癫痫型脑囊虫病患儿脑脊液中离子含量的变化

脑囊虫病患者癫痫发作的比例很高 ,对机体的损伤很大 ,对儿童患者造成不可逆的智力损害。在脑组织中寄生的囊虫其代谢产物通过囊虫的皮层扩散到脑脊液中 ,并随脑脊液进行循环 ,直接作用或间接影响到脑组织细胞 ,从而引起了脑囊虫病患者的癫痫发作。本实验经对脑脊液中离子的测定 ,证明钾、钠、氯、钙离子是囊虫很重要的代谢产物 ,尤其是钙离子 ,在脑囊虫病的癫痫发作中起了一定的作用。材料和方法1　分组和诊断标准1.1　实验组　癫痫型脑囊虫病患儿 10例 ,年龄 0～ 14岁。1有脑部症状和体征 ,如癫痫发作 ,头疼 ,颅内压增高。并排除其它原因…     

癫痫型脑囊虫病患者抑郁状态分析

脑囊虫病患者特别是癫痫型脑囊虫病患者多伴抑郁状态,且严重影响了患者的康复。为此,我们对50例本病患者进行了抑郁状态检测,并与正常组进行了比较分析。检测对象1997年3月～1999年7月在本院及山东省寄生虫病防治研究所清华医院门诊就诊及住院的癫痫型脑囊虫病病人50例为病例组,均经颅脑CT、血或脑脊液囊虫酶联免疫吸附试验确诊,且病程在3周以上,意识清楚,调查合作,无失语及智能障碍,并排除肝脏、甲状腺、肾上腺皮质、垂体等疾病,既往无精神障碍及家族史阳性者,其中男28例,女22例,年龄18～50岁。在同期健康人群中选50人为对照组,其中男30例…     

7例脑囊虫病病例临床资料分析

采用描述性流行病学方法对7例脑囊虫病患者临床资料进行了回顾性分析。7例患者中3例有绦虫病史,均有头晕、头痛症状。其他症状表现为:癫痫、肢体麻木、发作性眩晕、视物模糊、记忆力下降等,其中4例患者脑脊液压力增高。7例患者血清特异性囊虫抗体均阳性。头颅CT和MRI对于诊断脑囊虫病具有重要的价值。脑囊虫病的治疗应首选阿苯达唑。     

脑囊虫病患者脑脊液常规和生化检查与循环抗原检测的比较

本文对408例脑囊虫病患者脑脊液循环抗原检测与脑脊液常规检查和生化分析进行了比较.研究发现循环抗原强阳性组和弱阳性组脑脊液中出现嗜酸粒细胞者所占的比例高于阴性组(分别是50.43%、41.26%和17.65%).274例进行脑脊液生化分析,氯化物基本正常.循环抗原强阳性组葡萄糖含量降低的发生率(14.71%)高于阴性组(3.85%).脑脊液蛋白增高者所占的比例明显高于弱阳性组,弱阳性组又明显高于阴性组(分别为89.70%、71.43%和50.00%).23例原发性癫痫患者脑脊液中CAg均阴性,脑脊液常规和生化分析结果正常.     

癫痫型脑囊虫病患者细胞免疫功能状态的研究

虫体蛋白等刺激产生的异物反应可导致脑囊虫病患者机体免疫功能状态发生紊乱。免疫介质不仅参与了脑囊虫病的发病，可能还与癫痫发生机制密切相关。本研究通过对癫痫型脑囊虫病患者外周血T细胞亚群、NK细胞、白细胞介素-2受体（mIL-2R）变化的观察，探讨细胞免疫状态在脑囊虫病及癫痫发作中的临床意义。     

McAb检测囊尾蚴循环抗原诊断脑囊虫病试剂盒的研制

本文报道了McAb(4F_2)ELISA检测囊尾蚴循环抗原诊断脑囊虫病试剂盒的研制。实验对227例脑囊虫病患者脑脊液进行检测,循环抗原阳性率为84.58％,其中活动型脑囊虫病患者171例,循环抗原阳性率为93.57％。56例非活动型脑囊虫病患者,循环抗原阳性率为57.14％,前者的循环抗原强度也明显高于后者。83例患有其它中枢神经系统疾病的患者,1例阳性,阴性符合率为98.80％。本试验方法简便,结果客观,对脑囊虫病特别是活动型脑囊虫病敏感性高、特异性强。     

脑囊虫病患者心理分析与护理对策

脑囊虫病为猪带绦虫的幼虫一囊尾蚴寄生在脑组织所致，因其寄生部位不同而出现不同的症状和体征，患者有癫痫发作、颅内高压、精神障碍等。因此在较长的病程中，患者会出现各种心理问题，给患者本人和家属带来沉重的精神和经济负担。为了解脑囊虫病患者的心理变化，对2001年1月～2002年6月来我所住院的236例脑囊虫病患者进行了调查，以期为脑囊虫病患者心理护理提供依据。     

Dot—ELISA在脑囊虫病诊断中的应用

本文报告用Dot-ELISA法检测脑囊虫病患者的血清和脑脊液的抗体。108例确诊为脑囊虫病患者的血清阳性率为81.6～96.1％,14例确诊为脑囊虫病患者脑脊液的阳性率为85.7～100％。54例正常人血清在1:40稀释度以上,均未出现假阳性;与并殖吸虫病患者及华支睾吸虫病患者血清均未出现交叉反应;与包虫病及脑血管疾病患者血清有一定的交叉反应。     

231例脑囊虫病患者脑脊液中循环抗原检测分析

本文报告应用抗猪囊尾蚴单克隆抗体４Ｆ８－ＥＬＩＳＡ对２３１例脑囊虫病患者脑脊液中循环抗原检测的结果。经与患者病史、临床分型和脑ＣＴ检查结果比较，发现脑脊液中ＣＡｇ与有无绦虫史无关。脑型合并皮下结节患者脑脊液中ＣＡｇ的阳性率明显高于单纯型脑囊虫病和皮下结节消失组的患者。ＣＡｇ检测的结果与囊尾蚴和脑部寄生的数量，病灶的新旧与部位等病理情况有关。表明ＭｃＡｂ（４Ｆ８）－ＥＬＩＳＡ不仅可用于脑囊虫病的诊断     

脑囊虫病患者癫痫的预防护理

脑囊虫病患者癫痫的预防护理山东省寄生虫病防治研究所（济宁２７２１３３）李惠，于秀欣近１０年来我所收治囊虫病患者４６００人次，其中８０％左右为脑囊虫病。在脑囊虫病中癫痫型占５０％～９３．５％。部分患者癫痫发作凶险，呈癫痫持续状态，甚至导致脑水肿、脑疝而...     

Observations on the cyclic nucleotide concentrations in human cerebrospinal fluid.

Previous studies have shown that the concentrations of 3', 5' cyclic adenosine monophosphate (cAMP) and 3', 5' cyclic guanosine monophosphate (cGMP) in cerebrospinal fluid (CSF), brain, or both, are increased by melanotropic peptides and catechol amines, and by cholinergic agents. The present study measured the concentrations of cAMP, cGMP, and melanotropic activity in the CSF of normal patients and in 136 subjects with various neurologic diseases. In normal lumbar CSF, concentrations (ave +/- SD) were: cAMP, 21 +/- 8 mM; cGMP, 2.4 +/- 0.5 mM; melanotropic activity, 17 +/- 6 units/100 ml. Concentrations of cAMP, cGMP, and melanotropic activity did not differ significantly (P is less than .05) from normal in the following categories of adult and pediatric patients: back pain due to vertigo of unknown cause; cerebral atrophy; cerebral vascular disease; and brain tumor subdural hematoma not causing increased ventricular pressure. Nine children with retarded psychomotor development caused by diffuse brain disease (infection, trauma, hemorrhage, degenerative process, long-standing hydrocephalus with thinning of the cerebral mantle) had subnormal levels of cAMP and melanotropic activity. These two variables were significantly correlated in the entire series of CSF samples (r=+0.55, P is less than .005). cGMP was elevated in the ventricular fluid of adult and pediatric patients when the ventricular pressure was abnormally elevated. The nucleotide's level rose as high as 50 X normal when ventricular pressure exceeded 300 mm H2O. The concentration of ventricular cGMP was proportional to that of ventricular pressure (r=+0.76, P is less than .005). The correlation was similar regardless of the type of hydrocephalus (congenital or acquired, communicating or obstructive), the age of the patient, or the nature of the underlying disease.     

Elevation of Guanosine 3′,5′-Cyclic Phosphate in Rat Heart after Perfusion with Acetylcholine

The levels of guanosine 3',5'-cyclic phosphate (cGMP) and adenosine 3',5'-cyclic phosphate (cAMP) were measured in rat hearts after perfusion with acetylcholine to determine if parallel or independent changes occurred in the levels of these two cyclic nucleotides. It was found that after perfusion with the cholinergic agent tissue, cGMP levels increased as much as 140%. This was accompanied by no change or slight decreases in cardiac cAMP concentrations. The increases observed in cGMP levels were found to parallel the negative inotropic but not the negative chronotropic effects of acetylcholine. Perfusion with isoproterenol led to increases in the rate and force of cardiac contractility and a lowering of cGMP levels. It was concluded that the tissue concentrations of cGMP and cAMP in the perfused rat heart can vary independently and that these two tissue cyclic nucleotides probably do not share the same metabolic or functional role in this tissue.     

Effect of thymic immunomodulators on the system of cyclic nucleotides of splenic T-lymphocytes after BCG vaccination

The experiments on guinea pigs was performed to study the effects of thymogen , thymalin and vilosene on the activity of cAMP, cGMP, adenylate cyclase, guanylate cyclase, cAMP- and cGMP-phosphodiesterases in T lymphocytes during BCG vaccination. It was shown that the disease was accompanied by increased activity of enzymes of anabolism and catabolism of cyclic nucleotides. Thymogen and thymalin mainly activated the synthesis of cGMP, thus causing the shift of cAMP/cGMP value below the reference level. At the same time vilosene increased this value in the process of a repeated BCG injection.     

In vitro tropic action of ACTH upon adrenocortical cyclic nucleotide (cAMP, cGMP) production and corticosterone output in blue (Prionace glauca Linnaeus) and in mako (Isurus oxyrinchus Rafinesque) sharks.

The evolutionary origin of the ACTH-cyclic nucleotide-adrenocorticoid relationship was investigated in vitro. The adrenocortical production of cAMP and cGMP as well as corticosterone output in response to ACTH were examined in the blue (Prionace glauca) and the mako (Isurus oxyrinchus) sharks. Basal (control) cAMP levels remained relatively constant in both species, but were higher in the blue shark adrenal. Initially undetectable basal cGMP levels were increased with incubation time. A basal level of corticosterone output was present in both species. Porcine ACTH significantly increased shark adrenocortical cAMP and cGMP levels. Increased cGMP levels preceded cAMP elevation. Elevation of both cyclic nucleotides preceded increased steroid output. The mako shark adrenal corticosterone response to a given ACTH dose was 100% greater than that of the blue shark. The steroid response was inversely related to the total amount of cAMP generated and the temporal duration of the cAMP response. Both cyclic nucleotides may participate in the events preceding and ultimately determining the duration of the steroid response. The results indicate that the ACTH-cyclic nucleotide-steroid output relationship is established early in the evolution of adrenocortical tissue.     

Cyclic nucleotides in the blood plasma in arterial hypertension]

The reaction of cyclic nucleotides in blood to an orthostatic position, furosemid administration, and submaximal bicycle ergometry load was studied in 20 healthy individuals and in 50 patients with hypertensive disease. A special group was composed of 25 patients the disease in whom was marked by crises. It is shown that a walk of one hour and intravenous infusion of 40 mg of furosemid caused an increase in the blood cAMP but did not change the level of cGMP. During a bicycle ergometry load the levels of cGMP and cGMP increased to an equal measure and returned to their initial values 30 min after its cessation. In patients with arterial hypertension the cGMP system becomes most functionally mobile, whereas the cAMP level, if it increases, does so at a later term after the effect of the stimulus begins. The increased cGMP level is maintained for quite a lengthy period of time after the load is discontinued. In patients suffering from hypertensive disease with crises the cAMP/cGMP ratio, which is reduced at rest also, diminishes still more in an orthostatic position and particularly during a crisis. The role of changes in the metabolism of cyclic nucleotides and their sensitivity to regulatory factors in the pathogenesis of arterial hypertension is discussed.     

The prognostic significance of plasma cyclic nucleotides in patients with congestive heart failure]

The relationship between plasma levels of cyclic nucleotides and mortality was studied in 108 patients with congestive heart failure (CHF) in whom plasma cAMP and cGMP, were determined by radioimmunoassay and were followed-up for 36 to 48 months. 29 patients died. The plasma concentrations of cAMP and cGMP in the dead group were significantly higher than those in the survival group (27.41 +/- 6.11 and 31.11 +/- 18.23 vs 21.56 +/- 5.37 and 17.45 +/- 9.35 nmol/L, respectively, mean +/- s, P < 0.001). Compared with patients with cAMP concentrations below the median value of 22.31 nmol/L, those with higher levels of cAMP had a higher mortality rate (46.3% vs 7.4%, P < 0.001). Patients with cGMP levels above the median value of 17.24 nmol/L also had a higher mortality rate than those with lower levels (40.7% vs 13.0%, P < 0.01). Multivariate stepwise regression analysis including age, cardiac function classification, heart rate, serum potassium and sodium, plasma cAMP, cGMP and cAMP/cGMP was carried out and revealed that only plasma cAMP and cGMP could provide independent prognostic information. Thus plasma levels of cyclic nucleotides was considered the excellent predictor for patients with CHF.     

Cyclic nucleotide content in the adipocytes of rats with spontaneous genetic hypertension. Variations revealed by adrenalectomy]

The basal content of cAMP and cGMP in isolated adipose cells of rats with spontaneous genetic hypertension (SHR) was studied. No differences were found between SHR rats and animals with normal pressure in the content of cyclic nucleotides. Adrenalectomy changes essentially the content of cAMP and cGMP in the adipocytes, reducing the cAMP/cGMP ratio in the cells to about one half; the content of cAMP and cGMP is greater in the adipocytes of adrenalectomized SHR rats than in those of adrenalectomized animals with normal pressure.     

Cyclic nucleotides and somatomedin action in cartilage

The role of cyclic nucleotides was evaluated in the stimulation of cartilage metabolism by somatomedin-C (Sm-C). The effects of cAMP and cyclic guanosine monophosphate (cGMP) analogs on matrix synthesis were evaluated. The effects of Sm-C on tissue concentrations of these cyclic nucleotides were investigated. Likewise, the direct effects of Sm-C on the activities of cartilage adenylate cyclase, guanylate cyclase, and phosphodiesterase were determined. We found that tissue concentrations of cAMP in cartilage declined rapidly during organ culture, despite the presence of serum or Sm-C, cGMP concentrations in cartilage declined rapidly during control incubations but were augmented significantly at 30 and 60 min of incubation with the addition of serum or Sm-C. Thereafter, cGMP concentrations declined toward the levels of incubated control cartilages. Sm-C had no effect on phosphodiesterase activity. N6-Monobutyryl cAMP stimulated sulfate uptake, but dibutyryl cGMP did not. Sm-C did not stimulate adenylate cyclase in purified plasma membranes from chondrocytes, whereas it stimulated both plasma membrane and cytosol guanylate cyclase at concentrations of Sm-C as low as 10(-12) M. These data would indicate that cAMP is not the intracellular second messenger for Sm-C in cartilage. The data for cGMP are provocative and suggest it as a candidate for a second messenger mediating a portion of Sm's stimulation of cartilage metabolism.     

Effect of oral melatonin administration on melatonin, 5-hydroxyindoleacetic acid, indoleacetic acid, and cyclic nucleotides in human cerebrospinal fluid

Melatonin was given orally to patients undergoing diagnostic pneumoencephalography and various compounds were measured in the lumbar and cisternal CSF. Melatonin markedly increased plasma and CSF melatonin concentrations. The plasma: CSF melatonin ratios were similar in patients who received, and in those who did not receive, melatonin. This supports the idea that melatonin is released from pineal to blood and gets into the CSF via the blood. Melatonin did not affect CSF 5-hydroxyindoleacetic acid, which indicates that it has no effect on 5-hydroxytryptamine metabolism. Melatonin increased CSF indoleacetic acid significantly, indicating increased metabolism of tryptamine. Melatonin did not affect CSF cAMP levels, but increased cGMP levels. The effect on indoleacetic acid and cGMP was seen in both lumbar and cisternal CSF, suggesting that melatonin can have generalized actions throughout the CNS.     

Cyclic nucleotide concentrations in tissue and perfusate of isolated rat lung

Cyclic nucleotide content of lung tissue is altered by anesthesia, ventilatory pattern, and pharmacologic manipulation (e.g., isoproterenol). In addition the lung releases cyclic nucleotides into its circulation, but little is known about factors that might alter this release. We isolated and perfused rat lungs (IPL) to determine: 1) if cyclic nucleotides are released into the perfusate in the control state; and 2) if their release changes after alteration of the ventilatory pattern or the addition of isoproterenol. We demonstrated that the rat IPL releases both cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) into the perfusate. Isoproterenol has no effect on cGMP release but increases cAMP release dramatically. Perfusate cAMP is not affected by ventilatory pattern, but perfusate cGMP is higher during high-pressure ventilation than it is in nonventilated or normally ventilated lungs.