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Mallon, D.

Publications and source records attributed to Mallon, D..

5 recordsLinked to original sources

Disproportionate regulation of wildlife trade

An increasing number of countries in the Global North have enacted, or are considering, import bans on hunting trophies with the aim of protecting wildlife. We interrogate key arguments used to characterize trophy hunting and associated trade by proponents of such bans, using data from the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) over 25 years (2000-2024), the International Union for Conservation of Nature (IUCN) Red List of Threatened Species, and empirical research. Contrary to claims by proponents of bans, we show that trophy hunting is not a major threat to any CITES-listed species traded as a hunting trophy in 2000-2024. Arguments used to support bans often mischaracterize trophy hunting and its impacts and fail to recognize the benefits it can, and does, have for wildlife and people. Countries that have enacted or are considering import bans account for 64% of global trade in hunting trophies of CITES-listed species taken from the wild. Combined, these policies would restrict approximately one-fifth of this trade, likely with significant implications for conservation. We question whether these legislative actions are proportionate and discuss policy solutions. Wildlife trade solutions may appear simple, but evidence-based, just policies are needed to conserve biodiversity and avoid harming people.

ecology↗

Evaluating key evidence and formulating regulatory alternatives regarding the UK Hunting Trophies (Import Prohibition) Bill

Public policy addressing biodiversity loss is most likely to be effective when it is informed by appropriate evidence and considers potential unintended consequences. We evaluate key evidence relating to the Hunting Trophies (Import Prohibition) Bill that was discussed in the UK Parliament between 2022 and 2024. We characterize the UKs role in international hunting trophy trade by analyzing CITES trade data for 2000-2021 and 2015-2021. For CITES-listed species imported to/exported from the UK as hunting trophies in these periods we use data from the International Union for Conservation of Nature Red List of Threatened Species to determine whether hunting designated as "trophy hunting" is i) likely a major threat contributing to species being of elevated conservation concern, ii) likely or possibly causing localized declines, or iii) not a threat. We then use the Red List to determine whether such hunting provides, or potentially provides, benefits for species and/or people. Finally, we evaluate the UK Governments impact assessment of the bill. In 2000-2021 an estimated 3494 hunting trophies from 73 CITES-listed species and subspecies were exported to the UK involving an estimated 2549 whole organism equivalents (WOEs), i.e. individual animals. Imports involved 158.86 {+/-} 66.53 (mean {+/-} SD) trophies/year (115.83 {+/-} 32.27 WOEs/year). In 2015-2021, 79% of imports were from countries where populations of the hunted species are stable, increasing, or abundant. Legal hunting for trophies is not a major threat to any of the species or subspecies imported to the UK, but likely or possibly represents a local threat to some populations of nine species. This hunting does, or could potentially, benefit 20 species and subspecies, and people. Among other concerns, the impact assessment failed to adequately consider the costs and benefits to local communities in countries where such hunting occurs. Informed by these analyses we discuss alternative regulatory options.

ecology↗

Rare SH2B3 coding variants identified in lupus patients impair B cell tolerance and predispose to autoimmunity

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease, with a clear genetic component. While most SLE patients carry rare gene variants in lupus risk genes, little is known about their contribution to disease pathogenesis. Amongst them, SH2B3 - a negative regulator of cytokine and growth factor receptor signaling - harbors rare coding variants in over 5% of SLE patients. Here we show that unlike the variant found exclusively in healthy controls, most SH2B3 rare variants found in lupus patients are predominantly hypomorphic alleles. Generation of two mouse lines carrying variants orthologous to those found in patients revealed SH2B3 is important to limit the numbers of immature and transitional B cells. Furthermore, hypomorphic SH2B3 was shown to impair negative selection of immature/transitional self-reactive B cells and accelerate autoimmunity in sensitized mice, at least in part due to increased IL-4R signaling and BAFF-R expression. This work identifies a previously unappreciated role for SH2B3 in human B cell tolerance and lupus risk. SummaryZhang et al. reveal a role for hypomorphic SH2B3 in lupus risk. The study shows rare and damaging variants identified in lupus patients enable breach of B cell immune tolerance checkpoints and suggests involvement for dysregulated IL-4R signaling and BAFF-R expression.

immunology↗

Preventing extinctions post-2020 requires recovery actions and transformative change

Stopping human-induced extinctions will require strong policy commitments that comprehensively address threats to species. In 2021, a new Global Biodiversity Framework will be agreed by the Convention on Biological Diversity. Here we investigate how the suggested targets could contribute to reducing threats to threatened vertebrates, invertebrates, and plants, and assess the importance of a proposed target to implement recovery actions for threatened species. We find that whilst many of the targets benefit species, extinction risk for over one third of threatened species would not be reduced sufficiently without a target on recovery actions, including ex situ conservation, reintroductions and other species-specific interventions. A median of 41 threatened species per country require such actions, and they are found in most countries of the world. To prevent future extinctions, policy commitments must include recovery actions for the most threatened species in addition to broader transformative change.

ecology↗

Rewiring of Th-memory-associated gene co-expression networks underlie immunotherapy-induced changes in symptom expression in mite-sensitised atopics

BackgroundMultiple regulatory mechanisms have been identified employing conventional hypothesis-driven approaches as contributing to allergen-specific immunotherapy outcomes, but understanding of how these integrate to maintain immunological homeostasis is incomplete. ObjectiveTo explore the potential for unbiased systems-level gene co-expression network analysis to advance understanding of immunotherapy mechanisms. MethodsWe profiled genome-wide allergen-specific Th-memory responses prospectively across 24mths of subcutaneous immunotherapy (SCIT) in 25 rhinitics, documenting changes in immunoinflammatory pathways and associated co-expression networks and their relationships to symptom scores to 36mths. ResultsPrior to immunotherapy, mite-specific Th-memory response networks involved multiple discrete co-expression modules including those related to Th2-, Type1-IFN-, Inflammation-, and FOXP3/IL2-associated signalling. A signature comprising 109 genes correlated with symptom scores, and these mapped to cytokine signalling/T-cell activation-associated pathways, with upstream drivers including hallmark Th1/Th2-and inflammation-associated genes. Reanalysis after 3.5mths SCIT updosing detected minimal changes to pathway/upstream regulator profiles despite 32.5% reduction in symptoms, however network analysis revealed underlying merging of FOXP3/IL2-with Inflammation-and Th2-associated modules. By 12mths on SCIT, symptoms had reduced by 41% without further significant changes to pathway/upstream regulator or network profiles. Continuing SCIT to 24mths stabilised symptoms at 47% of baseline, accompanied by upregulation of the Type1-IFN-associated network module and its merging into the Th2/FOXP3/IL2/Inflammation module. ConclusionsSCIT stimulates progressive integration of Th-memory-associated Th2-,FOXP3/IL2-, Inflammation-, and Type1-IFN-signalling subnetworks, forming a single highly integrated co-expression network module, maximising potential for stable homeostatic control of allergen-specific Th2 responses via cross-regulation. Th2-anatogonistic Type1-IFN signalling may play a key role in stabilising clinical effects of SCIT. Clinical ImplicationStabilisation of the clinical effectiveness of SCIT involves recruitment of Th2-antagonistic Type 1 IFN-dependent signalling into the overall gene co-expression network underlying the allergen-specific Th-memory response, and this does not occur until the 2nd year of treatment. Capsule summarySCIT-induced rewiring of the gene network governing allergen-specific Th2-memory, as opposed to selective upregulation of genes associated with regulatory functions, underlies the clinical effectiveness of immunotherapy.

immunology↗