海人酸诱导的颞叶癫痫小鼠慢性期行为学变化

目的:研究海人酸(Kainic acid)所致的颞叶癫痫小鼠慢性期行为学改变及意义。方法:用海人酸构建癫痫小鼠模型作为实验组,对照组用生理盐水处理,2个月后分别进行Morris水迷宫实验、条件恐惧实验、高架十字实验和旷场实验。结果:Morris水迷宫实验中,后3d实验组小鼠的定位航行潜伏期长于对照组(P0.01),实验组目标象限滞留时间短于对照组(P0.01);条件恐惧实验中,场景联系性记忆实验实验组小鼠僵直时间百分比小于对照组(P0.01),声音联系性记忆实验实验组小鼠僵直时间百分比小于对照组(P0.01);旷场实验中,实验组小鼠活动路程长于对照组(P0.01),实验组小鼠中间区域滞留时间短于对照组(P0.01),实验组小鼠大小便次数比对照组多(P0.01);高架十字实验中,实验组和对照组小鼠进入开臂的次数比无显著差别(P0.05),两组小鼠在开臂的活动时间比较也无差异(P0.05),但实验组小鼠进入两种臂的总次数较对照组小鼠多(P0.05)。结论:海人酸诱导的颞叶癫痫小鼠慢性期有认知功能和情绪方面的障碍。     

血清铁和血清铁蛋白检测在肝脏疾病中的应用

目的探讨血清铁和血清铁蛋白与肝脏常见疾病的关系。方法用电化学发光法和紫外分光光度法分别检测病毒性肝炎、肝硬化和肝细胞癌患者和正常对照组血清铁、血清铁蛋白水平。结果病毒性肝炎、肝硬化血清铁均高于正常对照组（P〈0．05）。肝癌患者血清铁无明显升高。3组血清铁蛋白则明显高于正常对照组（P〈0．05）。结论血清铁和血清铁蛋白可作为肝脏疾病的重要参考指标,对于判断病情,了解预后有着重要意义。     

非酒精性脂肪肝患者血清铁、转铁蛋白、血清铁蛋白水平测定

目前研究发现,铁作为一种独立的危险因素,在非酒精性脂肪肝(NAFL)的发生发展过程中起着一定的作用[1]:启动脂质过氧化反应,导致机体组织细胞损伤。但国内研究相对较少,本文就不同程度的NAFL和血清铁的关系加以研究,旨在为本病诊断提供重要指标。1材料和方法2001年6月~2004年3月     

血清铁蛋白与红细胞铁蛋白联合检测对铁缺乏贫血诊断价值

目的:探讨血清铁蛋白(S-Fer)与红细胞铁蛋白(RBC-Fer)在原发和继发性铁缺乏贫血诊疗中的价值,特别是S-Fer增高的慢性病贫血合并铁缺乏的诊断,拓展铁蛋白(Fer)诊断的价值和特异性。方法:用放射免疫方法测定60例单纯性缺铁性贫血补铁前后及154例肝硬化、肝癌、白血病、慢性肾衰及慢性病贫血患者S-Fer和RBC-Fer,用t检验比较各组差异性。结果:单纯性缺铁性贫血组(IDA):与正常人比较,S-Fer下降显著(P<0.01);RBC-Fer:轻、中度患者下降显著(P<0.05),重度患者下降更显著(P<0.01);与治疗前比较:治疗两周后S-Fer上升差异无显著性(P>0.05),RBC-Fer差异有显著性(P<0.01)。与正常人比较:慢性病贫血患者S-Fer升高差异有显著性(P<0.01);RBC-Fer:轻、中度贫血患者差异无显著性(P>0.05),重度贫血患者下降差异有显著性(P<0.05)。结论:(1)S-Fer是铁缺乏的最敏感的指标。(2)RBC-Fer下降是贮铁竭尽的指标,上升是补铁显效的敏感指标,增高是铁负荷过多的指标。(3)RBC-Fer是S-Fer正常和升高慢性病贫血患者伴铁缺乏的特异诊断指标与铁缺乏程度呈正相关。两者联合检测可以提高Fer检测特异性。     

血清铁、铁蛋白和铁染色对缺铁性贫血诊断价值的研究

目的探究血清铁、铁蛋白和铁染色对缺铁性贫血的诊断价值。方法选取笔者所在医院2010年12月～2011年10月确诊为缺铁性贫血患者60例为缺铁性贫血组、非缺铁性贫血患者150例为非缺铁性贫血组,健康患者40例为对照组进行研究。对所选标本采用全自动生化分析法、电化学发光法和普鲁士蓝反应法进行血清铁、铁蛋白和细胞内外铁检测。结果与非缺铁性贫血组以及健康对照组比较,缺铁性贫血组的血清铁、铁蛋白和骨髓细胞内、外铁含量均减少,差异有统计学意义(P<0.01);与缺铁性贫血组以及健康对照组比较,非缺铁性贫血组的血清铁、铁蛋白和骨髓细胞内、外铁含量均增高,差异有统计学意义(P<0.01)。结论血清铁、铁蛋白和骨髓细胞内、外铁对于缺铁性贫血的诊断灵敏性高,可以有效反映体内铁贮存和利用情况,对缺铁性贫血的诊断和鉴别诊断具有重要意义。     

放射免疫测定血清铁蛋白评价儿童铁营养状态的分析

本文采用放射免疫法(RIA)对不同类型地区的2418名6个月—6岁儿童的血清铁蛋白(SF)进行测定。结果缺铁者占30.60％,缺铁性贫血(IDA)占25.35%。儿童血清铁蛋白水平坝区(68.53±41.89μg/L)明显高于山区(18.24±18.89μg/L)。山区缺铁率64.10％,远高于坝区的缺铁率9.09％,缺铁率以6个月—1岁组为高(为83.83％)随年龄增长有下降趋势,(Y=-0.886 P<0.01)。SF与Hb和RBC诊断缺铁性贫血符合率为44.33％。     

左乙拉西坦对海人酸致痫大鼠血清NSE和MBP变化的影响

目的:建立海人酸(KA)致痫大鼠模型并观察癫痫大鼠血清神经元特异性烯醇酶(NSE)和髓鞘碱性蛋白(MBP)的变化及左乙拉西坦(LEV)对其水平的影响,以探讨左乙拉西坦在癫痫脑损伤中是否具有保护的作用。方法:清结级Wistar雄性4~5周龄幼鼠72只,随机分为对照组24只,立体定向右侧海马注射生理盐水,KA组24只,注射海人酸,LEV治疗组24只,注射KA造模成功前12h胃管内注入LEV200mg/kg,以后未处死大鼠均每日给药一次。分别于致痫后6h、24h、72h处死,采用ELISA法检测各组大鼠血清NSE和MBP含量。结果:(1)大鼠癫痫行为;对照组无大鼠癫痫发作,其余组均有行为学改变。LEV组幼鼠癫痫发作程度与KA组类似,但潜伏期较KA组延长。(2)血清NSE变化:KA组和LEV组血清NSE于在致痫后6h升高,24h达高峰,与对照组相比有差异(P<0.05),LEV组与KA组的NSE比较无显著差异(P>0.05)。(3)MBP变化:KA组和LEV组血清MBP于致痫后6h升高,72h达高峰,与对照组相比差异有统计学意义(P<0.05),LEV组与KA组的MBP比较无显著差异(P>0.05)。结论:KA致痫大鼠血清NSE、MBP水平显著增高,提示癫痫发作可造成一过性脑损伤,血清NSE、MBP可能作为判断癫痫脑损伤程度的敏感指标,LEV对KA致痫大鼠血清NSE、MBP水平无影响,提示LEV不能减轻亦不加重癫痫发作引起的脑损伤。     

冠心病,高血压病患者血清铁,铁蛋白的检测与临床研究

为评价冠心病，高血压患者全体血清铁、铁蛋白水平，我们对８６例冠心病、１０４例高血压病、１１５例其他疾病及１１０例正常人的血清铁和铁蛋白进行检测对比研究。结果发现，不论是冠心病组，还是高血压病组其血清铁和铁蛋白水平均较其他疾病组和对照组增高，其中冠心病组的血清铁和铁蛋白病水平又高于高血压病组，而其他疾病组的血清铁和铁蛋白水平虽稍有增高，但与正常对照组相比，差异不大。笔者认为，血清铁和铁蛋白在冠心病、     

血清铁、铁蛋白在骨髓增生异常综合征无效造血中的应用

目的研讨血清铁、铁蛋白对骨髓增生异常综合征无效造血中的临床意义。方法测定我院45例初诊为MDS患者(未对输血形成依赖)、33例再生障碍性贫血(AA)患者、45例健康体检者的SI、SF水平,并将分为MDS组、AA组、健康组,比较三组的检测结果。结果MDS组SI水平低于AA组(P<0.05),略高于健康组(P>0.05),MDS组SF明显低于AA组,高于健康组,均有统计学意义(P<0.05);MDS组中环形铁粒幼细胞贫血4例(8.89%),而AA组均未发生,MDS组细胞外铁异常11例(24.44%),骨髓小粒可染铁基本均为球菌状存在,AA组11例(33.33%),骨髓小粒可染铁基本均为球状或块状存在。结论未对输血形成依赖的MDS患者SF显著升高,但仍低于AA,故通过SF的变化,能明确骨髓无效造血的特征,为临床诊断、病情监测及预后提供有利数据。     

妊娠期女性血清铁蛋白水平现况调查

目的 调查河南省不同妊娠阶段女性血清铁蛋白水平,探讨妊娠期铁缺乏与过量现况。方法 收集2018年1月至2020年12月期间就诊于郑州大学第三附属医院健康妊娠期女性13 756例,分析不同妊娠时期血清铁蛋白水平分布情况。参考中华医学会妊娠期铁缺乏和缺铁性贫血诊治指南定义血清铁蛋白<20μg/L为铁缺乏,多数文献中定义>200μg/L为铁过量,分析不同妊娠时期血清铁蛋白缺乏和过量情况。结果 13 756例妊娠期女性血清铁蛋白呈偏态分布,血清铁蛋白水平为25.20(11.70,50.80)μg/L。5 813例妊娠早期血清铁蛋白为47.00(28.10,76.00)μg/L,铁缺乏为891例(占比15.33%),铁过量为111例(占比1.91%);4 760例妊娠中期铁蛋白为18.90(10.20,35.20)μg/L,铁缺乏者2 512例(占比52.77%),铁过量29例(占比0.61%);3 183例妊娠晚期血清铁蛋白水平为11.30(7.60,20.40)μg/L,铁缺乏者2373例(占比74.32%),铁过量7例(占比0.22%)。血清铁蛋白随妊娠的进展而明显下降,妊娠早...     

Effects of morphine and nalorphine on kainic acid-induced hypothermia in rats

Intraventricular administration of kainic acid at the dose of 0.1 g induces a significant depression of rectal temperature followed rapidly by its slight elevation. Morphine (40.0 mg·kg^-1 IP), which by itself elicited biphasic effect on the body temperature of rats—initially hypothermia followed by hyperthermia—slightly increased the kainic acid-induced hypothermia. Kainic acid did not cause any changes in the hyperthermic effect of low doses of morphine (10.0 mg·kg^-1). Pretreatment of rats with nalorphine enhanced the kainic acid-induced hypothermia. On the contrary, nalorphine reversed the hypothermic effect produced by morphine at the dose of 40.0 mg·kg^-1. The results suggest that morphine and kainic acid-induced hypothermia are not mediated by the influence on the same type of receptors.     

Effects of some antiepileptic and proconvulsant drugs on kainic acid-induced limbic epilepsy in cats

The effects of parenteral administration of diazepam (3 mg/kg), DL-C-allylglycine (60–80 mg/kg), and ketamine (20 mg/kg) on kainic acid (KA)-induced limbic seizures were investigated in cats. Single microinjections of KA (1–4 μg) into the amygdaloid complex were followed by local sustained paroxysmal discharges in the limbic system. Seizures consisted of tonic clonic EEG discharges accompanied by orienting reaction to the ipsilateral side of injection and masticatory movements, facial jerks, and aggressive behaviour. Ictal discharges occurred every 5–10 min during the first hours after KA injection and then progressively disappeared within 1 wk. Interictal discharges remained for longer periods, but after 3 or 4 wk they were abolished. Diazepam completely blocked limbic seizures but not high-frequency discharges in the site of injection and the ipsilateral hippocampus. The animals were protected for 30 to 60 min. At the same time, diazepam decreased multiple-unit activity in the pontine reticular formation and the lateral geniculate nucleus and produced a general hypotonia state. DL-C-allylglycine activated KA amygdaloid focus during the remission state and ketamine produced independent epileptiformlike activity which interfered with that produced by KA injection.     

Effect of anticonvulsant treatment on kainic acid-induced increases in peptide levels

The influence of anticonvulsant treatment upon (1) chronically increased seizure susceptibility, (2) on late increases in peptide levels and (3) on seizure-induced brain damage was investigated during various stages of acute kainic acid (10 mg/kg i.p.)-induced seizures. The seizures were interrupted at various stages of the syndrome (50 min to 24 h after injection of the toxin) by injecting thiopental (50 mg/kg i.p.) or the excitatory amino acid antagonist, MK-801 (10 mg/kg i.p.). The increase in neuropeptide Y and somatostatin levels in the frontal cortex could be prevented by early injection of either anticonvulsant (up to 180 min after kainic acid). No protection against the increase in peptide levels was observed when the anticonvulsants were applied later. Kainic acid-induced neuronal damage in the amygdala, with glutamate decarboxylase as a neurochemical marker, was entirely prevented by interrupting seizures up to 2 h after kainic acid. Partial protection (about 40-50%) was even found when the anticonvulsant treatment was applied after the acute syndrome, as late as 8 h after kainic acid injection. Chronically increased seizure susceptibility induced by kainic acid was not prevented, even by early injection (90 min after kainic acid) of the anticonvulsant drugs. The data indicate that (1) the late increase in seizure susceptibility may be initiated early after injection of kainic acid. (2) the late increase in peptide levels may be related to the frequency of acute seizures rather than to a change in seizure threshold or brain damage and (3) even late anticonvulsant therapy may antagonize seizure-induced brain damage in the amygdala.     

Serum ferritin levels in iron deficient children

A group of 42 iron deficient children had serum ferritin levels in the range of 0-19 micrograms/l, with a mean figure of 7.2 micrograms/l. A control group had levels of 11 micrograms/l to 130 micrograms/l with a mean of 39.8 micrograms/l. The use of this assay has particular relevance whilst iron deficiency anaemia continues to be a common disorder in New Zealand children.     

Protective effect of trans-resveratrol against kainic acid-induced seizures and oxidative stress in rats.

Overexcitation of excitatory amino acid is an important mechanism in seizure genesis wherein free radicals have recently been suggested to play a critical role. Thus, intervention by antioxidants can be a potential beneficial approach in the treatment of epilepsy. The present study was undertaken to see the effect of trans-resveratrol, a potent antioxidant, against kainic acid-induced seizures, and effect on markers of oxidative stress in brain. Kainic acid, 10 mg/kg ip, induced long-lasting seizures and associated symptoms. The brain level of malondialdehyde (MDA) was found to be significantly raised after kainic acid administration (295 +/- 18 nmol/g wet tissue) as compared to control (195 +/- 26 nmol/g wet tissue). Pretreatment (5 min) of single dose of trans-resveratrol (40 mg/kg i.p.) could not inhibit the convulsions though the latency was significantly increased. When multiple doses of trans-resveratrol were injected in two-dose schedules in different animals (20 and 40 mg/kg ip, 5 min prior and repeated 30 and 90 min after kainic acid), there was significant reduction in incidence of convulsions in both treatment schedules. The brain MDA levels were found to be significantly attenuated in the trans-resveratrol-treated groups (multiple doses of 20 and 40 mg/kg) as compared to the kainic acid alone. However, the glutathione level in control, kainic acid- and trans-resveratrol-treated animals were not significantly different. The protective effect of trans-resveratrol against kainic acid-induced convulsions and the attenuation of raised MDA level suggest the potential use of antioxidants at least as adjunct therapy in epilepsy.     

缺铁性贫血患者血清红细胞生成素 铁蛋白等相关指标及T淋巴细胞水平的检测及分析

目的分析缺铁性贫血(IDA)患者血清红细胞生成素、铁蛋白、叶酸、维生素B12及T淋巴细胞水平的变化,为该病的诊断、治疗提供临床依据。方法收集2015年7月至2017年7月我院收治的缺铁性贫血患者80例为IDA组;同期慢性疾病性贫血患者80例为ACD组;同期于我院体检的健康志愿者80名为健康对照组。检测各组患者血清中红细胞生成素、铁蛋白、叶酸、维生素B12及T淋巴细胞水平。结果 IDA组及慢性疾病性贫血(ACD)组患者血清中红细胞生成素水平显著高于健康对照组,且IDA组患者血清中红细胞生成素水平显著高于ACD组,差异均有统计学意义(P<0.05)。IDA组患者血清铁蛋白水平明显低于健康对照组,ACD组患者血清铁蛋白水平明显高于健康对照组,差异有统计学意义(P<0.05)。IDA组及ACD组患者血清叶酸、维生素B12、CD3+、CD4+、CD4+/CD8+水平显著低于对照组,CD8+水平明显高于健康对照组,差异均有统计学意义(P<0.05)。IDA组患者血清叶酸、维生素B12水平显著低于ACD组,差异有统计学意义(P<0.05)。结论缺铁性贫血会导致患者红细胞生成及铁代谢障碍,维生素水平显著降低、细胞免疫紊乱。血清铁蛋白含量可作为区分缺铁性贫血及慢性疾病性贫血的指标。     

Montelukast potentiates the protective effect of rofecoxib against kainic acid-induced cognitive dysfunction in rats

There is an evolving consensus that mild cognitive impairment (MCI) serves as a prodrome to Alzheimer's disease. Antioxidants and COX-2 (cyclo-oxygenase-2) inhibitors have also been reported to have beneficial effects against conditions of memory impairment. Newer drugs like cysteinyl leukotriene inhibitors have shown neuroprotective effect in animal models of ischemia. Thus, the present study purports to explore the potential role of montelukast (a cysteinyl leukotriene inhibitor) in concert with rofecoxib (COX-2 inhibitor) and caffeic acid (a 5-LOX inhibitor and potent antioxidant) against kainic acid induced cognitive dysfunction in rats. In the experimental protocol, kainic acid (0.4 μg/2 μl) in artificial cerebrospinal fluid (ACSF) was given intrahippocampally (CA3 region) to induce a condition similar to MCI. Memory performance was measured on days 10-14 and the locomotor activity was measured on days 1, 7 and 14. For estimation of biochemical, mitochondrial and histopathological parameters, animals were sacrificed on day 14, stored at − 80 °C and the estimation was done on the 15th day. The treatment groups consisting of montelukast (0.5 and 1 mg/kg), rofecoxib (5 and 10 mg/kg) and caffeic acid (5 and 10 mg/kg) showed significant improvement in memory performance, oxidative stress parameters and mitochondrial function as compared to that of control (kainic acid treated), however, combination of montelukast with rofecoxib showed significant improvement in their protective effect. Thus the present study emphasizes the positive modulation of cysteinyl leukotriene receptor inhibition on COX (cyclooxygenase) and LOX (lipoxygenase) pathways in the control of the neuroinflammation in kainic acid induced cognitive dysfunction in rats.     

Occurrence of bicuculline-, NMDA- and kainic acid-induced seizures in prenatally methamphetamine-exposed adult male rats

Stimulant drugs are often associated with increased seizure susceptibility. Inhibitory γ-aminobutyric acid (GABA) and excitatory N-methyl-D-aspartate (NMDA) systems play an important role in the effect of stimulants on epileptic seizures. No studies investigating the effect of prenatal methamphetamine (MA) exposure on seizures are available. In this study, bicuculline (GABA_A receptor antagonist), NMDA (NMDA receptor agonist) and kainic acid (non-NMDA receptor agonist) were used to induce seizures in adult male rats. Three groups of animals were tested in each seizure test: prenatally MA- (5 mg/kg) exposed, prenatally saline-exposed, and absolute controls without any prenatal exposure. In bicuculline-induced seizures, the latency to onset of tonic–clonic seizures was shorter in MA-exposed rats than in controls, but it did not differ from saline-exposed rats. There were no differences in clonic seizure onset between groups. In NMDA-induced seizures, the latency to onset of clonic–tonic seizures was shorter in prenatally MA-exposed rats than in controls; however, the latency to onset of saline-exposed animals did not differ from either MA-exposed or from control rats. There were no differences in seizure susceptibility in kainic acid-induced clonic seizures. There were no differences in seizure incidences or stereotypical behavior in any seizure model. The question remains as to how much the present data demonstrate the effect of prenatal drug exposure on seizure susceptibility per se, and how much they may be explained by the effect of prenatal stress or by other mechanism(s).     

Effects of salicylic acid in glutamate- and kainic acid-induced neurotoxicity in cerebellar granular cell culture of rats

Glutamate (10(-7)m) and one of its non-NMDA receptor agonists, kainic acid (10(-4)m), were administered to rat cerebellar granular cell cultures, and the neuroprotective role of salicylic acid was examined. Glutamate induced 38.58 +/- 1.45% neuronal cell death while kainic acid induced only 21.4 +/- 2.01% despite being 1000 times more concentrated. The most effective dose for the neuroprotective effect of salicylate in glutamate-induced neurotoxicity was 10(-5)m and it had no protective effect at 10(-7)m. With kainic acid-induced toxicity, 10(-6)m salicylate had no protective effect but 10(-5)m and. 10(-4)m salicylic acid were very effective against kainic acid-induced toxicity. As an OH-trapping agent, salicylate had a protective role in NMDA and non-NMDA receptor-activated neuronal cell death. The present study gives some important clues about oxygen free radical generation having an important role in glutamate- and kainic acid-induced neurotoxicity. On the other hand, the neuroprotective effects of salicylic acid in the present study may depend on the pH alterations in salicylic acid solutions.