Design features of the orb web of the spider, Araneus diadematus

Analysis of orb webs of the garden cross spider (Araneus diadematus)showed that these vertical webs have a significant up/down asymmetry.Experiments demonstrated that the spider runs down faster thanup, and thus confers a relatively higher foraging value to sectionsbelow the hub. Simulations suggested that the density of capturespiral spacing, prey size, and the density of prey should allaffect the capture efficiency of a web. Webs lose effectivecapture area because of overlap of the capture zone around eachthread; the smaller the prey, the finer the mesh can be withoutlosing effective area. Lower sectors of the web have a particularmesh size (height and length of capture spiral segments) throughout,whereas in the upper sectors the mesh size changes, wideningfrom the hub towards the periphery.     

恒河猴艾滋病模型中枢神经系统及淋巴结病变的电镜观察

目的观察恒河猴艾滋病模型不同感染阶段中枢神经系统及淋巴结的超微结构改变,探讨艾滋病的发病机制和病理改变的发展过程。方法 15只恒河猴,1只为正常对照,其余14只静脉注射感染SIVmac239猴艾滋病病毒,分别于感染后1周,2周,1个月,2个月,12个月,18个月取腹股沟淋巴结及下丘脑组织进行透射电镜检查。结果感染后1周即可出现淋巴结内淋巴细胞病变,表现为线粒体肿胀,嵴溶解,出现自噬体等。感染后2周及1个月时淋巴细胞病变主要表现为线粒体肿胀,嵴溶解;感染2个月时淋巴细胞细胞核形态出现明显改变。感染后12个月淋巴结内多数淋巴细胞出现病变,细胞肿胀,细胞器正常形态大部分消失;部分细胞出现溶解性坏死的特征。至感染后期（18个月时）,淋巴结内局部淋巴细胞稀疏,细胞核肿胀或形态不规则。中枢神经系统的病变在感染后1周出现,表现为神经纤维肿胀,感染后2周出现神经元的病变,表现为神经元线粒体肿胀,粗面内质网脱颗粒,尼氏体消失;神经纤维内出现空泡。感染后12个月及18个月时,神经元和神经纤维的病变加重。结论在SIV感染早期,淋巴结内淋巴细胞及中枢神经系统即可出现病变,维持一段相对稳定的时间后,至疾病后期,病变加重。中枢神经系统与淋巴结的超微结构病变发展规律有一定的相似性。     

Cytokine Actions in the Central Nervous System

Cytokines and chemokines have been implicated in contributing to the initiation, propagation and regulation of immune and inflammatory responses. Also, these soluble mediators have important roles in contributing to a wide array of neurological diseases such as multiple sclerosis, AIDS Dementia Complex, stroke and Alzheimers disease. Cytokines and chemokines are synthesized within the central nervous system by glial cells and neurons, and have modulatory functions on these same cells via interactions with specific cell-surface receptors. In this article, I will discuss the ability of glial cells and neurons to both respond to, and synthesize, a variety of cytokines. The emphasize will be on three select cytokines; interferon-gamma (IFN-γ), a cytokine with predominantly proinflammatory effects; interleukin-6 (IL-6), a cytokine with both pro- and anti-inflammatory properties; and transforming growth factor-beta (TGF-β), a cytokine with predominantly immunosuppressive actions. The significance of these cytokines to neurological diseases with an immunological component will be discussed.     

Riboflavin Homeostasis in the Central Nervous System

Abstract: The mechanisms by which riboflavin, which is not synthesized in mammals, enters and leaves brain, CSF, and choroid plexus were investigated by injecting [¹⁴C]riboflavin intravenously or intraventricularly. Tracer amounts of [¹⁴C]riboflavin with or without FMN were infused intravenously at a constant rate into normal, starved, or probenecid-pretreated rabbits. At 3 h, [¹⁴C]riboflavin readily entered choroid plexus and brain, and, to a much lesser extent, CSF. Over 85% of the [¹⁴C]riboflavin in brain and choroid plexus was present as [¹⁴C]FMN and [¹⁴C]FAD. The addition of 0.2 mmol/kg FMN to the infusate markedly depressed the relative entry of [¹⁴C]riboflavin into brain, choroid plexus, and, less so, CSF, whereas starvation increased the relative entry of [¹⁴C]riboflavin into brain and choroid plexus. After intraventricular injection (2 h), most of the [¹⁴C]riboflavin was extremely rapidly cleared from CSF into blood. Some of the [¹⁴C]riboflavin entered brain, where over 85% of the ¹⁴C was present as [¹⁴C]FMN plus [¹⁴C]FAD. The addition of 1.2³μmol FAD (which was rapidly hydrolyzed to riboflavin) to the injectate decreased the clearance of [¹⁴C]riboflavin from CSF and the phosphorylation of [¹⁴C]riboflavin in brain. Probenecid in the injectate also decreased the clearance of [¹⁴C]riboflavin from CSF. These results show that the control of entry and exit of riboflavin is the mechanism, at least in part, by which total riboflavin levels in brain cells and CSF are regulated. Penetration of riboflavin through the blood-brain barrier, saturable efflux of riboflavin from CSF, and saturable entry of riboflavin into brain cells are three distinct parts of the homeostatic system for total riboflavin in the central nervous system.     

TWEAK and the Central Nervous System

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a member of the tumor necrosis factor superfamily that acts on responsive cells via binding to a cell surface receptor named fibroblast growth factor-inducible 14 (Fn14). TWEAK can regulate numerous cellular responses in vitro and in vivo. Recent studies have indicated that TWEAK and Fn14 are expressed in the central nervous system (CNS), and that in response to a variety of stimuli, including cerebral ischemia, there is an increase in TWEAK and Fn14 expression in perivascular astrocytes, microglia, endothelial cells, and neurons with subsequent increase in the permeability of the blood–brain barrier (BBB) and cell death. Furthermore, there is a growing body of evidence indicating that TWEAK induces the activation of the NF-κB in the CNS with release of proinflammatory cytokines and matrix metalloproteinases. In addition, inhibition of TWEAK activity by either treatment with a Fn14-Fc fusion protein or neutralizing anti-TWEAK antibodies has shown therapeutic efficacy in animal models of ischemic stroke, cerebral edema, and multiple sclerosis.     

Cytokine-Induced Inflammation in the Central Nervous System Revisited

Cytokines play an essential role as mediators of the immune response. They usually function as part of a network of interactive signals that either activate, enhance, or inhibit the ensuing reaction. An important contribution of this cytokine cascade is the induction of an inflammatory response that recruits and activates subsets of leukocytes that function as effector cells in the response to the sensitizing antigen. Proinflammatory cytokines activate endothelial cells (EC) to express adhesion molecules and induce the release of members of the chemokine family, thus focusing and directing the inflammatory response to sites of antigen recognition. However, the vasculature of the central nervous system (CNS) is highly specialized and restricts the access of components of the immune system to the CNS compartment. In this review, we address the question as to whether endothelial cells in the CNS respond differently to specific cytokines known to induce either a proinflammatory effect or a regulatory effect in systemic vascular beds.     

Electroneutral Cation-Chloride Cotransporters in the Central Nervous System

Several members of the cation-chloride cotransporter (solute carrier family 12, SLC12) gene family are expressed within the central nervous system, with one family member, the K+-Cl- cotransporter KCC2, exclusive to neurons. These transporters are best known for their roles in cell volume regulation and epithelial salt transport, but are increasingly receiving attention in neuroscience. In particular, intracellular chloride activity and hence the neuronal response to GABA and glycine appears to be determined by a balance between chloride efflux and influx through KCC2 and the Na+-K+-2Cl- cotransporter NKCC1, respectively. This relationship has important implications for neuronal development, sensory perception, neuronal excitability, and the response to neuronal injury. Finally, the association between loss of function in the K+-Cl- cotransporter KCC3, with a severe peripheral neuropathy associated with agenesis of the corpus callosum, has revealed an unexpected role for K+-Cl- cotransport in the development and/or maintenance of both the central and peripheral nervous systems.