High intake of sweet foods and low life satisfaction can act as risk factors for acute coronary syndrome through synergistic interaction.

Purpose: Dietary and psychological status contributes to the development of coronary artery disease. However, these lifestyle factors may vary depending on ethnic and environmental background, and secondary prevention programs dealing with these factors in a specific population are not well-established. We aimed to assess dietary and psychological characteristics in Korean patients with acute coronary syndrome (ACS) and analyze their interactions as independent risk factors for ACS. Methods: Ninety-two patients with ACS (29 acute myocardial infarction and 63 unstable angina) and 69 controls were subjected to dietary and psychological analyses. Dietary intake was assessed by a food frequency questionnaire. Psychological depression and perceived stress were assessed using the Patient Health Questionnaire-9 and the Perceived Stress Scale, respectively. Eight domains of life satisfaction (marital/love relationship, leisure, standard of living, job, health, family life, sex life, and self) were assessed using the Domain Satisfaction Questionnaire (DSQ). Results: The ACS group had a higher consumption of sweets and fish/seafood, as well as higher levels of depressive symptoms. Additionally, they had lower DSQ scores in total, and all eight individual domains compared with the control group. In multivariate logistic regression analysis, sweet intake (OR 4.57, 95% CI: 1.94-11.40) and total DSQ scores (OR 0.34, 95% CI: 0.14-0.81) were identified as independent risk factors for ACS. Furthermore, these factors, which displayed a significant inverse correlation (ρ = -0.23, p = 0.01), were determined as having a synergistic contribution to the development of ACS. Conclusion: High sweet food intake and low life satisfaction can act as risk factors for ACS through a synergistic interaction, which emphasizes a demand for a more comprehensive approach to secondary prevention of ACS. In addition, these data highlight the role of positive psychological wellbeing factors in cardiovascular health.

Thermocatalytic conversion of wood-plastic composite over HZSM-5 catalysts.

Air gasification of the Wood-Plastic Composite (WPC) was performed over Ni-loaded HZSM-5 catalysts to generate H2-rich gas. Increasing SiO2/Al2O3 ratio (SAR) of HZSM-5 adversely affected catalytic activity, where the highest gas yield (51.38 wt%) and H2 selectivity (27.01 vol%) were acquired using 20 %Ni/HZSM-5(30) than those produced over 20 %Ni/HZSM-5(80) and 20 %Ni/HZSM-5(280). Reducing SAR was also favorably conducive to increasing the acyclic at the expense of cyclic compounds in oil products. These phenomena are attributed to enhanced acid strength and Ni dispersion of 20 %Ni/HZSM-5(30) catalyst. Moreover, catalytic activity in the terms of gas yield and H2 selectivity enhanced with growing Ni loading to 20 %. Also, the addition of promoters (Cu and Ca) to 20 %Ni/HZSM-5(30) boosted the catalytic efficiency for H2-rich gas generation. Raising temperature indicated a positive relevance with the gas yield and H2 selectivity. WPC valorization via gasification technology would be an outstanding outlook in the terms of a waste-to-energy platform.

Combination of metformin/efavirenz/fluoxetine exhibits profound anticancer activity via a cancer cell-specific ROS amplification.

The possible anticancer activity of combination (M + E + F) of metformin (M), efavirenz (E), and fluoxetine (F) was investigated in normal HDF cells and HCT116 human colon cancer cells. Metformin increased cellular FOXO3a, p-FOXO3a, AMPK, p-AMPK, and MnSOD levels in HDFs but not in HCT116 cells. Cellular ATP level was decreased only in HDFs by metformin. Metformin increased ROS level only in HCT116 cells. Transfection of si-FOXO3a into HCT116 reversed the metformin-induced cellular ROS induction, indicating that FOXO3a/MnSOD is the key regulator for cellular ROS level. Viability readout with M, E, and F alone decreased slightly, but the combination of three drugs dramatically decreased cell survival in HCT116, A549, and SK-Hep-1 cancer cells but not in HDF cells. ROS levels in HCT116 cells were massively increased by M + E + F combination, but not in HDF cells. Cell cycle analysis showed that of M + E + F combination caused cell death only in HCT116 cells. The combination of M + E + F reduced synergistically mitochondrial membrane potential and mitochondrial electron transport chain complex I and III activities in HCT116 cells when compared with individual treatments. Western blot analysis indicated that DNA damage, apoptosis, autophagy, and necroptosis-realated factors increased in M + E + F-treated HCT116 cells. Oral administration with M + E + F combination for 3 weeks caused dramatic reductions in tumor volume and weight in HCT116 xenograft model of nude mice when compared with untreated ones. Our results suggest that M + E + F have profound anticancer activity both in vitro and in vivo via a cancer cell-specific ROS amplification (CASRA) through ROS-induced DNA damage, apoptosis, autophagy, and necroptosis.

Lipid Polysaccharides have a Detrimental Effect on the Function of the Ovaries and Uterus in Mice through Increased Pro-Inflammatory Cytokines.

As the number of coronavirus disease 2019 (COVID-19) vaccinations increases, various side effects are being reported, and menstrual abnormalities have been reported as a side effect in women. However, it is still unclear whether the COVID-19 vaccine has detrimental effects on the female reproductive system. Therefore, we investigated the effect of excessive immune response on reproductive function by administering Lipopolysaccharides (LPS) instead of the COVID-19 vaccine. The immune response in mice was induced by injection of LPS. Mice injected with saline 5 times were used as a control group, and mice injected with LPS 5 times were used as an experimental group. Repeated administration of LPS significantly reduced the number of corpus luteum (CL). On the other hand, the injection of LPS did not affect the development of follicles leading before the CL. The expression of the apoptosis-related genes Fas and Fas-L increased in the experimental group. In addition, the expression of the inflammation-related genes increased in the experimental group. In this study, we confirmed that LPS had detrimental effects on the uterus and ovaries in mice. These results suggest that injection of LPS can cause immune reactions within the uterus and ovaries and cause hormonal changes, which can have adverse effects such as abnormal operation or bleeding of the menstrual cycle. These results are expected to help determine the cause of decreased reproductive function, infertility, or physiological disorders caused by the COVID-19 vaccine.

A Prosthetic Socket with Active Volume Compensation for Amputated Lower Limb.

Typically, the actual volume of the residual limb changes over time. This causes the prosthesis to not fit, and then pain and skin disease. In this study, a prosthetic socket was developed to compensate for the volume change of the residual limb. Using an inflatable air bladder, the proposed socket monitors the pressure in the socket and keeps the pressure distribution uniform and constant while walking. The socket has three air bladders on anterior and posterior tibia areas, a latching type 3-way pneumatic valve and a portable control device. In the paper, the mechanical properties of the air bladder were investigated, and the electromagnetic analysis was performed to design the pneumatic valve. The controller is based on a hysteresis control algorithm with a closed loop, which keeps the pressure in the socket close to the initial set point over a long period of time. In experiments, the proposed prosthesis was tested through the gait simulator that can imitate a human's gait cycle. The active volume compensation of the socket was successfully verified during repetitive gait cycle using the weight loads of 50, 70, and 90 kg and the residual limb model with a variety of volumes. It was confirmed that the pressure of the residual limb recovered to the initial state through the active control. The pressure inside the socket had a steady state error of less than 0.75% even if the volume of the residual limb was changed from -7% to +7%.

Social defeat as a mediator of the relationship between childhood trauma and paranoid ideation.

Social defeat, the subjective experience of viewing oneself as a failure or social outsider, is associated with various psychiatric disorders. Recent studies suggest that social defeat may play an important role in the development of psychotic disorders. This study examined the role of social defeat in the relationship between childhood trauma and paranoid ideation, a symptom of psychosis, in non-psychotic mental disorders. Psychiatric patients (N = 199) completed the Korean version of the Childhood Trauma Questionnaire, the Korean version of the Defeat Scale, and Restructured Clinical Scale 6 (Ideas of Persecution) of the Korean version of the Minnesota Multiphasic Personality Inventory-2. A partial correlation analysis revealed that childhood trauma was significantly related to social defeat and paranoid ideation after controlling for age and gender. Structural equation modeling confirmed that the relationship between childhood trauma and paranoid ideation was partially mediated by social defeat. Thus, social defeat is a possible psychological mechanism underlying the association between childhood trauma and paranoia.

Poor health-related quality of life and proactive primary control strategy may act as risk factors for acute coronary syndrome.

BACKGROUND AND OBJECTIVES: Increasing evidence supports that psychological factors may be related to development of coronary artery disease (CAD). Although psychological well-being, ill-being, and control strategy factors may play a significant role in CAD, rarely have these factors been simultaneously examined previously. We assessed comprehensive psychological factors in patients with acute coronary syndrome (ACS). SUBJECTS AND METHODS: A total of 85 ACS patients (56 unstable angina, 29 acute myocardial infarction; 52.6±10.2 years; M/F=68/17) and 63 healthy controls (48.7±6.7 years, M/F=43/20) were included. Socio-demographic information, levels of psychological maladjustment, such as anxiety, hostility, and job stress, health-related quality of life (HRQoL), and primary and secondary control strategy use were collected through self-report questionnaires. RESULTS: There was no significant difference between the ACS group and control group in levels of anxiety, hostility, and job stress. However, ACS patients had significantly lower scores on the general health perception and bodily pain subscales of HRQoL than the control group. The ACS group, as compared with the controls, tended to use primary control strategies more, although not reaching statistical significance by univariate analysis. Multivariate logistic regression analysis after adjusting age and gender identified the physical domain of HRQoL {odds ratio (OR)=0.40}, primary control strategy (OR=1.92), and secondary control strategy (OR=0.53) as independent predictors of ACS. CONCLUSION: Poor HRQoL and primary control strategy, proactive behaviors in achieving ones' goal, may act as risk factors for ACS, while secondary control strategy to conform to current situation may act as a protective factor for ACS.

Trans-placental transfer of thirteen perfluorinated compounds and relations with fetal thyroid hormones.

While the results of animal studies have shown that perfluorinated compounds (PFCs) can modulate concentrations of thyroid hormones in blood, limited information is available on relationships between concentrations of PFCs in human blood serum and fetal thyroid hormones. The relationship between concentrations of PFCs in blood and fetal thyroid hormone concentrations or birth weight, and ratios of major PFCs between maternal and fetal serum were determined. Concentrations of PFCs were measured in blood serum of pregnant women (n = 44), fetal cord blood serum (n = 43) and breast milk (n = 35). Total concentrations of thyroxin (T4), triiodothyronin (T3) and thyroid stimulating hormone (TSH) in blood serum were also quantified. The ratios of major PFCs in maternal versus fetal serum were 1:1.93, 1.02, 0.72, and 0.48 for perfluorotridecanoic acid (PFTrDA), perfluorooctanoic acid (PFOA), perfluorohexane sulfonate (PFHxS), and perfluorooctane sulfonate (PFOS), respectively. Fetal PFOS, PFOA, PFTrDA and maternal PFTrDA were correlated with fetal total T4 concentrations, but after adjusting for major covariates, most of the relationships were no longer statistically significant. However, the significant negative correlations between maternal PFOS and fetal T3, and maternal PFTrDA and fetal T4 and T3 remained. Since thyroid hormones are crucial in the early development of the fetus, its clinical implication should be evaluated. Given the observed trans-placental transfer of PFCs, efforts should be also made to elucidate the exposure sources among pregnant women.

Genotoxicity and endocrine-disruption potentials of sediment near an oil spill site: two years after the Hebei Spirit oil spill.

The Hebei Spirit oil spill episode (December 7, 2007) has affected the western coastal area of South Korea; however, there is limited information on the potential toxicity of the oil spill to the ecosystem or humans. The potential toxicity of sediments collected from the affected area (n = 22) 2 years after the spill was evaluated. Acute lethal toxicity tests using Vibrio fischeri and Moina macrocopa and tests for genotoxicity and alteration of steroidogenesis using chicken DT40 cells and H295R cells, respectively, were conducted. Both crude and weathered oil extracts were evaluated in order to link the observed toxicity in the sediment extracts to the oil spill. Whereas toxicity to bacteria and daphnids was observed in only two elutriate samples, 10 of the 22 sediment extracts showed genotoxic potential in DT40 cells. The mechanisms of genotoxicity involved nucleotide excision repair (XPA(-/)), homologous recombination (RAD54(-/-)), and translesion synthesis pathways (REV3(-/-)). In addition, nine sediment extracts caused significantly greater production of E2 in H295R cells, and significant up-regulation of CYP19, CYP11B2, and 3ßHSD2 by sediment extracts was observed. The pattern of toxicities observed in both crude and weathered oil samples was similar to that observed in the sediment extracts. The genotoxicicity and endocrine-disruption potential of the sediment extracts suggest a need for long-term followup for such toxicity in humans and wildlife in this area.