[Effects of Fear of Coronavirus Disease 2019 and Social Distancing on Women's Suicidal Ideation: Mediating Effect of Depression].

PURPOSE: This study aimed to identify the mediating effects of depression amid the influence of fear and social distancing arising from Coronavirus disease 2019 (COVID-19) in Korean women's suicidal ideation. METHODS: A descriptive correlation study was conducted. Study participants, recruited by Hankook Research from March 2 to March 5, 2021, included 300 women aged 19 to 49 living in South Korea, and 100 people were randomly allocated and enlisted for each age group out of 700,000 Hankook Research Panels recruited in advance from 17 cities and provinces nationwide. Data were collected through a self-reported questionnaire and analyzed using Pearson's correlation coefficient and Hayes' Process Macro Model 4 with 95% bias-corrected bootstrap confidence interval via SPSS statistics 27.0. RESULTS: Suicidal ideation was significantly correlated with fear of COVID-19 (r = .16, p = .006) and depression (r = .65, p < .001). The mediation effect of depression in the relationship between the fear of COVID-19 and suicidal ideation was found to be significant (B = 0.40, boot 95% CI: 0.21~0.61). However, social distancing did not significantly affect suicidal ideation via depression (B = -0.79, boot 95% CI: -1.94~0.26). CONCLUSION: It is necessary to develop and apply interventions to prevent depression and suicidal behaviors by continuously observing and reducing the negative psychological responses caused by COVID-19.

Au-Embedded and Carbon-Doped Freestanding TiO2 Nanotube Arrays in Dye-Sensitized Solar Cells for Better Energy Conversion Efficiency.

Dye-sensitized solar cells (DSSCs) are fabricated with freestanding TiO2 nanotube arrays (TNTAs) which are incorporated with Au nanoparticles (NPs) and carbon materials via electrodeposition and chemical vapor deposition (CVD) method to create a plasmonic effect and better electron transport that will enhance their energy conversion efficiency (ECE). The ECE of DSSCs based on the freestanding TNTAs is 5.87%. The ECE of DSSCs, based on the freestanding TNTAs with Au NPs or carbon materials, is 6.57% or 6.59%, respectively, and the final results of DSSCs according to the freestanding TNTAs with Au NPs and carbon materials is increased from 5.87% to 7.24%, which is an enhancement of 23.34% owing to plasmonic effect and better electron transport. Au NPs are incorporated into the channel of freestanding TNTAs and are characterized by CS-corrected-field emission transmission electron microscope (Cs-FE-TEM) and elemental mapping. Carbon materials are also well-incorporated in the channel of freestanding TNTAs and are analyzed by Raman spectroscopy.

Wild Nutria (Myocastor coypus) Is a Potential Reservoir of Carbapenem-Resistant and Zoonotic Aeromonas spp. in Korea.

The emergence and spread of antibiotic-resistant Aeromonas spp. is a serious public and animal health concern. Wild animals serve as reservoirs, vectors, and sentinels of these bacteria and can facilitate their transmission to humans and livestock. The nutria (Myocastor coypus), a semi-aquatic rodent, currently is globally considered an invasive alien species that has harmful impacts on natural ecosystems and carries various zoonotic aquatic pathogens. This study aimed to determine the prevalence of antibiotic-resistant zoonotic Aeromonas spp. in wild invasive nutrias captured in Korea during governmental eradication program. Three potential zoonotic Aeromonas spp. (A. hydrophila, A. caviae, and A. dhakensis) were identified among isolates from nutria. Some strains showed unexpected resistance to fluoroquinolones, third-generation cephalosporins, and carbapenems. In carbapenem-resistant isolates, the cphA gene, which is related to intrinsic resistance of Aeromonas to carbapenems, was identified, and phylogenetic analysis based on this gene revealed the presence of two major groups represented by A. hydrophila (including A. dhakensis) and other Aeromonas spp. These results indicate that wild nutrias in Korea are a potential reservoir of zoonotic and antibiotic-resistant Aeromonas spp. that can cause infection and treatment failure in humans. Thus, measures to prevent contact of wild nutrias with livestock and humans are needed.

Low-Temperature Growth of Indium Oxide Thin Film by Plasma-Enhanced Atomic Layer Deposition Using Liquid Dimethyl(N-ethoxy-2,2-dimethylpropanamido)indium for High-Mobility Thin Film Transistor Application.

Low-temperature growth of In2O3 films was demonstrated at 70-250 °C by plasma-enhanced atomic layer deposition (PEALD) using a newly synthesized liquid indium precursor, dimethyl(N-ethoxy-2,2-dimethylcarboxylicpropanamide)indium (Me2In(EDPA)), and O2 plasma for application to high-mobility thin film transistors. Self-limiting In2O3 PEALD growth was observed with a saturated growth rate of approximately 0.053 nm/cycle in an ALD temperature window of 90-180 °C. As-deposited In2O3 films showed negligible residual impurity, film densities as high as 6.64-7.16 g/cm3, smooth surface morphology with a root-mean-square (RMS) roughness of approximately 0.2 nm, and semiconducting level carrier concentrations of 1017-1018 cm-3. Ultrathin In2O3 channel-based thin film transistors (TFTs) were fabricated in a coplanar bottom gate structure, and their electrical performances were evaluated. Because of the excellent quality of In2O3 films, superior electronic switching performances were achieved with high field effect mobilities of 28-30 and 16-19 cm2/V·s in the linear and saturation regimes, respectively. Furthermore, the fabricated TFTs showed excellent gate control characteristics in terms of subthreshold swing, hysteresis, and on/off current ratio. The low-temperature PEALD process for high-quality In2O3 films using the developed novel In precursor can be widely used in a variety of applications such as microelectronics, displays, energy devices, and sensors, especially at temperatures compatible with organic substrates.

Activation of NLRP3 and AIM2 inflammasomes in Kupffer cells in hepatic ischemia/reperfusion.

Inflammasome activation by danger signals in ischemia/reperfusion (I/R) injury is responsible for the sterile inflammatory response. Signals triggering formation and activation of the inflammasome involve the generation of oxidative stress. The aim of this study was to examine the molecular mechanisms of inflammasome activation and the involvement of reactive oxygen species in hepatic I/R. I/R induced the formation of nucleotide-binding domain leucine-rich repeat containing family pyrin domain containing 3 (NLRP3) and absent in melanoma 2 (AIM2) inflammasomes and the subsequent serum release of interleukin 1ß. Pannexin-1 inhibitor and anti-cathepsin B antibody attenuated I/R-induced inflammasome activation and hepatic injury. The expression of the thioredoxin-interacting protein gene and the interaction between NLRP3 and the thioredoxin-interacting protein increased after I/R. Treatment with the antioxidant N-acetylcysteine significantly attenuated protein conversion of interleukin 1ß after hepatic I/R. Moreover, pannexin-1 protein expression and cathepsin B release were strongly attenuated by N-acetylcysteine. The depletion of Kupffer cells with gadolinium chloride markedly decreased NLRP3 and AIM2 inflammasome expression and activation of their signaling pathways, and also reduced the level of caspase-1 protein in F4/80-positive cells. Our findings suggest that reactive-oxygen-species-mediated activation of NLRP3 and AIM2 inflammasomes leads to I/R-induced inflammatory responses in which Kupffer cells play a crucial role.

Protective Effects of Geniposide and Genipin against Hepatic Ischemia/Reperfusion Injury in Mice.

Geniposide is an active product extracted from the gardenia fruit, and is one of the most widely used herbal preparations for liver disorders. This study examined the cytoprotective properties of geniposide and its metabolite, genipin, against hepatic ischemia/reperfusion (I/R) injury. C57BL/6 mice were subjected to 60 min of ischemia followed by 6 h of reperfusion. Geniposide (100 mg/kg) and genipin (50 mg/kg) were administered orally 30 min before ischemia. In the I/R mice, the levels of serum alanine aminotransferase and hepatic lipid peroxidation were elevated, whereas hepatic glutathione/glutathione disulfide ratio was decreased. These changes were attenuated by geniposide and genipin administration. On the other hand, increased hepatic heme oxygenase-1 protein expression was potentiated by geniposide and genipin administration. The increased levels of tBid, cytochrome c protein expression and caspase-3 activity were attenuated by geniposide and genipin. Increased apoptotic cells in the I/R mice were also significantly reduced by geniposide and genipin treatment. Our results suggest that geniposide and genipin offer significant hepatoprotection against I/R injury by reducing oxidative stress and apoptosis.

Protective effects of HV-P411 complex against D-galactosamine-induced hepatotoxicity in rats.

This study examined the hepatoprotective effect of the HV-P411 complex, an herbal extract mixture from the seeds of Vitis vinifera, Schisandra chinensis and Taraxacum officinale, against D-galactosamine (D-GalN)-induced hepatitis. Hepatotoxicity was induced by D-GalN (700 mg/kg, i.p.), and the HV-P411 complex was administered orally 48, 24, and 2 h before and 6 h after D-GalN injection. Increases in serum aminotransferase activity and lipid peroxidation and a decrease in hepatic glutathione content were attenuated by the HV-P411 complex 24 h after D-GalN treatment. The HV-P411 complex attenuated the increases in serum tumor necrosis factor-α, interleukin (IL)-6 level and cyclooxygenase-2 protein production and their mRNA expressions, while increases in serum IL-10 level and heme oxygenase-1 protein production and their mRNA expressions were augmented by the HV-P411 complex. The increased translocation of nuclear factor-κB and c-Jun phosphorylation were attenuated by treatment with the HV-P411 complex. Our results suggest that the HV-P411 complex prevents D-GalN-induced hepatotoxicity via antioxidative and anti-inflammatory activities.

Ferulic acid attenuates ischemia/reperfusion-induced hepatocyte apoptosis via inhibition of JNK activation.

Ferulic acid (FA), a phenolic compound found in various medicinal plants, has hepatoprotective effects against oxidative stress and inflammation. Here, we investigated the protective effects and the specific mechanisms of FA against hepatocyte apoptosis caused by ischemia/reperfusion (I/R). Mice were treated intraperitoneally with vehicle or FA 30 min prior to 60 min of ischemia. After 5h of reperfusion, serum aminotransferase activities and hepatic lipid peroxidation were elevated and hepatic glutathione content was depleted. These alterations were attenuated by FA. I/R increased caspase-3 activity and release of cytochrome c, and these were suppressed by FA. FA also attenuated the increases in the serum tumor necrosis factor (TNF)-α levels and TNF receptor type 1-associated DEATH domain protein and TNF receptor-associated factor 2 protein expressions. The cytosolic levels of Bcl-2-associated X protein (Bax), truncated BH3 interacting domain death agonist (tBid), and Bcl-2-like protein 11 were upregulated after reperfusion. The increases in Bax and tBid protein expression were attenuated by FA. Moreover, I/R induced c-Jun N-terminal kinase 1 (JNK1) and JNK2 phosphorylation, and FA attenuated the JNK activation. FA protects against I/R-induced hepatocyte apoptosis by attenuating oxidative stress and JNK activation.

Ferulic acid protects against carbon tetrachloride-induced liver injury in mice.

Ferulic acid (FA), isolated from the root of Scrophularia buergeriana, is a phenolic compound possessing antioxidant, anticancer, and antiinflammatory activities. Here, we have investigated the hepatoprotective effect of FA against carbon tetrachloride (CCl(4))-induced acute liver injury. Mice were treated intraperitoneally with vehicle or FA (20, 40, and 80mg/kg) 1h before and 2h after CCl(4) (20µl/kg) injection. The serum activities of aminotransferases and the hepatic level of malondialdehyde were significantly higher after CCl(4) treatment, while the concentration of reduced glutathione was lower. These changes were attenuated by FA. The serum level and mRNA expression of tumor necrosis factor-α significantly increased after CCl(4) treatment, and FA attenuated these increases. The levels of inducible nitric oxide synthase and cyclooxygenase-2 protein and mRNA expression after CCl(4) treatment were significantly higher and FA reduced these increases. CCl(4)-treated mice showed increased nuclear translocation of nuclear factor-κB (NF-κB), and decreased levels of inhibitors of NF-κB in cytosol. Also, CCl(4) significantly increased the level of phosphorylated JNK and p38 mitogen-activated protein (MAP) kinase, and nuclear translocation of activated c-Jun. FA significantly attenuated these changes. We also found that acute CCl(4) challenge induced TLR4, TLR2, and TLR9 protein and mRNA expression, and FA significantly inhibited TLR4 expression. These results suggest that FA protects from CCl(4)-induced acute liver injury through reduction of oxidative damage and inflammatory signaling pathways.

Protective effects of Moutan Cortex Radicis against acute hepatotoxicity.

This study evaluated the potential beneficial effect of Moutan Cortex Radicis (MCR) in a murine model of carbon tetrachloride (CCl(4))-, D-galactosamine (GalN)- and α-naphthylisothiocyanate (ANIT)-induced liver injury. Acute hepatotoxicity was induced by intraperitoneal injection of CCl(4) (10 µL/kg), GalN (700 mg/kg), and ANIT (40 mg/kg). Animals received MCR (30, 100, and 300 mg/kg ) orally at 48, 24, and 2 h before and 6 h after administration of CCl(4), GalN, and ANIT. Serum activities of aminotransferase were significantly higher at 24 h after CCl(4) or GalN treatment. These changes were attenuated by MCR. Histopathological analysis revealed multiple and extensive areas of portal inflammation, hepatocellular necrosis, and an increase in inflammatory cell infiltration. These changes were inhibited by MCR. Serum total bilirubin concentration increased and bile flow decreased significantly 48 h after ANIT treatment, which was attenuated by MCR. Our results suggest that MCR has a protective effect on acute liver injury.

Protective effects of human placenta extract on cartilage degradation in experimental osteoarthritis.

This study investigated the effect of human placenta extract (HPE) on cartilage degradation in vitro MG-63 cells, articular cartilage explants, and in vivo monoiodoacetate (MIA)-induced osteoarthritis (OA). Matrix metalloproteinase (MMP)-2 activity was measured in HPE-treated osteoblastic MG-63 cells. Articular cartilage explants in rabbit were cultured, and the degree of proteoglycan (PG) degradation was assessed by measuring the amount of glycosaminoglycan (GAG) released into the culture medium. Experimental osteoarthritis was induced by intra-articular injection of 3 mg MIA in rats. Beginning 14 d post-MIA injection, HPE was administered intra-articularly once a day for 14 d. The knee joints were assessed by roentgenography, histology, and gelatinase activity. HPE inhibited PG degradation in articular cartilage explants. HPE significantly reduced deformity of knee joints and suppressed the histological change in MIA-induced OA. HPE inhibited MMP-2 activity in MG-63 cells. MMP-2 and -9 activities were also reduced in the cartilages of HPE-treated knee joints. Our results indicate that HPE has therapeutic effects on OA by protecting cartilage.

Expression of the homeobox gene, HOPX, is modulated by cell differentiation in human keratinocytes and is involved in the expression of differentiation markers.

Homeodomain only protein X (HOPX), an unusual homeodomain protein, was originally identified as a key regulator of cardiac development. We first demonstrated that the expression of HOPX was dependent on the differentiation of human keratinocytes and has an effect on the expression of differentiation markers. HOPX was suppressed in proliferating human keratinocytes and was gradually induced by calcium-triggered differentiation of human keratinocytes. In the epidermis, HOPX is highly expressed in the terminally differentiated suprabasal layers. Among the transcript variants of HOPX, the variant 3 driven by promoter A was the main transcript and it was regulated by cell differentiation in human keratinocytes. The expression of HOPX was induced through the phorbol-12-myristate-13-acetate (PMA)-dependent protein kinase C (PKC) signaling pathway, and not by the demethylating agent, 5-aza-dC (5-aza-2'-deoxycitidine) suggesting the suppression of HOPX is not associated with DNA methylation in human keratinocytes. The RNA interference (RNAi) silencing experiment showed that the knockdown of HOPX expression resulted in the increase of such differentiation markers as involucrin and loricrin. Exogenous expression of HOPX down-regulated the expression of differentiation marker genes in immortalized human keratinocytes (HaCaT). Collectively, HOPX is modulated by cell differentiation in human keratinocytes and this might contribute to homeostasis of keratinocytes by controlling differentiation-dependent genes.

Hepatoprotective effect of pinoresinol on carbon tetrachloride-induced hepatic damage in mice.

Forsythiae Fructus is known to have diuretic, anti-bacterial, and anti-inflammatory activities. This study examined the hepatoprotective effects of pinoresinol, a lignan isolated from Forsythiae Fructus, against carbon tetrachloride (CCl(4))-induced liver injury. Mice were treated intraperitoneally with vehicle or pinoresinol (25, 50, 100, and 200 mg/kg) 30 min before and 2 h after CCl4 (20 microl/kg) injection. In the vehicle-treated CCl(4 )group, serum aminotransferase activities were significantly increased 24 h after CCl4 injection, and these increases were attenuated by pinoresinol at all doses. Hepatic glutathione contents were significantly decreased and lipid peroxidation was increased after CCl4 treatment. These changes were attenuated by 50 and 100 mg/kg of pinoresinol. The levels of protein and mRNA expression of inflammatory mediators, including tumor necrosis factor-alpha, inducible nitric oxide synthase, and cyclooxygenase-2, were significantly increased after CCl4 injection; and these increases were attenuated by pinoresinol. Nuclear translocation of nuclear factor-kappaB (NF-kappaB) and phosphorylation of c-Jun, one of the components of activating protein 1 (AP-1), were inhibited by pinoresinol. Our results suggest that pinoresinol ameliorates CCl4)-induced acute liver injury, and this protection is likely due to anti-oxidative activity and down-regulation of inflammatory mediators through inhibition of NF-kappaB and AP-1.

Cracking Down On Youth Tobacco May Influence Drug Use.

This study evaluated the influence of tobacco Possession-Use-Purchase (PUP) law enforcement and illicit drug use and offers. Twenty-four towns were randomly assigned into two conditions. Both conditions focused on reducing minors' access to commercial sources of tobacco. The communities assigned to the experimental condition also increased their PUP law enforcement, whereas among communities in the control condition, PUP law enforcement remained at low levels. A Hierarchical Linear Modeling analytical approach was selected due to the multilevel data and nested design. The likelihood of a child currently using drugs, ever having used drugs, or illicit drug offers was lower in the experimental versus control conditions. These outcomes suggest that police efforts to reduce specific substance use behaviors (i.e., underage tobacco use) may have a positive spillover effect and help reduce teen drug use and illicit drug offers.

Immunomodulating effects of Korean mistletoe lectin in vitro and in vivo.

The immunomodulatory effects of Korean mistletoe lectin (KML), one of the major active components in Viscum album L. var. coloratum, were investigated in vitro in immune cell proliferation and natural killer (NK) cell- and macrophage-mediated cytotoxicity, and in vivo in the forced swim test and cold stress. In mitogen-induced lymphocyte proliferation of murine splenocytes, concanavalin A and lipopolysaccharide significantly increased the proliferation of T cell and B cell lymphocytes, respectively. KML exposure increased lymphocyte proliferation in response to mitogen. KML also increased the splenic NK cell and macrophage activities in vitro. Exposure to KML increased production of cytokines such as interleukin-1 and interleukin-6 by macrophages. Two-week treatment with KML (30, 100, 300 and 600 microg/kg) increased the recruitment of lymphocytes, monocytes and macrophages. In the forced swim test, the immobility time was significantly attenuated by treatment with KML (300 and 600 microg/kg). In a cold stress experiment, spleen and thymus weight increased in KML-treated mice, while the weight of adrenal gland was lower than that in vehicle-treated mice. The levels of serum aminotransferases, lactate dehydrogenase and alkaline phosphatase were decreased by KML treatment. KML treatment also induced increases in the percentages of CD4(+) and CD8(+) cells in thymus. Our results suggest that KML enhances the immune system through modulation of lymphocytes, NK cells, and macrophages.