Han Byul Jang

Particulate matter (PM), a key component of air pollution, is globally associated with adverse health effects, including premature mortality. Although the majority of the human lifespan is spent indoors, knowledge on the effects of indoor exposure to aerosol particles remains limited. Therefore, we aimed to investigate the effects of exposure to PM _2.5 (≤ 2.5 μ m) generated during indoor cooking on Alzheimer’s disease (AD). To investigate the signaling pathways activated by pork combustion PM _2.5 (PC‐PM _2.5 ), 2‐month‐old 5× FAD mice were exposed to whole‐body inhalation five times a week for 1 month. PC‐PM _2.5 ‐exposed mice were evaluated using the airway hyperresponsiveness test, novel object location recognition (NLR) task, and Y‐maze task, and glial cell localization was observed in the hippocampal brain regions. Additionally, cognition‐related markers (BDNF and CREB), amyloid beta (A β ) accumulation, pro‐inflammatory response, post‐synapse 95 (PSD95), and Wnt/GSK3 β signaling pathway expression were measured in hippocampal lysates to evaluate pathological changes. PC‐PM _2.5 treatment considerably increased A β accumulation and airway hyperresponsiveness and decreased cognitive function in 5× FAD mice. PC‐PM _2.5 treatment accelerated A β accumulation and pro‐inflammatory cytokine expression, as well as GFAP ⁺ localization, and reduced cognition‐related markers and synaptic plasticity in the hippocampus. Additionally, in the PC‐PM _2.5 ‐treated group, Wnt expression was lower than that in 5× FAD mice, GSK3 β phosphorylation increased, and nuclear translocation of β ‐catenin decreased. Therefore, this study confirmed that exposure to PC‐PM _2.5 , which is common in daily life, accelerates cognitive decline as a risk factor for AD and suggests that regulating the Wnt/GSK3 β / β ‐catenin pathway may be a potential prevention strategy. In summary, this study elucidates the changes and molecular signaling pathways activated by PM exposure and provides insights into the mechanistic links between air pollution and neurodegenerative diseases such as AD.

Background: Glutamate is a major neurotransmitter, although it causes cytotoxicity and inflammation in nonneuronal organs. This study aimed to investigate the metabolic disorders in which glutamate, associated with type 2 diabetes onset, is induced in the liver.Methods: An analysis of Korean community‐based Ansan‐Ansung cohort study data as well as functional research using in vitro and mouse models were performed.Results: Groups with high plasma glutamate levels (T2, T3) had a significantly increased risk of diabetes incidence after 8 years, compared to the group with relatively low glutamate levels (T1). Analysis of the effect of glutamate on diabetes onset in vitro showed that glutamate induces insulin resistance by increasing glucose‐related protein 78 (GRP78) and phosphoenolpyruvate carboxykinase (PEPCK) expression in SK‐Hep‐1 human liver cells. In addition, three different genes, FRMB4B, PLG, and PARD3, were significantly associated with glutamate and were identified via genome‐wide association studies. Among glutamate‐related genes, plasminogen (PLG) levels were most significantly increased in several environments in which insulin resistance was induced, and was also upregulated by glutamate. Glutamate‐induced increase in PLG in liver cells was caused by metabotropic glutamate receptor 5 activation, and PLG levels were also upregulated after extracellular secretion. Moreover, glutamate increased the expression of plasminogen activator inhibitor‐1 (PAI‐1). Thus, extracellular secreted PLG cannot be converted to plasmin (fibrinolytic enzyme) by increased PAI‐1.Conclusions: Increased glutamate is closely associated with the development of diabetes, and it may cause metabolic disorders by inhibiting the fibrinolytic system, which plays an important role in determining blood clots, a hallmark of diabetes.

The prevalence of obesity among children and adolescents with autism spectrum disorder (ASD) is higher than that among typically developing children and adolescents. However, very few studies have explored the genetic factors associated with obesity in children and adolescents with ASD. Thus, the aim of this study was to examine the associations between 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) gene polymorphisms and obesity among children and adolescents with ASD. The study participants consisted of 33 children and adolescents with ASD and 271 age- and sex-matched typically developing controls. We compared the metabolic traits (body mass index, blood pressure, triglyceride, high-density lipoprotein, and fasting glucose levels) between the ASD and control group. Furthermore, we assessed the genotypes of rs12654264 in the HMGCR gene within the participants with ASD, and compared metabolic traits among the different allele subgroups. The mean body mass index (BMI) and triglyceride level of the ASD group were significantly higher than those of the control group. Within the ASD group, the triglyceride level of participants with rs12654264-T alleles was significantly higher than that of participants with A-alleles. A pattern of increasing values in the BMI and fasting glucose was also observed in participants with T allele. This is the first study to show that obesity in children and adolescents with ASD is associated with the cholesterol synthesis pathway. Future studies are needed to further clarify the molecular mechanisms by which the HMGCR gene influences metabolic traits.

We conducted a retrospective study of Middle East respiratory syndrome coronavirus (MERS-CoV) viral load kinetics using data from patients hospitalized with MERS-CoV infection between 19 May and 20 August 2015. Viral load trajectories were considered over the hospitalization period using 1714 viral load results measured in serial respiratory specimens of 185 patients. The viral load levels were significantly higher among nonsurvivors than among survivors (P = .003). Healthcare workers (P = .001) and nonspreaders (P < .001) had significantly lower viral loads. Viral RNA was present on the day of symptom onset and peaked 4–10 days after symptom onset.

Kim J, et al. Nutr Res Pract. 2020 Jun;14(3):262-275. https://doi.org/10.4162/nrp.2020.14.3.262

Background: Behavioral modification on healthy eating and lifestyle is required to improve metabolically healthy status in severe obese child and adolescents. We aimed to develop tailored nutritional education programs to find barriers on dietary and lifestyle for severe obese adolescents and their caregivers. Methods: Focused on theoretical framework approaches are effective to change behavior and achieve goals. To develop four monthly contents, social cognitive theory and transtheoretical model were applied to this program. All sessions were designed to give nutritional knowledge and practical mission in a real life for individual goal setting and self‐control. In the 1st and 2nd sessions, my meal planning and portion control were emphasized based on five food groups for diet and health outcome expectations. The 3rd and 4th sessions were build up skills to choose healthy snacks and cook with fruit and vegetables. 103 participants aged 8 to 16 years will be participated in a 16 week intervention program. During the each sessions, the participants and their family will be interviewed by nutritional expert for further tailored nutritional education and counselling. Results: Each 20‐min individual face to face nutritional education and counselling will be offered every month for the participants and their parents; monthly phone contact and txt message for social support and online food recipe to emphasize having breakfast and vegetable and fruit consumption. Following as the monthly contents, individual dietary goal setting will be attained by every participants with their family. Promoting healthy eating practices resources; an educational book, practice posters, food diaries and a water bottle will be provided to all intervention participants to motivate healthy lifestyle behaviors. Discussion: This nutritional intervention program might be assist to implement further researches in severe obese adolescents' population. Support or Funding Information Preparation of this article was supported by Grant 2015‐ER6401‐00 from the Division of Metabolic disease, Center for Biomedical science, Korea National Institute of Health.