全文获取类型
收费全文 | 247篇 |
免费 | 25篇 |
国内免费 | 1篇 |
专业分类
儿科学 | 14篇 |
妇产科学 | 2篇 |
基础医学 | 51篇 |
口腔科学 | 17篇 |
临床医学 | 6篇 |
内科学 | 58篇 |
皮肤病学 | 1篇 |
神经病学 | 23篇 |
特种医学 | 6篇 |
外科学 | 44篇 |
综合类 | 2篇 |
一般理论 | 1篇 |
预防医学 | 10篇 |
眼科学 | 2篇 |
药学 | 25篇 |
中国医学 | 2篇 |
肿瘤学 | 9篇 |
出版年
2023年 | 5篇 |
2022年 | 3篇 |
2020年 | 4篇 |
2019年 | 6篇 |
2018年 | 4篇 |
2017年 | 5篇 |
2016年 | 10篇 |
2015年 | 7篇 |
2014年 | 14篇 |
2013年 | 17篇 |
2012年 | 20篇 |
2011年 | 12篇 |
2010年 | 9篇 |
2009年 | 15篇 |
2008年 | 16篇 |
2007年 | 12篇 |
2006年 | 10篇 |
2005年 | 15篇 |
2004年 | 4篇 |
2003年 | 9篇 |
2002年 | 7篇 |
2001年 | 9篇 |
2000年 | 8篇 |
1999年 | 3篇 |
1998年 | 2篇 |
1996年 | 2篇 |
1992年 | 1篇 |
1991年 | 2篇 |
1990年 | 3篇 |
1988年 | 2篇 |
1987年 | 8篇 |
1986年 | 3篇 |
1985年 | 6篇 |
1982年 | 2篇 |
1981年 | 1篇 |
1979年 | 1篇 |
1978年 | 1篇 |
1976年 | 1篇 |
1975年 | 2篇 |
1974年 | 2篇 |
1973年 | 1篇 |
1972年 | 1篇 |
1971年 | 2篇 |
1969年 | 1篇 |
1968年 | 4篇 |
1967年 | 1篇 |
排序方式: 共有273条查询结果,搜索用时 15 毫秒
1.
Nerve dysfunction after trauma around the elbow can lead to significant long-term pain and functional deficit. Fortunately, most of these injuries are neurapraxias that will recover spontaneously after conservative treatment. The necessity and time frame for surgical intervention for specific patterns of nerve dysfunction remains controversial. Often surgical exploration exacerbates rather than alleviates the presenting nerve problem. Distal humeral shaft fractures, elbow dislocations, Monteggia fracture-dislocations, supracondylar fractures in children, and proximal forearm trauma all have been associated with various types of nerve injuries with a variable degree of recovery. The early recognition of nerve dysfunction combined with appropriate treatment measures is the key to successful outcome. 相似文献
2.
Maja Misirkic Kristina Janjetovic Ljubica Vucicevic Gordana Tovilovic Biljana Ristic Urosh Vilimanovich Ljubica Harhaji-Trajkovic Mirjana Sumarac-Dumanovic Dragan Micic Vladimir Bumbasirevic Vladimir Trajkovic 《Pharmacological research》2012,65(1):111-119
The role of autophagy, a process in which the cell self-digests its own components, was investigated in glioma cell death induced by the hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase-inhibiting drug simvastatin. Induction of autophagy and activation of autophagy-regulating signalling pathways were analyzed by immunoblotting. Flow cytometry/fluorescent microscopy was used to assess autophagy-associated intracellular acidification and apoptotic markers (phosphatidylserine exposure, DNA fragmentation and caspase activation). Cell viability was determined by crystal violet, MTT or LDH release assay. Simvastatin treatment of U251 and C6 glioma cell lines caused the appearance of autophagolysosome-like intracytoplasmic acidic vesicles. The induction of autophagy in U251 cells was confirmed by the upregulation of autophagosome-associated LC3-II and pro-autophagic beclin-1, as well as by the downregulation of the selective autophagic target p62. Simvastatin induced the activation of AMP-activated protein kinase (AMPK) and its target Raptor, while simultaneously downregulating activation of Akt. Mammalian target of rapamycin (mTOR), a major AMPK/Akt downstream target and a major negative autophagy regulator, and its substrate p70 S6 kinase 1 were also inhibited by simvastatin. Mevalonate, the product of HMG-CoA reductase enzymatic activity, AMPK siRNA or pharmacological inactivation of AMPK with compound C suppressed, while the inhibitors of Akt (10-DEBC hydrochloride) and mTOR (rapamycin) mimicked autophagy induction by simvastatin. Inhibition of autophagy with bafilomycin A1, 3-methyladenine and LC3β shRNA, as well as AMPK inhibition with compound C or AMPK siRNA, markedly increased apoptotic death of simvastatin-treated U251 cells. These data suggest that inhibition of AMPK-dependent autophagic response might sensitize glioma cells to statin-induced apoptotic death. 相似文献
3.
4.
Tasic V Korneti P Gucev Z Hoppe B Blau N Cheong HI 《Pediatric nephrology (Berlin, Germany)》2008,23(7):1177-1181
Primary distal renal tubular acidosis (dRTA) is an inherited disease characterized by the inability of the distal tubule to lower urine pH <5.50 during systemic acidosis. We report two male siblings who presented with severe hyperchloremic metabolic acidosis, high urinary pH, nephrocalcinosis, growth retardation, sensorineural hearing loss, and hypokalemic paralysis. Laboratory investigations revealed proximal tubular dysfunction (low molecular weight proteinuria, generalized hyperaminoaciduria, hypophosphatemia with hyperphosphaturia, and hypouricemia with hyperuricosuria). There was significant hyperoxaluria and laboratory evidence for mild rhabdomyolysis. Under potassium and alkali therapy, proximal tubular abnormalities, muscular enzymes, and oxaluria normalized. A homozygous mutation in the ATP6V1B1 gene, which is responsible for dRTA with early hearing loss, was detected in both siblings. In conclusion, proximal tubular dysfunction and hyperoxaluria may be found in children with dRTA and are reversible under appropriate therapy. 相似文献
5.
Hypomagnesemia with hypercalciuria and nephrocalcinosis: case report and a family study 总被引:1,自引:0,他引:1
Tasic V Dervisov D Koceva S Weber S Konrad M 《Pediatric nephrology (Berlin, Germany)》2005,20(7):1003-1006
A 7-month-old male infant was referred for investigation after a documented febrile urinary tract infection. His past medical history was characterized by episodes of unexplained fever and mild dehydration. The ultrasound examination of his kidneys demonstrated bilateral diffuse medullary nephrocalcinosis. His serum and urine biochemistry revealed hypomagnesemia (0.4 mmol/l), hyperuricaemia (506 µmol/l), mildly increased iPTH (71 pg/ml) and hypercalciuria (16.0 mg/kg/day). The diagnosis of familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) was confirmed by mutational analysis of the CLDN16 gene, encoding paracellin-1. Sequencing displayed a homozygous Leu151Phe exchange affecting the first extracellular loop of paracellin-1. There were eight family relatives who underwent biochemical analysis, renal ultrasound and genetic investigation for CLDN16 mutations. Five of them were found to be heterozygous for the Leu151Phe mutation. Two heterozygotes (the mother and the maternal grandfather) presented with hypercalciuria. The grandfather had a history of recurrent passage of calculi. These findings point to the role of heterozygous CLDN16 gene mutations in renal pathophysiology. In conclusion, patients suspected of having FHHNC should be screened for CLDN16 mutations, especially with respect to genetic counseling. In addition, heterozygotes at risk should be clinically assessed in order to prevent renal complications of hypercalciuria. 相似文献
6.
Cardiac Rhythm and Conduction Disturbances: What is the Role of Autoimmune Mechanisms? 总被引:3,自引:0,他引:3
The immunopathogenesis of cardiac rhythm and conduction disorders has been underestimated. Therefore, the aim of this review is to analyze the current data and controversial issues in this area. The incidence of autoantibodies to human conducting tissue has been analyzed in sick sinus syndrome, bradyarrhythmia, and hypersensitive carotid sinus syndrome. Patients with anti-sinus node antibodies (ASNab) have a 10-fold higher risk of developing sick sinus syndrome, compared to age-matched controls. The risk of acquiring an atrioventricular block was up to 3-fold in patients with anti-atrioventricular node antibodies (AAVNab) in comparison to controls. The incidence of anti His antibodies (AHISab) was low both in patients and controls. Anti-cardiac Purkinje cell antibodies (ACPCab) seemed to be an epiphenomenon and not a pathogenetic marker of conduction disorders. In congenital heart block association with HLA-B27 and HLA-DR3 is a possible prerequisite in the pathophysiology of the disease, although transplacental passage of various antibodies and immune complexes is widely recognized. The main autoantibodies detected both in children with congenital heart block and their mothers are anti-Ro/SS-A and anti-La/SS-B antibodies. The cross-reactivity of laminin with anti-La antibodies could be important in the initiation of the autoimmune process. Autoantibodies against adrenoceptors and muscarinic cholinergic receptors of neonatal heart and human endogenous retrovirus-3 expressed in fetal cardiac tissue could also play a role in the pathogenesis of the congenital heart block. Of note, apoptosis could be one of the possible mechanisms of the progression of the congenital conduction disturbances to the complete heart block. In addition, evidence is compiling that cellular activation and cellular cytotoxicity specific for a given target tissue appears to be at least equally important in the pathogenesis of the disease as the humoral response. In conclusion, the immunopathogenesis of certain cardiac rhythm and conduction disorders is well established in sick sinus syndrome, congenital heart block, and connective tissue diseases. ASNab, AAVNab, anti-Ro/SS-A, and anti-La/SS-B antibodies can be regarded as diagnostic and prognostic markers. 相似文献
7.
Improved glycaemic control with dipeptidyl peptidase-4 inhibition in patients with type 2 diabetes: vildagliptin (LAF237) dose response 总被引:7,自引:0,他引:7
OBJECTIVE: A novel treatment option for diabetic patients is the enhancement of incretin hormone activity by inhibition of the enzyme dipeptidyl peptidase-4 (DPP-4). This study was designed to establish a dose of the DPP-4-inhibitor vildagliptin (LAF237) that was effective in reducing HbA1c levels and was safe and well tolerated in patients with type 2 diabetes. PATIENTS AND METHODS: The study of 279 patients with type 2 diabetes consisted of a 4-week run-in phase where patients received placebo and a 12-week active treatment phase where they received one of the following dosages of vildagliptin: 25 mg twice daily, 25, 50 or 100 mg once daily (qd), or placebo. RESULTS: There was a statistically significant reduction in HbA1c levels in the vildagliptin 50 mg qd (p=0.003) and 100 mg qd groups (p=0.004) compared with the placebo group. The mean 4-h postprandial glucose level was significantly reduced from placebo in the vildagliptin 50 mg qd group (p = 0.012) and mean 4-h postprandial insulin was significantly increased from baseline vs. placebo in the vildagliptin 100 mg qd group (p=0.022). The assessment of beta-cell function (HOMA-B) was significantly increased in the vildagliptin 100 mg qd treatment group (p=0.007). The incidence of adverse events was similar in all treatment groups including placebo. CONCLUSIONS: Vildagliptin, at 50 and 100 mg qd, was effective in reducing HbA1c levels compared with placebo in patients with type 2 diabetes. Vildagliptin at dosages up to 100 mg qd appeared safe and well tolerated. 相似文献
8.
9.
Velibor Tasic Zoran Gucev Nadica Ristoska-Bojkovska Aleksandra Janchevska Hermann-Josef Lüdecke 《Renal failure》2014,36(4):619-622
Introduction: The tricho-rhino-phalangeal syndrome type III (TRPS III) is a rare autosomal dominantly inherited condition. The main clinical features are sparse and slow-growing hair and nails, a pear-shaped nose with a bulbous tip, elongated and flat philtrum, thin upper lip, cone-shaped epiphyses of the phalanges, and short stature. All patients have a point mutation in the TRPS1 gene. Case report: In this paper, we present a 13-year-old female with the typical clinical features of TRPS III, extreme growth retardation, severe deformities of both proximal radii resulting in limited extension of the elbows, and chronic renal failure (CRF) in addition. Molecular diagnostics revealed a missense mutation in exon 6 of TRPS1 that she inherited from her father who is also affected with TRPS III, but does not have CRF. In the index patient, the CRF was found to be due to bilateral renal hypodysplasia (RHD). Conclusion: Beside the renal dysplasia, the girl had severe deformities of the proximal radii – findings which have not been reported so far in TRPS III. 相似文献
10.
Biljana Z. Ristic Marina M. Milenkovic Ivana R. Dakic Biljana M. Todorovic-Markovic Momir S. Milosavljevic Milica D. Budimir Verica G. Paunovic Miroslav D. Dramicanin Zoran M. Markovic Vladimir S. Trajkovic 《Biomaterials》2014
Synthesis of new antibacterial agents is becoming increasingly important in light of the emerging antibiotic resistance. In the present study we report that electrochemically produced graphene quantum dots (GQD), a new class of carbon nanoparticles, generate reactive oxygen species when photoexcited (470 nm, 1 W), and kill two strains of pathogenic bacteria, methicillin-resistant Staphylococcus aureus and Escherichia coli. Bacterial killing was demonstrated by the reduction in number of bacterial colonies in a standard plate count method, the increase in propidium iodide uptake confirming the cell membrane damage, as well as by morphological defects visualized by atomic force microscopy. The induction of oxidative stress in bacteria exposed to photoexcited GQD was confirmed by staining with a redox-sensitive fluorochrome dihydrorhodamine 123. Neither GQD nor light exposure alone were able to cause oxidative stress and reduce the viability of bacteria. Importantly, mouse spleen cells were markedly less sensitive in the same experimental conditions, thus indicating a fairly selective antibacterial photodynamic action of GQD. 相似文献