Differential Death Rates Research Articles

Evaluation of the pathogenicity of Pseudomonas aeruginosa isolates to strains of mice under stressful conditions

Pseudomonas aeruginosa (Pa) is an opportunistic pathogen that threatens the health, especially in immunocompromised individuals. Pseudomonas aeruginosa survives everywhere, including in a shuttle of spaceflights. Survival and starvation of Pa in water probably increase or decrease the degree of pathogenicity or virulence, but it is not well discovered. To promote our understanding of the mechanisms of Pa long-term survival in water, investigations on survival kinetics and its pathogenicity to mice are under investigation in our laboratory. Data has shown that under starvation conditions in water, Pa can lead to (i) survival for over 15 years in water; (ii) distinct changes in colony morphology, including loss of pigmentation. This study also aimed to determine the pathogenicity of clinical and environmental isolates of Pa in water under starved conditions. We hypothesized that the starvation of Pa isolates in water results in different survival curves, morphological, that may enhance pathogenicity in mice. Mice infected with starved isolates showed a lesser death rate than non-starved isolates. This project compared the susceptibility of BALB/c, C57BL/6J, and DBA/2 J in lung infection. Our data shows the vulnerability of DBA/2J was high compared to BALB/c or C57BL/6J. Hindlimb-unloading increased the death rate in DBA/2J compared to BALB/c strains. Lung infection of different Pa isolates shows a differential death rate, with the highest death rate caused by non-starved isolates in mice. Overall, long-term starvation of Pa isolates exits may lead to a reduced mortality rate of mice.

Geographic Disparities in Liver Availability: Accidents of Geography, or Consequences of Poor Social Policy?

Recently, a redistricting proposal intended to equalize Model for End-stage Liver Disease score at transplant recommended expanding liver sharing to mitigate geographic variation in liver transplantation. Yet, it is unclear whether variation in liver availability is arbitrary and a disparity requiring rectification or reflects differences in access to care. We evaluate the proposal's claim that organ supply is an "accident of geography" by examining the relationship between local organ supply and the uneven landscape of social determinants and policies that contribute to differential death rates across the United States. We show that higher mortality leading to greater availability of organs may in part result from disproportionate risks incurred at the local level. Disparities in public safety laws, health care infrastructure, and public funding may influence the risk of death and subsequent availability of deceased donors. These risk factors are disproportionately prevalent in regions with high organ supply. Policies calling for organ redistribution from high-supply to low-supply regions may exacerbate existing social and health inequalities by redistributing the single benefit (greater organ availability) of greater exposure to environmental and contextual risks (e.g. violent death, healthcare scarcity). Variation in liver availability may not be an "accident of geography" but rather a byproduct of disadvantage.

Stability of differential susceptibility and infectivity epidemic models.

We introduce classes of differential susceptibility and infectivity epidemic models. These models address the problem of flows between the different susceptible, infectious and infected compartments and differential death rates as well. We prove the global stability of the disease free equilibrium when the basic reproduction ratio R0≤1 and the existence and uniqueness of an endemic equilibrium when R0>1. We also prove the global asymptotic stability of the endemic equilibrium for a differential susceptibility and staged progression infectivity model, when R0>1. Our results encompass and generalize those of Hyman and Li (J Math Biol 50:626-644, 2005; Math Biosci Eng 3:89-100, 2006).

Senescence effects in an extremely long-lived bird: the grey-headed albatrossThalassarche chrysostoma

Studies attempting to document reproductive or other pre-lethal senescence effects in wild birds typically face an array of problems, including flaws in statistical analyses, non-adaptive philopatry to deteriorating environments, confounding effects arising from cohort heterogeneity and differential death rates of phenotypes and the frequent pairing of old birds to younger mates. Furthermore, recent studies suggest that birds could maintain a high level of physical fitness until old age, before being struck by a catastrophic illness leading quickly to their demise. The presence of terminally ill individuals in most datasets (and their greater incidence in older age categories) may therefore provide a false impression of progressive senescence in cross-sectional analyses. This study was designed explicitly to avoid all the known pitfalls linked to the demonstration of progressive senescence in wild populations, and involved one of the very longest-lived bird species. We show that, during incubation, old (aged 35 years and over) male grey-headed albatrosses Thalassarche chrysostoma make longer foraging trips, and have lower daily mass gains, than experienced mid-aged individuals (aged up to 28 years). This is, to our knowledge, the first report documenting reduced foraging performance with old age. Hatching and breeding success of pairs composed of two old individuals were reduced in comparison to mid-aged pairs. Overall results were very similar when analyses were repeated using only individuals known to have survived 1 or 2 years beyond field measurements (hence probably not suffering from the effects of an advanced terminal illness). We conclude that extremely long-lived individuals usually experience some degree of general physical deterioration, leading to reduced foraging and breeding performance, long before their final demise.

A delayed chemostat model with general nonmonotone response functions and differential removal rates

A chemostat model with general nonmonotone response functions is considered. The nutrient conversion process involves time delay. We show that under certain conditions, when n species compete in the chemostat for a single resource that is allowed to be inhibitory at high concentrations, the competitive exclusion principle holds. In the case of insignificant death rates, the result concerning the attractivity of the single species survival equilibrium already appears in the literature several times (see [H.M. El-Owaidy, M. Ismail, Asymptotic behavior of the chemostat model with delayed response in growth, Chaos Solitons Fractals 13 (2002) 787–795; H.M. El-Owaidy, A.A. Moniem, Asymptotic behavior of a chemostat model with delayed response growth, Appl. Math. Comput. 147 (2004) 147–161; S. Yuan, M. Han, Z. Ma, Competition in the chemostat: convergence of a model with delayed response in growth, Chaos Solitons Fractals 17 (2003) 659–667]). However, the proofs are all incorrect. In this paper, we provide a correct proof that also applies in the case of differential death rates. In addition, we provide a local stability analysis that includes sufficient conditions for the bistability of the single species survival equilibrium and the washout equilibrium, thus showing the outcome can be initial condition dependent. Moreover, we show that when the species specific death rates are included, damped oscillations may occur even when there is no delay. Thus, the species specific death rates might also account for the damped oscillations in transient behavior observed in experiments.

Global Dynamics of a Mathematical Model of Competition in the Chemostat: General Response Functions and Differential Death Rates

A model of exploitative competition of n species in a chemostat for a single, essential, nonreproducing, growth-limiting resource is considered. S. B. Hsu [SIAM J. Appl. Math., 34 (1978), pp. 760–763] applies LaSalle’s extension theorem of Lyapunov stability theory to study the asymptotic behavior of solutions in the special case that the response functions are modeled by Michaelis–Menten dynamics. G. J. Butler and G. S. K. Wolkowicz [SIAM J. Appl. Math., 45 (1985), pp. 138–151], on the other hand, allow more general response functions (including monotone and nonmonotone functions), but their analysis requires the assumption that the death rates of all the species are negligible in comparison with the washout rate, and hence can be ignored. By means of Lyapunov stability theory, the global dynamics of the model for a large class of response functions are studied, including both monotone and nonmonotone functions (though it is not as general as the class studied by Butler and Wolkowicz) and the results in ...

Failure of W/Wv Mouse-Derived Cultured Mast Cells to Enter S Phase Upon Contact With NIH/3T3 Fibroblasts

Although W/Wv mutant mice are profoundly deficient in tissue mast cells, these mice do have cells with similar features of mast cells that develop from their bone marrow cells as efficiently as those from congenic +/+ mice in pokeweed mitogen-stimulated spleen cell-conditioned medium (PWM-SCM). With cultured mast cells (CMCs), we analyzed the mechanism of mast-cell deficiency in tissues of W/Wv mice. CMCs were established from bone marrow cells of W/Wv and congenic +/+ mice with PWM-SCM, and then co-cultured with various mouse fibroblast cell lines without PWM-SCM. All the examined mouse embryo-derived fibroblast cell lines maintained CMCs derived from +/+ mice, but not CMCs from W/Wv mice, for greater than 2 weeks. Mast cells in S phase were observed only in CMCs derived from +/+ mice under these conditions. The poor survival of W/Wv CMCs as compared with +/+ CMCs was not owing to a differential death rate but to the inability of W/Wv CMCs to continue active proliferation on fibroblasts without PWM-SCM. By synchronizing CMCs at the G1 phase of the cell cycle, the defect in W/Wv CMCs was further characterized as a failure to transit G1 and enter the S phase upon contact with fibroblasts. This finding indicates the indispensable function of the W gene product(s) for this response.

Failure of W/Wv mouse-derived cultured mast cells to enter S phase upon contact with NIH/3T3 fibroblasts

Although W/Wv mutant mice are profoundly deficient in tissue mast cells, these mice do have cells with similar features of mast cells that develop from their bone marrow cells as efficiently as those from congenic +/+ mice in pokeweed mitogen-stimulated spleen cell- conditioned medium (PWM-SCM). With cultured mast cells (CMCs), we analyzed the mechanism of mast-cell deficiency in tissues of W/Wv mice. CMCs were established from bone marrow cells of W/Wv and congenic +/+ mice with PWM-SCM, and then co-cultured with various mouse fibroblast cell lines without PWM-SCM. All the examined mouse embryo-derived fibroblast cell lines maintained CMCs derived from +/+ mice, but not CMCs from W/Wv mice, for greater than 2 weeks. Mast cells in S phase were observed only in CMCs derived from +/+ mice under these conditions. The poor survival of W/Wv CMCs as compared with +/+ CMCs was not owing to a differential death rate but to the inability of W/Wv CMCs to continue active proliferation on fibroblasts without PWM-SCM. By synchronizing CMCs at the G1 phase of the cell cycle, the defect in W/Wv CMCs was further characterized as a failure to transit G1 and enter the S phase upon contact with fibroblasts. This finding indicates the indispensable function of the W gene product(s) for this response.

Models for describibg shape and allometry, illustrated by studies of Australian species of <I>Uca</I> (Brachyura : Ocypodidae)

<P>Morphometric data for males of three species of <I>Uca</I> and females of two species have been summarized in terms of concepts of shape and allometry using the multivariate linear model. Differences among species are greatest in the males where <I>U. vocans</I> develops a major chela with broad palm, greatly elongated fingers and large gape, while <I>U. lactea</I> produces a long narrow palm with long, widely separated fingers. The major chela of U. polita is approximately intermediate in shape between that of <I>U. vocans</I> and <I>U. lactea</I>. Differences among the patterns of development in the meral lengths of the supporting pereiopods are also marked and these relate not so much to the morphometric details of the major chela but to the crab's use of the major chela in agonistic interactions. </P><P>Because the study is cross-sectional, the observed differences do not entirely describe growth patterns. Biases almost certainly exist due to differential death rates of given sizes and sampling difficulties. </P><P>In this work there has been an emphasis on statistical procedures which reflects our expository aim.</P>

Effect of Infection Density On Sex Ratio of Heterodera Glycines 1)

Approximately equal numbers of males and females of Heterodera glycines Ichinohe developed in roots of soybean seedlings at low infection densities. High infection densities significantly increased the male to female ratio, first in the secondary and tertiary roots and then in the primary root. Infection density of secondary roots influenced nematode sex ratio in tertiary roots. Increased male to female ratios were attributed to differential death-rate of male and female larvae under conditions of food stress created by crowding.

Observations on the epidemiology of prostatic hyperplasia in Wales.

SUMMARY Analysis of the data on benign prostatic hyperplasia in Wales shows an excess of this condition in the Principality as a whole, an excessive differential death–rate within Wales related to the proportion of Welsh–speaking men in the population, and an excess of men with Welsh names in the geographically localised region of Swansea. Jt is concluded that there is a greater susceptibility, mediated by genetic factors, to prostatic hyperplasia among Welshmen.

Reversal of Symmetry in Campeloma rufum, a Fresh-Water Snail

(1) About 1.03 per cent. of free living Campeloma rufum in the Salt Fork River at Homer Park, Illinois, have sinistral shells. (2) Among uterine young about 5.83 per cent. are sinistral. (3) After birth there is a differential death rate tending to eliminate the sinistrals before they reach an age of one year. (4) Few sinistrals ever reach bearing age. (5) Sinistrality in this species seems to be accompanied by lethal factors.

Evidences of a Differential Death Rate of the Sexes Among Animals

Evidences of a Differential Death Rate of the Sexes Among Animals

On Criteria for the Existence of Differential Deathrates

On Criteria for the Existence of Differential Deathrates