Ross’ epidemic model describing the transmission of malaria uses two classes of infection, one for humans and one for mosquitoes. This paper presents a stochastic extension of a deterministic vector-borne epidemic mo...Ross’ epidemic model describing the transmission of malaria uses two classes of infection, one for humans and one for mosquitoes. This paper presents a stochastic extension of a deterministic vector-borne epidemic model based only on the class of human infectious. The consistency of the model is established by proving that the stochastic delay differential equation describing the model has a unique positive global solution. The extinction of the disease is studied through the analysis of the stability of the disease-free equilibrium state and the persistence of the model. Finally, we introduce some numerical simulations to illustrate the obtained results.展开更多
The presenilin genes(PSEN1 and PSEN2)are mainly responsible for causing early-onset familial Alzheimer’s disease,harboring~300 causative mutations,and representing~90%of all mutations associated with a very aggressiv...The presenilin genes(PSEN1 and PSEN2)are mainly responsible for causing early-onset familial Alzheimer’s disease,harboring~300 causative mutations,and representing~90%of all mutations associated with a very aggressive disease form.Presenilin 1 is the catalytic core of theγ-secretase complex that conducts the intramembranous proteolytic excision of multiple transmembrane proteins like the amyloid precursor protein,Notch-1,N-and E-cadherin,LRP,Syndecan,Delta,Jagged,CD44,ErbB4,and Nectin1a.Presenilin 1 plays an essential role in neural progenitor maintenance,neurogenesis,neurite outgrowth,synaptic function,neuronal function,myelination,and plasticity.Therefore,an imbalance caused by mutations in presenilin 1/γ-secretase might cause aberrant signaling,synaptic dysfunction,memory impairment,and increased Aβ42/Aβ40 ratio,contributing to neurodegeneration during the initial stages of Alzheimer’s disease pathogenesis.This review focuses on the neuronal differentiation dysregulation mediated by PSEN1 mutations in Alzheimer’s disease.Furthermore,we emphasize the importance of Alzheimer’s disease-induced pluripotent stem cells models in analyzing PSEN1 mutations implication over the early stages of the Alzheimer’s disease pathogenesis throughout neuronal differentiation impairment.展开更多
Professor du Xiaoquan is a famous Chinese medicine in Shaanxi Province,a master's tutor,a professor of Shaanxi University of traditional Chinese Medicine,a director of the Department of traditional Chinese Medicin...Professor du Xiaoquan is a famous Chinese medicine in Shaanxi Province,a master's tutor,a professor of Shaanxi University of traditional Chinese Medicine,a director of the Department of traditional Chinese Medicine,and a professor of Shen Shuwen,a national famous old Chinese medicine.展开更多
Mice have frequently been used to model human diseases involving immune dysregulation such as autoimmune and inflammatory diseases.These models help elucidatethe mechanisms underlying the disease and in the developmen...Mice have frequently been used to model human diseases involving immune dysregulation such as autoimmune and inflammatory diseases.These models help elucidatethe mechanisms underlying the disease and in the development of novel therapies.However,if mice are deficient in certain cells and/or effectors associated with human diseases,how can their functions be investigated in this species?Mucosal-associated invariant T(MAIT)cells,a novel innate-like T cell family member,are a good example.MAIT cells are abundant in humans but scarce in laboratory mice.MAIT cells harbor an invariant T cell receptor and recognize nonpeptidic antigens vitamin B2metabolites from bacteria and yeasts.Recent studies have shown that MAIT cells play a pivotal role in human diseases such as bacterial infections and autoimmune and inflammatory diseases.MAIT cells possess granulysin,a human-specific effector molecule,but granulysin and its homologue are absent in mice.Furthermore,MAIT cells show poor proliferation in vitro.To overcome these problems and further our knowledge of MAIT cells,we have established a method to expand MAIT cells via induced pluripotent stem cells(iP SCs).In this review,we describe recent advances in the field of MAIT cell research and our approach for human disease modeling with iP SCderived MAIT cells.展开更多
Intercellular communication via gap junctions allows cells within multicellular organisms to share small molecules. The effect of such interactions has been elucidated using mouse gene knockout strategies. Although se...Intercellular communication via gap junctions allows cells within multicellular organisms to share small molecules. The effect of such interactions has been elucidated using mouse gene knockout strategies. Although several mutations in human gap junction-encoding connexin(Cx) have been described, Cx mutants in mice do not always recapitulate the human disease. Among the 20 mouse Cxs, Cx26, Cx43, and Cx45 play roles in early cardiac or placental development, and disruption of the genes results in lethality that hampers further analyses. Embryonic stem cells(ESCs) that lack Cx43 or Cx45 have made analysis feasible in both in vitro differentiated cell cultures and in vivo chimeric tissues. The success of mouse ESCs studies is leading to the use of induced pluripotent stem cells to learn more about the pathogenesis of human Cx diseases. This review summarizes the current status of mouse Cx disruption models and ESC differentiation studies, and discusses their implication for understanding human Cx diseases.展开更多
The novel Coronavirus COVID-19 emerged in Wuhan,China in December 2019.COVID-19 has rapidly spread among human populations and other mammals.The outbreak of COVID-19 has become a global challenge.Mathematical models o...The novel Coronavirus COVID-19 emerged in Wuhan,China in December 2019.COVID-19 has rapidly spread among human populations and other mammals.The outbreak of COVID-19 has become a global challenge.Mathematical models of epidemiological systems enable studying and predicting the potential spread of disease.Modeling and predicting the evolution of COVID-19 epidemics in near real-time is a scientific challenge,this requires a deep understanding of the dynamics of pandemics and the possibility that the diffusion process can be completely random.In this paper,we develop and analyze a model to simulate the Coronavirus transmission dynamics based on Reservoir-People transmission network.When faced with a potential outbreak,decision-makers need to be able to trust mathematical models for their decision-making processes.One of the most considerable characteristics of COVID-19 is its different behaviors in various countries and regions,or even in different individuals,which can be a sign of uncertain and accidental behavior in the disease outbreak.This trait reflects the existence of the capacity of transmitting perturbations across its domains.We construct a stochastic environment because of parameters random essence and introduce a stochastic version of theReservoir-Peoplemodel.Then we prove the uniqueness and existence of the solution on the stochastic model.Moreover,the equilibria of the system are considered.Also,we establish the extinction of the disease under some suitable conditions.Finally,some numerical simulation and comparison are carried out to validate the theoretical results and the possibility of comparability of the stochastic model with the deterministic model.展开更多
文摘Ross’ epidemic model describing the transmission of malaria uses two classes of infection, one for humans and one for mosquitoes. This paper presents a stochastic extension of a deterministic vector-borne epidemic model based only on the class of human infectious. The consistency of the model is established by proving that the stochastic delay differential equation describing the model has a unique positive global solution. The extinction of the disease is studied through the analysis of the stability of the disease-free equilibrium state and the persistence of the model. Finally, we introduce some numerical simulations to illustrate the obtained results.
基金supported by the Consejo Nacional de Ciencia y Tecnología Scholarship 711893(to MAH)and 711874(to EER)。
文摘The presenilin genes(PSEN1 and PSEN2)are mainly responsible for causing early-onset familial Alzheimer’s disease,harboring~300 causative mutations,and representing~90%of all mutations associated with a very aggressive disease form.Presenilin 1 is the catalytic core of theγ-secretase complex that conducts the intramembranous proteolytic excision of multiple transmembrane proteins like the amyloid precursor protein,Notch-1,N-and E-cadherin,LRP,Syndecan,Delta,Jagged,CD44,ErbB4,and Nectin1a.Presenilin 1 plays an essential role in neural progenitor maintenance,neurogenesis,neurite outgrowth,synaptic function,neuronal function,myelination,and plasticity.Therefore,an imbalance caused by mutations in presenilin 1/γ-secretase might cause aberrant signaling,synaptic dysfunction,memory impairment,and increased Aβ42/Aβ40 ratio,contributing to neurodegeneration during the initial stages of Alzheimer’s disease pathogenesis.This review focuses on the neuronal differentiation dysregulation mediated by PSEN1 mutations in Alzheimer’s disease.Furthermore,we emphasize the importance of Alzheimer’s disease-induced pluripotent stem cells models in analyzing PSEN1 mutations implication over the early stages of the Alzheimer’s disease pathogenesis throughout neuronal differentiation impairment.
文摘Professor du Xiaoquan is a famous Chinese medicine in Shaanxi Province,a master's tutor,a professor of Shaanxi University of traditional Chinese Medicine,a director of the Department of traditional Chinese Medicine,and a professor of Shen Shuwen,a national famous old Chinese medicine.
文摘Mice have frequently been used to model human diseases involving immune dysregulation such as autoimmune and inflammatory diseases.These models help elucidatethe mechanisms underlying the disease and in the development of novel therapies.However,if mice are deficient in certain cells and/or effectors associated with human diseases,how can their functions be investigated in this species?Mucosal-associated invariant T(MAIT)cells,a novel innate-like T cell family member,are a good example.MAIT cells are abundant in humans but scarce in laboratory mice.MAIT cells harbor an invariant T cell receptor and recognize nonpeptidic antigens vitamin B2metabolites from bacteria and yeasts.Recent studies have shown that MAIT cells play a pivotal role in human diseases such as bacterial infections and autoimmune and inflammatory diseases.MAIT cells possess granulysin,a human-specific effector molecule,but granulysin and its homologue are absent in mice.Furthermore,MAIT cells show poor proliferation in vitro.To overcome these problems and further our knowledge of MAIT cells,we have established a method to expand MAIT cells via induced pluripotent stem cells(iP SCs).In this review,we describe recent advances in the field of MAIT cell research and our approach for human disease modeling with iP SCderived MAIT cells.
文摘Intercellular communication via gap junctions allows cells within multicellular organisms to share small molecules. The effect of such interactions has been elucidated using mouse gene knockout strategies. Although several mutations in human gap junction-encoding connexin(Cx) have been described, Cx mutants in mice do not always recapitulate the human disease. Among the 20 mouse Cxs, Cx26, Cx43, and Cx45 play roles in early cardiac or placental development, and disruption of the genes results in lethality that hampers further analyses. Embryonic stem cells(ESCs) that lack Cx43 or Cx45 have made analysis feasible in both in vitro differentiated cell cultures and in vivo chimeric tissues. The success of mouse ESCs studies is leading to the use of induced pluripotent stem cells to learn more about the pathogenesis of human Cx diseases. This review summarizes the current status of mouse Cx disruption models and ESC differentiation studies, and discusses their implication for understanding human Cx diseases.
文摘The novel Coronavirus COVID-19 emerged in Wuhan,China in December 2019.COVID-19 has rapidly spread among human populations and other mammals.The outbreak of COVID-19 has become a global challenge.Mathematical models of epidemiological systems enable studying and predicting the potential spread of disease.Modeling and predicting the evolution of COVID-19 epidemics in near real-time is a scientific challenge,this requires a deep understanding of the dynamics of pandemics and the possibility that the diffusion process can be completely random.In this paper,we develop and analyze a model to simulate the Coronavirus transmission dynamics based on Reservoir-People transmission network.When faced with a potential outbreak,decision-makers need to be able to trust mathematical models for their decision-making processes.One of the most considerable characteristics of COVID-19 is its different behaviors in various countries and regions,or even in different individuals,which can be a sign of uncertain and accidental behavior in the disease outbreak.This trait reflects the existence of the capacity of transmitting perturbations across its domains.We construct a stochastic environment because of parameters random essence and introduce a stochastic version of theReservoir-Peoplemodel.Then we prove the uniqueness and existence of the solution on the stochastic model.Moreover,the equilibria of the system are considered.Also,we establish the extinction of the disease under some suitable conditions.Finally,some numerical simulation and comparison are carried out to validate the theoretical results and the possibility of comparability of the stochastic model with the deterministic model.
