Benjamin Bolker

Prof. Benjamin Bolker


Research Focus & Metrics

Academic Career Length

34Years (1993-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 March 2009 in Trends in Ecology & Evolution
Verified
Journal Article
Closed access
BBBenjamin Bolker
Benjamin Bolker
MBMollie E. Brooks
Mollie E. Brooks
CCConnie J. Clark
Connie J. Clark
SGShane W. Geange
Shane W. Geange
JPJohn R. Poulsen
John R. Poulsen
JWJada-Simone S. White
Jada-Simone S. White

25 June 2003
Verified
Dataset
Closed access
DBDouglas Bates
Douglas Bates
MMMartin Maechler
Martin Maechler
BBBenjamin Bolker
Benjamin Bolker
SWSteven Walker
Steven Walker
ALAnna Ly
Anna Ly
MJMikael Jagan
Mikael Jagan

28 January 2000 in Science
Verified
Journal Article
Closed access
PDF file
DEDavid J. D. Earn
David J. D. Earn
PRPejman Rohani
Pejman Rohani
BBBenjamin Bolker
Benjamin Bolker
BGBryan T. Grenfell
Bryan T. Grenfell
Dramatic changes in patterns of epidemics have been observed throughout this century. For childhood infectious diseases such as measles, the major transitions are between regular cycles and irregular, possibly chaotic epidemics, and from regionally synchronized oscillations to complex, spatially incoherent epidemics. A simple model can explain both kinds of transitions as the consequences of changes in birth and vaccination rates. Measles is a natural ecological system that exhibits different dynamical transitions at different times and places, yet all of these transitions can be predicted as bifurcations of a single nonlinear model.

3 December 2004 in Ecology Letters
Verified
Journal Article
Closed access
FCFrancisco De Castro
Francisco De Castro
BBBenjamin Bolker
Benjamin Bolker

1 January 2008 in Discrete and Continuous Dynamical Systems
Verified
Journal Article
Open access
PDF file
LALinda Allen
Linda Allen
BBBenjamin Bolker
Benjamin Bolker
YLYuan Lou
Yuan Lou
ANA. L. Nevai
A. L. Nevai
To understand the impact of spatial heterogeneity of environment and movement of individuals on the persistence and extinction of a disease, a spatial SIS reaction-diffusion model is studied, with the focus on the existence, uniqueness and particularly the asymptotic profile of the steady-states. First, the basic reproduction number $\R_{0}$ is defined for this SIS PDE model. It is shown that if $\R_{0} < 1$, the unique disease-free equilibrium is globally asymptotic stable and there is no endemic equilibrium. If $\R_{0} > 1$, the disease-free equilibrium is unstable and there is a unique endemic equilibrium. A domain is called high (low) risk if the average of the transmission rates is greater (less) than the average of the recovery rates. It is shown that the disease-free equilibrium is always unstable $(\R_{0} > 1)$ for high-risk domains. For low-risk domains, the disease-free equilibrium is stable $(\R_{0} < 1)$ if and only if infected individuals have mobility above a threshold value. The endemic equilibrium tends to a spatially inhomogeneous disease-free equilibrium as the mobility of susceptible individuals tends to zero. Surprisingly, the density of susceptibles for this limiting disease-free equilibrium, which is always positive on the subdomain where the transmission rate is less than the recovery rate, must also be positive at some (but not all) places where the transmission rates exceed the recovery rates.

1 December 1997 in Theoretical Population Biology
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Journal Article
Closed access
BBBenjamin Bolker
Benjamin Bolker
SPStephen W Pacala
Stephen W Pacala