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Wild parrots represent one of the greatest commercial interests in the legal trade in wild birds. Although it is difficult to quantify, there is a considerable illegal trade in wild parrots. Thirty-six per cent of the world's parrot species are listed by the International Union for the Conservation of Nature as threatened or near threatened, and 55% of these are threatened to some degree by trade. In this paper, we investigate the impact of protection on the number of nests that failed because of nestlings being taken by humans (hereafter nest take) and on nesting success in parrots. We collate data on parrot nest take from published and unpublished studies from Africa, Asia and Australasia, including countries and sites with and without national and local parrot protection measures in place. Nest take was insignificant in Australia, where all studies were from areas with both local and national protection. For less developed countries, levels of nest take were variable between studies, spanning the whole range from 0 to 100%. Protection significantly reduced nest take and correspondingly increased nesting success. Our results corroborate those for the Neotropics; thus, the advantages of protection appear to be independent of geographical location or political and economic conditions. We analysed data on legal trade in wild-caught parrots before and after implementation of the 1992 Wild Bird Conservation Act (which practically eliminated import of parrots to the USA) and found that there was no apparent shift in parrot imports to other global regions from the Neotropics. We suggest that conservation of parrots globally would benefit from similar legislation introduced in other regions, such as the EU (15), which is responsible for more than 60% of global imports of wild parrots. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) is a debilitating disease with no current therapies outside of acute clinical management. While acute, controlled inflammation is important for debris clearance and regeneration after injury, chronic, rampant inflammation plays a significant adverse role in the pathophysiology of secondary brain injury. Immune cell therapies hold unique therapeutic potential for inflammation modulation, due to their active sensing and migration abilities. Macrophages are particularly suited for this task, given the role of macrophages and microglia in the dysregulated inflammatory response after TBI. However, maintaining adoptively transferred macrophages in an anti-inflammatory, wound-healing phenotype against the proinflammatory TBI milieu is essential. To achieve this, we developed discoidal microparticles, termed backpacks, encapsulating anti-inflammatory interleukin-4, and dexamethasone for ex vivo macrophage attachment. Backpacks durably adhered to the surface of macrophages without internalization and maintained an anti-inflammatory phenotype of the carrier macrophage through 7 days in vitro. Backpack-macrophage therapy was scaled up and safely infused into piglets in a cortical impact TBI model. Backpack-macrophages migrated to the brain lesion site and reduced proinflammatory activation of microglia in the lesion penumbra of the rostral gyrus of the cortex and decreased serum concentrations of proinflammatory biomarkers. These immunomodulatory effects elicited a 56% decrease in lesion volume. The results reported here demonstrate, to the best of our knowledge, a potential use of a cell therapy intervention for a large animal model of TBI and highlight the potential of macrophage-based therapy. Further investigation is required to elucidate the neuroprotection mechanisms associated with anti-inflammatory macrophage therapy., (© The Author(s) 2023. Published by Oxford University Press on behalf of National Academy of Sciences.)

Background and Objective: Enterobacteriaceae (EB) spp. family is known to include potentially multidrug-resistant (MDR) microorganisms, and remains as an important cause of community-acquired pneumonia (CAP) associated with high mortality. The aim of this study was to determine the prevalence and specific risk factors associated with EB and MDR-EB in a cohort of hospitalized adults with CAP., Methods: We performed a multinational, point-prevalence study of adult patients hospitalized with CAP. MDR-EB was defined when ≥3 antimicrobial classes were identified as non-susceptible. Risk factors assessment was also performed for patients with EB and MDR-EB infection., Results: Of the 3193 patients enrolled with CAP, 197 (6%) had a positive culture with EB. Fifty-one percent (n = 100) of EB were resistant to at least one antibiotic and 19% (n = 38) had MDR-EB. The most commonly EB identified were Klebsiella pneumoniae (n = 111, 56%) and Escherichia coli (n = 56, 28%). The risk factors that were independently associated with EB CAP were male gender, severe CAP, underweight (body mass index (BMI) < 18.5) and prior extended-spectrum beta-lactamase (ESBL) infection. Additionally, prior ESBL infection, being underweight, cardiovascular diseases and hospitalization in the last 12 months were independently associated with MDR-EB CAP., Conclusion: This study of adults hospitalized with CAP found a prevalence of EB of 6% and MDR-EB of 1.2%, respectively. The presence of specific risk factors, such as prior ESBL infection and being underweight, should raise the clinical suspicion for EB and MDR-EB in patients hospitalized with CAP., (Published 2019. This article is a U.S. Government work and is in the public domain in the USA.)

Fibrosing mediastinitis is a rare disorder characterized by the invasive proliferation of fibrous tissue within the mediastinum. This fibrosis can result in compression of intrathoracic structures including the pulmonary vasculature leading to clinical symptoms and complications like pulmonary hypertension. Here, we present two cases of young patients with fibrosing mediastinitis complicated by pulmonary artery stenosis requiring medical and endovascular management with excellent results., Competing Interests: The authors declare no competing interests., (© 2019 Published by Elsevier Ltd.)

There is continuing controversy relating to the primary afferent neurotransmitter that conveys itch signals to the spinal cord. Here, we investigated the DRG and spinal cord expression of the putative primary afferent-derived "itch" neurotransmitter, gastrin-releasing peptide (GRP). Using ISH, qPCR, and immunohistochemistry, we conclude that GRP is expressed abundantly in spinal cord, but not in DRG neurons. Titration of the most commonly used GRP antiserum in tissues from wild-type and GRP mutant mice indicates that the antiserum is only selective for GRP at high dilutions. Paralleling these observations, we found that a GRPeGFP transgenic reporter mouse has abundant expression in superficial dorsal horn neurons, but not in the DRG. In contrast to previous studies, neither dorsal rhizotomy nor an intrathecal injection of capsaicin, which completely eliminated spinal cord TRPV1-immunoreactive terminals, altered dorsal horn GRP immunoreactivity. Unexpectedly, however, peripheral nerve injury induced significant GRP expression in a heterogeneous population of DRG neurons. Finally, dual labeling and retrograde tracing studies showed that GRP-expressing neurons of the superficial dorsal horn are predominantly interneurons, that a small number coexpress protein kinase C gamma (PKCγ), but that none coexpress the GRP receptor (GRPR). Our studies support the view that pruritogens engage spinal cord "itch" circuits via excitatory superficial dorsal horn interneurons that express GRP and that likely target GRPR-expressing interneurons. The fact that peripheral nerve injury induced de novo GRP expression in DRG neurons points to a novel contribution of this peptide to pruritoceptive processing in neuropathic itch conditions., (Copyright © 2015 Solorzano et al.)