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11.
附子理中丸方药的药物动力学研究 总被引:13,自引:0,他引:13
附子理中丸是中医治疗脾胃虚寒、脘腹冷痛、呕吐泄泻、手足不温的常用成药。本文通过小白鼠急性死亡实验,测得ip LD_(50)=42.4870g/kg;运用药物累积法对该复方方药进行了药物动力学研究。结果表明:附子理中丸在小鼠体内按一级动力学消除,呈二房室开放式模型分布。测得其t_(1/2)α=0.1922h,t_(1/2)β=11.2888h等动力学参数。阐明了该药的体内动态过程,为评价该药的内在质量及临床安全合理应用提供了参考依据。 相似文献
12.
Naoki Sugawara Koji Arizono Toshiichi Kitajima Hideaki Inoue Yu-Rong Lai 《Archives of toxicology》1997,71(5):336-339
A new mutant, the Eisai hyperbilirubinemic (EHB) rat, shows no inherent expression of the canalicular isoform of the multidrug
resistance protein (cMrp) in the liver. It has defective biliary secretion of organic anions such as bilirubin glucuronides,
bromosulfophthalein (BSP), cysteinyl leukotrienes, glutathione (GSH) and bile acid sulfate and glucuronides. When rats were
injected intravenously with CdCl2, biliary excretion of Cd over 30 min was 0.28% and 0.004% of the total dose in Sprague-Dawley (SD) and EHB rats, respectively.
Six SD rats and five EHB rats were fed a diet containing Cd. Bile Cd was detected at the level of 2 ng/20 min in SD rats,
but not in EHB rats. There was no significant difference of hepatic Cd concentration between SD and EHB rats. Furthermore,
there were no significant differences of renal and intestinal Cd, and hepatic and renal metallothionein (MT) concentrations
between the SD and EHB groups. Biliary excretion of reduced-GSH for 20 min was 1.3 ± 0.3 mg and 3.6 ± 0.9 μg in SD and EHB
rats, respectively. Our results suggest that hepatobiliary excretion of exogenous Cd is mediated mainly via carrier transport,
including a cMrp or GSH carrier, but that the lack of the transport pathway does not contribute to abnormal accumulation of
Cd in the liver.
Received: 12 August 1996 / Accepted 7 November 1996 相似文献
13.
Nina M. Griffiths Chehrazade Brick-Ghannam Sylvie Siaume-Perez Danielle Chabardès 《Pflügers Archiv : European journal of physiology》1993,422(6):577-584
The effects of calcitonin, vasoactive intestinal peptide (VIP), parathyroid hormone (PTH) and isoprenaline on intracellular cAMP accumulation were determined in the distal tubule (DCT) microdissected from collagenase-treated rabbit kidney. In DCTb (the initial bright portion) calcitonin (10 ng/ml) elicited a highly reproducible response 203.7±19.1 fmol cAMP mm–1 4 min–1 (SE, N=13) whereas VIP-induced cAMP accumulation was less and more variable from one experiment to another (1 M, 97.2±17.8 fmol mm–1 4 min–1, SE, N=12). When used in combination, these two agonists were non-additive, indicating stimulation of a single pool of cAMP in DCTb. In DCTg, (granular) which consists of at least two cell types, PTH (100 nM) elicited a marked, reproducible accumulation of cAMP (154.3±27.0 fmol mm–1 4 min–1; SE, N=5). Isoprenaline (1 M) and VIP (1 M) induced much smaller increases in cAMP levels 20.9±2.7 and 29.4±4.1 fmol mm–1 4 min–1 (SE, N=5) respectively, and, when used in combination, were non-additive, demonstrating that VIP and isoprenaline are active on the same cell type. In DCTb, prostaglandin E2 (PGE2) inhibited both calcitoninand VIP-stimulated cAMP accumulation (calcitonin 57.8±2.7% inhibition, SE, N=16; VIP, 80.6±2.1% inhibition, SE, N=5). The EC50 values for calcitonin were 1.21±0.33 ng/ml and 1.83±0.25 ng/ ml (SD, N=3) in the absence and presence of PGE2 (300 nM) respectively with an IC50 for PGE2 of 26.3±6.3 nM (SE, N=4). In contrast, no effects of PGE2 were seen in DCTg vis à vis PTH, isoprenaline or VIP. The percentage inhibition of calcitonin-stimulated cAMP accumulation by PGE2 was of the same order in the presence of isobutylmethylxanthine (an inhibitor of all types of phosphodiesterase), Ro 20-1724 (inhibitor of low-K
m cAMP-specific phosphodiesterase) or in the absence of inhibitor. Preincubation of DCTb with pertussis toxin for up to 8 h in different experimental conditions did not relieve the inhibition by PGE2. Protein kinase C activation by phorbol ester did not attenuate calcitonin responses. These data demonstrate that the inhibition by PGE2 of cAMP production is restricted to the initial portion (DCTb) of the distal convoluted tubule and is effective on both calcitonin and VIP responses. When tested in the presence of Ro 20-1724, ionomycin, A1-adenosine, 2-adrenergic and muscarinic agonists were without effect on calcitoninand PTH-stimulated cAMP accumulation in DCTb and DCTg respectively. 相似文献
14.
Krustrup P Söderlund K Mohr M González-Alonso J Bangsbo J 《Pflügers Archiv : European journal of physiology》2004,449(1):56-65
To investigate recruitment of slow-twitch (ST) and fast-twitch (FT) muscle fibres, as well as the involvement of the various quadriceps femoris muscle portions during repeated, intense, one-legged knee-extensor exercise, 12 healthy male subjects performed two 3-min exercise bouts at ~110% maximum thigh O2 consumption (EX1 and EX2) separated by 6 min rest. Single-fibre metabolites were determined in successive muscle biopsies obtained from the vastus lateralis muscle (n=6) and intra-muscular temperatures were continuously measured at six quadriceps muscle sites (n=6). Creatine phosphate (CP) had decreased (P<0.05) by 27, 73 and 88% in ST fibres and 25, 71 and 89% in FT fibres after 15 and 180 s of EX1 and after 180 s of EX2, respectively. CP was below resting mean–1 SD in 15, 46, 84 and 100% of the ST fibres and 9, 48, 85 and 100% of the FT fibres at rest, after 15 and 180 s of EX1 and after 180 s of EX2, respectively. A significant muscle temperature increase (Tm) occurred within 2–4 s at all quadriceps muscle sites. Tm varied less than 10% between sites during EX1, but was 23% higher (P<0.05) in the vastus lateralis than in the rectus femoris muscle during EX2. Tm in the vastus lateralis was 101 and 109% of the mean quadriceps value during EX1 and EX2, respectively. We conclude that both fibre types and all quadriceps muscle portions are recruited at the onset of intense knee-extensor exercise, that essentially all quadriceps muscle fibres are activated during repeated intense exercise and that metabolic measurements in the vastus lateralis muscle provide a good indication of the whole-quadriceps muscle metabolism during repeated, intense, one-legged knee-extensor exercise. 相似文献
15.
16.
Seiler Petra; Fischer Bernd; Lindenau Antje; Beier Henning M. 《Human reproduction (Oxford, England)》1994,9(10):1920-1926
The commercial polychlorinated biphenyl (PCB) formulation Aroclor1260 (4 mg/kg body weight), technical grade dichlorodiphenyltrichloroethane(DDT; 3 mg) and Lindane (-hexachlorocyclohexane; 0.8 mg) wereadministered orally, either separately or in combination, tosexually mature female rabbits three times per week for 1215weeks. Oviductal and uterine luminal fluid, cleavage stage embryos(day 1 post coitum), blastocysts (day 6), fetuses, exocoelicfluid and placentae (day 11) were analysed, firstly for chlorinatedhydrocarbon residues, and secondly for embryonic and fetal development.The doses applied were well tolerated by the treated animals.PCB and DDT accumulated in uterine secretions (day 6) but notin oviductal luminal fluid (day 1). Both chlorinated hydrocarbonswere found in preimplantation blastocysts. Residues in day 11fetuses were 16- (DDT) or 18-fold (PCB) higher than in day 6blastocysts. Significant amounts were also detected in placentaltissue and in exocoelic fluid. A specific accumulation of thehighly chlorinated biphenyl congener no. 180 was noted in fetuses,placentae and exocoelic fluid. The clear accumulation of thechlorinated hydrocarbon compounds in luminal fluid and embryonictissue is contrasted by rather weak effects on fertility. Nostatistically significant differences between treated animalsand controls were observed for fertilization rate and pre- andpost-implantation (up to day 11 post coitum) losses. However,in females exposed to PCB, a 20% higher loss of blastocystswas noticed, as compared with controls (P > 0.05). This effectwas shown on day 6 of embryonic development and may be due tothe embryotoxic activities of PCB. 相似文献
17.
V. V. Tertov I. A. Sobenin Z. A. Gabbasov E. G. Popov A. N. Orekhov 《Bulletin of experimental biology and medicine》1990,110(1):882-885
Institute of Experimental Cardiology, All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Smirnov.) Translated from Byulleten's Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 7, pp. 34–36, July, 1990. 相似文献
18.
Savitskii VP Zorin VP Potapnev MP Potapenko AY 《Bulletin of experimental biology and medicine》2004,138(2):158-162
We studied accumulation of porphyrin photosensitizers chlorine e6, hematoporphyrin, and their derivatives by different lymphocyte subpopulations. The intensity of staining of B lymphocytes and natural killer cells with photosensitizers was higher compared to T lymphocytes. T cell subpopulation differed by their ability to bind photosensitizers. Relative accumulation of dimethyl esters of chlorine e6 and hematoporphyrin in cells surpassed that of nonesterified porphyrins. 相似文献
19.
Lotfi Aarab Sylvie Siaume-Perez Danielle Chabardès 《Pflügers Archiv : European journal of physiology》1993,425(5-6):417-425
Previous studies have demonstrated that prostaglandin E2 (PGE2) inhibits arginine vasopressin-(AVP)dependent adenosine 3,5-cyclic monophosphate (cAMP) accumulation in microdissected rat outer medullary collecting tubules (OMCD), by a mechanism unrelated to the inhibition of cAMP synthesis. The potential role of the activation of protein kinase C (PKC) to explain the negative regulation elicited by PGE2 was investigated in this study. Single OMCD samples were pre-incubated (10 min, 30°C) in the presence or absence of either activators of PKC, phorbol 12-myristate 13-acetate (PMA), 1-oleoyl-2-acetyl-glycerol (OAG), dioctanoylglycerol (DOG) or an inhibitor of PKC, staurosporine (SSP). These compounds were present also with the agonists tested during the incubation period (4 min, 35°C). In contrast to PGE2, activators of PKC did not decrease AVP-dependent cAMP accumulation (mean ±SEM): 1nM AVP=47.1±6.8 fmol · mm–1· 4 min–1; AVP + 0.3 M PGE2=20.1±2.7, P<0.01 versus AVP; AVP + 10 nM PMA=42.0±4.7, NS versus AVP; AVP + 50 g/ml OAG=44.1±4.8. NS versus AVP, N= 5 experiments. However, 10 nM PMA prevented PGE2-induced inhibition: AVP + PGE2= 44.2±3.5% of the response to AVP and 90.3±3.2% without and with PMA respectively, N= 16. Similar results were obtained with either 50 g/ml OAG or 25 g/ ml DOG (AVP + PGE2 + OAG=92.9±6.6% of the response to AVP, N= 8; AVP + PGE2 + DOG=94.1 ±5.3%, N= 7). OAG, DOG, PMA or PMA + PGE2 had no intrinsic agonist activity in the rat OMCD and the addition of an inactive phorbol ester did not prevent PGE2-induced inhibition. SSP, 50 nM or 0.1 M, did not affect the inhibition due to PGE2 but abolished the reversion by PMA of PGE2-induced inhibition. A similar regulation was observed on forskolin-(FK)dependent cAMP accumulation: 5 M FK + 0.3 M PGE2= 37.7±6.2% of the response to FK; FK + PGE2 + 10 nM PMA=89.5±6.7%; FK + PGE2 + PMA + 0.1 M SSP=43.1±7.9%, N= 4. The inhibition induced by an
2-adrenergic agonist, clonidine 1 M, was not blocked by the activation of PKC. In fura-2-loaded OMCD samples, 10nM PMA decreased by 63.3±5.0% and by 57.2±7.1% the peak and plateau phases, respectively, of the increase in intracellular calcium concentration ([Ca2+]i) obtained with PGE2 when compared to control responses in the same tubules (n=12) and did not affect the increase in [Ca2+]i induced by 0.1 mM carbachol. It is concluded that: (1) in the rat OMCD the activation of PKC by PMA or analogues of diacylglycerol did not reproduce PGE2-induced inhibition of AVP- or FK-dependent cAMP accumulation, but prevented specifically this inhibitory action; and (2) this reversion might be the consequence of the effect of PKC activation which impaired the rises in [Ca2+]i induced by PGE2. 相似文献
20.
Severe hypoxia decreases oxygen uptake relative to intensity during submaximal graded exercise 总被引:1,自引:0,他引:1
J. Ibañez R. Rama M. Riera M. T. Prats L. Palacios 《European journal of applied physiology》1993,67(1):7-13
Summary The effect of severe acute hypoxia (fractional concentration of inspired oxygen equalled 0.104) was studied in nine male subjects performing an incremental exercise test. For power outputs over 125 W, all the subjects in a state of hypoxia showed a decrease in oxygen consumption (
O2) relative to exercise intensity compared with normoxia (P < 0.05). This would suggest an increased anaerobic metabolism as an energy source during hypoxic exercise. During submaximal exercise, for a given
O2, higher blood lactate concentrations were found in hypoxia than in normoxia (P < 0.05). In consequence, the onset of blood lactate accumulation (OBLA) was shifted to a lower
O2 (
O2 1.77 l·min–1 in hypoxia vs 3.10 l·min–1 in normoxia). Lactate concentration increases relative to minute ventilation (
E) responses were significantly higher during hypoxia than in normoxia (P < 0.05). At OBLA,
E during hypoxia was 25% lower than in the normoxic test. This study would suggest that in hypoxia subjects are able to use an increased anaerobic metabolism to maintain exercise performance. 相似文献