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71.
Effects of Ethanol in an Experimental Model of Combined Traumatic Brain Injury and Hemorrhagic Shock 总被引:3,自引:2,他引:1
Brian J. Zink MD Susan A. Stern MD Xu Wang MD Carl C. Chudnofsky MD 《Academic emergency medicine》1998,5(1):9-17
Objectives: Given that clinical and laboratory studies suggest that ethanol and hemorrhagic shock (HS) potentiate traumatic brain injury (TBI), the authors studied the effects of ethanol in a model of combined TBI and HS.
Methods: A controlled porcine model of combined TBI and HS was evaluated for the effect of ethanol on survival time, hemodynamic function, and cerebral tissue perfusion. Anesthetized swine (17–24 kg) were instrumented, splenectomized, and subjected to fluid percussion TBI with concurrent 25-mL/kg graded hemorrhage over 30 minutes. Two groups were studied: control ( n = 11) and ethanol ( n = 11). Ethanol, 3.5 g/kg intragastric, was given 100 minutes prior to TBI/HS. Systemic and cerebral physiologic and metabolic parameters were monitored for 2 hours without resuscitation. Regional cerebral blood flow (rCBF) and renal blood flow were measured with dye-labeled microspheres. Data were analyzed with 2-sample t-test and repeated-measures ANOVA.
Results: Ethanol levels at the time of injury were 162 ± 68 mg/dL. Average TBI was 2.65 ± 0.35 atm. Survival time was significantly shorter in the ethanol group (60 ± 27 min vs 94 ± 28 min, p = 0.011). The ethanol group had significantly lower mean arterial pressure, cerebral perfusion pressure, and cerebral venous
O2 saturation in the postinjury period. Cerebral O2 extraction ratios and cerebral venous lactate levels were significantly higher in the ethanol group. A trend toward lower postinjury rCBF in all brain regions was observed in the ethanol group.
Conclusion: In this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion. 相似文献
Methods: A controlled porcine model of combined TBI and HS was evaluated for the effect of ethanol on survival time, hemodynamic function, and cerebral tissue perfusion. Anesthetized swine (17–24 kg) were instrumented, splenectomized, and subjected to fluid percussion TBI with concurrent 25-mL/kg graded hemorrhage over 30 minutes. Two groups were studied: control ( n = 11) and ethanol ( n = 11). Ethanol, 3.5 g/kg intragastric, was given 100 minutes prior to TBI/HS. Systemic and cerebral physiologic and metabolic parameters were monitored for 2 hours without resuscitation. Regional cerebral blood flow (rCBF) and renal blood flow were measured with dye-labeled microspheres. Data were analyzed with 2-sample t-test and repeated-measures ANOVA.
Results: Ethanol levels at the time of injury were 162 ± 68 mg/dL. Average TBI was 2.65 ± 0.35 atm. Survival time was significantly shorter in the ethanol group (60 ± 27 min vs 94 ± 28 min, p = 0.011). The ethanol group had significantly lower mean arterial pressure, cerebral perfusion pressure, and cerebral venous
O
Conclusion: In this TBI/HS model, ethanol administration decreased survival time, impaired the hemodynamic response, and worsened measures of cerebral tissue perfusion. 相似文献
72.
73.
Sources of P300 attenuation after head injury: Single-trial amplitude, latency jitter, and EEG power
Single trial amplitude, latency jitter, and electroencephalographic (EEG) power were examined as sources of the group difference in averaged P300 amplitude among 15 traumatically brain injured and 20 control individuals in an auditory oddball paradigm. Mean amplitude of the individual trials was highly correlated with the amplitude of the averaged P300, with little additional unique variance attributable to latency jitter or EEG power. The group difference in P300 amplitude was also explained by the mean amplitude of the single trials. These results support the robustness of the event-related potential averaging technique within the paradigm used. 相似文献
74.
金丹肝泰1号对大鼠急性肝损伤防治作用的实验研究 总被引:2,自引:0,他引:2
用D-氨基半乳糖(D-GaIN)制备大鼠急性肝损伤模型。方法:检测血清丙氨酸氨基转氨酶(ALT)和血清天门冬氨酸氨基转氨酶(AST)的活性,观察光镜下肝组织的病理学改变,探讨对急性肝损伤的保护作用。结果:口服浸膏可显降低急性肝损伤大鼠血清ALT和AST水平,减轻肝细胞的变性坏死,其作用强度与肝炎宁相当,但弱于联苯双酯。 相似文献
75.
卢利 《中国医科大学学报》1997,26(1):49-52
用100、45、15g力的血管夹,夹闭大白鼠股动静脉20、60和120min,24h后观察其通畅情况,并经扫描电镜和光学显微镜观察股动静脉内皮细胞的损伤程度和血管内血栓形成。结果显示:前两种压力的血管夹在对股动脉只产生轻微损伤的情况下,对伴行股静脉可造成内皮细胞脱落,微小血栓形成等病理损伤。随夹闭血管时间的延长,内皮细胞损伤加重,血小板沉积和微血栓增多。血管夹对静脉的损伤和对其通畅率的影响尤应引起注意。 相似文献
76.
1992~1993年间为180例冠脉病变的病人施行冠脉搭桥术,全部病人均采用核甙抑制剂利多氟嗪预处理和低温(28℃)间断缺血心停搏进行术中心肌保护。平均每例病人作冠状动脉端吻合3~4个,每个吻合口用9分钟,主动脉阻断累加时间约25分钟,体外循环时间90分钟,术后医院死亡率1.6%(3/180),无术后心梗发生。作者认为,冠脉搭桥术的术中心肌保护可采用核甙抑制剂和间断缺血心停搏方法,而不用心肌停搏液。 相似文献
77.
狗脊髓截除自体隐神经大网膜移植的初步观察 总被引:3,自引:0,他引:3
实验用6只狗于T13处切除脊髓8mm,局部用隐神经、大网膜移植。对照组6只狗单纯切除脊髓8mm。术后3个月、6个月实验组动物全部恢复到C/Ⅲ级功能,组织学切片见移植神经有不同程度存活,可记录到股四头肌、胫前肌电位。对照组动物仅达到0/0~A/I织功能,组织学切片见脊髓缺损处为结缔组织,诱电位波形消失。分析了影响脊髓神经功能恢复的原因。 相似文献
78.
神经移位修复臂丛神经根性撕脱伤 总被引:3,自引:2,他引:1
1987年7月~1994年6月,对21例臂丛神经根性撕脱伤采用神经移位修复。其中复合移位4组神经(膈神经、副神经、颈丛运动支、肋间神经)者1例,3组(膈神经、副神经、颈丛运动支)者6例,2组(膈神经、副神经)者9例,1组(膈神经或颈丛运动支或肋间神经)者5例。术中发现臂丛神经变异1例,对4例合并锁骨下动脉损伤者,在神经移位的同时进行血管修复,促进患肢的血液循环,有利于神经的康复。随访到19例,随访时间为8个月~6年2个月,优良率达73.7%。认为,神经移位术是修复神经根性撕裂伤的常规方法,合并血管损伤者也应同时修复,对促进神经功能恢复有利 相似文献
79.
刘达恩 《中国修复重建外科杂志》1997,11(2):83-85
总结胸腹轴型皮瓣早期修复上肢不同部位的深度蛇伤溃疡的经验,评价其应用价值。本组16例,胸脐皮瓣2例,侧胸腹皮瓣1例,髂腰皮瓣5例,下腹皮瓣6例,下腹分叶皮瓣1例,髂腰加下腹Y形皮瓣1例。术后1例皮瓣远端坏死,3例轻度感染,16例断蒂后全部成活。随访3个月~7年,皮瓣质地和弹性均好,手功能基本恢复。认为,带蒂胸腹轴型皮瓣是修复上肢深度蛇伤溃疡理想的方法。 相似文献
80.
KETAN A. SHAH SANDRA SHUREY & COLIN J. GREEN 《International journal of experimental pathology》1997,78(5):355-363
Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline ( n = 6) or modified University of Wisconsin solution ( n = 6) at 4 °C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury. 相似文献