Legumain deficiency halts atherogenesis by modulating T cell receptor signaling.

Atherosclerosis is an age-related pathological process associated with elevated levels of legumain in plaques and plasma. However, the underlying mechanisms remain unclear. The aim of this study was to investigate the role of legumain in the progression of atherosclerotic plaques, with a particular focus on functional and phenotypic changes in CD4 T cells.

Lymphocytes in autoimmune encephalitis: Pathogenesis and therapeutic target.

Autoimmune encephalitis (AE) is an inflammatory disease of the central nervous system characterized by the production of various autoimmune antibodies targeting neuronal proteins. The pathogenesis of AE remains elusive. Accumulating evidence suggests that lymphocytes, particularly B and T lymphocytes, play an integral role in the development of AE.

CircTLK1: A novel regulator involved in VSMC phenotypic switching and the developmental process of atherosclerosis.

Phenotypic switching of vascular smooth muscle cells (VSMCs) is essential for atherosclerosis development. Circular RNA (circRNA) is a specific non-coding RNA that is produced as a closed-loop structure in mammals, and its specific expression pattern is closely related to its cell type and tissue. To clarify the roles of circTLK1 in VSMC phenotypic switching, we performed qRT-PCR, immunoblotting, and immunostaining.

Movement disorders in autoimmune encephalitis: an update.

Autoimmune encephalitis (AE) is a form of encephalitis resulting from an immune response targeting central nervous system antigens, which is characterized by cognitive impairment, neuropsychiatric symptoms, seizures, movement disorders (MDs), and other encephalopathy symptoms. MDs frequently manifest throughout the progression of the disease, with recurrent involuntary movements leading to discomfort and, in some cases, necessitating admission to the intensive care unit. Prompt identification and management of MDs can aid in the diagnosis and prognosis of AE.

The Role of Lipid Subcomponents in the Development of Atherosclerotic Plaques.

Atherosclerosis (AS) is a long-standing cardiovascular and cerebrovascular disease. Its occurrence and development are related to the pathophysiology of lipids including cholesteryl ester (CE), cholesterol, triacylglycerol (TG), and phospholipid (PL). In this review, we focus on the roles and possible mechanisms of different lipid subcomponents in the process of AS, and provide new ideas for the prevention, diagnosis and treatment of AS.

TREM2 promotes cholesterol uptake and foam cell formation in atherosclerosis.

Disordered lipid accumulation in the arterial wall is a hallmark of atherosclerosis. Previous studies found that the expression of triggering receptor expressed on myeloid cells 2 (TREM2), a transmembrane receptor of the immunoglobulin family, is increased in mouse atherosclerotic aortic plaques. However, it remains unknown whether TREM2 plays a role in atherosclerosis.

The emerging role of Th1 cells in atherosclerosis and its implications for therapy.

Atherosclerosis is a chronic progressive inflammatory disease of the large and medium-sized artery walls. The molecular mechanisms regulating the onset and progression of atherosclerosis remain unclear. T cells, one of the most common immune cell types in atherosclerotic plaques, are increasingly recognized as a key mediator in the pathogenesis of atherosclerosis.

Time window and "tissue window": two approaches to assist decision-making in strokes.

Intravenous alteplase given in an appropriate time window has been recommended in guidelines and effects are on the decline over time. In general, the clinical decision is primarily based on whether ischemic stroke patients are sent to hospitals within the time window. However, some patients sent to the hospital over time limitations are eligible to receive intervention for recanalization due to good collateral circulation.

[A quantitative study of the synaptic alterations in spinal dorsal horn during the induction and maintenance of long-term potentiation].

By using stereological morphometric techniques, we examined the ultrastructure of synapses in lamine II of the spinal dorsal horn of Sprague Dawley rats 30 min, 3 h and 5 h after long-term potentiation (LTP) induction. We found that the numerical density per unit volume (Nv) of total synapses, the thickness of the postsynaptic density (PSD), width of the synaptic cleft increased significantly after the establishment of LTP. (1) Thirty minutes after the formation of LTP, the thickness of the PSD increased from 0.