广州市至灵学校167名学员智残原因的调查分析

本文以广州市至灵学校（智低）167名学员为研究对象，完成智力测验、体格检查和染色体分析．并且追溯围产期和出生后的种种异常．询查智力低下的家族史。综合分析有关资料，显示围产期的某些不利因素、遗传与先天疾病，以及婴幼儿中枢神经系统疾病是主要的发病原因。从而指出，加强优生咨询、重视围产期保健、提高产前诊断和产程中的监护水平、早期防治胎婴儿中枢神经系统损伤和疾病等，是降低智残儿发生率的重要措施。     

过敏性紫癜急性期血液流变性改变及其临床意义

为了研究过敏性紫癜（ＨＳＰ）急性期血液流变性改变及其临床意义，采用ＮＸＥ－Ｉ型锥板式粘度计，测定了２１例ＨＳＰ急性期血液流变学各项指标。结果表明，ＨＳＰ组全血粘度、血浆粘度、红细胞聚集性增多显著高于对照组；氧释放系数ＯＤ值较对照组明显降低；ＨＳＰ患儿红细胞压积、血小板计数、血清ＩｇＡ和ＩｇＭ呈明显升高。提示ＨＳＰ时存在明显的血液流变性异常，其发生与血液浓缩、高Ｉｇ血症等因素有关。及时治疗ＨＳＰ高粘滞血症对减轻症状、防止复发是十分有益的     

Pathogenesis of the low cardiac output syndrome in postresuscitation states

Acute hypervolemia induced in experiments on dogs by infusion of dextran, did not produce decompensation of the circulation in animals whose cardiac output was sharply depressed in the postresuscitation period after circulatory arrest lasting 15 min. The increase in the venous return and change in the conditions of the peripheral circulation as a result of dextran administration temporarily increased the central venous pressure, caused a lasting increase in the arterial pressure, cardiac output, stroke volume, work of the left ventricle, and total oxygen consumption by the body, and lowered the peripheral vascular resistance. In model experiments on dogs subjected to isolated compression ischemia of the brain for 20 min, a low cardiac output syndrome also developed.Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 7, pp. 787–789, July, 1976.     

Atrial fibrillation: a new explanation of the old phenomenon

We propose a new mechanism of atrial fibrillation basing on the results of 30 series of acute experiments on anesthetized cats. In brief, combination of two or more arrhythmogenic factors shortens the interval between the inward and outward ionic currents in cardiomyocytes to a critical value. Under these conditions repolarization of cardiomyocyte membrane reaches the excitation threshold before complete inactivation of the depolarizing currents. This inevitably results in autoexcitation of myocytes (or extrasystole), that in turn promotes repolarization. Once occurred, autoexcitation turns into self-triggering activity resembling tachyarrhythmia paroxysm.     

Case of postradiation osteosarcoma with a short latency period of 3 years

Osteosarcoma is one of the neoplasms that may occur following exposure to radiation. A case of osteosarcoma arising in the craniofacial bone with a short latency period of 3 years after radiotherapy for maxillary squamous cell carcinoma is described. A 64-year-old-man underwent right partial maxillectomy and chemoradiotherapy due to squamous cell carcinoma of his right maxillary sinus. Histologically, the tumor was composed of moderately differentiated squamous cell carcinoma with a component of spindle cell carcinoma. Three years later, osteosarcoma developed in the craniofacial bone within the irradiation field of the first tumor. Detailed histological examination demonstrated that there was no component of osteosarcoma in the first tumor or squamous cell carcinoma in the second tumor. Radiation-induced osteosarcoma usually occurs after a long latency period of more than 10 years after the radiotherapy. In this case, osteosarcoma was possibly a radiation-induced osteosarcoma with a short latency period of 3 years.     

Delayed responses to electrical stimuli reflect C-fiber responsiveness in human microneurography

The slowing of impulse conduction during the relative refractory period has often been used to assess activation of C-fibers, in particular, in human microneurography. This study aimed to evaluate the sensitivity of this method and the factors affecting it. Thirty cutaneous C-fibers were recorded from the peroneal nerves of healthy human subjects. Intracutaneous electrical stimulation in the receptive field at 4 s intervals, after some minutes of adaptation, induced spike discharges at constant latency. One or more conditioning stimulus pulses were interpolated at different intervals and the increase in latency after the subsequent regular pulse was assessed. The latency shift was found to depend on the number of interposed pulses, on the time interval between conditioning and conditioned stimulus, and on the conduction velocity of the C-unit. The increase in latency was larger with greater distance between stimulating and recording electrodes, indicating a contribution of the conductile membrane over its whole length. On the other hand, slowing was more pronounced, on average, in slower conducting C-units and conduction velocities were slower when recordings were performed more distally. These findings indicate that the slower terminal nerve branches contribute most to the latency increases. Even a single additional spike in between two regular pulses caused a reliable latency shift of 1.2±0.2 ms (mean ±SEM) and additional pulses lead to an approximately linear latency increase (2 pulses: 2.3±0.3 ms; 4 pulses: 5.9±0.7 ms). In contrast to the number of interposed stimuli, different intervals between interposed and regular stimuli had only a minor impact on the latency shifts. It is concluded that latency shifts are reliable indicators of C-fiber activation, being sensitive enough to detect even single spike responses. Furthermore, latency increases may be used as a relative measure of C-fiber activation, e.g., when comparing responses to stimuli of different strength.     

Maintained pregnancy levels of oestrogen afford complete protection from post-partum exacerbation of collagen-induced arthritis.

Pregnancy is known to influence the course of rheumatoid arthritis (RA) in women, as well as type II collagen-induced arthritis (CIA) in DBA/1 mice. A characteristic feature is the remission during gestation and the exacerbation of the diseases during the post-partum period. In the case of CIA in DBA 1 mice, two hormonal changes have been assumed to be critical for the induction of the post-partum flare: (i) the fall in steroid hormone levels from those present during pregnancy; and (ii) surges of prolactin (PRL) release at and after delivery. Our results show that treatment with oestradiol during a short period immediately after parturition protects the mouse from a post-partum flare of the disease, and that treatment with bromocriptine, a drug known to inhibit the endogenous PRL release, has a significant though less marked effect. Studies of lactating (i.e. animals with physiological stimulation of endogenous PRL release) and non-lactating arthritic mice revealed no clear-cut differences, indicating that PRL is of minor importance for the induction of the post-partum flare. Some steroids other than oestradiol, which may be implicated in the exacerbation of arthritis, namely progesterone and hydrocortisone, had no clinical effect. Analyses of agalactosyl IgG levels in mice with CIA, and anti-collagen II antibodies in sera collected at the end of the experiments revealed no significant differences between the oestradiol and the control groups. The successful oestradiol treatment of the mice indicates that the drop in endogenous oestradiol levels prior to delivery ends the oestrogen-mediated protection against arthritis during pregnancy.     

Cardiovascular indices of physiological arousal in boys with fragile X syndrome

In this study, the relationship between physiological arousal, as indexed by heart rate variability, was examined in boys with fragile X syndrome (FXS) and typically developing boys matched on chronological age. In addition, the relationship of heart activity to clinical and molecular factors in the group of boys with FXS was examined. Results suggest that boys with FXS have higher levels of heart activity during the passive phases, as reflected in shorter heart periods. This high level of heart activity appears to be due to increased sympathetic activity and reduced parasympathetic activity. Boys with FXS did not display the expected patterns of heart activity in response to phases of increasing challenge, and sympathetic and parasympathetic systems did not appear coordinated in these boys with FXS. Clinical factors may be related to neural regulation of heart activity while molecular factors do not appear to be.     

围产期母亲和胎儿心动周期信号分析

同时分析围产期胎儿和孕妇心动周期信号的数字特征(混沌和谱特征)以评价自主神经系统功能。用可视化程序设计的方法实现提取和分析围产期母亲和胎儿心动周期信号。受试者取仰卧位，心电信号从置于腹壁下部耻骨联合导联获得。胎儿心电信号用小波分解进行信号预处理。采用本实验室已经完成开发的技术实现心动周期信号数字特征的分析。该系统可以评价胎儿和孕妇的自主神经系统功能，特别是分别定量评价交感和副交感神经系统功能；该系统还可用以预测胎儿窘迫。胎儿和其它年龄段的心动周期信号数字特征随年龄的变化提示了自主神经系统的发育、成熟和衰老的生理过程，基于这一点我们可以寻找抗衰老的方法；胎儿的心动周期信号数字特征介于新生儿和成人之间，提示胎儿的自主神经系统的调节可能受母体神经内分泌系统的影响。     

Ultrastructure of the neuroglial fatty metamorphosis (virchow) in the perinatal period

Summary The ultrastructure of neuroglial fatty metamorphosis (GFM) has been investigated in the telencephalic white matter of 12 premature and mature infants (gestational age 22–40 weeks; survival 0–96 days). GFM was found in all cases apart from a 22-week-old fetus, and involves predominantly astrocytic cells (68.8%), then glioblasts (43.5%), but only 7.4% of oligodendrocytes. GFM, therefore, seems to be independent of the myelination process and indicates the vulnerability of the immature neuroglial population in the metabolic and circulatory disorders of the perinatal period. Since GFM is found in almost all children dying within the early postnatal period, this subtle alteration reflects a special form of minimal brain damage. The relationship between GFM, astrocytic hypertrophy and periventricular leucomalacia and their role in the telencephalic leucoencephalopathy are discussed.

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Zusammenfassung Die Gliazellverfettung im unreifen Großhirn-Marklager wurde bei 12 Kindern ultrastrukturell untersucht (Gestationsalter 22–40 Wochen; Überlebenszeit 0–96 Tage). Die fettige Metamorphose der Neuroglia (Virchow) fand sich in allen Fällen, ausgenommen den 22 Wochen alten Feten, und betrifft vorwiegend junge Astrozyten (68,8%), ferner zu 43,5% unreife Vorstufen, jedoch nur zu 7.4% die (z.Z. der Geburt erst in Erscheinung tretende) Oligodendroglia. Die Fett-Metamorphose der unreifen Glia stellt einen sensiblen Indikator für metabolisch-zirkulatorische Störungen der Perinatalperiode dar und erfolgt unabhängig von dem Prozeß der Markscheidenbildung. Zusammen mit einer oft auffälligen Astroglia-Proliferation ist die intracytoplasmatische Akkumulation nicht membrangebundener Lipide Ausdruck einer temporären Differenzierungsstörung der unreifen Neuroglia. Die resultierende Reifungsdissoziation mit Unterdrückung der oligodendrozytären Zellinie führt zur retardierten Markscheidenbildung und dem Bild der telencephalen Leucoencephalopathie.