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1.
In quantitative analysis of repeated coronary angiograms, a variable vasomotor tone of the epicardial coronary arteries may influence the accuracy of the results. Therefore, we evaluated the extent and reproducibility of coronary artery dilation with nitrocompounds. In 32 patients with coronary artery disease, the vasodilatory response of angiographically normal coronary segments to different nitrocompounds was analyzed with the computer-assisted contour detection system CAAS. Twenty patients received 5 mg or 10 mg of isosorbide dinitrate sublingually. After 10 to 15 min, a maximal diameter increase was measured with an average of 16 +/- 11% (5 mg: P less than 0.01) and 28 +/- 13% (10 mg: P less than 0.001) from control. Another 12 patients received 0.025 mg per kg body weight of SIN-1, the active metabolite of molsidomine, as an intravenous infusion over 5 min. A comparable maximal dilation (29 +/- 5%; P less than 0.001) occurred after 10 to 15 min and could not be enhanced further with 0.8 mg nitroglycerin administered sublingually (28 +/- 7%; n.s.). One hour after square root of Sin-1, coronary dilation was still 24 +/- 8% (P less than 0.001 compared with control), and 0.8 mg of nitroglycerin sublingually reestablished the previous maximal dilation of 28 +/- 8%. We conclude that high doses of nitrocompounds induce a reproducible maximal coronary dilation that eliminates a substantial source of error in quantitative analysis of repeated coronary angiograms. At present, sublingual administrations of either 10 mg isosorbide dinitrate once or 0.8 mg nitroglycerin repeatedly seem to represent the easiest practicable modes to achieve maximal coronary vasodilation for an adequate period.  相似文献   
2.

Objectives

This study assessed the prognostic significance of remote zone native T1 alterations for the prediction of clinical events in a population with ST-segment elevation myocardial infarction (STEMI) who were treated by primary percutaneous coronary intervention (PPCI) and compared it with conventional markers of infarct severity.

Background

The exact role and incremental prognostic relevance of remote myocardium native T1 mapping alterations assessed by cardiac magnetic resonance (CMR) after STEMI remains unclear.

Methods

We included 255 consecutive patients with STEMI who were reperfused within 12 h after symptom onset. CMR core laboratory analysis was performed to assess left ventricular (LV) function, standard infarct characteristics, and native T1 values of the remote, noninfarcted myocardium. The primary endpoint was a composite of death, reinfarction, and new congestive heart failure within 6 months (major adverse cardiac events [MACE]).

Results

Patients with increased remote zone native T1 values (>1,129 ms) had significantly larger infarcts (p = 0.012), less myocardial salvage (p = 0.002), and more pronounced LV dysfunction (p = 0.011). In multivariable analysis, remote zone native T1 was independently associated with MACE after adjusting for clinical risk factors (p = 0.001) or other CMR variables (p = 0.007). In C-statistics, native T1 of remote myocardium provided incremental prognostic information beyond clinical risk factors, LV ejection fraction, and other markers of infarct severity (all p < 0.05). The addition of remote zone native T1 to a model of prognostic CMR parameters (ejection fraction, infarct size, and myocardial salvage index) led to net reclassification improvement of 0.82 (95% confidence interval: 0.46 to 1.17; p < 0.001) and to an integrated discrimination improvement of 0.07 (95% confidence interval: 0.02 to 0.13; p = 0.01).

Conclusions

In STEMI patients treated by PPCI, evaluation of remote zone alterations by quantitative noncontrast T1 mapping provided independent and incremental prognostic information in addition to clinical risk factors and traditional CMR outcome markers. Remote zone alterations may thus represent a novel therapeutic target and a useful parameter for optimized risk stratification. (Effect of Conditioning on Myocardial Damage in STEMI [LIPSIA-COND]; NCT02158468)  相似文献   
3.
Recent published data suggest that performing carotid endarterectomy (CEA) in patients with renal dysfunction is associated with a prohibitively high perioperative stroke and death rate. On the basis of our experience, we hypothesized that CEA is a safe procedure in patients with renal insufficiency. A retrospective review of one surgeon's CEA experience from 1988 to 1998 was performed. A total of 398 procedures performed on 370 patients were reviewed for patient demographics and adverse events in the 30-day perioperative period. Risk factors, indications for procedure, and degree of stenosis, as well as intraoperative use of shunts, patch angioplasty, drains, completion angiography, and EEG monitoring were compared. Patients were categorized by preoperative creatinine (Cr) levels as normal (Cr 1.5). All data were subjected to statistical analysis. Our results showed that CEA can be performed safely in patients with renal dysfunction with no increase in perioperative stroke or death rate. Performing CEA in patients with renal insufficiency does require preoperative cardiac evaluation and close cardiac monitoring, as there appears to be an increased rate of myocardial infarction in our series.  相似文献   
4.
Prolonged administration of the anorectic drug chlorphentermine causes an accumulation of “foam cells” in pulmonary alveoli of guinea pigs, mice, and rabbits. Ultrastructurally, the “foam cells” correspond to enlarged alveolar macrophages, packed with lamellated cytoplasmic inclusions. Lamellar bodies of the same type also occur in increased numbers within nearly all other pulmonary cell types and in the cells of adrenal cortex of all three animal species. These cellular alterations are interpreted to result from an intralysosomal accumulation of phospholipids. In view of the present findings and of the bulk of experimental evidence from the literature, it is concluded that the presence of alveolar “foam cells” in animals treated with an amphiphilic drug is not an isolated occurrence, but rather an indication for a generalized phenomenon, which is believed to be due to a drug-induced phospholipidosis.  相似文献   
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The inflammatory cytokine tumor necrosis factor alpha (TNFalpha) is controversially discussed in ischemia/reperfusion damage of the heart. Purpose of this study was to elucidate cellular sources of TNFalpha and parameters which possibly influence its release in the heart following ischemia. Isolated hearts of mice were subjected to 15 min of global ischemia and 90 min of reperfusion. We employed hearts of various mice knock-out strains (interleukin-6(-/-), matrix metalloprotease-7(-/-), mast-cell deficient WBB6F1-Kit(W)/Kit(W-v), TNF-R1(-/-)) and wildtype mice, the latter perfused without and with infusion of cycloheximide or TNFalpha-cleaving-enzyme inhibitor (TAPI-2). Normoxic control hearts showed basal release of TNFalpha during the whole experiment. Immunohistology identified cardiac mast cells, macrophages and endothelial cells as main sources. TNFalpha release was stimulated during postischemic reperfusion, occurring in a two-peak pattern: directly after ischemia (0-10 min) and again after 60-90 min. The first peak mainly reflects tissue washout of TNFalpha accumulated during ischemia. The second, protracted peak arose continuously from the basal level and was abolished by protein synthesis inhibitor cycloheximide. Both properties are characteristic for de novo synthesis of TNFalpha, e.g., in cardiac muscle cells. However, immunohistological staining for TNFalpha failed in cardiomyocytes after 90 min of reperfusion. In contrast to hearts of TNF-R1(-/-) and Kit(W/W-v)-mice, those of IL-6(-/-) and MMP-7(-/-) mice lacked the late TNFalpha peak. TAPI did not suppress release of TNFalpha. While autostimulation via TNF-R1 also does not seem obligatory and mast cell can be ignored as source of the second peak, IL-6 may support de novo synthesis of TNFalpha. Additionally, TNFalpha release may essentially involve cleavage of membrane bound TNFalpha by MMP-7.  相似文献   
10.
Carotid interposition grafts (CIP) for carotid artery revascularization can be a viable alternative to carotid endarterectomy (CEA) or carotid artery stenting (CAS) for complex carotid disease. This is a retrospective review of the UCLA 17-year experience with CIP for carotid reconstruction. Carotid operations performed between 1988 and 2005 revealed 41 CIP procedures in 39 patients using polytetrafluoroethylene (PTFE, n = 31) or reversed greater saphenous vein (Vein) (n = 10). Perioperative data and long-term follow-up for each conduit were statistically compared. There were no significant differences in demographics, risk factors, operative indications, complications, or 30-day perioperative deaths. There was one postoperative stroke in each group, for an overall stroke rate of 4.9% (PTFE 3.2%, Vein 10%). There was one asymptomatic occlusion and there were two high-grade restenoses in the PTFE group compared with one asymptomatic occlusion and one high-grade restenosis in the Vein group. Overall primary patency was 90% and the assisted primary patency was 97% for the PTFE group (mean follow-up 50 months), whereas primary patency was 80% (mean follow-up 30 months) in the Vein group. CIP is a safe and effective technique with excellent long-term follow-up for complex carotid reconstruction when CEA or CAS may be contraindicated.  相似文献   
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