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81.
Background and aim of the workCardiovascular mortality and morbidity are significantly higher among uremic patients. Although the carotid intimal–medial thickness (C-IMT) as a predictor of endothelial dysfunction (ED) has a prognostic value that has been well demonstrated as an independent predictor of future cardiovascular events, its value in uremic patients need to be re-assisted in our locality. The aim of the work is to investigate a correlation between the brachial artery reactivity test (BART) and the carotid intimal–medial thickening (C-IMT) and their value as independent predictors of endothelial dysfunction in uremic patients.Subjects and methodsThe study involved 70 uremic patients, 40 men and 30 women, 36–56 years old, 40 of them on regular hemodialysis (HD) and 30 on conservative therapy, in addition to 30 healthy persons as a control group. They were selected from the General Medicine and Nephrology Departments, Al-Azhar Assiut University and Assiut University Hospitals over a period of 2 years. All of them were subjected to detailed history, thorough clinical examination, laboratory investigations including complete blood picture, renal function tests (urine analysis, blood urea, and serum creatinine), lipid profile, serum calcium and serum phosphorus, parathyroid hormone (PTH), fasting blood glucose, electrocardiography (ECG), high resolution B-mode ultra-sonography for C-IMT evaluation and brachial artery reactivity test (BART), and abdominal ultra-sonography.ResultsThe results of the present study showed: (1) uremic patients are at an increased risk for carotid atherosclerotic lesions, with significant increase in C-IMT than controls with more significant increase in HD patients. (2) Uremic patients are characterized by impaired endothelium dependent dilatation of the brachial artery (highly significant reduction in flow-mediated dilatation (FMD%)), an abnormality related to the renal failure severity and to the hemodialysis doses. The endothelial dysfunction in the brachial artery was more pronounced in HD patients than in patients on conservative therapy. (3) Significant positive correlation between increased C-IMT and reduction of the brachial FMD%. (4) Significant relation between C-IMT and plaque prevalence and HD duration, while no relations recorded between brachial FMD with HD duration.Conclusion(1) The study confirmed that carotid IMT and brachial artery FMD can be used in interventional studies in which cardiovascular risk is modified and increased in the uremic patients. (2) There was negative correlation between brachial FMD and C-IMT in the uremic patients. 相似文献
82.
T. Liu M. David M. Batstone J. Clark T.-H. Low D. Goldstein A. Hope A. Hosni B. Chua 《International journal of oral and maxillofacial surgery》2021,50(2):143-150
The effectiveness of postoperative radiotherapy (PORT) in improving outcomes remains debatable for oral squamous cell carcinoma (OSCC) patients with pathological intermediate-risk factors (IRFs) after surgery. A retrospective analysis was conducted on 432 intermediate-risk OSCC patients defined by histological reporting of close margin (<5 mm), early nodal disease (pN1), depth of invasion/tumour thickness ≥5 mm, perineural invasion, and/or lymphovascular invasion. Outcomes measured were disease-free survival (DFS), disease-specific survival (DSS), and overall survival (OS). PORT was associated with an improvement in 5-year DFS on univariable analysis (80% vs 71%; P = 0.044), but this did not remain significant on multivariable analysis. PORT was not associated with differences in DSS or OS. The surgical salvage rate was similar in the PORT and surgery-only groups (41% vs 47%; P = 0.972). Perineural invasion was found to be an independent predictor of inferior DSS (hazard ratio (HR) 2.19), DFS (HR 1.89), and OS (HR 1.97). Significantly worse outcomes were observed for patients with ≥4 concurrent IRFs. The application of PORT was associated with lower rates of recurrence, but the benefit was less apparent on mortality. Patients with perineural invasion and multiple concurrent IRFs were found to be at greatest risk, representing a subset of intermediate-risk OSCC patients who may benefit from PORT. 相似文献
83.
Salah AM Said Rikke HM Schiphorst Richard Derksen Lodewijk Wagenaar 《World journal of cardiology》2013,5(9):329-336
This is a case series and review of the literature adding11 new cases.Coronary-cameral fistulas(CCFs)are infrequent anomalies which are in general co-incidentally found during diagnostic coronary angiography(CAG).To delineate the characteristics of congenital and acquired CCFs in adults,we performed a PubMed search for papers dealing with congenital or acquired CCFs in adults.Publications on coronary-vascular fistulas or paediatric subjects were not included.From the world literature,a total of 243 adult patients were identified who had congenital(65%)or acquired(35%)CCFs.In this review,which is part one of a two-part series on CCFs,we describe and discuss the congenital fistulas,give an overview on the published literature and report details of our own series of 11 patients with MMFs and solitary macro CCFs.Of the congenital group,56%were small or large solitary macro CCFs(cut-off 1.5mm)and 9%were coronary artery-ventricular multiple micro-fistulas(MMFs).Apical hypertrophic cardiomyopathy was reported in some of the reviewed subjects with MMFs(3/24=13%)but not was seen in our own series.Conservative medical management was generally the treatment of choice in congenital MMFs;prophylactic implantable cardioverter defibrillators(ICD)were implanted in 2/24(8%)of subjects,especially when extensive micro-fistulisations were involved.None of the patients of our own series required an ICD,as the MMFs were of limited size.Congenital or acquired CCFs in adults are infrequent anomalies having a wide spectrum of clinical presentation may varies from asymptomatic to severely devastating states requiring different treatment modalities. 相似文献
84.
Talpaz M; Kantarjian HM; McCredie KB; Keating MJ; Trujillo J; Gutterman J 《Blood》1987,69(5):1280-1288
Fifty-one patients with previously untreated or minimally treated chronic myelogenous leukemia in chronic phase received human alpha interferon 3 to 9 X 10(6) units intramuscularly (IM) daily until complete hematologic remission, then at doses ranging from 3 X 10(6) units every other day to 9 X 10(6) units daily. Forty-one (80%) patients achieved a hematologic response, 36 (71%) of them attaining a complete hematologic remission with normal peripheral WBC and differential counts. Responding patients showed continuous but slow normalization of several other blood and marrow parameters including platelet counts, serum lactic dehydrogenase and B12 levels, and marrow cellularity and maturation index. Suppression of the Philadelphia chromosome on serial cytogenetic studies of marrow metaphases was documented in 20 of the 36 patients who achieved complete hematologic remission (56%; 39% of total group), eight of whom (22%) had a decrease of the Philadelphia chromosome-positive metaphases to less than 35%. These changes were persistent for 6 months or longer in 18 patients, seven of whom had continuous suppression of the Philadelphia chromosome to less than 90% for a median of 30+ months (range 21+ to 39+ months). After a median follow-up period of 37 months, 25 patients remain in continued disease control with interferon therapy. The projected 3-year survival rate is 76%, with a yearly death rate of 6%, 9%, and 9% in the first 3 years. Response, Philadelphia chromosome suppression, and survival were significantly better among patients in the low-risk category compared to intermediate- and high-risk categories, as defined by a multivariate analysis-derived prognostic model. The projected 3- year survival rate was 94% for patients who achieved a complete hematologic remission on interferon therapy and 45% for those who did not. Thirteen patients have developed blastic crisis, six with lymphoid and three with undifferentiated morphology. We conclude that human leukocyte alpha interferon effectively controls chronic myeloid leukemia and allows reappearance of diploid hemopoietic cells in some patients. 相似文献
85.
p16INK4A and p15INK4B gene deletions in primary leukemias 总被引:4,自引:0,他引:4
Haidar MA; Cao XB; Manshouri T; Chan LL; Glassman A; Kantarjian HM; Keating MJ; Beran MS; Albitar M 《Blood》1995,86(1):311-315
The 9p21 locus has been deleted at a high frequency in a wide variety of tumors. Recently, two genes, p16INK4A and p15INK4B (also called MTS1 and MTS2), have been localized in close proximity at the 9p21 locus, encoding cyclin-dependent kinases 4/6 inhibitors of relative molecular mass 16 kD and 15 kD, respectively and also found to be deleted at a high frequency in tumor cell lines. We analyzed p16INK4A and p15INK4B genes in 178 cases of primary leukemias including 81 cases of chronic lymphocytic leukemia (CLL), seven of hairy cell leukemia (HCL), seven of chronic myelogenous leukemia (CML), 43 of acute myelogenous leukemia (AML), 27 of acute lymphoblastic leukemia (ALL), and 13 of myelodysplastic syndrome (MDS) by Southern blot analyses. The ALL cases showed a relatively high frequency of homozygous deletions (22%, 6 of 27) at the p16INK4A gene locus. Interestingly, of the six cases with p16INK4A homozygous deletions, only three showed homozygous deletions at the p15INK4B gene. In 81 CLL patients, we detected one homozygous and five heterozygous deletions at both the p16INK4A and p15INK4B genes and two heterozygous deletions at the p16INK4A gene alone. Deletion of these two genes in AML cases is relatively low (9%). We did not detect deletions in any of the MDS, HCL, and CML cases examined. Sequence analyses of p16INK4A gene of six CLL cases with heterozygous deletion at this locus showed a 27-bp deletion at the splice acceptor site of intron 1 in one case and changes in the coding sequence in three other cases. The data presented in this report showed that (1) p16INK4A and p15INK4B genes are preferentially deleted homozygously in ALL and heterozygously in CLL cases with frequent mutation in the second allele, and (2) p16INK4A gene appears to be more frequently deleted than p15INK4B gene. 相似文献
86.
Dercksen MW; Weimar IS; Richel DJ; Breton-Gorius J; Vainchenker W; Slaper- Cortenbach CM; Pinedo HM; von dem Borne AE; Gerritsen WR; van der Schoot CE 《Blood》1995,86(10):3771-3782
In the present study, we show by adhesion assays and ultrastructural studies that platelets can bind to CD34+ cells from human blood and bone marrow and that this interaction interferes with the accurate detection of endogenously expressed platelet glycoproteins (GPs). The interaction between these cells was found to be reversible, dependent on divalent cations, and mediated by P-selectin. Enzymatic characterization showed the involvement of sialic acid residues, protein(s). The demonstration of mRNA for the P-selectin glycoprotein ligand 1 (PSGL-1) in the CD34+ cells by polymerase chain reaction (PCR) analysis suggests that this molecule is present in these cells. Under conditions that prevent platelet adhesion, a small but distinct subpopulation of CD34+ cells diffusely expressed the platelet GPIIb/IIIa complex. These cells were visualized by immunochemical studies. Furthermore, synthesis of mRNA for GPIIb and GPIIIa by CD34+ cells was shown using PCR analysis. The semiquantitative PCR results show relatively higher amounts of GPIIb mRNA than of PF4 mRNA in CD34+CD41+ cells in comparison with this ratio in platelets. This finding is a strong indication that the PCR results are not caused by contaminating adhering platelets. MoAbs against GPIa GPIb alpha, GPV, P- selectin, and the alpha-chain of the vitronectin receptor did not react with CD34+ cells. The number of CD34+ cells expressing GPIIb/IIIa present in peripheral blood stem cell (PBSC) transplants was determined and was correlated with platelet recovery after intensive chemotherapy in 27 patients. The number of CD34+CD41+ cells correlated significantly better with the time of platelet recovery after PBSC transplantation (r = .83, P = .04) than did the total number of CD34+ cells (r = .55). Statistical analysis produced a threshold value for rapid platelet recovery of 0.34 x 10(6) CD34+CD41+ cells/kg. This study suggests that if performed in the presence of EDTA the flow cytometric measurement of GPIIb/IIIa on CD34+ cells provides the most accurate indication of the platelet reconstitutive capacity of the PBSC transplant. 相似文献
87.
Verschraegen CF; Talpaz M; Hirsch-Ginsberg CF; Pherwani R; Rios MB; Stass SA; Kantarjian HM 《Blood》1995,85(10):2705-2710
The purpose of this report was to evaluate scintigraphy analysis of Southern blot hybridization as a method to quantify the breakpoint cluster region (BCR) rearrangement of Philadelphia chromosome (Ph)+ chronic myelogenous leukemia (CML). Cytogenetic and molecular studies performed simultaneously on 474 bone marrow and/or blood samples from 300 patients treated with alpha-interferon-based therapy were compared. Molecular results were expressed as the percentage of rearranged BCR bands versus the total scintigraphic signal. The percentage of Ph+ metaphases was calculated on 25 metaphases. The results of molecular studies obtained on both peripheral blood and bone marrow samples were identical. The rank correlation between the BCR quantification and the percentage of Ph positivity in 465 samples was excellent (r = .78). However, of 99 samples with a normal karyotype, 24% had a BCR rearrangement. Of 86 samples with no BCR rearrangement, 13% showed a Ph chromosome. Of 49 samples with partial cytogenetic remission (Ph+ metaphases, 1% to 34%), 23% had no BCR rearrangement. In samples with a minor or no cytogenetic response (Ph+ metaphases, > 34%), BCR analysis overestimated the degree of response in 73 of 326 samples (22%). Nevertheless, survival analysis by BCR quantification level showed statistically better outcome for patients in complete or partial molecular response (P < .01). Molecular quantification of BCR was useful in monitoring the course of Ph+ CML. This method, which can be used on peripheral blood, detected residual disease not shown by cytogenetic analysis and was prognostically relevant as a measure of disease suppression. 相似文献
88.
Collagen-induced arthritis in rhesus monkeys: evaluation of markers for inflammation and joint degradation 总被引:1,自引:0,他引:1
't Hart BA; Bank RA; De Roos JA; Brok H; Jonker M; Theuns HM; Hakimi J; Te Koppele JM 《Rheumatology (Oxford, England)》1998,37(3):314-323
The objective of this study was to analyse parameters in rhesus monkey
collagen-induced arthritis (CIA) with which the inflammation and
destruction of the joints can be described in quantitative terms. CIA was
induced in genetically susceptible and resistant monkeys, which can be
distinguished on the basis of the dominant resistance marker Mamu- A26. The
disease course was monitored daily using a semiquantitative scoring system.
Plasma samples were collected once or twice weekly and analysed for
C-reactive protein (CRP). Urines were collected overnight once a week and
analysed for excretion rates of the collagen cross- links
hydroxylysylpyridinoline (HP) and lysylpyridinoline (LP). The results show
that periods of active CIA are characterized by substantial weight loss and
increased plasma CRP levels, followed shortly thereafter by increased
excretion rates of the collagen cross- links HP and LP. Remission of the
disease can be recognized by a decline in plasma CRP levels and especially
an increase in body weight. The highest CRP levels were found in the most
severely arthritic monkeys, indicating a possible relationship of the
absolute plasma CRP levels to the severity of inflammation. During periods
of active arthritis, increased excretion rates of collagen cross-links HP
and LP in the urine were found. In particular, the major collagen
cross-link in articular cartilage, HP, showed a strong increase (9- to
15-fold). The excretion rates of LP, which is considered as a bone-specific
degradation marker, only increased 4- to 6-fold, thus indicating
predominant destruction of cartilage and less of bone. In conclusion, the
severity of CIA can be monitored in a quantitative manner using plasma CRP
levels, urinary excretion rates of HP and LP, and body weights,
superimposed on semiquantitative clinical scores. The parameters also
facilitate a more objective assessment of the effect of anti-arthritic
drugs in the model than with the clinical scores alone.
相似文献
89.
Ferguson JJ Fathy Waly HM Le D Thomakos N Wilson JM 《The Journal of invasive cardiology》1998,10(6):318-322
Considerable controversy exists as to the appropriate dosing of heparin for PTCA. We retrospectively reviewed records of 335 patients undergoing PTCA to determine: 1) the effects of correcting for weight and body surface area (BSA) on the heparin dose-response distribution; and 2) the average dose of heparin (standard, weight-based, and BSA-based) required to achieve an activated clotting time (ACT) of 300 seconds. For each patient, height, weight, BSA, baseline ACT (HemoTec), bolus heparin dose, and post-heparin ACT were recorded and the heparin response calculated. There were no significant differences in the distributions of standard (SD =.017 +/- 006 sec/U, 34% of mean), weight-based (SD = 1.41 +/- 0.46 sec/U/kg, 33% of mean), and BSA-based (SD = 0.033 +/- 0.011 sec/U/m2, 32% of mean) heparin response. There were slight, but significant correlations between heparin response and weight (r = 0.37) and heparin response and BSA (r = 0.36). The estimated doses of heparin to achieve a HemoTec ACT of 300 seconds were 10,650 +/- 1270 U, 130 +/- 15 U/kg, and 5390 +/- 640 U/m2. CONCLUSIONS: There are slight but significant correlations between heparin response and both weight and BSA. The distributions of weight- and BSA-corrected heparin response are similar to that of standard heparin dosing. Thus, weight adjusted heparin dosing would not appear to be likely to provide a more reliable ACT response to bolus doses of heparin. 相似文献
90.
Previous studies on the association of ankylosing spondylitis and
abnormalities of the lung parenchyma have been based largely on plain
radiography and pulmonary function testing. This study, although
uncontrolled, is the first to use high-resolution computed tomography to
examine the entire lung parenchyma in ankylosing spondylitis patients, and
to correlate the findings with clinical assessment, plain radiography and
pulmonary function testing. The study population comprised 26 patients
meeting the New York criteria for idiopathic ankylosing spondylitis who
attended the out-patient department at our institution. High-resolution
computed tomography examination revealed abnormalities in 19 patients
(70%): these included interstitial lung disease (n = 4), bronchiectasis (n
= 6), emphysema (n = 4), apical fibrosis (n = 2), mycetoma (n = 1) and
non-specific interstitial lung disease (n = 12). Plain radiography was
abnormal in only four patients and failed to identify any patient with
interstitial lung disease. All patients with interstitial lung disease on
high-resolution computed tomography had respiratory symptoms and three of
the four had evidence of a restrictive process on pulmonary function
testing. This study raises, for the first time, the possible association
between interstitial lung disease and ankylosing spondylitis, and
highlights the use of high-resolution computed tomography in detecting such
disease in ankylosing spondylitis patients.
相似文献