广义LESLIE矩阵模型的稳定年龄结构及其性质

〔1〕提出了一个描述生物种群动态的矩阵模型——广义Leslie矩阵模型。这个模型是Leslie矩阵模型的一个推广,它考虑了昆虫发育过程中个体在虫态发育历期上的差异。因此与普通Leslie矩阵模型相比,该模型更适于描述昆虫种群的动态。〔2〕对广义Leslie矩阵模型的渐近性质做了分析,给出了相应的稳定年龄结构的表达式,同时从马氏链的观点出发,给出了种群年龄结构渐近稳定或周期变化的充要条件。本文是〔2〕的继续,将给     

川西地区岷江柏种群生命表与生存分析

岷江柏 (CupressuschengianaS .Y .Hu)是国家II级保护植物 ,处于渐危状态 ,由于缺乏种群结构的研究限制了对该种的全面认识和有效保护。本文调查分析了岷江柏种群的年龄结构 ,编制了岷江柏种群的特定时间生命表 ,绘制了种群的存活曲线、死亡率曲线和消失率曲线 ,并用 4个生存函数对该种群进行了生存分析。结果表明 ,川西地区岷江柏种群处于中龄林阶段 ,种群存活曲线属Deevey III型 ,年龄结构呈增长型 ,死亡率曲线与消失率曲线变化趋势基本一致。在这一发育过程中有两个死亡高峰 ,一个出现在幼苗向幼树的过渡期(5～ 15a) ,环境胁迫是幼苗高死亡率的关键 ,另一个出现在从中龄向老龄过渡的阶段 (130～ 2 30a) ,环境制约以及人为砍伐是高死亡率的根本原因。种群生存分析表明 ,岷江柏种群累计死亡率单调增加 ,生存率单调下降 ,130年以后种群的累计死亡率均超过 95 % ,生存率都不足 5 % ,危险率超过了生存率 ;种群发育过程总体表现为前期增长 ,中期稳定 ,后期衰退。对大小结构与年龄结构的对比分析表明 ,目前广泛采用的大小结构代替年龄结构的分析方法对岷江柏这样的长寿慢生树种误差较大。     

污染与捕获对Logistic种群的影响

本文研究污染与捕获并存时Logistic种群的β生存问题．证明了种群若不永远β生存，则必在有限时间内绝灭．给出了种群β生存、β绝灭条件，并对临界情况作了讨论．     

一个竞争模型的一致持续生存

本文研究一个带有时滞的竞争模型的一致持续生存。首先证明了离散时滞不影响种群的一致持续生存,接着在种群增长率是周期的假设下讨论了正周期解的存在性,最后给出了连续时滞模型一致持续生存的充分条件。     

具有时间依赖转移率的昆虫种群的稳定性理论

研究Leslie种群的稳定性一直是种群动态研究中的重要课题。近几年,这项工作已得到比较完满的解决。考虑到昆虫个体在发育历期上的差异,〔1〕对Leslie模型进行了推广,提出了广义Leslie矩阵模型。〔2〕在转移率为常数的情况下,讨论了有关广义Leslie种群的渐近稳定性等方面的问题。本文将研究具有时间依赖转移率的广义Leslie种群的稳定性,给出一个具有时间依赖转移率的昆虫种群渐近于一个稳定的年龄分布的充分条件。     

污染环境中的Smith系统生存分析

研究了环境污染对Smith系统中种群生存的长期影响,考虑到种群数量的变化对种群个体体内毒素浓度和环境中毒素浓度的影响,对传统的Smith系统进行了修正,并且给出了一些种群弱平均持续生存和绝灭的充分条件．在一定条件下得到了弱平均持续生存与绝灭的阈值．     

毒素对种群生存的影响

本文总结了近年来我们关于污染环境中毒素对种群生存影响这一重要课题的研究成果,利用我们提出的积分均值法,给出了新的持续生存概念,对一些模型得到了种群持续生存与绝灭的阈值,我们的工作是从单个种群到ｎ维食物链,从简化模型到未简化模型、从无限时间到有限时间逐步展开的;另外,我们还讨论了一些模型解的稳定性与吸收域。     

濒危树种五莲杨种群结构与动态特征

五莲杨（Populus wulianensis）为山东特有种，属于极小种群野生植物。以昆嵛山国家级自然保护区内的五莲杨种群为研究对象，旨在通过建立静态生命表，绘制种群存活曲线来描述其种群的结构特征，使用4个生存函数进行种群的生存分析，运用数量动态指数定量描述种群的数量动态特征，并采用谱分析方法揭示种群年龄结构更替过程的周期性和结构的波动性。结果表明：（1）五莲杨种群龄级结构呈基部极宽顶部狭窄的金字塔形，种群存活曲线趋近于Deevey-Ⅲ型，幼龄个体数量丰富但存活率极低，种群增长性低；（2）死亡率和消失率曲线呈现"降低-增长-降低-增长"的复杂动态变化，种群在Ⅰ龄级死亡率最高；（3）生存分析表明该种群生存力低，具有前期锐减，中期和后期衰退的特点，呈现衰退特征；（4）种群数量动态指数显示种群呈增长趋势，但种群稳定性差且抗干扰能力弱；（5）谱分析表明该种群除受到基波影响外还受到个别小周期波动的显著影响。繁殖策略、有限的空间和资源是限制五莲杨种群增长的主要因素。建议对五莲杨种群进行原地保护的同时，通过输入实生苗防止种群在多个世代后因无性繁殖而导致抗性和遗传多样性降低。     

稻纵卷叶螟(Cnaphalocrocis medinalis)种群动态的电子计算机模拟

本文试图用电子计算机模拟预测稻纵卷叶螟种群变化。根据本校昆虫研究所对该虫生命表研究的结果及其有效积温的观察,用22个子式组建了该虫种群的预测式。整个工作过程按照昆虫生活史的发育顺序进行。发生期根据有效积温计算,发生量主要根据生命表的累计存活率计算。为了消除原始调查数据的随机误差,还采用两倍三天移动平均的方法来对原始数据进行修匀。本文给出计算例子,经过上机实际计算,说明基本上达到设计要求,但此式尚未在生产实践中进行过实际的预测检验。     

昆虫种群的生长──扩散模型研究

根据昆虫种群生长规律和空间扩散规律,本文提出了建立昆虫种群生长-扩散统一模型的条件,并提出了12种可能的生长-扩散统一模型．其中的模型包括了指数增长（减少）,逻辑斯蒂增长和威布尔生长规律,同时包括幂率衰减,指数衰减和随机扩散等扩散规律;同时这些模型可以单独描述单一的生长过程或扩散过程。文中以水稻害虫青翘蚁形隐翘虫的扩散和种群数量消长为例,研究了文中模型的应用问题,结果表明本文的模型用于描述昆虫种群的方向性扩散一指数衰减生长的过程是合适的。     

How to compare the lower developmental thresholds

According to the hypothesis of isomorphy rate, all the lower developmental thresholds of different developmental stages of an insect are equal. However, there is lack of a formal statistical method for testing whether there is a significant difference among the lower developmental thresholds on the basis of the traditional linear model describing developmental rate as a linear function of temperature. For comparing the lower developmental thresholds of different developmental stages, a new method based on the Chow test is proposed in the current study. Another feasible way based on the linear model proposed by Ikemoto and Takai is also proposed. The lower developmental thresholds can be compared by the analysis of covariance on this linear model. The current study can be used to test the hypothesis of isomorphy rate. When comparing the lower developmental thresholds of different geographical populations for one insect species, the two methods proposed here are also applicable.     

Do Insect Populations Die at Constant Rates as They Become Older? Contrasting Demographic Failure Kinetics with Respect to Temperature According to the Weibull Model

Temperature implies contrasting biological causes of demographic aging in poikilotherms. In this work, we used the reliability theory to describe the consistency of mortality with age in moth populations and to show that differentiation in hazard rates is related to extrinsic environmental causes such as temperature. Moreover, experiments that manipulate extrinsic mortality were used to distinguish temperature-related death rates and the pertinence of the Weibull aging model. The Newton-Raphson optimization method was applied to calculate parameters for small samples of ages at death by estimating the maximum likelihoods surfaces using scored gradient vectors and the Hessian matrix. The study reveals for the first time that the Weibull function is able to describe contrasting biological causes of demographic aging for moth populations maintained at different temperature regimes. We demonstrate that at favourable conditions the insect death rate accelerates as age advances, in contrast to the extreme temperatures in which each individual drifts toward death in a linear fashion and has a constant chance of passing away. Moreover, slope of hazard rates shifts towards a constant initial rate which is a pattern demonstrated by systems which are not wearing out (e.g. non-aging) since the failure, or death, is a random event independent of time. This finding may appear surprising, because, traditionally, it was mostly thought as rule that in aging population force of mortality increases exponentially until all individuals have died. Moreover, in relation to other studies, we have not observed any typical decelerating aging patterns at late life (mortality leveling-off), but rather, accelerated hazard rates at optimum temperatures and a stabilized increase at the extremes.In most cases, the increase in aging-related mortality was simulated reasonably well according to the Weibull survivorship model that is applied. Moreover, semi log- probability hazard rate model illustrations and maximum likelihoods may be usefully in defining periods of mortality leveling off and provide clear evidence that environmental variability may affect parameter estimates and insect population failure rate. From a reliability theory standpoint, failure rates vary according to a linear function of age at the extremes indicating that the life system (i.e., population) is able to eliminate earlier failure and/or to keep later failure rates constant. The applied model was able to identify the major correlates of extended longevity and to suggest new ideas for using demographic concepts in both basic and applied population biology and aging.     

Mathematical hazard models of mortality: an alternative to model life tables

A five-parameter competing hazard model of the age pattern of mortality is described, and methods of fitting it to survivorship, death rate, and age structure data are developed and presented. The methods are then applied to published life table and census data to construct life tables for a Late Woodland population, a Christian period Nubian population, and the Yanomama. The advantage of this approach over the use of model life tables is that the hazard model facilitates life-table construction without imposing a particular age pattern of mortality on the data. This development makes it possible to use anthropological data to extend the study of human variation in mortality patterns to small populations.     

Estimating developmental and mortality rates and stage recruitment from insect stage-frequency data

A model for the analysis of insect stage-frequency data is developed which includes stage-specific variable developmental periods and stage-specific daily survival rates. The model can predict the development of an insect population through its developmental stages and consequently may form the basis for a simulation model of the population.     

A motoneuron spared from steroid-activated developmental death by removal of descending neural inputs exhibits stable electrophysiological properties and morphology

Neurons die during the development of nervous systems. The death of specific, idenified motoneuros during metamorphosis of the tobacco hornworm, Manduca sexta, provides an accessible model system in which to study the regulation of postembryonic neuronal death. Hormones and descending neural inputs have been shown toinfluence the survival of abdominal motoneurons during the first few days of adult life in this insect. Motoneurons prevented from undergoing the normal process of developmental degeneration by removal of neural inputs were examined at the physiological and structural levels using several cell imaging techniques. Although these neurons lost their muscle targets and experienced the endocrine cue that normally triggers death, they showed no overt electrophysiological or morphological signs of degeneration. Thus, by appropriate intervention, the MN-12 motoneuron can be spared from developmental neuronal death and remain as a functioning supernumerary element in the mature nervous system. © 1995 John Wiley & Sons, Inc.     

Effects of Infection on Honey Bee Population Dynamics: A Model

We propose a model that combines the dynamics of the spread of disease within a bee colony with the underlying demographic dynamics of the colony to determine the ultimate fate of the colony under different scenarios. The model suggests that key factors in the survival or collapse of a honey bee colony in the face of an infection are the rate of transmission of the infection and the disease-induced death rate. An increase in the disease-induced death rate, which can be thought of as an increase in the severity of the disease, may actually help the colony overcome the disease and survive through winter. By contrast, an increase in the transmission rate, which means that bees are being infected at an earlier age, has a drastic deleterious effect. Another important finding relates to the timing of infection in relation to the onset of winter, indicating that in a time interval of approximately 20 days before the onset of winter the colony is most affected by the onset of infection. The results suggest further that the age of recruitment of hive bees to foraging duties is a good early marker for the survival or collapse of a honey bee colony in the face of infection, which is consistent with experimental evidence but the model provides insight into the underlying mechanisms. The most important result of the study is a clear distinction between an exposure of the honey bee colony to an environmental hazard such as pesticides or insecticides, or an exposure to an infectious disease. The results indicate unequivocally that in the scenarios that we have examined, and perhaps more generally, an infectious disease is far more hazardous to the survival of a bee colony than an environmental hazard that causes an equal death rate in foraging bees.     

A statistical model for red blood cell survival

A statistical model for the survival time of red blood cells (RBCs) with a continuous distribution of cell lifespans is presented. The underlying distribution of RBC lifespans is derived from a probability density function with a bathtub-shaped hazard curve, and accounts for death of RBCs due to senescence (age-dependent increasing hazard rate) and random destruction (constant hazard), as well as for death due to initial or delayed failures and neocytolysis (equivalent to early red cell mortality). The model yields survival times similar to those of previously published studies of RBC survival and is easily amenable to inclusion of drug effects and haemolytic disorders.     

昆虫发育速率与温度关系的数学模型研究

一、前言 昆虫生长发育过程中,温度是影响最显著的一个生态因子。对于昆虫发育历期与环境温度间的定量关系,前人提出过不少经验公式,分别在不同程度上反映了发育历期与温度间的密切依赖关系。     

Effect of low serum concentrations (0%-2.5%) on growth, production, and shear sensitivity of hybridoma cells

In a stirred culture of hybridoma cells, the effects of serum reduction from 2.5% to 0% on growth and monoclonal antibody porduction have been investigated. The shear sensitivity of cells from the same culture has been tested in a bubble column. Serum reduction does not greatly affect viable-cell concentrations, but cell specific monoclonal-antibody production rate shows a decreasing trend. A gradual increase in sensitivity for sparging, which is nor the result of a long-term biological effect, has beeen measured in a bubble column at decreasing fetal calf serum concentrations. Finally, the hypothetical killing-volume model describing the death rate of insect cells in bubble columns has now been completely validated for the pertinent hybridoma-cell line.     

Correcting for heterogeneity and non-comparability bias in multicenter clinical trials with a rescaled random-effect excess hazard model

In the presence of competing causes of event occurrence (e.g., death), the interest might not only be in the overall survival but also in the so-called net survival, that is, the hypothetical survival that would be observed if the disease under study were the only possible cause of death. Net survival estimation is commonly based on the excess hazard approach in which the hazard rate of individuals is assumed to be the sum of a disease-specific and expected hazard rate, supposed to be correctly approximated by the mortality rates obtained from general population life tables. However, this assumption might not be realistic if the study participants are not comparable with the general population. Also, the hierarchical structure of the data can induces a correlation between the outcomes of individuals coming from the same clusters (e.g., hospital, registry). We proposed an excess hazard model that corrects simultaneously for these two sources of bias, instead of dealing with them independently as before. We assessed the performance of this new model and compared it with three similar models, using extensive simulation study, as well as an application to breast cancer data from a multicenter clinical trial. The new model performed better than the others in terms of bias, root mean square error, and empirical coverage rate. The proposed approach might be useful to account simultaneously for the hierarchical structure of the data and the non-comparability bias in studies such as long-term multicenter clinical trials, when there is interest in the estimation of net survival.