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time of recovery
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  恢复时间
     The time of recovery of renal function in basiliximab group(4.7±s 2.1) d was earlier than that in OKT3 group (9±5) d (P< 0.05).
     巴利昔单抗组肌酐恢复时间(4.7±s2.1)d,明显短于OKT3组(9±5)d(P<0.05)。
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     The average time of recovery of bowel activity was 3.5 (2-5)days, 3.4 (2-5) days and that for oral intake was 4.5(3-6) days after operation.
     术后病人平均胃肠功能恢复时间为3.5(2~5)d,下床活动时间为3.4(2~5)d,进流质时间4.5(3~6)d;
短句来源
     The response time of the system is 5 s and the time of recovery is shorter than 10 s.
     该系统的响应时间仅为 5 s,恢复时间在 10 s之内
短句来源
     The responding time of the system is 5 s and the time of recovery is within 10 s.
     该系统的响应时间仅为 5 s,恢复时间在 10 s之内
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     Multiplicity logistic regression model analysis showed time of recovery to EEG and duration of seizures were the risk factors of secondary epilepsy after viral encephalitis (P < 0.05).
     Logistic回归分析显示惊厥持续时间及EEG恢复时间为病毒性脑炎继发癫癎的危险因素(P<0.05)。
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  “time of recovery”译为未确定词的双语例句
     The time of recovery from anesthesia was between 3.2 and 35.5 min,with the average being 7.9 min.
     麻醉时间为3.2~35.5min,平均为7.9min。
短句来源
     C group were treated with Bifid Triple Viable Powderand semecta. Then the effect of tree groups were compared. Results The cured rate of three groups were 63.33%,66.67%,93.33%,the time of recovery were(75.21±3.28)h,(73.33±5.05)h,(57.51±5.72)h,respectively.
     结果A、B、C组的总有效率分别为63·33%、66·67%、93·33%,平均止泻时间分别为(75·21±3·28)h、(73·33±5·05)h、(57·51±5·72)h。
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     The time of recovery to the normal platelet count was 1 31 days (median 6 days) in the control cycle, and 0 13 days (median 2 days) in the treatment cycle ( P =0.00).
     从出现血小板最低值到恢复正常的天数,对照周期中位值为6(1~31)d,治疗周期为2(0~13)d,差异有统计学意义(P=0.00)。
短句来源
     Results: The cured rate of treatment group was 92.4%,and of the control group was 73.3%. The time of recovery was(48.92 ± 3.02) h and(100.23 ± 3.16) h,respectively. There was a statistic difference(P < 0.05).
     结果:治疗组和对照组的总有效率分别为92.4%和73.3%,平均止泻时间分别为(48.92±3.02)d和(100.23±3.16)d,差异有统计学意义(P<0.05)。
短句来源
     The indication,choice of temperature,duration of mild hypothermia and time of recovery,monitoring,treatment of complication were discussed.
     结合治疗体会,讨论了亚低温治疗的适应症、温度的选择、亚低温持续的时间和复温时机、亚低温治疗的监测和辅助治疗及其并发症的处理。
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  相似匹配句对
     Time
     时间(英文)
短句来源
     Time
     时间
短句来源
     THE FROM OF TIME
     时间的形状 从多丽丝·塞尔萨多的作品谈材料处理与时间体验
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     In the Eye of Time
     光阴的眼中
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     Recovery of "the Other"
     “他者”的复苏
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  time of recovery
Analysis of qI (photoinhibition dependent quenching) showed that the half-time of recovery of qI increases steeply below an Fv/Fm of 0.65.
      
Two non-dimensional parameters, determining the dynamics of the model, are T, the ratio of the disturbance interval to the time of recovery and S, the ratio of the size of the disturbance to the size of the landscape.
      
Both d-methionine and gold chloride accelerated the time of recovery from glutamate-induced motility impairment, possibly through their antioxidant activities.
      
Both d-methionine and gold chloride accelerated the time of recovery from glutamate-induced motility impairment, possibly through their antioxidant activities.
      
The putrescine-catabolizing ability returns with a half-time of recovery of 15-18 h, corresponding to the estimates ofShaff andBeaven [36] for recovery of intestinal DAO activity following administration of heparin or cycloheximide.
      
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Male and female mice treated with a dose of antabuse (120 mg/kg, p.o.) 2—12 hours beforehand slept longer than control animals after an injection of pentobarbital. Similar but less pronounced effects were observed in rats. The initial prolongation of pentobarbital sleeping time was not followed by a late shortening of the duration of the hypnotic action as had been shown in the case of SKF-525A. The whole-body levels of pentobarbital in antabuse-treated mice were significantly higher than those in the untreated...

Male and female mice treated with a dose of antabuse (120 mg/kg, p.o.) 2—12 hours beforehand slept longer than control animals after an injection of pentobarbital. Similar but less pronounced effects were observed in rats. The initial prolongation of pentobarbital sleeping time was not followed by a late shortening of the duration of the hypnotic action as had been shown in the case of SKF-525A. The whole-body levels of pentobarbital in antabuse-treated mice were significantly higher than those in the untreated control animals 1 hour after pentobarbital administration. This suggests that the rate of biotransformation of pentobarbital was lowered by antabuse administration. On the other hand, at the time of recovery from narcosis, the whole-body levels of pentobarbital in mice pretreated wikh antabuse were not significantly different from those in control animals. The fact that neither the ED-50 of pentobarbital action, nor the diethylbarbital (a drug not metabolized in vivo) sleeping time was changed by antabuse administration offers further evidence against a central action of antabuse. The effects of antabuse on the rate of biotransformation of pentobarbital, chlorpromazine and p-nitrobenzoic acid were also studied using rat liver slices. The concentration of antabuse that produced 50 por cent inhibition of pentobarbital metabolism was found to be 6.9×10~(-5) M. Only a slight inhibition of chlorpromazine metabolism was observed while no inhibition of p-nitrobenzoic acid biotransformation was obtained when antabuse was added up to a concentration of 2×10~(-4)M. The inhibitory effect of antabuse on pentobarbital metabolism was not antagonized by glutathione, cysteine or ascorbic acid. Kinetic studies suggest that the inhibition was competitive in nature. When an oral does of 120 mg/kg was given to mice 2 hours previously, antabuse was found to decrease the hepatic glycogen content. Practically no change of liver ascorbic acid level was observed 2—72 hours after antabuse administration.

在給予小鼠安他布斯(120毫克/公斤,口服)2小时后,戊巴比妥鈉睡眠时間显著延长,同时肝糖元含量下降;24小时后作用消失。由于本药能延緩戊巴比妥鈉自小鼠体內消失而不改变維持动物睡眠所必須的最低催眠药水平,可見安他布斯这种“延长”效应是因为抑制了催眠药的生物轉化,而并非通过中樞协同机制。安他布斯并不改变小鼠戊巴比妥鈉的ED_(50)及二乙基巴比妥(一个在体內不經轉化的催眠药)睡眠时間,也支持这个論断。大鼠体外肝切片試驗表明,当安他布斯濃度为6.6×10~(-5)M时即抑制戊巴比妥鈉轉化的50%。安他布斯对药酶的抑制作用属于竞爭性,谷胱甘肽、半胱氨酸及維生素C不能对抗此作用。安他布斯对氯丙嗪的氧化影响不大,对对硝基苯甲酸的还原无抑制作用。

Thioacetamide is a hepatotoxic agent.In this paper,the effects of thioacetamide on the pentobarbital sleeping time and the rate of hepatic drug metabo- lism in mice and rats are reported. Mice treated with a dose of thioacetamide (60mg/kg s.c.) 48 hours prior to an in- jection of pentobarbital slept much longer than untreated animals.Similar results were obtained in rats treated 12-72 hours previous to injection.One hour after pentobarbital administration,whole-body levels of the hypnotic in thioacetamide-treated...

Thioacetamide is a hepatotoxic agent.In this paper,the effects of thioacetamide on the pentobarbital sleeping time and the rate of hepatic drug metabo- lism in mice and rats are reported. Mice treated with a dose of thioacetamide (60mg/kg s.c.) 48 hours prior to an in- jection of pentobarbital slept much longer than untreated animals.Similar results were obtained in rats treated 12-72 hours previous to injection.One hour after pentobarbital administration,whole-body levels of the hypnotic in thioacetamide-treated mice were significantly higher than those in control animals.The rate of biotransformation of pentobarbital in vitro by liver slices from rats pretreated with thioacetamide was found to be less rapid than those from control animals.These facts indicate that the hepatic metabolism of pentobarbital was lowered by thioacetamide pretreatment,and thus may explain,at least in part,the prolonging effect of thioacetamide on pentobarbital sleeping time.On the other hand,at the time of recovery from narcosis,the whole body levels of pentobarbital in thioacetamide pretreated mice as well as the concentrations of bar- biturate in the brain of rats pretreated similarly,were significantly lower than those in control animals.In addition,it was found that the ED-50 of pentobarbital action was decreased,and that the diethylbarbital sleeping time was increased by pretreatment with thioacetamide.It appears,therefore,that an extra-hepatic mechanism of the effect of thioacetamide on pentobarbital action is also involved. In in vitro experiments using liver slices from rats treated with thioacetamide 48 hours previously,only a slight decrease in the rate of metabolism of chlorpromazine was observed,while the rate of biotransformation of p-nitrobenzoic acid was not sig- nificantly affected.When added in vitro,thioacetamide was shown to exert no inhibitory effect on pentobarbital metabolism.The decrease in the pentobarbital-metabolizing ability of liver slices from rats pretreated with thioacetamide was found to correlate to a certain extent with the fall of hepatic glycogen and aseorbic acid contents,as well as with the histological changes induced by this hepatotoxic agent. Thioacetamide was shown not to block completely the shortening of phenobarbital sleeping time or the increase in hepatic aseorbio acid content induced by phenobarbital pretreatment.

给小鼠皮下注射硫代乙酰胺60毫克/公斤后48小时戊巴比妥钠睡眠时间明显延长;同剂量的硫代乙酰胺给大鼠后在12—72小时内戊巴比妥钠睡眠时间也都明显延长,而以48小时者最为明显。进一步实验发现48小时前接受一剂硫代乙酰胺处理的小鼠,戊巴比妥钠自体内消失的速率比正常动物者明显减慢;12—72小时前曾接受一剂硫代乙酰胺的大鼠肝切片转化戊巴比妥钠的速率比正常动物肝切片者小,此与戊巴比妥钠睡眠时间的延长相一致。可见,经硫代乙酰胺处理的动物的戊巴比妥钠睡眠时间延长的原因之一,是由于硫代乙酰胺抑制了肝脏对戊巴比妥钠的转化。另一方面,48小时前曾接受过硫代乙酰胺处理的小鼠,睡眠刚醒时,体内戊巴比妥钠含量明显地低于对照组;曾经硫代乙酰胺处理的大鼠刚醒时,脑组织的戊巴比妥钠含量明显低于对照组者。在经硫代乙酰胺处理后的小鼠,戊巴比妥钠引起睡眠的 ED_(50)明显减小;二乙基巴比妥钠的睡眠时间亦明显延长。这些结果说明硫代乙酰胺处理也增加了动物中枢对戊巴比妥类药物的敏感性。

110 patients under three years of age with pneumonia were admitted to this hospital in a period from August of 1982 to March of 1983. There were 68 males and 42 females. The patients were randomly divided into Group A and Group B .The symptoms and signs, the laboratory data, and the severity and duration of the illness of the patients of both groups were similar.After admission, laboratory examinations including WBC counts, throat swab cultures and determinations of immunity function were performed and chest...

110 patients under three years of age with pneumonia were admitted to this hospital in a period from August of 1982 to March of 1983. There were 68 males and 42 females. The patients were randomly divided into Group A and Group B .The symptoms and signs, the laboratory data, and the severity and duration of the illness of the patients of both groups were similar.After admission, laboratory examinations including WBC counts, throat swab cultures and determinations of immunity function were performed and chest x-ray films were taken for all the patients. Regular treatments were given to all of them but the patients of Group A received TDP radiation in addition.After comparing the clinical courses of the two groups, the authors found that TDP could cause more rapid disappearance of cough and moist rales in the lungs, shorten the time of recovery and the whole course of hospitalization, and hasten the absorption of pulmonary infiltrations as seen from the x-ray films. Furthermore, TDP is helpful to promote the immunity function by raising many immune indices. And the rate of lymphocyte transformation was also increased. Its influence on the bringing down of the fever to normal is not very remarkable.It is concluded that TDP radiation is a simple, safe and effective treatment for pneumonia and it is suitable to be used in children.

以1982年8月~1983年3月间住院的小儿肺炎110例为对象,年龄3岁以下,男68例,女42例,随机分为甲、乙两组,每组各55例。 两组除按常规治疗外,甲组加用TDP,乙组不用TDP。并检测了白细胞计数,咽拭子培养,免疫功能测定和X线胸部照片。 从临床资料分析:治疗前两组的临床症状、体征、病情、病期基本相同,可比性较强。 治疗后结果:体温恢复正常时间两组差异不显著。咳嗽消失时间、肺湿罗音消失时间、治愈时间和总病程时间,治疗组均比对照组为短,有显著差异。X线完全吸收和吸收好转也明显优于对照组。免疫功能方面,治疗组免疫指标增加项目比对照组多。两组第二次淋巴细胞转化率治疗组明显高于对照组。 对比结果可见TDP有促进肺炎吸收,加速肺炎治愈的效果,并对免疫功能可能发生有利的影响。 TDP治疗方法简单、安全、有效,可作为治疗小儿肺炎的方法之一,加以推广使用。

 
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