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71.
D. Freymond R. Guignet P. Lhote A.‐C. Passaquin U. T. Rüegg 《Acta physiologica (Oxford, England)》2002,176(4):283-292
The modulation of glucose uptake by cytosolic calcium and the role of insulin on calcium homeostasis in insulin‐target cells are incompletely understood and results are contradictory. To address this issue, we used the C2C12 murine skeletal muscle cell line model and examined the influence of caffeine and 4‐chloro‐m‐cresol, two ryanodine receptor agonists known to mobilize intracellular calcium stores and increase cytosolic free calcium concentration. We followed 45calcium efflux, a validated indicator of cytosolic calcium concentration, and 3‐O‐methyl‐[1–3H]‐d ‐glucose uptake in parallel. We also determined if insulin incubation affected 45calcium influx rate. A 30‐min treatment by 1 μm insulin highly significantly increased 45calcium efflux by 8.5% (P = 0.0014), despite a significant reduction of 45Ca2+ influx already measurable after 20 and 30 min of insulin stimulation (?16.6%, P = 0.0119 and ?21.3%, P = 0.0047, respectively). Caffeine (1–20 mm ) and 4‐chloro‐m‐cresol (0.05–10 mm ) concentration‐dependently increased 45calcium efflux, the latter being more potent and efficacious. These agents, in a concentration‐dependent manner, inhibited both basal and, more potently, insulin‐stimulated glucose uptake. This resulted in a negative correlation of glucose uptake and 45calcium efflux (r > 0.95, P < 0.001). This effect was ~5 times greater for caffeine than for 4‐chloro‐m‐cresol, suggesting a calcium‐independent part of the glucose uptake inhibition by caffeine. In our in vitro model of cultured muscle cells, insulin appears to prevent calcium overload by both stimulating efflux and inhibiting cell storage. This effect, taken together with the observed inhibitory, inverse relationship between 45calcium efflux and glucose uptake, contributes to describing the complex insulin–calcium interplay involved in target cells. 相似文献
72.
J. SVEDENHAG J. HENRIKSSON A. JUHLIN-DANNFELT K. ASANO 《Acta physiologica (Oxford, England)》1984,120(1):77-86
The effect of chronic β-adrenergic blockade on central circulatory adaptations to physical training was investigated. 16 healthy sedentary males (20–31 yrs) trained on cycle ergometers 40 min/day, 4 days a week for 8 weeks at a work load that during the last 5 weeks corresponded to 75% of the pretraining VO2 max. In a single blind way, 8 subjects were during the training period treated with the β-adrenergic receptor blocker propranolol (160 mg/day), while the remaining 8 received placebo tablets. Pretraining tests were performed before the start of medication and posttraining tests were performed 6 days after the last day of training and medication. The training program resulted in a similar increase (8%) in VO2 max in both groups (p<0.01). The resting heart rate (-4 beats/min; p<0.05) as well as the exercise heart rate at a moderate work load (120 W: -11 beats/min; p<0.01) decreased with training, and no significant difference was seen between the 2 groups. At a high work load (180 W), however, the heart rate decreased significantly more with training in the placebo group as compared with the β-blockade group (-19 vs.-7 beats/min; p<0.05). The oxygen pulse (VO2/HR) increased in both groups at 120 W (+6%; p<0.01). At 180 W the oxygen pulse increased only in the placebo group (+8%; p<0.05). The estimated stroke volume at 120 and 180 W, as determined by impedance cardiography, did not change significantly with training although there was a tendency towards an increase in the placebo group only. The resting left ventricular wall thickness and diameter, as determined by echocardiography, did not change significantly with training in either group.—In conclusion, the present study indicates that a moderate degree of β-adrenergic blockade does not prevent or impair the training-induced increase in the maximal oxygen uptake. During submaximal work, however, the circulatory adaptation may be less apparent if training has been performed during partial blockade of the sympathoadrenal system. 相似文献
73.
Bo Hellman Janove Sehlin Inge-Bert Täljedal 《Pflügers Archiv : European journal of physiology》1978,378(2):93-97
Microdissected pancreatic islets of noninbredob/ob-mice were used to study ionic effects on the lanthanum-nondisplaceable45Ca2+ uptake by islet cells. Omission of Mg2+ from the incubation medium had no effect, but the45Ca2+ uptake was increased by omission of Na+ and decreased by omission of K+. Excess Mg2+ (1.2–15 mM) inhibited and excess K+ (4.7–25 mM) stimulated the45Ca2+ uptake in a concentration-dependent manner. Stimulation of45Ca2+ uptake in Na+-deficient islets was associated with an enhancement of the basal insulin release. Total abolishment of glucose-stimulated45Ca2+ uptake in K+-deficient islets did not preclude a significant secretory response to glucose. It is concluded that the lanthanum-nondisplaceable45Ca2+ uptake shows a partial correlation to insulin release. 相似文献
74.
Carlo Capelli Guglielmo Antonutto Paola Zamparo Massimo Girardis Pietro Enrico di Prampero 《European journal of applied physiology》1993,66(3):189-195
Summary The mechanical power (Wtot, W·kg–1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO2max)] of 20–40 min duration. The oxygen uptake [VO2 (W·kg–1, 1 ml O2 = 20.9 J)] and venous blood lactate concentration ([la]b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, Wtot decreased linearly with the intensity of the priming exercise (Wtot = 11.9–0.25·VO2). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO2max, Wtot, VO2 and [la]b remained constant until the end of the exercise. For exercise intensities greater than 60% VO2max, VO2 and [la]b showed continuous upward drifts and Wtot continued decreasing. Under these conditions, the rate of decrease of Wtot was linearly related to the rate of increase of V [(d Wtot/dt) (W·kg–1·s–1) = 5.0·10–5 –0.20·(d VO2/dt) (W·kg–1·s–1)] and this was linearly related to the rate of increase of [la]b [(d VO2/dt) (W·kg–1·s–1) = 2.310–4 + 5.910–5·(d [la]b/dt) (mM·s–1)]. These findings would suggest that the decrease of Wtot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO2 (upwards) and of Wtot (downwards) during intense exercise at constant Wtot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles). 相似文献
75.
Bavo Vanden Eynde Dirk Vienne Magda Vuylsteke-Wauters Dirk Van Gerven 《European journal of applied physiology》1988,57(4):430-434
Summary To determine the cardiorespiratory response to maximal exercise before, during and after the pubescent growth spurt, thirty boys were tested at yearly intervals over a period of six consecutive years. For each individual, peak height velocity (PHV) was determined. The age at PHV (¯X= 13.6 years) was taken as a standard of maturation. The results from all subjects at 1.5 and 0.5 years before and 0.5 and 1.5 years after PHV are presented. The highest oxygen uptake (
) obtained during an incremental bicycle ergometer test to voluntary exhaustion was taken as peak oxygen uptake (
peak). Across each of the four years studied, mean
peak (min=49.6; max=52.5 ml·kg–1·min–1) and mean heart rate (HR) at
peak (min=190; max=192) did not change significantly as a function of PHV. On the other hand, the respiratory quotient at
peak increased considerably from mean minima and maxima of 0.99 and 1.01 before PHV to 1.07 and 1.10 after PHV. Ventilatory equivalent for
(
), taken as an indicator of ventilatory economy, seemed to be unaffected by the maturation process. The steepest increase in circumpubertal oxygen pulse was found one year after PHV. Average stability coefficients (¯r), calculated from the inter-years correlations were high for height (¯r=0.95), weight (¯r=0.92), HR at
peak (¯r=0.74),
peak in 1/min (¯r=0.71), oxygen pulse (¯r=0.68) and tidal volume (¯r=0.64). 相似文献
76.
We studied the effects of aging on the [3H]-choline uptake, acetylation, [3H]-ACh release and muscarinic modulation of [3H]-ACh release in cortical synaptosomes prepared from Fischer 344 male rats. Our results indicate that 6 and 24 month old rats take up and acetylate [3H]-choline to a similar extent, but that the older animals release significantly less [3H]-ACh in response to K+-depolarization than the young adults do. This difference in K+-induced release is not due to a difference in presynaptic muscarinic receptor inhibitory activity since the older animals appear to be, if anything, slightly less sensitive to oxotremorine than the younger animals are. Atropine (1 μM) had no effect on ACh-release but blocked oxotremorine-induced modulation. Our results suggest that acetylcholine release is decreased in synaptosomes prepared from old rats although the presynaptic muscarinic regulation of release is functional. Thus, muscarinic receptor-mediated release-modulation is a potential site for pharmacologically altering ACh release. 相似文献
77.
[3H]2-Deoxy-d-glucose (2-DG) was used to investigate the glucose uptake in cultured rat Schwann cells from postnatal Sprague-Dawley rat sciatic nerves. The glucose uptake of Schwann cells slightly increased in a time- and dose-dependent manner. However, the maximal uptake level was much lower than that of ethylnitrosourea (ENU)-induced transformed rat schwannoma-like cells and fibroblasts. By autoradiography of the cultured system, we were able to visualize the accumulation of [3H]2-DG grains in the schwannoma-like cells and fibroblasts, but not in Schwann cells. 相似文献
78.
Luis Gandía Baldomero Lara Julita S. Imperial Mercedes Villarroya Almudena Albillos Rosario Maroto A. G. García Baldomero M. Olivera 《Pflügers Archiv : European journal of physiology》1997,435(1):55-64
The characteristics of the binding sites for the Conus magus toxins ω-conotoxin MVIIC and ω-conotoxin MVIID, as well as their effects on K+-evoked 45Ca2+ entry and whole-cell Ba2+ currents (I
Ba), and K+-evoked catecholamine secretion have been studied in bovine adrenal chromaffin cells. Binding of [125I] ω-conotoxin GVIA to bovine adrenal medullary membranes was displaced by ω-conotoxins GVIA, MVIIC and MVIID with IC50 values of around 0.1, 4 and 100 nM, respectively. The reverse was true for the binding of [125I] ω-conotoxin MVIIC, which was displaced by ω-conotoxins MVIIC, MVIID and GVIA with IC50 values of around 30, 80 and 1.200 nM, respectively. The sites recognized by ω-conotoxins MVIIC and MVIID in bovine brain
exhibited higher affinities (IC50 values of around 1 nM). Both ω-conotoxin MVIIC and MVIID blocked I
Ba by 70–80%; the higher the [Ba2+]o of the extracellular solution the lower the blockade induced by ω-conotoxin MVIIC. This was not the case for ω-conotoxin
MVIID; high Ba2+ (10 mM) slowed down the development of blockade but the maximum blockade achieved was similar to that obtained in 2 mM Ba2+. A further difference between the two toxins concerns their reversibility; washout of ω-conotoxin MVIIC did not reverse the
blockade of I
Ba while in the case of ω-conotoxin MVIID a partial, quick recovery of current was produced. This component was irreversibly
blocked by ω-conotoxin GVIA, suggesting that it is associated with N-type Ca2+ channels. Blockade of K+-evoked 45Ca2+ entry produced results which paralleled those obtained by measuring I
Ba. Thus, 1 μM of each of ω-conotoxin GVIA and MVIIA inhibited Ca2+ uptake by 25%, while 1 μM of each of ω-conotoxin MVIIC and MVIID caused a 70% blockade. K+-evoked catecholamine secretory responses were not reduced by ω-conotoxin GVIA (1 μM). In contrast, at 1 μM both ω-conotoxin
MVIIC and MVIID reduced the exocytotic response by 70%. These data strengthen the previously established conclusion that Q-type
Ca2+ channels that contribute to the regulation of secretion and are sensitive to ω-conotoxins MVIIC and MVIID are present in
bovine chromaffin cells. These channels, however, seem to possess binding sites for ω-conotoxins MVIIC and MVIID whose characteristics
differ considerably from those described to occur in the brain; they might represent a subset of Q-type Ca2+ channels or an entirely new subtype of voltage-dependent high-threshold Ca2+ channel.
Received: 16 April 1997 / Received after revision: 10 July 1997 / Accepted: 23 July 1997 相似文献
79.
Summary The purpose of this study was to investigate the validity of heart rate (f
c) and ratings of perceived exertion (RPE) as indices of exercise intensity in a group of children while swimming. Six healthy male swimmers, aged 10–12, swam tethered using the breast-stroke in a flume. The resistance started at 1.0 kg and increased in 1.0 kg steps up to the point of their exhaustion. The subjects swam for 5 min during each period, with a rest of 10–20 min until they had returned to their resting f
c level. The last exercise intensity was with the maximal mass the subjects could support for 2 min. The last min of oxygen consumption (VO2) and 30 s of f
c were measured during each exercise period. The subjects gave their RPE assessment at the end of exercise.The individual relationships between f
c and VO2, and percentage maximal oxygen consumption (% VO2max, were linear with a high correlation r=0.962–0.996 and r=0.962–0.996, respectively. Therefore, it was concluded that f
c was valid as an index of the exercise intensity of children while swimming. Compared to the results found in adults using a similar protocol, the children's f
c were 8.3–26.9 beats·min–1 higher than those of the adults at the given % VO2max. The present study showed two different patterns in the relationship between VO2 and RPE in individuals. In two subjects the RPE increased linearly with VO2 while in the other four subjects the increase was discontinuous. If f
c and RPE were to be applied to the setting and evaluation of exercise intensity during swimming, it would seem that f
c would be a more useful guide than RPE for some children. 相似文献
80.
Abstract Data on the metabolic responses to repeated endurance exercise sessions are limited. Thus, the aims of this study were to examine (1) the impact of prior exercise on metabolic responses to a subsequent exercise session and (2) the effect of different recovery periods between two daily exercise sessions on metabolic responses to the second bout of exercise. Nine male elite athletes participated in four 25-h trials: one bout of exercise (ONE), two bouts of exercise separated by 3 h of rest and one meal (SHORT), two bouts of exercise separated by 6 h of rest and two meals (LONG), and a trial with no exercise (REST). All exercise bouts consisted of 10 min cycling at 50% followed by 65 min at 75% of maximal O2 uptake. Compared to no prior exercise (ONE), a previous bout of exercise (SHORT) was followed by higher mean O2 uptake, heart rate (HR), rectal temperature (TR), excess post-exercise oxygen consumption and lower respiratory exchange ratio (R) during and after a similar exercise session 3 h later. A longer rest interval between the two exercise bouts (6 h versus 3 h) and an additional meal resulted in a decrease in O2 uptake, HR, TR and an increase in R during the second bout of exercise, but no effects on post-exercise metabolism were found. Thus, augmented metabolic stress was observed when strenuous exercise was repeated after only 3 h of recovery, but this was attenuated when a longer recovery period including an additional meal was provided between the exercise sessions. 相似文献