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11.
L-硝基精氨酸甲酯对实验性葡萄膜炎的影响 总被引:1,自引:0,他引:1
目的:观察一氧化氮(NO)含量含量在葡萄炎房东水及玻璃体中的变化及L-硝基精氨酸甲酯(N^G-nitro-L-arginine methyl earter,L-NAME)的治疗效果。方法;采用兔眼玻璃2本内注射内毒素脂多糖(LPS)制备葡萄膜炎模型,以检测房水蛋白浓度,结果:葡萄为房水及玻璃体及玻璃体中显著增高,即刻使用L NAME;显著降低了NO水平,同时其蛋白浓度、细胞数目及组织炎症程度明显降 相似文献
12.
Karen B Jourdan Timothy W Evans Nicholas P Curzen Jane A Mitchell 《British journal of pharmacology》1997,120(7):1280-1285
- 8-Iso prostaglandin F2α (8-iso PGF2α) is one of a series of prostanoids formed independently of the cyclo-oxygenase pathway. It has been shown to be upregulated in many conditions of oxidant stress where its formation is induced by free radical-catalysed actions on arachidonic acid. As 8-iso PGF2α is formed in vivo in diseases in which oxidant stress is high such as septic shock, we have assessed the relative potency and efficacy of this compound in pulmonary arteries from control and lipopolysaccharide (LPS)-treated rats.
- Several studies have characterized the contractile actions of 8-iso PGF2α on various smooth muscle preparations, but its potential dilator actions have not been addressed. Thus these studies examined both the contractile and dilator actions of 8-iso PGF2α in rat pulmonary artery rings. The thromboxane mimetic U46619, PGE2 sodium nitroprusside (SNP) and acetyl choline (ACh) were used for comparison. Each prostanoid had to be dissolved in ethanol to a maximum concentration of 1×10−2 M. At high concentrations, ethanol directly contracted pulmonary vessels. We were therefore limited by the actions of the vehicle such that we were unable to add prostanoids at concentrations higher than 1×10−4 M. In some cases this meant that maximum responses were not achieved and in these cases the Emax and pD2 values are apparent estimates.
- The following rank order of potency was obtained from contractile studies; U46619>8-iso PGF2α>PGE2, each prostanoid producing concentration-dependent contractions (10−103×10−4 M, 10−910−4 M, 10−810−4 M, respectively). As has been shown previously for other smooth muscle preparations, the thromboxane receptor (TP) antagonist ICI 192605, (1×10−6, 1×10−5 and 1×10−4 M), inhibited the contractions of 8-iso PGF2α in a concentration-dependent fashion.
- The nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 1×10−4 M), enhanced the contractile function of both 8-iso PGF2α and PGE2, but had no effect on that caused by U46619. Similarly, L-NAME inhibited the dilator function of all agents tested except the exogenous nitric oxide (NO) donor SNP, indicating that PGE2 and 8-iso PGF2α like ACh, act through the release of NO. The specificity of the effects of L-NAME were confirmed in studies with the inactive enantiomer D-NAME (1×10−4 M), which did not affect the contractile or the dilator actions of 8-iso PGF2α. Furthermore, ICI 192605 enhanced the dilator actions of 8-iso PGF2α, suggesting that the dilator component of 8-iso PGF2α was achieved via activation of a non-TP receptor.
- Isoprostanes may modulate vascular tone by a direct action on TP receptors to cause contraction and via a distinct receptor leading to the release of NO to cause dilatation.
13.
Masato Kochi Shuichi Takaki Jun -ichi Kuratsu Hiroshi Seto Isao Kitamura Yukitaka Ushio 《Journal of neuro-oncology》1994,19(3):239-244
Summary Ventriculolumbar perfusion of methyl 6-[3-(2-chloroethyl)-3-nitrosoureido]-6-deoxy-alpha-D-glucopyranoside (MCNU), a water soluble nitrosourea with log P-0.71, may be efficacious in the treatment of subarachnoid dissemination of malignant glioma. We used 2 dogs to study the neurotoxicity and pharmacokinetics of MCNU. MCNU (1 mg), dissolved in 10 ml of artificial CSF, was administered via the right lateral ventricle during a period of 18 to 42 min and the CSF was drained by lumbar puncture. The perfusion was repeated once a week for 10 consecutive weeks. No neurological and systemic symptoms were noted after perfusion. Histological examination of the brain and spinal cord showed local denudation of the ependyma and local subependymal spongy degeneration and gliosis in the lateral ventricle into which MCNU was administered in one dog and local denudation of the ependyma in the other. When administration was over a period of 21 to 38 min, the MCNU concentration in the lumbar CSF peaked at 11.11 to 50.67 g/ml, in 28 to 78 min. The area under the drug concentration-time curve (AUC) was 1152 g×min/ml on average, significantly larger than that of ACNU. The elimination phase followed linear kinetics and the half-time was 41.1 min on average, significantly longer than that of ACNU. These findings suggest that ventriculolumbar perfusion of MCNU may be effective in the treatment of subarachnoid dissemination of malignant glioma notwithstanding some local histological changes. 相似文献
14.
应用北京医科大学培育的听源性癫痫易感大鼠P77PMC,以癫痫不易感大鼠Wistar为对照,系统研究了NMDA受体亚单位Ⅰ(NR1)与白细胞介素1(IL1)在癫痫发生发展中的作用及相互关系。实验在整体、脑片、神经细胞培养及分子水平进行。所得较有意义的结果如下:(1)在听源性惊厥易感大鼠P77PMC整个发育过程中脑内NR1mRNA的表达,以及成年鼠脑内NMDA受体活性(MK801结合)都高于对照组Wistar大鼠。惊厥后P77PMC脑内NR1mRNA的表达呈时间依赖性增加,惊厥后24h比惊厥前增加111%~202%;NR1反义寡核苷酸脑室注射(每μl10μg)可显著减轻P77PMC大鼠惊厥程度,并可对谷氨酸引起的体外神经细胞的损伤有保护作用,抑制谷氨酸导致的神经毒性作用。由此证实NR1参与惊厥的发生发展,并与P77PMC大鼠的遗传性癫痫易感性关系密切。(2)在神经细胞培养中IL1β可明显剂量依赖性地(1~25U·ml1)提高NR1mRNA的表达,白细胞介素1受体拮抗剂(IL1ra)可阻断此效应;IL1β可剂量依赖性地提高NR1受体活性,因此提示IL1具有兴奋性神经调质的作用,其作 相似文献
15.
小檗碱对体外培养大鼠大脑皮层神经元损伤的保护作用 总被引:2,自引:0,他引:2
体外培养大鼠胎鼠大脑皮层神经细胞,观察小檗碱(berberine,Ber)对N-甲基-D-门冬氨酸(N-methyl-D-aspar-tate,NMDA)、过氧化氢(H2O2)及撤血清培养引起的细胞损伤的保护作用。结果表明,培养的大鼠胚胎大脑皮层神经细胞在NMDA500μmol/L作用10min、或H2O2100μmol/L24h、或无血清培养48h后,细胞的死亡率及乳酸脱氢酶(LDH)漏出率明显增加,抗氧化酶SOD、谷胱甘肽过氧化酶(GSH-Px)活性显著降低,而脂质过氧化物丙二醛(MDA)生成增多。Ber10、30μmol/L能显著降低细胞死亡率、LDH漏出率及MDA的生成,且能明显提高抗氧化酶活性。提示:Ber可拮抗NMDA、H2O2及撤血清培养引起的神经细胞损伤,其机理可能与其减少膜脂质过氧化物生成,提高抗氧化酶活性有关 相似文献
16.
Arezo Nahavandi Ahmad Reza Dehpour Ali Reza Mani Homayoun Homayounfar Ali Abdoli 《European journal of pharmacology》1999,370(3):1170
In this study the effect of nitric oxide (NO) synthesis inhibition on ethanol-induced gastric damage was evaluated in bile duct-ligated, sham-operated and unoperated rats. The animals were injected intraperitoneally with saline,
-arginine (200 mg/kg) or NG-nitro-
-arginine methylester (
-NAME) in doses of 5, 15 and 30 mg/kg, 30 min before ethanol administration. The animals were killed 1 h after ethanol administration and their stomachs were removed for measurement of gastric mucosal damage. The results showed that
-NAME significantly enhanced the development of gastric mucosal lesions in sham-operated and unoperated rats, while in bile duct-ligated animals,
-NAME decreased and
-arginine enhanced the potentiation of ethanol-induced gastric mucosal damage. The plasma level of nitrite and nitrate was also measured and was significantly higher in bile duct-ligated rats than in control groups. The results suggest that inhibition of NO synthase with
-NAME has different effects on ethanol-induced gastric damage in cholestatic groups and in normal rats and that these effects can be explained by overproduction of NO in bile duct-ligated animals. 相似文献
17.
The capacity of N-oxidized metabolites of 4,4-methylenebis(2-chloroaniline) (MBOCA) to form hemoglobin (Hb) adducts was determined in vitro, and the formation of Hb adducts following in vivo administration of MBOCA was assessed with or without prior induction of cytochrome P-450 enzymes with phenobarbital or -naphthoflavone. Hb adduct formation was determined by electron-capture GLC of MBOCA as the heptafluorobutyryl derivative following mild acid hydrolysis of protein-bound MBOCA. The method was confirmed by gas chromatography-mass spectrometry with selected ion monitoring. N-hydroxy- and mononitroso-MBOCA, but not MBOCA itself, formed adducts to rat and human Hb in vitro in a dose-related manner. Binding was inhibited by cysteine and glutathione but not oxidized glutathione or methionine. Intravenous administration of as little as 0.04 mol/kg N-hydroxy-MBOCA to rats resulted in measurable formation of MBOCA-Hb adducts (0.9 ng/50 mg Hb). Intraperitoneal administration of 0.5–50 mg/kg MBOCA to rats, and subcutaneous administration of 5–500 mg/kg MBOCA to rats and 4–100 mg/kg to guinea pigs resulted in dose-related formation of Hb adducts. MBOCA-Hb remained elevated in blood for greater than 10 weeks following a single subcutaneous dose in guinea pigs. Pretreatment of rats with phenobarbital induced microsomal benzphetamine N-demethylase (BND) activity and resulted in a small increase in in vitro N- andortho- hydroxylation of MBOCA, but did not increase in vivo Hb adducts. Pretreatment of rats with -naphthoflavone induced microsomal aryl hydrocarbon hydroxylase as well as ethoxyresorufin-O-deethylase, and increased in vitro N- but notortho-hydroxylation of MBOCA. -Naphthoflavone pretreatment increased the formation of MBOCA-Hb adducts when rats were dosed with MBOCA at 100 and 500 mg/kg, but not 20 mg/kg subcutaneously. 相似文献
18.
HPLC法测定冠心通络片中橙皮苷的含量 总被引:1,自引:0,他引:1
目的:建立冠心通络片中橙皮苷含量的测定方法。方法:采用高效液相色谱法,色谱柱为HypersilODSC18(5μm,4.6mm×100mm);流动相为甲醇-5%醋酸溶液(30∶70);检测波长为283nm;柱温为30℃;流速为1.0mL/min。结果:橙皮苷在419.2~2096μg(r=0.9998,n=5)范围内呈良好的线性关系;平均回收率98.71%;RSD为1.13%。结论:本法检测快速,定量准确,可用于冠心通络片的定量分析。 相似文献
19.
目的 :寻找简单、方便、有效的预防产后出血的方法。方法 :将 30 0例无合并症产妇分成 3组 ,均于胎儿娩出后立即给药。A组 10 0例给缩宫素 2 0U ,静脉注射 ;B组 10 0例给米索前列醇 4 0 0μg ,口服 ;C组 10 0例给卡前列甲酯栓 1mg置入直肠内。比较 3组产后 2h出血量。结果 :A组的产后 2h出血量为 (2 5 1±s 71)mL ,B组和C组的产后 2h出血量分别为 (15 9± 6 7)mL和 (15 0± 73)mL ,A组明显多于B组和C组 ,差异有显著意义 (P<0 .0 1)。而B组和C组间差异无显著意义 (P >0 .0 5 )。结论 :米索前列醇、卡前列甲酯栓均能有效预防产后出血 相似文献
20.
丙泊酚对N-甲基-D-天冬氨酸所致PC12细胞损伤的保护作用 总被引:8,自引:0,他引:8
目的 探讨静脉麻醉药丙泊酚 (PPF)脑保护作用的可能机制。方法 乳酸脱氢酶 (LDH)法及MTT比色法判断细胞损伤程度及细胞存活率 ,Fura 2 /AM荧光标记法测定细胞内Ca2 + 浓度 ( [Ca2 + ]i)的变化 ,分光光度法测定细胞一氧化氮合酶 (NOS)活性。结果 N 甲基 D 天冬氨酸 (NMDA) 3 0 0 μmol·L-1处理4h可明显导致PC1 2细胞的损伤 ,表现为LDH释放量明显增加 ,吸光度值A570nm明显降低 ,细胞存活率降低 ,同时 [Ca2 + ]i 和NOS活性则明显增加。PPF6.2 5 ,2 5 ,1 0 0 ,40 0 μmol·L-1与NMDA同时处理PC1 2细胞则使LDH释放量显著降低 ,细胞存活率增加。PPF 1 2 .5和 1 2 5 μmol·L-1可显著降低NMDA诱导的[Ca2 + ]i 水平及NOS活性的提高。结论 PPF对NMDA所致的PC1 2细胞损伤有明显的保护作用 ,其机制可能与其抑制NMDA受体的功能 ,降低 [Ca2 + ]i,减弱Ca2 + 超载 ,并降低NMDA诱导的NOS活性增加有关。提示PPF可能是通过抑制NMDA受体 Ca2 + NOS通路的功能而产生细胞保护效应 相似文献