Spatial transcriptomics and neurofilament light chain reveal changes in lesion patterns in murine autoimmune neuroinflammation.

Objective: Ongoing neuroaxonal damage is a major contributor to disease progression and long-term disability in multiple sclerosis. However, spatio-temporal distribution and pathophysiological mechanisms of neuroaxonal damage during acute relapses and later chronic disease stages remain poorly understood.

Methods: Here, we applied immunohistochemistry, single-molecule array, spatial transcriptomics, and microglia/axon co-cultures to gain insight into spatio-temporal neuroaxonal damage in experimental autoimmune encephalomyelitis (EAE).

Prediction of beef tenderness and juiciness using consumer and descriptive sensory attributes.

The impact of different cooking methods, degree of doneness, cuts, and marbling scores on beef juiciness and tenderness have been examined. However, relationships between tenderness and juiciness, the two major components of beef texture, for descriptive and consumer sensory data with Warner-Bratzler shear force (WBSF) and overall consumer liking have not been elucidated using US consumers recently. The objective was to use two data sets that measured consumer sensory and beef descriptive tenderness and juiciness attributes to understand relationships between consumer and trained descriptive tenderness and juiciness attributes, and Warner-Bratzler shear force (WBSF) and overall consumer liking.

Activation of non-classical NMDA receptors by glycine impairs barrier function of brain endothelial cells.

Blood-brain barrier (BBB) integrity is necessary to maintain homeostasis of the central nervous system (CNS). NMDA receptor (NMDAR) function and expression have been implicated in BBB integrity. However, as evidenced in neuroinflammatory conditions, BBB disruption contributes to immune cell infiltration and propagation of inflammatory pathways.

Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

T helper (Th)17 cells are considered to contribute to inflammatory mechanisms in diseases such as multiple sclerosis (MS). However, the discussion persists regarding their true role in patients. Here, we visualized central nervous system (CNS) inflammatory processes in models of MS live in vivo and in MS brains and discovered that CNS-infiltrating Th17 cells form prolonged stable contact with oligodendrocytes.