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81.
Gloria Bustos Maria Luisa Ferrándiz Maria Jesús Sanz Miguel Payá Maria José Alcaraz 《Naunyn-Schmiedeberg's archives of pharmacology》1995,351(3):298-304
We have evaluated the effects of the novel anti-inflammatory agent florifenine, 2-(1-Pyrrolidinyl)ethyl N-[7-(trifluoromethyl)-4-quinolyl]anthranilate, on topical inflammation in mice, free radical-mediated reactions, arachidonic acid metabolism and some neutrophil functions. Topical administration of florifenine produced dose-related anti-inflammatory activity in 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced ear oedema and with a lower potency, in the response induced by arachidonic acid (AA). Florifenine also inhibited neutrophil migration and PGE2 content in the inflammed ears. In human whole blood, florifenine was a potent and selective inhibitor of TXB2 generation. This anti-inflammatory agent did not exert antioxidant effects but inhibited elastase release in human neutrophils without affecting superoxide anion generation. Florifenine administration to mice dose-dependently inhibited leukocyte migration and PGE2 levels in the air pouch inflammation induced by zymosan. These results demonstrate the topical anti-inflammatory activity of florifenine and provide a basis for understanding the mechanisms involved in the inhibitory effects of this agent on inflammatory responses. 相似文献
82.
Mickleborough TD Gotshall RW Kluka EM Miller CW Cordain L 《European journal of applied physiology》2001,85(5):450-456
Dietary sodium chloride (NaCl) has been shown to alter the severity of exercise-induced asthma, but it is not known if the
sodium and chloride ions have independent effects in this regard. The hypothesis tested in the present study was that both
a low sodium, low chloride diet and a high sodium, low chloride diet would improve post-exercise pulmonary function in subjects
with exercise-induced asthma (EIA) compared to a normal NaCl diet (NSD); but that neither of these diets would have an effect
on post-exercise pulmonary function in control (non-EIA) subjects. Eight subjects who suffered from EIA and eight subjects
who did not (control) took part in a double-blind crossover study. Pre- and post-exercise pulmonary function was assessed
after 2 weeks on a NSD, a low NaCl diet (LSD, low sodium, low chloride) or a sodium bicarbonate diet (NaHCO3 diet, high sodium, low chloride). A 1 week washout period occurred between diets. Altering dietary sodium or chloride had
no effect on pre-exercise (baseline) pulmonary function in either group or on post-exercise pulmonary function in control
subjects. However, both the LSD and the NaHCO3 diet lessened the deterioration in post-exercise pulmonary function in EIA subjects. Comparing results from pre- to post-exercise,
forced expiratory volume in 1 s (FEV1) at 15 min post-exercise differed significantly (P<0.05) between diets [mean (SEM) 7 (4)% on the LSD, 14 (4)% on the NaHCO3 diet, and 19 (2)% on the NSD]. Similar patterns were observed for forced vital capacity (FVC), forced expiratory flow rate
at 25%–75% FVC and peak expiratory flow rate. The NaHCO3 diet lessened the deterioration of post-exercise pulmonary function, but not to the extent of LSD. These data suggest that
both sodium and chloride contribute to the worsening of EIA symptoms seen after consuming a normal or high NaCl diet.
Electronic Publication 相似文献
83.
花生四烯酸产物对系膜细胞增殖作用的研究 总被引:3,自引:1,他引:3
用[3H]胸腺嘧啶核甙([3H-thymidine,[3H]-TdR)掺入法测定花生四烯酸产物对体外培养的大鼠肾小球系膜细胞的增殖作用。前列腺素E2(prostaglandin,PG)抑制血清所致的系膜细胞增殖。血栓素A2(thromboxane,Tx)类似物U46619、白三烯(leukotuiene,LT)C4、LTD、12-羟二十碳四烯酸(12-hydroxyeicosatetraenoicacid,12-HETE)、15-HETE促进静息的系膜细胞增殖,LTB4及5-HETE无此作用。用特异性蛋白激酶C(proteinkinaseC,PKc)抑制剂可抑制U46619、LTC4、LTD4及12-HETE的促增殖作用。PGF2α、U46619、LTC4、LTD4促进系膜细胞合成二脂酰甘油(diacylglycerol,DAG)。PGF2α及LTD4刺激系膜细胞合成三磷酸肌醇(inositoltriphosphate,IP3)。提示部分花生四烯酸产物活化PKC而促进系膜细胞增殖。 相似文献
84.
Nogueira-Neto Fde S Amorim RL Brigatte P Picolo G Ferreira WA Gutierrez VP Conceição IM Della-Casa MS Takahira RK Nicoletti JL Cury Y 《Pharmacology, biochemistry, and behavior》2008,91(2):252-260
Crotoxin (CTX), a neurotoxin isolated from the venom of the South American rattlesnake Crotalus durissus terrificus, induces analgesia. In this study, we evaluated the antinociceptive effect of CTX in a model of neuropathic pain induced by rat sciatic nerve transection. Hyperalgesia was detected 2 h after nerve transection and persisted for 64 days. Immersion of proximal and distal nerve stumps in CTX solution (0.01 mM for 10 s), immediately after nerve transection, blocked hyperalgesia. The antinociceptive effect of CTX was long-lasting, since it was detected 2 h after treatment and persisted for 64 days. CTX also delayed, but did not block, neurectomy-induced neuroma formation. The effect of CTX was blocked by zileuton (100 mg/kg, p.o.) and atropine (10 mg/kg, i.p.), and reduced by yohimbine (2 mg/kg, i.p.) and methysergide (5 mg/kg, i.p.). On the other hand, indomethacin (4 mg/kg, i.v.), naloxone (1 mg/kg, i.p.), and N-methyl atropine (30 mg/kg, i.p.) did not interfere with the effect of CTX. These results indicate that CTX induces a long-lasting antinociceptive effect in neuropathic pain, which is mediated by activation of central muscarinic receptors and partially, by activation of α-adrenoceptors and 5-HT receptors. Eicosanoids derived from the lipoxygenase pathway modulate the action of crotoxin. 相似文献
85.
Mary W. Wilson L. Travis Lay Ching K. Chow Hsin -Hsiung Tai Larry W. Robertson Howard P. Glauert 《Archives of toxicology》1995,69(7):491-497
Several hypolipidemic drugs, plasticizers, and other chemicals induce hepatic peroxisome proliferation and hepatocellular
carcinomas in rodents. These agents induce and promote hepatocarcinogenesis by unknown mechanisms, since most studies have
not found them to be genotoxic. Peroxisome proliferators increase the expression of several genes, including those for the
enzymes of the peroxisomal β-oxidation pathway and the cytochrome P-450 4A family, which metabolize lipids, including eicosanoids
and their precursor fatty acids. The peroxisome proliferators ciprofibrate and perfluorodecanoic acid (PFDA) were therefore
examined for their ability to alter hepatic eicosanoid concentrations. Rats received injections of 3 or 10 mg PFDA/kg body
weight every 14 days or were fed 0.01% ciprofibrate for 10 days, 24 days, 6 weeks, 26 weeks, or 54 weeks. The activity of
the peroxisomal enzyme fatty acyl CoA oxidase was significantly increased by both ciprofibrate and PFDA at all times. Hepatic
concentrations of prostaglandins E2 and F2α (PGE2, PGF2α), thromboxane B2 (TXB2), and leukotriene C4 (LTC4) were measured by immunoassay. Concentrations of PGE2, PGF2α, and TXB2 were decreased in livers of rats receiving ciprofibrate or PFDA compared to livers of control rats, with ciprofibrate exerting
a greater effect than PFDA at the doses used. Hepatic LTC4 concentrations were significantly increased by ciprofibrate at 10 days and PFDA at 54 weeks, and significantly decreased
by PFDA at 26 weeks. These alterations in eicosanoid concentrations may be important in the natural history of peroxisome
proliferator-induced hepatocarcinogenesis.
Received: 15 September 1994/Accepted: 15 December 1994 相似文献