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51.
Rebecca M. Crocker Kelly N.B. Palmer David G. Marrero Tze-Woei Tan 《Journal of diabetes and its complications》2021,35(8):107960
AimsDiabetic foot ulcers (DFUs) and ulceration are complex and lifelong problems for patients with diabetes which dramatically increase mortality rates. This qualitative study sought to capture detailed personal accounts and insights from patients with a clinical history of DFUs and amputations to better understand patient experiences.MethodsFifteen patients from a tertiary referral center that treats diabetic foot problems were approached for participation. Inclusion criteria included having at least one DFU and being of white, Native American, or Hispanic background. Interviews were conducted by telephone by study staff trained in qualitative data gathering and audio recorded.ResultsThe main themes that emerged around impacts included the heavy burden of managing care, significant loss of ambulatory function, economic stress due to medical care costs and job loss, and emotional suffering tied to these stressors.ConclusionsThese data illuminate common social and personal impacts of diabetic foot problems across an ethnically and racially diverse and predominantly low-income US sample that expand our understanding of related declines in well-being. Our results indicate a need for proactive mental health assessment post DFUs diagnosis and the diversification of hospital and community-based support systems. 相似文献
52.
53.
Meerkin D Tardif JC Crocker IR Arsenault A Joyal M Lucier G King SB Williams DO Serruys PW Bonan R 《Circulation》1999,99(13):1660-1665
BACKGROUND: Endovascular radiation is emerging as a potential solution for the prevention and treatment of restenosis. Its effects on the morphology of unstented vessels cannot be determined by angiography and therefore require the use of intravascular ultrasound. METHODS AND RESULTS: Through a 5F noncentered catheter for delivery of a 90Sr/Y source train, 12, 14, or 16 Gy at 2 mm was delivered to native coronary arteries after successful balloon angioplasty in 30 patients. Four patients required stent deployment in the first week. Quantitative coronary angiography and IVUS were performed during the initial procedure and at 6-month follow-up. Binary angiographic restenosis was present in 3 of 30 patients, with target lesion and vessel revascularization performed in 3 and 5 patients, respectively. Angiographic late loss was -0.02+/-0.60 mm, with a -0.09+/-0.46 loss index. IVUS demonstrated no significant reduction in lumen area (from 5.69+/-1.72 mm2 after treatment to 6. 04+/-2.63 mm2 at follow-up), with no significant change in external elastic membrane area (13.71+/-4.54 to 14.22+/-4.71 mm2) over the 6-month follow-up. Wall area was 8.01+/-3.85 mm2 after radiation therapy and 8.19+/-3.44 mm2 at follow-up (P=NS). No significant differences were noted between the different dose groups. CONCLUSIONS: beta-Radiation therapy resulted in a low restenosis rate with negligible late loss by angiography. By IVUS, beta-radiation was shown to inhibit neointima formation, with no reduction of total vessel area at 6-month follow-up. 相似文献
54.
SG Lindquist M Duno M Batbayli A Puschmann H Braendgaard S Mardosiene K Svenstrup LH Pinborg K Vestergaard LE Hjermind J Stokholm BB Andersen P Johannsen JE Nielsen 《Clinical genetics》2013,83(3):279-283
Recently, a hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72 was reported as the cause of chromosome 9p21‐linked frontotemporal dementia‐amyotrophic lateral sclerosis (FTD‐ALS). We here report the prevalence of the expansion in a hospital‐based cohort and associated clinical features indicating a wider clinical spectrum of C9ORF72 disease than previously described. We studied 280 patients previously screened for mutations in genes involved in early onset autosomal dominant inherited dementia disorders. A repeat‐primed polymerase chain reaction amplification assay was used to identify pathogenic GGGGCC expansions. As a potential modifier, confirmed cases were further investigated for abnormal CAG expansions in ATXN2. A pathogenic GGGGCC expansion was identified in a total of 14 probands. Three of these presented with atypical clinical features and were previously diagnosed with clinical olivopontocerebellar degeneration (OPCD), atypical Parkinsonian syndrome (APS) and a corticobasal syndrome (CBS). Further, the pathogenic expansion was identified in six FTD patients, four patients with FTD‐ALS and one ALS patient. All confirmed cases had normal ATXN2 repeat sizes. Our study widens the clinical spectrum of C9ORF72related disease and confirms the hexanucleotide expansion as a prevalent cause of FTD‐ALS disorders. There was no indication of a modifying effect of the ATXN2 gene. 相似文献
55.
Ahmed Z Elmaadawi Peter S Jensen L Eugene Arnold Brooke SG Molina Lily Hechtman Howard B Abikoff Stephen P Hinshaw Jeffrey H Newcorn Laurence Lee Greenhill James M Swanson Cathryn A Galanter 《World Journal of Psychiatry》2015,5(4):412-424
AIM: To determine the prevalence of bipolar disorder (BD) and sub-threshold symptoms in
children with attention deficit hyperactivity disorder (ADHD) through 14 years’
follow-up, when participants were between 21-24 years old.METHODS: First, we examined rates of BD type I and II diagnoses in youth
participating in the NIMH-funded Multimodal Treatment Study of ADHD (MTA). We used the
diagnostic interview schedule for children (DISC), administered to both parents (DISC-P) and
youth (DISCY). We compared the MTA study subjects with ADHD (n = 579) to a
local normative comparison group (LNCG, n = 289) at 4 different assessment
points: 6, 8, 12, and 14 years of follow-ups. To evaluate the bipolar variants, we compared
total symptom counts (TSC) of DSM manic and hypomanic symptoms that were generated by DISC in
ADHD and LNCG subjects. Then we sub-divided the TSC into pathognomonic manic (PM) and
non-specific manic (NSM) symptoms. We compared the PM and NSM in ADHD and LNCG at each
assessment point and over time. We also evaluated the irritability as category A2 manic symptom
in both groups and over time. Finally, we studied the irritability symptom in correlation with
PM and NSM in ADHD and LNCG subjects.RESULTS: DISC-generated BD diagnosis did not differ significantly in rates between ADHD
(1.89%) and LNCG 1.38%). Interestingly, no participant met BD diagnosis more than once in the 4
assessment points in 14 years. However, on the symptom level, ADHD subjects reported
significantly higher mean TSC scores: ADHD 3.0; LNCG 1.7; P < 0.001. ADHD
status was associated with higher mean NSM: ADHD 2.0 vs LNCG 1.1;
P < 0.0001. Also, ADHD subjects had higher PM symptoms than LNCG, with PM
means over all time points of 1.3 ADHD; 0.9 LNCG; P = 0.0001. Examining both
NSM and PM, ADHD status associated with greater NSM than PM. However, Over 14 years, the NSM
symptoms declined and changed to PM over time (df 3, 2523; F = 20.1; P <
0.0001). Finally, Irritability (BD DSM criterion-A2) rates were significantly higher in ADHD
than LNCG (χ2 = 122.2, P < 0.0001), but irritability was
associated more strongly with NSM than PM (df 3, 2538; F = 43.2; P <
0.0001).CONCLUSION: Individuals with ADHD do not appear to be at significantly greater risk for
developing BD, but do show higher rates of BD symptoms, especially NSM. The greater linkage of
irritability to NSM than to PM suggests caution when making BD diagnoses based on irritability
alone as one of 2 (A-level) symptoms for BD diagnosis, particularly in view of its frequent
presentation with other psychopathologies. 相似文献
56.
Cyclin-dependent kinase 5 is a mediator of dopaminergic neuron loss in a mouse model of Parkinson's disease 总被引:6,自引:0,他引:6
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Smith PD Crocker SJ Jackson-Lewis V Jordan-Sciutto KL Hayley S Mount MP O'Hare MJ Callaghan S Slack RS Przedborski S Anisman H Park DS 《Proceedings of the National Academy of Sciences of the United States of America》2003,100(23):13650-13655
Recent evidence indicates that cyclin-dependent kinases (CDKs, cdks) may be inappropriately activated in several neurodegenerative conditions. Here, we report that cdk5 expression and activity are elevated after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that damages the nigrostriatal dopaminergic pathway. Supporting the pathogenic significance of the cdk5 alterations are the findings that the general cdk inhibitor, flavopiridol, or expression of dominant-negative cdk5, and to a lesser extent dominant-negative cdk2, attenuates the loss of dopaminergic neurons caused by MPTP. In addition, CDK inhibition strategies attenuate MPTP-induced hypolocomotion and markers of striatal function independent of striatal dopamine. We propose that cdk5 is a key regulator in the degeneration of dopaminergic neurons in Parkinson's disease. 相似文献
57.
PurposeTo evaluate the effect of Haishengsu (HSS), a protein extract from Tegillarca granosa, on multidrug-resistance genes mdr1, BCR/ABL and sorcin in transplanted tumors.Material/MethodsMice were inoculated subcutaneously with a drug resistant leukemia cell line K562/ADM. Tumor-bearing animals were divided into control, adriamycin, HSS and combination therapy (adriamycin plus HSS) groups. Flow cytometry was used to detect apoptosis of tumor cells, and RT-PCR was used to evaluate the expression of mdr1, BCR/ABL and sorcin.ResultsThe apoptosis rate in the high (71.8%), medium (72.3%) and low doses HSS group (72.4%) was higher than in control (1.2%, p<0.01), adriamycin (34.4%, p<0.05) or combination therapy group (46.4%, p<0.05). The mean optical density of mdr1, BCR/ABL and sorcin in HSS groups was lower than in control, adriamycin and combination therapy group (p<0.01). The optical density of the three genes in high HSS group was lower than in medium and low HSS group (p<0.01).ConclusionsHaishengsu promotes apoptosis of drug-resistant K562/ADM tumors in mice in a dose-dependent manner. The pro-apoptotic effect of Haishengsu may be related to a reduced expression of multidrug-resistance genes mdr1, BCR/ABL and sorcin. 相似文献
58.
Amelioration of coxsackievirus B3-mediated myocarditis by inhibition of tissue inhibitors of matrix metalloproteinase-1 总被引:1,自引:0,他引:1
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Crocker SJ Frausto RF Whitmire JK Benning N Milner R Whitton JL 《The American journal of pathology》2007,171(6):1762-1773
Coxsackievirus B3 (CVB3) is a major cause of acute myocarditis, a serious condition that is refractory to treatment. Myocardial damage results in tissue remodeling that, if too extensive, may contribute to disease. Remodeling is achieved by extracellular proteolysis mediated by the matrix metalloproteinases (MMPs), and MMP activity is counterbalanced by tissue inhibitors of MMPs (TIMPs). We show herein that TIMP-1 expression is induced in the myocardium by CVB3 infection. Surprisingly, TIMP-1 knockout mice exhibited a profound attenuation of myocarditis, with increased survival. The amelioration of disease in TIMP-1 knockout mice was not attributable to either an altered T-cell response to the virus or to reduced viral replication. These data led us to propose a novel function for TIMP-1: its highly localized up-regulation might arrest the MMP-dependent migration of inflammatory cells at sites of infection, thereby anatomically focusing the adaptive immune response. The benefits of TIMP-1 blockade in treating viral myocarditis were confirmed by administering, to wild-type animals, TIMP-1-specific siRNA or polyclonal antisera, both of which diminished CVB3-induced myocarditis. These unexpected findings indicate that increased TIMP-1 expression exacerbates, rather than ameliorates, CVB3-induced myocarditis and, thus, that TIMP-1 may represent a target for the treatment of virus-induced heart disease. 相似文献
59.
60.
S Mukherjee C Pringle M Crocker 《Annals of the Royal College of Surgeons of England》2014,96(4):266-270