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Age affects outcomes in chronic kidney disease   总被引:1,自引:0,他引:1  
Chronic kidney disease (CKD) is common among the elderly. However, little is known about how the clinical implications of CKD vary with age. We examined the age-specific incidence of death, treated end-stage renal disease (ESRD), and change in estimated glomerular filtration rate (eGFR) among 209,622 US veterans with CKD stages 3 to 5 followed for a mean of 3.2 years. Patients aged 75 years or older at baseline comprised 47% of the overall cohort and accounted for 28% of the 9227 cases of ESRD that occurred during follow-up. Among patients of all ages, rates of both death and ESRD were inversely related to eGFR at baseline. However, among those with comparable levels of eGFR, older patients had higher rates of death and lower rates of ESRD than younger patients. Consequently, the level of eGFR below which the risk of ESRD exceeded the risk of death varied by age, ranging from 45 ml/min per 1.73 m(2) for 18 to 44 year old patients to 15 ml/min per 1.73 m(2) for 65 to 84 year old patients. Among those 85 years or older, the risk of death always exceeded the risk of ESRD in this cohort. Among patients with eGFR levels <45 ml/min per 1.73 m(2) at baseline, older patients were less likely than their younger counterparts to experience an annual decline in eGFR of >3 ml/min per 1.73 m(2). In conclusion, age is a major effect modifier among patients with an eGFR of <60 ml/min per 1.73 m(2), challenging us to move beyond a uniform stage-based approach to managing CKD.  相似文献   
94.
Helicobacter pylori (H. pylori) is an infectious agent influencing as much as 50% of the world’s population. It is the causative agent for several diseases, most especially gastric and duodenal peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma of the stomach. A number of other, extragastric manifestations also are associated with H. pylori infection. These include neurological disorders, such as Alzheimer’s disease, demyelinating multiple sclerosis and Parkinson’s disease. There is also evidence for a relationship between H. pylori infection and such dermatological diseases as psoriasis and rosacea as well as a connection with infection and open-angle glaucoma. Generally little is known about the relationship between H. pylori infection and diseases of the pancreas. Most evidence about H. pylori and its potential role in the development of pancreatic diseases concerns pancreatic adenocarcinoma and autoimmune forms of chronic pancreatitis. There is data (albeit not fully consistent) indicating modestly increased pancreatic cancer risk in H. pylori-positive patients. The pathogenetic mechanism of this increase is not yet fully elucidated, but several theories have been proposed. Reduction of antral D-cells in H. pylori-positive patients causes a suppression of somatostatin secretion that, in turn, stimulates increased secretin secretion. That stimulates pancreatic growth and thus increases the risk of carcinogenesis. Alternatively, H. pylori, as a part of microbiome dysbiosis and the so-called oncobiome, is proven to be associated with pancreatic adenocarcinoma development via the promotion of cellular proliferation. The role of H. pylori in the inflammation characteristic of autoimmune pancreatitis seems to be explained by a mechanism of molecular mimicry among several proteins (mostly enzymes) of H. pylori and pancreatic tissue. Patients with autoimmune pancreatitis often show positivity for antibodies against H. pylori proteins. H. pylori, as a part of microbiome dysbiosis, also is viewed as a potential trigger of autoimmune inflammation of the pancreas. It is precisely these relationships (and associated equivocal conclusions) that constitute a center of attention among pancreatologists, immunologists and pathologists. In order to obtain clear and valid results, more studies on sufficiently large cohorts of patients are needed. The topic is itself sufficiently significant to draw the interest of clinicians and inspire further systematic research. Next-generation sequencing could play an important role in investigating the microbiome as a potential diagnostic and prognostic biomarker for pancreatic cancer.  相似文献   
95.
BACKGROUND/AIMS: Persistent postoperative dysphagia diminishes the good effect of laparoscopic anti-reflux surgery. An excessive increase of the intraoperative lower esophageal sphincter pressure (LESp) is supposed to be related to the persistent postoperative dysphagia and its knowledge could lead to the modification of the surgical technique followed by improved clinical outcomes. This study aims to describe the relation between the intraoperative LESp increase and the incidence of postoperative dysphagia and to find whether a combination of intraoperative manometry and mechanical calibration of the wrap is able to decrease the incidence of the persistent postoperative dysphagia. METHODOLOGY: The randomized, prospective, two-branch study included 39 patients suffering from symptoms of gastroesophageal reflux disease. All patients underwent pre- and postoperative manometry, 24-hour pH-metry and laparoscopic anti-reflux surgery. The intraoperative LESp was measured in the study arm only. RESULTS: A higher incidence of persistent postoperative dysphagia was revealed in patients with the intraoperative LESp increase more than 15 mmHg. This complication was not found in patients with the LESp increase under 8 mmHg with no impact on the efficacy of the surgery. The combination of the intraoperative manometry and the mechanical calibration of the wrap seems to bring the benefit only to a small number of the patients. CONCLUSIONS: According to our results, the intraoperative LESp measurement proved to be a useful supplementary method which was easy to perform, and which enables a modification of the surgical technique to decrease the incidence of the persistent postoperative dysphagia.  相似文献   
96.

Background

The systolic variation of mitral regurgitation (MR) is a pitfall in its quantification. Current recommendations advocate using quantitative echocardiographic techniques that account for this systolic variation. While prior studies have qualitatively described patterns of systolic variation no study has quantified this variation.

Methods

This study includes 41 patients who underwent cardiovascular magnetic resonance (CMR) evaluation for the assessment of MR. Systole was divided into 3 equal parts: early, mid, and late. The MR jets were categorized as holosystolc, early, or late based on the portions of systole the jet was visible. The aortic flow and left ventricular stroke volume (LVSV) acquired by CMR were plotted against time. The instantaneous regurgitant rate was calculated for each third of systole as the difference between the LVSV and the aortic flow.

Results

The regurgitant rate varied widely with a 1.9-fold, 3.4-fold, and 1.6-fold difference between the lowest and highest rate in patients with early, late, and holosystolic jets respectively. There was overlap of peak regurgitant rates among patients with mild, moderate and severe MR. The greatest variation of regurgitant rate was seen among patients with mild MR.

Conclusion

CMR can quantify the systolic temporal variation of MR. There is significant variation of the mitral regurgitant rate even among patients with holosystolic MR jets. These findings highlight the need to use quantitative measures of MR severity that take into consideration the temporal variation of MR.  相似文献   
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98.
Dopaminergic cell transplantation is an experimental therapy for Parkinson's disease (PD). It has many potential theoretical advantages over current treatment strategies such as providing continuous local dopaminergic replenishment, eliminating motor fluctuations and medication-induced dyskinesias, slowing down disease progression or even reversing disease pathology in the host. Recent studies also show that dopaminergic cell transplants provide long-term neuromodulation in the basal ganglia that simulates the combined effects of oral dopaminergic therapy and surgical therapies like deep brain stimulation, the contemporary therapeutic approach to advanced PD. However, dopaminergic cell transplantation in PD as not been optimized and current experimental techniques have many drawbacks. In published experiments to date of attempted dopaminergic grafting in PD, the major challenges are unacceptable graft-induced dyskinesias or failure of such grafts to exceed the benefits afforded by sham surgery. A deleterious host immune response to the transplant has been implicated as a major putative cause for these adverse outcomes. This article focuses on recent advances in understanding the immunology of the transplantation in PD and possible methods to overcome adverse events such that we could translate cell replacement strategies into viable clinical treatments in the future.  相似文献   
99.
Spontaneous intramural duodenal haematoma develops mostly as a complication of anticoagulation therapy. Other causes were reported only as case reports. CT diagnostics has some typical features in an intramural haematoma of the small bowel. This is especially hyperdensity of the bowel wall during the first 10 days from the onset of symptoms (30-80 HU), which could contribute to the differentiation from other infiltrative processes. These features are fully expressed only in a certain part of patients. We reported a 54 year-old female treated for epigastric pain. The patient's history, laboratory data, ultrasonography and CT findings resulted in a mistaken diagnosis of acute pancreatitis, necrosis of the pancreatic body with a subsequent development of pancreatic pseudocyst. The CT guided drainage was performed. The correct diagnosis was made one year later--surgical treatment was indicated for clinical signs of GI obstruction and CT findings of pseudocyst recurrence. During the operation, there was a finding of intramural haematoma in the duodenojejunal border. We performed an evacuation of the haematoma and gastroenteroanastomosis.  相似文献   
100.

Background

Consumer credit may reflect financial hardship that patients face due to cancer treatment, which in turn may impact ability to manage health after cancer; however, credit’s relationship to economic burden and health after cancer has not been evaluated.

Methods

From May to September 2015, 123 women with a history of breast cancer residing in Pennsylvania or New Jersey completed a cross-sectional survey of demographics, socioeconomic position, comorbidities, SF-12 self-rated health, economic burden since cancer diagnosis, psychosocial stress, and self-reported (poor to excellent) credit quality. Ordinal logistic regression evaluated credit’s contribution to economic burden and self-rated health.

Results

Mean respondent age was 64 years. Mean year from diagnosis was 11.5. Forty percent of respondents were Black or Other and 60% were White. Twenty-four percent self-reported poor credit, and 76% reported good to excellent credit quality. In adjusted models, changing income, using savings, borrowing money, and being unable to purchase a health need since cancer were associated with poorer credit. Better credit was associated with 7.72 ([1.22, 14.20], p =?0.02) higher physical health t-score, and a ??2.00 ([??3.92, ??0.09], p =?0.04) point change in psychosocial stress.

Conclusions

This exploratory analysis establishes the premise for consumer credit as a marker of economic burden and health for breast cancer survivors. Future work should validate these findings in larger samples and for other health conditions.

Implications for Cancer Survivors

Stabilizing and monitoring consumer credit may be a potential intervention point for mitigating economic burden after breast cancer.
  相似文献   
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