Social interactions are important for how societies function, conferring robustness and resilience to environmental changes. The structure of social interactions can shape the dynamics of information and goods transmission. In addition, the availability and types of resources that are transferred might impact the structure of interaction networks. For example, storable resources might reduce the required speed of distribution and altering interaction structure can facilitate such change. Here, we use Camponotus fragilis ants as a model system to examine how social interactions are impacted by group size, food availability, and food type. We compare global- and individual-level network measures across experiments in which groups of different sizes received limited or unlimited food that is either favorable and cannot be stored (carbohydrates), or unfavorable but with a potential of being stored (protein). We found that in larger groups, individuals interacted with more social partners and connected more individuals, and interaction networks became more compartmentalized. Furthermore, the number of individuals that ants interacted with and the distance they traveled both increased when food was limited compared to when it was unlimited. Our findings highlight how biological systems can adjust their interaction networks in ways that relate to their function. The study of such biological flexibility can inspire novel and important solutions to the design of robust and resilient supply chains.
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http://dx.doi.org/10.1242/bio.060422 | DOI Listing |
J Med Internet Res
January 2025
Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, MA, United States.
Background: Twitter (subsequently rebranded as X) is acknowledged by US health agencies, including the US Centers for Disease Control and Prevention (CDC), as an important public health communication tool. However, there is a lack of data describing its use by state health agencies over time. This knowledge is important amid a changing social media landscape in the wake of the COVID-19 pandemic.
View Article and Find Full Text PDFGeroscience
January 2025
Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St, Durham, NC, 27705, USA.
Genetics is the second strongest risk factor for Alzheimer's disease (AD) after age. More than 70 loci have been implicated in AD susceptibility so far, and the genetic architecture of AD entails both additive and nonadditive contributions from these loci. To better understand nonadditive impact of single-nucleotide polymorphisms (SNPs) on AD risk, we examined individual, joint, and interacting (SNPxSNP) effects of 139 and 66 SNPs mapped to the BIN1 and MS4A6A AD-associated loci, respectively.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Social Science Research Institute, Duke University, Durham, NC, USA.
Background: Results of recent analyses indicate that axon demyelination may play an important role in AD pathology. The MBP gene encodes a myelin basic protein involved in axon myelination in the nervous system including the central nervous system. Polymorphisms in this gene, as well as variations in expression, have been associated with multiple sclerosis (MS).
View Article and Find Full Text PDFBackground: African Americans (AA) and Latin Americans (LA) are at a higher risk of developing AD compared to non-Hispanic whites (NHW) but are traditionally underrepresented in AD research. The disproportionate risk is likely multifactorial including differences in co-morbidities and structural and social determinants of health (SSDoH). AD risk is thought to result from multiple genetic and environmental factors, and their interactions (GxE).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Texas A&M Health Science Center, Bryan, TX, USA.
Background: Traumatic brain injury (TBI) is a serious societal concern and is considered a major risk factor for the development of Alzheimer's disease (AD) and related dementias. Identifying shared pathological mediators that contribute to the progression of AD following TBI may allow therapeutic targeting to reduce the likelihood of developing AD following TBI. Cerebrovascular dysfunction is present in both AD and TBI, and thrombin has been implicated as a mediator of cerebrovascular dysfunction and inflammation.
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