首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 15 毫秒
1.
The effect of oxidative stress on the process of spermatogenesis in terms of hsp70 expression was studied. For creating different oxidative stressed mice, three selenium (Se) levels viz., deficient (group I), adequate (group II) and excess (group III) were fed for 8 weeks in a yeast-based diet. After completion of diet feeding, Se level was significantly decreased in group I and significantly increased in group III, as compared to group II. Glutathione peroxidase (GSH-Px) activity was significantly decreased in both liver and testis in group I animals; however, the activity was comparable in groups II and III. Significant increase in the testis glutathione-S-transferase (GST) activity was observed in group I. No change was seen in group III, when compared to group II. Histological analysis of testis revealed a significant decrease in the germ cell population in group I, as compared to group II, with a predominant effect on spermatid and mature sperm numbers. In group III, displacement of germ cell population was observed. ELISA assays for hsp70 level showed increase in group I as compared to group II, whereas no significant change was observed in group III, as compared to group II. Immunohistochemical analysis revealed intense localization of hsp70 only in spermatid and sperm cells. The expression in groups II and III was homogeneous with slightly increased expression around lumen in group III. The data indicate that excessive oxidative stress in Se deficient group, affects the spermatogenesis process, especially affecting the mature sperm number which in turn leads to infertility.  相似文献   

2.
目的应用手持激光器作为光源建立光化学法局灶性脑梗死动物模型。方法将36只SD大鼠随机分为4组,即A组:开骨窗至硬脑膜,不注射玫瑰红,手持激光器照射5rain;B组:开骨窗至硬脑膜,注射玫瑰红,手持激光器照射5min;C组:保留颅骨内板,注射玫瑰红,手持激光器照射5min;D组:开骨窗至硬脑膜,注射玫瑰红,冷光源照射40rain。于术后24、48h对各组大鼠进行神经功能的行为学评分,进行MR扫描,术后48h处死动物,TTC染色测量梗死体积,光镜下观察病理改变,比较各组的模型制作成功率。结果不同方法进行动物模型制作时,24h神经功能的行为学评分有显著性差异,48h后差异消失。头部MR扫描显示,A组未见脑梗死形成,B组、c组全部有脑梗死灶形成,D组仅部分大鼠形成梗死灶,但体积明显较B、C组小,另外C组有2例合并硬膜外血肿。TTC染色A组未见梗死灶形成,B组、C组可见恒定的梗死灶,D组仅部分形成梗死灶。B、C、D组模型制作成功率分别为100%、80%、50%,将B组、C组合并为手持激光器组,与冷光源组(D组)比较,两种方法间有显著性差异(P=0.026)。结论应用手持激光器作为照射光源与冷光源相比,有更高的模型制作成功率。  相似文献   

3.
Crowded tadpoles in a limited volume grow to divide into two groups, a normally growing group and a stunted group, even if there are a plenty of food. This phenomenon was found to be interpreted by a model involving a mutual inhibition of the growth among individuals. It was assumed that the growth curve of an individual was modelled by a Gompertz growth equation. Through mathematical analysis and computer simulation of the model, it was shown that the average growth rate of the group was a decreasing function of the population density and that the group segregated into two subgroups, a normally growing group and a stunted group in a certain range of density. A theoretical prospect that the population of normally growing group is proportionate to the volume of the aquarium was obtained.  相似文献   

4.
目的:探讨miR-34a在幼鼠海马神经元细胞增殖凋亡中的作用。方法:分离幼鼠海马神经元细胞,转染miR-34a抑制剂(miR-34a inhibitor)、抑制剂对照(inhibitor control)、miR-34a模拟物(miR-34a mimics)、模拟物对照(mimics control),RT-PCR检测细胞中miR-34a表达水平。MTT检测转染后细胞增殖情况。流式细胞仪检测细胞凋亡情况。Western blot检测细胞中Cleaved-caspase-3、Bcl-2、Bax的表达水平。结果:转染miR-34a inhibitor可以抑制miR-34a的表达,miR-34a mimics可以促进miR-34a的表达。miR-34a mimics对细胞增殖抑制率明显高于mimics control组(P0.05),miR-34a inhibitor组抑制率明显低于inhibitor control组(P0.05)。miR-34a inhibitor组神经元细胞凋亡率明显低于inhibitor control组(P0.05),miR-34a mimics组神经元细胞凋亡率明显高于mimics control组(P0.01),inhibitor control组和mimics control组神经元细胞凋亡率差异不显著(P0.05)。miR-34a inhibitor组Cleaved-caspase-3、Bax蛋白表达量低于inhibitor control组,差异显著(P0.05);miR-34a inhibitor组Bcl-2蛋白表达量高于inhibitor control组,差异显著(P0.05);miR-34a mimics组Cleaved-caspase-3、Bax蛋白表达量高于mimics control,差异显著(P0.05);miR-34a mimics组Bcl-2蛋白表达量低于mimics control,差异显著(P0.05)。结论:miR-34a抑制海马神经元细胞增殖,促进细胞凋亡,其作用机制可能与调控Cleaved-caspase-3、Bcl-2、Bax表达有关。  相似文献   

5.
Birth rate and immature survival rate in group living primates have been predicted to vary as a function of group size. These predictions were tested with data from a wild population of lion-tailed macaques in the Anamalai Wildlife Sanctuary, Tamil Nadu (India). Group size and composition, births, and mortality were monitored from eight groups for one to six years. The rate of growth of groups, birth rate, and survival rate were examined in relation to group size. The rate of growth of a group was a decreasing function of group size. Birth rate was also a decreasing function of group size and the number of adult females in the group. The sample size for survival rate of adults was too small to test for their dependence on group size. Immature survival was independent of group size, but the analysis was based on a very small sample. It is possible that the nature of dependence of net growth rate, birth rate, and survival rate on group size could be different outside the range of group sizes on which the analysis was based. The stronger relationship between birth rate and group size in the lion-tailed macaque, in relation to other primates, might be the result of its low birth rate as well as the relatively low temporal variation in resources in the rain forest. Limited data available from other sites indicate that the observed relationship between birth rate and group size might be spatially stable.  相似文献   

6.
摘要 目的:研究miR-124和MAPK/ERK途径对脑梗死大鼠神经细胞凋亡的影响及其可能的机制。方法:本研究将SD大鼠随机分为假手术组(Sham组)、模型组(CI组)、miR-124组(miR组)、脑梗死+miR-124组(CI+miR组)和脑梗死+MEK/ERK阻滞剂组(CI+U0126组),采用mNSS评分法评估大鼠神经功能损伤程度,采用TTC染色检测脑梗死体积,采用尼式染色检查脑组织的病理情况,采用TUNEL染色法检测大鼠脑神经细胞凋亡,TRIzol法提取总RNA,RT-PCR检测miR-124、ERK1和ERK2基因表达,蛋白质免疫印迹法检测Caspase-3、Bax、Bcl-2、MEK2和ERK1蛋白表达水平。结果:与Sham组和miR组相比,CI组、CI+miR组和CI+U0126组大鼠的脑梗死体积、mNSS评分和脑含水量均显著增加(P<0.01)。Sham组、miR组、CI+miR组和CI+U0126组大鼠的脑组织中尼式体的数量显著高于CI组,模型组大鼠的脑神经元结构被破坏且出现核移位和细胞坏死等病理变化;与Sham组和miR组相比,CI组大鼠中miR-124的表达水平显著降低(P<0.01),CI+miR组和CI+U0126组大鼠中miR-124的表达水平显著上调(P<0.01)。TUNEL染色结果显示,与模型组相比,CI+miR组和CI+U0126组大鼠中凋亡数量显著减少(P<0.01),ERK1和ERK2的mRNA相对表达水平均显著下调(P<0.01)。与模型组相比,CI+miR组和CI+U0126组大鼠脑组织中Caspase-3和Bax蛋白表达水平显著下调,Bcl-2蛋白的表达水平显著上调(P<0.01)。与模型组相比,CI+miR组和CI+U0126组大鼠脑组织中磷酸化的p-MEK-2和p-ERK1/2蛋白表达水平均显著下调(P<0.01)。结论:miR-124可能通过抑制MAPK/ERK信号通路的激活,减少脑梗死大鼠的神经细胞的凋亡,最终发挥保护作用。  相似文献   

7.
为探讨小球藻保护大鼠运动因运动造成的心肌损伤,为小球藻科学合理的应用和推广提供理论依据,本研究将60只SD大鼠随机分为5组:对照组(C组)、运动对照组(S组)、运动+低剂量小球藻组(SCL组)、运动+高剂量小球藻组(SCH组),每组12只大鼠。所有参与实验的大鼠每天自由饮水择食,小球藻的摄入采用灌胃器每日灌胃一次。小球藻各组灌胃体积为5 m L/kg,其他组灌入等量生理盐水。安静对照组(C组)笼内自由活动,不进行额外运动,运动对照组(S组)、运动+低剂量小球藻组(SCL组)、运动+高剂量小球藻组(SCH组)进行8周的跑台跑步训练,每周6次。1~4周进行中等强度训练,5~8周进行高强度训练。本研究发现,在大鼠血清谷丙转氨酶、乳酸脱氢酶、肌酸激酶、α-羟丁酸脱氢酶含量水平,S组较C组均显著升高(p<0.05)。血清谷丙转氨酶、乳酸脱氢酶、肌酸激酶含量,SCL组和SCH组显著低于S组(p<0.05),SCL组和SCH组组间无显著性差异(p>0.05),且随剂量增加而递减。鼠心肌SOD活性方面,S组显著低于C组(p<0.05);SCL组和SCH组显著高于S组(p<0.05),组间随剂量增加而递增;SCH组显著高于SCL组(p<0.05)。血清、心肌CGRP水平,S组显著低于C组(p<0.05);SCL组和SCH组显著低于S组均显著降低(p<0.05)。本研究认为摄入小球藻能够有效消除机体由于长期高强度大负荷运动下产生的过量的自由基;提高机体免疫力,增强血管原生性一氧化氮合酶活性。  相似文献   

8.
黑龙江东部马鹿集群行为的初步观察   总被引:7,自引:2,他引:5  
张明海  钟立成 《兽类学报》1992,12(4):243-247
本文根据野外观察到的112群马鹿,初步研究了马鹿的集群行为。野生鹿群大小范围为2—19头,平均群内头数为3.55,鹿群在各季节具有明显的变化。通过对3种类型鹿群的观察分析,发现母仔群是主要的鹿群类型,该类型在各季节中所占比例较大(26%—53%),且在产仔期和哺乳期群内分化较高。而在妊娠期群内分化较低。公鹿群在全年比较稳定,混合群在各季节变化较大,每群平均数4.58头,为3种鹿群类型中最大者。  相似文献   

9.
目的:探讨人参皂甙Rb1(GRb1)对香烟烟雾诱导的大鼠神经细胞凋亡和细胞内Ca^2±浓度的影响。方法:雄性Wistar大鼠48只,随机分为对照组、吸烟组和GRb1组,每组16只。吸烟组和GRbI组连续吸烟12周制作吸烟大鼠模型,期间每周给予GRb1组和吸烟组大鼠分别腹腔注射40mg/kg的GRb1和等量生理盐水,对照组不做任何处理。提取大鼠大脑皮层组织,TUNEL法检测各组细胞凋亡情况,荧光分光光度法检测细胞内Ca^2±浓度变化情况。结果:TUNEL法检测表明,未经香烟烟雾处理的对照组大鼠大脑皮层细胞自然凋亡率为2.54±0.92个/视窗。连续吸烟12周,吸烟组大鼠大脑皮层细胞凋亡率较对照组显著升高,达20.62±2.13个/视窗(q=35.72,P〈0.01)。GRb1组细胞凋亡率虽也有增加,为11.48±2.37个/视窗,明显低于吸烟组(q=15.39,P〈0.01)。对照组、吸烟组和GRb1组大鼠大脑皮层细胞内Ca^2±浓度分别为236.62±12.52ng/L、636.37±18.63ng/L和353.61±13.72ng/L.GRb1组Ca^2+浓度显著低于吸烟组(q=54.73,P〈0.01)。结论:GRb1对吸烟大鼠脑损伤的保护作用可能与抑制细胞内的Ca^2+超载、降低香烟烟雾诱导的神经细胞凋亡有关。  相似文献   

10.
We investigated the effect of prostaglandin E1 on human polymorphonuclear leukocytes, in vivo. Polymorphonuclear leukocytes of a prostaglandin E1 and placebo study group were harvested and their function, as production of oxygen-derived metabolites and adherence to human cultured endothelial cells, was compared. Additionally, data obtained from polymorphonuclear leukocytes of a prostaglandin E1 and placebo group were compared with data obtained from polymorphonuclear leukocytes from 28 blood donors, who served as a control group. Production of oxygen-derived metabolites by polymorphonuclear leukocytes during contact with endothelial cells was measured by chemiluminescence. Chemiluminescence was significantly (p < 0.01) increased in the placebo group in comparison to the control group decreasing to values of control group after 6 d (post-trauma). Chemiluminescence response was not significantly suppressed in patients treated with prostaglandin E1 in comparison to the placebo group. Adherence of polymorphonuclear leukocytes (placebo group) to endothelial cells was significantly increased (p < 0.01) within the first 6 d post-trauma Following day 6, values were in the same range as values for the control group. Adherence was not significantly suppressed in patients treated with prostaglandin E1 in comparison to the placebo group. In conclusion, prostaglandin E1 at a dose of 20 ng/kg bw/min does not influence production of oxygenderived metabolites and adherence in polytraumatized patients in comparison to a placebo group. Additionally, production of oxygen-derived metabolites by polymorphonuclear leukocytes in response to endothelial cells is shown and it is evident that endothelial cells might influence production of oxygen derived metabolites by polymorphonuclear leukocytes.  相似文献   

11.
Pallial fluid buffering capacity of the sea mussel Mytilus galloprovincialis was investigated to establish the potential of this biological parameter to serve as a biomarker. Four groups of 15 animals were used in a 72-h toxicity test. Group 1, the aerobic control group, was placed in a filtered aerated natural seawater aquarium. Groups 2-4 were subjected to hypoxic conditions by removal from water after animals were injected with a single dose of the following: group 2 (anaerobic control) was administered 10 microl of UV-treated filtered natural seawater; group 3 (anaerobic solvent control) was injected with 10 microl of acetonitrile and group 4 (PAH exposed group) with 10 microl of 2 mM anthracene. Pallial fluid was taken from all the animals following seawater immersion or air exposure. Pallial fluid from each individual was extracted, adjusted to pH 5.0 and titrated with NaOH until reaching pH 6.0. The buffering capacity index (beta), defined as the amount of mu equivalents of NaOH needed to change in one unit the pH of a 5-ml sample of pallial fluid, was calculated for each group. Values were: for group 1, beta = 3.17 (+/- 0.782); for group 2, beta=15.713 (+/-2.992); group 3 was beta=18.124 (+/-2.288); and group 4 was beta=28.109 (+/-11.398). The statistically significant increase (P<0.05) in group 4 compared with the other groups indicates that the buffering capacity index (beta) is a worthy biological parameter to be further explored as a biomarker for ecotoxicological monitoring programs. The increase in buffering capacity is discussed and a biochemical link between anaerobic metabolism and the exposure to PAH is suggested to explain changes of this biological parameter.  相似文献   

12.
高凤娟  李丕鹏  陆宇燕 《蛇志》2016,(3):256-259
目的为了探究化肥磷酸二铵对两栖类幼体发育的影响。方法以花背蟾蜍(Bufo raddei)蝌蚪为研究对象,用化肥磷酸二铵(DAP)进行染毒培育,并依据Gosner(1960)分期标准,将蝌蚪分为G0实验组和G20实验组,分别暴露于浓度为0.045g/L、0.135g/L、0.225g/L的DAP水溶液中,直至蝌蚪完成变态发育,并对孵化率、死亡率、畸形率以及发育时程等参数进行统计分析。结果随着化肥DAP浓度的升高,孵化率逐渐下降,但对照组与各侵染组之间均无显著性差异;侵染组蝌蚪死亡率均高于对照组,均呈极显著性差异(P0.01),且G20侵染组明显高于G0侵染组;蝌蚪畸形可分为四大类,侵染组蝌蚪畸形率均高于对照组,且均呈极显著性差异(P0.01),畸形率随着DAP浓度的升高而增加;完成变态发育所用时程,侵染组明显长于对照组。结论化肥磷酸二铵对蝌蚪发育具有显著影响及损伤。  相似文献   

13.
基于熵权的北京城市生态系统健康模糊综合评价   总被引:51,自引:3,他引:51  
周文华  王如松 《生态学报》2005,25(12):3244-3251
采用基于熵权的模糊数学评价方法,借助于相对隶属度的概念评价了北京城市生态系统在某一特定时间内(1996~2003年)的相对健康状态。方法避免了主观判断城市生态系统健康标准的不确定性。评价结果表明:(1)1996~2003年,北京市相对健康状态整体呈上升趋势,最优年为2003年,最差年为1996年;(2)按照最大隶属度原则,人类健康要素的最大隶属度0.967(2002),生物群落的最大隶属度1.000(2003),社会的最大隶属度1.000(2003),经济的最大隶属度0.938(2003),人工环境的最大隶属度1.000(2003),自然环境的最大隶属度0.795(1998),自然与社会经济的相互作用的最大隶属度0.916(2002),对区域的影响的最大隶属度1.000(1996)。各评价要素的最大隶属度主要集中于2003年,其概率为37.5%。  相似文献   

14.
Lysinomicin, a naturally-occurring pseudodisaccharide, inhibits translation in prokaryotes. We report that lysinomicin (and three related compounds) are able to inhibit the self-splicing of group I introns, thus identifying pseudodisaccharides as a novel class of group I intron splicing inhibitors. Lysinomicin inhibited the self-splicing of the sunY intron of phage T4 with a Ki of 8.5 microM (+/- 5 microM) and was active against other group I introns. Inhibition was found to be competitive with the substrate guanosine, unlike aminoglycoside antibiotics, which act non-competitively to inhibit the splicing of group I introns. Competitive inhibitors of group I intron splicing known to date all contain a guanidino group that was thought to be required for inhibition; lysinomicin lacks a guanidino group.  相似文献   

15.
为了探讨白芍总苷治疗干燥综合征的作用机制,本实验以BALB/c小鼠为正常对照组,将8周龄雌性NOD小鼠24只随机分为模型组、羟氯喹组、白芍总苷组、联合组,每组各6只,白芍总苷组每日灌胃白芍总苷稀释液0.4 mL,羟氯喹组每日灌胃羟氯喹稀释液0.4 mL,联合组每日灌胃白芍总苷+羟氯喹稀释液0.4 mL,模型组和正常组灌...  相似文献   

16.
酪酸梭菌活菌散治疗婴幼儿病毒性腹泻疗效观察   总被引:1,自引:0,他引:1  
目的观察和评价酪酸梭菌活菌散治疗婴幼儿病毒性腹泻的临床疗效。方法将200例病毒性腹泻患儿随机分为观察组和对照组。观察组120例,服用酪酸梭菌活菌散,首次1 000 mg,以后500 mg/次,4次/d,疗程3~7 d,对照组80例,应用蒙脱石散治疗,观察疗效和不良反应。结果观察组总有效率为92.5%,对照组总有效率为71.25%,差异有统计学意义(P<0.01)。结论酪酸梭菌活菌散治疗婴幼儿病毒性腹泻疗效显著,且未见不良反应,值得临床推广应用。  相似文献   

17.
Choi JH  Rhee IK  Park KY  Park KY  Kim JK  Rhee SJ 《Life sciences》2003,73(12):1479-1489
The purpose of this study was to investigate the effects of green tea catechin on bone metabolic disorders and its mechanism in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100+/-10 g were randomly assigned to one control group and three cadmium-poisoned groups. The cadmium groups included a catechin free diet (Cd-0C) group, a 0.25% catechin diet (Cd-0.25C) group and a 0.5% catechin diet (Cd-0.5C) group according to their respective levels of catechin supplement. After 20 weeks, the deoxypyridinoline and crosslink values measured in urine were significantly increased in the Cd-0C group. Cadmium intoxication seemed to lead to an increase in bone resorption. In the catechin supplemented group (Cd-0.5C group), these urinary bone resorption marks, were decreased. The serum osteocalcin content in the cadmium-poisoned group was significantly increased as compared with the control group. In the catechin supplemented group serum osteocalcin content values were lower than the control group. The cadmium-intoxicated group (Cd-0C group), had lower bone mineral density than the control group (total body, vertebra, pelvis, tibia and femur). The catechin supplement increased bone mineral density to about the same as the control group. Bone mineral content showed a similar trend to total bone mineral density. Therefore, the bone mineral content of the Cd-0C group at the 20th week was significantly lower than the control group. The catechin supplemented group (Cd-0.5C group) was about the same as the control group. The cause of decreasing bone mineral density and bone mineral content by cadmium poisoning was due to the fast bone turnover rate, where bone resorption occurred at a higher rate than bone formation. The green tea catechin aided in normalizing bone metabolic disorders in bone mineral density, bone mineral content and bone calcium content caused by chronic cadmium intoxication.  相似文献   

18.
We investigated the histopathological effects of methotrexate (MTX), a chemotherapeutic agent, and beta glucan (BG), an antioxidant, on rat testis. We used four groups of Sprague-Dawley male rats: MTX, MTX + BG, BG, and control. The MTX group was exposed to a single dose of MTX on the first day of experiment. The MTX + BG group was exposed to a single dose of MTX and BG on the first day of experiment followed by BG for 4 additional days. The BG group was exposed to BG for 5 days. The control group was given saline for 5 days. On day five, all animals were sacrificed and testicular tissue was evaluated for histopathology and the terminal deoxynucleotidyl transferase (TdT) deoxyuridine triphosphate nick-end labeling assay (TUNEL) was used to detect apoptosis. The apoptotic index (AI) and testicular damage increased in the MTX group compared to the other three groups. Histopathology was reduced in the MTX + BG group compared to the MTX group. Seminiferous tubule diameter was reduced in the MTX group compared to the BG group; we found no difference between control and BG groups. The thickness of th e germinal epithelium was reduced in the MTX group compared to the other groups. We found no difference in testicular weight among the groups. We compared body weight before and after the experiment; weights in the MTX and MTX + BG groups were significantly reduced compared to controls. In the control groups, we found a statistically significant increase in body weight, whereas there was no change in the BG group. We found that MTX causes deleterious effects on testicular tissue and that beta glucan may be protective.  相似文献   

19.
建立大脑中动脉闭塞(model of middle cerebral artery occlusion,MCAO)大鼠模型,研究阿加曲班对大鼠不同时间脑缺血再灌注损伤血小板功能的影响。将120只健康雄性SD大鼠随机分为假手术组(Sham)、模型组(Model)和阿加曲班给药组(Argatroban),其中Argatroban组分为4组:Argatroban+30 min组、Argatroban+1 h组、Argatroban+3 h组和Argatroban+7 h组,Sham组和Model组40只,其余各组每组10只。线栓法制备大鼠MCAO模型,术中输注Argatroban,剂量为0.3μg·kg^-1·min^-1,完成手术前5 min停止输注。手术完成后,Sham组和Model组分别于术后30 min、1 h、3 h和7 h处死10只取样;Argatroban给药组5个时间点处死取样。检测大鼠血浆血细胞数量,并计数骨髓有核细胞数的变化。采用流式细胞仪检测血小板-白细胞聚集体(platelet-leukocyte aggregates,PLA)表达水平,观察活化部分凝血活酶时间(activated partial thromboplastin time,APTT)、血小板计数变化,ELISA检测血浆D-二聚体和TAT。结果显示,与Sham组相比,Model组大鼠的红细胞(RBC)、白细胞(WBC)、血红蛋白含量(HGB)和中性粒细胞(GR)数都显著升高(p<0.05),且与给药组没有统计学差异。Sham组、Model组和Argatroban给药组的骨髓有核细胞数也没有统计学差异。与Sham组相比,Model组PLA表达水平极显著升高(p<0.01),Argatroban+30 min组PLA表达水平却低于Sham组,但没有统计学差异,Argatroban+1 h组高于Sham组和Argatroban+30 min组(p<0.05),Argatroban+3 h组和Argatroban+7 h组高于Argatroban+1 h组低于Sham组。术后各组的血小板计数均高于Sham组(p<0.05),Argatroban各组的血小板计数要低于Model组(p<0.05),并在30 min时达到最低,30 min以后血小板升高,但是1 h以后血小板不再升高,趋于稳定。Argatroban各组PT和APTT虽略有降低,但是与Sham组和Model组并没有统计学差异。造模后各组TAT、D-二聚体水平显著升高,Argatroban各组TAT水平较模型组明显降低(p<0.05),Argatroban+30 min组水平最低。MCAO模型大鼠血液呈现高凝状态,凝血功能和纤维蛋白溶解功能亢进,血小板活化增强,阿加曲班可对此起到改善作用。  相似文献   

20.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号