Cell kinetics and radiation pathology

Conclusion Radiation pathology is a general term describing the damage that occurs in tissues after irradiation. After the very low doses, received by the normal working population, no major pathology is seen. There is a hazard of cancer induction if DNA damage that has been inflicted in an individual cell is repaired in such a way that the DNA remains intact but rearranged. This radiation carcinogenesis is however a low risk compared with many chemical carcinogens in the environment and in cancer chemotherapy.The treatment of cancer by radiation is now commonly accepted as one of the most effective forms of treatment. It can kill tumour cells effectively, but the dose that can be given is limited by the normal tissues that are inevitably included in the beam. Cell function is maintained for some time even after very large doses. However normal tissues show a loss of function and structure because the proliferating subcompartment of each tissue is depleted as the radiation injured cells fail to divide and die. The time at which the cell deficit is detected varies from hours in some tissues to months or years in others. It depends upon the normal rate of cell turnover. The apparent sensitivity of each tissue therefore depends upon the time at which the assessment is made. Lung and kidney would appear very resistant at 1–3 months post irradiation, but would seem very radiosensitive at 6–12 months as their latent damage is expressed.The ultimate expression of radiation pathology is the death of the whole animal as the essential organ function fails. The time of this death is only comprehensible if the time sequence and the proliferation kinetics of the target cells are taken into account. It must be recognised that it is initial damage to the clonogenic cells, not to the differentiated cells per se that is important.     

Human MutY: gene structure,protein functions and interactions,and role in carcinogenesis

Faithful maintenance of the genome is crucial to the individual and the species. Oxidative DNA damage, such as 8-oxo-7,8-dihydroguanine (8-oxoG), poses a major threat to genomic integrity. 8-OxoG can mispair with 2-deoxycytidine 5-triphosphate or with 2-deoxyadenosine triphosphate during DNA replication, forming C8-oxoG and A8-oxoG mispairs. Human MutY is responsible for recognition and removal of the inappropriately inserted adenine in an A8-oxoG mispair. If unrepaired, the A8-oxoG mispairs can result in deleterious C:G to A:T transversions. Human MutY functions in a postreplication repair pathway and is targeted to the newly synthesized daughter strand of DNA for removal of the adenine base. The human MutY protein is targeted to both the mitochondria and the nucleus and associates with the proliferating cell nuclear antigen, apurinic/ apyrimidinic endonuclease 1, replication protein A and mutS homolog 6 proteins. Mutations in the human MutY gene and defective activity of the human MutY protein have been detected in cancer. A direct correlation between defective A8-oxoG repair and increased levels of genomic 8-oxoG has now been established.Received 10 February 2003; received after revision 7 April 2003; accepted 14 April 2003     

Fibrocytes: a unique cell population implicated in wound healing

Following tissue damage, host wound healing ensues. This process requires an elaborate interplay between numerous cell types which orchestrate a series of regulated and overlapping events. These events include the initiation of an antigen-specific host immune response, blood vessel formation, as well as the production of critical extracellular matrix molecules, cytokines and growth factors which mediate tissue repair and wound closure. Connective tissue fibroblasts are considered essential for successful wound healing; however, their origin remains a mystery. A unique cell population, known as fibrocytes, has been identified and characterized. One of the unique features of these blood-borne cells is their ability to home to sites of tissue damage. This article reviews the identification and characterization of fibrocytes, summarizes the potential role of fibrocytes in the numerous steps of the wound-healing process and highlights the potential role of fibrocytes in fibrotic disease pathogenesis.Received 25 November 2002; received after revision 31 December 2002; accepted 16 January 2003     

自然费用下设备更换和维修的最优化

本文在更自然的费用结构下,用马尔柯夫决策规刻,证明了设备更换和维修问题对折扣目标和平均目标都存在一种特殊的最优策略——控制限策略。     

政企联合储备模式下应急物资储备及采购定价研究

为提高灾害发生后应急物资的供给能力，降低政府单独储备应急物资时承担的风险及成本，文章设计了一个基于政府主导的政企联合储备应急物资模型，并对合作中的两个关键问题——物资储备量及采购定价进行了研究.在考虑政企双方同时参与现货市场的情形下，文章通过逆序推导法给出了企业最优储备量决策及政府最优采购定价，并与政府单独储备模式进行了对比分析，发现联合储备模式能够有效降低政府采购成本，提高企业收益，实现双方合作共赢.此外，文章还进一步分析了灾害事件发生概率，政府自身储备量等因素对政企双方决策，各自成本收益及增减变化的影响，发现随着灾害事件发生概率和现货市场采购价格的增加，联合储备模式的优越性越发明显，而过多的政府自身储备量及企业参与现货市场的行为则会阻碍企业参与合作的积极性，削弱联合储备的优越性.文章的研究为政府联合企业开展应急物资储备工作提供了操作策略和指导法则.     

F-风险入侵生成与承灾类特征

基于公共突发事件的动态性和不确定性，利用单向S-粗集，定义了承灾类与承灾元的概念，讨论了承灾类F-风险入侵生成、F-风险入侵损失和F-入侵风险度。提出了F-风险入侵损失与入侵风险度关系定理、F-风险入侵损失规律与入侵风险度规律关系定理，以及F-风险入侵分辨定理和入侵风险度分辨定理。给出了一个研究F-入侵风险度规律识别准则及其应用的简单案例。     

危险源扩散环境下救援物资协同调度问题

面对生物恐怖威胁,为提高应急救援系统应对潜在危险源的能力,围绕危险源扩散环境下的潜在需求网络,研究确定需留后备救援物资的储备库,为每个疫区储备库计算需保留的救援物资量及疫区周围各储备库调配物资量.在此基础上,引入出救风险系数概念,研究建立了储备网络资源协同动态调度优化模型.通过数值仿真验证了模型的有效性,实现了储备网络中应急救援物资协同调度优化.合理调度应急救援物资,既可满足规定的应急服务水平,又可增强救援系统应急能力.     

基于城际多HUB的应急物流网络协同动力学模型分析

为了提高应急物流在生物反恐体系中的应急物资配送水平,完善城际应急物流系统,根据生物危险源扩散规律,建立了多层次的城际多HUB应急物流网络协同模型,分析了城际多HUB应急物流网络协同状态下,处理危机的流程.从系统动力学角度建立了传染病模型,并讨论了多HUB物流网络协同状态下,应急物资在最短时间内,以最合适的量配送到疫区的方法.研究表明,根据城际多HUB应急物流网络协同性的研究,能够有效控制生物危险源的扩散,提高应急系统多个城市之间的应急管理水平.     

急性颅内血肿并静脉窦损伤15例报告

目的探讨急性颅内血肿并静脉窦损伤诊断、治疗、手术方法。方法急性颅内血肿清除时修补静脉窦损伤,术中行明胶海棉压迫,硬脑膜悬吊8例,上矢状窦前1/3损伤断裂结扎1例,间断缝合、骨膜、硬脑膜翻转修补缝合5例,术中修补硬脑膜6例。结果本组治愈11例,上肢感觉障碍2例,死亡2例,1例死亡于手术中。结论对于静脉窦损伤患者尽量做到早诊断、早治疗,抢救患者的生命,提高治愈率。     

城市公共安全应急系统中一维洪水演进及其可视化研究

基于圣维南方程组建立河渠一维洪水演进模型,用Matlab编制程序进行计算并将结果数据导入到Arc-GIS中,实现各断面水位和流量的实时动态显示,同时利用Matlab的作图功能绘制每个断面的水位、流量随时间变化的过程图,从而实现了城市公共安全应急系统中一维洪水演进的实时可视化.