Multi-modal analysis reveals tumor and immune features distinguishing EBV-positive and EBV-negative post-transplant lymphoproliferative disorders.

The oncogenic Epstein-Barr virus (EBV) can drive tumorigenesis with disrupted host immunity, causing malignancies including post-transplant lymphoproliferative disorders (PTLDs). PTLD can also arise in the absence of EBV, but the biological differences underlying EBV(+) and EBV(-) B cell PTLD and the associated host-EBV-tumor interactions remain poorly understood. Here, we reveal the core differences between EBV(+) and EBV(-) PTLD, characterized by increased expression of genes related to immune processes or DNA interactions, respectively, and the augmented ability of EBV(+) PTLD B cells to modulate the tumor microenvironment through elaboration of monocyte-attracting cytokines/chemokines.

The use of phosphate rock and plant growth promoting microorganisms for the management of (Stapf.) R.D. Webster in acidic soils.

Background: Forage production in tropical soils is primarily limited by nutrient deficiencies, especially nitrogen (N) and phosphorus (P). The use of phosphate rock by plants is limited by its low and slow P availability and microbial phosphate solubilization is the main mechanism for P bioavailability in the soil-root system. The objectives of this study were (i) select a nitrogen-fixing bacteria which could be used as a co-inoculant with the IR94MF1 phosphate-solubilizing fungus and (ii) evaluate under field conditions the effect of inoculation combined with phosphate rock (PR) application on yield and nutrient absorption of a pasture which was previously established in a low-fertility, acidic soil.

Graft-derived extracellular vesicles transport miRNAs to modulate macrophage polarization after heart transplantation.

Heart transplantation, a crucial intervention for saving lives of those with end-stage cardiac failure, often faces complications from acute allograft rejection. This study focuses on the intricate dynamics of immune cell interactions and specific communication pathways between organs, which are not yet well understood. Our study investigates this interplay using a murine heterotopic transplant model, using single-cell RNA sequencing to examine CD45 immune cells from both the heart grafts and spleens.

CCDC28A deficiency causes head-tail coupling defects and immotility in murine spermatozoa.

Male infertility presents a substantial challenge in reproductive medicine, often attributed to impaired sperm motility. The present study investigates the role of CCDC28A, a protein expressed specifically in male germ cells, whose paralog CCDC28B has been implicated in ciliogenesis. We identify unique expression patterns for CCDC28A and CCDC28B within the mouse testes, where CCDC28A is expressed in germ cells, whereas CCDC28B is expressed in supporting somatic cells.