Some cytochemical peculiarities of the rat brain motor system after space flight

The results of cytochemical cytometry of rat brain suggest that a 9-day exposure of rats to microgravitation conditions lowers the activity of monoaminoxidase in the fibrous structures of layer V of the somatosensory cortex and in the head ofnucleus caudatus, as well as the activity of acetylcholine esterase in the bodies of neurons forming the head ofn. caudatus. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 3, pp. 288–290, March, 1995 Presented by the late O. S. Adrianov, Member of the Russian Academy of Medical Sciences     

Effect of the factors of space flight on erythropoiesis

After orbital flight for 19–22 days on the satellites Kosmos-605 and Kosmos-782 erythropoiesis of rats was inhibited and the morphology of their megakaryocytes was modified. These changes disappeared by the 25th–27th day after the flight.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 2, pp. 238–240, February, 1977.     

The effect of repetitive spreading depression on neuronal damage in juvenile rat brain

Spreading depression (SD) is pronounced depolarization of neurons and glia that travels slowly across brain tissue followed by massive redistribution of ions between intra- and extracellular compartments. There is a relationship between SD and some neurological disorders. In the present study the effects of repetitive SD on neuronal damage in cortical and subcortical regions of juvenile rat brain were investigated. The animals were anesthetized and the electrodes as well as cannula were implanted over the brain. SD-like event was induced by KCl injection. The brains were removed after 2 or 4 weeks after induction of 2 or 4 SD-like waves (with interval of 1 week), respectively. Normal saline was injected instead of KCl in sham group. For stereological study, paraffin-embedded brains were cut in 5 μm sections. The sections were stained with Toluidine Blue to measure the volume-weighted mean volume of normal neurons and the numerical density of dark neurons. The volume-weighted mean volume of normal neurons in the granular layer of the dentate gyrus and layer V of the temporal cortex in SD group were significantly decreased after four repetitive SD. Furthermore, densities of dark neurons in the granular layer of the dentate gyrus (after 2 weeks), the caudate–putamen, and layer V of the temporal cortex (after 4 weeks) were significantly increased in SD group. Repetitive cortical SD in juvenile rats may cause neuronal damage in cortical and subcortical areas of the brain. This may important in pathophysiology of SD-related neurological disorders.     

Protective effect of growth hormone on neuronal apoptosis after hypoxia-ischemia in the neonatal rat brain

Recent studies have shown that growth hormone (GH) can reduce neuronal loss after hypoxic-ischemic injury (HI) in neonatal and juvenile rat brains. Here, we investigated whether GH exerts its neuroprotective role through an anti-apoptotic effect in neonatal rat brains damaged by severe HI. Gross and histological observations showed that the extent of brain damage was found to be reduced in GH-treated brain at E7 after injury. In a terminal transferase-mediated dUTP nick-end-labeling (TUNEL) study, TUNEL-positive apoptotic cells were localized only at the damaged region in animals treated with saline, which was confirmed by an electron microscopy. In an immunohistochemical study with anti-bcl-2, -bax, -bad, -neuronal nitric oxide synthase (nNOS), -inducible NOS (iNOS) and -endothelial NOS (eNOS) antibodies, we observed that bax, bad, iNOS and eNOS were elevated in the saline-treated group. This study thus suggests that the protective role of GH against HI injury is mediated thorough an anti-apoptotic effect, which offers the possibility of a GH application for the treatment of neonatal HI encephalopathy.     

Immunochemical analysis of glial and neuronal fractions of rat brain

A method of obtaining antineuronal and antiglial immune sera is described. The results of a quantitative immunochemical analysis of antigens of neuronal and glial fractions of rat brain are given. Neurons were shown to contain four, and glia three brain-specific proteins; in addition, one or two proteins are common to these cellular fractions.Department of Normal Physiology, Moscow Medical Stomatological Institute. Course of Physiology, Medico-Biological Faculty, N. I. Pirogov Second Moscow Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. A. Fedorov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 83, No. 2, pp. 156–158, February, 1977.     

Multivariate multipoint linkage analysis of quantitative trait loci

Resolution of the genetic components of complex disorders may require simultaneous analysis of the contribution of individual quantitative trait loci (QTLs) to multiple variables. A likelihood approach is used to illustrate how the complexities of multivariate data may be resolved with multipoint linkage analysis. Sibling pair data were simulated from a model in which two QTLs and trait-specific polygenic effects explained all the sibling resemblance within and between five variables. Multipoint linkage analysis was used to obtain individual pair probabilities of having zero, one, or two alleles identical by descent, and these probabilities were applied in a weighted maximum-likelihood fit function. The results were compared with those obtained using conventional linear structural equation modeling to estimate the contribution of latent genetic factors to the genetic covariance in the multiple measures. Both analyses were conducted using the Mx package. Relatively poor agreement was found between genetic factors defined in purely statistical terms by varimax rotation of the first two factors of the genetic covariance matrix and the structure obtained by fitting a model jointly to the phenotypic and the multipoint linkage data.     

Use of tissue culture models to study neuronal regulatory trophic and toxic factors in the aged brain

Dementia is believed to result from the loss of selective neurons within the brain, but approaches for systematic study of that degenerative process are hampered by the complexity of the neuronal milieu. Tissue culture models provide a means to reduce dramatically the variables inherent in the study of neuronal plasticity. Three levels of complexity can be described: cellular and molecular diversity; primary and secondary interconnections; and finally, the dynamics influenced by age. The following review discusses the advantages and disadvantages of tissue culture models for the detailed study of neuronal trophic and toxic factors. Our selection of factors is broadened to include ions, intermediate metabolites, antioxidants, steroids, neuropeptides, gangliosides, metals, neurotransmitters, brain extracts, and protein molecules. Most of these factors have been shown to be altered in the aged brain, to have a significant effect on cultured neurons, or both. This multilevel analysis provides the reader with an overview of the events regulating neuronal survival, differentiation and death. An understanding of these basic questions is necessary to sequence the molecular events resulting in neuronal death.     

Multivariate genetic analysis of twin-family data on fears: Mx models

We describe the implementation of multivariate models of familial resemblance with the Mx package. The structural equation models allow for the effects of assortative mating, additive and dominant genes, common and specific environment, and both genetic and cultural transmission between generations. Two approaches are compared: a correlational one based on Fulker and a factor model described by Phillips and Fulker. Both are illustrated by application to published data on social fears and fear of leadership measured in monozygotic and dizygotic twins and their parents. In the example data, genetic dominance yields a more parsimonious explanation of the data than does cultural transmission, although neither is needed to obtain a good fit to the data. A model of reduced genetic correlation between generations also fits the data but has inherent limitations in this sample. Extensions to sex-limitation and more complex models are discussed.     

Statistical issues in the analysis of neuronal data

Analysis of data from neurophysiological investigations can be challenging. Particularly when experiments involve dynamics of neuronal response, scientific inference can become subtle and some statistical methods may make much more efficient use of the data than others. This article reviews well-established statistical principles, which provide useful guidance, and argues that good statistical practice can substantially enhance results. Recent work on estimation of firing rate, population coding, and time-varying correlation provides improvements in experimental sensitivity equivalent to large increases in the number of neurons examined. Modern nonparametric methods are applicable to data from repeated trials. Many within-trial analyses based on a Poisson assumption can be extended to non-Poisson data. New methods have made it possible to track changes in receptive fields, and to study trial-to-trial variation, with modest amounts of data.     

正常门腔间隙前后径大小及其影响因素的CT影像学研究

目的 探讨影响成人肝脏尾状叶下缘平面门腔间隙(PCS-IHCL)前后径大小的因素。方法 收集2011年1月—2016年7月潍坊医学院附属医院影像中心行腹部增强CT检查无椎体及门腔间隙(PCS)病变的64例患者的临床资料进行回顾性分析。其中男35例、女29例,年龄23～64(46.8±10.8)岁。在轴位增强CT图像上,测量PCS-IHCL最小前后径、门静脉最大前后径、下腔静脉最大短径、最大淋巴结前后径、邻近椎体最大横径、肝脏尾状叶最大前后径以及脐部水平的腹壁脂肪厚度,分析PCS-IHCL最小前后径与其他测量数值的相关性,并得出回归方程。结果 在轴位CT图像上,PCS-IHCL最小前后径为(0.345±0.246) cm;门静脉最大前后径为(1.277±0.126) cm,下腔静脉最大短径为(1.633±0.339) cm,邻近椎体最大横径为(4.214±0.455) cm;PCS-IHCL水平,PCS内共有11例显示有13个淋巴结,最大淋巴结前后径为(0.627±0.100) cm。PCS内肝脏尾状叶的最大前后径为(2.325±0.533) cm,脐部水平的腹壁脂肪厚度为(1.594±0.601) cm。PCS-IIHCL最小前后径与性别、年龄、门静脉的最大前后径、下腔静脉的最大短径、最大淋巴结前后径及邻近椎体的最大横径均无相关性(P值均＞0.05);与肝脏尾状叶前后径及腹壁脂肪的厚度呈正相关(t=4.649、2.403,P值均<0.05)。以PCS-IHCL最小前后径(＾Y)为应变量,以PCS内肝脏尾状叶的最大前后径(X₁)、脐部腹壁脂肪厚度(X₂)为自变量,得回归方程为:＾Y=-0.689+0.180X₁+0.122X₂,R²=0.472。结论 PCS-IHCL具有自身的解剖特点,肝脏尾状叶的最大前后径和腹壁脂肪含量是影响PCS-IHCL最小前后径的主要因素。在CT图像上注重PCS-IHCL的观察和测量,对PCS内病变及邻近脏器病变的诊断和治疗具有指导意义。     

应用改变的Golgi-Cox染色方法检测纹状体内神经元的结构与形态(英文)

为了改变传统的Golgi-Cox染色方法,使其在纹状体神经元形态与结构的研究中更加稳定和有效,本实验将昆明小鼠随机分为两组,一组采用传统的Golgi-Cox染色法,另一组采用改良的Golgi-Cox染色法。改良方法在传统方法的基础上,改变了几个关键环节,包括溶液的配制、固定、包埋、切片和定影等,然后对两种方法进行统计学比较和分析。在所有的数据采集工作完成之前,切片上的标记是封闭的。通过统计学分析比较,发现改良方法能够稳定地显示更多的树突分支(增加50%)、树突棘(增加63%)和胞体(增加一倍)。改良的Golgi-Cox染色方法比传统的Golgi-Cox染色方法更加稳定和敏感,在纹状体神经元树突和树突棘形态与结构研究中是一种可靠的技术方法。     

The neuronal organization of the periamygdaloid cortex in the rat brain

Cytoarchitectonic peculiarities and neuronal organization of periamygdaloid cortex (PAC) of rat brain was studied at three levels: rostral and caudal regions of central part and in posterior part of amygdala using Nissl and Golgi methods. Neuronal composition characteristic for each level and interrelations between neurons of different layers were determined. Different levels of PAC vary in architecture of neurons. Periamygdaloid cortex at the rostral level of central region is characterized with more simple organization.     

Alpha-Phenyl-n-tert-butyl-nitrone attenuates lipopolysaccharide-induced neuronal injury in the neonatal rat brain

Although white matter damage is a fundamental neuropathological feature of periventricular leukomalacia (PVL), the motor and cognitive deficits observed later in infants with PVL indicate the possible involvement of cerebral neuronal dysfunction. Using a previously developed rat model of white matter injury induced by cerebral lipopolysaccharide (LPS) injection, we investigated whether LPS exposure also results in neuronal injury in the neonatal brain and whether alpha-phenyl-n-tert-butyl-nitrone (PBN), an antioxidant, offers protection against LPS-induced neuronal injury. A stereotactic intracerebral injection of LPS (1 mg/kg) was performed in Sprague-Dawley rats (postnatal day 5) and control rats were injected with sterile saline. LPS exposure resulted in axonal and neuronal injury in the cerebral cortex as indicated by elevated expression of beta-amyloid precursor protein, altered axonal length and width, and increased size of cortical neuronal nuclei. LPS exposure also caused loss of tyrosine hydroxylase positive neurons in the substantia nigra and the ventral tegmental areas of the rat brain. Treatments with PBN (100 mg/kg) significantly reduced LPS-induced neuronal and axonal damage. The protection of PBN was associated with an attenuation of oxidative stress induced by LPS as indicated by the reduced number of 4-hydroxynonenal, malondialdehyde or nitrotyrosine positive cells in the cortical area following LPS exposure, and with the reduction in microglial activation stimulated by LPS. The finding that an inflammatory environment may cause both white matter and neuronal injury in the neonatal brain supports the possible anatomical correlate for the intellectual deficits and the other cortical and deep gray neuronal dysfunctions associated with PVL. The protection of PBN may indicate the potential usefulness of antioxidants for treatment of these neuronal dysfunctions.     

Multivariate behavioral genetic analysis of twin data on scholastic abilities

Multivariate behavioral genetic analyses may employ either genetic and environmental correlations or phenotypically standardized covariances to assess the structure of genetic and environmental influences. Correlations and phenotypically standardized covariances answer different questions—correlations are appropriate for understanding the nature of genetic and environmental influences, whereas covariances are approapriate for determining the etiology of phenotypic correlations. The ratio of the genetic and environmental covariances to the phenotypic correlation yields estimates of bivariate heritability and environmentality, measures of the extent to which observed phenotypic covariance is due to genetic and environmental influences. Multivariate analyses of genetic and environmental correlations and covariances are illustrated with twin data on scholastic abilities. Factor analyses of correlations suggest that the same set of genes affects the major areas of academic achievement and that the environmental influences are similarly structured. Analyses of phenotypically standardized covariances indicate that the structures of genetic and environmental influences as they contribute to phenotypic resemblance among scholastic abilities are both similar and simple: there are one general genetic factor and one general environmental factor. Bivariate heritabilities and environmentalities are similar in magnitude, indicating that the strong phenotypic relationship among scholastic abilities is due roughly equally to genetic and environmental influences.Preparation of this article was supported in part by NICHD Research Grant HD-10333 and by N/AAA K01-AA00041.     

Multivariate behavioral genetic analysis of correlations vs. phenotypically standardized covariances

Factor analysis is frequently employed in multivariate behavioral genetic analyses to explore the underlying structures of genetic and environmental influences. Different but related questions are addressed when genetic and environmental correlations versus phenotypically standardized genetic and environmental covariances are factor analyzed. The resulting factor loadings are related in that phenotypically standardized covariance factor loadings are the loadings obtained from the correlation matrix weighted by the square roots of the corresponding heritabilities or environmentalities. This relationship can aid in understanding the differences in factor structures obtained from genetic and environmental correlation matrices and from the corresponding phenotypically standardized genetic and environmental covariance matrices.