This study investigated the molecular mechanism of phenotypic switching of vascular smooth muscle cells (VSMCs), which play a crucial role in vascular remodeling using 9H-Carbazol-3-yl 4-aminobenzoate (CAB). CAB significantly attenuated platelet-derived growth factor (PDGF)-induced VSMC proliferation and migration. CAB suppressed PDGF-induced STAT3 activation by directly binding to the SH2 domain of STAT3. Downregulation of STAT3 phosphorylation by CAB attenuated CIAPIN1/JAK2/STAT3 axis through a decrease in CIAPIN1 transcription. Furthermore, abrogated CIAPIN1 decreased KLF4-mediated VSMC dedifferentiation and increased CDKN1B-induced cell cycle arrest and MMP9 suppression. CAB inhibited intimal hyperplasia in injury-induced neointima animal models by inhibition of the CIAPIN1/JAK2/STAT3 axis. However, CIAPIN1 overexpression attenuated CAB-mediated suppression of VSMC proliferation, migration, phenotypic switching, and intimal hyperplasia. Our study clarified the molecular mechanism underlying STAT3 inhibition of VSMC phenotypic switching and vascular remodeling and identified novel active CAB. These findings demonstrated that STAT3 can be a major regulator to control CIAPIN1/JAK2/STAT3 axis that may be a therapeutic target for treating vascular proliferative diseases.

Objective: Even minor sacral slanting can influence T1 tilt and shoulder balance. Yet, the relationship between sacral slanting and postoperative shoulder imbalance (PSI) has not been previously explored. To determine risk factors for PSI in Lenke 2A adolescent idiopathic scoliosis (AIS) patients, with an emphasis on sacral slanting. Methods: The study encompassed 96 consecutive patients who had undergone posterior correction and fusion surgery for Lenke type 2A AIS. Patients were grouped into PSI(+) and PSI(-) based on postoperative outcomes. Additionally, they were classified into left-sided slanting, no slanting, and right-sided slanting groups according to the degree of sacral slanting. Various radiological measures were compared. Results: Patients in the PSI(+) group exhibited a smaller preoperative proximal thoracic curve and a higher main thoracic curve correction rate than those in the PSI(-) group. The presence or absence of sacral slanting did not exhibit a significant variation in PSI occurrence. However, the right-sided sacral slanting group showed a larger delta radiologic shoulder height compared to the other 2 groups (7.1 mm vs. 1.5 & 3.3 mm). Conclusion Sacral slanting was not directly linked to the development of PSI. Despite the common postoperative elevation of the left shoulder, the shoulder height differences decreased over the follow-up period. Especially in cases with a right-sided tilted sacrum, the PSI demonstrated progressive improvement, with an associated increase in the rightward distal wedging angle, leading to distal adding-on.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

Objective: Even minor sacral slanting can influence T1 tilt and shoulder balance. Yet, the relationship between sacral slanting and postoperative shoulder imbalance (PSI) has not been previously explored. To determine risk factors for PSI in Lenke 2A adolescent idiopathic scoliosis (AIS) patients, with an emphasis on sacral slanting. Methods: The study encompassed 96 consecutive patients who had undergone posterior correction and fusion surgery for Lenke type 2A AIS. Patients were grouped into PSI(+) and PSI(-) based on postoperative outcomes. Additionally, they were classified into left-sided slanting, no slanting, and right-sided slanting groups according to the degree of sacral slanting. Various radiological measures were compared. Results: Patients in the PSI(+) group exhibited a smaller preoperative proximal thoracic curve and a higher main thoracic curve correction rate than those in the PSI(-) group. The presence or absence of sacral slanting did not exhibit a significant variation in PSI occurrence. However, the right-sided sacral slanting group showed a larger delta radiologic shoulder height compared to the other 2 groups (7.1 mm vs. 1.5 & 3.3 mm). Conclusion Sacral slanting was not directly linked to the development of PSI. Despite the common postoperative elevation of the left shoulder, the shoulder height differences decreased over the follow-up period. Especially in cases with a right-sided tilted sacrum, the PSI demonstrated progressive improvement, with an associated increase in the rightward distal wedging angle, leading to distal adding-on.

Objective: Even minor sacral slanting can influence T1 tilt and shoulder balance. Yet, the relationship between sacral slanting and postoperative shoulder imbalance (PSI) has not been previously explored. To determine risk factors for PSI in Lenke 2A adolescent idiopathic scoliosis (AIS) patients, with an emphasis on sacral slanting. Methods: The study encompassed 96 consecutive patients who had undergone posterior correction and fusion surgery for Lenke type 2A AIS. Patients were grouped into PSI(+) and PSI(-) based on postoperative outcomes. Additionally, they were classified into left-sided slanting, no slanting, and right-sided slanting groups according to the degree of sacral slanting. Various radiological measures were compared. Results: Patients in the PSI(+) group exhibited a smaller preoperative proximal thoracic curve and a higher main thoracic curve correction rate than those in the PSI(-) group. The presence or absence of sacral slanting did not exhibit a significant variation in PSI occurrence. However, the right-sided sacral slanting group showed a larger delta radiologic shoulder height compared to the other 2 groups (7.1 mm vs. 1.5 & 3.3 mm). Conclusion Sacral slanting was not directly linked to the development of PSI. Despite the common postoperative elevation of the left shoulder, the shoulder height differences decreased over the follow-up period. Especially in cases with a right-sided tilted sacrum, the PSI demonstrated progressive improvement, with an associated increase in the rightward distal wedging angle, leading to distal adding-on.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

Objective: Even minor sacral slanting can influence T1 tilt and shoulder balance. Yet, the relationship between sacral slanting and postoperative shoulder imbalance (PSI) has not been previously explored. To determine risk factors for PSI in Lenke 2A adolescent idiopathic scoliosis (AIS) patients, with an emphasis on sacral slanting. Methods: The study encompassed 96 consecutive patients who had undergone posterior correction and fusion surgery for Lenke type 2A AIS. Patients were grouped into PSI(+) and PSI(-) based on postoperative outcomes. Additionally, they were classified into left-sided slanting, no slanting, and right-sided slanting groups according to the degree of sacral slanting. Various radiological measures were compared. Results: Patients in the PSI(+) group exhibited a smaller preoperative proximal thoracic curve and a higher main thoracic curve correction rate than those in the PSI(-) group. The presence or absence of sacral slanting did not exhibit a significant variation in PSI occurrence. However, the right-sided sacral slanting group showed a larger delta radiologic shoulder height compared to the other 2 groups (7.1 mm vs. 1.5 & 3.3 mm). Conclusion Sacral slanting was not directly linked to the development of PSI. Despite the common postoperative elevation of the left shoulder, the shoulder height differences decreased over the follow-up period. Especially in cases with a right-sided tilted sacrum, the PSI demonstrated progressive improvement, with an associated increase in the rightward distal wedging angle, leading to distal adding-on.

Objective: Previous studies have reported that vitamin D deficiency increased the risk of Alzheimer’s disease (AD) dementia in older adults. However, little is known about how vitamin D is involved in the pathophysiology of AD. Thus, this study aimed to examine the association and interaction of serum vitamin D levels with in vivo AD pathologies including cerebral beta-amyloid (Aβ) deposition and neurodegeneration in nondemented older adults. Methods: 428 Nondemented older adults were recruited from the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease, a prospective cohort that began in 2014. All participants underwent comprehensive clinical assessments, measurement of serum 25-hydroxyvitamin D (25[OH]D), and multimodal brain imaging including Pittsburgh compound B (PiB) positron emission tomography and magnetic resonance imaging. Global PiB deposition was measured for the Aβ biomarker. Intracranial volume-adjusted hippocampal volume (HVa) was used as a neurodegeneration biomarker. Results: Overall, serum 25(OH)D level was not associated with either Aβ deposition or HVa after controlling for age, sex, apolipoprotein E ε4 positivity, and vascular risk factors. However, serum 25(OH)D level had a significant moderating effect on the association between Aβ and neurodegeneration, with lower serum 25(OH)D level significantly exacerbating cerebral Aβ-associated hippocampal volume loss (B = 34.612, p = 0.008). Conclusion Our findings indicate that lower serum vitamin D levels may contribute to AD by exacerbating Aβ-associated neurodegeneration in nondemented older adults. Further studies to explore the potential therapeutic effect of vitamin D supplementation on the progression of AD pathology will be necessary.

Objective: Even minor sacral slanting can influence T1 tilt and shoulder balance. Yet, the relationship between sacral slanting and postoperative shoulder imbalance (PSI) has not been previously explored. To determine risk factors for PSI in Lenke 2A adolescent idiopathic scoliosis (AIS) patients, with an emphasis on sacral slanting. Methods: The study encompassed 96 consecutive patients who had undergone posterior correction and fusion surgery for Lenke type 2A AIS. Patients were grouped into PSI(+) and PSI(-) based on postoperative outcomes. Additionally, they were classified into left-sided slanting, no slanting, and right-sided slanting groups according to the degree of sacral slanting. Various radiological measures were compared. Results: Patients in the PSI(+) group exhibited a smaller preoperative proximal thoracic curve and a higher main thoracic curve correction rate than those in the PSI(-) group. The presence or absence of sacral slanting did not exhibit a significant variation in PSI occurrence. However, the right-sided sacral slanting group showed a larger delta radiologic shoulder height compared to the other 2 groups (7.1 mm vs. 1.5 & 3.3 mm). Conclusion Sacral slanting was not directly linked to the development of PSI. Despite the common postoperative elevation of the left shoulder, the shoulder height differences decreased over the follow-up period. Especially in cases with a right-sided tilted sacrum, the PSI demonstrated progressive improvement, with an associated increase in the rightward distal wedging angle, leading to distal adding-on.