Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation. Targeting CD36 pathways has emerged as a promising therapeutic strategy. Oral hypoglycemic agents, such as metformin, teneligliptin, and pioglitazone, have shown protective effects on β-cells by enhancing antioxidant defenses. These agents reduce glucotoxicity via mechanisms such as suppressing CD36 expression and stabilizing mitochondrial function. Additionally, novel insights into the glutathione antioxidant system and its role in β-cell survival underscore its therapeutic potential. This review focuses on the key contribution of oxidative stress and CD36 to β-cell impairment, the therapeutic promise of antioxidants, and the need for further research to apply these findings in clinical practice. Promising strategies targeting these mechanisms may help preserve β-cell function and slow T2DM progression.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation. Targeting CD36 pathways has emerged as a promising therapeutic strategy. Oral hypoglycemic agents, such as metformin, teneligliptin, and pioglitazone, have shown protective effects on β-cells by enhancing antioxidant defenses. These agents reduce glucotoxicity via mechanisms such as suppressing CD36 expression and stabilizing mitochondrial function. Additionally, novel insights into the glutathione antioxidant system and its role in β-cell survival underscore its therapeutic potential. This review focuses on the key contribution of oxidative stress and CD36 to β-cell impairment, the therapeutic promise of antioxidants, and the need for further research to apply these findings in clinical practice. Promising strategies targeting these mechanisms may help preserve β-cell function and slow T2DM progression.

Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation. Targeting CD36 pathways has emerged as a promising therapeutic strategy. Oral hypoglycemic agents, such as metformin, teneligliptin, and pioglitazone, have shown protective effects on β-cells by enhancing antioxidant defenses. These agents reduce glucotoxicity via mechanisms such as suppressing CD36 expression and stabilizing mitochondrial function. Additionally, novel insights into the glutathione antioxidant system and its role in β-cell survival underscore its therapeutic potential. This review focuses on the key contribution of oxidative stress and CD36 to β-cell impairment, the therapeutic promise of antioxidants, and the need for further research to apply these findings in clinical practice. Promising strategies targeting these mechanisms may help preserve β-cell function and slow T2DM progression.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Type 2 diabetes mellitus (T2DM) is marked by chronic hyperglycemia, gradually worsening β-cell failure, and insulin resistance. Glucotoxicity and oxidative stress cause β-cell failure by increasing reactive oxygen species (ROS) production, impairing insulin secretion, and disrupting transcription factors such as pancreatic and duodenal homeobox 1 (PDX-1) and musculoaponeurotic fibrosarcoma oncogene family A (MafA). Cluster determinant 36 (CD36), an essential glycoprotein responsible for fatty acid uptake, exacerbates oxidative stress and induces the apoptosis of β-cells under hyperglycemic conditions through pathways involving ceramide, thioredoxin-interacting protein (TXNIP), and Rac1-nicotinamide adenine dinucleotide phosphate oxidase (NOX)-mediated redoxosome formation. Targeting CD36 pathways has emerged as a promising therapeutic strategy. Oral hypoglycemic agents, such as metformin, teneligliptin, and pioglitazone, have shown protective effects on β-cells by enhancing antioxidant defenses. These agents reduce glucotoxicity via mechanisms such as suppressing CD36 expression and stabilizing mitochondrial function. Additionally, novel insights into the glutathione antioxidant system and its role in β-cell survival underscore its therapeutic potential. This review focuses on the key contribution of oxidative stress and CD36 to β-cell impairment, the therapeutic promise of antioxidants, and the need for further research to apply these findings in clinical practice. Promising strategies targeting these mechanisms may help preserve β-cell function and slow T2DM progression.

Background: It is unclear whether long-term use of proton pump inhibitors (PPIs) has a potential carcinogenic effect on the colorectum. Methods: We reviewed a consecutive series of neurosurgery outpatients who underwent two or more colonoscopies between January 2014 and April 2023. Patients in whom the timing of endoscopy was not in accordance with the guidelines and those without a history of previous endoscopy were excluded. In the second colonoscopy, the risk of adenomatous colon polyps was evaluated depending on whether the patient had taken a PPI. Results: In total, 520 patients were enrolled. In the multivariate analysis related to the risk of adenomatous colon polyps, age and aspirin use for >5 years were identified as significant factors. After excluding patients who had taken aspirin for >5 years, the patients were divided into three groups: those who had taken PPIs for >12 months, those who had taken PPIs for >3 months but <12 months, and those who had not taken PPIs. The risk of adenomatous colon polyps in these groups was 35.2%, 32.8%, and 22.8%, respectively (p=0.10). In the post-hoc analysis, there was a significant difference between patients who took PPIs and those who did not (p=0.03). In the multivariate analysis, a history of PPI use for >12 months was a significant risk factor for the development of advanced colon polyps (p=0.03). Conclusion Prolonged PPI use appears to increase the risk of developing adenomatous and advanced colon polyps.

Background: It is well known that a large number of patients with diabetes also have dyslipidemia, which significantly increases the risk of cardiovascular disease (CVD). This study aimed to evaluate the efficacy and safety of combination drugs consisting of metformin and atorvastatin, widely used as therapeutic agents for diabetes and dyslipidemia. Methods: This randomized, double-blind, placebo-controlled, parallel-group and phase III multicenter study included adults with glycosylated hemoglobin (HbA1c) levels >7.0% and <10.0%, low-density lipoprotein cholesterol (LDL-C) >100 and <250 mg/dL. One hundred eighty-five eligible subjects were randomized to the combination group (metformin+atorvastatin), metformin group (metformin+atorvastatin placebo), and atorvastatin group (atorvastatin+metformin placebo). The primary efficacy endpoints were the percent changes in HbA1c and LDL-C levels from baseline at the end of the treatment. Results: After 16 weeks of treatment compared to baseline, HbA1c showed a significant difference of 0.94% compared to the atorvastatin group in the combination group (0.35% vs. −0.58%, respectively; P<0.0001), whereas the proportion of patients with increased HbA1c was also 62% and 15%, respectively, showing a significant difference (P<0.001). The combination group also showed a significant decrease in LDL-C levels compared to the metformin group (−55.20% vs. −7.69%, P<0.001) without previously unknown adverse drug events. Conclusion The addition of atorvastatin to metformin improved HbA1c and LDL-C levels to a significant extent compared to metformin or atorvastatin alone in diabetes and dyslipidemia patients. This study also suggested metformin’s preventive effect on the glucose-elevating potential of atorvastatin in patients with type 2 diabetes mellitus and dyslipidemia, insufficiently controlled with exercise and diet. Metformin and atorvastatin combination might be an effective treatment in reducing the CVD risk in patients with both diabetes and dyslipidemia because of its lowering effect on LDL-C and glucose.

Background: Left ventricular assist devices (LVADs) are widely employed as a therapeutic option for end-stage heart failure. We evaluated the outcomes associated with centrifugal-flow LVAD implantation, comparing 2 device models: the Heartmate 3 (HM3) and the Heartware Ventricular Assist Device (HVAD). Methods: Data were collected from patients who underwent LVAD implantation between June 1, 2015 and December 31, 2022. We analyzed overall survival, first rehospitalization, and early, late, and LVAD-related complications. Results: In total, 74 patients underwent LVAD implantation, with 42 receiving the HM3 and 32 the HVAD. A mild Interagency Registry for Mechanically Assisted Circulatory Support score was more common among HM3 than HVAD recipients (p=0.006), and patients receiving the HM3 exhibited lower rates of preoperative ventilator use (p=0.010) and extracorporeal membrane oxygenation (p=0.039). The overall early mortality rate was 5.4% (4 of 74 patients), with no significant difference between groups. Regarding early right ventricular (RV) failure, HM3 implantation was associated with a lower rate (13 of 42 [31.0%]) than HVAD implantation (18 of 32 [56.2%], p=0.051). The median rehospitalization-free period was longer for HM3 recipients (16.9 months) than HVAD recipients (5.3 months, p=0.013).Furthermore, HM3 recipients displayed a lower incidence of late hemorrhagic stroke (p=0.016). In the multivariable analysis, preoperative use of continuous renal replacement therapy (odds ratio, 22.31; p=0.002) was the only significant predictor of postoperative RV failure. Conclusion The LVAD models (HM3 and HVAD) demonstrated comparable overall survival rates. However, the HM3 was associated with a lower risk of late hemorrhagic stroke.