Purpose: To compare the macular and peripapillary vascular parameters between the primary angle closure suspect (PACS) eyes and normal control eyes using optical coherence tomography angiography (OCTA). Methods: In this retrospective study, 42 PACS subjects and 38 normal individuals are included. Vessel density (VD) and perfusion density (PD) of the macular area and peripapillary area, and fovea avascular zone parameter were analyzed using OCTA and compared between two groups after adjustment for the axial length. Results: There were no statistically significant differences in sex ratio, age, refractive errors and intraocular pressures between both groups. In the peripapillary area, inferior VD and PD in the outer zone were significantly lower in the PACS eyes, while the retinal nerve fiber layer thicknesses were similar between groups (p = 0.032, 0.026). In the macular superficial capillary plexus, inferior VD and PD in the inner zone, inferior VD and PD, nasal VD and PD in the outer zone were significantly lower in the PACS eyes, whereas ganglion cell inner plexiform layer thickness were similar between both groups (all p < 0.005). Conclusions The VDs and PDs of retinal capillaries in PACS eyes, which have no glaucomatous changes in the retinal nerve fiber layer and optic nerve disc, were significantly lower compared to normal eyes.

Purpose: To compare the macular and peripapillary vascular parameters between the primary angle closure suspect (PACS) eyes and normal control eyes using optical coherence tomography angiography (OCTA). Methods: In this retrospective study, 42 PACS subjects and 38 normal individuals are included. Vessel density (VD) and perfusion density (PD) of the macular area and peripapillary area, and fovea avascular zone parameter were analyzed using OCTA and compared between two groups after adjustment for the axial length. Results: There were no statistically significant differences in sex ratio, age, refractive errors and intraocular pressures between both groups. In the peripapillary area, inferior VD and PD in the outer zone were significantly lower in the PACS eyes, while the retinal nerve fiber layer thicknesses were similar between groups (p = 0.032, 0.026). In the macular superficial capillary plexus, inferior VD and PD in the inner zone, inferior VD and PD, nasal VD and PD in the outer zone were significantly lower in the PACS eyes, whereas ganglion cell inner plexiform layer thickness were similar between both groups (all p < 0.005). Conclusions The VDs and PDs of retinal capillaries in PACS eyes, which have no glaucomatous changes in the retinal nerve fiber layer and optic nerve disc, were significantly lower compared to normal eyes.

Background: Histone deacetylase (HDAC) inhibition offers potential anticancer effects across diverse cancers due to HDAC's significant role in cancer development and progression. Consequently, we demonstrated the therapeutic efficacy of the novel HDAC inhibitor, CG-745, in comparison with existing inhibitors such as suberoylanilide hydroxamic acid (SAHA) in non-small cell lung cancer (NSCLC) cells. Methods: CG-745's effect on apoptosis and reactive oxygen species (ROS)-dependent mitochondrial dysfunction was investigated using annexin V assay, MitoSoX, and Western blot in human A549 and H460 cells. Additionally, HDAC expression was analyzed through real-time polymerase chain reaction. We also evaluated the inhibitory effect of CG-745 on epithelial-mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) via Western blot, scratch analysis, and matrigel invasion analysis. Results: Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3, and HDAC8. It also induced apoptosis, ROS, and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT triggered by TGF-β1 in A549 and H460 cells, and curtailed the migration and invasion enhanced by TGF-β1. CG-745 has demonstrably inhibited EMT and induced apoptosis in NSCLC cells. Conclusion CG-745 may represent a novel therapeutic strategy for NSCLC treatment.

Background: Histone deacetylase (HDAC) inhibition offers potential anticancer effects across diverse cancers due to HDAC's significant role in cancer development and progression. Consequently, we demonstrated the therapeutic efficacy of the novel HDAC inhibitor, CG-745, in comparison with existing inhibitors such as suberoylanilide hydroxamic acid (SAHA) in non-small cell lung cancer (NSCLC) cells. Methods: CG-745's effect on apoptosis and reactive oxygen species (ROS)-dependent mitochondrial dysfunction was investigated using annexin V assay, MitoSoX, and Western blot in human A549 and H460 cells. Additionally, HDAC expression was analyzed through real-time polymerase chain reaction. We also evaluated the inhibitory effect of CG-745 on epithelial-mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) via Western blot, scratch analysis, and matrigel invasion analysis. Results: Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3, and HDAC8. It also induced apoptosis, ROS, and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT triggered by TGF-β1 in A549 and H460 cells, and curtailed the migration and invasion enhanced by TGF-β1. CG-745 has demonstrably inhibited EMT and induced apoptosis in NSCLC cells. Conclusion CG-745 may represent a novel therapeutic strategy for NSCLC treatment.

Background: Histone deacetylase (HDAC) inhibition offers potential anticancer effects across diverse cancers due to HDAC's significant role in cancer development and progression. Consequently, we demonstrated the therapeutic efficacy of the novel HDAC inhibitor, CG-745, in comparison with existing inhibitors such as suberoylanilide hydroxamic acid (SAHA) in non-small cell lung cancer (NSCLC) cells. Methods: CG-745's effect on apoptosis and reactive oxygen species (ROS)-dependent mitochondrial dysfunction was investigated using annexin V assay, MitoSoX, and Western blot in human A549 and H460 cells. Additionally, HDAC expression was analyzed through real-time polymerase chain reaction. We also evaluated the inhibitory effect of CG-745 on epithelial-mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) via Western blot, scratch analysis, and matrigel invasion analysis. Results: Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3, and HDAC8. It also induced apoptosis, ROS, and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT triggered by TGF-β1 in A549 and H460 cells, and curtailed the migration and invasion enhanced by TGF-β1. CG-745 has demonstrably inhibited EMT and induced apoptosis in NSCLC cells. Conclusion CG-745 may represent a novel therapeutic strategy for NSCLC treatment.

Background: Histone deacetylase (HDAC) inhibition offers potential anticancer effects across diverse cancers due to HDAC's significant role in cancer development and progression. Consequently, we demonstrated the therapeutic efficacy of the novel HDAC inhibitor, CG-745, in comparison with existing inhibitors such as suberoylanilide hydroxamic acid (SAHA) in non-small cell lung cancer (NSCLC) cells. Methods: CG-745's effect on apoptosis and reactive oxygen species (ROS)-dependent mitochondrial dysfunction was investigated using annexin V assay, MitoSoX, and Western blot in human A549 and H460 cells. Additionally, HDAC expression was analyzed through real-time polymerase chain reaction. We also evaluated the inhibitory effect of CG-745 on epithelial-mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) via Western blot, scratch analysis, and matrigel invasion analysis. Results: Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3, and HDAC8. It also induced apoptosis, ROS, and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT triggered by TGF-β1 in A549 and H460 cells, and curtailed the migration and invasion enhanced by TGF-β1. CG-745 has demonstrably inhibited EMT and induced apoptosis in NSCLC cells. Conclusion CG-745 may represent a novel therapeutic strategy for NSCLC treatment.

Purpose: To compare the macular and peripapillary vascular parameters between the primary angle closure suspect (PACS) eyes and normal control eyes using optical coherence tomography angiography (OCTA). Methods: In this retrospective study, 42 PACS subjects and 38 normal individuals are included. Vessel density (VD) and perfusion density (PD) of the macular area and peripapillary area, and fovea avascular zone parameter were analyzed using OCTA and compared between two groups after adjustment for the axial length. Results: There were no statistically significant differences in sex ratio, age, refractive errors and intraocular pressures between both groups. In the peripapillary area, inferior VD and PD in the outer zone were significantly lower in the PACS eyes, while the retinal nerve fiber layer thicknesses were similar between groups (p = 0.032, 0.026). In the macular superficial capillary plexus, inferior VD and PD in the inner zone, inferior VD and PD, nasal VD and PD in the outer zone were significantly lower in the PACS eyes, whereas ganglion cell inner plexiform layer thickness were similar between both groups (all p < 0.005). Conclusions The VDs and PDs of retinal capillaries in PACS eyes, which have no glaucomatous changes in the retinal nerve fiber layer and optic nerve disc, were significantly lower compared to normal eyes.

Background: Histone deacetylase (HDAC) inhibition offers potential anticancer effects across diverse cancers due to HDAC's significant role in cancer development and progression. Consequently, we demonstrated the therapeutic efficacy of the novel HDAC inhibitor, CG-745, in comparison with existing inhibitors such as suberoylanilide hydroxamic acid (SAHA) in non-small cell lung cancer (NSCLC) cells. Methods: CG-745's effect on apoptosis and reactive oxygen species (ROS)-dependent mitochondrial dysfunction was investigated using annexin V assay, MitoSoX, and Western blot in human A549 and H460 cells. Additionally, HDAC expression was analyzed through real-time polymerase chain reaction. We also evaluated the inhibitory effect of CG-745 on epithelial-mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) via Western blot, scratch analysis, and matrigel invasion analysis. Results: Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3, and HDAC8. It also induced apoptosis, ROS, and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT triggered by TGF-β1 in A549 and H460 cells, and curtailed the migration and invasion enhanced by TGF-β1. CG-745 has demonstrably inhibited EMT and induced apoptosis in NSCLC cells. Conclusion CG-745 may represent a novel therapeutic strategy for NSCLC treatment.

Pedicle ossification is a rare but significant complication following mandibular reconstruction using a fibular free flap (FFF), a technique widely employed in maxillofacial surgery due to its reliable vascularized bone supply and low donor site morbidity. The FFF supports dental implantation and prosthetic rehabilitation, with its vascularized periosteum enhancing osteogenic potential. Despite these advantages, unexpected ossification of the flap’s vascular pedicle may occur, potentially mimicking tumor recurrence and causing diagnostic uncertainty. This case report describes a 38-year-old male with left buccal squamous cell carcinoma treated by wide excision, modified radical neck dissection, and reconstruction using a radial forearm free flap. Postoperative radiotherapy led to complications including trismus and alveolar bone exposure, culminating in a pathological mandibular fracture. Mandibular reconstruction was performed using an FFF. Over 4 years of follow-up, computed tomography revealed ossification within the vascular pedicle. Notably, the patient remained asymptomatic, maintaining normal speech and swallowing without functional impairment. Pedicle ossification may present radiographically as a suspicious bony change misinterpreted as tumor recurrence. Routine follow-up imaging such as computed tomography is essential for differentiation. Although trismus, bony swelling, or pain may occur, surgical intervention is typically deferred unless symptoms develop. Therefore, careful clinical assessment and monitoring remain crucial.

Pedicle ossification is a rare but significant complication following mandibular reconstruction using a fibular free flap (FFF), a technique widely employed in maxillofacial surgery due to its reliable vascularized bone supply and low donor site morbidity. The FFF supports dental implantation and prosthetic rehabilitation, with its vascularized periosteum enhancing osteogenic potential. Despite these advantages, unexpected ossification of the flap’s vascular pedicle may occur, potentially mimicking tumor recurrence and causing diagnostic uncertainty. This case report describes a 38-year-old male with left buccal squamous cell carcinoma treated by wide excision, modified radical neck dissection, and reconstruction using a radial forearm free flap. Postoperative radiotherapy led to complications including trismus and alveolar bone exposure, culminating in a pathological mandibular fracture. Mandibular reconstruction was performed using an FFF. Over 4 years of follow-up, computed tomography revealed ossification within the vascular pedicle. Notably, the patient remained asymptomatic, maintaining normal speech and swallowing without functional impairment. Pedicle ossification may present radiographically as a suspicious bony change misinterpreted as tumor recurrence. Routine follow-up imaging such as computed tomography is essential for differentiation. Although trismus, bony swelling, or pain may occur, surgical intervention is typically deferred unless symptoms develop. Therefore, careful clinical assessment and monitoring remain crucial.