This study aimed to assess the utilization trends of pulmonary rehabilitation (PR) among lung cancer patients in Korea using the National Health Insurance Service (NHIS) database (2017 to 2021). PR was introduced and covered under the NHIS in 2016, primarily for chronic obstructive pulmonary disease, but recent evidence suggests its benefits for lung cancer patients. Data extraction was based on Korea Informative Classification of Diseases 8th revision codes C33 and C34, with PR prescriptions identified by codes MM440 and MM290.Descriptive statistical analysis was performed, and propensity score matching was used for comparison between PR and non-PR groups. Results showed a significant increase in PR utilization, with the number of patients receiving PR (MM440) rising from 1,002 in 2017 to 3,723 in 2021, indicating a 3.7-fold increase. However, the proportion of patients receiving PR remained low at 2.9% in 2021. Enhanced access to PR services and improved evaluation strategies are essential for optimizing patient outcomes.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

This study aimed to assess the utilization trends of pulmonary rehabilitation (PR) among lung cancer patients in Korea using the National Health Insurance Service (NHIS) database (2017 to 2021). PR was introduced and covered under the NHIS in 2016, primarily for chronic obstructive pulmonary disease, but recent evidence suggests its benefits for lung cancer patients. Data extraction was based on Korea Informative Classification of Diseases 8th revision codes C33 and C34, with PR prescriptions identified by codes MM440 and MM290.Descriptive statistical analysis was performed, and propensity score matching was used for comparison between PR and non-PR groups. Results showed a significant increase in PR utilization, with the number of patients receiving PR (MM440) rising from 1,002 in 2017 to 3,723 in 2021, indicating a 3.7-fold increase. However, the proportion of patients receiving PR remained low at 2.9% in 2021. Enhanced access to PR services and improved evaluation strategies are essential for optimizing patient outcomes.

This study aimed to assess the utilization trends of pulmonary rehabilitation (PR) among lung cancer patients in Korea using the National Health Insurance Service (NHIS) database (2017 to 2021). PR was introduced and covered under the NHIS in 2016, primarily for chronic obstructive pulmonary disease, but recent evidence suggests its benefits for lung cancer patients. Data extraction was based on Korea Informative Classification of Diseases 8th revision codes C33 and C34, with PR prescriptions identified by codes MM440 and MM290.Descriptive statistical analysis was performed, and propensity score matching was used for comparison between PR and non-PR groups. Results showed a significant increase in PR utilization, with the number of patients receiving PR (MM440) rising from 1,002 in 2017 to 3,723 in 2021, indicating a 3.7-fold increase. However, the proportion of patients receiving PR remained low at 2.9% in 2021. Enhanced access to PR services and improved evaluation strategies are essential for optimizing patient outcomes.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

This study aimed to assess the utilization trends of pulmonary rehabilitation (PR) among lung cancer patients in Korea using the National Health Insurance Service (NHIS) database (2017 to 2021). PR was introduced and covered under the NHIS in 2016, primarily for chronic obstructive pulmonary disease, but recent evidence suggests its benefits for lung cancer patients. Data extraction was based on Korea Informative Classification of Diseases 8th revision codes C33 and C34, with PR prescriptions identified by codes MM440 and MM290.Descriptive statistical analysis was performed, and propensity score matching was used for comparison between PR and non-PR groups. Results showed a significant increase in PR utilization, with the number of patients receiving PR (MM440) rising from 1,002 in 2017 to 3,723 in 2021, indicating a 3.7-fold increase. However, the proportion of patients receiving PR remained low at 2.9% in 2021. Enhanced access to PR services and improved evaluation strategies are essential for optimizing patient outcomes.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

BACKGROUND: The repair of large bone defects remains a significant challenge in clinical practice and requires bone grafts or substitute materials. In this study, we developed a unique hybrid bone scaffold comprising a three dimensional (3D)-printed metal plate for weight bearing and a biodegradable polymer tube serving as bone conduit. We assessed the long-term effect of the hybrid bone scaffold in repairing radial bone defects in a beagle model. METHODS: Bone defects were created surgically on the radial bone of three beagle dogs and individually-tailored scaffolds were used for reconstruction with or without injection of autologous bone and decellularized extracellular matrix (dECM). The repaired tissue was evaluated by X-ray, micro-computed tomography, and histological observation 6 months after surgery. The functional integrity of hybrid bone scaffold-mediated reconstructions was assessed by gait analysis. RESULTS: In vivo analysis showed that the hybrid bone scaffolds maintained the physical space and bone conductivity around the defect. New bone was formed adjacent to the scaffolds. Addition of autologous bone and dECM in the polymer tube improved healing by enhancing bone induction and osteoconduction. Furthermore, the beagles’ gait appeared normal by 4 months. CONCLUSION The future of bone healing and regeneration is closely related to advances in tissue engineering. Bone production using autologous bone and dECM loaded on 3D-printed hybrid bone scaffolds can successfully induce osteogenesis and provide mechanical force for functional bone regeneration, even in large bone defects.