Peripheral nerve phospholipids in acrylamide neuropathy

Treatment of cats with acrylamide, either 7.5 or 15 mg/kg IM, once a day for 10 days, resulted in increases of 31 and 47% in the phospholipid content of sciatic nerve, respectively, from a control level of 41.1±2.7 mg/kg wet weight. Determination of the distribution of individual phospholipids indicated no significant differences between control cats and those receiving a cumulative dose of 150 mg/kg acrylamide. In a separate experiment, cats were treated with the 150 mg/kg dose of acrylamide and the sciatic nerve was divided into proximal and distal portions at the level of the triceps surae nerve. Significant increases in phospholipid content were observed in both the proximal and distal portions of peripheral nerve of the acrylamide-intoxicated cats. This effect was present even when the phospholipid content was expressed in terms of total protein, dry weight or total lipid. Total weight of nerve segments, however, was significantly decreased in the neuropathic animals. The data are consistent with a focal degeneration of axons with relative sparing of phospholipids.This work was supported by U.S. Public Health Service NIH Grant NS-11948, ES-02405 and 5-S07 RR05393 (Biomedical Research Support)     

Effects of ganglioside therapy on experimental CS2 neuropathy

Both in animals and in man the inhalation of CS2 vapor induces a chronic polyneuropathy with primary lesions in the axons of peripheral nerves. Since it was reported in several studies that the administration of gangliosides improves nerve regeneration and the functional recovery of nerves damaged by section as well as cryodegeneration, a study was undertaken to evaluate the effects of bovine-brain gangliosides administration on the experimental CS2 neuropathy in the rat. One hundred and fifty male rats were intoxicated with CS2 by a discontinuous inhalation exposure to 700 ppm for 12 weeks until a clear neuropathy developed. Thereafter the animals were subdivided at random into five groups and treated in different ways: 10 mg/kg BW gangliosides, 0.5 mg/kg gangliosides, 0.5 mg/kg vitamin B1, and 1 mg/kg vitamin B6, physiological solution, and controls without any treatment. The recovery from neuropathy was controlled for 18 weeks of treatment and assessed periodically by means of clinical, electromyographic, and morphological examination. The results of morphological studies showed more pronounced regeneration activity in the rats treated with the high dose of gangliosides than in all others, while no differences among the groups could be observed as far as clinical and neurophysiological parameters are concerned. The mechanism supporting this ganglioside-induced effect has so far not been ascertained, and further studies on this subject are in progress.     

Ganglioside treatment of vincristine-induced neuropathy. An electrophysiologic study

A 5-week treatment with vincristine (0.20 or 0.25 mg/kg, i.v., once/week) in the rabbit produced a peripheral neuropathy characterized by both morphologic and electrophysiologic alterations. In particular, electrophysiologic recordings demonstrated that the amplitude, area and conduction velocity of compound action potential (CAP) were consistently reduced in a dose-dependent manner. The simultaneous daily administration of 50 mg/kg ganglioside mixture counteracted significantly this functional impairment, area and amplitude of the monophasic CAP being maintained closer to control values. These results suggest that the loss of functional nerve fibers can be reduced, in vincristine-induced neuropathy, by ganglioside treatment.     

Modification of acrylamide neuropathy in rats by selected factors

A modified rotarod technique was used to determine whether dietary deficiencies in pyridoxine or thiamine, bilateral adrenalectomy or cortisol treatment and pretreatment with microsomal enzyme inducers (DDT or phenobarbital) would modify the course of onset and recovery from functional acrylamide neuropathy in rats. Neither pyridoxine or thiamine deficiency nor daily injections of cortisol had any measurable effect on the cumulative dose of acrylamide required to produce functional impairment. Although adrenalectomized animals were more susceptible to acrylamide, the effect seemed nonspecific. The total cumulative doses of acrylamide required to produce neurologic deficit in DDT- and phenobarbital-pretreated rats were 520 and 600 mg/kg, respectively, compared to 360 mg/kg for the controls. Hepatic in vitro metabolism of acrylamide was studied to determine whether the observed delay could be explained by an increased capacity of the liver to detoxify acrylamide. There was a greater loss of acrylamide from incubation mixtures containing 9000 g supernatants from phenobarbital-pretreated rat livers than from control livers. Histologic studies of peripheral nerves from acrylamide-treated rats revealed that at the time of onset of functional impairment young and phenobarbital-pretreated adult rats had severe peripheral nerve damage, while no discernible peripheral nerve injury was seen in unpretreated adult rats.     

Studies on drug-induced neuropathies. III. Motor nerve deficit in cats with experimental acrylamide neuropathy.

To assess motor nerve and motor nerve terminal function in acrylamide neuropathy, cats were given i.m. injections of acrylamide (15 mg/kg) daily for 10 days to induce a peripheral neuropathy. Tests of function were performed on the day of the 10th injection (day 0) and 7, 21 and 35 days thereafter. In untreated animals tetanic conditioning evoked stimulus-bound repetition (SBR) in 85% of soleus alpha-motoneurones. Following administration of acrylamide, the percent of axons elaborating SBR were: day 0 -- 79%, day 7 -- 71%, day 21 -- 31%, day 35 -- 22%. The response of soleus muscle to SBR is normally a post-tetanic potentiation (PTP) of contractile tension which is proportional to the tetanic conditioning frequency; during the development of the neuropathy, PTP in response to all tetanic frequencies progressively declined, concomitant with and as a result of the declining incidence of SBR. These data indicate that initial functional alterations in motor nerves during acrylamide neuropathy occurs at the level of the nerve terminal, preceding alterations in conduction velocities in the axons. However, the motor nerve deficit is not adequate, in either time to onset or severity, to account for the clinical manifestations of the neuropathy. The possible contribution to clinical signs of the neuropathy made by lesions to other peripheral nerves is discussed.     

Survey on spontaneous peripheral neuropathy in aging mice.

The incidence of peripheral neuropathy in CD-1 mice (caesarean-derived) obtained from long term studies over a 10 year period is reported. The survey included peripheral nerve samples of 15,223 males and 15,075 females. The incidence of peripheral neuropathy is 8% in untreated males and 12% in untreated females aged 80 to 104 weeks. The total incidence in all mice in the survey was higher in females than males and was age-related. The present survey also showed interstrain differences. The peripheral neuropathy in CD-1 strain was low in incidence compared to B6C3F1 (cross between C57 BL/C6NCLB and C3H/HENCRLB). The peripheral neuropathy was spontaneous in origin and was age-related.     

丙烯酰胺对小鼠生殖细胞毒性的研究

丙烯酰胺(Acrylamide,AA),是一种用途广泛的重要工业化合物,可用于饮水净化、食品加工、采矿业及用于生产聚丙烯酰胺等.AA可经皮肤快速吸收,职业人员长期接触可导致中枢神经系统损害、皮肤红斑和四肢乏力等中毒症状[1].     

依达拉奉联合神经节苷酯治疗血管源性帕金森综合征的临床观察

目的观察依达拉奉联合单唾液酸四己糖神经节苷酯（GMl）治疗血管源性帕金森综合征的临床疗效。方法选择96例郑州人民医院收治的血管源性帕金森综合征患者,随机分为2组。两组均予美多巴、拜阿司匹林等基础治疗,对照组给予依达拉奉30mg／次、2次／d治疗,试验组在依达拉奉的基础上加用GMl80mg／次,10：／a静脉滴注,3周一疗程。观察两组患者治疗前后帕金森病综合评分量表（UP-DRS）积分改善情况。结果试验组患者精神、行为、情绪、13常活动及运动功能评分均优于对照组（P〈0．05）。而两组并发症积分差异无统计学煮义（P〉0．05）．结诊依扶村塞联合GMl治疗向管源忡帕会套综合秤且右掂杯的临床痒特     

神经节苷脂联合血塞通注射液治疗脑梗死的临床研究

目的考察单唾液酸四己糖神经节苷脂钠注射液联合血塞通注射液治疗脑梗死的临床疗效。方法选择2016年1月—2017年1月上海市第四康复医院治疗的92例脑梗死患者作为研究对象,将患者随机分为对照组和治疗组,每组各46例。对照组患者静脉滴注血塞通注射液,600 mg加入到生理盐水250 mL中,1次/d。治疗组在对照组治疗的基础上给予静脉滴注单唾液酸四己糖神经节苷脂钠注射液,100 mg加入到生理盐水250 mL中,1次/d。两组患者均连续治疗14 d。观察两组患者的临床疗效,同时比较两组治疗前后的神经功能缺损评分、生活质量评分和炎症因子水平。结果治疗后,治疗组的总有效率为76.1%,显著高于对照组的60.8%,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者的生理功能、生理职能、情感职能、社会功能、活力、躯体疼痛、精神健康、总体健康评分和总分均显著升高,同组治疗前后比较差异具有统计学意义(P0.05);且治疗后治疗组生活质量各项评分和总分均明显高于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组患者NIHSS评分显著降低,同组治疗前后比较差异具有统计学意义(P0.05);治疗后治疗组NIHSS评分显著低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者的血浆C反应蛋白(CRP)和纤维蛋白原(Fg)水平均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);且治疗后治疗组血浆CRP和Fg水平均明显低于对照组,两组比较差异具有统计学意义(P0.05)。结论单唾液酸四己糖神经节苷脂钠注射液联合血塞通注射液治疗脑梗死具有较好的临床疗效,可显著改善患者的神经功能和生活质量,能降低炎症因子水平,具有一定的临床推广应用价值。     

gamma-diketone peripheral neuropathy. I. Quality morphometric analyses of axonal atrophy and swelling

Quantitative morphometric analysis was used to characterize expression of myelinated axon swelling and atrophy in rat peripheral nerve during 2,5-hexanedione (HD) intoxication. HD was administered by gavage according to different daily dosing regiments (100, 175, 250, or 400 mg/kg/day) and four proximodistal nerve regions (5th lumbar spinal nerve, proximal and distal sciatic nerve, and tibial nerve) were examined morphometrically. Morphometric determinations were made at four behavioral endpoints (unaffected, slight, moderate, and severe toxicity) and were correlated to electrophysiologic measurements of peripheral nerve function. Results show that, for all HD dose rates, onsets of behavioral neurotoxicity and nerve dysfunction were generally related to development of abundant axon atrophy. The proximodistal manifestation of atrophy was dependent upon the dosing rate; i.e., the atrophy response produced by subacute intoxication with higher daily dosing rates (250 and 400 mg/kg/day) was restricted to distal nerve regions whereas subchronic induction with lower dosing rates (100 and 175 mg/kg/day) produced abundant fiber atrophy in all proximodistal areas. In contrast to atrophy, axonal swellings constituted an inconsistent minor morphologic response, the expression of which was dependent upon subchronic dosing rates (100-250 mg/kg/day). Subacute HD administration (400 mg/kg/day) produced significant changes in neurobehavior and nerve electrophysiologic parameters in the absence of peripheral axon swelling. Thus, conditional expression of swellings suggests they are an epiphenomenon related to low-dose induction rates. Fiber atrophy, however, was numerically dominant, correlated with nerve dysfunction, and occurred at all dosing levels. These characteristics suggest atrophy is a neurotoxicologically significant feature of gamma-diketone peripheral neuropathy.     

Clomipramine vs desipramine vs placebo in the treatment of diabetic neuropathy symptoms. A double-blind cross-over study.

1. The effect of clomipramine and desipramine on diabetic neuropathy symptoms was examined in a double-blind, randomised, placebo controlled, cross-over study for 2 + 2 + 2 weeks. Drug doses were adjusted according to the sparteine phenotype, i.e. extensive metabolisers were treated with 75 mg clomipramine day-1 and 200 mg desipramine day-1 whereas poor metabolisers were treated with 50 mg day-1 of both drugs. Nineteen patients completed the study. 2. Plasma concentration of clomipramine plus desmethylclomipramine was 70-510 nM in extensive metabolisers, vs 590 and 750 nM in two poor metabolisers. Desipramine levels were 130-910 nM, vs 860 and 880 nM. 3. Both clomipramine and desipramine significantly reduced the symptoms of neuropathy as measured by observer- and self rating in comparison with placebo. Clomipramine tended to be more efficacious than desipramine. Patients with a weak or absent response on clomipramine had lower plasma concentrations (clomipramine plus desmethyl-clomipramine less than 200 nM) than patients with a better response. For desipramine a relationship between plasma concentration and effect was not established. 4. Side effect ratings did not differ for clomipramine and desipramine and on both drugs three patients withdrew due to side effects. 5. Compared with earlier results obtained with imipramine dosed on the basis of plasma level monitoring, clomipramine and desipramine on fixed doses appeared less efficacious whereas the side effect profiles were the same. At least for clomipramine, appropriate dose adjustment on the basis of plasma level monitoring may increase the efficacy.     

脑心通胶囊联合神经节苷脂治疗急性脑梗死的临床研究

目的探讨脑心通胶囊联合单唾液酸四己糖神经节苷脂钠注射液治疗急性脑梗死的临床疗效。方法选取2016年4月—2017年12月在荆门市中医医院接受治疗的急性脑梗死患者128例为研究对象,将所有患者根据随机数字表法分为对照组和治疗组,每组各64例。对照组静脉滴注单唾液酸四己糖神经节苷脂钠注射液,40 mg加入到0.9%氯化钠溶液250 mL中,1次/d;治疗组在对照组治疗的基础上口服脑心通胶囊,4粒/次,3次/d。两组患者均连续治疗2周。观察两组的临床疗效,比较两组的NIHSS评分、血液流变学指标和血清学指标同型半胱氨酸(Hcy)、超敏C反应蛋白(hs-CRP)、S100β蛋白、血管内皮生长因子(VEGF)水平。结果治疗后,对照组和治疗组的总有效率分别为75.00%、90.63%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者NIHSS评分均明显降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组NIHSS评分明显低于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组患者全血高切黏度、全血低切黏度、HCT、FIB和红细胞聚集指数均显著降低,同组治疗前后比较差异有统计学意义(P0.05);且治疗组血液流变学指标显著低于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组患者血清Hcy、hs-CRP、S100β蛋白水平均明显降低,VEGF水平明显升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组上述指标明显优于对照组,两组比较差异有统计学意义(P0.05)。结论脑心通胶囊联合单唾液酸四己糖神经节苷脂钠注射液治疗急性脑梗死的疗效显著,可改善血液流变学指标,减轻炎症反应,抑制血栓形成,促进患者神经功能的恢复,具有一定的临床推广应用价值。     

葛根素注射液联合神经节苷脂钠治疗突发性耳聋的临床研究

目的探讨葛根素注射液联合神经节苷脂钠治疗突发性耳聋的临床疗效。方法选取2015年10月—2017年2月在宜兴市人民医院进行治疗的100例突发性耳聋患者为研究对象,根据用药的差别分为对照组(50例)和治疗组(50例)。对照组静脉滴注单唾液酸四己糖神经节苷脂钠注射液,40 mg加入生理盐水100 m L,1次/d。治疗组在对照组的基础上静脉滴注葛根素注射液,400 mg加入生理盐水250 m L,1次/d。两组患者均治疗10 d。评价两组患者临床疗效,同时比较治疗前后两组患者血清细胞因子水平、血液流变学指标和力阈值。结果治疗后,对照组和治疗组总有效率分别为80.00%和96.00%,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者血浆内皮素(ET)、可溶性血管细胞间黏附分子-1(s VCAM-1)水平降低,降钙素基因相关肽(CGRP)水平增高,同组比较差异具有统计学意义(P0.05);且治疗组患者血清细胞因子水平显著优于对照组(P0.05)。治疗后,两组患者血浆黏度(PV)、全血黏度高切(HS)、红细胞聚集指数(EAI)、纤维蛋白原(FIB)均显著降低(P0.05);且治疗组患者血液流变学指标明显低于对照组(P0.05)。治疗后,两组患者听力阈值均显著下降(P0.05);且治疗组患者听力阈值明显低于对照组(P0.05)。结论葛根素注射液联合神经节苷脂钠治疗突发性耳聋可有效改善血液流变学指标和血管内皮功能,有利于听力恢复,具有一定的临床推广应用价值。     

Somatofugal axonal atrophy precedes development of axonal degeneration in acrylamide neuropathy

Somatofugal axonal atrophy is part of the neuronal perikaryal response to axonal injury (axon reaction). Chronic administration of acrylamide (AC) produces proximal atrophy in virtually all sensory fibers in lumbar dorsal root ganglion (DRG) despite the presence of many intact axons in the distal portion of the sciatic nerve. This suggests that the development of axonal atrophy in AC-intoxicated animals is not solely due to a toxic chemical-induced axonal degeneration (axotomy). In this study, we asked whether axonal atrophy arises before onset of axonal degeneration. Rats were given a single intraperitoneal (i.p.) high dose of AC (75 mg/kg), which blocks retrograde axonal transport, followed by daily intraperitoneal injections (30 mg/kg, for 4 days). At 5 days, sensory fibers in the L4 and L5 DRG appeared smaller in caliber and less circular in shape compared to fibers from age-matched normal animals. Axonal diameters of sensory fibers in the L5 dorsal root were significantly (p<0.05) reduced at distances up to 2 mm from the DRG. Quantitative electron microscopy demonstrated that the reduction in caliber was due to a decreased neurofilament (NF) content. Axonal degeneration was not present in the distal portion of both centrally (dorsal root) and peripherally (sciatic nerve) projecting sensory fibers at this time, although primary afferent terminals in muscles of the hindfeet were packed with NFs. The somatofugal progression of the atrophy was evident following more prolonged exposures (10–28 days). It is suggested that AC produces somatofugal axonal atrophy by inhibiting the delivery of a retrogradely transported target-derived “trophic” signal to the neuronal perikaryon.     

三七通舒胶囊联合神经节苷脂治疗急性脑梗死的临床研究

目的研究三七通舒胶囊联合单唾液酸四己糖神经节苷脂钠注射液治疗急性脑梗死的临床疗效。方法选取2016年8月—2018年8月延安大学咸阳医院收治的85例急性脑梗死患者为研究对象,将所有患者随机分为对照组(42例)和治疗组(43例)。对照组患者静脉滴注单唾液酸四己糖神经节苷脂钠注射液,40 mg加入到0.9%氯化钠注射液250 mL中,1次/d;治疗组在对照组基础上口服三七通舒胶囊,1粒/次,3次/d。两组患者持续治疗4周。观察两组的临床疗效,比较两组的美国国立卫生研究院卒中量表(NHISS)评分,以及丙二醛(MDA)、神经元特异性烯醇化酶(NSE)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、脑源性神经营养因子(BDNF)和谷胱甘肽过氧化物酶(GSH-Px)水平。结果治疗后,对照组和治疗组的总有效率分别为83.33%、95.35%,两组比较差异有统计学意义(P0.05)。治疗后,两组MDA、NSE、TNF-α、IL-6水平均显著降低,同组治疗前后比较差异有统计学意义(P0.05);并且治疗组MDA、NSE、TNF-α、IL-6水平明显低于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组患者NIHSS评分显著降低,同组治疗前后比较差异有统计学意义(P0.05);并且治疗组患者NIHSS评分明显低于对照组,两组比较差异有统计学意义(P0.05)。治疗后,两组患者BDNF和GSH-Px水平均显著升高,同组治疗前后比较差异有统计学意义(P0.05);并且治疗组患者BDNF和GSH-Px水平明显高于对照组,两组比较差异有统计学意义(P0.05)。结论三七通舒胶囊联合单唾液酸四己糖神经节苷脂钠注射液治疗急性脑梗死具有较好的临床疗效,能改善神经功能缺损情况,调节MDA、NSE、TNF-α、IL-6、BDNF和GSH-Px水平,具有一定的临床推广应用价值。     

Effect of trapidil on neuropathy in diabetic mice

Long term oral administration of trapidil at the doses of 20 and 60 mg/kg/day restored the decrease in motor nerve conduction velocity in genetically diabetic mice (C57BL/KsJ db+/db+). Trapidil also suppressed the increase in sorbitol content and the decrease in myoinositol content in the sciatic nerve. The elevation of serum total cholesterol level and the decrease in the ratio of serum HDL-cholesterol level to total cholesterol level were suppressed by trapidil. The blood glucose level and the serum triglyceride level were not affected by the drug administration. These results suggest that trapidil may restore the decrease in nerve conduction velocity in diabetic mice through amelioration of the metabolite abnormalities in nerve and microcirculatory disorders.     

安宫牛黄丸联合神经节苷脂治疗儿童病毒性脑炎的临床研究

目的观察安宫牛黄丸联合单唾液酸四己糖神经节苷脂钠注射液治疗儿童病毒性脑炎的临床疗效。方法选取2016年12月—2017年12月新乡市中心医院收治的128例病毒性脑炎患儿作为研究对象,采用随机数表法将所有患儿随机分为对照组和治疗组,每组各64例。对照组静脉滴注单唾液酸四己糖神经节苷脂钠注射液,20 mg加入10%的葡萄糖溶液100 mL中,1次/d。治疗组在对照组的基础上口服或鼻饲安宫牛黄丸,3岁以下患儿每次1/4丸,4～6岁每次1/2丸,7～13岁每次1丸,生理盐水15～20mL研成匀浆,每日1～2次。两组患儿均连续治疗2周。观察两组患者的临床疗效,同时比较两组治疗前后的临床症状、体征改善情况、神经功能指标、炎症因子水平和脑脊液检查结果。结果治疗后,对照组和治疗组的总有效率分别为76.57%、96.88%,两组比较差异具有统计学意义(P0.05)。治疗后,治疗组呕吐消失时间、意识清醒时间、头痛消失时间、锥体束征消失时间均显著短于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组血清S100β蛋白、神经元特异性烯醇化酶(NSE)、神经生长因子(NGF)、髓磷脂碱性蛋白(MBP)水平均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);治疗后治疗组S100β、NSE、NGF、MBP水平显著低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组血清白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)水平均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);治疗后治疗组血清IL-1、TNF-α、CRP水平显著低于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组总细胞数、单核细胞数、蛋白含量均显著降低,同组治疗前后比较差异具有统计学意义(P0.05);治疗后治疗组总细胞数、蛋白含量显著低于对照组,两组比较差异具有统计学意义(P0.05)。结论安宫牛黄丸联合单唾液酸四己糖神经节苷脂钠注射液可显著提高病毒性脑炎临床疗效,改善患儿的临床症状和神经功能,减轻炎症反应,具有一定的临床推广应用价值。     

A simple, sensitive, and objective method for early assessment of acrylamide neuropathy in rats

A simple, quantitative, sensitive, and objective method of early assessment of the degree of disability of rats with acrylamide-induced neuropathy by the measurement of landing foot-spread is described.     

An absorption study of dietary administered acrylamide in swine.

Acrylamide is a food toxicant suspected to be carcinogenic to humans. It is formed in the heat processing of carbohydrate-rich food. A current issue in food safety is whether acrylamide actually represents a risk for human health. At present, available information is insufficient to reach any conclusions. Inter alias, a still unclear matter is the fraction of acrylamide ingested by food that is absorbed and metabolized. This study compared the in vivo relative absorption of acrylamide formed in cooked food with that of the pure compound dissolved in drinking water using the pig (25 Italian Large White females) as the animal model. Acrylamide intakes of about 0.8 and 8 microg kg(-1) pig body wt day(-1) equal to one and ten times, respectively, the maximum average acrylamide daily intake for humans from the diet (expressed on a body wt basis) in industrialized countries, were chosen for the study. Adducts with the N-terminal valine of haemoglobin formed by acrylamide and its epoxide metabolite glycidamide, were used as exposure markers. Analyses were carried out by gas chromatography/mass spectrometry following in-house method validation. Both for the low and the high dose regimen, the glycidamide adduct levels in swine globins were lower of the limit of quantification of the method. As concerns acrylamide adducts, it was found that the relative absorption of acrylamide from feed and water was the same and that there is a direct proportionality between the adduct concentration and acrylamide intake.     

复方脑肽节苷脂联合多奈哌齐治疗阿尔茨海默症的临床研究

目的探讨复方脑肽节苷脂联合盐酸多奈哌齐治疗阿尔茨海默症患者的临床疗效。方法选取2016年7月—2017年7月在首都医科大学附属北京康复医院治疗的阿尔茨海默症患者105例,随机分成对照组(52例)和治疗组(53例)。对照组患者口服盐酸多奈哌齐片,1片/次,1次/d。治疗组患者在对照组的基础上静脉滴注复方脑肽节苷脂注射液,10 m L加入300 m L生理盐水,1次/d。两组患者均治疗2周。观察两组患者临床疗效,同时比较治疗前后两组患者精神状态、生活自理能力、阿尔茨海默相关的神经丝蛋白(AD7C-NTP)和tau蛋白水平。结果治疗后,对照组和治疗组的总有效率分别为78.85%和94.34%,两组比较差异具有统计学意义(P0.05)。治疗后,两组患者MMSEE评分和BI指数均显著升高(P0.05),且治疗后治疗组患者精神状态和生活自理能力明显优于对照组(P0.05)。治疗后,两组患者AD7c-NTP和tau蛋白水平均显著降低(P0.05),且治疗后治疗组患者AD7c-NTP和tau蛋白水平明显低于对照组(P0.05)。结论复方脑肽节苷脂联合盐酸多奈哌齐治疗阿尔茨海默症患者疗效显著,安全性高,具有一定的临床推广应用价值。