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61.
Jordi Landier Guillaume Constantin de Magny Andres Garchitorena Jean-Fran?ois Guégan Jean Gaudart Laurent Marsollier Philippe Le Gall Tamara Giles-Vernick Sara Eyangoh Arnaud Fontanet Ga?tan Texier 《Emerging infectious diseases》2015,21(8):1414-1417
To determine when risk for Buruli ulcer is highest, we examined seasonal patterns in a highly disease-endemic area of Cameroon during 2002–2012. Cases peaked in March, suggesting that risk is highest during the high rainy season. During and after this season, populations should increase protective behaviors, and case detection efforts should be intensified. 相似文献
62.
Summary The fasting plasma growth hormone (GH) concentration and the plasma growth hormone response to sustained hyperglycemia was
examined in 8 chronically uremic subjects before and after hemodialysis employing the hyperglycemic clamp technique. The plasma
glucose concentration was actuely raised and maintained at +125 mg/100 ml above basal levels. Since the glucose concentration
was held constant, the glucose infusion rate is an index of glucose metabolism (M) and M divided by the plasma insulin response
(I) is a measure of tissue sensitivity to insulin. Predialysis, the fasting GH concentration, 4.0±1.0 ng/ml, was significantly
greater than controls, 0.3±0.1 ng/ml (p<0.01), and failed to suppress normally following sustained hyperglycemia. Both M,
4.23±0.36 mg/kg·min, and M/I, 5.05±0.79 mg/kg·min per μU/ml, were significantly reduced compared to controls (p<0.001). There
was no correlation between either the fasting GH concentration or the GH response to sustained hyperglycemia and either M
or M/I. Following dialysis both M, 6.30±0.64 mg/kg·min, and M/I, 8.39±1.06 mg/kg·min per μU/ml, increased (p<0.01) without
significant change in either the fasting GH level, 4.0 ± 1.2 ng/ml, or the plasma GH response to hyperglycemia. It is concluded
that while deranged GH physiology is a common accompaniment of the uremic state, it is not responsible for the glucose intolerance
and tissue insensitivity to insulin observed in uremia.
The middle of the weight range for subjects of medium frame from the 1959 Metropolitan Life Insurance Company table for desirable
weight was used. 相似文献
63.
In rabbits intravenous administration of antibodies to lung angiotensin converting enzyme (ACE) results in a rapid redistribution of ACE on the plasma membrane of pulmonary endothelium with fixation of complement and development of fatal pulmonary edema. In survivors given daily injections of antibodies, ACE disappears from the lung ("antigenic modulation") and the rabbits become resistant to further immune injury. To test the hypothesis that these events depend on a functionally intact mechanism of cell activation, rabbits received, in addition to anti-ACE antibodies, chlorpromazine, a drug that inhibits calmodulin and protein kinase C and decreases plasma membrane fluidity. Initially, chlorpromazine inhibited antigen redistribution, fixation of complement, and development of pulmonary edema. In rabbits maintained on chlorpromazine and receiving daily anti-ACE antibodies this effect became attenuated and the rabbits eventually developed ACE redistribution, complement fixation, and pulmonary edema. We conclude that chlorpromazine temporarily inhibits antigenic modulation in vivo, presumably through its action on calcium-mediated antibody-cell surface antigen interaction. 相似文献
64.
Predictors and consequences of aggressive behavior by community-based dementia patients 总被引:1,自引:0,他引:1
The frequency, nature, context, and caregivers' reactions to aggressive behavior in 213 dementia patients residing in the community was studied. Aggression was reported in 57.2% of the patients and in 10.6% of the caregivers. Predictors of patient aggression were greater frequency of behavior and memory problems, premorbid aggression, and a more troubled premorbid social relationship between patient and caregiver. Patient aggression predicted the decision to discontinue home care. 相似文献
65.
66.
Metabolic syndrome amplifies the age-associated increases in vascular thickness and stiffness 总被引:13,自引:0,他引:13
Scuteri A Najjar SS Muller DC Andres R Hougaku H Metter EJ Lakatta EG 《Journal of the American College of Cardiology》2004,43(8):1388-1395
OBJECTIVES: We sought to evaluate whether the clustering of multiple components of the metabolic syndrome (MS) has a greater impact on these vascular parameters than individual components of MS. BACKGROUND: Intima-media thickness (IMT) and vascular stiffness have been shown to be independent predictors of adverse cardiovascular events. The MS is defined as the clustering of three or more of the cardiovascular risk factors of dysglycemia, hypertension, dyslipidemia, and obesity. METHODS: Carotid IMT and stiffness were derived via B-mode ultrasonography in 471 participants from the Baltimore Longitudinal Study on Aging, who were without clinical cardiovascular disease and not receiving antihypertensive therapy. RESULTS: The MS conferred a disproportionate increase in carotid IMT (+16%, p < 0.0001) and stiffness (+32%, p < 0.0001), compared with control subjects. Multiple regression models, which included age, gender, smoking, low-density lipoprotein, as well as each individual component of MS as continuous variables, showed that MS was an independent determinant of both IMT (p = 0.002) and stiffness (p = 0.012). The MS was associated with a greater prevalence of subjects whose values were in the highest quartiles of IMT, stiffness, or both. CONCLUSIONS: Even after taking into account each individual component of MS, the clustering of at least three of these components is independently associated with increased IMT and stiffness. This suggests that the components of MS interact to synergistically impact vascular thickness and stiffness. Future studies should examine whether the excess cardiovascular risk associated with MS is partly mediated through the amplified alterations in these vascular properties. 相似文献
67.
Elevation of endothelial microparticles, platelets, and leukocyte activation in patients with venous thromboembolism 总被引:5,自引:0,他引:5
Chirinos JA Heresi GA Velasquez H Jy W Jimenez JJ Ahn E Horstman LL Soriano AO Zambrano JP Ahn YS 《Journal of the American College of Cardiology》2005,45(9):1467-1471
OBJECTIVES: The purpose of this research was to determine the levels of platelet, leukocyte, and endothelial activation and markers of cellular interactions in patients with venous thromboembolism (VTE). BACKGROUND: The details of interactions between endothelium, platelets, and leukocytes in VTE are not well understood. METHODS: We studied 25 patients with VTE and compared 25 healthy controls. We used flow cytometry to measure: 1) endothelial microparticles (EMP) identified by CD31+/CD42b- (EMP(31)) or E-selectin (EMP(62E)); 2) platelet microparticles (CD31+/CD42b+); 3) surface expression of P-selectin in platelets and CD11b in leukocytes; 4) EMP-monocyte conjugates (percentage of monocytes positive for E-selectin); and 5) platelet-leukocyte conjugates (PLC) expressed as percentage of leukocytes positive for CD41. RESULTS: Patients with VTE had marked elevations of EMP(31) (2,193 vs. 383 counts/microl; p = 0.003), EMP(62E) (368 vs. 223 counts/microl; p = 0.001), and EMP-monocyte conjugates (3.3% vs. 2.5%; p = 0.002), as well as increased activation of platelets (35.2 vs. 5.0 fluorescence intensity units for P-selectin; p < 0.0001) and leukocytes (13.9 vs. 7.7 U for CD11b; p = 0.004). Also elevated in VTE were PLC (61.7% vs. 39.6%; p = 0.01). Expression of CD11b in leukocytes strongly correlated with PLC (r = 0.74; p < 0.0001). CONCLUSIONS: Marked activation of endothelium, platelets, and leukocytes occurs in VTE, and VTE, or the accompanying inflammatory process, involves the release of EMP and formation of EMP-monocyte conjugates and PLC. These findings support prior studies suggesting that release of EMP and their binding to monocytes are key events in thrombogenesis. Our findings also support the concept that the formation of PLC regulates leukocyte activation and participates in linking thrombosis with inflammation. 相似文献
68.
69.
Fulvia Milena Cribi Roberta Erra Lorenza Pugni Carlota Rubio-Perez Lidia Alonso Sara Simonetti Giorgio Alberto Croci Garazi Serna Andrea Ronchi Carlo Pietrasanta Giovanna Lunghi Anna Maria Fagnani Maria Piana Matthias Matter Alexandar Tzankov Luigi Terracciano Andres Anton Enrico Ferrazzi Stefano Ferrero Enrico Iurlaro Joan Seoane Paolo Nuciforo 《The Journal of clinical investigation》2021,131(6)
70.
Mutations in leucine rich repeat kinase 2 (LRRK2) are a major cause of familial Parkinson's disease (PD) and a risk factor for its sporadic form. LRRK2 hyperactivity has also been reported in sporadic PD, making LRRK2 an appealing target for PD small-molecule therapeutics. At a cellular level, increasing evidence suggests that LRRK2 regulates membrane trafficking. Under some conditions LRRK2 also associates with microtubules, the cellular tracks used by dynein and kinesin motors to move membranes. At a structural level, however, relatively little was known about LRRK2. An important step toward bridging this gap took place last year with the publication of structures of LRRK2's cytosolic and microtubule-bound forms. Here, we review the main findings from these studies and discuss what we see as the major challenges going forward with a focus on areas that will require structural information. We also introduce the structural techniques—cryo-electron microscopy and cryo-electron tomography—that were instrumental to solving the structures of LRRK2. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society 相似文献