Project description:Theoretical studies of ecosystem models have generally concluded that large numbers of species will not stably coexist if the species are all competing for the same limited set of resources. Here, we describe a simple multi-trait model of competition where the presence of N resources will lead to the stable coexistence of up to 2 N species. Our model also predicts that the long-term dynamics of the population will lie on a neutral attractor hyperplane. When the population shifts within the hyperplane, its dynamics will behave neutrally, while shifts which occur perpendicular to the hyperplane will be subject to restoring forces. This provides a potential explanation of why complex ecosystems might exhibit both niche-like and neutral responses to perturbations. Like the neutral theory of biodiversity, our model generates good fits to species abundance distributions in several datasets but does so without needing to evoke inter-generational stochastic effects, continuous species creation or immigration dynamics. Additionally, our model is able to explain species abundance correlations between independent but similar ecosystems separated by more than 1400 km inside the Amazonian forests.
Project description:The increasing number of reported scarlet fever cases during 2011‒2016 in the National Notifiable Infectious Disease database in South Korea occurred because of increased overall reporting and expanded reporting criteria rather than because of increasing scarlet fever incidence. Further increases are anticipated because of other expansions in reporting requirements.
Project description:In this study, we investigated the correlation between the microbiological characteristics of Clostridium difficile clinical isolates and the recurrence of C. difficile-associated disease (CDAD). Twenty C. difficile isolates recovered from 20 single infection cases and 53 isolates from 20 recurrent cases were analyzed by pulsed-field gel electrophoresis (PFGE) and PCR ribotyping, and the cytotoxicity, antimicrobial susceptibility, and sporulation/germination rates of the isolates were examined. Recurrent cases were divided into relapse or reinfection cases by the results of C. difficile DNA typing. Among the 20 recurrent cases, 16 cases (80%) were identified to be relapse cases caused by the initial strain and the remaining 4 cases (20%) were identified to be reinfection cases caused by different strains. All 73 isolates were susceptible to both vancomycin and metronidazole, but resistance against clindamycin, ceftriaxone, erythromycin, and ciprofloxacin was found in 87.7%, 93.2%, 87.7%, and 100% of the isolates, respectively. No correlations between DNA typing group, cytotoxicity, and sporulation rate of isolates and infection status, i.e., single, relapse, or reinfection, were observed. However, the isolates recovered from relapse cases showed a significantly higher germination rate when incubated in medium lacking the germination stimulant sodium taurocholate. These results indicate that the germination ability of C. difficile may be a potential risk factor for the recurrence of CDAD.
Project description:ObjectivesWe study changes in average disability over nearly two decades for a large epidemiological cohort of older Americans. As some people exit by mortality, do average disability levels for the living cohort rise rapidly, rise gradually, stay steady, or decline?MethodData are from the Study of Asset and Health Dynamics Among the Oldest Old (AHEAD) cohort for 1993-2010. Cohort members are aged 70+ in 1993 (mean = 77.5 years), and the survivors are aged 87+ in 2010 (mean = 90.2 years). Personal care disability (activities of daily living), household management disability (instrumental activities of daily living), and physical limitations are studied. We study average disability for the living cohort over time and the disability histories for decedent and survivor groups.ResultsAverage disability rises gradually over time for the living cohort. Earlier decedent groups have higher average disability than later ones. Near death, disability rises sharply for all decedent groups. Longer surviving groups have less average disability, and slower disability increases, than shorter surviving groups. All results are repeated for younger cohort members (baseline age = 70-79 years), older ones (baseline age = 80+ years), women, and men.DiscussionAs a cohort ages, average disability among living members increases gradually, signaling behavioral, psychological, and biological fitness in very old persons.
Project description:We estimate the number of COVID-19 cases from newly reported deaths in a population without previous reports. Our results suggest that by the time a single death occurs, hundreds to thousands of cases are likely to be present in that population. This suggests containment via contact tracing will be challenging at this point, and other response strategies should be considered. Our approach is implemented in a publicly available, user-friendly, online tool.
Project description:Copy number variants (CNVs) were detected and analyzed in 14 probands with autism and intellectual disability with self-injurious behavior (SIB) resulting in tissue damage. For each proband we obtained a clinical history and detailed behavioral descriptions. Genetic anomalies were observed in all probands, and likely clinical significance could be established in four cases. This included two cases having novel, de novo copy number variants and two cases having variants likely to have functional significance. These cases included segmental trisomy 14, segmental monosomy 21, and variants predicted to disrupt the function of ZEB2 (encoding a transcription factor) and HTR2C (encoding a serotonin receptor). Our results identify variants in regions previously implicated in intellectual disability and suggest candidate genes that could contribute to the etiology of SIB.
Project description:We estimate the number of COVID-19 cases from newly reported deaths in a population without previous reports. Our results suggest that by the time a single death occurs, hundreds to thousands of cases are likely to be present in that population. This suggests containment via contact tracing will be challenging at this point, and other response strategies should be considered. Our approach is implemented in a publicly available, user-friendly, online tool.
Project description:COVID-19 is an emerging respiratory infectious disease caused by the coronavirus SARS-CoV-2. It was first reported on in early December 2019 in Wuhan, China and within three months spread as a pandemic around the whole globe. Here, we study macro-epidemiological patterns along the time course of the COVID-19 pandemic. We compute the distribution of confirmed COVID-19 cases and deaths for countries worldwide and for counties in the US and show that both distributions follow a truncated power-law over five orders of magnitude. We are able to explain the origin of this scaling behavior as a dual-scale process: the large-scale spread of the virus between countries and the small-scale accumulation of case numbers within each country. Assuming exponential growth on both scales, the critical exponent of the power-law is determined by the ratio of large-scale to small-scale growth rates. We confirm this theory in numerical simulations in a simple meta-population model, describing the epidemic spread in a network of interconnected countries. Our theory gives a mechanistic explanation why most COVID-19 cases occurred within a few epicenters, at least in the initial phase of the outbreak. By combining real world data, modeling, and numerical simulations, we make the case that the distribution of epidemic prevalence might follow universal rules.
Project description:Clostridium difficile infection (CDI) is the most common cause of hospital-acquired infection in the United States. Host susceptibility and the severity of infection are influenced by disruption of the microbiota and the immune response. However, how the microbiota regulate immune responses to mediate CDI outcome remains unclear. Here, we have investigated the role of the microbiota-linked cytokine IL-25 during infection. Intestinal IL-25 was suppressed during CDI in humans and mice. Restoration of IL-25 reduced CDI-associated mortality and tissue pathology even though equivalent levels of C. difficile bacteria and toxin remained in the gut. IL-25 protection was mediated by gut eosinophils, as demonstrated by an increase in intestinal eosinophils and a loss of IL-25 protection upon eosinophil depletion. These findings support a mechanism whereby the induction of IL-25-mediated eosinophilia can reduce host mortality during active CDI. This work may provide targets for future development of microbial or immune-based therapies.