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31.
Busserolles J Payá M D'Auria MV Gomez-Paloma L Alcaraz MJ 《Biochemical pharmacology》2005,69(10):1433-1440
Proinflammatory mediators, namely eicosanoids, reactive oxygen and nitrogen species and cytokines, are clearly involved in the pathogenesis of intestinal bowel disease. bolinaquinone (BQ) and petrosaspongiolide M (PT), two marine products with potent anti-inflammatory action, have been shown to control the production of mediators in acute and chronic inflammatory processes. Hence, we have tested here the hypothesis that BQ and PT could ameliorate inflammation and oxidative stress parameters in 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colitis in Balb/c mice. BQ and PT were given orally in doses of 10 or 20mg/kg/day. Treatment of the animals with BQ or PT at the highest dose significantly protected against TNBS-induced inflammation, as assessed by a reduced colonic weight/length ratio and histological scoring. Neutrophilic infiltration, interleukin (IL)-1beta and prostaglandin E(2) (PGE(2)) levels, as well as cyclooxygenase-2 (COX-2) protein expression were inhibited by both compounds. Colonic nitrite and nitrate levels and protein expression of inducible nitric oxide synthase (iNOS) were also lower in the treated groups in comparison to the TNBS control. BQ and PT reduced nitrotyrosine immunodetection and colonic superoxide anion production. Neither compound inhibited the expression of the protective protein heme oxygenase-1 (HO-1), although they reduced the extension of apoptosis. Our study also indicated that PT could interfere with the translocation of p65 into the nucleus, a key step in nuclear factor-kappaB (NF-kappaB) activation. Altogether, the results suggest that BQ and PT can have potential protective actions in intestinal inflammatory diseases. 相似文献
32.
Kawakami T Mitsuhata H Saitoh J Takeuchi H Hasome N Hiruta M Horikawa Y Seo N 《Journal of anesthesia》2003,17(1):22-29
Purpose. The present study was done to investigate the role of endothelin-1 (ET-1) in hypotension and bronchospasm provoked by anaphylaxis
in rabbits in vivo.
Methods. Forty-five rabbits sensitized to horse serum were randomly allocated to five groups: Group 1 (n = 10) received 0.5 nmol·kg−1 of ET-1; Group 2 (n = 10) received 0.5 nmol·kg−1 of ET-1 and 200 nmol·kg−1 of a selective ETA receptor antagonist, BQ 610, without anaphylaxis; Group 3 (n = 5) received 200 nmol·kg−1 of BQ 610 alone without anaphylaxis; Group 4 (n = 10) received normal saline alone before being antigen challenged to induce anaphylaxis; Group 5 (n = 10) received 200 nmol·kg−1 of BQ 610 before antigen challenge.
Results. Mean arterial pressure (MAP) values were significantly different between Groups 1 and 2. Heart rate (HR), central venous
pressure (CVP), dynamic pulmonary compliance (Cdyn), and pulmonary airway resistance (RL) did not differ significantly between Groups 1 and 2. MAP values were significantly decreased compared with baseline in both
Groups 4 and 5; however, the values were not significantly different between two groups. CVP values were significantly different
between Groups 4 and 5 only at the 15-min time point following antigen challenge. HR, RL, and Cdyn values were not significantly different between Groups 4 and 5, nor were the survival rates.
Conclusion. BQ 610 does not improve hypotension or survival rates in systemic aggregated anaphylactic rabbits in vivo, implying that
circulating ET-1 may not play an important role in anaphylaxis, although direct proof of production of circulating ET-1 or
activation of ETA receptors is lacking in this study.
Received: October 15, 2001 / Accepted: August 20, 2002
Address correspondence to: T. Kawakami 相似文献
33.
Zusammenfassung 1. Bei Diabetikern mit und ohne Gefäßkomplikationen wurden die Serumkonzentrationen des sauren 1-Glykoproteins, der gruppen-spezifischen Komponente (Gc), des 2-Makroglobulins und des Hämopexins mit der Immuno-Diffusions-Methode nachMancini und Mitarb. quantitativ bestimmt. — 2. Das 2- Makroglobulin ist bei Diabetikern vermehrt, bei 276 Patienten fand sich ein Mittelwert von 242 mg% gegenüber einem Mittelwert von 186 mg% bei 98 nicht-diabetischen Blutspendern. Diese Differenz ist statistisch hochsignifikant. Der Konzentrationsanstieg ist bei jugendlichen Diabetikern stärker ausgeprägt als bei Altersdiabetikern. Bei Patienten mit Retinopathie findet sich eine deutlichere Vermehrung als bei Patienten ohne Retinopathie. Auch geht der Anstieg des 2-Makroglobulins mit dem Schweregrad arteriosklerotischer Veränderungen der peripheren Gefäße parallel. — 3. Die Konzentrationen des sauren 2-Glykoproteins und der gruppen-spezifischen Komponente sind in Seren von Diabetikern gegenüber gesunden Blutspendern nur unwesentlich vermehrt. — 4. Die Hämopexin Konzentration ist bei Diabetikern mit einem Mittelwert von 92 mg% gegenüber gesunden Blutspendern mit einem Mittelwert von 77 mg% gering erhöht; dieser geringe Unterschied ist statistisch hochsignifikant.
Serum, glycoproteins in diabetes mellitus; quantitative immunological determination of acid 1-glycoprotein, Gc, 2-macroglobulin and haemopexin in diabetics with and without angiopathy
Summary 1. Serum concentrations of acid 1-glycoprotein, Gc, 2-macroglobulin and haemopexin were determined in diabetics with and without vascular complications by the immunological assay method ofMancint and co-workers. — 2. 2-macroglobulin concentrations were increased in sera of diabetics. The mean value was 242 mg% in 276 patients compared with the mean value of 186 mg% in a sample of 98 healthy blood-donors. This difference is statistically highly significant. The increase was more pronounced in juvenile diabetes than in late-onset diabetes. The increase was also more pronounced in patients with retinopathy than in patients without retinopathy. There was also an increase of 2- macroglobulin concentrations in relation to the degree of arteriosclerotic changes of the peripheral vessels. — 3. Serum concentrations of acid 1-glycoprotein and Gc were only slightly increased in diabetics compared with blood-donors. — 4. There was a small, but statistically highly significant increase of haemopexin concentrations in sera of diabetics. The mean value in 243 diabetics was 92 mg%, in 15 healthy blood-donors a mean value of only 77 mg% was found.
Mit Unterstützung durch die Deutsche Forschungsgemeinschaft 相似文献
34.
Wenzel RR Rüthemann J Bruck H Schäfers RF Michel MC Philipp T 《British journal of clinical pharmacology》2001,52(2):151-157
AIMS: Endothelin-1 (ET-1) is a potent vasoconstrictor produced by the vascular endothelium. The interactions of ET with the mediators of the sympathetic nervous system and the renin-angiotensin-system in humans are unclear. METHODS: We studied the effects of the ETA-selective antagonist BQ-123 and the ETB-selective antagonist BQ-788 (both 10(-10)-10(-8) M) on ET-1 (10(-16)-10(-10) M), angiotensin II (AT, 10(-16)-10(-10) M) and noradrenaline (NA, 10(-16)-10(-10) M) induced vasoconstriction in the human skin microcirculation in vivo in 25 healthy male volunteers using laser Doppler flowmetry and double injection technique. RESULTS: BQ-123 caused a dose-dependent vasodilatation (maximum effect: + 949 +/- 84 AUC-PU, P < 0.001), whereas BQ-788 induced mild vasoconstriction (maximum effect: -388 +/- 96 AUC-PU, P < 0.01). In the presence of BQ-123, but not BQ-788, ET-1, AT and NA caused markedly less vasoconstriction at any tested agonist dose; the effect was most pronounced on ET-1 (maximum effect at 10(-14) M: + 814 +/- 93 AUC-PU vs ET alone, P < 0.001), followed by noradrenaline (maximum effect at 10(-16) M: +580 +/- 107 AUC-PU vs NA alone, P < 0.01) and angiotensin II (maximum effect at 10(-14) M: + 493 +/- 111 AUC-PU vs AT alone, P < 0.001). CONCLUSIONS: ETA-selective antagonism inhibits vasoconstriction to AT and NA in vivo in healthy subjects. This beneficial effect may be useful for the treatment of patients with cardiovascular disease including hypertension especially in combination therapy with sympatholytic agents and inhibitors of the renin-angiotensin system. 相似文献
35.
36.
Effects of natural free radical scavengers on peripheral nerve and neurovascular function in diabetic rats 总被引:5,自引:1,他引:5
Summary Increased generation of reactive oxygen species, coupled with impaired endogenous scavenging mechanisms, plays a prominent role in the aetiology of neurovascular abnormalities in experimental diabetes mellitus. We examined the efficacy of the natural anti-oxidants vitamins C, E and -carotene in preventing nerve conduction and nutritive blood flow deficits in streptozotocin-diabetic rats. One month of diabetes caused a 19.1% reduction in sciatic motor conduction velocity (p<0.001). This was approximately prevented 80–90% by high-dose (1000 mg · kg–1 · day–1) vitamin E and -carotene treatments (p<0.001). Vitamin C had lesser effects; the maximum protection found for motor conduction velocity was 36% using a dose of 150 mg · kg–1 · day–1 (p<0.001). High dose (500 mg · kg–1 · day–1) vitamin C had a lesser effect on conduction than intermediate doses. Joint vitamin C and lower dose (500 mg · kg–1 · day–1) vitamin E treatment had a predominantly additive preventive effect against nerve dysfunction. Resistance to hypoxic conduction failure for sciatic nerve in vitro was markedly increased by diabetes and this remained relatively unaffected by treatment. Sciatic nutritive endoneurial blood flow, measured using microelectrode polarography and hydrogen clearance, was reduced 46.1% by 1 month of diabetes (p<0.001). This was prevented to the extent of 87%, 36% and 98% by vitamins E, C and -carotene, respectively (p<0.01). These data emphasize the role of oxidative stress in the development of early neurovascular changes in experimental diabetes and show that naturally available scavengers have a neuroprotective action.Abbreviations NCV
Nerve conduction velocity
- NO
nitric oxide
- ROS
reactive oxygen species 相似文献
37.
内皮素-1引起热痛觉过敏的研究 总被引:2,自引:1,他引:1
目的研究内皮素-1(ET-1)在局部引起热痛觉过敏的表现及机制。方法小鼠分为生理盐水对照组(NS组)、ET-1组(ET组)、ETA受体拮抗剂BQ123加ET-1组(BE组),每组6例。NS足底注射生理盐水,ET组足底注射10pmolET-1,BE组注射3nmolBQ12320min后再注射ET-1。测量注药前后15min、30min、45min及60min热痛阈值。结果NS组热痛阈值无明显变化,ET组热痛阈值降低,60min时热痛阈值基本恢复,BE组热痛阈值无明显变化。结论ET-1可在局部通过与ETA受体结合引起动物的热痛觉过敏。 相似文献
38.
C. R. W. Kuhlmann A. K. Most F. Li B. M. Münz C. A. Schaefer S. Walther T. Raedle‐Hurst B. Waldecker H. M. Piper H. Tillmanns J. Wiecha 《Acta physiologica (Oxford, England)》2005,183(2):161-169
Aims: Endothelin‐1 (ET‐1) promotes endothelial cell growth. Endothelial cell proliferation involves the activation of Ca2+‐activated K+ channels. In this study, we investigated whether Ca2+‐activated K+ channels with big conductance (BKCa) contribute to endothelial cell proliferation induced by ET‐1. Methods: The patch‐clamp technique was used to analyse BKCa activity in endothelial cells derived from human umbilical cord veins (HUVEC). Endothelial proliferation was examined using cell counts and measuring [3H]‐thymidine incorporation. Changes of intracellular Ca2+ levels were examined using fura‐2 fluorescence imaging. Results: Characteristic BKCa were identified in cultured HUVEC. Continuous perfusion of HUVEC with 10 nmol L?1 ET‐1 caused a significant increase of BKCa open‐state probability (n = 14; P < 0.05; cell‐attached patches). The ETB‐receptor antagonist (BQ‐788, 1 μmol L?1) blocked this effect. Stimulation with Et‐1 (10 nmol L?1) significantly increased cell growth by 69% (n = 12; P < 0.05). In contrast, the combination of ET‐1 (10 nmol L?1) and the highly specific BKCa blocker iberiotoxin (IBX; 100 nmol L?1) did not cause a significant increase in endothelial cell growth. Ca2+ dependency of ET‐1‐induced proliferation was tested using the intracellular Ca2+‐chelator BAPTA (10 μmol L?1). BAPTA abolished ET‐1 induced proliferation (n = 12; P < 0.01). In addition, ET‐1‐induced HUVEC growth was significantly reduced, if cells were kept in a Ca2+‐reduced solution (0.3 mmol L?1), or by the application of 2 aminoethoxdiphenyl borate (100 μmol L?1) which blocks hyperpolarization‐induced Ca2+ entry (n = 12; P < 0.05). Conclusion: Activation of BKCa by ET‐1 requires ETB‐receptor activation and induces a capacitative Ca2+ influx which plays an important role in ET‐1‐mediated endothelial cell proliferation. 相似文献
39.
40.