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1.
石英纤维桩在后牙残根残冠修复中的应用   总被引:3,自引:0,他引:3  
目的研究固位增强温控变色石英纤维桩在后牙残根残冠修复中的效果。方法选择81例患者共109颗需修复的上下颌患牙,随机分为实验组和对照组,实验组62颗患牙,对照组47颗患牙,实验组采用固位增强温控变色石英纤维桩进行桩核修复,对照组采用金属桩核修复,观察16~24个月,通过临床和X线检查评价修复体的效果。结果实验组62颗患牙中,1颗桩冠脱落,1颗桩冠松动,成功率为96.8%。对照组47颗患牙中,4颗桩冠脱落,3颗桩冠松动,成功率为85.1%。实验组和对照组经卡方检验,两组之间有统计学意义(P<0.05)。结论固位增强温控变色石英纤维桩与金属桩相比有较高的成功率,是一种效果良好的后牙残根残冠修复方式。  相似文献
2.
Aims Endothelin is a peptide produced by endothelial cells with many biological properties. In the human skin microcirculation endothelin induces neurogenic vasodilation associated with burning pruritus. We investigated the mechanisms involved in this response.
Methods The effects of prolonged pretreatment with capsaicin, a specific inhibitor of polimodal nociceptor fibres, and of the nitric oxide synthase inhibitor l-NMMA on endothelin-1-induced vasodilation were studied in 15 human subjects. Furthermore, we investigated the effects of the ETA -selective antagonist PD147953 on bradykinin-induced vasodilation.
Results After local injection, endothelin-1 caused vasoconstriction at the injection site and a profound vasodilation in the surrounding area (flare reaction, P <0.01). This response was specific and not induced by saline, albumin, acetylcholine or an ET-antagonist. Prolonged capsaicin pretreatment inhibited endothelin-1 induced vasodilation in the area surrounding the injection site, but not the central vasoconstriction at the injection site. Bradykinin also induced a marked vasodilation in the area surrounding the injection site; this was not inhibited by an ETA -selective antagonist, while the flare reaction was. l-NMMA applied at the site of the flare reaction prevented endothelin-1-induced vasodilation.
Conclusions Endothelin-1 in the human skin microcirculation stimulates polimodal nociceptor fibres leading to the release of nitric oxide. This response may play a pathophysiological role in inflammatory processes in the human skin.  相似文献
3.
The popularity of testosterone among drug users is due to its powerful effects on muscle strength and mass. Important mechanisms behind the myotrophic effects of testosterone were uncovered both in athletes using steroids for several years and in short-term controlled studies. Both long-term and short-term steroid usage accentuates the degree of fibre hypertrophy in human skeletal muscle by enhancing protein synthesis. A mechanism by which testosterone facilitates the hypertrophy of muscle fibres is the activation of satellite cells and the promotion of myonuclear accretion when existing myonuclei become unable to sustain further enhancement of protein synthesis. Interestingly, long-term steroid usage also enhances the frequency of fibres with centrally located myonuclei, which implies the occurrence of a high regenerative activity. Under the action of testosterone, some daughter cells generated by satellite cell proliferation may escape differentiation and return to quiescence, which help to replenish the satellite cell reserve pool. However, whether long-term steroid usage induces adverse effects of satellite cells remains unknown. Testosterone might also favour the commitment of pluripotent precursor cells into myotubes and inhibit adipogenic differentiation. The effects of testosterone on skeletal muscle are thought to be mediated via androgen receptors expressed in myonuclei and satellite cells. Some evidence also suggests the existence of an androgen-receptor-independent pathway. Clearly, testosterone abuse is associated with an intense recruitment of multiple myogenic pathways. This provides an unfair advantage over non-drug users. The long-term consequences on the regenerative capacity of skeletal muscle are unknown.  相似文献
4.
Protein, fibre and blood pressure: potential benefit of legumes   总被引:1,自引:0,他引:1  
1. Prevention of hypertension and improved blood pressure control can be achieved through dietary modification. In particular, population studies and randomised controlled trials have indicated a beneficial effect of both dietary protein and dietary fibre on level of blood pressure. 2. A large population study indicates that an increase in 37 g/day of protein leads to a decrease in mean systolic and diastolic blood pressure by approximately 3 and 2.5 mmHg, respectively. This protective effect is independent of the source of dietary protein. 3. Meta-analysis suggests that a fibre increase of approximately 17 g/day will decrease systolic blood pressure by 1.15 mmHg and diastolic blood pressure by 1.65 mmHg, with soluble fibre showing a stronger effect than insoluble fibre. 4. Protein and dietary fibre may have additive effects to lower blood pressure. One feasible approach to increasing both protein and fibre in the daily diet could be through the incorporation of legumes, a protein- and fibre-rich food. 5. This review assesses the evidence for effects of protein and fibre to reduce blood pressure and the potential of incorporation of legumes into the daily diet as a feasible approach to achieving such benefits for blood pressure.  相似文献
5.
Summary Rabbits were given an infusion of 10 mg/kg (–)- or 30 mg/kg (+)--methyldopamine and killed after 135 min. The noradrenaline content of the heart was decreased to 26±5 and 34±2%, respectively, of the control value. After infusion of the (+)-isomer the missing noradrenaline was replaced by (–)--methylnoradrenaline. Electrical stimulation of the sympathetic nerves or infusion of acetylcholine plus atropine caused an output of noradrenaline and (–)--methylnoradrenaline from the isolated heart. The two amines were released in the same proportion as they were stored in the heart and the total output of both amines equalled the output of noradrenaline from control hearts. Nerve stimulation caused frequency-dependent increases in the rate and tension of cardiac contraction. There was no significant difference between the frequency-response curves obtained from untreated hearts and those treated with (+)--methyldopamine.After pretreatment with (–)--methyldopamine the noradrenaline lost from the heart was substituted by the infused amine;-methylnoradrenaline was not detected. Nerve stimulation or infusion of acetylcholine plus atropine caused an output of noradrenaline and (–)--methyldopamine at the same proportion as the amines were stored. Electrical stimulation of the sympathetic nerves caused an undiminished output of noradrenaline although the cardiac noradrenaline was decreased. It is suggested that the (–)--methyldopamine released during nerve stimulation interferes with the membranal re-uptake and therefore increases the overflow of the catecholamines. Pretreatment with (–)--methyldopamine shifted the frequencyresponse curves for rate and tension to the right.It concluded that treatment with (+)--methyldopamine failed to inhibit adrenergic transmission because the cardiostimulant activity of its metabolite, (–)--methylnoradrenaline, does not differ from that of noradrenaline, and the false transmitter released fully balances the decrease of noradrenaline output. In contrast, admixture of a large proportion of a weak cardiostimulant amine such as (–)--methyldopamine inhibits the actions of the physiological transmitter released by nerve stimulation probably by a postjunctional effect.This work was supported by the Deutsche Forsehungsgcmeinschaft. We wish to thank Dr. phil. et reed. Petra Netter (Institut für Medizinische Statistik und Dokumentation, Mainz) for her advice in the statistical analysis, and Dr. C. A. Stone (Merck, Sharpe and Dohme) for the donation of (–)- and (+)--methyldopamine. The technical assistance of Miss B. Hering and Miss H. Zappe is gratefully acknowledged.  相似文献
6.
Summary The influence of phentolamine on the uptake of exogenous noradrenaline infused into the aortic cannula and on the overflow of endogenous noradrenaline caused by sympathetic nerve stimulation was investigated in the isolated perfused rabbit heart. 10–6 M phentolamine doubled the overflow of endogenous noradrenaline, but did not change noradrenaline uptake. 10–5 M phentolamine increased the stimulation-induced overflow of noradrenaline 4-fold and inhibited amine uptake by about 50%. 10–4 M phentolamine elevated the overflow of noradrenaline less than 10–5 and 3×10–5 M did. The augmentation of transmitter overflow was only partly reversed by 13 min perfusion with drug-free medium.Pretreatment of hearts with 1.5×10–5 M cocaine or with 10–7 or 10–6 M desipramine did not change the effect of phentolamine on the overflow of noradrenaline evoked by nerve impulses. Pretreatment of hearts with 10–5 M, but not with 10–6 M, phentolamine prevented the increase of transmitter overflow by cocaine.It is concluded that low concentrations of phentolamine potentiate the overflow of noradrenaline during nerve stimulation by a mechanism different from that of cocaine, i.e. different from inhibition of neuronal re-uptake. The nature of this mechanism is discussed.This work was supported by the Deutsche Forsehungsgemeinschaft. We have the pleasure to thank Mrs. Ch. Arts, Miss B. Piel and Mr. E. Hagelskamp for skilful technical assistance.  相似文献
7.
A study has been made of the effect of diphenylhydantoin on the electrogenic component of the sodium pump in non-myelinated fibres of the desheathed rabbit vagus nerve. Acute or chronic administration of this drug did not affect the excitability, nor the membrane permeability, nor the activity of the sodium pump of the nerve fibres.  相似文献
8.
Summary Membrane and action potentials, electrical thresholds and isometric contractions of isolated guinea-pig papillary muscles were measured before and during exposure to sparteine in concentrations of 10–5 to 10–3 M. The rates of rise and fall of the action potential were slowed, the duration prolonged, the overshoot decreased. The resting potential decreased at concentrations of >5×10–4 M. Electrical threshold for eliciting a contraction was increased. Isometric force and rate of force development were increased, the time to peak of contraction and the relaxation time remained almost unchanged. All drug effects progressed the faster the higher the concentration and were reversible on washout.This work was supported by the Deutsche Forschungsgemeinschaft  相似文献
9.
Summary The release of endogenous acetylcholine (ACh) has been investigated in 9 human papillary muscles. In the isolated preparation, transmitter substances were released by high voltage stimulation and simultaneous application of trains of stimuli during the abolute refractory period of the myocardium.In the pharmacologically untreatet human heart muscle the negative inotropic effect of ACh was superimposed on the positive inotropic effect of simultaneously released catecholamines. After treatment with guanethidine, high voltage stimulation reduced the amplitude of isometric contraction by an average of 14%. After contractility had been increased by noradrenaline, isoprenaline, orciprenaline or theophylline high voltage stimulation reduced the amplitude of contraction by 23%. These negative inotropic effects were increased up to 47% by neostigmine, diminished by hemicholinium and prevented by atropine, Blockade of intramural nerve endings by tetrodotoxin abolished completely the positive as well as negative inotropic effects of high voltage stimuli.These findings indicate the possibility of a release of endogenous ACh from intramural nerve endings also in human ventricular myocardium. The negative inotropic effect of endogenous ACh is most pronounced during positive inotropic effects of sympathominetic agents or of theophylline.
Ein Teil der Ergebnisse wurde anläßlich der 39. Tagung der Deutschen Physiologischen Gesellschaft als vorläufige Mitteilung publiziert (Sieber et al., 1972).  相似文献
10.
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