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Lea Tenenholz Grinberg Xuehua Wang Chao Wang Peter Dongmin Sohn Panos Theofilas Manu Sidhu John Benjamin Arevalo Helmut Heinsen Eric J. Huang Howard Rosen Bruce L. Miller Li Gan William W. Seeley 《Acta neuropathologica》2013,125(4):581-593
Post-translational modifications play a key role in tau protein aggregation and related neurodegeneration. Because hyperphosphorylation alone does not necessarily cause tau aggregation, other post-translational modifications have been recently explored. Tau acetylation promotes aggregation and inhibits tau’s ability to stabilize microtubules. Recent studies have shown co-localization of acetylated and phosphorylated tau in AD and some 4R tauopathies. We developed a novel monoclonal antibody against acetylated tau at lysine residue 274, which recognizes both 3R and 4R tau, and used immunohistochemistry and immunofluorescence to probe 22 cases, including AD and another eight familial or sporadic tauopathies. Acetylated tau was identified in all tauopathies except argyrophilic grain disease (AGD). AGD is an age-associated, common but atypical 4R tauopathy, not always associated with clinical progression. Pathologically, AGD is characterized by neuropil grains, pre-neurofibrillary tangles, and oligodendroglial coiled bodies, all recognized by phospho-tau antibodies. The lack of acetylated tau in these inclusions suggests that AGD represents a distinctive tauopathy. Our data converge with previous findings to raise the hypothesis that AGD could play a protective role against the spread of AD-related tau pathology. Tau acetylation as a key modification for the propagation tau toxicity deserves further investigation. 相似文献
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Incidence and prognosis of intraabdominal hypertension in a mixed population of critically ill patients: a multiple-center epidemiological study 总被引:1,自引:0,他引:1
Malbrain ML Chiumello D Pelosi P Bihari D Innes R Ranieri VM Del Turco M Wilmer A Brienza N Malcangi V Cohen J Japiassu A De Keulenaer BL Daelemans R Jacquet L Laterre PF Frank G de Souza P Cesana B Gattinoni L 《Critical care medicine》2005,33(2):315-322
OBJECTIVE: Intraabdominal hypertension is associated with significant morbidity and mortality in surgical and trauma patients. The aim of this study was to assess, in a mixed population of critically ill patients, whether intraabdominal pressure at admission was an independent predictor for mortality and to evaluate the effects of intraabdominal hypertension on organ functions. DESIGN: Multiple-center, prospective epidemiologic study. SETTING: Fourteen intensive care units in six countries. PATIENTS: A total of 265 consecutive patients admitted for >24 hrs during the 4-wk study period. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Intraabdominal pressure was measured twice daily via the bladder. Data recorded on admission were the patient demographics with Simplified Acute Physiology Score II, Acute Physiology and Chronic Health Evaluation II score, and type of admission; during intensive care stay, Sepsis-Related Organ Failure Assessment score and intraabdominal pressure were measured daily together with fluid balance. Nonsurvivors had a significantly higher mean intraabdominal pressure on admission than survivors: 11.4 +/- 4.8 vs. 9.5 +/- 4.8 mm Hg. Independent predictors for mortality were age (odds ratio, 1.04; 95% confidence interval, 1.01-1.06; p = .003), Acute Physiology and Chronic Health Evaluation II score (odds ratio, 1.1; 95% confidence interval, 1.05-1.15; p < .0001), type of intensive care unit admission (odds ratio, 2.5 medical vs. surgical; 95% confidence interval, 1.24-5.16; p = .01), and the presence of liver dysfunction (odds ratio, 2.5; 95% confidence interval, 1.06-5.8; p = .04). The occurrence of intraabdominal hypertension during the intensive care unit stay was also an independent predictor of mortality (relative risk, 1.85; 95% confidence interval, 1.12-3.06; p = .01). Patients with intraabdominal hypertension at admission had significantly higher Sepsis-Related Organ Failure Assessment scores during the intensive care unit stay than patients without intraabdominal hypertension. CONCLUSIONS: Intraabdominal hypertension on admission was associated with severe organ dysfunction during the intensive care unit stay. The mean intraabdominal pressure on admission was not an independent risk factor for mortality; however, the occurrence of intraabdominal hypertension during the intensive care unit stay was an independent outcome predictor. 相似文献
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Wojciech Dabrowski Todd T. Schlegel Jaroslaw Wosko Radoslaw Rola Ziemowit Rzecki Manu L.N.G. Malbrain Andrzej Jaroszynski 《Journal of electrocardiology》2018,51(3):499-507
Introduction
Traumatic brain injury (TBI) affects cardiac electrical function, and several extra-cerebral factors, including intra-abdominal pressure (IAP), might further modulate this brain-heart interaction. The purpose of this study was to investigate the impact of TBI, and of increased IAP during TBI, on cardiac electrical function as measured by vectorcardiographic (VCG) variables.Methods
Survival, IAP and changes in VCG variables including spatial QRS-T angle and QTc interval were measured in consecutive adult patients with either isolated TBI (iTBI), or with TBI accompanied by polytrauma to the abdomen and/or limbs (pTBI). For all patients, observations were performed just after the admission to the ICU (baseline) and at 24, 48, 72 and 96 h after admission.Results
74 patients aged 45 ± 18 were studied. 44 were treated for iTBI and 30 for pTBI. In all patients, spatial QRS-T angle and QTc interval increased after TBI (p < 0.001), relatively more so in patients with pTBI. Compared to survivors, non-survivors also ultimately had greater widening of the spatial QRS-T angle (p < 0.001), most notably just before foraminal herniation. Wider spatial QRS-T angle and longer QTc interval were also noted in patients with IAP > 12 mmHg (p < 0.001), and with right compared to left hemispheric injury (p < 0.001). ST segment level at the J point decreased 24 and 48 h after TBI in leads I, II, III, aVR, aVF, V1, V2, V3 and V6, and increased in lead V1, especially in non-survivors.Conclusions
Spatial QRS-T angle and QTc interval increase after TBI. If foraminal herniation complicates TBI, further widening of the spatial QRS-T angle typically precedes it, followed by notable narrowing thereafter. Increased IAP also intensifies TBI-associated increases in spatial QRS-T angle and QTc interval. 相似文献38.
Manu Tomar Raghavendra Pralhada Rao Palaniyamma Dorairaj Abhishek Koshta Sowbhagya Suresh Mohamed Rafiq Rajesh Kumawat Rangesh Paramesh Babu U. V K. V. Venkatesh 《RSC advances》2019,9(39):22288
Correction for ‘A clinical and computational study on anti-obesity effects of hydroxycitric acid’ by Manu Tomar et al., RSC Adv., 2019, 9, 18578–18588.The authors regret that the name of one of the authors (Raghavendra Pralhada Rao) was shown incorrectly in the original article. The corrected author list is as shown above.The Royal Society of Chemistry apologises for these errors and any consequent inconvenience to authors and readers. 相似文献
39.
Anju Rani Anuj Kumar Ankita Lal Manu Pant 《International journal of environmental health research》2014,24(4):378-399
Cadmium is a widespread toxic pollutant of occupational and environmental concern because of its diverse toxic effects: extremely protracted biological half-life (approximately 20–30 years in humans), low rate of excretion from the body and storage predominantly in soft tissues (primarily, liver and kidneys). It is an extremely toxic element of continuing concern because environmental levels have risen steadily due to continued worldwide anthropogenic mobilization. Cadmium is absorbed in significant quantities from cigarette smoke, food, water and air contamination and is known to have numerous undesirable effects in both humans and animals. Cadmium has a diversity of toxic effects including nephrotoxicity, carcinogenicity, teratogenicity and endocrine and reproductive toxicities. At the cellular level, cadmium affects cell proliferation, differentiation, apoptosis and other cellular activities. Current evidence suggests that exposure to cadmium induces genomic instability through complex and multifactorial mechanisms. Most important seems to be cadmium interaction with DNA repair mechanism, generation of reactive oxygen species and induction of apoptosis. In this article, we have reviewed recent developments and findings on cadmium toxicology. 相似文献