Endothelial Progenitor Cells Induce Angiogenesis: a Potential Mechanism Underlying Neovascularization in Encephaloduroarteriosynangiosis.

Encephaloduroarteriosynangiosis (EDAS) is one of the most commonly used indirect vascular reconstruction methods. EDAS aids in the formation of collateral vessels from the extracranial to the intracranial circulation in patients with moyamoya disease (MMD). However, the underlying mechanism of collateral vessel formation is not well understood.

Endoplasmic reticulum stress-dependent activation of iNOS/NO-NF-κB signaling and NLRP3 inflammasome contributes to endothelial inflammation and apoptosis associated with microgravity.

Exposure to microgravity results in vascular remodeling and cardiovascular dysfunction. To elucidate the mechanism involved in this condition, we investigated whether endoplasmic reticulum (ER) stress during simulated microgravity induced endothelial inflammation and apoptosis in human umbilical vein endothelial cells (HUVECs). Microgravity was simulated by clinorotation in the current study.

Combination of olfactory ensheathing cells and human umbilical cord mesenchymal stem cell-derived exosomes promotes sciatic nerve regeneration.

Olfactory ensheathing cells (OECs) are promising seed cells for nerve regeneration. However, their application is limited by the hypoxic environment usually present at the site of injury. Exosomes derived from human umbilical cord mesenchymal stem cells have the potential to regulate the pathological processes that occur in response to hypoxia.

TRADD Mediates RIPK1-Independent Necroptosis Induced by Tumor Necrosis Factor.

As a programmed necrotic cell death, necroptosis has the intrinsic initiators, including receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed-lineage kinase domain-like protein (MLKL), which combine to form necroptotic signaling pathway and mediate necroptosis induced by various necroptotic stimuli, such as tumor necrosis factor (TNF). Although chemical inhibition of RIPK1 blocks TNF-induced necroptosis, genetic elimination of RIPK1 does not suppress but facilitate necroptosis triggered by TNF. Moreover, RIPK3 has been reported to mediate the RIPK1-independent necroptosis, but the involved mechanism is unclear.

[Progress in the application of high-flow nasal cannula oxygenation in immunosuppressed patients with acute respiratory failure].

High-flow nasal cannula oxygenation (HFNC) characterized as a new non-invasive respiratory support technology, has been widely used in recent years. Compared with conventional oxygen therapy (COT), non-invasive ventilation (NIV), HFNC can offset patient discomforts, and effectively arrest the deterioration of acute respiratory failure (ARF) in immunosuppressed patients. Although there is no benefit of HFNC over COT on reducing mortality in immunocompromised patients with ARF, HFNC is associated with a lower intubation rate and the improved prognosis of transplant recipients and solid cancer patients.

Follicular Helper T Cell Derived Exosomes Promote B Cell Proliferation and Differentiation in Antibody-Mediated Rejection after Renal Transplantation.

Follicular helper T cells (Tfh cells) are closely related to the occurrence and development of antibody-mediated rejection (AMR) after renal transplantation. Exosomes play a key role in the rejection after organ transplantation. However, whether Tfh-derived exosomes are involved in AMR has not been reported.

Elevated expression of interleukin-33 in myasthenia gravis patients.

Myasthenia gravis (MG) is an archetypal autoimmune disorder of the neuromuscular junction. The imbalance of inflammatory cytokines are involved in the pathogenesis of MG. IL-33, a member of the IL-1 family, plays a key immune-modulation role in several autoimmune disease.