An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

An excess of amyloid beta (Aβ) led to a rise in ROS production, which in turn caused inflammatory reactions and mitochondrial dysfunction, both of which accelerate the progression of Alzheimer’s disease (AD).Natural flavonoids are proposed as possible agents for neurodegeneration. Pectolinarin is an important flavone mainly found in Cirsium species. In this study, we explored the potential neuroprotective effect of pectolinarin in Aβ25-35 -induced SH-SY5Y cells. The result demonstrated that pectolinarin enhanced cell viability. Pectolinarin treatment inhibited Aβ25-35 -induced ROS generation. Pectolinarin also suppressed NO generation by inhibiting the translocation of NF-ĸB and downregulating protein expression of iNOS and COX-2. Moreover, the expression of Bcl-2 increased while BAX protein decreased when the cells were exposed to pectolinarin, resulting in a decrease in the BAX/Bcl-2 ratio. Pectolinarin treatment also increased BDNF and its receptor TrkB protein expression. In conclusion, pectolinarin neuroprotected Aβ25-35 -induced inflammation and apoptosis. These findings suggest that pectolinarin may be a promising neuroprotective functional food in the protection of the neurodegenerative diseases, including AD.

Objectives: . The supine sleep position and the rapid eye movement (REM) stage are widely recognized to exacerbate the severity of obstructive sleep apnea (OSA). Position-dependent OSA is generally characterized by an apnea-hypopnea index (AHI) that is at least twice as high in the supine position compared to other sleep positions. However, this condition can be misdiagnosed if a particular sleep stage—REM or non-REM (NREM)—predominates in a specific position. We explored the impact of the sleep stage on positional dependency in OSA. Methods: . Polysomnographic data were retrospectively analyzed from 111 patients with OSA aged 18 years or older, all of whom had an AHI exceeding five events per hour and slept in both supine and non-supine positions for at least 5% of the total sleep time. The overall ratio of non-supine AHI to supine AHI (NS/S-AHI ratio) was compared between total, REM, and NREM sleep. Additionally, a weighted NS/S-AHI ratio, reflecting the proportion of time spent in each sleep stage, was calculated and compared to the original ratio. Results: . The mean NS/S-AHI ratio was consistent between the entire sleep period and the specific sleep stages. However, the NS/S-AHI ratios for individual patients displayed poor agreement between total sleep and the specific stages. Additionally, the weighted NS/S-AHI ratio displayed poor agreement with the original NS/S-AHI ratio, primarily due to discrepancies in patients with mild to moderate OSA. Conclusion . The weighted NS/S-AHI ratio may help precisely assess positional dependency.

OBJECTIVES: The escalating burden of cardiovascular disease (CVD) is a critical public health issue worldwide. CVD, especially acute myocardial infarction (AMI) and stroke, is the leading contributor to morbidity and mortality in Korea. We aimed to develop algorithms for identifying AMI and stroke events from the National Health Insurance Service (NHIS) database and validate these algorithms through medical record review. METHODS: We first established a concept and definition of “hospitalization episode,” taking into account the unique features of health claims-based NHIS database. We then developed first and recurrent event identification algorithms, separately for AMI and stroke, to determine whether each hospitalization episode represents a true incident case of AMI or stroke. Finally, we assessed our algorithms’ accuracy by calculating their positive predictive values (PPVs) based on medical records of algorithm- identified events. RESULTS: We developed identification algorithms for both AMI and stroke. To validate them, we conducted retrospective review of medical records for 3,140 algorithm-identified events (1,399 AMI and 1,741 stroke events) across 24 hospitals throughout Korea. The overall PPVs for the first and recurrent AMI events were around 92% and 78%, respectively, while those for the first and recurrent stroke events were around 88% and 81%, respectively. CONCLUSIONS We successfully developed algorithms for identifying AMI and stroke events. The algorithms demonstrated high accuracy, with PPVs of approximately 90% for first events and 80% for recurrent events. These findings indicate that our algorithms hold promise as an instrumental tool for the consistent and reliable production of national CVD statistics in Korea.

Anterior cruciate ligament (ACL) rupture leads to weakened quadriceps muscle strength and a decline in proprioception, impairing the neuromuscular control of the lower extremities. ACL reconstruction, aimed at addressing such structural and functional instability, has become a primary treatment method for young and active patients. Consequently, there have been significant advancements in surgical techniques, resulting in improved clinical outcomes. However, achieving successful outcomes after ACL reconstruction is not solely dependent on the surgery itself; pre- and postoperative rehabilitation and management are equally crucial. A well-designed functional recovery program based on medical evidence before and after ACL reconstruction plays a vital role in restoring function to preinjury levels. The process of the functional recovery program, from presurgery to sports return, should adhere to certain principles. These principles involve prompt and accurate clinical diagnosis and patient classification after injury, systematic programs addressing joint swelling and inflammation control, reduction of arthrogenic muscle inhibition, restoration of range of motion, muscle strength recovery, and proprioception restoration. Postoperatively, it is essential to go beyond traditional methods (such as range of motion restoration and muscle strengthening) by implementing a functional recovery program that includes enhancement of proprioception and neuromuscular control system from the early stages, considering the biological healing response of the graft. This comprehensive approach is vital for achieving optimal outcomes in the recovery of function after ACL reconstruction.

n patients who have undergone knee joint surgery or suffer from osteoarthritis, weakened quadriceps muscle strength is often observed. This can lead to various pathological issues in the long term, such as abnormal gait and persistent knee pain. Due to the need to protect against pain or surgical site complications, high-intensity exercise is often restricted for most patients with muscle atrophy in the knee joint due to surgery or osteoarthritis or surgery. To overcome this challenge, various methods are being attempted, including exercise combined with neuromuscular electrical stimulation, blood flow restriction (BFR) exercise, and biofeedback exercise. Recently, BFR exercise has garnered attention in line with these strategic trends. Applying low-intensity BFR exercise to patients who have undergone anterior cruciate ligament reconstruction surgery or suffer from knee joint osteoarthritis, most studies report improvements in strength, muscle mass, and functional enhancement of the knee joint. Compared to non-BFR high-intensity exercise, it has been reported that increases in maximal strength and muscle mass are similar, but pain reduction is superior with BFR exercise. Engaging in low-intensity BFR exercise for a sufficient duration can minimize the risk of injury associated with high-intensity exercise while maximizing the exercise’s effectiveness, leading to symptom improvement and enhancement of knee joint function. Furthermore, when conducted according to specified manuals, the likelihood of cardiovascular imbalance, muscle damage, thrombosis, and embolism due to BFR is low, making it a safe rehabilitation method.

Inflammation is a series of host defense processes in response to microbial infection and tissue injury. Inflammatory processes frequently cause extracellular acidification in the inflamed region through increased glycolysis and lactate secretion. Therefore, the immune cells infiltrating the inflamed region encounter an acidic microenvironment. Extracellular acidosis can modulate the innate immune response of macrophages; however, its role for inflammasome signaling still remains elusive. In the present study, we demonstrated that macrophages exposed to an acidic microenvironment exhibited enhanced caspase-1 processing and IL-1β secretion compared with those under physiological pH. Moreover, exposure to an acidic pH increased the ability of macrophages to assemble the NLR family pyrin domain containing 3 (NLRP3) inflammasome in response to an NLRP3 agonist.This acidosis-mediated augmentation of NLRP3 inflammasome activation occurred in bone marrow-derived macrophages but not in bone marrow-derived neutrophils. Notably, exposure to an acidic environment caused a reduction in the intracellular pH of macrophages but not neutrophils. Concordantly, macrophages, but not neutrophils, exhibited NLRP3 agonist-mediated translocation of chloride intracellular channel protein 1 (CLIC1) into their plasma membranes under an acidic microenvironment. Collectively, our results demonstrate that extracellular acidosis during inflammation can increase the sensitivity of NLRP3 inflammasome formation and activation in a CLIC1-dependent manner. Thus, CLIC1 may be a potential therapeutic target for NLRP3 inflammasome-mediated pathological conditions.