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.

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: Internal hernia after gastrectomy is a rare but potentially life-threatening condition without surgical intervention. Clinical risk factors of internal hernia should, hence, be reviewed after gastrectomy.From 2008 to 2018, patients who underwent gastrectomy for gastric cancer were investigated. Methods: Abdominal computed tomography (CT) was used to screen for internal hernia, and surgical exploration was performed to confirm the diagnosis. Using retrospective statistical analysis, the incidence, characteristics, and risk factors were identified, and the characteristics of the internal hernia group were reviewed. Results: The overall incidence of internal hernia was 0.9%. From statistical analysis, it was found that laparoscopic surgery was almost five times riskier than open gastrectomy (odds ratio [OR], 4.947; 95% confidence interval [CI], 1.308–18.710; p = 0.019). Body mass index < 25 kg/m2 (OR, 4.596; 95% CI, 1.056– 20.004; p = 0.042) and proximal gastrectomy (OR, 4.238; 95% CI, 1.072–16.751; p = 0.039) were also associated with internal hernia. Among 20 patients with internal hernia, 12 underwent laparotomy, and five had their bowels removed due to ischemia. All patients with bowel resected had suffered from short bowel syndrome. Conclusion Suspecting an internal hernia should be an important step when a patient with a history of laparoscopic gastrectomy visits for medical care. When suspected, emergent screening through CT scan and surgical intervention should be considered as soon as possible to prevent lifetime complications accordingly.

Background: Femoral internal rotation in total knee arthroplasty (TKA) is well known as one of the main causes of patellar maltracking. Although femoral internal rotation in TKA is considered unacceptable due to the risk of patellar maltracking, it is sometimes required for ligament balancing. We evaluated the influence of femoral internal rotation on patellar tracking in TKA performed using the gap technique. Methods: From April 2008 to May 2018, 1,612 cases of TKA were done. Among them, 245 cases of TKA for osteoarthritis were followed up for at least 1 year and included in this study. We compared patellar tracking in two groups; group I consisted of 99 cases whose femoral rotation was less than 0° and group II consisted of 146 cases whose femoral rotation was 3°–5° external rotation. Preoperative femoral rotation was measured with the condylar twist angle (CTA) by using computed tomography. The patella was replaced in all cases. Patellar tracking was evaluated with patellar tilt angle (lateral tilt [+] and medial tilt [–]) in the merchant radiograph. Statistical analysis was done using Mann-Whitney U-test. Clinical assessment was performed using the Knee Society clinical rating system. Results: The preoperative CTA was 5.3° ± 1.6° in group I and 5.4° ± 1.6° in group II, showing no statistically significant difference between groups (p = 0.455). Intraoperative femoral rotation was –0.5° ± 0.8° in group I and 3.9° ± 0.8° in group II when the gap technique was used (p < 0.001). The postoperative patellar tilt angle was –0.4° ± 3.6° in group I and 0.1° ± 4.1° in group II with no statistically significant difference (p = 0.251). Conclusions Compared with femoral external rotation, femoral internal rotation with ligament balance in TKA was not more associated with patellar maltracking. Therefore, patellar tracking might be related with ligament balance in flexion regardless of the anatomic femoral rotational alignment.

Background: Femoral internal rotation in total knee arthroplasty (TKA) is well known as one of the main causes of patellar maltracking. Although femoral internal rotation in TKA is considered unacceptable due to the risk of patellar maltracking, it is sometimes required for ligament balancing. We evaluated the influence of femoral internal rotation on patellar tracking in TKA performed using the gap technique. Methods: From April 2008 to May 2018, 1,612 cases of TKA were done. Among them, 245 cases of TKA for osteoarthritis were followed up for at least 1 year and included in this study. We compared patellar tracking in two groups; group I consisted of 99 cases whose femoral rotation was less than 0° and group II consisted of 146 cases whose femoral rotation was 3°–5° external rotation. Preoperative femoral rotation was measured with the condylar twist angle (CTA) by using computed tomography. The patella was replaced in all cases. Patellar tracking was evaluated with patellar tilt angle (lateral tilt [+] and medial tilt [–]) in the merchant radiograph. Statistical analysis was done using Mann-Whitney U-test. Clinical assessment was performed using the Knee Society clinical rating system. Results: The preoperative CTA was 5.3° ± 1.6° in group I and 5.4° ± 1.6° in group II, showing no statistically significant difference between groups (p = 0.455). Intraoperative femoral rotation was –0.5° ± 0.8° in group I and 3.9° ± 0.8° in group II when the gap technique was used (p < 0.001). The postoperative patellar tilt angle was –0.4° ± 3.6° in group I and 0.1° ± 4.1° in group II with no statistically significant difference (p = 0.251). Conclusions Compared with femoral external rotation, femoral internal rotation with ligament balance in TKA was not more associated with patellar maltracking. Therefore, patellar tracking might be related with ligament balance in flexion regardless of the anatomic femoral rotational alignment.

Objective: To evaluate the construction reproducibility of a composite tooth model (CTM) composed of an intraoral-scanned crown and a cone-beam computed tomography (CBCT)-scanned root. Methods: The study assessed 240 teeth (30 central incisors, 30 canines, 30 second premolars, and 30 first molars in the maxillary and mandibular arches) from 15 young adult patients whose pre-treatment intraoral scan and CBCT were available. Examiner-Reference (3 years’ experience in CTM construction) and Examiners-A and Examiner-B (no experience) constructed the individual CTMs independently by performing the following steps: image acquisition and processing into a three-dimensional model, integration of intraoral-scanned crowns and CBCT-scanned teeth, and replacement of the CBCT-scanned crown with the intraoral-scanned crown. The tooth axis angle in terms of mesiodistal angulation and buccolingual inclination of the CTMs constructed by the three examiners were measured. To assess the construction reproducibility of CTMs, intraclass correlation coefficient (ICC) assessments were performed. Results: The ICC values of mesiodistal angulation and buccolingual inclination among the 3 examiners showed excellent agreement (0.950–0.992 and 0.965–0.993; 0.976–0.994 and 0.973–0.995 in the maxillary and mandibular arches, respectively). Conclusions The CTM showed excellent construction reproducibility in mesiodistal angulation and buccolingual inclination regardless of the construction skill and experience levels of the examiners.

BACKGROUND: Plasma epidermal growth factor receptor (EGFR) mutation tests are less invasive than tissue EGFR mutation tests. We determined which of two kits is more efficient: cobas EGFR Mutation test v2 (cobasv2; Roche Molecular Systems, Pleasanton, CA, USA) or PANAMutyper-R-EGFR (Mutyper; Panagene, Daejeon, Korea). We also evaluated whether pleural effusion supernatant (PE-SUP) samples are assayable, similar to plasma samples, using these two kits. METHODS: We analyzed 156 plasma and PE-SUP samples (31 paired samples) from 116 individuals. We compared the kits in terms of accuracy, assessed genotype concordance (weighted κ with 95% confidence intervals), and calculated Spearman's rho between semi-quantitatively measured EGFR-mutant levels (SQIs) measured by each kit. We also compared sensitivity using 47 EGFR-mutant harboring samples divided into more-dilute and less-dilute samples (dilution ratio: ≥ or <1:1,000). RESULTS: cobasv2 tended to have higher accuracy than Mutyper (73% vs 69%, P=0.53), and PE-SUP samples had significantly higher accuracy than plasma samples (97% vs 55–71%) for both kits. Genotype concordance was 98% (κ=0.92, 0.88–0.96). SQIs showed strong positive correlations (P<0.0001). In less-dilute samples, accuracy and sensitivity did not differ significantly between kits. In more-dilute samples, cobasv2 tended to have higher sensitivity than Mutyper (43% vs 20%, P=0.07). CONCLUSIONS: The kits have similar performance in terms of EGFR mutation detection and semi-quantification in plasma and PE-SUP samples. cobasv2 tends to outperform Mutyper in detecting less-abundant EGFR-mutants. PE-SUP samples are assayable using either kit.
Epidermal Growth Factor ; Genotype ; Plasma ; Pleural Effusion ; Receptor, Epidermal Growth Factor