Abnormal Silicon Etching Behaviors in Nanometer-Sized Channels.

Modern semiconductor fabrication is challenged by difficulties in overcoming physical and chemical constraints. A major challenge is the wet etching of dummy gate silicon, which involves the removal of materials inside confined spaces of a few nanometers. These chemical processes are significantly different in the nanoscale and bulk. Previously, electrical double-layer formation, bubble entrapment, poor wettability, and insoluble intermediate precipitation have been proposed. However, the exact suppression mechanisms remain unclear due to the lack of direct observation methods. Herein, we investigate limiting factors for the etching kinetics of silicon with tetramethylammonium hydroxide at the nanoscale by using liquid-phase transmission electron microscopy, three-dimensional electron tomography, and first-principles calculations. We reveal suppressed chemical reactions, unstripping phenomena, and stochastic etching behaviors that have never been observed on a macroscopic scale. We expect that solutions can be suggested from this comprehensive insight into the scale-dependent limiting factors of fabrication.

A bipedicled keystone perforator island flap: Pedicle division technique with enhanced advancement potential for chronic wound coverage.

Since the first description of the keystone perforator island flap (KPIF) in 2003, several modifications have been suggested to enhance its coverage ability. However, locoregional flaps have limited its use in chronic wounds due to decreased elasticity around the defect. We investigated the use of a bipedicled KPIF (bKPIF), which covers a defect while completely elevating the median part of the flap from the fascia. A retrospective chart review of 20 consecutive patients who underwent classical type I KPIF (n = 10) or bKPIF (n = 10) reconstruction from June 2020 to December 2022 was performed. Baseline characteristics, indications, operative details, healing time, and complications were analyzed and compared between the two groups. The average defect size was 30 cm2 in type I KPIF and 36.6 cm2 in bKPIF, and an average flap size of 86.5 cm2 was covered in type I KPIF, larger than bKPIF at 73.8 cm2. The flap/defect ratio was significantly lower in the bKPIF group (p < 0.02), with an average of only 55% pedicular area. The average advancement distance in the bKPIF group was 1.85 cm (standard deviation 0.78) greater than that in the type 1 KPIF group. There was no significant difference between the groups in terms of operation time, complete healing time, and complications. All ten bKPIFs were successful without any flap necrosis. Even though the mean pedicular area in the bKPIF group was nearly half compared with that in the type I KPIF group, it was sufficient to perfuse the entire flap without any major complications. This novel technique using bKPIF has potential clinical relevance, as evidenced by the enhanced ability to cover chronic defects with severe scarring. Lateralizing the hotspots to the bilateral corners of the flap is the mechanism that facilitates this potential.

Comparative transcriptome analysis of periodontitis and peri-implantitis in human subjects.

BACKGROUND: Peri-implantitis is similar to periodontitis, but there are some differences. For the effective control of peri-implantitis, it is necessary to clarify its similarities and differences with periodontitis in terms of gene expression. METHODS: This cross-sectional study included 20 participants (10 healthy subjects and 10 patients with periodontitis and peri-implantitis). Gingival tissue samples (10 healthy, 10 periodontitis, and 10 peri-implantitis tissues) were collected, RNAs were extracted, and RNA sequencing and analysis were performed. RESULTS: Differentially expressed gene (DEG) analysis identified 757 upregulated and 159 downregulated genes common between periodontitis and peri-implantitis. Periodontitis tissues uniquely showed 186 overexpressed and 22 suppressed genes compared with peri-implantitis and healthy tissues, while peri-implantitis had 1974 and 642, respectively. Each common and unique differential gene set showed distinct enriched biological features between periodontitis and peri-implantitis after the pathway enrichment analysis. The expression pattern of selected DEGs focused on the representability of the disease was validated by RT-qPCR. CONCLUSIONS: Although periodontitis and peri-implantitis showed common gene expression that was clearly differentiated from healthy conditions, there were also unique gene patterns that were differentially expressed only in peri-implantitis. These findings will help elucidate the mechanisms involved in the progression of peri-implantitis.

Comprehensive Clinical Characterization of Decade-Long Survivors of Metastatic Breast Cancer.

BACKGROUND: Elucidating the clinical features of metastatic breast cancer (MBC) patients with an exceptionally favorable prognosis may offer insights to improve the survival of more typical patients. METHODS: We collected comprehensive real-world data on clinicopathologic characteristics, treatments, and outcomes of 110 consecutive MBC patients who survived for over ten years from the clinical data warehouse of Samsung Medical Center. RESULTS: The cohort included 54 hormone receptor (HR)-positive/HER2-negative (HR+/HER2-), 21 HR+/HER2+, 16 HR-/HER2+, and 14 triple-negative breast cancer (TNBC) patients. The median age at MBC diagnosis was 48.5 years. Approximately 70% of patients initially had a single-organ metastasis. The most common site of metastasis was the lung (46.4%), followed by distant lymph nodes (37.3%). During a median follow-up of 14.6 years, the median duration of systemic therapy was 11, 8.4, 7.3, and 0.8 years in the HR+/HER2-, HR+/HER2+, HR-/HER2+, and TNBC subgroups, respectively. Seven HER2+ and ten TNBC patients received systemic treatment for less than two years and remained treatment-free for most of the follow-up period, suggesting a potential chance of cure. The TNBC subtype (p < 0.001) and local treatment with curative intent within 1 year of MBC diagnosis (p = 0.002) were significantly associated with long-term treatment-free survival. The survival of HER2+ MBC and TNBC patients, but not that of HR+/HER2- patients, plateaued approximately 13 years after MBC diagnosis. CONCLUSIONS: A small subset of patients with HER2+ MBC and metastatic TNBC may be curable with multimodality therapy. Prospective studies integrating clinical and genomic data may identify unique clinicogenomic features of MBC patients who can achieve durable disease control without prolonged chemotherapy.

The effect of oral bacterial infection on DNA damage response in host cells.

Maintaining and transferring intact genomes from one generation to another plays a pivotal role in all living organisms. DNA damage caused by numerous endogenous and exogenous factors must be adequately repaired, as unrepaired and accumulated DNA mutations can cause severe deleterious effects, such as cell death and cancer. To prevent adverse consequences, cells have established DNA damage response mechanisms that address different forms of DNA damage, including DNA double-strand breaks, mismatches, nucleotide excision, and base excision. Among several sources of exogenous DNA damage, bacterial infections cause inflammation in the host, generating reactive oxygen species (ROS) and causing oxidative DNA damage. Recent studies have revealed the importance of the oral microbiome in inflammation and several systemic host diseases. Dysbiosis of oral bacteria can induce chronic inflammation, which enhances ROS-induced DNA damage, and improperly repaired damage can lead to carcinogenesis. This review describes the various DNA repair pathways that are affected by chronic inflammation and the discovery of the DNA damage response induced by oral bacteria such as Porphyromonas gingivalis and Fusobacterium nucleatum.

MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1.

DNA double-strand break (DSB) repair via homologous recombination is initiated by end resection. The extent of DNA end resection determines the choice of the DSB repair pathway. Nucleases for end resection have been extensively studied. However, it is still unclear how the potential DNA structures generated by the initial short resection by MRE11-RAD50-NBS1 are recognized and recruit proteins, such as EXO1, to DSB sites to facilitate long-range resection. We found that the MSH2-MSH3 mismatch repair complex is recruited to DSB sites through interaction with the chromatin remodeling protein SMARCAD1. MSH2-MSH3 facilitates the recruitment of EXO1 for long-range resection and enhances its enzymatic activity. MSH2-MSH3 also inhibits access of POLθ, which promotes polymerase theta-mediated end-joining (TMEJ). Collectively, we present a direct role of MSH2-MSH3 in the initial stages of DSB repair by promoting end resection and influencing the DSB repair pathway by favoring homologous recombination over TMEJ.

METTL3 regulates alternative splicing of cell cycle-related genes via crosstalk between mRNA m6A modifications and splicing factors.

N6-methyladenosine (m6A) modification in RNA affects various aspects of RNA metabolism and regulates gene expression. This modification is modulated by many regulatory proteins, such as m6A methyltransferases (writers), m6A demethylases (erasers), and m6A-binding proteins (readers). Previous studies have suggested that alterations in m6A regulatory proteins induce genome-wide alternative splicing in many cancer cells. However, the functional effects and molecular mechanisms of m6A-mediated alternative splicing have not been fully elucidated. To understand the consequences of this modification on RNA splicing in cancer cells, we performed RNA sequencing and analyzed alternative splicing patterns in METTL3-knockdown osteosarcoma U2OS cells. We detected 1,803 alternatively spliced genes in METTL3-knockdown cells compared to the controls and found that cell cycle-related genes were enriched in differentially spliced genes. A comparison of the published MeRIP-seq data for METTL14 with our RNA sequencing data revealed that 70-87% of alternatively spliced genes had an m6A peak near 1 kb of alternative splicing sites. Among the 19 RNA-binding proteins enriched in alternative splicing sites, as revealed by motif analysis, expression of SFPQ highly correlated with METTL3 expression in 12,839 TCGA pan-cancer patients. We also found that cell cycle-related genes were enriched in alternatively spliced genes of other cell lines with METTL3 knockdown. Taken together, we suggest that METTL3 regulates m6A-dependent alternative splicing, especially in cell cycle-related genes, by regulating the functions of splicing factors such as SFPQ.

Effect of Substitutional Oxygen on Properties of Ti3 C2 Tx MXene Produced Using Recycled TiO2 Source.

MXenes are an emerging class of 2D materials with unique properties including metallic conductivity, mechanical flexibility, and surface tunability, which ensure their utility for diverse applications. However, the synthesis of MXenes with high crystallinity and atomic stoichiometry in a low-cost process is still challenging because of the difficulty in controlling the oxygen substitute in the precursors and final products of MXenes, which limits their academic understanding and practical applications. Here, a novel cost-effective method is reported to synthesize a highly crystalline and stoichiometric Ti3 C2 Tx MXene with minimum substitutional oxygen impurities by controlling the amount of excess carbon and time of high-energy milling in carbothermal reduction of recycled TiO2 source. The highest used content (2 wt%) of excess-carbon yields TiC with the highest carbon content and minimal oxygen substitutes, which leads to the Ti3 AlC2 MAX phase with improved crystallinity and atomic stoichiometry, and finally Ti3 C2 Tx MXene with the highest electrical conductivity (11738 S cm-1 ) and superior electromagnetic shielding effectiveness. Additionally, the effects of carbon content and substitutional oxygen on the physical properties of TiC and Ti3 AlC2 are elucidated by density-functional-theory calculations. This inexpensive TiO2 -based method of synthesizing high-quality Ti3 C2 Tx MXene can facilitate large-scale production and thus accelerate global research on MXenes.

Role of Oxygen in the Ti3AlC2 MAX Phase in the Oxide Formation and Conductivity of Ti3C2-Based MXene Nanosheets.

Ti3C2Tx MXene, a two-dimensional transition metal carbide, has attracted substantial interest due to its unique physical properties and a wide range of potential applications. Although the properties of devices using MXene have been substantially enhanced in recent years, it is not fully understood how the oxygen concentration in Ti3AlC2 MAX affects oxide formation in Ti3C2-based MXene nanosheets and their fundamental properties. To this end, we compared two types of MAX phases: MAX with low oxygen content (LO-MAX) and MAX synthesized by a conventional process. Since the conventional MAX synthesis employs metal (Ti) as a primary material, it is referred to as metal-based MAX (MB-MAX) from here. The oxygen content of the LO-MAX was only 0.56 wt %, which was about 20% compared to that of MAX synthesized using conventional methods. We compared the properties of MXene nanosheets prepared from the LO-MAX with MXene nanosheets obtained from the MB-MAX. Microscopic and chemical analyses revealed smooth and wrinkle-free morphology and small amounts of oxygen in MXene nanosheets prepared from LO-MAX (LO-MXene). The LO-MXene nanosheet film exhibited an exceptionally high conductivity of 10,540 S/cm and an ultralow surface roughness of 1.7 nm, which originated from inhibited surface oxide formation. Moreover, the inhibition of oxide formation strengthened the function of -O or -OH groups on the surface of MXene, thereby facilitating strong hydrogen bonding to the polymer with hydroxyl groups. To clearly reveal these properties, we prepared a pressure sensor by coating these MXene nanosheets on nylon/polyester fibers. The fabricated sensor exhibited a high sensitivity of up to 85.6/kPa and excellent stretch stability and reliability. These results clearly revealed that lowering the oxygen content in MAX can make a decisive contribution to improving the fundamental properties of MXene nanosheets prepared therefrom.

Regulation of BRCA1 stability through the tandem UBX domains of isoleucyl-tRNA synthetase 1.

Aminoacyl-tRNA synthetases (ARSs) have evolved to acquire various additional domains. These domains allow ARSs to communicate with other cellular proteins in order to promote non-translational functions. Vertebrate cytoplasmic isoleucyl-tRNA synthetases (IARS1s) have an uncharacterized unique domain, UNE-I. Here, we present the crystal structure of the chicken IARS1 UNE-I complexed with glutamyl-tRNA synthetase 1 (EARS1). UNE-I consists of tandem ubiquitin regulatory X (UBX) domains that interact with a distinct hairpin loop on EARS1 and protect its neighboring proteins in the multi-synthetase complex from degradation. Phosphomimetic mutation of the two serine residues in the hairpin loop releases IARS1 from the complex. IARS1 interacts with BRCA1 in the nucleus, regulates its stability by inhibiting ubiquitylation via the UBX domains, and controls DNA repair function.

Mesenchymal stem cells target microglia via galectin-1 production to rescue aged mice from olfactory dysfunction.

Olfactory loss has been considered as the earliest complication for the aging process while underlying mechanisms and therapeutic strategies remain unclear. Given the correlation between microglial activation and olfactory dysfunction, here we investigated whether the immunomodulatory action of mesenchymal stem cells (MSCs) can rescue the olfactory impairment in old mice. The intranasal delivery of MSCs limited microglial activation and neuronal apoptosis in the olfactory bulb (OB), leading to improvement in olfaction. MSCs down-regulated the proportion of CD86+ microglia and prevented the maturation of cathepsin S, one of the inflammatory mediators in olfactory impairment, via the suppression of p38 MAPK signaling. Notably, old astrocytes could not prevent excessive microgliosis because the endogenous production of Galectin-1 (Gal1), one of the key microglia regulators secreted by astrocytes, was not sufficiently upregulated in the aged brain despite the presence of reactive astrogliosis. Considering that Gal1 is known as a potent paracrine factor of MSCs, we investigated whether MSC-derived Gal1 could compensate for defective astrocyte function in terms of microglial regulation. MSCs and their culture supernatant (MSC-CM) could regulate the direction of microglial differentiation by impeding the polarization towards the pro-inflammatory M1 type; notably, a selective Gal1 inhibitor OTX008 could hinder this phenomenon, indicating that Gal1 is involved in immunomodulation exerted by MSCs. Also, acute microglial activation within the OB upon LPS infusion was attenuated by MSC-CM in a Gal1-dependent manner. Our study demonstrates the therapeutic benefit of MSCs on age-related olfactory dysfunction and suggests Gal1 as a key mediator of the anti-inflammatory action of MSCs.

Improved Prediction of Survival Outcomes Using Residual Cancer Burden in Combination With Ki-67 in Breast Cancer Patients Underwent Neoadjuvant Chemotherapy.

We developed a model for improving the prediction of survival outcome using postoperative Ki-67 value in combination with residual cancer burden (RCB) in patients with breast cancer (BC) who underwent neoadjuvant chemotherapy (NAC). We analyzed the data from BC patients who underwent NAC between 2010 and 2019 at Samsung Medical Center and developed our residual proliferative cancer burden (RPCB) model using semi-quantitative Ki-67 value and RCB class. The Cox proportional hazard model was used to develop our RPCB model according to disease free survival (DFS) and overall survival (OS). In total, 1,959 patients were included in this analysis. Of 1,959 patients, 905 patients were excluded due to RCB class 0, and 32 were due to a lack of Ki-67 data. Finally, an RPCB model was developed using data from 1,022 patients. The RPCB score was calculated for DFS and OS outcomes, respectively (RPCB-DFS and RPCB-OS). For further survival analysis, we divided the population into 3 classes according to the RPCB score. In the prediction of DFS, C-indices were 0.751 vs 0.670 and time-dependent areas under the receiver operating characteristic curves (AUCs) at 3-year were 0.740 vs 0.669 for RPCB-DFS and RCB models, respectively. In the prediction of OS, C-indices were 0.819 vs 0.720 and time-dependent AUCs at 3-year were 0.875 vs 0.747 for RPCB-OS and RCB models, respectively. The RPCB model developed using RCB class and semi-quantitative Ki-67 had superior predictive value for DFS and OS compared with that of RCB class. This prediction model could provide the basis to decide risk-stratified treatment plan for BC patients who had residual disease after NAC.

Crosstalk between different DNA repair pathways for DNA double strand break repairs.

DNA double strand breaks (DSBs) are the most threatening type of DNA lesions and must be repaired properly in order to inhibit severe diseases and cell death. There are four major repair pathways for DSBs: non-homologous end joining (NHEJ), homologous recombination (HR), single strand annealing (SSA) and alternative end joining (alt-EJ). Cells choose repair pathway depending on the cell cycle phase and the length of 3' end of the DNA when DSBs are generated. Blunt and short regions of the 5' or 3' overhang DNA are repaired by NHEJ, which uses direct ligation or limited resection processing of the broken DNA end. In contrast, HR, SSA and alt-EJ use the resected DNA generated by the MRN (MRE11-RAD50-NBS1) complex and C-terminal binding protein interacting protein (CtIP) activated during the S and G2 phases. Here, we review recent findings on each repair pathway and the choice of repair mechanism and highlight the role of mismatch repair (MMR) protein in HR.

Melatonin and verteporfin synergistically suppress the growth and stemness of head and neck squamous cell carcinoma through the regulation of mitochondrial dynamics.

The prevalence of head and neck squamous cell carcinoma (HNSCC) has continued to rise for decades. However, drug resistance to chemotherapeutics and relapse, mediated by cancer stem cells (CSCs), remains a significant impediment in clinical oncology to achieve successful treatment. Therefore, we focused on analyzing CSCs in HNSCC and demonstrated the effect of melatonin (Mel) and verteporfin (VP) on SCC-25 cells. HNSCC CSCs were enriched in the reactive oxygen species-low state and in sphere-forming cultures. Combination treatment with Mel and VP decreased HNSCC viability and increased apoptosis without causing significant damage to normal cells. Sphere-forming ability and stem cell population were reduced by co-treatment with Mel and VP, while mitochondrial ROS level was increased by the treatment. Furthermore, the expression of mitophagy markers, parkin and PINK1, was significantly decreased in the co-treated cells. Mel and VP induced mitochondrial depolarization and inhibited mitochondrial function. Parkin/TOM20 was localized near the nucleus and formed clusters of mitochondria in the cells after treatment. Moreover, Mel and VP downregulated the expression of markers involved in epithelial-mesenchymal transition and metastasis. The migration capacity of cells was significantly decreased by co-treatment with Mel and VP, accompanied by the down-regulation of MMP-2 and MMP-9 expression. Taken together, these results indicate that co-treatment with Mel and VP induces mitochondrial dysfunction, resulting in the apoptosis of CSCs. Mel and VP could thus be further investigated as potential therapies for HNSCC through their action on CSCs.

Elevated Level of Nerve Growth Factor (NGF) in Serum-Derived Exosomes Predicts Poor Survival in Patients with Breast Cancer Undergoing Neoadjuvant Chemotherapy.

Neoadjuvant chemotherapy (NAC) is a standard treatment strategy for patients with locally advanced breast cancer (LABC). However, there are no established predictors of chemosensitivity and survival in LABC patients who undergo NAC. Many studies have demonstrated that exosomes and cytokines are important players in intercellular communication between tumors and their environments, and are involved in chemotherapy resistance. Recently, it was reported that cytokines can be packaged into exosomes, but whether exosomal cytokines serve as biomarkers in breast cancer patients is still unclear. In this study, we examined the roles of cytokines in both serum and exosomes as prognostic biomarkers for long-term outcomes in patients with breast cancer who undergo NAC. We isolated exosomes from the blood of 129 patients with early breast cancer who were receiving neoadjuvant chemotherapy between 2008 and 2011 at Samsung Medical Center. The levels of cytokines and growth factors in serum and exosomes were measured with ProcartaPlex immune-related panels. We investigated correlations between clinic-pathologic variables and patient survival, and Cox proportional hazards regression analysis was performed for prognostic evaluation. We detected significant differences in expression patterns between serum cytokines and exosomal cytokines. In both serum and exosomes, many cytokines were positively correlated with age. In univariate analysis, patients with high serum IP-10, serum MMP-1, and exosomal NGF had shorter overall survival. Exosomal NGF showed significantly poorer overall survival in multivariate analysis. These findings suggest that exosomal NGF is useful for identifying patients with poor survival outcomes.

Which Clinicopathologic Parameters Suggest Primary Resistance to Palbociclib in Combination With Letrozole as the First-Line Treatment for Hormone Receptor-Positive, HER2-Negative Advanced Breast Cancer?

In this study, we evaluated clinical parameters to predict the primary resistance of palbociclib in combination with endocrine therapy as the first-line treatment in patients with hormone receptor (HR)+, human epidermal growth factor receptor 2 (HER2)- metastatic breast cancer (MBC). We performed a data analysis of patients diagnosed with HR+, HER2-MBC who received palbociclib plus letrozole as the first-line treatment in the metastatic setting from the clinical data warehouse in Samsung Medical Center. In this study, 305 patients were included in the final data analysis. The median follow-up duration was 31 months, and we observed 123 cases of disease progression. The median progression-free survival (PFS) was 28.7 months, and 38 patients (12.5%) had less than a 6-month PFS. The multivariate analysis suggested that primary resistance to adjuvant endocrine therapy (ET) (hazard ratio: 1.91), presence of liver metastasis (hazard ratio: 2.17), initial elevation of serum CA-15-3 (hazard ratio: 1.99), weak positivity of estrogen receptor (ER) (hazard ratio: 2.28), Ki-67 3+ or 4+ (hazard ratios: 2.58 and 10.28), and presence of mutation (hazard ratio: 9.59) were associated with a short PFS duration. A further prediction model was developed with data from 256 patients and 33 cases of disease progression in 6 months. This model included five factors-primary resistance to adjuvant ET (odds ratio, OR: 1.14), liver metastasis (OR: 1.56), initial CA-15-3 elevation (OR: 1.51), weak ER expression (OR: 2.22), and BRCA2 mutation (OR: 2.85)-and the area under the receiver operating characteristic curve was 0.842 (95% CI: 0.775, 0.909; p < 0.001). Finally, we divided them into four risk groups according to the prediction model with the five risk factors. These four groups had different PFS (p < 0.001) and primary resistance of palbociclib with letrozole [OR of group 2 vs. group 1 (ref): 2.18 (p = 0.002), OR of group 3: 3.91 (p < 0.001), and OR of group 4: 4.25 (p < 0.001)]. We developed a prediction model of primary resistance to palbociclib with letrozole as the first-line treatment for HR+, HER2-MBC. Our prediction model might be helpful for considering the first-line treatment strategies. Further well-designed clinical trials would be warranted to validate our prediction model.

RNF126 is a positive regulator of TRAF3 ubiquitination.

Ubiquitination and deubiquitination of signaling molecules are critical regulatory mechanisms in various biological contexts such as inflammatory signaling and the DNA damage response. Thus, finely tuned regulation of protein ubiquitination is essential for maintaining cellular homeostasis. Here, we showed that the RING finger protein RNF126 interacts with TRAF3 and promotes its K63-linked polyubiquitination, which is a crucial step in the TRAF3-dependent antiviral response. We found that RNF126 also interacts with OTUB1, a deubiquitinating enzyme that negatively regulates K63-linked ubiquitination of TRAF3. RNF126 promotes ubiquitination of OTUB1, leading to reduced deubiquitinating activity toward TRAF3. Moreover, RNF126 promotes ubiquitination of OTUB1 on cysteine 91, which is reportedly required for its catalytic activity. Taken together, our results suggest that RNF126 positively regulates the antiviral response by directly promoting K63-linked polyubiquitination of TRAF3 and by reducing OTUB1 activity.

One-Way Continuous Deposition of Monolayer MXene Nanosheets for the Formation of Two Confronting Transparent Electrodes in Flexible Capacitive Photodetector.

MXenes based on titanium carbide are promising next-generation transparent electrode materials due to their high metallic conductivity, optical transparency, mechanical flexibility, and abundant hydrophilic surface functionality. MXene electrodes offer a much wider conductive surface coverage than metal nanowires, thereby gaining popularity as flexible electrode materials in supercapacitors and energy devices. However, given that monolayer MXene nanosheets are only a few nanometers thick, meticulous surface treatments and deposition technologies are required for a practical implementation of these transparent electrodes. Unfortunately, a capacitor produced by forming high-quality transparent MXene electrodes on both sides of a film has not yet been reported. We report the successful development of a one-way continuous deposition technology to form high-quality MXene nanosheet-based transparent electrodes on both surfaces of a polymer film without large physical stresses on the MXene nanosheets. One transparent electrode was formed by transferring MXene nanosheets predeposited on a temporary glass substrate to the film surface, while the other was directly deposited on the exposed film surface. The Ti3AlC2 precursor (MAX) was synthesized via a spark plasma sintering crystallization, and the MXene nanosheets were prepared via a subsequent Al-selective etching and delamination. We used this material to implement a capacitive photodetector consisting of two layers of opposing transparent electrodes. The flexible photodetector was based on poly(vinyl butyral) (PVB), which was solidly bonded with MXene nanosheets to serve as a free-standing binder for the Cu-doped ZnS semiconductor particles. The fabricated device exhibited excellent mechanical stability due to the high affinity between the MXene nanosheets and PVB. Furthermore, the device exhibited an initial capacitance of 2 nF, photosensitivity of 12.5 µF/W, and rise and decay times of 0.031 and 0.751 s, respectively. All these parameters were 1 to 2 orders of magnitude higher or faster than reported capacitive photodetectors. Overall, the proposed approach resolves the core issues associated with existing metal nanowire-based electrodes, and it is a breakthrough in the development of next-generation flexible devices comprising two layers of confronting transparent electrodes.

Clerodendrum trichotomum extract improves metabolic derangements in high fructose diet-fed rats.

Clerodendrum trichotomum has been reported to possess beneficial properties for human health, but its effects on metabolic syndrome have not been reported. In this study, we investigated the effect of C. trichotomum leaf extract (CT) on the metabolic derangements induced by a high-fructose (HF) diet. Sprague-Dawley rats were fed with a 46% carbohydrate diet (HC group), 60% high-fructose diet (HF group), or HF diet supplemented with CT (500 mg/kg of body weight/day, CT group) via drinking water for 16 weeks. Results showed that CT alleviated HF diet-induced insulin resistance, dyslipidemia, and hepatic steatosis In liver tissues, CT affected the signaling pathways of AMP-activated protein kinase, peroxisome proliferator-activated receptor α (PPARα), and sterol regulatory element binding protein 1. CT enriched the genes that were mainly involved in cytokine-cytokine receptor interaction, PPAR, PI3K-Akt signaling pathways, and fatty acid metabolism pathway. These results suggest that CT is a promising therapeutic against metabolic disorders.