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We investigated the protective effect and mechanisms of apigenin against cognitive impairments in a scopolamine-injected mouse model. Our results showed that intraperitoneal (i.p.) injection of scopolamine leads to learning and memory dysfunction, whereas the administration of apigenin (synthetic compound, 100 and 200 mg/kg/day) improved cognitive ability, which was confirmed by behavioral tests such as the T-maze test, novel objective recognition test, and Morris water maze test in mice. In addition, scopolamine-induced lipid peroxidation in the brain was attenuated by administration of apigenin. To further evaluate the protective mechanisms of apigenin on cognitive and memory function, Western blot analysis was carried out. Administration of apigenin decreased the B-cell lymphoma 2-associated X/B-cell lymphoma 2 (Bax/Bcl-2) ratio and suppressed caspase-3 and poly ADP ribose polymerase cleavage. Furthermore, apigenin down-regulated the β-site amyloid precursor protein-cleaving enzyme, along with presenilin 1 (PS1) and PS2 protein levels. Apigenin-administered mice showed lower protein levels of a receptor for advanced glycation end-products, whereas insulin-degrading enzyme, brain-derived neurotrophic factor (BDNF), and tropomyosin receptor kinase B (TrkB) expression were promoted by treatment with apigenin. Therefore, this study demonstrated that apigenin is an active substance that can improve cognitive and memory functions by regulating apoptosis, amyloidogenesis, and BDNF/TrkB signaling pathways.

Amyloid-beta (Aβ) aggregation and deposition have been identified as a critical feature in the pathology of Alzheimer’s disease (AD), with a series of functional alterations including neuronal oxidative stress and apoptosis. N-feruloyl serotonin (FS) is a plant-derived component that exerts antioxidant activity. This study investigated the protective effects of FS on Aβ25–35-treated neuronal damage by regulation of oxidative stress and apoptosis in human neuroblastoma SH-SY5Y cells. The radical scavenging activities increased with the concentration of FS, exhibiting in vitro antioxidant activity. The Aβ25–35-treated SH-SY5Y cells exerted neuronal cell injury by decreased cell viability and elevated reactive oxygen species, but that was recovered by FS treatment. In addition, treatment of FS increased anti-apoptotic factor B-cell lymphoma protein 2 (Bcl-2) and decreased the pro-apoptotic factor Bcl-2-associated X protein. The FS attenuated Aβ-stimulated neuronal apoptosis by regulations of mitogen-activated protein kinase signaling pathways. Moreover, activated CREB-BDNF signaling was observed by the treatment of FS in Aβ25–35-induced SH-SY5Y cells. These results demonstrate that FS shows potential neuroprotective effects on Aβ25–35-induced neuronal damage by attenuation of oxidative stress and apoptosis, and suggest that FS may be considered a promising candidate for the treatment of AD.

Tantalum-oxide-based bi-layered resistance-change memories (RRAMs) have recently improved greatly with regard to their memory performances. The formation and rupture of conductive filaments is generally known to be the mechanism that underlies resistive switching. The nature of the filament has been studied intensively and several phenomenological models have consistently predicted the resistance-change behavior. However, a physics-based model that describes a complete bi-layered RRAM structure has not yet been demonstrated. Here, a complete electro-thermal resistive switching model based on the finite element method is proposed. The migration of oxygen vacancies is simulated by the local temperature and electric field derived from carrier continuity and heat equations fully coupled in a 3-D geometry, which considers a complete bi-layered structure that includes the top and bottom electrodes. The proposed model accurately accounts for the set/reset characteristics, which provides an in-depth understanding of the nature of resistive switching.

Deposition of amyloid-beta (Aβ) in the aging brain has been often observed and is thought to be a pathological feature of Alzheimer’s disease. The use of natural products for disease prevention and treatment is gaining attention worldwide. Carthamus tinctorius L. seed and Taraxacum coreanum have been used as traditional medicines in Asian countries, where they have been reported to exert anti-inflammatory and anti-oxidative effects. It has been demonstrated that the combination of C. tinctorius L. seed and T. coreanum has an effect on cognitive enhancement, indicating a ratio of 5:5 synergistically enhancing learning and memory abilities in comparison with a single treatment. Here, we aimed to investigate the protective effect of C. tinctorius L. seed and T. coreanum mixture (CT) at different concentrations on cognition in Aβ25-35-infused mice. CT-administered mice showed significant cognitive improvement in the T-maze, novel object recognition, and Morris water maze tests. Moreover, amyloidogenesis-related proteins, such as β-secretase and γ-secretase, were detected and their protein levels decreased after treatment with CT. Our study shows that CT attenuates cognitive dysfunction by improving learning and memory capability and regulating Aβ-related proteins in Aβ25-35-injected mice. These findings suggest that CT might be a candidate for functional food on cognitive improvement.

Regular surveillance for hepatocellular carcinoma (HCC) in chronic hepatitis B (CHB) patients is essential to detect HCC earlier and to improve prognosis. This study investigated whether prescription of oral medication contributes to adherence to surveillance, early tumor detection, and overall survival (OS). A total of 401 CHB patients who were newly diagnosed with HCC were included: 134 patients received no medication (group 1), 151 received hepatoprotective agents such as ursodeoxycholic acid and silymarin (group 2), and 116 received antiviral agents (group 3) at two years before HCC diagnosis. The primary endpoint was OS, and secondary endpoints were compliance to regular surveillance and HCC status at diagnosis. Compared to group 1, both group 2 and 3 had higher rates of good compliance to regular surveillance (defined as participation in >80% of imaging intervals being ≤6 months) (58.2%, 90.1%, and 97.4%, respectively; P<0.001), more HCC diagnosed at a very early stage (20.9%, 32.5%, and 36.2%; P = 0.019) and smaller tumor size (2.8±2.4cm, 1.9±1.1cm, and 1.8±0.9cm; P<0.001). Finally, compared to group 1, both group 2 (hazard ratio, 0.63; 95% confidence interval, 0.41-0.97; P = 0.035) and group 3 (hazard ratio, 0.40; 95% confidence interval, 0.22-0.71; P = 0.002) had significantly longer OS. In mediation analysis, prolonged OS is resulted considerably from indirect effect mediated by shorter imaging interval (>100% in group 2 and 14.5% in group 3) rather than direct effect of medication itself. Prescription of oral medication improves compliance to surveillance and enables early detection of HCC, which is associated with enhanced survival.

Insulin like-growth factor-1 (IGF-1) reflects hepatic synthetic function and plays a major role in the development and progression of various cancers. In the present study, we investigated whether baseline serum IGF-1 levels predict time-to-progression (TTP) and overall survival (OS) in hepatocellular carcinoma (HCC) patients treated with transarterial chemoembolization (TACE). A total of 155 consecutive treatment-naive patients with HCC who had undergone TACE as initial treatment were included from a prospective cohort. Baseline serum IGF-1 levels were analyzed with regard to their associations with disease progression and survival. During a median follow-up period of 41.8 months, patients with low IGF-1 levels showed significantly shorter TTP (median, 6.0 months; 95% confidence interval [CI], 4.5-7.6) than patients with high IGF-1 levels (median, 16.5 months; 95% CI, 4.9-28.1; p = 0.003). In the multivariate analysis, BCLC stage, serum vascular endothelial growth factorlevels, and IGF-1 levels were independent risk factors for disease progression. The hazard ratio (HR) of progression for each 10 ng/mL decrease in IGF-1 level was 1.072 (95% CI, 1.029-1.117; p = 0.001). Furthermore, together with tumor size, stage, and treatment response, IGF-1 levels were an independent predictor of poorer survival (for each 10 ng/mL decrease in IGF-1 level; HR, 1.057; 95% CI, 1.001-1.115; p = 0.045). In conclusion, low baseline IGF-1 levels independently correlated with shorter TTP and poorer OS in patients with HCC who underwent TACE.

Amyloid-beta (Aβ) aggregation and deposition have been identified as a critical feature in the pathology of Alzheimer’s disease (AD), with a series of functional alterations including neuronal oxidative stress and apoptosis. N-feruloyl serotonin (FS) is a plant-derived component that exerts antioxidant activity. This study investigated the protective effects of FS on Aβ[sub.25–35]-treated neuronal damage by regulation of oxidative stress and apoptosis in human neuroblastoma SH-SY5Y cells. The radical scavenging activities increased with the concentration of FS, exhibiting in vitro antioxidant activity. The Aβ[sub.25–35]-treated SH-SY5Y cells exerted neuronal cell injury by decreased cell viability and elevated reactive oxygen species, but that was recovered by FS treatment. In addition, treatment of FS increased anti-apoptotic factor B-cell lymphoma protein 2 (Bcl-2) and decreased the pro-apoptotic factor Bcl-2-associated X protein. The FS attenuated Aβ-stimulated neuronal apoptosis by regulations of mitogen-activated protein kinase signaling pathways. Moreover, activated CREB-BDNF signaling was observed by the treatment of FS in Aβ[sub.25–35]-induced SH-SY5Y cells. These results demonstrate that FS shows potential neuroprotective effects on Aβ[sub.25–35]-induced neuronal damage by attenuation of oxidative stress and apoptosis, and suggest that FS may be considered a promising candidate for the treatment of AD.

Long-term discharge of turbid water from reservoirs after flood events is a major socioenvironmental problem in many countries, including Korea. This study used a suite of mathematical models to simulate the fate of turbidity flows in the Soyanggang Reservoir in Korea, an important source of drinking water for the Seoul Capital Area, in response to extreme floods based on the Representative Concentration Pathway 4.5 climate scenario. It evaluated the effectiveness of the selective withdrawal facility (SWF), installed recently in the Soyanggang Reservoir to control persistent turbidity. Extreme floods with a maximum daily inflow rate greater than the historical maximum observed in 2006 were projected to occur four times in this century. The fate and transport of turbidity flows were highly influenced by both the thermal stability of the reservoir and the season in which the flood event occurred. Thus, SWF operations should consider the timing of extreme events (i.e., the imminence of the autumn turnover) to mitigate the impact of high turbidity on the water supply and downstream ecosystem. It was found to be ineffective under extreme events if these occurred in two consecutive years. Current reservoir operations, which rely heavily on the SWF, are likely to be inadequate to overcome the negative effects of extreme-turbidity events on reliably providing safe water supplies. Coping with the worst event expected to occur in the future would require additional countermeasures such as bypassing high-turbidity water.

Amyloid-beta (Aβ) aggregation and deposition have been identified as a critical feature in the pathology of Alzheimer's disease (AD), with a series of functional alterations including neuronal oxidative stress and apoptosis. -feruloyl serotonin (FS) is a plant-derived component that exerts antioxidant activity. This study investigated the protective effects of FS on Aβ -treated neuronal damage by regulation of oxidative stress and apoptosis in human neuroblastoma SH-SY5Y cells. The radical scavenging activities increased with the concentration of FS, exhibiting in vitro antioxidant activity. The Aβ -treated SH-SY5Y cells exerted neuronal cell injury by decreased cell viability and elevated reactive oxygen species, but that was recovered by FS treatment. In addition, treatment of FS increased anti-apoptotic factor B-cell lymphoma protein 2 (Bcl-2) and decreased the pro-apoptotic factor Bcl-2-associated X protein. The FS attenuated Aβ-stimulated neuronal apoptosis by regulations of mitogen-activated protein kinase signaling pathways. Moreover, activated CREB-BDNF signaling was observed by the treatment of FS in Aβ -induced SH-SY5Y cells. These results demonstrate that FS shows potential neuroprotective effects on Aβ -induced neuronal damage by attenuation of oxidative stress and apoptosis, and suggest that FS may be considered a promising candidate for the treatment of AD.

Parkinson’s disease (PD) is one of the most common neurodegenerative diseases. The mechanisms underlying PD remain to be fully elucidated, and research into treatments for this condition is ongoing. Recent advances in genetic research have shed light on the mechanisms underlying PD. In this study, we used PD and control mesenchymal stem cells (MSCs) obtained from adipose tissues to confirm the differences between groups at the cellular and molecular levels. The results revealed that in PD MSCs, cell viability was clearly lower, and the rate of cell senescence was higher compared to the controls. Next, to compare the gene expression in PD and control cells, transcriptome analysis was performed. Genes in pathways, including extracellular matrix (ECM) receptor interaction, P53 signaling, and focal adhesion, were down-regulated in PD. Among genes related to ECM receptor interaction, RELN gene expression was markedly decreased in PD cells; however, after being treated with recombinant Reelin protein, a significant increase in cell viability and a decrease in α-Synuclein aggregation and cell senescence were observed. In conclusion, Reelin affects PD by positively influencing the cell characteristics. Our findings will facilitate research into new treatments for PD.