急性颅脑损伤患者外周血C-反应蛋白和IL-6水平的

目的检测急性颅脑损伤后患者外周血C-反应蛋白(CRP)和IL-6水平的动态变化,探讨其临床意义.方法选择77例不同病情的急性颅脑损伤患者作为研究对象,32例健康体检者作为对照组.采用免疫浊度法检测血浆CRP,ELISA法检测IL-6水平.结果急性颅脑损伤患者血浆CRP和IL-6水平均显著高于正常人对照组(P<0.01),且患者CRP和IL-6水平与病情呈正相关;各组患者在入院当天IL-6和CRP水平有所升高,并在入院1 d后继续升高,IL-6于3 d达最高水平,以后逐渐下降,CRP在1 d达高峰,随即开始下降;患者IL-6水平与CRP呈正相关(r＝0.556,P<0.01).结论急性颅脑损伤患者外周血IL-6和CRP水平的变化与病情严重程度密切相关,IL-6在急性颅脑损伤中可能通过促进肝脏合成CRP,在一定程度上对神经系统起保护作用.     

Regional astrocyte allocation regulates CNS synaptogenesis and repair

Astrocytes, the most abundant cell population in the central nervous system (CNS), are essential for normal neurological function. We show that astrocytes are allocated to spatial domains in mouse spinal cord and brain in accordance with their embryonic sites of origin in the ventricular zone. These domains remain stable throughout life without evidence of secondary tangential migration, even after acute CNS injury. Domain-specific depletion of astrocytes in ventral spinal cord resulted in abnormal motor neuron synaptogenesis, which was not rescued by immigration of astrocytes from adjoining regions. Our findings demonstrate that region-restricted astrocyte allocation is a general CNS phenomenon and reveal intrinsic limitations of the astroglial response to injury.     

Cyclic AMP-induced repair of zebrafish spinal circuits

Neurons in the human central nervous system (CNS) are unable to regenerate, as a result of both an inhibitory environment and their inherent inability to regrow. In contrast, the CNS environment in fish is permissive for growth, yet some neurons still cannot regenerate. Fish thus offer an opportunity to study molecules that might surmount the intrinsic limitations they share with mammals, without the complication of an inhibitory environment. We show by in vivo imaging in zebrafish that post-injury application of cyclic adenosine monophosphate can transform severed CNS neurons into ones that regenerate and restore function, thus overcoming intrinsic limitations to regeneration in a vertebrate.     

Interleukin-1 stimulates the secretion of hypothalamic corticotropin-releasing factor

There is now evidence that the immune system, during times of infectious challenge, can stimulate the secretion of glucocorticoids, the adrenal steroids that mediate important aspects of the response to stress. Specifically, secretion of interleukin-1 (IL-1), a monocyte lymphokine secreted after infection, appears at least in part responsible for this effect. Glucocorticoids are secreted in response to a neuroendocrine cascade involving, first, the brain, then the pituitary, and finally the adrenal gland. In this report, human IL-1 is shown to activate the adrenocortical axis at the level of the brain, stimulating the release of the controlling hormone corticotropin-releasing factor (CRF) from the hypothalamus. Infusion of IL-1 induced a significant secretion of CRF into the circulation exiting the hypothalamus, whereas immunoneutralization of CRF blocked the stimulatory effect of IL-1 on glucocorticoid secretion. IL-1 appeared to have no acute direct stimulatory effects on the pituitary or adrenal components of this system. Furthermore, IL-1 did not cause a nonspecific release of other hypothalamic hormones. Thus, the lymphokine acts in a specific manner to activate the adrenocortical axis at the level of the brain; this effect appears to be unrelated to the known pyrogenic effects of IL-1 within the hypothalamus.     

Deposits of amyloid beta protein in the central nervous system of transgenic mice.

Alzheimer's disease is characterized by widespread deposition of amyloid in the central nervous system. The 4-kilodalton amyloid beta protein is derived from a larger amyloid precursor protein and forms amyloid deposits in the brain by an unknown pathological mechanism. Except for aged nonhuman primates, there is no animal model for Alzheimer's disease. Transgenic mice expressing amyloid beta protein in the brain could provide such a model. To investigate this possibility, the 4-kilodalton human amyloid beta protein was expressed under the control of the promoter of the human amyloid precursor protein in two lines of transgenic mice. Amyloid beta protein accumulated in the dendrites of some but not all hippocampal neurons in 1-year-old transgenic mice. Aggregates of the amyloid beta protein formed amyloid-like fibrils that are similar in appearance to those in the brains of patients with Alzheimer's disease.     

川硬皮肿腿蜂雌蜂中枢神经系统解剖结构

应用解剖镜研究了川硬皮肿腿蜂Scleroderma sichuanensis雌蜂中枢神经系统的结构与分布.结果表明:川硬皮肿腿蜂中枢神经系统由脑和腹神经索组成,前中后脑分化不很明显,中脑相对于前后脑发达;腹神经索包括咽下神经节、2对胸神经节、5对腹神经节及纵贯各神经节的神经索;胸神经节位于前胸和中胸,腹神经节位于第1～6腹节节间膜下方.最后,比较了川硬皮肿腿蜂与其他膜翅目昆虫脑和咽下神经节的差异.图3参10     

Glial cell diversification in the rat optic nerve

A central challenge in developmental neurobiology is to understand how an apparently homogeneous population of neuroepithelial cells in the early mammalian embryo gives rise to the great diversity of nerve cells (neurons) and supporting cells (glial cells) in the mature central nervous system. Because the optic nerve is one of the several types of glial cells but no intrinsic neurons, it is an attractive place to investigate how neuroepithelial cells diversify. Studies of developing rat optic nerve cells in culture suggest that both cell-cell interactions and intrinsic cellular programs play important parts in glial cell diversification.     

急性脑梗塞与血清白细胞介素—6关系的初步探讨

用双抗体夹心ＥＬＩＳＡ法对４６例急性脑梗塞患者血清ＩＬ－６含量作了检测，结果显示：脑梗塞急性期和恢复期两组均明显高于健康人对照组（Ｐ＜０．００５，Ｐ＜０．０１）；恢复期组略低于急性期组，但无统计学意义（Ｐ＞０．０５）。急性期血清ＩＬ－６含量与脑梗塞估测体积呈正相关关系（ｒ＝０．６４，Ｐ＜０．０５），而与脑梗塞发生部位无关。脑梗塞体积越大，血清ＩＬ－６值越大，提示血清ＩＬ－６含量的测定可能作为早期判断急性脑梗塞脑损害程度的指标。     

Fate mapping analysis reveals that adult microglia derive from primitive macrophages

Microglia are the resident macrophages of the central nervous system and are associated with the pathogenesis of many neurodegenerative and brain inflammatory diseases; however, the origin of adult microglia remains controversial. We show that postnatal hematopoietic progenitors do not significantly contribute to microglia homeostasis in the adult brain. In contrast to many macrophage populations, we show that microglia develop in mice that lack colony stimulating factor-1 (CSF-1) but are absent in CSF-1 receptor-deficient mice. In vivo lineage tracing studies established that adult microglia derive from primitive myeloid progenitors that arise before embryonic day 8. These results identify microglia as an ontogenically distinct population in the mononuclear phagocyte system and have implications for the use of embryonically derived microglial progenitors for the treatment of various brain disorders.     

PirB restricts ocular-dominance plasticity in visual cortex

Experience can alter synaptic connectivity throughout life, but the degree of plasticity present at each age is regulated by mechanisms that remain largely unknown. Here, we demonstrate that Paired-immunoglobulin-like receptor B (PirB), a major histocompatibility complex class I (MHCI) receptor, is expressed in subsets of neurons throughout the brain. Neuronal PirB protein is associated with synapses and forms complexes with the phosphatases Shp-1 and Shp-2. Soluble PirB fusion protein binds to cortical neurons in an MHCI-dependent manner. In mutant mice lacking functional PirB, cortical ocular-dominance plasticity is more robust at all ages. Thus, an MHCI receptor is expressed in central nervous system neurons and functions to limit the extent of experience-dependent plasticity in the visual cortex throughout life. PirB is also expressed in many other regions of the central nervous system, suggesting that it may function broadly to stabilize neural circuits.     

Identification of a novel thyroid hormone receptor expressed in the mammalian central nervous system

A complementary DNA clone derived from rat brain messenger RNA has been isolated on the basis of homology to the human thyroid hormone receptor gene. Expression of this complementary DNA produces a high-affinity binding protein for thyroid hormones. Sequence analysis and the mapping of this gene to a distinct human genetic locus indicate the existence of multiple human thyroid hormone receptors. Messenger RNA from this gene is expressed in a tissue-specific fashion with highest levels in the central nervous system.     

Cell biology of synaptic plasticity

The nervous system of mammals retains throughout the animals' life-span the ability to modify the number, nature, and level of activity of its synapses. Synaptic plasticity is most evident after injury to the nervous system, and the cellular and molecular mechanisms that make it possible are beginning to be understood. Transplantation of brain tissue provides a powerful approach for studying mechanisms of synaptic plasticity. In turn, understanding the response of the central nervous system to injury can be used to optimize transplant survival and integration with the host brain.     

Alternative RNA processing: determining neuronal phenotype

On the basis of an analysis of the human and rat calcitonin genes and of a related gene, alternative RNA processing represents a developmental strategy of the brain to dictate tissue-specific patterns of polypeptide synthesis. This regulation allows the calcitonin gene to generate two messenger RNA's, one encoding the precursor of a novel neuropeptide, referred to as CGRP, which predominates in the brain, and the second encoding the precursor to the hormone calcitonin which predominates in thyroid C cells. The distribution of CGRP in the central and peripheral nervous system and in endocrine and other organ systems suggests potential functions in nociception, ingestive behavior, cardiovascular homeostasis, and mineral metabolism.     

Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1

Intraperitoneal administration of human recombinant interleukin-1 (IL-1) to rats can increase blood levels of corticosterone and adrenocorticotropic hormone (ACTH). The route by which IL-1 affects pituitary-adrenal activity is unknown. That the IL-1-induced pituitary-adrenal activation involves an increased secretion of corticotropin-releasing factor (CRF) is indicated by three lines of evidence. First, immunoneutralization of CRF markedly attenuated the IL-1-induced increase of ACTH blood levels. Second, after blockade of fast axonal transport in hypothalamic neurons by colchicine, IL-1 administration decreased the CRF immunostaining in the median eminence, indicating an enhanced release of CRF in response to IL-1. Third, IL-1 did not stimulate ACTH release from primary cultures of anterior pituitary cells. These data further support the notion of the existence of an immunoregulatory feedback circuit between the immune system and the brain.     

Hyperactivity and brain catecholamines in lead-exposed developing rats

Newborn rats that suckled mothers eating a diet containing 4 percent lead carbonate display hyperactivity, aggressiveness, and excessive stereotyped behavior starting at 4 weeks of age. There is an eightfold increase in the concentration of lead in brain, no change in norepinephrine, but a 20 percent decrease in dopamine relative to coetaneous controls. This suggests a relationship between central nervous system dysfunction due to lead and dopamine metabolism in brain.     

Brain barrier tissues: end organs for atriopeptins

Little is known about the pathophysiology of cerebral edema and other disturbances of water balance that involve the barrier tissues at the interface of blood and brain. The present experiments show that these barrier tissues contain receptors and second messenger systems for atriopeptins, recently identified cardiac peptides involved in peripheral water regulation. They also show that atriopeptins can alter the rate of cerebrospinal fluid production. Because the blood-brain and blood-cerebrospinal fluid barriers are involved in normal water movements in the central nervous system, these studies suggest that brain barrier tissues may be important end organs for the atriopeptins and that atriopeptins could have therapeutic application to disorders of water balance in the central nervous system. An isolated, purified population of atriopeptin receptor cells, obtained from choroid epithelium, was used in these experiments. This cell population may provide a valuable model system for investigating the intracellular biochemical mechanisms through which atriopeptins exert their actions.     

Cholecystokinin inhibits tail pinch-induced eating in rats

Peripheral administration of the COOH-terminal octapeptide of cholecystokinin in doses from 1 to 100 micrograms per kilogram of body weight (0.25 to 25.0 micrograms per rat) significantly antagonized tail pinch-induced eating in rats, an animal model for stress-induced human hyperphagia. Centrally administered cholecystokinin was effective only in high doses (3 micrograms into the cerebral ventricle). The finding that the minimal effective dose of cholecystokinin in suppressing stress-induced appetitive behavior is smaller after peripheral than central administration suggests that the peptide is acting on peripheral, as opposed to central nervous system, substrates.     

Identification and functional characterization of brainstem cannabinoid CB2 receptors

The presence and function of CB2 receptors in central nervous system (CNS) neurons are controversial. We report the expression of CB2 receptor messenger RNA and protein localization on brainstem neurons. These functional CB2 receptors in the brainstem were activated by a CB2 receptor agonist, 2-arachidonoylglycerol, and by elevated endogenous levels of endocannabinoids, which also act at CB1 receptors. CB2 receptors represent an alternative site of action of endocannabinoids that opens the possibility of nonpsychotropic therapeutic interventions using enhanced endocannabinoid levels in localized brain areas.     

Amacrine-signaled loss of intrinsic axon growth ability by retinal ganglion cells

The central nervous system (CNS) loses the ability to regenerate early during development, but it is not known why. The retina has long served as a simple model system for study of CNS regeneration. Here we show that amacrine cells signal neonatal rat retinal ganglion cells (RGCs) to undergo a profound and apparently irreversible loss of intrinsic axon growth ability. Concurrently, retinal maturation triggers RGCs to greatly increase their dendritic growth ability. These results suggest that adult CNS neurons fail to regenerate not only because of CNS glial inhibition but also because of a loss of intrinsic axon growth ability.