Integrating plant physiology into simulation of fire behavior and effects

Wildfires are a global crisis, but current fire models fail to capture vegetation response to changing climate. With drought and elevated temperature increasing the importance of vegetation dynamics to fire behavior, and the advent of next generation models capable of capturing increasingly complex physical processes, we provide a renewed focus on representation of woody vegetation in fire models. Currently, the most advanced representations of fire behavior and biophysical fire effects are found in distinct classes of fine-scale models and do not capture variation in live fuel (i.e. living plant) properties. We demonstrate that plant water and carbon dynamics, which influence combustion and heat transfer into the plant and often dictate plant survival, provide the mechanistic linkage between fire behavior and effects. Our conceptual framework linking remotely sensed estimates of plant water and carbon to fine-scale models of fire behavior and effects could be a critical first step toward improving the fidelity of the coarse scale models that are now relied upon for global fire forecasting. This process-based approach will be essential to capturing the influence of physiological responses to drought and warming on live fuel conditions, strengthening the science needed to guide fire managers in an uncertain future

Isolation and Mutagenesis of a Capsule-Like Complex (CLC) from Francisella tularensis, and Contribution of the CLC to F. tularensis Virulence in Mice

BACKGROUND: Francisella tularensis is a category-A select agent and is responsible for tularemia in humans and animals. The surface components of F. tularensis that contribute to virulence are not well characterized. An electron-dense capsule has been postulated to be present around F. tularensis based primarily on electron microscopy, but this specific antigen has not been isolated or characterized. METHODS AND FINDINGS: A capsule-like complex (CLC) was effectively extracted from the cell surface of an F. tularensis live vaccine strain (LVS) lacking O-antigen with 0.5% phenol after 10 passages in defined medium broth and growth on defined medium agar for 5 days at 32°C in 7% CO₂. The large molecular size CLC was extracted by enzyme digestion, ethanol precipitation, and ultracentrifugation, and consisted of glucose, galactose, mannose, and Proteinase K-resistant protein. Quantitative reverse transcriptase PCR showed that expression of genes in a putative polysaccharide locus in the LVS genome (FTL_1432 through FTL_1421) was upregulated when CLC expression was enhanced. Open reading frames FTL_1423 and FLT_1422, which have homology to genes encoding for glycosyl transferases, were deleted by allelic exchange, and the resulting mutant after passage in broth (LVSΔ1423/1422_P10) lacked most or all of the CLC, as determined by electron microscopy, and CLC isolation and analysis. Complementation of LVSΔ1423/1422 and subsequent passage in broth restored CLC expression. LVSΔ1423/1422_P10 was attenuated in BALB/c mice inoculated intranasally (IN) and intraperitoneally with greater than 80 times and 270 times the LVS LD₅₀, respectively. Following immunization, mice challenged IN with over 700 times the LD₅₀ of LVS remained healthy and asymptomatic. CONCLUSIONS: Our results indicated that the CLC may be a glycoprotein, FTL_1422 and -FTL_1423 were involved in CLC biosynthesis, the CLC contributed to the virulence of F. tularensis LVS, and a CLC-deficient mutant of LVS can protect mice against challenge with the parent strain

This work was supported by The Department of the Interior Alaska Climate Adaptation Science Center, which is managed by the USGS National Climate Adaptation Science Center.

53 pages : color illustrations, color maps ; 28 cmThis report is designed as a living document to inform the community, decision makers, and academics and to serve as a learning and teaching tool. The nine key messages summarized on pages 6 and 7 are intended for use as a quick reference. Unique for this type of report, these key messages highlight actions by Juneau's civil society, including local nonprofit organizations.We thank the City and Borough of Juneau (CBJ) for its support in bringing this vital information on climate change to the Juneau community and to others. Thanks especially to all the co-authors and other contributors. The inclusion of such a diverse array of material, including local knowledge, was made possible by the many elders, scientists, and local experts who contributed their time and expertise. The report is online at acrc.alaska.edu/ juneau-climate-report. It is an honor to be the lead editor and project manager for this critical effort. We have a chance to save our world from the most extreme effects of climate change. Let us take it. Gunalchéesh, sincerely, James E. Powell (Jim), PhD, Alaska Coastal Rainforest Center, UASWelcome / Thomas F. Thornton -- Juneau's climate report: History and background / Bruce Botelho -- Using this report -- Acknowledgements / James E. Powell -- A regional Indigenous perspective on adaptation: The Central Council of Tlingit & Haida Indian Tribes of Alaska's Climate Change Adaptation Plan / Raymond Paddock -- Nine key messages -- What we're experiencing: Atmospheric, marine, terrestrial, and ecological effects. Climate. Setting and seasons / Tom Ainsworth -- More precipitation / Rick Thoman -- Higher temperatures / Rich Thoman -- Less snowfall / Eran Hood -- Ocean. Surface uplift and sea level rise / Eran Hood -- Extensive effects of a warming ocean / Heidi Pearson -- Increasing ocean acidification / Robert Foy -- Land. More landslides / Sonia Nagorski & Aaron Jacobs -- Mendenhall Glacier continues to retreat / Jason Amundson -- Tongass Forest impacts and carbon / Dave D'Amore -- Animals. Terrestrial vertebrates in A¿¿ak'w & T'aak¿łu Aani¿¿ / Richard Carstensen -- Three animals as indicators of change / Richard Carstensen -- Insects / Bob Armstrong -- What we're doing: Community response. Upgrading ifrastructure and mitigation / Katie Koester -- Upgrading utilities and other energy consumers / Alec Mesdag -- Growing demand for hydropower / Duff Mitchell -- Leading a shift in transportation / Duff Mitchell -- Maintaining mental health through community and recreation / Linda Kruger & Kevin Maier -- Food security / Darren Snyder & Jim Powell -- Large cruise ship air emissions / Jim Powell -- Tourists' views on climate change mitigation / Jim Powell -- Lowering greenhouse gas emissions / Jim Powell & Peggy Wilcox -- Residents taking action / Andy Romanoff & Jim Powell -- Summary and Recommendations -- References -- Graphics and data sources -- Appendix: Juneau nonprofit climate change organization

Global urban environmental change drives adaptation in white clover

Urbanization transforms environments in ways that alter biological evolution. We examined whether urban environmental change drives parallel evolution by sampling 110,019 white clover plants from 6169 populations in 160 cities globally. Plants were assayed for a Mendelian antiherbivore defense that also affects tolerance to abiotic stressors. Urban-rural gradients were associated with the evolution of clines in defense in 47% of cities throughout the world. Variation in the strength of clines was explained by environmental changes in drought stress and vegetation cover that varied among cities. Sequencing 2074 genomes from 26 cities revealed that the evolution of urban-rural clines was best explained by adaptive evolution, but the degree of parallel adaptation varied among cities. Our results demonstrate that urbanization leads to adaptation at a global scale

Growth Response of Whitebark Pine (Pinus albicaulis Engelm) Regeneration to Thinning and Prescribed Burn Treatments

Whitebark pine (Pinus albicaulis Engelm.) forests play a prominent role throughout high-elevation ecosystems in the northern Rocky Mountains, however, they are vanishing from the high mountain landscape due to three factors: exotic white pine blister rust (Cronartium ribicola Fischer) invasions, mountain pine beetle (Dendroctonus ponderosae Hopkins) outbreaks, and successional replacement by more shade-tolerant tree species historically controlled by wildfire. Land managers are attempting to restore whitebark pine communities using prescribed fire and silvicultural cuttings, but they are unsure if these techniques are effective. The objective of this study was to determine how whitebark pine regeneration responds to selective thinning and prescribed burn treatments. We studied changes in diameter growth after restoration treatments using ring width measurements obtained from 93 trees at four sites in Montana and Idaho that were treated in the late 1990s. Overall, the average annual radial growth rates of the trees in treated areas were greater than those of trees in control areas. Specifically, there were significant increases in the growth ratio (180%) in the two sites that were both thinned and later burned. Younger regeneration showed more response to the treatments than older regeneration. All sites showed high variability in post-treatment growth rates across individual trees, with greater variability for trees in treated areas than in trees from the control areas. Results suggest that whitebark pine regeneration can respond to thin and burn release treatments and that managers may see positive results in areas that are treated similarly

The selective Tie2 inhibitor rebastinib blocks recruitment and function of Tie2Hi macrophages in breast cancer and neuroendocrine pancreatic tumors

Tumor-infiltrating myeloid cells promote tumor progression by mediating angiogenesis, tumor cell intravasation and metastasis, which can offset the effects of chemotherapy, radiation, and anti-angiogenic therapy. Here, we show that the kinase switch control inhibitor rebastinib inhibits Tie2, a tyrosine kinase receptor expressed on endothelial cells and pro-tumoral Tie2-expressing macrophages in mouse models of metastatic cancer. Rebastinib reduces tumor growth and metastasis in an orthotopic mouse model of metastatic mammary carcinoma through reduction of Tie2+ myeloid cell infiltration, anti-angiogenic effects, and blockade of tumor cell intravasation mediated by perivascular Tie2(hi)/VegfA(hi) macrophages in the tumor microenvironment of metastasis (TMEM). The anti-tumor effects of rebastinib enhance the efficacy of microtubule inhibiting chemotherapeutic agents, either eribulin or paclitaxel, by reducing tumor volume, metastasis, and improving overall survival. Rebastinib inhibition of angiopoietin/Tie2 signaling impairs multiple pathways in tumor progression mediated by pro-tumoral Tie2+ macrophages, including TMEM-dependent dissemination and angiopoietin/Tie2-dependent angiogenesis. Rebastinib is a promising therapy for achieving Tie2 inhibition in cancer patients

2002 Research Honors Program Abstracts

Faculty in the College of Agriculture and Life Sciences at Cornell University mentor and guide undergraduate students who have chosen to pursue a research project and graduate with honors. These abstracts reflect the depth of their scholarship and intellectual ability. The research projects encompass work in animal science, biological science, entomology, natural resources, physical science, plant science, and social science

Lived experience of CamAPS FX closed loop system in youth with type 1 diabetes and their parents.

AIM: To examine changes in the lived experience of type 1 diabetes after use of hybrid closed loop (CL), including the CamAPS FX CL system. MATERIALS AND METHODS: The primary study was conducted as an open-label, single-period, randomized, parallel design contrasting CL versus insulin pump (with or without continuous glucose monitoring). Participants were asked to complete patient-reported outcomes before starting CL and 3 and 6 months later. Surveys assessed diabetes distress, hypoglycaemia concerns and quality of life. Qualitative focus group data were collected at the completion of the study. RESULTS: In this sample of 98 youth (age range 6-18, mean age 12.7 ± 2.8 years) and their parents, CL use was not associated with psychosocial benefits overall. However, the subgroup (n = 12) using the CamAPS FX system showed modest improvements in quality of life and parent distress, reinforced by both survey (p < .05) and focus group responses. There were no negative effects of CL use reported by study participants. CONCLUSIONS: Closed loop use via the CamAPS FX system was associated with modest improvements in aspects of the lived experience of managing type 1 diabetes in youth and their families. Further refinements of the system may optimize the user experience

Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036.

Acquired resistance to ABL1 tyrosine kinase inhibitors (TKIs) through ABL1 kinase domain mutations, particularly the gatekeeper mutant T315I, is a significant problem for patients with chronic myeloid leukemia (CML). Using structure-based drug design, we developed compounds that bind to residues (Arg386/Glu282) ABL1 uses to switch between inactive and active conformations. The lead "switch-control" inhibitor, DCC-2036, potently inhibits both unphosphorylated and phosphorylated ABL1 by inducing a type II inactive conformation, and retains efficacy against the majority of clinically relevant CML-resistance mutants, including T315I. DCC-2036 inhibits BCR-ABL1(T315I)-expressing cell lines, prolongs survival in mouse models of T315I mutant CML and B-lymphoblastic leukemia, and inhibits primary patient leukemia cells expressing T315I in vitro and in vivo, supporting its clinical development in TKI-resistant Ph(+) leukemia

Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036.

Acquired resistance to ABL1 tyrosine kinase inhibitors (TKIs) through ABL1 kinase domain mutations, particularly the gatekeeper mutant T315I, is a significant problem for patients with chronic myeloid leukemia (CML). Using structure-based drug design, we developed compounds that bind to residues (Arg386/Glu282) ABL1 uses to switch between inactive and active conformations. The lead "switch-control" inhibitor, DCC-2036, potently inhibits both unphosphorylated and phosphorylated ABL1 by inducing a type II inactive conformation, and retains efficacy against the majority of clinically relevant CML-resistance mutants, including T315I. DCC-2036 inhibits BCR-ABL1(T315I)-expressing cell lines, prolongs survival in mouse models of T315I mutant CML and B-lymphoblastic leukemia, and inhibits primary patient leukemia cells expressing T315I in vitro and in vivo, supporting its clinical development in TKI-resistant Ph(+) leukemia