👤 Yae Jung Hyun

This study aimed to identify different symptom profiles of complicated grief/bereavement-related posttraumatic stress disorder (PTSD) and examine the associations with social life factors, posttraumatic growth, and quality of life in a sample of parents whose children died in Sewol ferry accident. A total of 272 bereaved parents affected by the Sewol ferry accident participated and completed self-report scales about traumatic loss-related symptoms. The latent profile analysis (LPA) of complicated grief and posttraumatic symptoms was classified. To examine the predictors (interpersonal stress/familial conflict/social support) and outcomes (posttraumatic growth/quality of life) of the traumatic loss symptom profiles, an automatic three-step approach was chosen. The LPA identified three symptom profiles of complicated grief and posttraumatic stress: low symptomatology group (30.4%), moderate symptomatology group (49.6%), and high symptomatology group (20.0%). Higher perceived interpersonal stress significantly increased the odds of moderate and high symptomatology, while higher family stress was a significant predictor for high symptomatology compared to both low and moderate symptomatology groups. In addition, higher perceived social support significantly decreased the odds of being in both moderate and high symptomatology groups compared to the low group. The low symptomatology group showed the highest quality of life, followed by the moderate and high groups. Posttraumatic growth was also significantly different between the classes, with the moderate symptomatology group reporting higher growth than the low symptomatology group. Our findings suggest that managing the mental health of people who have experienced a traumatic loss will be a critical component of their quality of life in the future. In addition, interventions to help reduce family conflict and interpersonal stress may be necessary to reduce difficulties associated with psychopathology. Show less

MYD88 is a signal-transducing adaptor protein that plays a central role in Toll-like receptor and interleukin 1 receptor signalling through activation of the NF-κB pathway. The somatic L265P mutation in Show less

Muscle atrophy, including glucocorticoid-induced muscle wasting from treatments such as dexamethasone (DEX), results in significant reductions in muscle mass, strength and function. This study investigates the potential of lonafarnib, a farnesyltransferase inhibitor, to counteract DEX-induced muscle atrophy by targeting key signalling pathways. We utilized in vitro models with C2C12 myotubes treated with DEX and in vivo models with Caenorhabditis elegans and DEX-treated Sprague-Dawley rats. Myotube morphology was assessed by measuring area, fusion index and diameter. Muscle function was evaluated by grip strength and compound muscle action potential (CMAP) in the gastrocnemius (GC) and tibialis anterior (TA) muscles. Molecular mechanisms were explored through RNA sequencing and Western blotting to assess changes in mitochondrial function and muscle signalling pathways. Lonafarnib (2 μM) significantly improved myotube area (1.49 ± 0.14 × 10 Lonafarnib mitigates dexamethasone-induced muscle atrophy by enhancing mitochondrial function and activating anabolic pathways. These findings support further investigation of lonafarnib as a therapeutic agent for muscle atrophy in clinical settings. Show less

SORT1 (sortilin 1), a member of the the Vps10 (vacuolar protein sorting 10) family, is involved in hepatic lipid metabolism by regulating very low-density lipoprotein (VLDL) secretion and facilitating the lysosomal degradation of CES1 (carboxylesterase 1), crucial for triglyceride (TG) breakdown in the liver. This study explores whether SORT1 is targeted for degradation by chaperone-mediated autophagy (CMA), a selective protein degradation pathway that directs proteins containing KFERQ-like motifs to lysosomes via LAMP2A (lysosomal-associated membrane protein 2A). Silencing LAMP2A or HSPA8/Hsc70 with siRNA increased cytosolic SORT1 protein levels. Leupeptin treatment induced lysosomal accumulation of SORT1, unaffected by si Show less

Thin-cap fibroatheroma is a rupture-prone vulnerable plaque that leads to acute coronary syndrome (ACS). However, its underlying mechanisms are not fully understood. Several studies have investigated the clinical association between angiopoietin-like protein 4 (ANGPTL4) and coronary artery disease. Therefore, this study aimed to investigate the correlation of plasma ANGPTL4 in culprit lesion of ACS patients using intravascular ultrasound (IVUS) and virtual-histology IVUS (VH-IVUS). Fifty patients newly diagnosed with ACS between March to September 2021 were selected. Blood samples for baseline laboratory tests, including ANGPTL4, were collected before percutaneous coronary intervention (PCI), and all pre- and post-PCI IVUS examinations were performed of the culprit lesions. Linear regression analysis between plasma ANGPTL4 and grayscale IVUS/VH-IVUS parameters revealed that plasma ANGPTL4 was strongly correlated with the necrotic core (NC) of the minimal lumen site (r = -0.666, p = 0.003) and largest NC site (r = -0.687, p < 0.001), and patients with lower plasma ANGPTL4 levels showed a significantly higher proportion of TFCA. The present study further demonstrated the protective role of ANGPTL4 in the spectrum of atherosclerotic development in patients with ACS by culprit lesion morphology analysis using IVUS and VH-IVUS. Show less

Ferroptosis is an iron-dependent regulated necrosis mediated by lipid peroxidation. Cancer cells survive under metabolic stress conditions by altering lipid metabolism, which may alter their sensitivity to ferroptosis. However, the association between lipid metabolism and ferroptosis is not completely understood. In this study, we found that the expression of elongation of very long-chain fatty acid protein 5 (ELOVL5) and fatty acid desaturase 1 (FADS1) is up-regulated in mesenchymal-type gastric cancer cells (GCs), leading to ferroptosis sensitization. In contrast, these enzymes are silenced by DNA methylation in intestinal-type GCs, rendering cells resistant to ferroptosis. Lipid profiling and isotope tracing analyses revealed that intestinal-type GCs are unable to generate arachidonic acid (AA) and adrenic acid (AdA) from linoleic acid. AA supplementation of intestinal-type GCs restores their sensitivity to ferroptosis. Based on these data, the polyunsaturated fatty acid (PUFA) biosynthesis pathway plays an essential role in ferroptosis; thus, this pathway potentially represents a marker for predicting the efficacy of ferroptosis-mediated cancer therapy. Show less

Whereas the relation between apolipoprotein A5 (APOA5) gene polymorphisms and triglycerides (TG) levels is well established, the associations between apoA5 concentrations, TG and coronary artery disease (CAD) remain controversial. Therefore, we investigated these relations in the setting of a case-control study involving Korean males. ApoA5, TG, insulin, free fatty acid (FFA) and lipoprotein profiles were determined using a cross-sectional design in 777 healthy controls and 367 CAD patients. Plasma apoA5 concentration was lower in CAD patients than controls (192.7+/-5.2 vs. 237.2+/-3.7ng/ml, P<0.001). Values in the second and top tertiles of apoA5 were associated with a decreased odds ratio (OR) for CAD when compared with values in the bottom tertile; OR for apoA5 top tertile was 0.33 (95% CI, 0.23-0.47) in the age- and BMI-adjusted model and 0.35 (95% CI, 0.23-0.56) following additional adjustments for smoking, drinking status, blood pressure, TG and HDL-cholesterol. After adjustment for age and BMI, plasma apoA5 concentration was negatively correlated with serum TG (r=-0.188, P<0.001) and insulin (r=-0.185, P<0.001) in normotriglyceridemic controls (TG<150mg/dL, n=509) whereas apoA5 was positively correlated with serum TG in hypertriglyceridemic controls (TG> or =150mg/dL, n=268) (r=0.246, P<0.001) and total CAD patients (r=0.177, P<0.01). Regardless of TG levels and CAD status, apoA5 concentration was positively correlated with HDL-cholesterol and FFA levels. Our data supports an inverse association between plasma apoA5 concentrations and CAD risk, probably due to the observed negative correlations of apoA5 with TGs and insulin, although these correlations were affected by TG levels. Show less

The association between -1131T>C single nucleotide polymorphism (SNP) of the apolipoprotein A5 gene (APOA5) and hypertriglyceridemia raised the possibility that this SNP could be related to coronary artery disease (CAD) risk. Therefore, we investigated the association of this APOA5 -1131T>C SNP with circulating concentrations of APOA5, triglyceride and CAD in Koreans. CAD patients (n=741) and age-, sex-matched healthy controls (n=741) were genotyped for the APOA5 -1131T>C SNP. The main outcome measures were the odds ratio (OR) on CAD risk and lipid variables, APOA5 concentration and LDL particle size. The presence of the minor allele at the -1131T>C SNP was associated with an increased risk of CAD [OR 1.34 (95% CI, 1.09-1.65), P=0.007] after adjusting for BMI, alcohol consumption, systolic blood pressure and diastolic blood pressure. There was an association between the APOA5 concentration and the -1131T>C genotype in controls (T/T: 245+/-7 ng/ml, T/C: 220+/-6, C/C: 195+/-12; P=0.001) and CAD patients (T/T: 218+/-8 ng/ml, T/C: 185+/-7, C/C: 169+/-12; P<0.001). Subjects with T/C or C/C in control and CAD patient groups showed higher triglyceride than those with T/T genotype. Also, the -1131T>C polymorphism was associated with LDL particle size (P=0.003), with the T/C or C/C controls having smaller size than the T/T controls. The APOA5 -1131C allele is associated with reduced APOA5 concentration and with increased CAD risk. This is consistent with the observed association between the -1131C SNP, increased triglycerides as well as small LDL particle size. Show less