Research communications in chemical pathology and pharmacology最新文献

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Enhanced sensitivity of mdx mice to intramuscular injection of compound 48/80. 增强mdx小鼠肌肉注射复方48/80的敏感性。
J A Granchelli, M S Hudecki, C M Pollina
{"title":"Enhanced sensitivity of mdx mice to intramuscular injection of compound 48/80.","authors":"J A Granchelli,&nbsp;M S Hudecki,&nbsp;C M Pollina","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Species-specific differences in the inflammatory response, specifically with regard to mast cells, have been proposed to explain the phenotypic variation among dystrophin-deficient humans, and mdx mice (Gorospe et al., 1994). To test this hypothesis we have intramuscularly injected a mast cell secretogogue into both dystrophin-negative mdx and dystrophin-positive normal mice. Mast cell activity was determined by measuring the activity of mast cell tryptase, while creatine kinase activity was used to determine the course of muscle damage in vivo. Area of damage around the injection site was measured at autopsy, and used as an indication of relative sensitivity to the secretogogue effect of compound 48/80. Mdx mice exhibited more damage in response to intramuscular injection than normal control mice. In addition, mdx mice showed a substantial increase in plasma tryptase activity, followed by a large increase in muscle creatine kinase activity. On the other hand, dystrophin-positive normal controls injected with 48/80 liberated little CK or tryptase activity. These results are consistent with the hypothesis that species-specific differences in mast cell activity, or sensitivity to mast cell products could account for the variation in pathology seen in dystrophin-deficient animals.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"351-62"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Elevation of ceruloplasmin activity involved in changes of hepatic metal concentration in primary biliary cirrhosis. 原发性胆汁性肝硬化中铜蓝蛋白活性升高与肝金属浓度变化有关。
K Sogawa, T Yamada, Y Suzuki, T Masaki, S Watanabe, Y Uchida, K Arima, M Nishioka, K Matsumoto
{"title":"Elevation of ceruloplasmin activity involved in changes of hepatic metal concentration in primary biliary cirrhosis.","authors":"K Sogawa,&nbsp;T Yamada,&nbsp;Y Suzuki,&nbsp;T Masaki,&nbsp;S Watanabe,&nbsp;Y Uchida,&nbsp;K Arima,&nbsp;M Nishioka,&nbsp;K Matsumoto","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Primary biliary cirrhosis (PBC) patients showed increased ceruloplasmin activity and Cu content in the serum as compared to the control group. Moreover, Cu, Fe, and Zn contents were measured in the livers of autopsied cases. The PBC patients showed increased Cu content and reduced Fe and Zn levels. In PBC cases, Cu transportation via bile is disturbed due to collapse of the interlobular bile ducts and consequently Cu accumulates in the liver. Thus, it is likely that serum ceruloplasmin activity increases to metabolize the accumulated hepatic Cu and that Cu content increases in the serum as a ceruloplasmin-bound form. Furthermore, reduction of Fe and Zn contents in the liver of the PBC patients indicated the possible relationship of ceruloplasmin to Fe and Zn metabolism as well as Cu metabolism.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"367-70"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Blood cytokine and complement levels in patients with sepsis. 脓毒症患者血液细胞因子和补体水平的变化。
T Takakuwa, S Endo, H Nakae, M Kikuchi, N Baba, K Inada, M Yoshida
{"title":"Blood cytokine and complement levels in patients with sepsis.","authors":"T Takakuwa,&nbsp;S Endo,&nbsp;H Nakae,&nbsp;M Kikuchi,&nbsp;N Baba,&nbsp;K Inada,&nbsp;M Yoshida","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We measured serum levels of endotoxin, cytokines, and eicosanoids and investigated their relationship to serum complement levels in patients with sepsis. Serum endotoxin (Et) levels (5.3 +/- 2.4 pg/ml) were within the normal range, but levels of tumor necrosis factor-alpha (TNF-alpha, 114 +/- 104.94 pg/ml), interleukin 6 (IL-6, 86.7 +/- 50.9 pg/ml), interleukin 8 (IL-8, 86.8 +/- 49.7 pg/ml), type-II phospholipase A2 (type II PLA2, 211.3 +/- 193.9 ng/ml), leukotriene B4 (LTB4, 88.7 +/- 27.2 pg/ml), thromboxane B2 (TXB2, 58.7 +/- 50.9 pg/ml) and 6-keto-prostaglandin F1 alpha (PGF1 alpha, 21.0 +/- 11.0 pg/ml) levels were above normal. Levels of C3a (1088.4 +/- 83.8.7 ng/ml) and C4a (1951.5 +/- 1697.8 ng/ml) were also above normal; C3 (66.0 +/- 25.6 mg/dl) and C4 (23.6 +/- 5.3 mg/dl) were within the normal range, and C5a was lower than the detectable limit in all but one of the subjects. Serum TNF-alpha was significantly correlated with C3a (p < 0.001). Serum IL-6 had a significant negative correlation with C3 (p = 0.002) and C4 (p = 0.010). Type II PLA2 was significantly correlated with C3a (p < 0.001). There were no significant correlations between serum Et or IL-8 and serum C3, C4, C3a or C4a. Our findings suggest that increased levels of TNF-alpha, IL-6, and Type II PLA/ in patients with sepsis contribute to activation of the complement system.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"291-300"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Bradykinin induces generation of reactive oxygen species in bovine aortic endothelial cells. 缓激肽诱导牛主动脉内皮细胞产生活性氧。
S Shimizu, M Ishii, T Yamamoto, T Kawanishi, K Momose, Y Kuroiwa
{"title":"Bradykinin induces generation of reactive oxygen species in bovine aortic endothelial cells.","authors":"S Shimizu,&nbsp;M Ishii,&nbsp;T Yamamoto,&nbsp;T Kawanishi,&nbsp;K Momose,&nbsp;Y Kuroiwa","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We investigated the effects of bradykinin on intracellular oxidative stress in bovine aortic endothelial cells using a hydroperoxide-sensitive fluorescent dye, 2',7'-dichlorofluorescein (DCFH), and a laser scanning confocal microscope. Bradykinin induced an immediate increase in intracellular Ca2+ concentration, and stimulated the oxidation of DCFH in cultured endothelial cells. This bradykinin-induced oxidation of DCFH was inhibited by pretreatment with N-(2-mercaptopropionyl)-glycine (MPG) and 1,3-dimethyl-thiourea (DMTU), scavengers of hydroxyl radical, and the removal of extracellular Ca2+ but was unaffected by NG-nitro-L-arginine or NG-monomethyl-L-arginine, both inhibitors of nitric oxide (NO) synthase. On the other hand, pretreatment with indomethacin and aspirin, inhibitors of cyclooxygenase, inhibited bradykinin-induced oxidation of DCFH. These findings suggest that bradykinin increases intracellular Ca2+ and stimulates the generation of hydroxyl radical-like reactive oxygen species (scavenged by MPG or DMTU) via the cyclooxygenase pathway but not via the reaction of NO and superoxide anion.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"301-14"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18530938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Copper cytotoxicity impairs DNA synthesis but not protein phosphorylation upon growth stimulation in LEC mutant rat. 在LEC突变大鼠的生长刺激下,铜细胞毒性损害DNA合成,但不损害蛋白质磷酸化。
J K Kim, T Yamada, K Matsumoto
{"title":"Copper cytotoxicity impairs DNA synthesis but not protein phosphorylation upon growth stimulation in LEC mutant rat.","authors":"J K Kim,&nbsp;T Yamada,&nbsp;K Matsumoto","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Long-Evans Cinnamon (LEC) mutant rat, which possesses a genetic defect of the block of copper exclusion pathway in the hepatocytes, is a good model for studying the mechanism of cellular copper toxicity. We have examined effects of copper toxicity on DNA synthesis and protein phosphorylation upon growth stimulation by treating LEC rat primary-cultured hepatocytes with EGF and insulin. The proportion of DNA-synthesizing S-phase cells in LEC rat markedly decreased when compared to that of normal rat. However, the electrophoretic pattern and the signal intensity of 32P-labeled nuclear proteins in LEC rat were indistinguishable from those of normal rat. These results suggest that a cellular event other than protein phosphorylation required for the initiation of DNA synthesis upon growth stimulation is impaired by copper cytotoxicity.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"363-6"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Vasodilator effects of clonidine on the mesenteric arterial beds in normotensive and spontaneously hypertensive rats. 可乐定对正常血压和自发性高血压大鼠肠系膜动脉床的血管舒张作用。
K Kamata, T Numazawa, Y Kasuya
{"title":"Vasodilator effects of clonidine on the mesenteric arterial beds in normotensive and spontaneously hypertensive rats.","authors":"K Kamata,&nbsp;T Numazawa,&nbsp;Y Kasuya","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Clonidine, an alpha 2-agonist, caused a concentration-dependent vasodilation of the mesenteric arterial beds in both normotensive and hypertensive rats. The clonidine-induced vasodilation was inhibited by NG-nitro-L-arginine, and the inhibition was reversed by L-arginine. The concentration-dependent vasodilation was not significantly different between normotensive and hypertensive rats. These results suggest that clonidine has an endothelium-dependent vasorelaxant action in the resistance artery such as rat mesenteric arterial bed, and the endothelium-dependent vasodilator effects of clonidine in the mesentery may be involved in the depressor effect of the drug.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"371-4"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Relationships between plasma levels of type-II phospholipase A2, PAF-acetylhydrolase, leukotriene B4, complements, endothelin-1, and thrombomodulin in patients with sepsis. 脓毒症患者血浆ii型磷脂酶A2、paf -乙酰水解酶、白三烯B4、补体、内皮素-1和血栓调节蛋白水平的关系
T Takakuwa, S Endo, H Nakae, T Suzuki, K Inada, M Yoshida, M Ogawa, K Uchida
{"title":"Relationships between plasma levels of type-II phospholipase A2, PAF-acetylhydrolase, leukotriene B4, complements, endothelin-1, and thrombomodulin in patients with sepsis.","authors":"T Takakuwa,&nbsp;S Endo,&nbsp;H Nakae,&nbsp;T Suzuki,&nbsp;K Inada,&nbsp;M Yoshida,&nbsp;M Ogawa,&nbsp;K Uchida","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We determined the plasma levels of type-II phospholipase A2 (type II PLA2), platelet-activating factor acetylhydrolase (PAFAH) leukotriene B4 (LTB4) and of several complements (C3a, C4a, and C5a), which are considered to be among the cytokines and eicosanoids involved in vascular endothelial disorders and that vary in concentration during sepsis. We investigated the relationship between those levels and those of ET-1 and TM levels in plasma. Plasma levels of type II PLA2, PAFAH, LTB4, C3a, C4a, ET-1, and TM at the time that sepsis was diagnosed in 30 patients were 218.3 +/- 179.9 ng/ml, 23.92 +/- 9.66 nmol/min/ml, 90.35 +/- 31.49 pg/ml, 838.73 +/- 2.30 pg/ml, 1951.46 +/- 1697.78 pg/ml, 6.98 +/- 4.08 pg/ml and 7.80 +/- 3.34 ng/ml, respectively. The C5a plasma level was below the limit of detection in all cases. There were significant correlations between type II PLA2 and ET-1 plasma levels (r = 0.39, p = 0.032) and C3a and ET-1 plasma levels (r = 0.60, p = 0.03). There were also significant correlations between type II PLA2 and TM levels in plasma (r = 0.76, p = 0.0017), PAFAH and TM plasma levels (r = 0.53, p = 0.037), LTB4 and TM plasma levels (r = 0.46, p = 0.016) and C4a and TM plasma levels (r = 0.58, p = 0.037). Results suggest that the elevation of type II PLA2, PAFAH, LTB4 and complement in plasma is involved in vascular endothelial disorders in patients with sepsis.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"271-81"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Inhibition of antigen-induced airway hyperresponsiveness in rats: effects of ozagrel (a thromboxane A2 synthase inhibitor) and of CV-3988 (a platelet activating factor antagonist). 抑制大鼠抗原诱导的气道高反应性:奥扎格雷尔(一种血栓素A2合成酶抑制剂)和CV-3988(一种血小板活化因子拮抗剂)的作用
M Misawa, Y Chiba
{"title":"Inhibition of antigen-induced airway hyperresponsiveness in rats: effects of ozagrel (a thromboxane A2 synthase inhibitor) and of CV-3988 (a platelet activating factor antagonist).","authors":"M Misawa,&nbsp;Y Chiba","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effects of ozagrel, a thromboxane A2 (TXA2) synthase inhibitor, and CV-3988, a platelet activating factor (PAF) antagonist, was investigated on the repeatedly antigenic challenge-induced airway hyperresponsiveness (AHR) in rats. Rats were actively sensitized with DNP-Ascaris antigen and received 3 inhalations of antigen (challenges) or saline (sensitized control) every 48 hr. These animals were also pretreated with ozagrel (100 mg/kg, p.o., 30 min before), CV-3988 (3 mg/kg, i.v., 5 min before) or respective vehicle (water and saline, respectively) before each inhalation of antigen or saline. The in vivo airway responsiveness to cumulatively inhaled acetylcholine (ACh; 0.001-0.03%, each for 3 min) was measured 24 hr after the last inhalation of antigen or saline under anesthesia. A marked AHR was observed after repeated antigenic challenge when compared with the sensitized control group (5.5-9.5 times in order). This AHR was significantly, but partly, attenuated by pretreatment with ozagrel although this treatment alone had no effect on the airway responsiveness to inhaled ACh in sensitized control animals. On the other hand, CV-3988 had no inhibitory effect on this AHR. These findings suggest that TXA2, but not PAF, is one of the most important mediators participating in the pathogenesis of the antigen-induced AHR in rats.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"341-9"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Effects of the intracerebroventricular administration of ketamine on centrogenic arrhythmias in anesthetized rats. 脑室注射氯胺酮对麻醉大鼠心源性心律失常的影响。
A Filippelli, B Cuparencu, M Falciani, V de Novellis, L Safta, V Arustei, F Rossi
{"title":"Effects of the intracerebroventricular administration of ketamine on centrogenic arrhythmias in anesthetized rats.","authors":"A Filippelli,&nbsp;B Cuparencu,&nbsp;M Falciani,&nbsp;V de Novellis,&nbsp;L Safta,&nbsp;V Arustei,&nbsp;F Rossi","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In urethane anesthetized rats the icv (lateral cerebral ventricle) administration of ketamine, at the highest utilized doses, induced bradypnea and sinus bradycardia in spontaneously breathing rats. Moreover, it partially antagonized the arrhythmogenic activities of sodium glutamate and sodium aspartate, as well as desipramine and ouabain. From these results, we conclude that ketamine had an inhibitory effect on the centrogenic arrhythmias not only acting at the level of NMDA subtype receptor, but also at beta 1 adrenergic central receptors. Moreover at high doses, ketamine can also induce centrogenic arrhythmias in spontaneously breathing rats.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 3","pages":"331-40"},"PeriodicalIF":0.0,"publicationDate":"1994-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18935579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Dynamics of hepatic collagen synthesis and intracellular degradation of newly synthesized collagen during chronic carbon tetrachloride-induced liver injury in rats. 慢性四氯化碳肝损伤大鼠肝胶原合成动态及新合成胶原细胞内降解。
M Koda, Y Murawaki, H Yamamoto, H Kwasaki
{"title":"Dynamics of hepatic collagen synthesis and intracellular degradation of newly synthesized collagen during chronic carbon tetrachloride-induced liver injury in rats.","authors":"M Koda,&nbsp;Y Murawaki,&nbsp;H Yamamoto,&nbsp;H Kwasaki","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To clarify the significance of intracellular degradation of newly synthesized collagen during the progression of hepatic fibrosis, we measured the intracellular degradation of newly synthesized collagen at 2, 4 and 8 weeks after the administration of CCl4, together with the measurement of collagen synthesis and serum prolyl hydroxylase concentration. Hepatic collagen synthesis and serum prolyl hydroxylase concentration did not change until 4 weeks after the CCl4 administration, but was increased significantly at 8 weeks. Intracellular degradation of newly synthesized collagen was significantly increased at 2 weeks, was unchanged at 4 weeks, and was significantly decreased at 8 weeks compared with the individual control. The percentage of the intracellular degradation relative to the total amount of collagen synthesis did not change at 2 and 4 weeks, but was significantly decreased at 8 weeks, compared with the controls. These results suggest that the intracellular degradation system may prevent an accumulation of collagen at the early stage of hepatic injury, whereas at the stage of hepatic fibrosis, the combination of an increase in collagen synthesis and a reduction of intracellular degradation may lead to a rapid accumulation of collagen.</p>","PeriodicalId":21140,"journal":{"name":"Research communications in chemical pathology and pharmacology","volume":"84 2","pages":"233-44"},"PeriodicalIF":0.0,"publicationDate":"1994-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19083977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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