An NFAT1-C3a-C3aR Positive Feedback Loop in Tumor-Associated Macrophages Promotes a Glioma Stem Cell Malignant Phenotype.

Extensive infiltration by tumor-associated macrophages (TAM) in combination with myeloid-derived suppressor cells constitute the immunosuppressive microenvironment and promote the malignant phenotype of gliomas. The aggressive mesenchymal (MES)-subtype glioma stem cells (GSC) are prominent in the immunosuppressive microenvironment of gliomas. However, the underlying immune-suppressive mechanisms are still unknown.

Identification of common genetic characteristics of rheumatoid arthritis and major depressive disorder by bioinformatics analysis and machine learning.

Introduction: Depression is the most common comorbidity of rheumatoid arthritis (RA). In particular, major depressive disorder (MDD) and rheumatoid arthritis share highly overlapping mental and physical manifestations, such as depressed mood, sleep disturbance, fatigue, pain, and worthlessness. This overlap and indistinguishability often lead to the misattribution of physical and mental symptoms of RA patients to depression, and even, the depressive symptoms of MDD patients are ignored when receiving RA treatment.

NFAT2-HDAC1 signaling contributes to the malignant phenotype of glioblastoma.

Background: Deregulation of the nuclear factor of activated T cell (NFAT) pathway has been reported in several human cancers. Particularly, NFAT2 is involved in the malignant transformation of tumor cells and is identified as an oncogene. However, the role of NFAT2 in glioblastoma (GBM) is largely unknown.

Bumetanide: A review of its neuroplasticity and behavioral effects after stroke.

Stroke often leads to neuronal injury and neurological functional deficits. Whilst spontaneous neurogenesis and axon regeneration are induced by ischemic stroke, effective pharmacological treatments are also essential for the improvement of neuroplasticity and functional recovery after stroke. However, no pharmacological therapy has been demonstrated to be able to effectively improve the functional recovery after stroke.