Background: The time-consuming process of drug development contributes to unmet healthcare needs for rheumatoid arthritis (RA). Studies of Western populations suggest the potential use of antidiabetic drugs as an alternative to lower RA risk. We aimed to examine the possibility of repurposing antidiabetic drugs for RA by evaluating their causal associations with genetic antidiabetic drug target genes using Mendelian randomization (MR) of samples from an East Asian biobank. Methods: We conducted drug-targeting two-sample MR to estimate the association between the antidiabetic drug and RA risk using summary statistics of genome-wide association studies (GWAS). Six single-nucleotide polymorphisms (SNPs) were selected as independent genetic variants that encode the target proteins of the selected antidiabetic drugs (insulin/insulin analogues, thiazolidinediones, and sulfonylureas). Instrumental associations with fasting blood glucose and RA were extracted from the KoGES (Korean Genome and Epidemiology Study) and BBJ (BioBank Japan), respectively. Results: A decrease in fasting blood sugar level of 1 mmol (1.8 mg/dL) by the rs1801282 SNP in the PPARG gene reduced the incidence of RA by about 20%. Moreover, another SNP within the PPARG gene, rs35240997, reduced the incidence of RA about 16%. Conclusion SNPs within the anti-diabetic drug target genes lowered fasting blood sugar levels and the risk of RA. However, the results from this study require cautious interpretations due to weak instrument bias.

Background: The time-consuming process of drug development contributes to unmet healthcare needs for rheumatoid arthritis (RA). Studies of Western populations suggest the potential use of antidiabetic drugs as an alternative to lower RA risk. We aimed to examine the possibility of repurposing antidiabetic drugs for RA by evaluating their causal associations with genetic antidiabetic drug target genes using Mendelian randomization (MR) of samples from an East Asian biobank. Methods: We conducted drug-targeting two-sample MR to estimate the association between the antidiabetic drug and RA risk using summary statistics of genome-wide association studies (GWAS). Six single-nucleotide polymorphisms (SNPs) were selected as independent genetic variants that encode the target proteins of the selected antidiabetic drugs (insulin/insulin analogues, thiazolidinediones, and sulfonylureas). Instrumental associations with fasting blood glucose and RA were extracted from the KoGES (Korean Genome and Epidemiology Study) and BBJ (BioBank Japan), respectively. Results: A decrease in fasting blood sugar level of 1 mmol (1.8 mg/dL) by the rs1801282 SNP in the PPARG gene reduced the incidence of RA by about 20%. Moreover, another SNP within the PPARG gene, rs35240997, reduced the incidence of RA about 16%. Conclusion SNPs within the anti-diabetic drug target genes lowered fasting blood sugar levels and the risk of RA. However, the results from this study require cautious interpretations due to weak instrument bias.

Background: The time-consuming process of drug development contributes to unmet healthcare needs for rheumatoid arthritis (RA). Studies of Western populations suggest the potential use of antidiabetic drugs as an alternative to lower RA risk. We aimed to examine the possibility of repurposing antidiabetic drugs for RA by evaluating their causal associations with genetic antidiabetic drug target genes using Mendelian randomization (MR) of samples from an East Asian biobank. Methods: We conducted drug-targeting two-sample MR to estimate the association between the antidiabetic drug and RA risk using summary statistics of genome-wide association studies (GWAS). Six single-nucleotide polymorphisms (SNPs) were selected as independent genetic variants that encode the target proteins of the selected antidiabetic drugs (insulin/insulin analogues, thiazolidinediones, and sulfonylureas). Instrumental associations with fasting blood glucose and RA were extracted from the KoGES (Korean Genome and Epidemiology Study) and BBJ (BioBank Japan), respectively. Results: A decrease in fasting blood sugar level of 1 mmol (1.8 mg/dL) by the rs1801282 SNP in the PPARG gene reduced the incidence of RA by about 20%. Moreover, another SNP within the PPARG gene, rs35240997, reduced the incidence of RA about 16%. Conclusion SNPs within the anti-diabetic drug target genes lowered fasting blood sugar levels and the risk of RA. However, the results from this study require cautious interpretations due to weak instrument bias.

Background: The time-consuming process of drug development contributes to unmet healthcare needs for rheumatoid arthritis (RA). Studies of Western populations suggest the potential use of antidiabetic drugs as an alternative to lower RA risk. We aimed to examine the possibility of repurposing antidiabetic drugs for RA by evaluating their causal associations with genetic antidiabetic drug target genes using Mendelian randomization (MR) of samples from an East Asian biobank. Methods: We conducted drug-targeting two-sample MR to estimate the association between the antidiabetic drug and RA risk using summary statistics of genome-wide association studies (GWAS). Six single-nucleotide polymorphisms (SNPs) were selected as independent genetic variants that encode the target proteins of the selected antidiabetic drugs (insulin/insulin analogues, thiazolidinediones, and sulfonylureas). Instrumental associations with fasting blood glucose and RA were extracted from the KoGES (Korean Genome and Epidemiology Study) and BBJ (BioBank Japan), respectively. Results: A decrease in fasting blood sugar level of 1 mmol (1.8 mg/dL) by the rs1801282 SNP in the PPARG gene reduced the incidence of RA by about 20%. Moreover, another SNP within the PPARG gene, rs35240997, reduced the incidence of RA about 16%. Conclusion SNPs within the anti-diabetic drug target genes lowered fasting blood sugar levels and the risk of RA. However, the results from this study require cautious interpretations due to weak instrument bias.

Background: The time-consuming process of drug development contributes to unmet healthcare needs for rheumatoid arthritis (RA). Studies of Western populations suggest the potential use of antidiabetic drugs as an alternative to lower RA risk. We aimed to examine the possibility of repurposing antidiabetic drugs for RA by evaluating their causal associations with genetic antidiabetic drug target genes using Mendelian randomization (MR) of samples from an East Asian biobank. Methods: We conducted drug-targeting two-sample MR to estimate the association between the antidiabetic drug and RA risk using summary statistics of genome-wide association studies (GWAS). Six single-nucleotide polymorphisms (SNPs) were selected as independent genetic variants that encode the target proteins of the selected antidiabetic drugs (insulin/insulin analogues, thiazolidinediones, and sulfonylureas). Instrumental associations with fasting blood glucose and RA were extracted from the KoGES (Korean Genome and Epidemiology Study) and BBJ (BioBank Japan), respectively. Results: A decrease in fasting blood sugar level of 1 mmol (1.8 mg/dL) by the rs1801282 SNP in the PPARG gene reduced the incidence of RA by about 20%. Moreover, another SNP within the PPARG gene, rs35240997, reduced the incidence of RA about 16%. Conclusion SNPs within the anti-diabetic drug target genes lowered fasting blood sugar levels and the risk of RA. However, the results from this study require cautious interpretations due to weak instrument bias.

Background: The benefits of transradial access (TRA) over transfemoral access (TFA) for bifurcation percutaneous coronary intervention (PCI) are uncertain because of the limited availability of device selection. This study aimed to compare the procedural differences and the in-hospital and long-term outcomes of TRA and TFA for bifurcation PCI using secondgeneration drug-eluting stents (DESs). Methods: Based on data from the Coronary Bifurcation Stenting Registry III, a retrospective registry of 2,648 patients undergoing bifurcation PCI with second-generation DES from 21 centers in South Korea, patients were categorized into the TRA group (n = 1,507) or the TFA group (n = 1,141). After propensity score matching (PSM), procedural differences, in-hospital outcomes, and device-oriented composite outcomes (DOCOs; a composite of cardiac death, target vessel-related myocardial infarction, and target lesion revascularization) were compared between the two groups (772 matched patients each group). Results: Despite well-balanced baseline clinical and lesion characteristics after PSM, the use of the two-stent strategy (14.2% vs. 23.7%, P = 0.001) and the incidence of in-hospital adverse outcomes, primarily driven by access site complications (2.2% vs. 4.4%, P = 0.015), were significantly lower in the TRA group than in the TFA group. At the 5-year follow-up, the incidence of DOCOs was similar between the groups (6.3% vs. 7.1%, P = 0.639). Conclusion The findings suggested that TRA may be safer than TFA for bifurcation PCI using second-generation DESs. Despite differences in treatment strategy, TRA was associated with similar long-term clinical outcomes as those of TFA. Therefore, TRA might be the preferred access for bifurcation PCI using second-generation DES.

Background: Tea tree oil has antiviral, antimicrobial and antifungal effects and Mastic oil has antifungal and anticancer effects. For synergistic effects of oils, blending oil containing a mixture of two to three oils is recommended. This study aimed to determine the antibacterial effects of Tea tree oil, Mastic oil, and Blending oil containing the two oils in a mixture, to verify and suggest the potential use of these oils as a substance to prevent dental caries. Methods: Tea tree oil, Mastic oil, and Blending oil with a 1:1 blend of the two oils were diluted in liquid medium to 0% (negative control), 0.5%, 1.0%, and 2.0%. Streptococcus mutans was applied to each experimental group of the three diluted oils and after 8 h culture, the optical density (OD) was measured and the growth inhibition rate for S. mutans was estimated. Results: Tea tree oil had significantly low OD values across all concentrations (p<0.05) without significant variation among different concentrations (p>0.05). Mastic oil did not significantly vary in OD compared to the negative control across all concentrations (p>0.05) without significant variation among different concentrations (p>0.05). Blending oil, compared to the negative control, did not significantly vary in OD at 0.5% (p>0.05) but significant variation was found as the concentration increased (p<0.05). Additionally, for Tea tree oil and Mastic oil, the growth inhibition rate showed no significant variation according to concentration (p>0.05), whereas for Blending oil, the growth inhibition rate for S. mutans showed a significant difference at 1.0% (p<0.05) and at higher concentrations. Conclusion Blending oil containing a Tea tree oil and Mastic oil demonstrated a significant growth inhibition effect on S. mutans from the concentration of 1.0%, which suggested its potential use as an effective antibacterial agent for dental caries.

Plasmodium vivax exhibits dormant liver-stage parasites, called hypnozoites, which can cause relapse of malaria. The only drug currently used for eliminating hypnozoites is primaquine. The antimalarial properties of primaquine are dependent on the production of oxidized metabolites by the cytochrome P450 isoenzyme 2D6 (CYP2D6). Reduced primaquine metabolism may be related to P. vivax relapses. We describe a case of 4 episodes of recurrence of vivax malaria in a patient with decreased CYP2D6 function. The patient was 52-year-old male with body weight of 52 kg. He received total gastrectomy and splenectomy 7 months before the first episode and was under chemotherapy for the gastric cancer. The first episode occurred in March 2019 and each episode had intervals of 34, 41, and 97 days, respectively. At the first and second episodes, primaquine was administered as 15 mg for 14 days. The primaquine dose was increased with 30 mg for 14 days at the third and fourth episodes. Seven gene sequences of P. vivax were analyzed and revealed totally identical for all the 4 samples. The CYP2D6 genotype was analyzed and intermediate metabolizer phenotype with decreased function was identified.

Background: We assessed the myocardial infarction (MI), stroke, and all-cause death risks during follow-up according to the low-density lipoprotein cholesterol (LDL-C) levels among older adults. Methods: The Korean National Health Insurance Service datasets (2002 to 2020) were used for this population-based cohort study. The hazards of MI, stroke, and all-cause mortality during follow-up were analyzed according to LDL-C level in individuals aged ≥65 years without baseline cardiovascular diseases (n=1,391,616). Results: During a mean 7.55 years, 52,753 MIs developed; 84,224 strokes occurred over a mean 7.47 years. After a mean 8.50 years, 233,963 died. A decrease in LDL-C was associated with lower hazards of MI and stroke. The decreased hazard of stroke in lower LDL-C was more pronounced in statin users, and individuals with diabetes or obesity. The hazard of all-cause death during follow-up showed an inverted J-shaped pattern according to the LDL-C levels. However, the paradoxically increased hazard of mortality during follow-up in lower LDL-C was attenuated in statin users and individuals with diabetes, hypertension, or obesity. In statin users, lower LDL-C was associated with a decreased hazard of mortality during follow-up. Conclusion Among the elderly, lower LDL-C was associated with decreased risks of MI and stroke. Lower LDL-C achieved by statins in the elderly was associated with a decreased risk of all-cause death during follow-up, suggesting that LDL-C paradox for the premature death risk in the elderly should not be applied to statin users. Intensive statin therapy should not be hesitated for older adults with cardiovascular risk factors including diabetes.

Background: Low 25-hydroxyvitamin D (25OHD) levels are associated with the incidence of type 2 diabetes mellitus (T2DM). However, the association between 25OHD and metabolic health status or diabetic complications is inconclusive. We evaluated this relationship between vitamin D status and metabolic parameters and complications of T2DM. Methods: This study included 1,392 patients with T2DM who visited Eulji and Ewha Diabetes Center between January 2011 and August 2016. Anthropometric parameters and laboratory tests including glycated hemoglobin (HbA1c), lipid profile, liver and kidney function, and urinary albumin-to-creatinine ratio (UACR) were evaluated. Diabetic macro- and microvascular complications were determined through a medical record review. Serum 25OHD concentrations were measured by chemiluminescent immunoassay. Results: The mean 25OHD level was 16.8±9.6 ng/mL. Vitamin D deficiency (<20 ng/mL) and severe deficiency (<10 ng/mL) were observed in 990 (71.1%) and 351 (25.2%) participants, respectively. 25OHD level was positively correlated with age and highdensity lipoprotein cholesterol (HDL-C) level and negatively correlated with HbA1c, triglyceride level, and UACR. HDL-C and UACR were significantly associated with 25OHD after adjusting for other variables. Vitamin D deficiency was independently related to nephropathy after adjusting for confounding variables. Conclusion Vitamin D deficiency was common among Korean T2DM patients; it was independently associated with microalbuminuria and HDL level, and positively related to diabetic nephropathy.