX2 gene in these families suggests that mutations in other genes may also be responsible for this syndrome. 相似文献
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For the identification of early steps in the multiphasic processof human pancreas carcinogenesis we have developed a panel ofmonoclonal antibodies to normal and carcinogen-treated humanpancreas cells. One of these, an IgG3 with strong affinity fora membrane-associated 46 kd protein (p-46) in progenitor cellsof methyhiitrosourea (MNU)-treated human pancreas, was purifiedby h.p.l.c. and used to study the modulation of this markerin human pancreas carcinogenesis. This protein was undetectablein adult human pancreas, appeared on the cell surface of a smallsubpopulation of human pancreas explants exposed to MNU, persistedin proliferating cells in hyperplastic foci, and was abundantin anaplastic cells in this model. This marker was associatedwith cytoplasmic and nuclear membrane of all cells in nontumorigenicand tumorigenic cell lines derived from these explants. It waspresent in primary carcinomas of human pancreas but absent innormal pancreas adjacent to tumors. This p-46 marker appearsto be organ and species specific since it was undetectable inother normal tissues and their neoplastic counterparts. 相似文献
45.
Seunggu J. Han Isaac Yang Tarik Tihan Michael D. Prados Andrew T. Parsa 《Journal of neuro-oncology》2010,96(3):313-320
This report presents the historical experience, clinical presentation, treatment, prognosis, and pathogenesis of gliosarcoma
described to date in the English literature. PubMed query of term “gliosarcoma” was performed, followed by a rigorous review
of cited literature. Articles selected for analysis included: (1) case reports of gliosarcoma, (2) review articles of gliosarcoma,
and (3) studies of the pathogenesis or genetics of gliosarcoma in humans. Our review identified 219 cases of gliosarcoma in
34 reports and eight articles addressing the pathogenesis. Survival in larger series ranged 4–11.5 months. Features unique
to gliosarcoma compared to glioblastoma (GBM) include their temporal lobe predilection, potential to appear similar to a meningioma
at surgery, repeated reports of extracranial metastases, and infrequency of EGFR mutations. Published experience is limited
to small case series, and the pathogenesis remains unclear. Clinical and pathologic characteristics distinct from GBM suggest
that they may warrant specific treatment, separate from conventional GBM therapy. 相似文献
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Clonal cytogenetic abnormalities in Hodgkin's disease 总被引:3,自引:0,他引:3
M Ladanyi N Z Parsa K Offit M S Wachtel D A Filippa S C Jhanwar 《Genes, chromosomes & cancer》1991,3(4):294-299
Cytogenetic studies of Hodgkin's disease (HD), in contrast to those of non-Hodgkin's lymphoma (NHL), have been limited to small numbers of cases with infrequently recurring aberrations, underscoring the need for additional studies in establishing a coherent cytogenetic picture of HD. Over a 6 1/2-year period, we received 95 specimens of HD for cytogenetic analysis. Analyzable chromosome preparations were obtained in 70 cases, of which 57 (81%) showed only normal metaphases. In the remaining 13 cases (19%), karyotypic abnormalities were observed that were nonclonal in 3 and clonal in 10. The latter 10 cases included 6 of the nodular sclerosis subtype, 3 mixed cellularity, and 1 lymphocyte-depleted; 8 of the specimens were obtained pretreatment and 2 posttreatment. Two of the cases had a clonal numerical aberration, monosomy 17 in one and trisomy 13 in the other, as their sole abnormality. The remaining 8 cases showed complex karyotypes with multiple structural rearrangements; in 3 of these, the abnormal clone was near-tetraploid. Bands involved more than once included 1p36, 1q21, and 4q35, each in 2 cases. Arms involved more than once included 6q (6q13,6q23), 9p (9p13,9p21), and 5q (5q15,5q35). Three patients had loss of part or all of 6q (del(6)(q13),del(6)(q23),i(6p). Bands 14q32 and 18q21 were not involved in any case, contrary to some previous reports. Our results confirm the frequent occurrence of 1p, 1q, and 6q abnormalities in HD. In addition, we have identified a 5q35 breakpoint, which has recently been shown to be highly specific for Ki-1-positive NHL in a case of typical nodular sclerosis HD. Its presence in HD may represent a cytogenetic link between the two entities, which are immunophenotypically related but clinically and histologically distinct. 相似文献
48.
Fakhraddin Naghibalhossaini Pooneh Mokarram Islam Khalili 《Clinical chemistry and laboratory medicine》2008,46(7):987-989
BACKGROUND: 5,10-Methylenetetrahydrofolate reductase (MTHFR) plays a central role in folate metabolism. Previous studies have suggested an association between the MTHFR 1298A/C polymorphism and several diseases, such as cardiovascular and psychiatric diseases, neural tube defects, diabetes, and cancer. Currently, either PCR-restriction fragment length polymorphism (RFLP) technique or real-time PCR using Taqman assay are used to determine the MTHFR 1298 genotype. METHODS: We developed a simple and efficient approach that employs mutagenically separated PCR to genotype MTHFR 1298A/C polymorphism. Two forward mutagenic allele-specific primers of different lengths for MTHFR 1298A/C were paired with the same reverse primer in a one-tube assay to genotype 20 genomic DNA samples. RESULTS: Electrophoresis on 2.5% agarose gel showed two allele-specific fragments, a 113-bp A allele-specific and a 93-bp C allele-specific PCR product. The results were confirmed by the conventional PCR-RFLP method. CONCLUSIONS: We conclude that mutagenically separated PCR could be used as an alternative simple, reliable, and cost-effective method for the genotyping of MTHFR 1298A/C polymorphism. 相似文献
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Neurochemical and behavioural indices of exercise reward are independent of exercise controllability 下载免费PDF全文
Jonathan J. Herrera Sofiya Fedynska Parsa R. Ghasem Tyler Wieman Peter J. Clark Nathan Gray Esteban Loetz Serge Campeau Monika Fleshner Benjamin N. Greenwood 《The European journal of neuroscience》2016,43(9):1190-1202
Brain reward circuits are implicated in stress‐related psychiatric disorders. Exercise reduces the incidence of stress‐related disorders, but the contribution of exercise reward to stress resistance is unknown. Exercise‐induced stress resistance is independent of exercise controllability; both voluntary running (VR) and forced running (FR) protect rats against the anxiety‐like and depression‐like behavioural consequences of stress. Voluntary exercise is a natural reward, but whether rats find FR rewarding is unknown. Moreover, the contribution of dopamine (DA) and striatal reward circuits to exercise reward is not well characterized. Adult, male rats were assigned to locked wheels, VR, or FR groups. FR rats were forced to run in a pattern resembling the natural wheel running behavior of rats. Both VR and FR increased the reward‐related plasticity marker ΔFosB in the dorsal striatum and nucleus accumbens, and increased the activity of DA neurons in the lateral ventral tegmental area, as revealed by immunohistochemistry for tyrosine hydroxylase and pCREB. Both VR and FR rats developed conditioned place preference (CPP) to the side of a CPP chamber paired with exercise. Re‐exposure to the exercise‐paired side of the CPP chamber elicited conditioned increases in cfos mRNA in direct‐pathway (dynorphin‐positive) neurons in the dorsal striatum and nucleus accumbens in both VR and FR rats, and in tyrosine hydroxylase‐positive neurons in the lateral ventral tegmental area of VR rats only. The results suggest that the rewarding effects of exercise are independent of exercise controllability and provide insight into the DA and striatal circuitries involved in exercise reward and exercise‐induced stress resistance. 相似文献