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61.
脑内注射白细胞介素-1β对淋巴结细胞应激免疫抑制因子生成的影响 总被引:1,自引:0,他引:1
our previous work showed that a suppressive factor( a protein with largemolecular weight in serum was induced by restraint stress in mice and rats,which suppressed Con Ainduced lymphocyte proliferation.It was also found that the generation of serum suppressive factorwas under control of the central nervous system.Our further study showed thatintracerebroventricular(icv )injection of interleukin 1 receptor antagonist(IL-1Ra)antagonised thegeneration of serum suppressive factor induced by restraint stress and icv injection of interleukin-1β(IL-1β)increased the generation of the suppressive factor.Our experiment also showed that the serumsuppressive factor induced by restraint stress was first made in lymph tissue and then released intoblood.The present work was designed to investigate the role of IL-1 in the brain in generation of thesuppressive factor in lymph node in mice.Icv injection of IL-1β( 1 pg/mouse) was shown tosignificantly increase the generation of the suppressive factor in lymph node.Icv injection of IL-1Ra,however ,antagonised generation of the suppressive factor.In mice without restraint stress,both thesuppressive factor in serum and in lymph node were found to be induced in dose-dependent manner byicv injection of IL-1β.Taken together,these results suggest that IL-1β in brain played a veryimportant role in generation of the suppressive factor in lymph node.The positive correlation betweenthe suppressive action of lymph node and of serum added to the evidence that lymph tissue is probablythe source of the serum suppressive factor. 相似文献
62.
血小板激活因子对大鼠脑血管通透性的影响及药物的保护作用 总被引:1,自引:0,他引:1
颈内动脉注射血小板激活因子(PAF),再给伊文思蓝,可见脑实质染色程度加深,而颈内动脉只注射伊文思蓝,脑实质未见染色。而我们合成的新药SZ-1可剂量依赖性地抑制PAF诱导的脑实质伊文思蓝染色程度的加深。在体外培养的脑微血管平滑肌细胞上,PAF能显著刺激~(14)-花生四烯酸的释放,而SZ-1能剂量依赖性地抑制这种释放,提示PAF在脑内产生的损害除与其他因素相关外,还与其刺激花生四烯酸释放有密切关系,SZ-1对PAF引起的脑部损害有保护作用。 相似文献
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65.
Vissers YL von Meyenfeldt MF Braulio VB Luiking YC Deutz NE 《Clinical science (London, England : 1979)》2003,104(6):585-590
To measure actin/myosin protein breakdown, the 24 h excretion of N (tau)-methylhistidine (3MH) is used. However, in mice, this method is invalid. Therefore we have developed a liquid chromatography-MS technique to measure the tracer/tracee ratio and concentration of 3MH in plasma, enabling an in vivo primed constant infusion protocol with a deuterated stable isotope of 3MH. We tested this model by giving a primed constant infusion of L-[3-methyl-(2)H(3)]histidine, L-[phenyl-(2)H(5)]phenylalanine and L-[phenyl-(2)H(2)]tyrosine to three anaesthetized experimental groups: mice receiving saline intraperitoneally (i.p.) (CON), mice receiving saline i.p. and starved for 9 h (STA), and mice receiving lipopolysaccharide i.p. and starved for 9 h (STA+LPS). The contribution of myofibrillar to total protein breakdown was significantly lower in the STA group than the CON group (30+/-4% and 54+/-14% respectively; P <0.05), and was significantly higher in the STA+LPS group than the STA group (52+/-7% and 30+/-4% respectively; P <0.05). Whole-body myofibrillar protein breakdown, total protein breakdown, protein synthesis and net protein breakdown were not different between the groups. We conclude that this in vivo primed constant stable isotope-infusion protocol can give valuable information about the role of actin/myosin protein breakdown in mice. 相似文献
66.
Vissers YL von Meyenfeldt MF Luiking YC Dejong CH Deutz NE 《Metabolism: clinical and experimental》2008,57(7):896-902
Renal de novo arginine production has been suggested to be crucial for regulation of arginine production in disease. We investigated how the interorgan pathway for de novo arginine production is affected by the presence of malignant tumor and/or surgical trauma. Controls and methylcholanthrene-sarcoma-bearing mice were studied, both with and without undergoing laparotomy (n = 9-13 per group). One day after laparotomy, amino acid fluxes across the hindquarter, intestine, liver, and kidney were studied. In contrast to healthy mice, the liver of tumor-bearing mice took up citrulline (9 +/- 3 vs 1 +/- 2 nmol/[10 g min], P < .05), simultaneous with attenuated renal arginine output (4 +/- 3 vs 12 +/- 2 nmol/[10 g min], P < .05), despite increased intestinal conversion of glutamine to citrulline (15 +/- 3 vs 8 +/- 1 nmol/[10 g min], P < .05). In tumor-bearing mice undergoing surgery, intestinal citrulline output decreased (from 15 +/- 3 to 8 +/- 2 nmol/[10 g min], P < .05) and renal arginine output remained close to zero despite increased renal citrulline uptake (from 6 +/- 2 to 12 +/- 2 nmol/[10 g min], P < .05). In conclusion, the interorgan pathway for de novo arginine production was differently regulated depending on the pathophysiological situation. In methylcholanthrene-sarcoma-bearing mice, decreased de novo arginine production was accompanied by the presence of hepatic citrulline uptake, whereas tumor-bearing mice subjected to surgical trauma showed concomitant decreased intestinal citrulline output. 相似文献
67.
Polycystic ovarian syndrome: Assessment of approaches to diagnosis and cardiometabolic monitoring in UK primary care 下载免费PDF全文
68.
Wai Cho Yu Yiu Cheong Yeung Yiu Chang Ling Yuet Tsang Kwok Chu Kwong Hau Chung Kwok YC Gary Lee 《Journal of cardiothoracic surgery》2009,4(1):63
Spontaneous pneumothoraces are believed to arise when air from the supplying airway exit via a ruptured visceral pleural bleb
into the pleural cavity. Endobronchial one-way valves (EBVs) allow air exit (but not entry) from individual segmental airways.
Systematic deployment of EBVs was applied to three patients with secondary spontaneous pneumothoraces and persistent airleak.
In all cases, balloon-catheter occlusion of the upper lobe bronchus stopped the airleak. EBVs applied to individual upper
lobe segmental airways failed to terminate the airleak, which only stopped after placements of multiple EBVs to occlude all
upper lobe segments. The observation questions the traditional belief of 'one-airway-one-bleb-one-leak' in spontaneous pneumothorax. 相似文献
69.
Michael YC Tsang Simon W Rabkin 《Clinical and experimental pharmacology & physiology》2009,36(8):e12-e19
- 1 The aim of the present study was to investigate the role of p38 mitogen‐activated protein kinases (MAPK) in mediating the effect of noradrenaline (NA) on cardiomyocyte cell viability.
- 2 Cardiomyocytes from embryonic chick heart were treated with various concentrations of NA, phenylephrine or isoproterenol and p38 MAPK activation was determined by western blotting. Total cell death was assessed by the 3‐(4,5‐dimethyl‐2 thiazoyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay. Apoptosis was determined by specific DNA fragmentation.
- 3 At 100 µmol/L, NA produced a significant increase in cell death that was associated with microscopic changes and DNA fragmentation indicative of apoptosis. The p38 MAPK inhibitor SB202190 (at 1 µmol/L beginning 1 h before NA), reduced NA‐induced p38 MAPK activation and significantly accentuated NA‐induced cell death. In contrast, the mitogen‐activated protein kinase kinase ERK1/2 inhibitor PD98059 (at 1 µmol/L beginning 1 h before NA) did not significantly alter NA‐induced cell death. These effects of NA were mediated, in part, through α‐adrenoceptor because phenylephrine (100 µmol/L), like NA, also induced p38 MAPK activation. However, 100 µmol/L isoproterenol produced a sustained dephosphorylation of p38 MAPK.
- 4 These data show that NA‐induced p38 MAPK activation, through α‐adrenoceptor, has a protective role in cardiomyocytes to antagonize NA‐induced cell death. In contrast, β‐adrenoceptor stimulation produces dephosphorylation of p38 MAPK.
70.
YG Cao JG Chai YC Chen J Zhao J Zhou JP Shao C Ma XD Liu XQ Liu 《British journal of pharmacology》2009,157(3):482-490