Objective: The upper lumbar region has distinctive anatomical characteristics that contribute to the challenges of performing discectomy. We introduce far-lateral transforaminal unilateral biportal endoscopic (UBE) lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. Methods: We conducted retrospective review of the patients who underwent a far-lateral transforaminal UBE lumbar discectomy at our institution from January 2018 to September 2024. The electronic medical records, operative records, and radiologic images of the patients were reviewed. Results: A total of 27 patients underwent far-lateral transforaminal UBE lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. The patient had a mean age of 54.0 ± 13.7 years. Operation was performed at the L1–2 level in 3 patients (11.1%), L2–3 in 9 patients (33.3%), and L3–4 in 15 patients (55.6%). The patients were followed-up for a mean of 27.7 ± 19.3 months. The Oswestry Disability Index was significantly decreased from 36.3 ± 6.8 preoperatively to 3.7 ± 3.3 at last follow-up (p < 0.001). The visual analogue scale (VAS) back was significantly decreased from 7.8 ± 0.9 preoperatively to 3.1 ± 0.6 postoperative day 2 (p < 0.001). The VAS leg was significantly decreased from 8.1 ± 0.8 preoperatively to 2.3 ± 0.7 postoperative day 2 (p < 0.001). Conclusion The far-lateral transforaminal UBE lumbar discectomy would be a viable surgical option for upper lumbar disc herniations.

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.

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.

Objective: The upper lumbar region has distinctive anatomical characteristics that contribute to the challenges of performing discectomy. We introduce far-lateral transforaminal unilateral biportal endoscopic (UBE) lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. Methods: We conducted retrospective review of the patients who underwent a far-lateral transforaminal UBE lumbar discectomy at our institution from January 2018 to September 2024. The electronic medical records, operative records, and radiologic images of the patients were reviewed. Results: A total of 27 patients underwent far-lateral transforaminal UBE lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. The patient had a mean age of 54.0 ± 13.7 years. Operation was performed at the L1–2 level in 3 patients (11.1%), L2–3 in 9 patients (33.3%), and L3–4 in 15 patients (55.6%). The patients were followed-up for a mean of 27.7 ± 19.3 months. The Oswestry Disability Index was significantly decreased from 36.3 ± 6.8 preoperatively to 3.7 ± 3.3 at last follow-up (p < 0.001). The visual analogue scale (VAS) back was significantly decreased from 7.8 ± 0.9 preoperatively to 3.1 ± 0.6 postoperative day 2 (p < 0.001). The VAS leg was significantly decreased from 8.1 ± 0.8 preoperatively to 2.3 ± 0.7 postoperative day 2 (p < 0.001). Conclusion The far-lateral transforaminal UBE lumbar discectomy would be a viable surgical option for upper lumbar disc herniations.

Objective: The upper lumbar region has distinctive anatomical characteristics that contribute to the challenges of performing discectomy. We introduce far-lateral transforaminal unilateral biportal endoscopic (UBE) lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. Methods: We conducted retrospective review of the patients who underwent a far-lateral transforaminal UBE lumbar discectomy at our institution from January 2018 to September 2024. The electronic medical records, operative records, and radiologic images of the patients were reviewed. Results: A total of 27 patients underwent far-lateral transforaminal UBE lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. The patient had a mean age of 54.0 ± 13.7 years. Operation was performed at the L1–2 level in 3 patients (11.1%), L2–3 in 9 patients (33.3%), and L3–4 in 15 patients (55.6%). The patients were followed-up for a mean of 27.7 ± 19.3 months. The Oswestry Disability Index was significantly decreased from 36.3 ± 6.8 preoperatively to 3.7 ± 3.3 at last follow-up (p < 0.001). The visual analogue scale (VAS) back was significantly decreased from 7.8 ± 0.9 preoperatively to 3.1 ± 0.6 postoperative day 2 (p < 0.001). The VAS leg was significantly decreased from 8.1 ± 0.8 preoperatively to 2.3 ± 0.7 postoperative day 2 (p < 0.001). Conclusion The far-lateral transforaminal UBE lumbar discectomy would be a viable surgical option for upper lumbar disc herniations.

Objective: The upper lumbar region has distinctive anatomical characteristics that contribute to the challenges of performing discectomy. We introduce far-lateral transforaminal unilateral biportal endoscopic (UBE) lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. Methods: We conducted retrospective review of the patients who underwent a far-lateral transforaminal UBE lumbar discectomy at our institution from January 2018 to September 2024. The electronic medical records, operative records, and radiologic images of the patients were reviewed. Results: A total of 27 patients underwent far-lateral transforaminal UBE lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. The patient had a mean age of 54.0 ± 13.7 years. Operation was performed at the L1–2 level in 3 patients (11.1%), L2–3 in 9 patients (33.3%), and L3–4 in 15 patients (55.6%). The patients were followed-up for a mean of 27.7 ± 19.3 months. The Oswestry Disability Index was significantly decreased from 36.3 ± 6.8 preoperatively to 3.7 ± 3.3 at last follow-up (p < 0.001). The visual analogue scale (VAS) back was significantly decreased from 7.8 ± 0.9 preoperatively to 3.1 ± 0.6 postoperative day 2 (p < 0.001). The VAS leg was significantly decreased from 8.1 ± 0.8 preoperatively to 2.3 ± 0.7 postoperative day 2 (p < 0.001). Conclusion The far-lateral transforaminal UBE lumbar discectomy would be a viable surgical option for upper lumbar disc herniations.

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.

Objective: The upper lumbar region has distinctive anatomical characteristics that contribute to the challenges of performing discectomy. We introduce far-lateral transforaminal unilateral biportal endoscopic (UBE) lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. Methods: We conducted retrospective review of the patients who underwent a far-lateral transforaminal UBE lumbar discectomy at our institution from January 2018 to September 2024. The electronic medical records, operative records, and radiologic images of the patients were reviewed. Results: A total of 27 patients underwent far-lateral transforaminal UBE lumbar discectomy for central or paracentral disc herniations in the upper lumbar region. The patient had a mean age of 54.0 ± 13.7 years. Operation was performed at the L1–2 level in 3 patients (11.1%), L2–3 in 9 patients (33.3%), and L3–4 in 15 patients (55.6%). The patients were followed-up for a mean of 27.7 ± 19.3 months. The Oswestry Disability Index was significantly decreased from 36.3 ± 6.8 preoperatively to 3.7 ± 3.3 at last follow-up (p < 0.001). The visual analogue scale (VAS) back was significantly decreased from 7.8 ± 0.9 preoperatively to 3.1 ± 0.6 postoperative day 2 (p < 0.001). The VAS leg was significantly decreased from 8.1 ± 0.8 preoperatively to 2.3 ± 0.7 postoperative day 2 (p < 0.001). Conclusion The far-lateral transforaminal UBE lumbar discectomy would be a viable surgical option for upper lumbar disc herniations.

Background/Aims: Little is known about the practical clinical application of neuromodulators and psychiatric treatments in patients with functional gastrointestinal disorders (FGIDs). We investigate the knowledge, attitudes, and practices of Korean clinicians regarding the use of neuromodulators and psychiatric treatments for FGIDs. Methods: This prospective, online, cross-sectional study was conducted between May and August 2022. A questionnaire regarding the knowledge, attitude, and practice of neuromodulators and psychiatric treatments for FGIDs was developed and administered to primary care clinicians and gastroenterologists in university hospitals in Korea. Results: Overall, 451 clinicians from primary (n = 179, 39.7%), secondary (n = 113, 25.1%), and tertiary (n = 159, 35.3%) hospitals participated in the survey. Most of them considered that neuromodulators (98.7%) and psychiatric treatment (86.5%) were required for patients with FGIDs. However, approximately one-third of them did not prescribe neuromodulators, mainly due to unfamiliarity with the drugs, and only one-quarter considered psychiatric referral. Compared to gastroenterologists at university hospitals, primary care clinicians’ prescriptions had a lower rate (87.2% vs 64.2%, P < 0.001) and shorter duration of neuromodulator. The psychiatric referral rate was lower for primary care clinicians than for gastroenterologists at university hospitals (19.0% vs 34.2%, P < 0.001). Conclusions Knowledge, attitude, and practice levels regarding neuromodulators and psychiatric treatment among clinicians are inhomogeneous, and a knowledge gap exists between primary care clinicians and gastroenterologists at university hospitals. Encouraging ongoing education for Korean clinicians regarding the appropriate use of neuromodulators and psychiatric treatments in patients with FGIDs is suggested.