Recent progress and prospects of dimer and multimer acceptors for efficient and stable polymer solar cells.

High power conversion efficiency (PCE) and long-term stability are essential prerequisites for the commercialization of polymer solar cells (PSCs). Small-molecule acceptors (SMAs) are core materials that have led to recent, rapid increases in the PCEs of the PSCs. However, a critical limitation of the resulting PSCs is their poor long-term stability. Blend morphology degradation from rapid diffusion of SMAs with low glass transition temperatures (Tgs) is considered the main cause of the poor long-term stability of the PSCs. The recent emergence of oligomerized SMAs (OSMAs), composed of two or more repeating SMA units (i.e., dimerized and trimerized SMAs), has shown great promise in overcoming these challenges. This innovation in material design has enabled OSMA-based PSCs to reach impressive PCEs near 19% and exceptional long-term stability. In this review, we summarize the evolution of OSMAs, including their research background and recent progress in molecular design. In particular, we discuss the mechanisms for high PCE and stability of OSMA-based PSCs and suggest useful design guidelines for high-performance OSMAs. Furthermore, we reflect on the existing hurdles and future directions for OSMA materials towards achieving commercially viable PSCs with high PCEs and operational stabilities.

High-Performance Intrinsically Stretchable Polymer Solar Cell with Record Efficiency and Stretchability Enabled by Thymine-Functionalized Terpolymer.

Designing new polymer semiconductors for intrinsically stretchable polymer solar cells (IS-PSCs) with high power conversion efficiency (PCE) and durability is critical for wearable electronics applications. Nearly all high-performance PSCs are constructed using fully conjugated polymer donors (PD) and small-molecule acceptors (SMA). However, a successful molecular design of PDs for high-performance and mechanically durable IS-PSCs without sacrificing conjugation has not been realized. In this study, we design a novel thymine side chain terminated 6,7-difluoro-quinoxaline (Q-Thy) monomer and synthesize a series of fully conjugated PDs (PM7-Thy5, PM7-Thy10, PM7-Thy20) featuring Q-Thy. The Q-Thy units capable of inducing dimerizable hydrogen bonding enable strong intermolecular PD assembly and highly efficient and mechanically robust PSCs. The PM7-Thy10:SMA blend demonstrates a combination of high PCE (>17%) in rigid devices and excellent stretchability (crack-onset value >13.5%). More importantly, PM7-Thy10-based IS-PSCs show an unprecedented combination of PCE (13.7%) and ultrahigh mechanical durability (maintaining 80% of initial PCE after 43% strain), illustrating the promising potential for commercialization in wearable applications.

Performance Evaluation of a Multichannel All-In-One Phantom Dosimeter for Dose Measurement of Diagnostic X-ray Beam.

We developed a multichannel all-in-one phantom dosimeter system composed of nine sensing probes, a chest phantom, an image intensifier, and a complementary metal-oxide semiconductor (CMOS) image sensor to measure the dose distribution of an X-ray beam used in radiation diagnosis. Nine sensing probes of the phantom dosimeter were fabricated identically by connecting a plastic scintillating fiber (PSF) to a plastic optical fiber (POF). To measure the planar dose distribution on a chest phantom according to exposure parameters used in clinical practice, we divided the top of the chest phantom into nine equal parts virtually and then installed the nine sensing probes at each center of the nine equal parts on the top of the chest phantom as measuring points. Each scintillation signal generated in the nine sensing probes was transmitted through the POFs and then intensified by the image intensifier because the scintillation signal normally has a very low light intensity. Real-time scintillation images (RSIs) containing the intensified scintillation signals were taken by the CMOS image sensor with a single lens optical system and displayed through a software program. Under variation of the exposure parameters, we measured RSIs containing dose information using the multichannel all-in-one phantom dosimeter and compared the results with the absorbed doses obtained by using a semiconductor dosimeter (SCD). From the experimental results of this study, the light intensities of nine regions of interest (ROI) in the RSI measured by the phantom dosimeter were similar to the dose distribution obtained using the SCD. In conclusion, we demonstrated that the planar dose distribution including the entrance surface dose (ESD) can be easily measured by using the proposed phantom dosimeter system.

Human milk oligosaccharides 3'-sialyllactose and 6'-sialyllactose attenuate LPS-induced lung injury by inhibiting STAT1 and NF-κB signaling pathways.

Acute lung injury (ALI) is the leading cause of respiratory diseases induced by uncontrolled inflammation and cell death. Lipopolysaccharide (LPS) is a major trigger of ALI in the progression through macrophage differentiation and the accelerated release of pro-inflammatory cytokines. The present study aimed to investigate the protective effects of human milk oligosaccharides, specifically 3'-sialyllactose (3'-SL) and 6'-sialyllactose (6'-SL), on LPS-induced ALI and elucidate their underlying signaling pathways. The inhibitory effects of 3'-SL and 6'-SL on inflammation were evaluated using LPS-treated RAW 264.7 macrophages. To establish the ALI model, mice were treated with 10 mg/kg LPS for 24 h. Histological changes in the lung tissues were assessed using hematoxylin and eosin staining and immunofluorescence. LPS causes thickening of the alveolar wall infiltration of immune cells in lung tissues and increased serum levels of TNF-α, IL-1ß, and GM-CSF. However, these effects were significantly alleviated by 100 mg/kg of 3'-SL and 6'-SL. Consistent with the inhibitory effects of 3'-SL and 6'-SL on LPS-induced pro-inflammatory cytokine secretion in serum, 3'-SL and 6'-SL suppressed mRNA expression of TNF-α, IL-1ß, MCP-1, iNOS, and COX2 in LPS-induced RAW 264.7 cells. Mechanistically, 3'-SL and 6'-SL abolished LPS-mediated phosphorylation of NF-κB and STAT1. Interestingly, fludarabine treatment, a STAT1 inhibitor, did not affect LPS-mediated NF-κB phosphorylation. In summary, 3'-SL and 6'-SL protect LPS-induced macrophage activation and ALI through the STAT1 and NF-κB signaling pathways.

Ginsenoside-Rg2 exerts anti-cancer effects through ROS-mediated AMPK activation associated mitochondrial damage and oxidation in MCF-7 cells.

In this study, we investigated the anti-cancer effects of ginsenoside Rg2 (G-Rg2) and its underlying signaling pathways in breast cancer (BC) cells. G-Rg2 significantly induced cytotoxicity and reactive oxygen species (ROS) production in MCF-7 cells among various types of BC cells including HCC1428, T47D, and BT-549. G-Rg2 significantly inhibited protein and mRNA expression of cell cycle G1-S phase regulators, including p-Rb, cyclin D1, CDK4, and CDK6, whereas it enhanced the protein and mRNA expression of cell cycle arrest and apoptotic molecules including cleaved PARP, p21, p27, p53 and Bak through ROS production. These effects were abrogated by the antioxidant N-acetyl-I-cysteine, or NADPH oxidase inhibitors, such as diphenyleneiodonium chloride and apocynin. Interestingly, G-Rg2 induced mitochondrial damage by reducing the membrane potential. G-Rg2 further activated the ROS-sensor protein, AMPK and downstream targets of AMPK activation, including PGC-1α, FOXO1, and IDH2, and downregulated mTOR activation and antioxidant response element-driven luciferase activity. Together, our data demonstrate that G-Rg2 mediates anti-cancer effects by activating cell cycle arrest and signaling pathways related to mitochondrial damage-induced ROS production and apoptosis.

Protective effects of ginsenoside-Rg2 and -Rh1 on liver function through inhibiting TAK1 and STAT3-mediated inflammatory activity and Nrf2/ARE-mediated antioxidant signaling pathway.

Systemic or hepatic inflammation is caused by intraperitoneal application of lipopolysaccharide (LPS). In this study, we investigated anti-inflammatory and antioxidant properties of combination of ginsenoside-Rg2 (G-Rg2) and -Rh1 (G-Rh1) on liver function under LPS challenging. We first confirmed that G-Rg2 and -Rh1 at 100 µg/ml did not show cytotoxicity in HepG2 cells. G-Rg2 and -Rh1 treatment significantly inhibited activation of STAT3 and TAK1, and inflammatory factors including iNOS, TNF-α, and IL-1ß in peritoneal macrophages. In HepG2 cells, G-Rg2 and -Rh1 treatment inhibited activation of STAT3 and TAK1/c-Jun N-terminal kinase, and down-regulated nuclear translocation of NF-κB transcription factor. In addition, LPS-induced mitochondrial dysfunction was restored by treatment with G-Rg2 and -Rh1. Interestingly, pretreatment with G-Rg2 and -Rh1 effectively inhibited mitochondrial damage-mediated ROS production induced by LPS stimulation, and alterations of Nrf2 nuclear translocation and ARE promotor activity were involved in G-Rg2 and -Rh1 effects on balancing ROS levels. In liver tissues of LPS-treated mice, G-Rg2 and -Rh1 treatment protected liver damages and increased Nrf2 expression while reducing CD45 expression. Taken together, G-Rg2 and -Rh1 exerts a protective effect on liver function by increasing antioxidant through Nrf2 and anti-inflammatory activities through STAT3/TAK1 and NF-κB signaling pathways in liver cells and macrophages.

Ginsenoside-Rg2 affects cell growth via regulating ROS-mediated AMPK activation and cell cycle in MCF-7 cells.

BACKGROUND: Ginsenoside-Rg2 (G-Rg2) is a protopanaxatriol-type ginsenoside isolated from ginseng. It has been found to exhibit various pharmacological effects, including antioxidant, anti-inflammatory, and anticancer effects. PURPOSE: This study aimed to investigate the anticancer effects of G-Rg2 on estrogen receptor-positive MCF-7 breast cancer (BC) cells, and the underlying mechanisms involving in reactive oxygen species (ROS) production. STUDY DESIGN/METHODS: Cell viability, cell cycle distribution, apoptosis, and ROS production were measured following exposure to G-Rg2. The protein expression levels of p-ERK1/2, p-Akt, PARP, p-Rb, cyclin D1, CDK6, and p-AMPK were quantified using western blot analysis. The in vivo activity of G-Rg2 was assessed in a xenograft model. Immunohistochemistry staining for p-Rb and p-AMPK was performed in tumor tissues. RESULTS: G-Rg2 significantly decreased cell viability but increased cell apoptosis. In MCF-7 cells, G-Rg2 increased ROS production by inhibiting ERK1/2 and Akt activation. G-Rg2-induced ROS induced G0/G1 cell cycle arrest and AMPK phosphorylation. In the xenograft model, the 5 mg/kg G-Rg2-treated group showed decreased tumor volume and weight, similar to the 5 mg/kg 4-OHT-treated group, compared to the control group. Immunohistochemistry staining showed that G-Rg2 treatment decreased Rb phosphorylation, while increasing AMPK phosphorylation in tumor tissues. CONCLUSION: G-Rg2 has potential anticancer effects by increasing the ROS-AMPK signaling pathway and inhibiting ERK1/2 and Akt activation-mediated cell proliferation and cell cycle progression in MCF-7 BC cells.

Therapeutic effects of ginsenosides on breast cancer growth and metastasis.

Breast cancer is the most common cause of cancer-related deaths among women worldwide. Thus, the development of new and effective low-toxicity drugs is vital. The specific characteristics of breast cancer have allowed for the development of targeted therapy towards each breast cancer subtype. Nevertheless, increasing drug resistance is displayed by the changing phenotype and microenvironments of the tumor through mutation or dysregulation of various mechanisms. Recently, emerging data on the therapeutic potential of biocompounds isolated from ginseng have been reported. Therefore, in this review, various roles of ginsenosides in the treatment of breast cancer, including apoptosis, autophagy, metastasis, epithelial-mesenchymal transition, epigenetic changes, combination therapy, and drug delivery system, have been discussed.

Feasibility of a 12 Week Physical Intervention to Prevent Cognitive Decline and Disability in the At-Risk Elderly Population in Korea.

There is a need for measures that can prevent the onset of dementia in the rapidly aging population. Reportedly, sustained physical exercise can prevent cognitive decline and disability. This study aimed to assess the feasibility of a 12-week physical exercise intervention (PEI) for delay of cognitive decline and disability in the at-risk elderly population in Korea. Twenty-six participants (aged 67.9 ± 3.6 years, 84.6% female) at risk of dementia were assigned to facility-based PEI (n = 15) or home-based PEI (n = 11). The PEI program consisted of muscle strength training, aerobic exercise, balance, and stretching using portable aids. Feasibility was assessed by retention and adherence rates. Physical fitness/cognitive function were compared before and after the PEI. Retention and adherence rates were 86.7% and 88.3%, respectively, for facility-based PEI and 81.8% and 62.3% for home-based PEI. No intervention-related adverse events were reported. Leg strength/endurance and cardiopulmonary endurance were improved in both groups: 30 s sit-to-stand test (facility-based, p = 0.002; home-based, p = 0.002) and 2 -min stationary march (facility-based, p = 0.001; home-based, p = 0.022). Cognitive function was improved only after facility-based PEI (Alzheimer's Disease Assessment Scale-cognitive total score, p = 0.009; story memory test on Literacy Independent Cognitive Assessment, p = 0.026). We found that, whereas our PEI is feasible, the home-based program needs supplementation to improve adherence.