Fabrication and Characterization of Electrospun Cu-Doped TiO2 Nanofibers and Enhancement of Photocatalytic Performance Depending on Cu Content and Electron Beam Irradiation.

Titanium dioxide (TiO2) is a widely studied material with many attractive properties such as its photocatalytic features. However, its commercial use is limited due to issues such as deactivation in the visible spectrum caused by its wide bandgap and the short lifetime of photo-excited charge carriers. To overcome these challenges, various modifications could be considered. In this study, we investigated copper doping and electron beam treatment. As-spun TiO2 nanofibers were fabricated by electrospinning a TiO2 sol, which obtained viscosity through a polyvinylpyrrolidone (PVP) matrix. Cu-doped TiO2 nanofibers with varying dopant concentrations were synthesized by adding copper salts. Then, the as-spun nanofibers were calcined for crystallization. To evaluate photocatalytic performance, a photodegradation test of methylene blue aqueous solution was performed for 6 h. Methylene blue concentration was measured over time using UV-Vis spectroscopy. The results showed that Cu doping at an appropriate concentration and electron-beam irradiation showed improved photocatalytic efficiency compared to bare TiO2 nanofibers. When the molar ratio of Cu/Ti was 0.05%, photodegradation rate was highest, which was 10.39% higher than that of bare TiO2. As a result of additional electron-beam treatment of this sample, photocatalytic efficiency improved up to 8.93% compared to samples without electron-beam treatment.

Unlocking the Potential of Porous Bi2Te3-Based Thermoelectrics Using Precise Interface Engineering through Atomic Layer Deposition.

Porous thermoelectric materials offer exciting prospects for improving the thermoelectric performance by significantly reducing the thermal conductivity. Nevertheless, porous structures are affected by issues, including restricted enhancements in performance attributed to decreased electronic conductivity and degraded mechanical strength. This study introduces an innovative strategy for overcoming these challenges using porous Bi0.4Sb1.6Te3 (BST) by combining porous structuring and interface engineering via atomic layer deposition (ALD). Porous BST powder was produced by selectively dissolving KCl in a milled mixture of BST and KCl; the interfaces were engineered by coating ZnO films through ALD. This novel architecture remarkably reduced the thermal conductivity owing to the presence of several nanopores and ZnO/BST heterointerfaces, promoting efficient phonon scattering. Additionally, the ZnO coating mitigated the high resistivity associated with the porous structure, resulting in an improved power factor. Consequently, the ZnO-coated porous BST demonstrated a remarkable enhancement in thermoelectric efficiency, with a maximum zT of approximately 1.53 in the temperature range of 333-353 K, and a zT of 1.44 at 298 K. Furthermore, this approach plays a significant role in enhancing the mechanical strength, effectively mitigating a critical limitation of porous structures. These findings open new avenues for the development of advanced porous thermoelectric materials and highlight their potential for precise interface engineering through the ALD.

Newly isolated Lactobacillus paracasei strain modulates lung immunity and improves the capacity to cope with influenza virus infection.

BACKGROUND: The modulation of immune responses by probiotics is crucial for local and systemic immunity. Recent studies have suggested a correlation between gut microbiota and lung immunity, known as the gut-lung axis. However, the evidence and mechanisms underlying this axis remain elusive. RESULTS: In this study, we screened various Lactobacillus (L.) strains for their ability to augment type I interferon (IFN-I) signaling using an IFN-α/ß reporter cell line. We identified L. paracasei (MI29) from the feces of healthy volunteers, which showed enhanced IFN-I signaling in vitro. Oral administration of the MI29 strain to wild-type B6 mice for 2 weeks resulted in increased expression of IFN-stimulated genes and pro-inflammatory cytokines in the lungs. We found that MI29-treated mice had significantly increased numbers of CD11c+PDCA-1+ plasmacytoid dendritic cells and Ly6Chi monocytes in the lungs compared with control groups. Pre-treatment with MI29 for 2 weeks resulted in less weight loss and lower viral loads in the lung after a sub-lethal dose of influenza virus infection. Interestingly, IFNAR1-/- mice did not show enhanced viral resistance in response to oral MI29 administration. Furthermore, metabolic profiles of MI29-treated mice revealed changes in fatty acid metabolism, with MI29-derived fatty acids contributing to host defense in a Gpr40/120-dependent manner. CONCLUSIONS: These findings suggest that the newly isolated MI29 strain can activate host defense immunity and prevent infections caused by the influenza virus through the gut-lung axis. Video Abstract.

Upcycling green carbon black as a reinforcing agent for styrene-butadiene rubber materials.

This study reports the effects of recovered carbon black (produced in a clean and sustainable way) as a reinforcing agent on the physicochemical properties of a styrene-butadiene rubber (SBR) matrix. SBR-based composite materials are prepared with recovered green carbon black (GCB), and these are thoroughly compared to the composite materials containing conventional virgin carbon black (VCB) (produced by the incomplete combustion of petroleum products). The GCB-SBR composite materials generally show detectably inferior properties compared to the VCB-SBR composite under the same preparation conditions due to the limited functionality of the GCB filler. However, the introduction of a small amount of crosslinker, acrylate-functionalized POSS (polyhedral oligomeric silsesquioxane), into the GCB-SBR composite materials effectively enhances the overall physical properties, including the tensile strength, fracture elongation, and thermal stability. The degree of the crosslinking efficiency, thermal stability, and mechanical properties of the composite materials are optimized and thoroughly examined to demonstrate the possibility of replacing typical VCB with GCB, which can allow for upcycling the inexpensive and ecofriendly carbon black materials as effective reinforcing fillers.

Hypoxia-Responsive Azobenzene-Linked Hyaluronate Dot Particles for Photodynamic Tumor Therapy.

In this study, we developed ultra-small hyaluronate dot particles that selectively release phototoxic drugs into a hypoxic tumor microenvironment. Here, the water-soluble hyaluronate dot (dHA) was covalently conjugated with 4,4'-azodianiline (Azo, as a hypoxia-sensitive linker) and Ce6 (as a photodynamic antitumor agent), producing dHA particles with cleavable Azo bond and Ce6 (dHA-Azo-Ce6). Importantly, the inactive Ce6 (self-quenched state) in the dHA-Azo-Ce6 particles was switched to the active Ce6 (dequenched state) via the Azo linker (-N=N-) cleavage in a hypoxic environment. In vitro studies using hypoxia-induced HeLa cells (treated with CoCl2) revealed that the dHA-Azo-Ce6 particle enhanced photodynamic antitumor inhibition, suggesting its potential as an antitumor drug candidate in response to tumor hypoxia.

LKB1 in Intestinal Epithelial Cells Regulates Bile Acid Metabolism by Modulating FGF15/19 Production.

BACKGROUND & AIMS: Liver kinase B1 (LKB1) is a master upstream protein kinase involved in nutrient sensing and glucose and lipid metabolism in many tissues; however, its metabolic role in intestinal epithelial cells (IEC) remains unclear. In this study, we investigated the regulatory role of LKB1 on bile acid (BA) homeostasis. METHODS: We generated mice with IEC-specific deletion of LKB1 (LKB1ΔIEC) and analyzed the characteristics of IEC development and BA level. In vitro assays with small interfering RNA, liquid chromatography/mass spectrometry, metagenomics, and RNA-sequencing were used to elucidate the regulatory mechanisms underlying perturbed BA homeostasis. RESULTS: LKB1 deletion resulted in abnormal differentiation of secretory cell lineages. Unexpectedly, BA pool size increased substantially in LKB1ΔIEC mice. A significant reduction of the farnesoid X receptor (FXR) target genes, including fibroblast growth factor 15/19 (FGF15/19), known to inhibit BA synthesis, was found in the small intestine (SI) ileum of LKB1ΔIEC mice. We observed that LKB1 depletion reduced FGF15/19 protein level in human IECs in vitro. Additionally, a lower abundance of bile salt hydrolase-producing bacteria and elevated levels of FXR antagonist (ie, T-ßMCA) were observed in the SI of LKB1ΔIEC mice. Moreover, LKB1ΔIEC mice showed impaired conversion of retinol to retinoic acids in the SI ileum. Subsequently, vitamin A treatment failed to induce FGF15 production. Thus, LKB1ΔIEC mice fed with a high-fat diet showed improved glucose tolerance and increased energy expenditure. CONCLUSIONS: LKB1 in IECs manages BA homeostasis by controlling FGF15/19 production.

A High-Fat Diet Activates the BAs-FXR Axis and Triggers Cancer-Associated Fibroblast Properties in the Colon.

BACKGROUND & AIMS: Dietary signals are known to modulate stemness and tumorigenicity of intestinal progenitors; however, the impact of a high-fat diet (HFD) on the intestinal stem cell (ISC) niche and its association with colorectal cancer remains unclear. Thus, we aimed to investigate how a HFD affects the ISC niche and its regulatory factors. METHODS: Mice were fed a purified diet (PD) or HFD for 2 months. The expression levels of ISC-related markers, ISC-supportive signals, and Wnt2b were assessed with real-time quantitative polymerase chain reaction, in situ hybridization, and immunofluorescence staining. RNA sequencing and metabolic function were analyzed in mesenchymal stromal cells (MSCs) from PD- and HFD-fed mice. Fecal microbiota were analyzed by 16s rRNA sequencing. Bile salt hydrolase activity and bile acid (BA) levels were measured. RESULTS: We found that expression of CD44 and Wnt signal-related genes was higher in the colonic crypts of HFD-fed mice than in those fed a PD. Within the ISC niche, MSCs were expanded and secreted predominant levels of Wnt2b in the colon of HFD-fed mice. Of note, increased energy metabolism and cancer-associated fibroblast (CAF)-like properties were found in the colonic MSCs of HFD-fed mice. Moreover, colonic MSCs from HFD-fed mice promoted the growth of tumorigenic properties and accelerated the expression of cancer stem cell (CSC)-related markers in colon organoids. In particular, production of primary and secondary BAs was increased through the expansion of bile salt hydrolase-encoding bacteria in HFD-fed mice. Most importantly, BAs-FXR interaction stimulated Wnt2b production in colonic CAF-like MSCs. CONCLUSIONS: HFD-induced colonic CAF-like MSCs play an indispensable role in balancing the properties of CSCs through activation of the BAs-FXR axis.

Exposure of Metal Oxide Nanoparticles on the Bioluminescence Process of Pu- and Pm-lux Recombinant P. putida mt-2 Strains.

Comparison of the effects of metal oxide nanoparticles (NPs; CuO, NiO, ZnO, TiO2, and Al2O3) on different bioluminescence processes was evaluated using two recombinant (Pm-lux and Pu-lux) strains of Pseudomonas putida mt-2 with same inducer exposure. Different sensitivities and responses were observed according to the type of NPs and recombinant strains. EC50 values were determined. The negative effects on the bioluminescence activity of the Pm-lux strain was greater than for the Pu-lux strains for all NPs tested. EC50 values for the Pm-lux strain were 1.7- to 6.2-fold lower (corresponding to high inhibition) than for Pu-lux. ZnO NP caused the greatest inhibition among the tested NPs in both strains, showing approximately 11 times less EC50s of CuO, which appeared as the least inhibited. Although NPs showed different sensitivities depending on the bioluminescence process, similar orders of EC50s for both strains were observed as follows: ZnO > NiO, Al2O3 > TiO2 > CuO. More detailed in-depth systematic approaches, including in the field of molecular mechanisms, is needed to evaluate the accurate effect mechanisms involved in both bioluminescence metabolic processes.

Comparison of ocular surface assessment and adherence between preserved and preservative-free latanoprost in glaucoma: a parallel-grouped randomized trial.

Given that nonadherence is related to subject characteristics and drug tolerance and preserved eye drops tend to be more intolerable than preservative-free ones, we conducted a phase 4, parallel-grouped, investigator-blind, active-control, randomized, multicenter study. A total of 51 patients with intraocular pressure (IOP) ≥ 15 mmHg diagnosed with open-angle glaucoma or ocular hypertension were randomly assigned to the preserved latanoprost group (n = 26) and the preservative-free latanoprost group (n = 25). The efficacy variables were corneal/conjunctival staining grade, Ocular Surface Disease Index (OSDI), adherence at 12 weeks after the first administration; corneal/conjunctival staining grade at 4 weeks; and IOP, tear break-up time (TBUT), and hyperemia score at 4 and 12 weeks. The safety variables included visual acuity and drug tolerance questionnaire results. There was no statistically significant difference in corneal/conjunctival staining grade, OSDI, or TBUT between the groups at 4 and 12 weeks. However, the adherence rate was higher and the hyperemia score was lower in the preservative-free group than in the preserved group. The severity and duration of stinging/burning sensation were lower in the preservative-free group than in the preserved group. Overall, preservative-free latanoprost showed better ocular tolerance assessed by hyperemia scores and stinging/burning symptoms following higher adherence than preserved latanoprost.

Naa20, the catalytic subunit of NatB complex, contributes to hepatocellular carcinoma by regulating the LKB1-AMPK-mTOR axis.

N-α-acetyltransferase 20 (Naa20), which is a catalytic subunit of the N-terminal acetyltransferase B (NatB) complex, has recently been reported to be implicated in hepatocellular carcinoma (HCC) progression and autophagy, but the underlying mechanism remains unclear. Here, we report that based on bioinformatic analysis of Gene Expression Omnibus and The Cancer Genome Atlas data sets, Naa20 expression is much higher in HCC tumors than in normal tissues, promoting oncogenic properties in HCC cells. Mechanistically, Naa20 inhibits the activity of AMP-activated protein kinase (AMPK) to promote the mammalian target of rapamycin signaling pathway, which contributes to cell proliferation, as well as autophagy, through its N-terminal acetyltransferase (NAT) activity. We further show that liver kinase B1 (LKB1), a major regulator of AMPK activity, can be N-terminally acetylated by NatB in vitro, but also probably by NatB and/or other members of the NAT family in vivo, which may have a negative effect on AMPK activity through downregulation of LKB1 phosphorylation at S428. Indeed, p-LKB1 (S428) and p-AMPK levels are enhanced in Naa20-deficient cells, as well as in cells expressing the nonacetylated LKB1-MPE mutant; moreover, importantly, LKB1 deficiency reverses the molecular and cellular events driven by Naa20 knockdown. Taken together, our findings suggest that N-terminal acetylation of LKB1 by Naa20 may inhibit the LKB1-AMPK signaling pathway, which contributes to tumorigenesis and autophagy in HCC.

Deacetylation by SIRT1 promotes the tumor-suppressive activity of HINT1 by enhancing its binding capacity for ß-catenin or MITF in colon cancer and melanoma cells.

Histidine triad nucleotide-binding protein 1 (HINT1), which belongs to the evolutionarily conserved HIT superfamily, has been shown to possess a tumor-suppressive function by binding to and inhibiting several oncogenic transcription factors, such as ß-catenin and microphthalmia transcription factor (MITF), in various types of cancer cells. However, the regulatory mechanism that mediates the binding capacity of HINT1 for partner transcription factors remains elusive. Here, we report that HINT1 is acetylated by CBP at K21 and K30 and deacetylated by SIRT1. Deacetylation of HINT1 by SIRT1 increases the capacity of HINT1 to bind to ß-catenin or MITF. As a result, the tumor-suppressive function of HINT1 is increased. In support of this, the deacetylation mimetic HINT1 mutant HINT1 2KR was found to significantly reduce cellular proliferation in colon cancer and melanoma cells and tumorigenesis in xenograft assays. Thus, this study reveals an acetylation-dependent regulatory mechanism that governs the tumor-suppressive function of HINT1.

Effects of the Immobilization of the Upper Extremities on Spatiotemporal Gait Parameters during Walking in Stroke Patients: A Preliminary Study.

BACKGROUND: The purpose of this study was to investigate the effects of upper extremity immobilization and consequent walking speed on spatiotemporal gait parameters in stroke patients with hemiparesis. METHODS: The following variables were assessed or measured in 29 stroke patients: age, height, weight, disease duration, Korean version of the Mini-Mental State Examination (MMSE-K), Berg balance scale (BBS-K), functional gait assessment (FGA-K), cause of the disease (type of lesion), and hemiparetic side. The measurement of gait was performed using two pressure plates of 1.5 m to create a 3 m walking distance and leaving 1.5 m of extension at both start and end, to ultimately create a 6 m walking distance that the patient could walk through. The following gait patterns were randomly selected based on card draws: self-selected walk speed (SW), self-selected walk speed with immobilized upper extremities (SWI), fast walking (FW), and fast walking with immobilized upper extremities (FWI). Each patient was assessed for four different gait patterns, with three measurements per pattern (12 gait measurements in total). RESULTS: While there were significant differences in the stride length, step width, velocity, and step length of the paretic side between self-selected walk speed (SW) and SWI, FWI did not show significant changes in any of the tested parameters. CONCLUSIONS: Immobilization of the upper extremities may affect walking at self-selected walk speeds. A comprehensive training program including upper extremity movement should be established for gait rehabilitation. Clinical Trial Registration. This trial is registered at http://cris.nih.go.kr/cris.

Enzymatic Synthesis of Glucosyl Rebaudioside A and its Characterization as a Sweetener.

Rebaudioside A was modified via glucosylation by recombinant dextransucrase of Leuconostoc lactis EG001 in Escherichia coli BL21 (DE3), forming single O-α-D-glucosyl-(1″→6') rebaudioside A with yield of 86%. O-α-D-glucosyl-(1″→6') rebaudioside A was purified using HPLC and Diaion HP-20 and its properties were characterized for possible use as a food ingredient. Almost 98% of O-α-D-glucosyl-(1″→6') rebaudioside A was dissolved after 15 days of storage at room temperature, compared to only 11% for rebaudioside A. Compared to rebaudioside A, O-α-D-glucosyl-(1″→6') rebaudioside A showed similar or improved acidic or thermal stability in commercial drinks. Thus, O-α-D-glucosyl-(1″→6') rebaudioside A could be used as a highly pure and improved sweetener with high stability in commercial drinks. PRACTICAL APPLICATION: The proposed method can be used to generate glucosyl rebaudioside A by enzymatic glucosylation. Simple glucosyl rebaudioside A exhibited high acid/thermal stability and improved sweetener in commercialized drinks. This method can be applied to obtain high value-added bioactive compounds by enzymatic modification.

Kakkalide and irisolidone alleviate 2,4,6-trinitrobenzenesulfonic acid-induced colitis in mice by inhibiting lipopolysaccharide binding to toll-like receptor-4 and proteobacteria population.

The flower of Pueraria lobata (family Fabaceae) has been clinically used in traditional Chinese medicine to counteract symptoms associated with drinking alcohol and liver injury and to alleviate inflammatory diseases. Its major constituent kakkalide is metabolized to irisolidone by gut microbiota. This research study was undertaken to understand the anti-colitis mechanism of kakkalide and irisolidone in vitro and in vivo. Kakkalide and its metabolite irisolidone inhibited lipopolysaccharide (LPS)-stimulated NF-κB activation and TNF-α expression in macrophages. They also inhibited LPS-induced phosphorylation of IRAK1 and TAK1 and activation of NF-κB by inhibiting the binding of Alexa Fluor 488-conjugated LPS in vitro. Orally administered irisolidone or kakkalide alleviated colon shortening and myeloperoxidase activity in mice with 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis. Their treatments also protected epithelial cell disruption and infiltration of CD11b+/CD11c+ cells in the colon. Furthermore, they suppressed TNBS-induced expression of M1 macrophage markers TNF-α, CD80, CD86, and Arg2 expression while the expression of M2 macrophage markers Arg1, CD163, CD206, and IL-10 was induced. They also suppressed the fecal Proteobacteria population. Overall, the anti-colitic effects of irisolidone were superior to those of kakkalide. Kakkalide and its metabolite irisolidone inhibited inflammation in vitro and in vivo by inhibiting LPS binding to toll-like receptor 4 and gut proteobacteria population.