Association between High Blood Pressure and Intakes of Sodium and Potassium among Korean Adults: Korean National Health and Nutrition Examination Survey, 2007-2012

ABSTRACT Background The association between dietary sodium and potassium, the ratio of sodium to potassium, and blood pressure remains unclear. Objective We evaluated the associations between blood pressure and dietary sodium and potassium intake in terms of the amount and ratio in Korean adults. Design This cross-sectional study was based on data from the fourth and fifth Korean National Health and Nutrition Examination Survey, 2007Survey, -2012 Participants/setting A total of 24,096 adults (aged !19 years) without history of antihypertensive medication use were selected. The 24-hour recall method was used for dietary assessment. We categorized the subjects into four groups using median intakes of sodium and potassium, and defined the low sodium/high potassium intake group as the reference group. Main outcome measures High blood pressure (HBP) was defined as mean systolic or diastolic blood pressures of !140 or !90 mm Hg, respectively. Statistical analyses performed Multivariate logistic regression was performed to estimate the odds ratio and 95% CI to investigate the association between the four groups of sodium and potassium intakes and HBP. Results Sodium intake was positively associated with diastolic blood pressure, with an increase of 0.21 mm Hg per 1 mg/kcal increase in sodium (P<0.001). In contrast, potassium intake was negatively associated with systolic blood pressure, with a decrease of 1.01 mm Hg per 1 mg/kcal increase in potassium (P<0.001). After adjusting for confounders, the high sodium/low potassium (odds ratio 1.21, 95% CI 1.02 to 1.44) and low sodium/low potassium intake groups (odds ratio 1.19, 95% CI 1.01 to 1.40) were at higher risk of HBP than the reference group. The risk of HBP in the high sodium/high potassium group did not differ from that in the reference group. Conclusions Low potassium intake was associated with an increased risk of hypertension. These results suggest that increasing potassium intake might be beneficial for hypertension control among populations with low-potassium diets

Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males

The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA₂) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA₂ in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.PLA2G7 V279F genotypes were initially compared in 2890 male cases diagnosed with CAD before age 60 with 3128 male controls without CAD at age 50 and above and subsequently in a second independent male dataset of 877 CAD cases and 1230 controls. In the first dataset, the prevalence of the 279F null allele was 11.5% in cases and 12.8% in controls. After adjustment for age, body mass index, diabetes, smoking, glucose and lipid levels, the OR (95% CI) for CAD for this allele was 0.80 (0.66-0.97, p = 0.02). The results were very similar in the second dataset, despite lower power, with an allele frequency of 11.2% in cases and 12.5% in controls, leading to a combined OR of 0.80 (0.69-0.92), p = 0.002. The magnitude and direction of this genetic effect were fully consistent with large epidemiological studies on plasma Lp-PLA₂ activity and CAD risk.Natural deficiency in Lp-PLA₂ activity due to carriage of PLA2G7 279F allele protects from CAD in Korean men. These results provide evidence for a causal relationship between Lp-PLA₂ and CAD, and support pharmacological inhibition of this enzyme as an innovative way to prevent CAD

Carriage of the V279F Null Allele within the Gene Encoding Lp-PLA2 Is Protective from Coronary Artery Disease in South Korean Males

The Asia-specific PLA2G7 994G-T transversion leads to V279F substitution within the lipoprotein-associated phospholipase-A2 (Lp-PLA₂) and to absence of enzyme activity in plasma. This variant offers a unique natural experiment to assess the role of Lp-PLA₂ in the pathogenesis of coronary artery disease (CAD) in humans. Given conflicting results from mostly small studies, a large two-stage case-control study was warranted.PLA2G7 V279F genotypes were initially compared in 2890 male cases diagnosed with CAD before age 60 with 3128 male controls without CAD at age 50 and above and subsequently in a second independent male dataset of 877 CAD cases and 1230 controls. In the first dataset, the prevalence of the 279F null allele was 11.5% in cases and 12.8% in controls. After adjustment for age, body mass index, diabetes, smoking, glucose and lipid levels, the OR (95% CI) for CAD for this allele was 0.80 (0.66-0.97, p = 0.02). The results were very similar in the second dataset, despite lower power, with an allele frequency of 11.2% in cases and 12.5% in controls, leading to a combined OR of 0.80 (0.69-0.92), p = 0.002. The magnitude and direction of this genetic effect were fully consistent with large epidemiological studies on plasma Lp-PLA₂ activity and CAD risk.Natural deficiency in Lp-PLA₂ activity due to carriage of PLA2G7 279F allele protects from CAD in Korean men. These results provide evidence for a causal relationship between Lp-PLA₂ and CAD, and support pharmacological inhibition of this enzyme as an innovative way to prevent CAD

The disruption of proteostasis in neurodegenerative diseases

Cells count on surveillance systems to monitor and protect the cellular proteome which, besides being highly heterogeneous, is constantly being challenged by intrinsic and environmental factors. In this context, the proteostasis network (PN) is essential to achieve a stable and functional proteome. Disruption of the PN is associated with aging and can lead to and/or potentiate the occurrence of many neurodegenerative diseases (ND). This not only emphasizes the importance of the PN in health span and aging but also how its modulation can be a potential target for intervention and treatment of human diseases.info:eu-repo/semantics/publishedVersio

Machine Learning for Intelligent-Reflecting-Surface-Based Wireless Communication towards 6G: A Review

An intelligent reflecting surface (IRS) is a programmable device that can be used to control electromagnetic waves propagation by changing the electric and magnetic properties of its surface. Therefore, IRS is considered a smart technology for the sixth generation (6G) of communication networks. In addition, machine learning (ML) techniques are now widely adopted in wireless communication as the computation power of devices has increased. As it is an emerging topic, we provide a comprehensive overview of the state-of-the-art on ML, especially on deep learning (DL)-based IRS-enhanced communication. We focus on their operating principles, channel estimation (CE), and the applications of machine learning to IRS-enhanced wireless networks. In addition, we systematically survey existing designs for IRS-enhanced wireless networks. Furthermore, we identify major issues and research opportunities associated with the integration of IRS and other emerging technologies for applications to next-generation wireless communication

HLA-DRB1 is associated with cefaclor-induced immediate hypersensitivity

Background: Drug-induced hypersensitivity such as anaphylaxis is an important cause of drug-related morbidity and mortality. Cefaclor is a leading cause of drug induced type I hypersensitivity in Korea, but little is yet known about genetic biomarkers to predict this hypersensitivity reaction. We aimed to evaluate the possible involvement of genes in cefaclor induced type I hypersensitivity. Methods: Whole exome sequencing (WES) and HLA genotyping were performed in 43 patients with cefaclor induced type I hypersensitivity. In addition, homology modeling was performed to identify the binding forms of cefaclor to HLA site. Results: Anaphylaxis was the most common phenotype of cefaclor hypersensitivity (90.69%). WES results show that rs62242177 and rs62242178 located in LIMD1 region were genome-wide significant at the 5 × 10−8 significance level. Cefaclor induced type I hypersensitivity was significantly associated with HLA-DRB1∗04:03 (OR 4.61 [95% CI 1.51–14.09], P < 0.002) and HLA-DRB1∗14:54 (OR 3.86 [95% CI 1.09–13.67], P < 0.002). Conclusion: LIMD1, HLA-DRB1∗04:03 and HLA-DRB1∗14:54 may affect susceptibility to cefaclor induced type I hypersensitivity. Further confirmative studies with a larger patient population should be performed to ascertain the role of HLA-DRB1 and LIMD1 in the development of cefaclor induced hypersensitivity