食物不耐受及食物过敏与再发性腹痛患儿胃肠激素的相关性研究

目的探讨再发性腹痛患儿血清食物不耐受(FI)特异性IgG抗体和食物过敏特异性IgE抗体水平及其与P物质(SP)、胃动素(MLT)和生长抑素(SST)水平的相关性。方法本组研究50例符合条件的再发性腹痛患儿和50例体检健康儿童作为研究对象。Elisa法检测两组血清中食物不耐受特异性IgG抗体和食物过敏特异性IgE抗体及胃肠激素SP、MLT和SST水平。应用散射比浊法测定两组儿童血清总IgG。分析血清总IgG水平与SP、MLT和SST相关性。结果 55例再发性腹痛患儿出现食物特异性IgG抗体者39例,阳性率为70.91%,明显高于对照组的阳性率为30%(χ2=17.55,P<0.01)。两组儿童对食物过敏特异性IgE抗体阳性例数比较无统计学意义(P>0.05)。再发性腹痛患儿血清总IgG和SP、SST明显高于对照组,MLT明显低于对照组(P<0.01)。血清总IgG与SP和SST呈正相关,与MLT呈负相关(P<0.01)。结论 FI与儿童再发性腹痛联系密切,FI血清总IgG与再发性腹痛患儿胃肠激素SP、MLT和SST存在明显相关性。     

食物特异性IgG抗体检测在儿童再发性腹痛中的意义研究

目的探讨儿童再发性腹痛与食物过敏原特异性IgG的关系,指导其临床防治。方法选取2009年3月—2011年3月在佛山市第一人民医院儿科住院或门诊治疗的再发性腹痛患儿,经消化道钡餐、胃镜、腹部B超未发现器质性病变的患儿100例,随机分成腹痛1组和腹痛2组,分别60例和40例;同时选择20例健康体检者作为对照组。应用酶联免疫法检测血清中14种食物特异性IgG水平。结果腹痛1组食物过敏原特异性IgG抗体阳性54例,占90%,其中蛋清/蛋黄49例、牛奶41例;腹痛2组食物过敏原特异性IgG抗体阳性35例,占87.5%,其中蛋清/蛋黄30例、牛奶29例;对照组食物过敏原特异性IgG抗体阳性17例,其中蛋清/蛋黄15例,牛奶14例。3组比较差异无统计学意义(P>0.05)。腹痛1组根据检验结果,对相关食物进行回避治疗2周后,症状消失或明显改善35例,症状有改善9例,症状无改善或加重16例,总有效率73.33%;腹痛2组总有效率20%,两组比较差异有统计学意义(P<0.01)。结论食物不耐受可能是再发性腹痛的原因之一,再发性腹痛患儿有必要进行血清食物过敏原特异性IgG抗体检测,并进行食物回避治疗。     

儿童功能性胃肠病与食物过敏关系的研究

目的 探讨儿童功能性胃肠病与食物过敏的关系及近期预后.方法 选取108例功能性胃肠病患儿作为观察组,健康儿童36例为对照组.采用ELISA法对10种过敏食物进行IgG抗体浓度水平及血清总IgE水平进行检测,采用不同方法对患者进行健康饮食指导,3～6个月后比较两组的症状改善情况.结果 观察组1 ～10种不等的食物过敏原特异性IgG升高的患儿有90例,占83.3％,而对照组有9例,仅占25.0％(x2=20.87,P＜0.05).观察组中敏感性最高的是牛奶、蛋清/黄,分别为84例(77.8％)和60例(55.6％).两组比较,均P＜0.05.观察组与对照组血清总IgE水平比较,P＞0.05.经饮食指导后17例(15.7％)在1个月内症状有所改善,13例(12.1％)在3个月内症状改善21例(19.4％)患者症状在3个月后无改善.总有效率为80.6％.结论 功能性胃肠病患儿易发生食物过敏且以多种食物过敏为主,IgG抗体水平的检测能够正确反应两者的关系,合理饮食结构可改善功能性胃肠病症状.     

IgG抗体与食物过敏

目的：探讨IgG抗体与过敏反应的关系,并在此基础上进一步研究影响IgG抗体的相关因素。方法：为探讨IgG抗体在食物过敏反应中的作用,采用酶联免疫吸附试验（ELISA）和放射过敏原吸附试验（RAST）分别检测61例食物过敏者及269例非食物过敏的过敏者血清四种常见食物过敏原（花生、鸡蛋、牛奶、海蟹）特异性IgG、IgE抗体;正常对照组为65例无任何过敏史和家族史的健康志愿者。结果：除了食物过敏者以外,在非食物过敏的过敏病人血清中,也检测到了四种食物过敏原特异性IgG抗体。非食物过敏者血清花生、鸡蛋、牛奶特异性IgG抗体水平均高于食物过敏者（P〈0．05）,而且非食物过敏者食物特异性IgG抗体阳性率显著高于食物过敏者（P〈0．05）,但两组间IgE抗体阳性率无显著性差异（P〉0．05）。与正常对照组相比,食物过敏者血清四种食物过敏原特异性IgG抗体水平均无显著性差异;但非食物过敏者血清中,花生、鸡蛋、牛奶三种食物过敏原特异性IgG抗体均显著高于正常对照组（P〈0．05）。非食物过敏的过敏病人血清海蟹特异性IgG抗体与食物过敏者无显著性差异（P〉0．05）。结论：特异性IgG抗体在食物过敏反应中可能为保护性抗体：食物特异性IgG抗体与过敏原对过敏者的刺激有关。     

肠易激综合征患者血清食物不耐受特异性IgG和IgG4检测的意义

目的 探讨同步检测肠易激综合征(IBS)患者血清食物特异性抗体IgG和IgG4含量的临床意义.方法 采用ELISA法检测IBS组(n=88)、健康对照组(n=40)血清中常见的8种食物特异性抗体IgG和IgG4.结果 IBS组与健康对照组血清食物特异性抗体IgG和IgG4总阳性率差异有统计学意义(均P＜0.01),IBS组内IgG和IgG4阳性率差异无统计学意义(均P＞0.05).结论 机体内食物不耐受所引起的IgG和IgG4特异性抗体升高是导致IBS发生的重要原因,食物过敏原特异性IgG和IgG4的检测结果对削除不耐受食物以预防IBS发生有重要的临床意义.     

食物血清特异性IgG检测在变应性皮肤病中的相关性分析

目的探讨食物特异性IgG抗体与慢性3种变态反应性皮肤病的相关性。方法采用ELISA方法检测320例变态反应性皮肤病患者及对照组血清中14种食物特异性IgG抗体及检测不同分组的IgG抗体阳性率。结果 320例患者食物特异性IgG总阳性率72.8%高于对照组。特异性IgG阳性率较高(20%以上)的主要致敏食物有2种,分别为蛋黄/蛋清和牛奶。过敏性紫癜组患者敏感食物蛋黄/蛋清类的阳性率均明显高于荨麻疹及湿疹组。儿童组食物不耐受明显高于其他组。过敏性紫癜食物不耐受多见于儿童组。不同性别间食物不耐受无显著性差异。结论变态反应性皮肤病与血清食物特异性IgG抗体有明显相关性,儿童变态反应性皮肤病食物不耐受发生率较高,食物不耐受与儿童过敏性紫癜发病有密切关系。     

荨麻疹发病因素与食物特异性IgG抗体的相关性分析

目的探讨荨麻疹的发病原因与食物不耐受之间的相关性。方法选取2010年10月至2011年10月来我院皮肤科治疗荨麻疹的患者90例,采用ELISA法分别检测患者血清中的10种食物特异性IgG抗体。食物过敏原IgG检测阳性的患者根据结果调整饮食,食物过敏原IgG检测阴性的患者饮食结构不改变,于初次检测3个月、6个月之后再次检测,对比阳性率和IgG抗体浓度。结果 90例患者中,食物特异性IgG抗体检测存在阳性项目的患者62例,对这62例患者进行严格禁食3个月之后,患者全身症状明显好转者28例,治愈者10例,抗体检测阳性的患者下降到48例;禁食6个月之后,治愈患者21例,明显好转者32例,抗体检测阳性者下降到23例。90患者禁食前、禁食3个月、禁食6个月三次检测阳性率分别为67.78%、53.33%、25.56%,差异存在显著性(P<0.05)。结论部分荨麻疹患者的发病原因与食物不耐受有较大的相关性。对这部分患者,进行食物特异性IgG抗体检测可以了解患者是否对某些事物产生了不耐受,并以此为根据调整饮食,减轻荨麻疹症状,对预防和治疗荨麻疹具有重要的价值。     

慢性腹泻患儿血清食物不耐受IgG抗体检测

目的:测定慢性腹泻患儿血清食物不耐受特异性IgG抗体并进行脱敏治疗,观察脱敏治疗后患儿腹泻缓解情况.方法:采用血清特异性IgG抗体测定法检测59例慢性腹泻患儿血清食物不耐受特异性IgG抗体.结果:59例慢性腹泻患儿食物不耐受特异性IgG抗体检测阳性率迭93.22％.59例慢性腹泻惠儿经脱敏治疗1个月和3个月后总有效率分别为74.55％和82.69％.结论:食物不耐受可能为小儿慢性腹泻的原因之一,慢性腹泻患儿有必要进行血清食物不对受特异性IgG抗体测定并进行脱敏治疗.     

食物过敏在小儿迁延性慢性腹泻病中的检测研究

目的分析食物过敏在小儿迁延性慢性腹泻病中的检测情况。方法选择2018年1月至2018年6月我院收治的200例原因不明型迁延性慢性腹泻小儿患者为研究对象。依照受试者食物特异性IgG检查是否为阳性,分为过敏组以及非过敏组,每组100例。分析临床表现以及预后情况。结果和非过敏组相比,过敏组的IgG明显更高,P <0.05,其余指标无明显差异,P> 0.05。和非过敏组相比,过敏组的便潜血、便脂肪球、大便白细胞、大便红细胞、肠道菌群异常率无明显差异,食物特异性IgG阳性率比非过敏组高。在过敏组内,3种阳性人数最高,其次为4种阳性,再次为2种阳性,最后为1种阳性。过敏组患儿治疗有效率为93.00%,非过敏组为55.00%,过敏组的治疗有效率明显更高,P <0.05。结论大部分不明原因性迁延性慢性腹泻患儿存在食物过敏现象,其对于食物特异性IgG抗体敏感性高,开展此类IgG过敏原抗体检查,有助于尽早做出临床诊断,值得进一步推广。     

672例慢性荨麻疹血清食物特异性IgG抗体检测分析

目的：了解常见的血清中7种食物特异性IgG抗体与慢性荨麻疹的相关性,探讨检测食物过敏原特异性IgG抗体在一些慢性疾病的诊断与预防的意义。方法：采用酶联免疫吸附法（ELISA）检测672例慢性荨麻疹患者血清中7种食物特异性IgG抗体水平。结果：患者血清食物特异性IgG抗体总阳性率65.1%,7种食物特异性IgG抗体有不同程度增高,其中蛋清/蛋黄最高。不同年龄组过敏食物比较有一定特异性。结论：对慢性荨麻疹以及其他慢性病的病人应做食物不耐受抗体的检测。     

模式动物斑马鱼在神经退行性疾病研究中的应用

斑马鱼作为一种新型模式低等脊椎动物,具有发育周期短、体外受精、胚胎透明、突变种多等优势,被广泛应用于神经、心血管、消化等方面的研究中。神经退行性疾病包括帕金森病、阿尔茨海默病等,近年来发病率不断上升,且有年轻化的趋势,严重影响人们的身体健康和生活质量。因其发病机制复杂,至今仍缺乏治疗此类疾病的方法。本文综述近年来用斑马鱼制作神经退行性疾病模型的主要方式及可行性,为研究神经退行性疾病中斑马鱼模型的选择提供参考。     

Age related changes in cardiac and aortic phosphodiesterase activities in normotensive and hypertensive rats.

The activities of cAMP¹ and cGMP phosphodiesterase were studied in the aorta (freed of adventitia layer) and in the heart (ventricles) of normotensive and mincralocorticoid hypertensive rats of 8 or 16 weeks of age. The enzyme activities were determined at low (1 μM) and high (100 μM) substrate concentrations. The changes in activity were compared to the changes in organ weight, protein and DNA content. The increase in organ weight that occurred with both age and hypertensive treatment corresponded mostly to a marked elevation in protein content in the aorta, but not in the heart, where the DNA content increased without any significant variation in protein content. In both tissues. eGMP phosphodiesterase activity measured at low substrate concentration was sensitive to endogenous Ca²⁺-dependent activation and markedly increased with age. This increase was proportionally larger than the variations in DNA content of the tissues, but lower than those of total protein in the aorta. It could not be ascribed to an increase in the activator content of the tissues, which was in excess. By contrast. cGMP phosphodiesterase activity measured at high substrate concentration and cAMP phosphodiesterase activity, measured at either substrate concentration, were not sensitive to the Ca²⁺-dependent activation and did not undergo large changes with age except for a significant decrease in cAMP phosphodiesterase activity at high substrate concentration per mg heart cytosol protein. No relationship could be found between the elevation of blood pressure, due to age or to the influence of the mineralocorticoid treatment, and phosphodiesterase activities, which varied in a similar manner in control and hypertensive rats. The results are consistent with the view that a cGMP phosphodiesterase. which is sensitive to Ca²⁺-dependent endogenous activation, increases in aorta and heart cells with the age of the rat.     

Reasons that prevent the inclusion of Alzheimer's disease patients in clinical trials

Aim

To assess reasons that prevent Alzheimer''s disease (AD) patients from being included in clinical trials.

Methods

In 2009, we reviewed the Lille Memory Clinic''s case database to identify patients suitable for inclusion in four AD clinical trials. An initial selection was made on the basis of four criteria: (i) a diagnosis of AD (with or without white matter lesions [WML]), (ii) age, (iii) mini mental state examination (MMSE) score and (iv) symptomatic treatment of AD (cholinesterase inhibitors/memantine). Next, data on patients fulfilling these criteria were reviewed against all the inclusion/exclusion criteria for four clinical trials performed in 2009 at the Memory Clinic. Reasons for non-inclusion were analyzed.

Results

Two hundred and five patients were selected according to the four initial criteria. Reasons for subsequently not including some of patients in clinical trials were abnormalities on MRI (56.9%, 88.9% of which were WML), unauthorized medication (37.3%), the lack of a study partner/informant (37.1%), the presence of a non-authorized disease (24.4%), contraindication to MRI (9%), a change in diagnosis over time (3.9%), visual/auditory impairments (2.9%), alcohol abuse (2%) and an insufficient educational level (1%).

Conclusion

A high proportion of AD patients presented with vascular abnormalities on MRI. This was not unexpected, since the patients were selected from the database and, as shown in epidemiologic studies, cerebrovascular diseases are frequently associated with AD. The presence of a study partner is essential for enabling a patient to participate in clinical trials because of the need to record reliably primary and secondary outcomes.     

淫羊藿苷改善中枢神经系统疾病的研究进展

淫羊藿苷是淫羊藿中主要活性成分,具有抗肿瘤、抗炎、增强免疫、抗肝毒性、抗氧化等多种药理活性。淫羊藿苷可通过多靶点、多途径对中枢神经系统疾病产生保护作用,如淫羊藿苷具有抗抑郁作用,对阿尔茨海默病、帕金森病、缺血性脑卒中、多发性硬化具有保护作用。为了进一步扩大淫羊藿苷在临床治疗中的应用,综述了淫羊藿苷改善中枢神经系统疾病及其作用机制。     

Signs of Preclinical Wernicke's Encephalopathy and Thiamine Levels as Predictors of Neuropsychological Deficits in Alcoholism without Korsakoff's Syndrome

The purpose of this study was to determine whether meeting historical criteria for unsuspected Wernicke''s encephalopathy (WE), largely under-diagnosed in vivo, explains why some alcoholics have severe neuropsychological deficits, whereas others, with a similar drinking history, exhibit preserved performance. Demographic, clinical, alcohol related, and neuropsychological measures were collected in 56 abstinent alcoholics and 38 non-alcohol-dependent volunteers. Alcoholics were classified using the clinical criteria established by Caine et al (1997) and validated in their neuropathological study of alcoholic cases. Our alcoholics who met a single criterion were considered ‘at risk for WE'' and those with two or more criteria with ‘signs of WE''. Whole blood thiamine was also measured in 22 of the comparison group and 28 alcoholics. Of the alcoholics examined, 27% met no criteria, 57% were at risk for WE, and 16% had signs of WE. Neuropsychological performance of the alcoholic subgroups was graded, with those meeting zero criteria not differing from controls, those meeting one criterion presenting mild-to-moderate deficits on some of the functional domains, and those meeting two or more criteria having the most severe deficits on each of the domains examined. Thiamine levels were selectively related to memory performance in the alcoholics. Preclinical signs of WE can be diagnosed in vivo, enabling the identification of ostensibly ‘uncomplicated'' alcoholics who are at risk for neuropsychological complications. The graded effects in neuropsychological performance suggest that the presence of signs of WE explains, at least partially, the heterogeneity of alcoholism-related cognitive and motor deficits.     

瑞香素对阿尔茨海默病模型小鼠自噬的影响

目的 探讨瑞香素对阿尔茨海默病(Alzheimer’s disease,AD)自噬的影响以及对AD神经保护的作用机制。方法 选用APP/PS1双转基因模型小鼠,3个月龄后开始灌胃给药。药物治疗3个月后,通过Morris水迷宫试验观察瑞香素对AD模型小鼠空间探索和记忆能力的影响;采用ELISA试剂盒检测AD模型小鼠海马脑组织Aβ1-40、Aβ1-42水平;利用Western blotting检测瑞香素对AD模型小鼠海马组织微管相关蛋白轻链3Ⅱ(microtubule-associated proteins light chain 3Ⅱ,LC3-Ⅱ)、beclin-1及p62表达水平的影响。结果 Morris水迷宫试验显示,APP/PS1双转基因模型小鼠逃避潜伏期较对照组明显延长,原象限停留时间明显缩短;瑞香素组小鼠逃避潜伏期较模型组明显缩短,原象限停留时间明显延长。与对照组比较,APP/PS1双转基因模型小鼠脑组织中Aβ水平增多,而瑞香素减少模型小鼠Aβ水平;Western blotting结果显示AD模型小鼠海马区LC3-Ⅱ及beclin-1显著降低,p62显著增加,而瑞香素可上调AP...     

海藻糖治疗帕金森病的作用机制研究进展

帕金森病是一种常见的神经变性疾病,特征性病理改变主要是黑质多巴胺能神经元丢失和路易小体的形成。路易小体中主要成分是纤维化的α-突触核蛋白,研究表明多巴胺能神经元中异常的蛋白质沉积可能与溶酶体自噬途径的失调有关。自噬调节剂的治疗潜力已在帕金森病动物模型中得到证实。海藻糖是一种天然双糖,被认为是治疗神经退行性疾病的新候选药物。它具有类似伴侣活性,防止蛋白质错误折叠或聚集,并有助于通过促进自噬去除积聚的蛋白质。总结异常自噬在帕金森病疾病发展过程中的潜在机制,讨论使用海藻糖对抗帕金森病的促进自噬、蛋白质稳定和抗神经炎症作用。     

Graves病患者甲状腺肿大及眼征的影响因素分析

目的 探讨Graves病患者甲状腺肿大及眼征的影响因素。 方法 选取皖北煤电集团总医院内分泌科2011年1月至2013年12月就诊的Graves病患者154例。分别按照患者有无甲状腺肿及有无甲状腺眼征,分为甲状腺肿大组(A组)和无甲状腺肿大组(B组)以及有眼征组(C组)和无眼征组(D组)。应用化学发光法检测游离三碘甲状腺原氨酸(FT₃)、游离甲状腺素(FT₄)、促甲状腺激素(TSH)、甲状腺过氧化物酶抗体(TPOAb)、甲状腺球蛋白抗体(TGAb)、甲状腺激素受体抗体(TRAb)。分别比较两组患者的年龄、FT₃、FT₄、TSH、TPOAb、TGAb、TRAb 。 结果 154例患者中,甲状腺肿大者112例(72.7%),伴甲状腺眼征者62例(40.3%)。甲状腺肿大组的FT₃、FT₄、TPOAb和TRAb均高于无甲状腺肿大组(P<0.05),年龄小于无甲状腺肿大组(P<0.01)。有甲状腺眼征组的TPOAb、TGAb和TRAb均高于无甲状腺眼征组(P<0.05)。相关分析显示,甲状腺肿大与年龄、TPOAb、TRAb相关(相关系数分别为0.149、0.295、0.198,P<0.05)。甲状腺眼征与TGAb、TRAb相关(相关系数分别为0.280、0.228,P<0.05)。 结论 Graves病患者甲状腺肿与年龄、高滴度的TPOAb和TRAb相关,甲状腺眼征与高滴度的TGAb和TRAb相关。     

Increased thymidylate synthetase in 5-fluorodeoxyuridine resistant cultured hepatoma cells

A FdUrd resistant line of cultured mouse hepatoma cells has been obtained. The resistant cell line had 6- to 10-fold higher levels of thymidylate synthetase, but dihydrofolate reductase and thymidine kinase were unchanged. No impairment of FdUrd incorporation by the resistant cell line could be detected. The increased thymidylate synthetase in resistant cells had the same turnover number and I₅₀ for FdUMP as the enzyme found in sensitive cells, making it unlikely that a new gene product had been obtained. Sensitive cells could be completely rescued by the addition of thymidine, suggesting that the primary mode of drug action is to diminish thymidine metabolites. Resistant cells, removed from FdUrd for several generations, did not proliferate immediately upon reintroduction of the drug; however, loss of sensitivity was much more rapid than upon initial exposure. These results are interpreted in terms of a mechanism for resistance.