Background: Myasthenia gravis (MG) is the most common primary disorder of neuromuscular transmission, but the incidence of MG in China is unknown. We conducted the first nationwide study to determine the incidence and mortality rates of MG in all age groups at the national level in China.Methods: This national population-based registry study is based on the database of the Hospital Quality Monitoring System of National Health Commission, which covers 1665 hospitals providing myasthenia gravis care in 31 provinces and municipalities across China. 94,638 hospital admissions for 59,243 myasthenia gravis patients were identified from January 1st, 2016 to December 31st, 2018. Myasthenia gravis was identified by ICD-10 codes (G70). Incidence of myasthenia gravis was stratified by age, sex, and province.Findings: Of 59,243 patients, 30,503 individuals with myasthenia gravis were newly diagnosed. Age and sex adjusted incidence of myasthenia gravis was 0.68 per 10 0,0 0 0 person-years, with highest in the age group of 70-74 years. The incidence in females was 0.76 per 10 0,0 0 0 and 0.60 per 10 0,0 0 0 in males. The admission mortality rate was 14.69 ‰ . Respiratory failure was the leading cause of death in patients with myasthenic crisis. There were 14,840 patients with thymomas, encompassing 14,636 (26.5%) adults and 204 (7.1%) juveniles. 9453 (63.7%) patients with thymomas underwent thymomectomy. The median length of hospital stay was 8 days (interquartile range (IQR) 4 to 15 days

No abstract

Intracerebral hemorrhage (ICH), a devastating form of stroke, has a mortality of 40% and no available treatment. Inflammation contributes to the genesis and expansion of perihematomal edema (PHE) in ICH, thus driving secondary injury and subsequent neurological deterioration. This study was carried out to elucidate contributions of lymphocytes, specifically CD4 + cells in the formation of PHE and ICH-induced neural injury. Upon examination of brain sections of ICH patients, we observed abundant CD4 + T cells among the PHE-infiltrating immune cells as early as 24 hours post-ictus. Analogous findings in ICH mouse model induced with autologous blood or collagenase injection confirmed the phenomenon. Using anti-CD4 antibody to deplete CD4 + T cells, we find that brain-infiltrating CD4 + T cells exacerbates acute ICH injury in mice by reducing BBB integrity and promoting leukocytes recruitment with early and time-dependent CD4 + T cells activation. Brain infiltrating CD4 + T cells exhibit activated transcriptome signatures, promoting local inflammation via IL-17. In the hemorrhagic brain, CD4 + T cells induces CD31 + endothelial cell apoptosis via death receptor-ligands TRAIL-DR5 pathway; specific ablation of CD4 + T cells with depleting antibody results in reduced PHE volume and improved long-term neurological outcome. In all, these data sheds new lights on T cell-mediated immune responses contributing to PHE and brain injury in ICH.

No abstract

In the pathophysiology of hemorrhagic stroke, the perturbation of the neurovascular unit (NVU), a functional group of the microvascular and brain intrinsic cellular components, is implicated in the progression of secondary injury and partially informs the ultimate patient outcome. Given the broad NVU functions in maintaining healthy brain homeostasis through its maintenance of nutrients and energy substrates, partitioning central and peripheral immune components, and expulsion of protein and metabolic waste, intracerebral hemorrhage (ICH)-induced dysregulation of the NVU directly contributes to numerous destructive processes in the post-stroke sequelae. In ICH, the damaged NVU precipitates the emergence and evolution of perihematomal edema as well as the breakdown of the blood–brain barrier structural coherence and function, which are critical facets during secondary ICH injury. As a gateway to the central nervous system, the NVU is among the first components to interact with the peripheral immune cells mobilized toward the injured brain. The release of signaling molecules and direct cellular contact between NVU cells and infiltrating leukocytes is a factor in the dysregulation of NVU functions and further adds to the acute neuroinflammatory environment of the ICH brain. Thus, the interactions between the NVU and immune cells, and their reverberating consequences, are an area of increasing research interest for understanding the complex pathophysiology of post-stroke injury. This review focuses on the interactions of T-lymphocytes, a major cell of the adaptive immunity with expansive effector function, with the NVU in the context of ICH. In cataloging the relevant clinical and experimental studies highlighting the synergistic actions of T-lymphocytes and the NVU in ICH injury, this review aimed to feature emergent knowledge of T cells in the hemorrhagic brain and their diverse involvement with the neurovascular unit in this disease.