Background and Objectives: Outcomes of deferring percutaneous coronary intervention (PCI) without invasive physiologic assessment for intermediate coronary lesions is uncertain.We sought to compare long-term outcomes between medical treatment and PCI of intermediate lesions without invasive physiologic assessment. Methods: A total of 899 patients with intermediate coronary lesions between 50% and 70% diameter-stenosis were randomized to the conservative group (n=449) or the aggressive group (n=450). For intermediate lesions, PCI was performed in the aggressive group, but was deferred in the conservative group. The primary endpoint was major adverse cardiac events (MACE, a composite of all-cause death, myocardial infarction [MI], or ischemia-driven any revascularization) at 3 years. Results: The number of treated lesions per patient was 0.8±0.9 in the conservative group and 1.7±0.9 in the aggressive group (p=0.001). At 3 years, the conservative group had a significantly higher incidence of MACE than the aggressive group (13.8% vs. 9.3%; hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.00–2.21; p=0.049), mainly driven by revascularization of target intermediate lesion (6.5% vs. 1.1%; HR, 5.69; 95% CI, 2.20–14.73;p<0.001). Between 1 and 3 years after the index procedure, compared to the aggressive group, the conservative group had significantly higher incidence of cardiac death or MI (3.2% vs.0.7%; HR, 4.34; 95% CI, 1.24–15.22; p=0.022) and ischemia-driven any revascularization. Conclusions For intermediate lesions, medical therapy alone, guided only by angiography, was associated with a higher risk of MACE at 3 years compared with performing PCI, mainly due to increased revascularization.

Background and Objectives: Outcomes of deferring percutaneous coronary intervention (PCI) without invasive physiologic assessment for intermediate coronary lesions is uncertain.We sought to compare long-term outcomes between medical treatment and PCI of intermediate lesions without invasive physiologic assessment. Methods: A total of 899 patients with intermediate coronary lesions between 50% and 70% diameter-stenosis were randomized to the conservative group (n=449) or the aggressive group (n=450). For intermediate lesions, PCI was performed in the aggressive group, but was deferred in the conservative group. The primary endpoint was major adverse cardiac events (MACE, a composite of all-cause death, myocardial infarction [MI], or ischemia-driven any revascularization) at 3 years. Results: The number of treated lesions per patient was 0.8±0.9 in the conservative group and 1.7±0.9 in the aggressive group (p=0.001). At 3 years, the conservative group had a significantly higher incidence of MACE than the aggressive group (13.8% vs. 9.3%; hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.00–2.21; p=0.049), mainly driven by revascularization of target intermediate lesion (6.5% vs. 1.1%; HR, 5.69; 95% CI, 2.20–14.73;p<0.001). Between 1 and 3 years after the index procedure, compared to the aggressive group, the conservative group had significantly higher incidence of cardiac death or MI (3.2% vs.0.7%; HR, 4.34; 95% CI, 1.24–15.22; p=0.022) and ischemia-driven any revascularization. Conclusions For intermediate lesions, medical therapy alone, guided only by angiography, was associated with a higher risk of MACE at 3 years compared with performing PCI, mainly due to increased revascularization.

Background and Objectives: Outcomes of deferring percutaneous coronary intervention (PCI) without invasive physiologic assessment for intermediate coronary lesions is uncertain.We sought to compare long-term outcomes between medical treatment and PCI of intermediate lesions without invasive physiologic assessment. Methods: A total of 899 patients with intermediate coronary lesions between 50% and 70% diameter-stenosis were randomized to the conservative group (n=449) or the aggressive group (n=450). For intermediate lesions, PCI was performed in the aggressive group, but was deferred in the conservative group. The primary endpoint was major adverse cardiac events (MACE, a composite of all-cause death, myocardial infarction [MI], or ischemia-driven any revascularization) at 3 years. Results: The number of treated lesions per patient was 0.8±0.9 in the conservative group and 1.7±0.9 in the aggressive group (p=0.001). At 3 years, the conservative group had a significantly higher incidence of MACE than the aggressive group (13.8% vs. 9.3%; hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.00–2.21; p=0.049), mainly driven by revascularization of target intermediate lesion (6.5% vs. 1.1%; HR, 5.69; 95% CI, 2.20–14.73;p<0.001). Between 1 and 3 years after the index procedure, compared to the aggressive group, the conservative group had significantly higher incidence of cardiac death or MI (3.2% vs.0.7%; HR, 4.34; 95% CI, 1.24–15.22; p=0.022) and ischemia-driven any revascularization. Conclusions For intermediate lesions, medical therapy alone, guided only by angiography, was associated with a higher risk of MACE at 3 years compared with performing PCI, mainly due to increased revascularization.

Background and Objectives: Outcomes of deferring percutaneous coronary intervention (PCI) without invasive physiologic assessment for intermediate coronary lesions is uncertain.We sought to compare long-term outcomes between medical treatment and PCI of intermediate lesions without invasive physiologic assessment. Methods: A total of 899 patients with intermediate coronary lesions between 50% and 70% diameter-stenosis were randomized to the conservative group (n=449) or the aggressive group (n=450). For intermediate lesions, PCI was performed in the aggressive group, but was deferred in the conservative group. The primary endpoint was major adverse cardiac events (MACE, a composite of all-cause death, myocardial infarction [MI], or ischemia-driven any revascularization) at 3 years. Results: The number of treated lesions per patient was 0.8±0.9 in the conservative group and 1.7±0.9 in the aggressive group (p=0.001). At 3 years, the conservative group had a significantly higher incidence of MACE than the aggressive group (13.8% vs. 9.3%; hazard ratio [HR], 1.49; 95% confidence interval [CI], 1.00–2.21; p=0.049), mainly driven by revascularization of target intermediate lesion (6.5% vs. 1.1%; HR, 5.69; 95% CI, 2.20–14.73;p<0.001). Between 1 and 3 years after the index procedure, compared to the aggressive group, the conservative group had significantly higher incidence of cardiac death or MI (3.2% vs.0.7%; HR, 4.34; 95% CI, 1.24–15.22; p=0.022) and ischemia-driven any revascularization. Conclusions For intermediate lesions, medical therapy alone, guided only by angiography, was associated with a higher risk of MACE at 3 years compared with performing PCI, mainly due to increased revascularization.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

PURPOSE: This pilot study investigated the effect of surface roughness on osseointegration by comparing two types of commercial SLA-treated dental implants with different surface roughness levels: moderately rough (Sa = 1 – 2 µm) and rough surfaces (Sa > 2 µm). MATERIALS AND METHODS: Two implant groups were studied: TS (rough surface) and ADD (moderately rough surface) groups. Surface characteristics were analyzed using optical profilometry and SEM. In vitro studies using BRITER cells assessed cell adhesion, proliferation, and osteogenic differentiation through CCK-8 assay and qRT-PCR for osteopontin (OPN), osteocalcin (OCN), and alkaline phosphatase (ALP) expression. The in vivo study involved 12 implants (six per group) placed in mandibular defects of two beagle dogs. After 8 weeks, histomorphometric analysis evaluated bone to implant contact (BIC) and inter-thread bone density (ITBD). Statistical analysis used Student’s t-test and two-way ANOVA for in vitro data, and Mann-Whitney U test for in vivo data. RESULTS: Surface analysis revealed Sa values of 2.50 ± 0.27 µm for the TS group and 1.80 ± 0.06 µm for the ADD group. In vitro studies showed no significant differences in cell adhesion and proliferation between the groups (P > .05). However, gene expression patterns differed, with ADD group showing higher OPN expression (P < .001) and TS group showing higher ALP expression (P < .01). The in vivo study revealed no statistically significant differences in BIC and ITBD between the two groups (P > .05). CONCLUSION Surface roughness influenced osteoblast differentiation in vitro, but did not significantly affect osseointegration outcomes in vivo. Both moderately rough and rough surfaces appeared to support comparable levels of osseointegration. Larger studies are needed to confirm these findings and determine optimal implant surface characteristics.

Purpose: Recently, we developed allele-discriminating priming system (ADPS) technology. This method increases the sensitivity of conventional quantitative polymerase chain reaction up to 100 folds, with limit of detection, 0.01%, with reinforced specificity. This prospective study aimed to develop and validate the accuracy of ADPS epidermal growth factor receptor (EGFR) Mutation Test Kit using clinical specimens. Materials and Methods: In total 189 formalin-fixed paraffin-embedded tumor tissues resected from patients with non–small cell lung cancer were used to perform a comparative evaluation of the ADPS EGFR Mutation Test Kit versus the cobas EGFR Mutation Test v2, which is the current gold standard. When the two methods had inconsistent results, next-generation sequencing–based CancerSCAN was utilized as a referee. Results: The overall agreement of the two methods was 97.4% (93.9%-99.1%); the positive percent agreement, 95.0% (88.7%-98.4%); and the negative percent agreement, 100.0% (95.9%-100.0%). EGFR mutations were detected at a frequency of 50.3% using the ADPS EGFR Mutation Test Kit and 52.9% using the cobas EGFR Mutation Test v2. There were 10 discrepant mutation calls between the two methods. CancerSCAN reproduced eight ADPS results. In two cases, mutant allele fraction was ultra-low at 0.02% and 0.06%, which are significantly below the limit of detection of the cobas assay and CancerSCAN. Based on the EGFR genotyping by ADPS, the treatment options could be switched in five patients. Conclusion The highly sensitive and specific ADPS EGFR Mutation Test Kit would be useful in detecting the patients who have lung cancer with EGFR mutation, and can benefit from the EGFR targeted therapy.