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Background and aim: Bone marrow stem cells (BM-SCs) and their progeny play a central role in tissue repair and regeneration. In patients with chronic liver failure, bone marrow (BM) reserve is severally compromised and they showed marked defects in the resolution of injury and infection, leading to liver failure and the onset of decompensation. Whether BM failure is the cause or consequence of liver failure during cirrhosis is not known. In this study, we aimed to determine the underlying relationship between BM failure and regeneration failure in cirrhosis. Methodology: C57Bl/6(J) mice were used to develop chronic liver injury through intra-peritoneal administration of carbon tetrachloride (CCl4) for 15 weeks (0.1- 0.5 ml/kg). Animals were sacrificed to study the transition of cirrhosis and BM defects. To restore the BM-SC reserve; healthy BM cells were infused via intra- BM infusion and assessed for changes in liver injury, regeneration, and BMSC reserve. Results: Using a CCl4-induced animal - model of cirrhosis, we showed the loss of BM-SCs reserve occurred before regeneration failure and the onset of nonacute decompensation. Intra-BM infusion of healthy BM cells induced the repopulation of native hematopoietic stem cells (HSCs) in cirrhotic BM. Restoring BM-HSCs reserve augments liver macrophage-mediated clearance of infection and inflammation dampens neutrophil-mediated inflammation, accelerates fibrosis regression, enhances hepatocyte proliferation, and delays the onset of non-acute decompensation. Conclusion: These findings suggest that loss of BM-HSCs reserve underlies the compromised innate immune function of the liver, drives regeneration failure, and the onset of non-acute decompensation. We further provide the proof-ofconcept that rejuvenating BM-HSC reserve can serve as a potential therapeutic approach for preventing regeneration failure and transition to decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Few landscapes on earth remain free of human‐modification, which may influence resource selection in wildlife. To investigate the effects of anthropic pressure on wild boar (Sus scrofa) and explore management implications, we studied how diel resource selection of the species' main life stages changed with spatial variations of human access (e.g., for recreation), temporal changes in hunting pressure, and habitat type. Using 206,461 hourly GPS‐locations of 15 males, 11 females with dependent young, and 17 other females from south‐western Germany, we found anthropic pressure influenced resource selection more than ecological factors. All boars were more likely to select for low human‐access areas than high human‐access areas, regardless of habitat. Hunting pressure was most avoided by females with dependent piglets, followed by males and other females. Since both hunting activity and general human access affected resource selection, they should be considered simultaneously in wildlife management and conservation. We suggest the further establishment of wildlife reserves that are inaccessible to people where boar may remain more localized, thereby reducing the risk of disease transmission, and boar hunting to focus on open lands and refuge boundaries to reduce crop damage. This may also benefit overall human‐wildlife coexistence, animal welfare, and biodiversity conservation in anthropized environments. [ABSTRACT FROM AUTHOR]

Introduction: With evolving pandemic, a substantial proportion of patients are presenting with liver dysfunction as an extra-pulmonary manifestation of COVID-19 illness. We planned this study to evaluate the incidence of liver dysfunction in COVID-19 pneumonia and find an association between abnormal liver function and the severity of the disease. Method: We retrospectively analysed the hospital records of 344 patients with moderate to severe COVID-19 illness admitted to a Dedicated COVID Hospital in North India. Results: Out of 344 patients included in the study, 59.9% were males. The abnormal liver functions were present in 78.49% of patients at admission. Mean age of the patient with liver dysfunction was 53.41 ± 15.71 years. The incidence of elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and hypoalbuminemia was 82.96%, 74.91%, and 69.7%, respectively, in patients with COVID-19 at admission. A positive correlation was found between the levels of AST, ALT and hypoalbuminemia with severity of disease. Mortality was 33% in patients with liver dysfunction in comparison to 18.9% in patients with normal liver functions. Conclusion: More than 75% of the patient had abnormal liver functions at admission, and mortality was also high in this group. Mortality can be effectively reduced if laboratory parameters such as elevated AST and ALT and hypoalbuminemia are closely monitored at admission and during hospital stay in patients with risk factors like male, age <55 years and HTN. [ABSTRACT FROM AUTHOR]