Yonsei University · Medicine
Professor Bon-Nyeo Koo's research lab focuses on the pathophysiological mechanisms underlying cerebrovascular diseases, particularly ischemic stroke and related neuroinflammatory and neurodegenerative processes. The lab investigates the roles of immune cell activation, blood-brain barrier disruption, oxidative stress, and inflammatory signaling pathways—such as ASK1 and MMP-9—in ischemic brain injury. Additionally, the lab explores the impact of systemic inflammatory responses, including cytokine storms in conditions like severe COVID-19, on neurological outcomes. The research integrates molecular mechanisms with clinical implications, aiming to identify therapeutic targets and improve patient management in critical neurological conditions.
Figures are computed from collected data and may differ slightly.
This study demonstrated that venous air embolism during hepatic resection was more frequent and severe when using the Cavitron Ultrasonic Surgical Aspirator. Although we found no evidence of hemodynamic compromise, increased venous air embolism may increase the risk of paradoxical embolism in patients with liver cirrhosis.
Inflammation is implicated in ischemic stroke and is involved in abnormal homeostasis. Activation of the immune system leads to breakdown of the blood-brain barrier and, thereby, infiltration of immune cells into the brain. Upon cerebral ischemia, infiltrated macrophages and microglia (resident CNS immune cell) are activated, change their phenotype to M1 or M2 based on the microenvironment, migrate toward damaged tissue, and are involved in repair or damage. Those of M1 phenotype release pro-inf
Stroke has become a more common disease worldwide. Despite great efforts to develop treatment, little is known about ischemic stroke. Cerebral ischemia activates multiple cascades of cell type-specific pathomechanisms. Ischemic brain injury consists of a complex series of cellular reactions in various cell types within the central nervous system (CNS) including platelets, endothelial cells, astrocytes, neutrophils, microglia/macrophages, and neurons. Diverse cellular changes after ischemic injur
Conditions of increased oxidative stress including cerebral ischemia can lead to blood-brain barrier dysfunction via matrix metalloproteinase (MMP). It is known that MMP-9 in particular is released from brain endothelial cells is involved in the neuronal cell death that occurs after cerebral ischemia. In the intracellular signaling network, apoptosis signal-regulating kinase 1 (ASK1) is the main activator of the oxidative stress that is part of the pathogenesis of cerebral ischemia. ASK1 also pr
The outbreak of the coronavirus disease 2019 (COVID-19) began at the end of 2019. COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with COVID-19 may exhibit poor clinical outcomes. Some patients with severe COVID-19 experience cytokine release syndrome (CRS) or a cytokine storm-elevated levels of hyperactivated immune cells-and circulating pro-inflammatory cytokines, including interleukin (IL)-1β and IL-18. This severe inflammator
Based on the fluoroscopic findings, the weight-based doses for caudally administered 0.2% bupivacaine suggested by Armitage are also useful for ropivacaine to block the spinal level required for the different types of surgeries studied.
This guideline will aid decisions related to RBC transfusion in healthcare settings and minimize patient risk associated with unnecessary pRBC transfusion.
Although the anatomy of the spinal cord and its associated structures have been well defined, the effects of body position relevant to neuraxial blockade have not been elucidated. This study was designed to determine the effect of body position on the end of the dural sac in children. After induction of anaesthesia, ultrasound examination was performed to evaluate the location of the dural sac end in the lateral position with a straight back and knee, and in the lateral position with the knees,
The prevalence of OSD in children under 24 months of age with simple urogenital anomaly was higher than what was reported for the general population. Ultrasound examination of spinal structures before caudal block in children with urogenital anomaly should be considered.
AGM posttreatment reduced cerebral infarct size and neurological deficit expression in diabetic rats subjected to MCAO. The reduced infarct size was associated with a decrease in apoptosis and NOS expression.
Cognitive symptoms are prevalent in the elderly and are associated with an elevated risk of developing dementia. Disease-driven changes can cause cognitive disabilities in memory, attention, and language. The inflammasome is an innate immune intracellular complex that has a critical role in the host defense system, in that it senses infectious pathogen-associated and endogenous danger-associated molecular patterns. An unbalanced or dysregulated inflammasome is associated with infectious, inflamm
Hyperammonemia in HE may be involved in mtROS overproduction and subsequent NLRP3 inflammasome activation. Further studies using NLRP3-specific inhibitor or NLRP3 knockout mice are needed to elucidate the important role of NLRP3 inflammasome in HE development.
Preoperative MCI was seen in ~20% of surgical patients aged >70 years. POCD was seen in ~20% of patients with pre-existing MCI, and ~ 10% of those without. Benzodiazepine use, significant comorbidities, pre-existing MCI, and depressive tendencies were risk factors for POCD.
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