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Abstract Hematocrit (Hct) is a powerful tool often used in a clinical setting for the diagnosis of blood conditions such as anemia. It is also used in the research field as a hematological parameter in both human and mouse models. Measuring Hct, however, involves the use of expensive standardized equipment (such as a CritSpin™ Microhematocrit Centrifuge). Here, we describe a novel, simple, and affordable method to determine the Hct in untreated wild‐type (WT) mice and phenylhydrazine (PHZ)‐induced anemic mice with reasonable accuracy, using a benchtop centrifuge commonly available in laboratories. Hct of murine samples processed with a benchtop centrifuge, when compared to the standardized method CritSpin™, showed comparable results. This approach for determining Hct of murine can prove useful to research laboratories that cannot afford specialized equipment for Hct studies. © 2024 Wiley Periodicals LLC. Basic Protocol 1: Affordable Method for Hematocrit Determination in Murine Models Basic Protocol 2: Murine Sample Validation Support Protocol: Phenylhydrazine‐induced anemia in wild‐type (WT) mice 

OBJECTIVES:To identify triggering receptor expressed in myeloid cells-like transcript-1 positive (TLT-1⁺) microparticles (MPs) and evaluate if their presence is associated with clinical outcomes and/or disease severity in acute respiratory distress syndrome (ARDS). DESIGN:Retrospective cohort study. SETTING:ARDS Network clinical trials. PATIENTS:A total of 564 patients were diagnosed with ARDS. INTERVENTIONS:None. MEASUREMENTS AND MAIN RESULTS:Using flow cytometry, we demonstrated the presence of TLT-1⁺platelet-derived microparticles (PMP) that bind fibrinogen in plasma samples from fresh donors. We retrospectively quantified TLT-1, glycoprotein (Gp) 1b, or α_IIbβ_IIIaimmunopositive microparticles in plasma samples from patients with ARDS enrolled in the ARMA, KARMA, and LARMA (Studies 01 and 03 lower versus higher tidal volume, ketoconazole treatment, and lisofylline treatment Clincial Trials) ARDS Network clinical trials and evaluated the relationship between these measures and clinical outcomes. No associations were found between Gp1b⁺MPs and clinical outcomes for any of the cohorts. When stratified by quartile, associations were found for survival, ventilation-free breathing, and thrombocytopenia with α_IIbβ_IIIa⁺and TLT-1⁺MPs (χ²p< 0.001). Notably, 63 of 64 patients in this study who failed to achieve unassisted breathing had TLT⁺PMP in the 75th percentile. In all three cohorts, patients whose TLT⁺MP counts were higher than the median had higher Acute Physiology and Chronic Health Evaluation III scores, were more likely to present with thrombocytopenia and were 3.7 times (p< 0.001) more likely to die than patients with lower TLT⁺PMP after adjusting for other risk factors. CONCLUSIONS:Although both α_IIbβ_IIIa⁺and TLT⁺microparticles (α_IIbβ_IIIa, TLT-1) were associated with mortality, TLT-1⁺MPs demonstrated stronger correlations with Acute Physiology and Chronic Health Evaluation III scores, unassisted breathing, and multiple system organ failure. These findings warrant further exploration of the mechanistic role of TLT-1⁺PMP in ARDS or acute lung injury progression. 

Abstract Atmospheric heat transport (AHT) is an important piece of our climate system but has primarily been studied at monthly or longer time scales. We introduce a new method for calculating zonal-mean meridional AHT using instantaneous atmospheric fields. When time averaged, our calculations closely reproduce the climatological AHT used elsewhere in the literature to understand AHT and its trends on long time scales. In the extratropics, AHT convergence and atmospheric heating are strongly temporally correlated suggesting that AHT drives the vast majority of zonal-mean atmospheric temperature variability. Our AHT methodology separates AHT into two components (eddies and the mean meridional circulation) which we find are negatively correlated throughout most of the mid- to high latitudes. This negative correlation reduces the variance in the total AHT compared to eddy AHT. Last, we find that the temporal distribution of the total AHT at any given latitude is approximately symmetric. 

Abstract We investigate the linear trends in meridional atmospheric heat transport (AHT) since 1980 in atmospheric reanalysis datasets, coupled climate models, and atmosphere-only climate models forced with historical sea surface temperatures. Trends in AHT are decomposed into contributions from three components of circulation: (i) transient eddies, (ii) stationary eddies, and (iii) the mean meridional circulation. All reanalyses and models agree on the pattern of AHT trends in the Southern Ocean, providing confidence in the trends in this region. There are robust increases in transient-eddy AHT magnitude in the Southern Ocean in the reanalyses, which are well replicated by the atmosphere-only models, while coupled models show smaller magnitude trends. This suggests that the pattern of sea surface temperature trends contributes to the transient-eddy AHT trends in this region. In the tropics, we find large differences between mean-meridional circulation AHT trends in models and the reanalyses, which we connect to discrepancies in tropical precipitation trends. In the Northern Hemisphere, we find less evidence of large-scale trends and more uncertainty, but note several regions with mismatches between models and the reanalyses that have dynamical explanations. Throughout this work we find strong compensation between the different components of AHT, most notably in the Southern Ocean where transient-eddy AHT trends are well compensated by trends in the mean-meridional circulation AHT, resulting in relatively small total AHT trends. This highlights the importance of considering AHT changes holistically, rather than each AHT component individually.