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Bronchopulmonary dysplasia (BPD) is potentially one of the most devastating conditions in premature infants with longstanding consequences involving multiple organ systems including adverse effects on pulmonary function and neurodevelopmental outcome. Here we review recent studies in the field to summarize the progress made in understanding in the pathophysiology, prognosis, prevention, and treatment of BPD in the last decade. The work reviewed includes the progress in understanding its pathobiology, genomic studies, ventilatory strategies, outcomes, and therapeutic interventions. We expect that this review will help guide clinicians to treat premature infants at risk for BPD better and lead researchers to initiate further studies in the field.

The excellent cryogenic tensile properties of the CrMnFeCoNi alloy are generally caused by deformation twinning, which is difficult to achieve at room temperature because of insufficient stress for twinning. Here, we induced twinning at room temperature to improve the cryogenic tensile properties of the CrMnFeCoNi alloy. Considering grain size effects on the critical stress for twinning, twins were readily formed in the coarse microstructure by cold rolling without grain refinement by hot rolling. These twins were retained by partial recrystallization and played an important role in improving strength, allowing yield strengths approaching 1 GPa. The persistent elongation up to 46% as well as the tensile strength of 1.3 GPa are attributed to additional twinning in both recrystallized and non-recrystallization regions. Our results demonstrate that non-recrystallized grains, which are generally avoided in conventional alloys because of their deleterious effect on ductility, can be useful in achieving high-strength high-entropy alloys. CrMnFeCoNi high entropy alloys have high fracture toughness at cryogenic temperatures due to deformation twinning but twinning is not active in this alloy at room temperature. Here authors optimize composition and thermomechanical treatments to introduce non-recrystallized grains, producing high yield strength while maintaining good ductility.

Induction of tumor cell death is the therapeutic goal for most anticancer drugs. Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to augment therapeutic efficacy. Currently, the molecular hallmark of ICD features the release of damage-associated molecular patterns (DAMPs) by dying cancer cells. Here, we show that gemcitabine, a standard chemotherapy for various solid tumors, triggers hallmark immunostimualtory DAMP release (e.g., calreticulin, HSP70, and HMGB1); however, is unable to induce ICD. Mechanistic studies reveal gemcitabine concurrently triggers prostaglandin E 2 release as an inhibitory DAMP to counterpoise the adjuvanticity of immunostimulatory DAMPs. Pharmacological blockade of prostaglandin E 2 biosythesis favors CD103 + dendritic cell activation that primes a Tc1-polarized CD8 + T cell response to bolster tumor rejection. Herein, we postulate that an intricate balance between immunostimulatory and inhibitory DAMPs could determine the outcome of drug-induced ICD and pose COX-2/prostaglandin E 2 blockade as a strategy to harness ICD. Most chemotherapeutic agents, including gemcitabine, do not elicit immunogenic cell death, a phenomenon associated with the release of damage-associated molecule patterns (DAMPs). Here, the authors show that gemcitabine-treated dying cancer cells express hallmark DAMPs but their immunogenic properties are hindered by the concomitant release of the inhibitory DAMP PGE 2 .

Small mammals play a central role in northern ecosystems, yet their diversity and habitat associations remain poorly documented in the subarctic mountains of northwestern Canada. I assessed small mammal assemblages across elevational and habitat gradients in Tombstone Territorial Park, located in the Taiga Cordillera Ecozone. My objectives were to document small mammal diversity and habitat associations. In 2005, small mammals were sampled at 27 sites representing seven common habitat types, ranging from lowland boreal forest to subalpine shrublands and alpine tundra. Twelve species of voles, lemmings, mice, and shrews were captured. Species richness and relative abundance were highest in lowland habitats and declined with increasing elevation. Alpine habitats supported fewer, highly specialized species. Several species were restricted to lowland habitats, whereas two species occurred exclusively in alpine tundra. Canonical correspondence analysis revealed a separation of species assemblages based primarily on moisture. These findings demonstrated that moisture, elevation, and habitat type structured small mammal assemblages in this northern mountain landscape. As a first approximation of small mammal assemblages in the Taiga Cordillera Ecozone, I provide a historical baseline for detecting recent and future ecological change. Climate change may facilitate the range expansion of lowland species and alter alpine assemblages, with potential consequences for community composition, trophic interactions, and ecosystem processes, highlighting the importance of small mammal monitoring in a rapidly warming subarctic.

Bioactive herbicidal compounds produced by soil microorganisms might be used to creating a bioherbicide for biological weed control. A total of 1,300 bacterial strains were isolated and screened for herbicidal activity against grass and broadleaf weeds. Among primarily selected 102 strains, the herbicidal activity of bacterial fermentation broths from the following three isolates strain-101, strain-128, and strain-329 reduced the growth of D. sanguinalis by 66.7%, 78.3%, and 100%, respectively as compared with control. Phylogenetic analysis of 16S rRNA gene sequencing determined that the strain-329 has 99% similarity to Streptomyces anulatus (HBUM 174206). The potential bioherbicidal efficacy of Streptomyces strain-329 was tested on grass and broadleaf weeds for phytotoxic activity through pre- and post-emergence applications. At pre-emergence application, the phytotoxic efficacy to D. sanguinalis and S. bicolor on seed germination were 90.4% and 81.3%, respectively at the 2x concentration, whereas in the case of Solanum nigrum, 85.2% phytotoxic efficacy was observed at the 4x concentration. The efficacy of Streptomyces strain-329 was substantially higher at post-emergence application, presenting 100% control of grass and broadleaf weeds at the 1x concentration. Two herbicidal compounds coded as 329-C1 and 329-C3 were extracted and purified by column chromatography and high-performance liquid chromatography methods. The active compound 329-C3 slightly increased leaf electrolytic leakage and MDA production as concentration-dependent manner. These results suggest that new Streptomyces sp. strain-329 produced bioherbicidal metabolites and may provide a new lead molecule for production an efficient bioherbicide to regulate grass and broadleaf weeds.

Background:Gout has been widely associated with cardiovascular health, but its relationship with incident valvular heart disease (VHD) remains uncertain.Objectives:To investigate the association between gout and VHD, and further explore the role of weight management within this context.Methods:We identified 10,930 patients with gout from the UK Biobank Cohort based on the combination of self-report and/or hospital diagnostic codes. The risk of VHD associated with gout was assessed in the overall populations and across subgroups with differing metabolic profiles. To examine the impact of obesity on the incident VHD, the relative risk of VHD were analyzed based on body mass index and waist circumference.Results:The incidence rate of VHD was significantly higher in patients with gout than in participants without gout (Hazard ratio 2.53, 95% confidence interval 2.35-2.71). While a positive correlation was observed between SUA level and VHD risk in the general population, the significant higher incidence of VHD was observed only in patients with SUA levels higher than 10 mg/dL among gout population. The elevated risk of VHD associated with gout remained consistently across subgroups with differing metabolic profiles. The impact of obesity on the incident VHD was notable among gout patients with SUA below 9.0 mg/dL, but less pronounced in those with SUA exceeding 9.0 mg/dL.Conclusion:This finding suggests a significant association between gout and VHD, emphasizing the need for screening and preventive efforts in patients with gout to mitigate the risk of VHD.REFERENCES:[1] Messika-Zeitoun D, Baumgartner H, Burwash IG, Vahanian A, Bax J, Pibarot P, et al. Unmet needs in valvular heart disease. Eur Heart J 2023;44:1862-73.[2] Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med 2008;359:1811-21.[3] Lazzeroni D, Bini M, Camaiora U, Castiglioni P, Moderato L, Bosi D, et al. Serum uric acid level predicts adverse outcomes after myocardial revascularization or cardiac valve surgery. Eur J Prev Cardiol 2018;25:119-26.[4] Muiesan ML, Salvetti M, Virdis A, Masi S, Casiglia E, Tikhonoff V, et al. Serum uric acid, predicts heart failure in a large Italian cohort: search for a cut-off value the URic acid Right for heArt Health study. J Hypertens 2021;39:62-9.[5] Choi HK, McCormick N, Yokose C. Excess comorbidities in gout: the causal paradigm and pleiotropic approaches to care. Nat Rev Rheumatol 2022;18:97-111.Acknowledgements:This research was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (Grant Number: 2022R1F1A1072279).Disclosure of Interests:None declared.

From biological ecosystems to spin glasses, connectivity plays a crucial role in determining the function, dynamics, and resiliency of a network. In the realm of non-Hermitian physics, the possibility of complex and asymmetric exchange interactions (κij≠κji) between a network of oscillators has been theoretically shown to lead to novel behaviors like delocalization, skin effect, and bulk-boundary correspondence. An archetypical lattice exhibiting the aforementioned properties is that proposed by Hatano and Nelson in a series of papers in late 1990s. While the ramifications of these theoretical works in optics have been recently pursued in synthetic dimensions, the Hatano–Nelson model has yet to be realized in real space. What makes the implementation of these lattices challenging is the difficulty in establishing the required asymmetric exchange interactions in optical platforms. In this work, by using active optical oscillators featuring non-Hermiticity and nonlinearity, we introduce an anisotropic exchange between the resonant elements in a lattice, an aspect that enables us to observe the non-Hermitian skin effect, phase locking, and near-field beam steering in a Hatano–Nelson laser array. Our work opens up new regimes of phase-locking in lasers while shedding light on the fundamental physics of non-Hermitian systems.The Hatano–Nelson model with asymmetric couplings is demonstrated for the first time in phase locked laser arrays. The arrays exhibit steerable non-Hermitian skin effects.

mTORC2 phosphorylates AKT in a hydrophobic motif site that is a biomarker of insulin sensitivity. In brown adipocytes, mTORC2 regulates glucose and lipid metabolism, however the mechanism has been unclear because downstream AKT signaling appears unaffected by mTORC2 loss. Here, by applying immunoblotting, targeted phosphoproteomics and metabolite profiling, we identify ATP-citrate lyase (ACLY) as a distinctly mTORC2-sensitive AKT substrate in brown preadipocytes. mTORC2 appears dispensable for most other AKT actions examined, indicating a previously unappreciated selectivity in mTORC2-AKT signaling. Rescue experiments suggest brown preadipocytes require the mTORC2/AKT/ACLY pathway to induce PPAR-gamma and establish the epigenetic landscape during differentiation. Evidence in mature brown adipocytes also suggests mTORC2 acts through ACLY to increase carbohydrate response element binding protein (ChREBP) activity, histone acetylation, and gluco-lipogenic gene expression. Substrate utilization studies additionally implicate mTORC2 in promoting acetyl-CoA synthesis from acetate through acetyl-CoA synthetase 2 (ACSS2). These data suggest that a principal mTORC2 action is controlling nuclear-cytoplasmic acetyl-CoA synthesis. mTORC2 activates Akt, a regulator of cell growth and metabolism, however, the role of mTORC2 in adipocytes is incompletely understood. Here the authors report that a mTORC2-Akt axis specifically activates ACLY to promote lipid synthesis and histone acetylation during brown adipocyte differentiation.