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Biology subjects

Duncan, B.

Publications and source records attributed to Duncan, B..

4 recordsLinked to original sources

Internal decay in living trees: a quantitative tomography framework and its application in a temperate forest

Internal decay in living trees is an important component of carbon and nutrient cycling as well as species and structural diversity maintenance in forest ecosystems. We used sonic and electrical resistance tomography to evaluate and compare the prevalence and severity of stem decay in 57 living trees among four common species (Acer rubrum L., Nyssa sylvatica Marsh., Quercus rubra L., and Tsuga canadensis (L.) Carriere)) with overlapping and non-overlapping distributions across wetland and upland habitat types at the Harvard Forest in Petersham, MA, USA. Independent of tree size, site identity best explained variation in the prevalence of decay across trees sampled, whereas species identity best explained the severity of decay. We categorized trees as having no decay, incipient decay, active decay, or cavities based on combined sonic and electrical resistance metrics, the latter generated by a custom image analysis application. About 31% of wetland trees exhibited incipient decay (compared to 11% in the upland), whereas about 32% of upland trees exhibited active decay (compared to 10% in the wetland). Our study highlights a new quantitative framework for decay categorization through normalized principal component analysis (PCA) and decay analysis software that complements dual tomographic methodology for future investigations of ecological drivers of decay presence and susceptibility.

ecology↗

Contrasting controls on tree methane emissions in upland and wetland forests

Trees can produce, consume, transport, and emit methane (CH), yet the environmental controls and mechanisms underlying these fluxes remain poorly understood. We combined 1,640 stem-chamber observations (2023-2025) with tower-based meteorology, soil moisture and temperature networks, water table monitoring, and non-destructive tomography to test how hydrology, energy balance, species identity, and internal wood condition regulate stem CH flux. Wetland trees emitted approximately 40-fold more CH than upland trees (1.96 vs. 0.05 nmol m-{superscript 2} s-{superscript 1}). At the wetland, a three-way interaction between soil temperature, water table depth, and species explained 65% of flux variance, consistent with soil-derived CH transport through stems. The wetland specialist Nyssa sylvatica emitted an order of magnitude more CH than co-occurring generalists, likely reflecting flood-tolerance adaptations that enhance gas transport. In contrast, upland fluxes showed minimal environmental control (R{superscript 2} < 9%), with most variance occurring as unexplained temporal variation within individual trees--a pattern suggesting competing methanogenic and methanotrophic processes operating near equilibrium. Internal wood condition, assessed via acoustic and electrical resistance tomography, had opposite effects across sites: decay increased emissions in upland trees, likely by creating anaerobic microsites for in situ production, while decay decreased net emissions in wetland trees, likely by impairing transport of soil-derived CH more than it enhanced in situ production. Together, these results indicate that the dominant controls on tree CH flux differ fundamentally between wetland and upland forests, underscoring the need to represent hydrologic setting, species composition, and tree condition when scaling forest CH contributions to regional budgets.

ecology↗

Genetic diversity of Collaborative Cross mice enables the establishment of a novel Chlamydia muridarum female genital tract infection model

Chlamydial infection in women displays wide variation in bacterial burden, persistence, and risk of upper genital tract pathology, yet the host genetic factors underlying this heterogeneity remain poorly defined. We evaluated genital tract infection with Chlamydia muridarum across 20 Collaborative Cross (CC) strains, a recombinant inbred mouse panel that captures broad genetic diversity with high within-strain reproducibility. CC strains exhibited striking differences in early bacterial burden, time to clearance, and oviduct pathology, including prolonged low-inflammatory infections and burden-pathology discordance that mirror key features of human disease. Heritability analyses demonstrated that host genetics accounted for most of the variation observed in Day 7 bacterial burden and pathological outcomes. Genome-wide scans identified suggestive quantitative trait loci associated with both traits. Genes within the burden-associated locus converged on host pathways implicated in chlamydial intracellular growth, including membrane dynamics and lipid metabolism, ubiquitin signaling, host cell survival mechanisms, and immune regulatory signaling. In contrast, genes within the pathology-associated locus were enriched for pathways regulating inflammatory cell recruitment, inflammasome activation, and tissue remodeling, processes central to genital tract damage following infection. Cervical transcriptional profiling further revealed strain-dependent innate and adaptive immune programs associated with bacterial burden and disease phenotype. Together, these findings establish the CC as a powerful platform for dissecting the genetic architecture of chlamydial immunopathogenesis, and for improving preclinical evaluation of vaccines and therapeutics.

immunology↗

miRNA/mRNA analysis of increased TGF-β pathways drive epithelial-mesenchymal transition and regulatory T cell differentiation

Chlamydia trachomatis genital tract infection is linked to severe reproductive complications in women, including ectopic pregnancy, infertility, and adverse pregnancy outcomes. Mouse models of infection suggest that chlamydia-induced dysregulation of microRNAs (miRNAs) can drive harmful cytokine responses, pathogenic epithelial-mesenchymal transition (EMT), and fibrosis. To investigate these mechanisms in humans, we profiled miRNA and mRNA expression in endometrial biopsies from women with endometrial infection (Endo+) and compared them to profiles from women with cervix-only infection (Endo-) or no infection. Ingenuity Pathway Analysis (IPA) revealed that Endo+ tissues had upregulated genes associated with innate and adaptive immune response pathways, as well as EMT regulation, while downregulated genes were linked to cell cycle control. An integrative miRNA-mRNA analysis, which combined a review of published miRNA regulation in human infections and immune responses with IPAs miRNA target filter, identified differentially expressed miRNAs that modulate these pathways in the endometrium of Endo+ women. Functional annotation of these miRNAs showed a predominance of downregulated miRNAs that typically suppress EMT and regulatory T cell (Treg) differentiation, along with miRNAs that usually enhance Th17 responses. Comparisons with previously identified mRNA pathways in blood samples from women with endometrial Chlamydia infection indicated that alterations in TGF-{beta} signaling and EMT were specific to the endometrium. Overall, the miRNA-mRNA interactions inferred from Endo+ tissue suggest increased activity in TGF-{beta} pathways that promote enhanced EMT and Treg differentiation, while reducing Th17 activation. These changes highlight a dual potential for promoting tissue scarring while dampening inflammatory responses that could otherwise limit infection.

genomics↗