Identification and Functional Characterization of Abiotic Stress Tolerance-Related Transcription Factor Family in Barley ( L.).

Plant AT-rich sequence and zinc-binding proteins (PLATZs) are a novel category of plant-specific transcription factors involved in growth, development, and abiotic stress responses. However, the gene family has not been identified in barley. In this study, a total of 11 were identified in barley, and they were unevenly distributed on five of the seven chromosomes.

Reduced serum IgG galactosylation is associated with increased inflammation during relapses of neuromyelitis optica spectrum disorders.

Background And Objective: Post-translational modifications of antibodies, with a specific focus on galactosylation, have garnered increasing attention in the context of understanding the pathogenesis and therapeutic implications of autoimmune diseases. However, the comprehensive scope and the clinical significance of antibody galactosylation in the context of Neuromyelitis Optica Spectrum Disorder (NMOSD) remain enigmatic.The primary aim of this research was to discern disparities in serum IgG galactosylation levels between individuals in the acute stage of NMOSD relapse and their age- and sex-matched healthy counterparts.

A splicing site change between exon 5 and 6 of the nuclear-encoded chloroplast-localized gene results in reduced chlorophyll content and plant height in barley.

The chloroplast is an important cellular organelle and metabolic hub, which is not only responsible for plant photosynthesis but is also involved in the biosynthesis of pigments, fatty acids, and hormone metabolisms. Several genes that are responsible for rice leaf color variations have been reported to be directly or indirectly involved in chlorophyll biosynthesis and chloroplast development, whereas a few genes have been functionally confirmed to be responsible for leaf color changes in barley at the molecular level. In this study, we obtained a yellow leaf and dwarf mutant from the progeny of Morex (a variety of barley) seeds treated with EMS.

Receptor-Interacting Protein 3/Calmodulin-Dependent Kinase II/Proline-Rich Tyrosine Kinase 2 Pathway is Involved in Programmed Cell Death in a Mouse Model of Brain Ischaemic Stroke.

Neuronal necroptosis and apoptosis are the most important pathways for programmed cell death after brain ischaemic stroke. Although apoptosis signalling pathways have been extensively studied, molecular mechanisms underlying necroptosis remain unclear. In this study, we found that receptor-interacting protein 3 (RIP3) deficiency reduced cerebral infarction volume, neurological deficits, and neuronal ultrastructural damage in a mouse model of brain ischaemic stroke by inhibiting programmed cell death.

Maackiain Prevents Amyloid-Beta-Induced Cellular Injury via Priming PKC-Nrf2 Pathway.

Amyloid-beta (A) peptide induces neurotoxicity through oxidative stress and inflammatory response. Brain deposition of a large amount of amyloid-beta (A), in particular A , promotes the development of Alzheimer's disease (AD). Maackiain is extracted from traditional Chinese medicine peony root and possesses antioxidative, antiosteoporosis, antitumor, and immunoregulatory effects.

Ponesimod modulates the Th1/Th17/Treg cell balance and ameliorates disease in experimental autoimmune encephalomyelitis.

Sphingosine-1-phosphate receptor 1 (S1P1) plays an important role in autoimmune disease. Here, we evaluated whether ponesimod, an S1P1 modulator, affects inflammation in experimental autoimmune encephalomyelitis (EAE) and investigated Th1/Th2/Th17/Treg cell subsets. Ponesimod treatment ameliorated EAE and alleviated inflammatory infiltration.

Amlexanox attenuates experimental autoimmune encephalomyelitis by inhibiting dendritic cell maturation and reprogramming effector and regulatory T cell responses.

Background: Amlexanox (ALX), a TBK1 inhibitor, can modulate immune responses and has anti-inflammatory properties. To investigate its role in regulating the progression of experimental autoimmune encephalomyelitis (EAE), we studied the effect of ALX on the maturation of dendritic cells (DCs) and the responses of effector and regulatory T cells (Tregs).

Methods: In vitro, bone marrow-derived DCs (BMDCs) were cultured and treated with ALX.

Rapamycin and fingolimod modulate Treg/Th17 cells in experimental autoimmune encephalomyelitis by regulating the Akt-mTOR and MAPK/ERK pathways.

Rapamycin prevents experimental autoimmune encephalomyelitis (EAE) and activates the MAPK/ERK pathway in EAE. Thus, we hypothesized combining rapamycin and fingolimod treatments would have synergistic effects in EAE. We show that combination therapy ameliorated EAE and regulated spinal cord IL-17 and TGF-β levels in EAE mice.

Fingolimod ameliorates the development of experimental autoimmune encephalomyelitis by inhibiting Akt-mTOR axis in mice.

Fingolimod is a new immunosuppressive agent approved by Food and Drug Administration (FDA) for treating multiple sclerosis (MS). It acts as a functional antagonist to downregulate the S1P1 receptor, which is known to signal through the Akt-mTOR pathway. We investigated the mechanism of fingolimod action in the classical animal model of MS: experimental autoimmune encephalomyelitis (EAE).

[Anti-oxidative effects of dexamethasone on mice with experimental autoimmune encephalomyelitis].

Objective: To investigate the effects of dexamethasone (DXM) on the level of oxidative stress and antioxidant enzymes in mice with experimental autoimmune encephalomyelitis (EAE).

Methods: C57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) to induce EAE. The mice were randomly divided into control group, EAE group, DXM group, and their clinical symptoms were observed.

Sulforaphane ameliorates the development of experimental autoimmune encephalomyelitis by antagonizing oxidative stress and Th17-related inflammation in mice.

Sulforaphane (SFN) is an organosulfur compound present in vegetables and has potent anti-oxidant and anti-inflammatory activities. This study was aimed at investigating the effect of treatment with SFN on inflammation and oxidative stress, and the potential mechanisms underlying the action of SFN in experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice. Treatment with SFN significantly inhibited the development and severity of EAE in mice, accompanied by mitigating inflammatory infiltration and demyelination in the spinal cord of mice.