Browse Articles

CO2 and electrical stunning differentially affect energy metabolism in pigs

Abstract The use of CO₂ or electrical stunning to render pigs unconscious and insensible before exsanguination is a common practice. Although both methods are widely implemented, they differ fundamentally in their underlying mechanisms, and studies have produced conflicting results regarding their influence on meat quality. In the case of CO₂ stunning, impaired pulmonary gas exchange causes a rapid onset of systemic hypoxia, accompanied by hypercapnia, which in turn lowers blood pH and triggers additional physiological stress responses. Electrical stunning, by contrast, induces a generalized epileptic seizure by depolarizing neuronal cell membranes, markedly increasing oxygen consumption in both the brain and peripheral muscles. Coupled with apnea-induced cessation of respiration, this leads to rapid systemic hypoxia and associated metabolic disturbances. With this study, we aim to generate comprehensive metabolic data as a foundation for deeper understanding of the animal’s physiological responses depending on the stunning method used. We identified differences in metabolite pathways associated with the stunning method and evaluated potential influence on early post mortem processes relevant to meat quality development. After CO2 stunning, there was a marked increase in purine degradation into inosine (p < 0.0001) and hypoxanthine (p < 0.0001), along with increased levels of C4 intermediates (succinate, fumarate and malate, all p < 0.0001) in the tricarboxylic acid (TCA) cycle. In contrast, electrical stunning showed a higher rate of glycolysis, as indicated by reduced levels of C6 sugars (e.g. glucose p < 0.0001), and elevated levels of TCA cycle entry metabolites such as citrate (p = 0.0053) and aconitate (p = 0.0009). Our findings suggest that purinergic signaling acts as a rapid emergency response mechanism during gas stunning, reflected by pronounced purine catabolism. The distinct metabolite patterns likely result from different physiological stress responses, such as CO2-induced acidosis and variable oxygen availability. In addition, differences in cellular redox balance (NAD⁺/NADH) between stunning methods may further modulate glycolytic flux and TCA cycle activity. These divergent metabolic states at the time of death may, in turn, influence subsequent post mortem biochemical processes and ultimately influence meat quality development.

Case 20-2025: An 86-Year-Old Woman with Neck Swelling and Dysphagia

Effect of fuel feeding cycle adjustments on emissions in spruce pellet combustion with the application of a four-tube electrostatic precipitator

The Role of Public Health Agencies in Creating Vaccine Policy

New insights from the application of ZooMS to Late Pleistocene fauna from Grotta di Castelcivita, southern Italy

Abstract The Middle to Upper Paleolithic cave site of Grotta di Castelcivita (Campania, Southern Italy) contains a key archaeological sequence exhibiting Late Mousterian occupation followed by the Uluzzian techno-complex and an Aurignacian sequence (Protoaurignacian and Early Aurignacian). Abundant faunal remains are found throughout the sequence with variations in taxa present in each period. Previous studies of the morphologically identifiable faunal remains have provided valuable information on species abundance and diversity to reconstruct subsistence behaviour. However, like in many Pleistocene sequences, much of the faunal assemblage is fragmented and unidentifiable. Here we focus on these unidentified fragmentary bones to add greater dimension to the observed patterns. The application of collagen peptide mass fingerprinting (or Zooarchaeology by Mass Spectrometry; ZooMS) on 1263 unidentified bones revealed distinct changes in ZooMS NISP values in the Uluzzian and Protoaurignacian periods where equids and bovids nearly doubled in quantity compared to the original morphologically identified macrofaunal assemblage. New ZooMS identifications of rhinoceros, bear, and canids were made in layers deeper than previous recorded zooarchaeological analyses, extending the presence of these taxa at the site. The unexpectedly high level of collagen preservation in the bones from the cave confirms the potential for further applications of biomolecular approaches to Pleistocene bones from southern Italy.

On-Table Reanimation of a Pediatric Heart from Donation after Circulatory Death

Impact of dexamethasone therapy on mortality in critically ill patients with non-traumatic intracerebral hemorrhage: a propensity score-matched cohort study

Apixaban for Cancer-Associated Venous Thromboembolism

Research on aerodynamic characteristics and control method of rigid-flexible variable camber wing

First-Line Treatment of Pulmonary Sarcoidosis with Prednisone or Methotrexate

Fat-tailed failure strength distributions and manufacturing defects in advanced composites

Abstract This study investigates how manufacturing defects transform the statistical distribution of failure in carbon fiber-reinforced polymer composites under tension and compression loading. The analysis of tension and compression specimens reveals that defect-free composites exhibit relatively narrow, unimodal strength distributions. In contrast, specimens with porosity or fiber waviness develop more complex multimodal probability densities with fat-tailed distributions and substantially higher variability. Applying Jensen’s inequality demonstrates that this increased variability can be assessed to identify higher risk profiles. These findings indicate that defects in composites don’t simply reduce mean strength values but alter the statistical nature of composite failure, transforming thin-tailed, unimodal, well-behaved distributions into multimodal, fat-tailed ones. Such transformation necessitates more sophisticated probabilistic approaches for reliable design and strength prediction in safety-critical applications where understanding tail risk becomes crucial to proper risk management.

Acrometastases

Giant map details nerves across a mouse’s body: see stunning pics

International consensus statement on diagnosis, evaluation, and research of Richter transformation: the ERIC recommendations

Abstract Richter transformation (RT) is defined as an aggressive lymphoma emerging in patients with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL). Despite novel therapeutics developed in CLL, RT is associated with poor outcomes. In light of recent progress regarding the diagnostic procedures and therapeutic concepts of RT, an international group of experts, under the coordination of the European Research Initiative on CLL, has developed consensus recommendations for clinical procedures and future research on this disease. Patients with RT typically present with a rapid clinical decline, worsening B-symptoms, elevated lactate dehydrogenase, and/or rapidly enlarging lymphadenopathy. Workup should include a positron emission tomography–computed tomography scan for patients with suspected RT. An excisional biopsy should be taken from an accessible lesion, preferably with the highest fluorodeoxyglucose avidity, and analyzed for the presence of aggressive lymphoma. The molecular relationship to the original CLL clone(s) should be defined. Because no effective standard treatment for RT exists, patients should be treated in a clinical trial. Response of both RT and CLL should be assessed at an early time point, and survival end points should be prioritized in trial design. We hope that these recommendations can help to harmonize clinical and translational research and improve outcomes for patients with RT.

Platelet NLRP6: a hidden talent?

Africa’s chief diplomat for vaccine manufacturing

Clinical phenotype and pathophysiological mechanisms underlying qualitative low VWF

Abstract Previous reports have highlighted that some patients with low von Willebrand factor (VWF) with significant bleeding were diagnosed based on an isolated but persistent reduction in plasma VWF activity levels in the 30 to 50 IU/dL range. These patients had plasma VWF antigen (VWF:Ag) levels >50 IU/dL and thus had qualitative low VWF (low VWF–QL) rather than quantitative low VWF. Although the clinical importance of functional VWF defects in type 2 von Willebrand disease (VWD) is well recognized, the translational implications of mild functional defects in patients with low VWF–QL have not been defined. To address this clinically important question, we combined low VWF data sets from the low VWF in Ireland cohort and the low VWF in Erasmus MC studies. Overall, we observed that low VWF–QL was common and accounted for ∼50% of our combined low VWF cohort. Importantly, our findings demonstrated that many of these patients with mild isolated functional VWF defects in the 30 to 50 IU/dL range had significant bleeding phenotypes, although their plasma VWF:Ag levels were within the normal range. In addition, we further showed that low VWF–QL is a distinct clinicopathological entity compared to type 2 VWD. Finally, our studies highlighted that low VWF–QL is predominantly caused by abnormalities in VWF biosynthesis within endothelial cells that are occurring largely independent of identifiable pathological VWF sequence variants. Cumulatively, these novel observations have important clinical implications for the diagnosis and management of patients with mild functional VWF defects.

PROTACtion against BCL-xL in post-MPN AML

Secondary blastoid plasma cell leukemia: can an old dog learn new tricks?

An unbiased genomewide screen uncovers 7 genes that drive hematopoietic stem cell fate from mouse embryonic stem cells

Abstract Hematopoietic stem cells (HSCs) possess the ability to long term reconstitute all the blood lineages and generate all blood cell types. As such, the in vitro generation of HSCs remains a central goal in regenerative medicine. Despite many efforts and recent advancements in the field, there is still no robust, reproducible, and efficient protocol for generating bona fide HSCs in vitro. This suggests that certain regulatory elements have yet to be uncovered. Here, we present a novel and unbiased approach to identifying endogenous components to specify HSCs from pluripotent stem cells. We performed a genomewide CRISPR activator screening during mesodermal differentiation from mouse embryonic stem cells. After in vitro differentiation, mesodermal KDR+ precursors were transplanted into primary and secondary immunodeficient NSG mice. This approach led to the identification of 7 genes (Spata2, Aass, Dctd, Eif4enif1, Guca1a, Eya2, and Net1) that, when activated during mesoderm specification, induce the generation of hematopoietic stem and progenitor cells. These cells are capable of serial engraftment and multilineage output (erythroid, myeloid, and T and B lymphoid) in vivo. Single-cell RNA sequencing further revealed that activating these 7 genes biases the embryoid bodies toward intraembryonic development, instead of extraembryonic, increasing the number of mesodermal progenitors that can generate HSCs. Our findings underscore the importance of differentiation during the first germ layer specification to generate definitive blood stem cells.