首页 | 本学科首页   官方微博 | 高级检索  
文章检索
  按 检索   检索词:      
出版年份:   被引次数:   他引次数: 提示:输入*表示无穷大
  收费全文   301篇
  免费   7篇
  国内免费   10篇
化学   157篇
力学   10篇
综合类   9篇
数学   108篇
物理学   34篇
  2024年   12篇
  2023年   15篇
  2022年   36篇
  2021年   23篇
  2020年   25篇
  2019年   22篇
  2018年   5篇
  2017年   17篇
  2016年   15篇
  2015年   16篇
  2014年   8篇
  2013年   15篇
  2012年   10篇
  2011年   14篇
  2010年   9篇
  2009年   9篇
  2008年   7篇
  2007年   8篇
  2006年   5篇
  2005年   7篇
  2004年   7篇
  2003年   5篇
  2002年   7篇
  2001年   3篇
  2000年   5篇
  1999年   2篇
  1998年   3篇
  1997年   1篇
  1996年   2篇
  1995年   1篇
  1994年   1篇
  1991年   2篇
  1985年   1篇
排序方式: 共有318条查询结果,搜索用时 15 毫秒
261.
裴伟东  刘忠信  陈增强  袁著祉 《物理学报》2008,57(11):6777-6785
传统的病毒传播模型在无限大无标度网络上不存在病毒传播阈值,即无论病毒的传播速率多么低,病毒始终能够在网络中传播.但研究发现,这个结论是在网络中存在超级传染者的假设下得到的,然而许多真实的无标度网络中并不存在超级传染者.因此,文章提出了一个最大传染能力限定的病毒传播模型,并从理论上证明了在最大传染能力限定的无限大无标度网络上,病毒传播阈值是存在的;同时,也分析了最大传染能力限定下非零传播阈值与有限规模网络下非零传播阈值的本质区别,并解释了为什么人们总是认为传统病毒传播模型对许多真实网络病毒感染程度估计过高的关键词:无标度网络最大传染能力传播阈值感染程度  相似文献   
262.
We propose a two-species infection model, in which an infected aggregate can gain one monomer from a healthy one due to infection when they meet together. Moreover, both the healthy and infected aggregates may lose one monomer because of self-death, but a healthy aggregate can spontaneously yield a new monomer. Consider a simple system in which the birth/death rates are directly proportional to the aggregate size, namely, the birth and death rates of the healthy aggregate of size k are J1 k and J2k while the self-death rate of the infected aggregate of size k is J3k. We then investigate the kinetics of such a system by means of rate equation approach. For the J1 〉 J2 case, the aggregate size distribution of either species approaches the generalized scaling form and the typical size of either species increases wavily at large times. For the J1 = J2 case, the size distribution of healthy aggregates approaches the generalized scaling form while that of infected aggregates satisfies the modified scaling form. For the J1 〈 J2 case, the size distribution of healthy aggregates satisfies the modified scaling form, but that of infected aggregates does not scale.  相似文献   
263.
In this paper, a mathematical model for HILV-I infection of CD4+ T-cells is investigated. The force of infection is assumed be of a function in general form, and the resulting incidence term contains, as special cases, the bilinear and the saturation incidences. The model can be seen as an extension of the model [Wang et al. Mathematical analysis of the global dynamics of a model for HTLV-I infection and ATL progression, Math. Biosci. 179 (2002) 207-217; Song, Li, Global stability and periodic solution of a model for HTLV-I infection and ATL progression, Appl. Math. Comput. 180(1) (2006) 401-410]. Mathematical analysis establishes that the global dynamics of T-cells infection is completely determined by a basic reproduction number R0R0. If R0?1R0?1, the infection-free equilibrium is globally stable; if R0>1R0>1, the unique infected equilibrium is globally stable in the interior of the feasible region.  相似文献   
264.
实验应用双抗体夹心免疫吸附试验(Double Antibodies—ELISA ELISA)检测获得感染鼠血清的循环抗体,所用抗原由日本血吸虫成虫和虫卵抗原免疫长爪沙鼠而获得.实验结果证明,用该试验检测长爪沙鼠感染日本血吸虫后6周内各期的抗体有高度的特异性,可为日本血吸虫感染模型的建立和考核疗效提供参考.  相似文献   
265.
考虑具有周期传染率和垂直传染的S IR流行病模型,分析了该模型的动力学性态.对小振幅的周期垂直传染率模型,给出了模型周期解的近似表达式,证明了该周期解的稳定性,并做了数值模拟,显示出周期解可能是全局稳定的.  相似文献   
266.
    
We develop two numerical methods to approximate the solutions of a pioneer model of the lesions at the cervical cells caused by the human papillomavirus. Such model is given by a nonlinear advection–diffusion-reaction partial differential equation and the goal of the schemes is to analyze the behaviour of the evolution of infected cells. The developed schemes consist of two explicit non standard finite differences numerical schemes which satisfy positivity conditions. They are based on the subequation method in the context of the non standard scheme methodology. Our approach provides an alternative method to the early diagnosis of the disease and may open up new lines of research.  相似文献   
267.
    
In this work, we integrate both density‐dependent diffusion process and Beddington–DeAngelis functional response into virus infection models to consider their combined effects on viral infection and its control. We perform global analysis by constructing Lyapunov functions and prove that the system is well posed. We investigated the viral dynamics for scenarios of single‐strain and multi‐strain viruses and find that, for the multi‐strain model, if the basic reproduction number for all viral strains is greater than 1, then each strain persists in the host. Our investigation indicates that treating a patient using only a single type of therapy may cause competitive exclusion, which is disadvantageous to the patient's health. For patients infected with several viral strains, the combination of several therapies is a better choice. Copyright © 2017 John Wiley & Sons, Ltd.  相似文献   
268.
In the last forty years, the rise of HIV has undoubtedly become a major concern in the field of public health, imposing significant economic burdens on affected regions. Consequently, it becomes imperative to undertake comprehensive investigations into the mechanisms governing the dissemination of HIV within the human body. In this work, we have devised a mathematical model that elucidates the intricate interplay between CD4+T-cells and viruses of HIV,employing the principles of fractional calculus. The production rate of CD4+T-cells, like other immune cells depends on certain factors such as age, health status, and the presence of infections or diseases. Therefore, we incorporate a variable source term in the dynamics of HIV infection with a saturated incidence rate to enhance the precision of our findings. We introduce the fundamental concepts of fractional operators as a means of scrutinizing the proposed HIV model.To facilitate a deeper understanding of our system, we present an iterative scheme that elucidates the trajectories of the solution pathways of the system. We show the time series analysis of our model through numerical findings to conceptualize and understand the key factors of the system.In addition to this, we present the phase portrait and the oscillatory behavior of the system with the variation of different input parameters. This information can be utilized to predict the long-term behavior of the system, including whether it will converge to a steady state or exhibit periodic or chaotic oscillations.  相似文献   
269.
    
In this paper, two non-standard finite difference (NSFD) schemes are proposed for a mathematical model of hepatitis B virus (HBV) infection with spatial dependence. The dynamic properties of the obtained discretized systems are completely analyzed. Relying on the theory of M-matrix, we prove that the proposed NSFD schemes is unconditionally positive. Furthermore, we establish that the NSFD method used preserves all constant steady states of the corresponding continuous initial boundary value problem (IBVP) model. We prove that the conditions for those equilibria to be asymptotically stable are consistent with the continuous IBVP model independently of the numerical grid size. The global asymptotical properties of the HBV-free equilibrium of the proposed NSFD schemes are derived via the construction of a suitable discrete Lyapunov function, and coincides with the continuous system. This confirms that the discretized models are dynamically consistent since they maintain essential properties of the corresponding continuous IBVP model. Finally, numerical simulations are performed from which it is demonstrated that the proposed NSFD method is advantageous over the standard finite difference (SFD) method.  相似文献   
270.
    
Establishment or spread of a viral infection within healthy individuals depends on exposure to a viral source, either through virus particles or through cells that have been infected. We assume that a potential infection has reached the site of the healthy target cells and we apply stochastic within-host models and multitype branching processes to investigate whether a major infection becomes established. The model includes multiple latent and actively infected stages. It is shown that the probability of a major infection is generally more likely after the virus has entered the target cell and the cell is actively infected. In some cases, the probability of a major infection is less likely if the burst size of actively infected cells is small.  相似文献   
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号