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.

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.

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.

Purpose: This study aimed to develop and evaluate machine learning models, specifically CatBoost and extreme gradient boosting (XGBoost), for diagnosing lower urinary tract symptoms (LUTS) in male patients. The objective is to differentiate between bladder outlet obstruction (BOO) and detrusor underactivity (DUA) using a comprehensive dataset that includes patient-reported outcomes, uroflowmetry measurements, and ultrasound-derived features. Methods: The dataset used in this study was collected from male patients aged 40 and older who presented with LUTS and sought treatment at the urology department of Samsung Medical Center. We developed and trained CatBoost and XGBoost models using this dataset. These models incorporated features like prostate size, voiding parameters, and responses from questionnaires. Their performance was assessed using standard metrics such as accuracy, precision, recall, F1-score, and area under the receiver operating characteristic curve (AUROC). Results: The results indicated that the CatBoost models displayed greater sensitivity, rendering them effective for initial screenings by accurately identifying true positive cases. Conversely, the XGBoost models showed higher specificity and precision, making them more suitable for confirming diagnoses and reducing false positives. In terms of overall performance for both BOO and DUA, XGBoost surpassed CatBoost, achieving an AUROC of 0.826 and 0.819, respectively. Conclusions Integrating these machine learning models into the diagnostic workflow for LUTS can significantly enhance clinical decision-making by offering noninvasive, cost-effective, and patient-friendly diagnostic alternatives. The combined application of CatBoost and XGBoost models has the potential to improve diagnostic accuracy and provide customized treatment plans for patients, ultimately leading to better clinical outcomes.

Purpose: This study aimed to develop and evaluate machine learning models, specifically CatBoost and extreme gradient boosting (XGBoost), for diagnosing lower urinary tract symptoms (LUTS) in male patients. The objective is to differentiate between bladder outlet obstruction (BOO) and detrusor underactivity (DUA) using a comprehensive dataset that includes patient-reported outcomes, uroflowmetry measurements, and ultrasound-derived features. Methods: The dataset used in this study was collected from male patients aged 40 and older who presented with LUTS and sought treatment at the urology department of Samsung Medical Center. We developed and trained CatBoost and XGBoost models using this dataset. These models incorporated features like prostate size, voiding parameters, and responses from questionnaires. Their performance was assessed using standard metrics such as accuracy, precision, recall, F1-score, and area under the receiver operating characteristic curve (AUROC). Results: The results indicated that the CatBoost models displayed greater sensitivity, rendering them effective for initial screenings by accurately identifying true positive cases. Conversely, the XGBoost models showed higher specificity and precision, making them more suitable for confirming diagnoses and reducing false positives. In terms of overall performance for both BOO and DUA, XGBoost surpassed CatBoost, achieving an AUROC of 0.826 and 0.819, respectively. Conclusions Integrating these machine learning models into the diagnostic workflow for LUTS can significantly enhance clinical decision-making by offering noninvasive, cost-effective, and patient-friendly diagnostic alternatives. The combined application of CatBoost and XGBoost models has the potential to improve diagnostic accuracy and provide customized treatment plans for patients, ultimately leading to better clinical outcomes.

Purpose: This study aimed to develop and evaluate machine learning models, specifically CatBoost and extreme gradient boosting (XGBoost), for diagnosing lower urinary tract symptoms (LUTS) in male patients. The objective is to differentiate between bladder outlet obstruction (BOO) and detrusor underactivity (DUA) using a comprehensive dataset that includes patient-reported outcomes, uroflowmetry measurements, and ultrasound-derived features. Methods: The dataset used in this study was collected from male patients aged 40 and older who presented with LUTS and sought treatment at the urology department of Samsung Medical Center. We developed and trained CatBoost and XGBoost models using this dataset. These models incorporated features like prostate size, voiding parameters, and responses from questionnaires. Their performance was assessed using standard metrics such as accuracy, precision, recall, F1-score, and area under the receiver operating characteristic curve (AUROC). Results: The results indicated that the CatBoost models displayed greater sensitivity, rendering them effective for initial screenings by accurately identifying true positive cases. Conversely, the XGBoost models showed higher specificity and precision, making them more suitable for confirming diagnoses and reducing false positives. In terms of overall performance for both BOO and DUA, XGBoost surpassed CatBoost, achieving an AUROC of 0.826 and 0.819, respectively. Conclusions Integrating these machine learning models into the diagnostic workflow for LUTS can significantly enhance clinical decision-making by offering noninvasive, cost-effective, and patient-friendly diagnostic alternatives. The combined application of CatBoost and XGBoost models has the potential to improve diagnostic accuracy and provide customized treatment plans for patients, ultimately leading to better clinical outcomes.

Arterial thrombosis and its associated diseases are considered to constitute a major healthcare problem. Arterial thrombosis, defined as blood clot formation in an artery that interrupts blood circulation, is associated with many cardiovascular diseases. Oxidative stress is one of many important factors that aggravates the pathophysiological process of arterial thrombosis. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ref-1) has a multifunctional role in cells that includes the regulation of oxidative stress and anti-inflammatory function. The aim of this study was to investigate the therapeutic effect of adenovirus-mediated Ref-1 overexpression on arterial thrombosis induced by 60% FeCl3 solution in rats. Blood flow was measured to detect the time to occlusion, thrombus formation was detected by hematoxylin and eosin staining, reactive oxygen species (ROS) levels were detected by high-performance liquid chromatography, and the expression of tissue factor and other proteins was detected by Western blot. FeCl3 aggravated thrombus formation in carotid arteries and reduced the time to artery occlusion. Ref-1 significantly delayed arterial obstruction via the inhibition of thrombus formation, especially by downregulating tissue factor expression through the Akt-GSK3β-NF-κB signaling pathway. Ref-1 also reduced the expression of vascular inflammation markers ICAM-1 and VCAM-1, and reduced the level of ROS that contributed to thrombus formation. The results showed that adenovirus-mediated Ref-1 overexpression reduced thrombus formation in the rat carotid artery. In summary, Ref-1 overexpression had anti-thrombotic effects in a carotid artery thrombosis model and could be a target for the treatment of arterial thrombosis.

Arterial thrombosis and its associated diseases are considered to constitute a major healthcare problem. Arterial thrombosis, defined as blood clot formation in an artery that interrupts blood circulation, is associated with many cardiovascular diseases. Oxidative stress is one of many important factors that aggravates the pathophysiological process of arterial thrombosis. Apurinic/apyrimidinic endonuclease 1/redox factor-1 (Ref-1) has a multifunctional role in cells that includes the regulation of oxidative stress and anti-inflammatory function. The aim of this study was to investigate the therapeutic effect of adenovirus-mediated Ref-1 overexpression on arterial thrombosis induced by 60% FeCl3 solution in rats. Blood flow was measured to detect the time to occlusion, thrombus formation was detected by hematoxylin and eosin staining, reactive oxygen species (ROS) levels were detected by high-performance liquid chromatography, and the expression of tissue factor and other proteins was detected by Western blot. FeCl3 aggravated thrombus formation in carotid arteries and reduced the time to artery occlusion. Ref-1 significantly delayed arterial obstruction via the inhibition of thrombus formation, especially by downregulating tissue factor expression through the Akt-GSK3β-NF-κB signaling pathway. Ref-1 also reduced the expression of vascular inflammation markers ICAM-1 and VCAM-1, and reduced the level of ROS that contributed to thrombus formation. The results showed that adenovirus-mediated Ref-1 overexpression reduced thrombus formation in the rat carotid artery. In summary, Ref-1 overexpression had anti-thrombotic effects in a carotid artery thrombosis model and could be a target for the treatment of arterial thrombosis.