The D-lactate enigma: exploring the inflammatory influence of D-lactate in cattle.

D-lactic acidosis is associated with fermentative disturbances and is often marked by elevated levels of D-lactic acid in the blood, ruminal fluid, and synovial fluid in cattle. D-lactic acidosis is linked to various inflammatory manifestations, and although the causative factors have been extensively explored, the exact pathogenesis of the associated inflammation remains elusive. Notably, less attention has been given to D-lactate, a stereoisomer found in the plasma of affected animals, which may lead to D-lactic acidosis.

Soluble Antigen (Ag)-Induced NETs Under Hypoxic Conditions Exert Cytotoxic Effects on Hepatic Cells In Vitro.

is a parasitic trematode that causes fasciolosis in sheep, provoking a decrease in their reproductive capacity, weight gain, meat and milk production, and wool quality. In the pathogenesis of , the penetration and migration of parasitic stages through the liver provoke intense inflammatory immune responses and tissue damage. The aim of this study was to investigate the cytotoxic effects of -induced ovine NETs in exposed hepatocytes in vitro, and to analyze whether antigens (Ag) trigger the release of ovine NETs under hypoxic conditions as well as the roles of matrix metalloproteinase-9 (MMP-9) and CD11b in this cellular process in vitro.

Bone marrow microenvironment signatures associate with patient survival after guadecitabine and atezolizumab therapy in HMA-resistant MDS.

Almost 50% of patients with myelodysplastic syndrome (MDS) are refractory to first-line hypomethylating agents (HMAs), which presents a significant clinical challenge considering the lack of options for salvage. Past work revealed that immune checkpoint molecules on peripheral myeloblasts and immune cells are up-regulated after HMA treatment. Therefore, we conducted a Phase I/II clinical trial combining guadecitabine (an HMA) and atezolizumab (an immune checkpoint inhibitor) to treat HMA-relapsed or refractory (HMA-R/R) MDS patients.

Origin of Ewing sarcoma by embryonic reprogramming of neural crest to mesoderm.

Ewing sarcoma is a malignant small round blue cell tumor of bones and soft tissues caused by chromosomal translocations that generate aberrant fusion oncogenes, most frequently EWSR1::FLI1. The cell of origin and mechanisms of EWSR1::FLI1-driven transformation have remained unresolved, largely due to lack of a representative animal model. By developing a zebrafish Ewing sarcoma model, we provide evidence for a neural crest origin of this cancer.

Development of a prognostic model to predict 90-day mortality in hospitalised cancer patients (PROMISE tool): a prospective observational study.

Background: Prognostic factors for ambulatory oncology patients have been described, including Eastern Cooperative Oncology Group (ECOG), tumor stage and malnutrition. However, there is no firm evidence on which variables best predict mortality in hospitalized patients receiving active systemic treatment. Our main goal was to develop a predictive model for 90-day mortality upon admission.