Customizing Wettability of Defect-Rich CeO2/TiO2 Nanotube Arrays for Humidity-Resistant, Ultrafast, and Sensitive Ammonia Response.

In all their applications, gas sensors should satisfy several requirements, including low cost, reduced energy consumption, fast response/recovery, high sensitivity, and reliability in a broad humidity range. Unfortunately, the fast response/recovery and sensing reliability under high humidity conditions are often still missing, especially those working at room temperature. In this study, a humidity-resistant gas sensor with an ultrafast response/recovery rate was designed by integrating a defect-rich semiconducting sensing interface and a self-assembled monolayer (SAM) with controllable wettability. As a proof-of-concept application, ammonia (NH3), one of the atmospheric and indoor pollutants, was selected as the target gas. The decoration of interconnected defective CeO2 nanowires on spaced TiO2 nanotube arrays (NTAs) provided superior NH3 sensing performances. Moreover, we showed that manipulating the functional end group of SAMs is an efficient and simple method to adjust the wettability, by which 86% sensitivity retention with an ultrafast response (within 5 s) and a low limit of detection (45 ppb) were achieved even at 75% relative humidity and room temperature. This work provides a new route toward the comprehensive design and application of metal oxide semiconductors for trace gas monitoring under harsh conditions, such as those of agricultural, environmental, and industrial fields.

MoO2 Pump-Enhanced Flexible TiO2 Nanojungle-Based Chemiresistors for Rapid Room-Temperature Detection of H2S at Parts-per-Billion Levels.

In this study, we developed a gas sensing platform that can sensitively and specifically detect trace H2S in a high-humidity atmosphere at RT. Upon integrating a carbon nitride (C3N4) nanofilm and molybdenum dioxide (MoO2) nanosheets onto nanojungle-like TiO2 nanotube arrays (TiNTs), the fabricated chemiresistor showed rapid response (38 s)/recovery (58 s) abilities and remarkable detection sensitivity for H2S at concentrations down to 2 ppb, with an estimated detection limit of 1.13 ppb at RT and room-environmental light (REL). Importantly, the gas sensor exhibited satisfactory H2S sensing performance even in dark conditions with a response of 1.9 at 200 ppb. In this design, apart from the architectural advantages of the nanojungle-like TiNTs for accelerating the gas flow efficiency and the abundant sensing sites provided by the C3N4 film, the MoO2 nanosheets act as the essential electron pump not only for the H2S response but also for the subsequent recovery process in air. After employing the MoO2 pump onto C3N4/TiNTs, the response time and recovery time of the system are shortened to ∼35 and ∼11%, respectively. Moreover, we demonstrated the good performance of the flexible gas sensor in detecting trace H2S in human exhaled breath with good humidity resistance. These results highlight the possibility of designing chemiresistors operating in RT and REL conditions and to use these environmentally friendly TiO2-based sensors in real applications.

Rational Integration of SnMOF/SnO2 Hybrid on TiO2 Nanotube Arrays: An Effective Strategy for Accelerating Formaldehyde Sensing Performance at Room Temperature.

Formaldehyde is ubiquitously found in the environment, meaning that real-time monitoring of formaldehyde, particularly indoors, can have a significant impact on human health. However, the performance of commercially available interdigital electrode-based sensors is a compromise between active material loading and steric hindrance. In this work, a spaced TiO2 nanotube array (NTA) was exploited as a scaffold and electron collector in a formaldehyde sensor for the first time. A Sn-based metal-organic framework was successfully decorated on the inside and outside of TiO2 nanotube walls by a facile solvothermal decoration strategy. This was followed by regulated calcination, which successfully integrated the preconcentration effect of a porous Sn-based metal-organic framework (SnMOF) structure and highly active SnO2 nanocrystals into the spaced TiO2 NTA to form a Schottky heterojunction-type gas sensor. This SnMOF/SnO2@TiO2 NTA sensor achieved a high room-temperature formaldehyde response (1.7 at 6 ppm) with a fast response (4.0 s) and recovery (2.5 s) times. This work provides a new platform for preparing alternatives to interdigital electrode-based sensors and offers an effective strategy for achieving target preconcentrations for gas sensing processes. The as-prepared SnMOF/SnO2@TiO2 NTA sensor demonstrated excellent sensitivity, stability, reproducibility, flexibility, and convenience, showing excellent potential as a miniaturized device for medical diagnosis, environmental monitoring, and other intelligent sensing systems.

Single-Nanoparticle-Level Understanding of Oxidase-like Activity of Au Nanoparticles on Polymer Nanobrush-Based Proton Reservoirs.

Enzyme-mimicking nanoparticles play a key role in important catalytic processes, from biosensing to energy conversion. Therefore, understanding and tuning their performance is crucial for making further progress in biological applications. We developed an efficient and sensitive electrochemical method for the real-time monitoring of the glucose oxidase (GOD)-like activity of single nanoparticle through collision events. Using brush-like sulfonate (-SO3-)-doped polyaniline (PANI) decorated on TiO2 nanotube arrays (TiNTs-SPANI) as the electrode, we fabricated a proton reservoir with excellent response and high proton-storage capacity for evaluating the oxidase-like activity of individual Au nanoparticles (AuNPs) via instantaneous collision processes. Using glucose electrocatalysis as a model reaction system, the GOD-like activity of individual AuNPs could be directly monitored via electrochemical tests through the nanoparticle collision-induced proton generation. Furthermore, based on the perturbation of the electrical double layer of SPANI induced by proton injection, we investigated the relationship between the measured GOD-like activities of the plasmonic nanoparticles (NPs) and the localized surface plasmon resonance (LSPR) as well as the environment temperature. This work introduces an efficient platform for understanding and characterizing the catalytic activities of nanozymes at the single-nanoparticle level.

Target-Driven Z-Scheme Heterojunction Formation for ppb H2S Detection from Exhaled Breath at Room Temperature.

As a biomarker of periodontitis, sensitive and timely monitoring of hydrogen sulfide (H2S) in exhaled breath at room temperature (RT) is important for the early intervention of oral diseases. However, the required high operation temperature to achieve high sensitivity is still a technical challenge for directly monitoring exhaled breath. In this study, by integrating metal-organic frameworks (MOFs) into self-aligned TiO2 nanotube arrays (NTs), a chemiresistor gas sensor with outstanding sensitivity and selectivity was constructed for the detection of H2S at RT. The precise regulation of a Co(III)-based MOF CoBDC-NH2 (BDC-NH2 = 2-aminoterephthalic acid) not only induced more active surface for the preconcentration of the target gas but also caused a buildup of Z-scheme heterojunctions in the H2S atmosphere that induced an ultrahigh sensitivity at RT via 365 nm light-emitting diode irradiation. The response and recovery times decreased to ∼50 and ∼28%, respectively, when this system was exposed to UV light. The sensing chips based on the as-prepared TiO2/CoBDC-NH2 NTs exhibited the highest-ranking H2S sensing performance, i.e., a limit of detection of 1.3 ppb and excellent selectivity even to 100 times high concentration of interference gases, owing to the synergistic chemical environment provided by NH2-functionalized Co-MOFs and abundant photogenerated electrons provided by Z-scheme heterojunctions. This sensing chip was also used in a practical application for the timely monitoring of halitosis from direct exhaled breath. This study provides a reliable and sensitive design for clinically aiding the timely detection of H2S in a complex oral environment.

Circ-PRKCI Alleviates Lipopolysaccharide-induced Human Kidney 2 Cell Injury by Regulating miR-106b-5p/GAB1 Axis.

ABSTRACT: Circular RNAs act as vital regulators in diverse diseases. However, the investigation of circular RNAs in sepsis-engendered acute kidney injury remains dismal. We aimed to explore the effects of circular RNA protein kinase C iota (circ-PRKCI) in lipopolysaccharide (LPS)-mediated HK2 cell injury. Sepsis in vitro model was established by LPS treatment. Quantitative real-time polymerase chain reaction assay was conducted for determining the levels of circ-PRKCI, microRNA-106b-5p (miR-106b-5p), and growth factor receptor binding 2-associated binding protein 1 (GAB1). Cell viability and apoptosis were evaluated using Cell Counting Kit-8 assay and flow cytometry analysis, respectively. The concentrations of interleukin-6, interleukin-1ß, and tumor necrosis factor-α were measured with enzyme-linked immunosorbent assay kits. The levels of oxidative stress markers were determined using relevant commercial kits. Western blot assay was conducted for B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), and GAB1 protein levels. Dual-luciferase reporter assay and RNA immunoprecipitation assay were used to verify the association between miR-106b-5p and circ-PRKCI or GAB1. We found the Circ-PRKCI level was decreased in sepsis patients and LPS-induced human kidney 2 (HK-2) cells. LPS exposure inhibited cell viability and facilitated apoptosis, inflammation, and oxidative stress in HK-2 cells. Circ-PRKCI overexpression abrogated the effects of LPS on cell apoptosis, inflammation, and oxidative stress in HK-2 cells. Furthermore, circ-PRKCI was identified as the sponge for miR-106b-5p to positively regulate GAB1 expression. Overexpression of circ-PRKCI relieved LPS-mediated HK-2 cell damage by sponging miR-106b-5p. MiR-106b-5p inhibition ameliorated the injury of HK-2 cells mediated by LPS, whereas GAB1 knockdown reversed the effect. Collectively, Circ-PRKCI overexpression attenuated LPS-induced HK-2 cell injury by regulating miR-106b-5p/GAB1 axis.

Diminution of microRNA-98 alleviates renal fibrosis in diabetic nephropathy by elevating Nedd4L and inactivating TGF-ß/Smad2/3 pathway.

MicroRNAs (miRNAs) have already been documented to function in diabetic nephropathy (DN), yet little research has focused on the role of miR-98 in this disease. Here, we discuss the mechanism of miR-98 on the renal fibrosis in DN. Recombinant adeno-associated virus carrying miR-98 inhibitor or Nedd4L overexpression plasmid was injected into DN modeled rats to explore their roles in DN. Renal tubular epithelial cell injury models (NRK-52E cells) were induced by high glucose (HG). HG-treated NRK-52E cells were transfected with miR-98 inhibitor or Nedd4L overexpression plasmid for further verification. MiR-98 was upregulated, Nedd4L was downregulated and TGF-ß/Smad2/3 signaling was activated in kidney tissues of DN rats and HG-treated NRK-52E cells. miR-98 targeted Nedd4L mRNA 3'UTR. MiR-98 depletion and Nedd4L overexpression inactivated TGF-ß/Smad2/3 signaling pathway, alleviated pathological damage and fibrosis, ameliorated inflammation, and depressed cell apoptosis of kidney tissues of DN rats. MiR-98 depletion and Nedd4L overexpression inactivated TGF-ß/Smad2/3 signaling pathway, strengthened viability, and limited apoptosis of HG-treated renal tubular epithelial cells. Nedd4L overexpression reversed the effect of up-regulating miR-98 on DN rats and HG-treated renal tubular epithelial cells. Altogether, we find that miR-98 is upregulated in kidney tissues of DN rats, and miR-98 diminution and Nedd4L elevation attenuate renal fibrosis through inactivation of the TGF-ß/Smad2/3 pathway, which provides a novel therapy for DN.

Anti-hepatoma effect of taccalonolide A through suppression of sonic hedgehog pathway.

Taccalonolide A has been reported to have anti-tumour efficiency. However, the underlying mechanism for taccalonolides A therapy of hepatocellular carcinoma (HCC) is still obscure. Cell viability was evaluated by cell counting kit-8 (CCK-8) assay. Apoptosis was determined by flow cytometry. Protein expression of B cell lymphoma (Bcl-2), Bcl-2 associated X (Bax), sonic hedgehog (Shh), Smoothened (Smo) and Gli family zinc finger 1 (Gli1) was analyzed by western blot. The expression of Shh, Smo and Gli1 mRNA was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Results showed that taccalonolide A inhibited cell proliferation, induced apoptosis and cell cycle arrest at the G0/G1 phase, and improved the cytotoxicity of sorafenib in HCC cells. The expressions of Shh, Smo, Gli1 mRNA and protein were decreased after taccalonolide A treatment. More importantly, activation of the Shh pathway attenuated taccalonolide A-induced inhibition on cell viability and promotion on apoptosis and cell cycle arrest in HCC. Also, activation of the Shh pathway neutralized the effect of taccalonolide A on sorafenib cytotoxicity in HCC. We clarified that taccalonolide A suppressed cell viability facilitated apoptosis, and improved the cytotoxicity of sorafenib in HCC by inhibition of the activation of the Shh pathway, providing alternative treatments for HCC.

Mesenchymal Stem Cells Reverse Diabetic Nephropathy Disease via Lipoxin A4 by Targeting Transforming Growth Factor ß (TGF-ß)/smad Pathway and Pro-Inflammatory Cytokines.

BACKGROUND Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Mesenchymal stem cells (MSCs) treatment has been proved to be effective in DN models by protecting renal function and preventing fibrosis. However, the underlying mechanism is unclear. Previous research indicated diabetes and associated complications may be attributed to failed resolution of inflammation, which is deliberately regulated by pro-resolving lipids, including lipoxins (LXs), resolvins (Rv) D and E series, protectins, and maresins. In this study, we monitored pro-resolving mediators in a DN model to explore the mechanism of MSCs treatment. MATERIAL AND METHODS The DN model was induced by STZ injection in SD rats. UPLC-MS/MS was performed to determine pro-resolving lipids in kidney tissue and serum of DN model before and after MSCs treatment, as well as in supernatants of HBZY-1-MSCs co-culture. RESULTS LXA4 was highly accumulated in renal tissue of DN rats with MSCs treatment; ex vivo, LXA4 was significantly increased in the supernatants of HBZY-1 cells co-cultured with MSCs in a high-glucose (HG) medium. Western blot analysis indicated that ALX/FPR2, the receptor of LXA4, was markedly expressed in renal tissue of the DN-MSC group and HBZY-1 after incubating with MSCs in HG. Intraperitoneal injection of LXA4 inhibited renal fibrosis by targeting TGF-ß/Smad signaling and downregulated serum TNF-alpha, IL-6, IL-8, and IFN-γ in DN rats. Notably, all the protective effects induced by MSCs or LXA4 were abolished by ALX/FRP2 blocking. CONCLUSIONS Our results demonstrate that MSCs intervention prevented DN procession via the LXA4-ALX/FPR2 axis, which inhibited glomerulosclerosis and pro-inflammatory cytokines, eventually contributing to kidney homeostasis.

miR-215 Enhances HCV Replication by Targeting TRIM22 and Inactivating NF-κB Signaling.

PURPOSE: Hepatitis C virus (HCV) infection is a major cause of liver disease. Several miRNAs have been found to be associated with HCV infection. This study aimed to investigate the functional roles and possible molecular mechanisms of miR-215 in HCV replication. MATERIALS AND METHODS: The expression levels of miR-215 and TRIM22 were detected by quantitative real-time PCR (qRT-PCR) and western blot analysis in Con1b subgenomic genotype 1b HCV replicon cells (Con1b cells) and JFH1 full genome infecting Huh7.5.1 cells (Huh7.5.1 cells). HCV RNA levels were measured by qRT-PCR. The protein levels of NS3, NS5A, p65 subunit of NF-κB (p65), and phosphorylated p65 (p-p65) were determined by western blot analysis. The relationship between miR-215 and TRIM22 were explored by target prediction and luciferase reporter analysis. RESULTS: miR-215 overexpression enhanced HCV replication in Con1b cells, while miR-215 knockdown suppressed HCV replication in Huh7.5.1 cells. TRIM22 was confirmed to be a direct target of miR-215. TRIM22 upregulation resulted in a decline in HCV replication, while TRIM22 inhibition led to enhancement of HCV replication. Additionally, exogenous expression of TRIM22 reversed the facilitating effect of miR-215 on HCV replication, while TRIM22 downregulation counteracted the inhibitory effect of miR-215 knockdown on HCV replication. Furthermore, miR-215 targeted TRIM22 to block the NF-κB pathway, and exerted a positively regulatory role on HCV replication. CONCLUSION: miR-215 facilitated HCV replication via inactivation of the NF-κB pathway by inhibiting TRIM22, providing a novel potential target for HCV infection.

miR-200c targets nuclear factor IA to suppress HBV replication and gene expression via repressing HBV Enhancer I activity.

BACKGROUND: Hepatitis B virus (HBV) chronic infection is a health problem in the worldwide, with a underlying higher risk of liver cirrhosis and hepaticocellular carcinoma. A number of studies indicate that microRNAs (miRNAs) play vital roles in HBV replication. This study was designed to explore the potential molecular mechanism of miR-200c in HBV replication. METHODS: The expression of miR-200c, nuclear factor IA (NFIA) mRNA, HBV DNA, and HBV RNA (pregenomic RNA (pgRNA), and total RNA) were measured by qRCR. The levels of HBsAg and HBeAg were detected by ELISA. NFIA expression at protein level was measured by western blot. The direct interaction between miR-200c and NFIA were identified by Targetscan software and Dual-Luciferase reporter analysis. Enhance I activity were detected by Dual-Luciferase reporter assay. RESULTS: miR-200c expression was prominently reduced in pHBV1.3-tranfected Huh7 and in stable HBV-producing cell line (HepG2.2.15). The enforced expression of miR-200c significantly suppressed HBV replication, as demonstrated by the reduced levels of HBV protein (HBsAg and HBeAg) and, DNA and RNA (pgRNA and total RNA) levels. NFIA was proved to be a target of miR-200c and NFIA overexpression notably stimulated HBV replication. In addition, the inhibitory effect of miR-200c on HBV Enhance I activity was abolished following restoration of NFIA. CONCLUSIONS: miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.

Clinical observation of umbilical cord mesenchymal stem cell transplantation for treating patients receiving peritoneal dialysis.

BACKGROUND: This study aims to observe the outcome and safety of umbilical cord-mesenchymal stem cell (UC-MSC) treatment for continuous ambulatory peritoneal dialysis (CAPD) patients. METHODS: A total of 24 CAPD patients, who underwent UC-MSC treatment from June 2011 to December 2012, were selected for this study. These patients were followed up until June 2015. RESULTS: Results revealed a significant increase in hemoglobin, erythropoietin and albumin levels, a decrease in C-reactive protein levels, and marked improvement in cystatin C and urine volume within three months after UC-MSC transplantation; and the difference was statistically significant (P<0.05). However, the difference in residual glomerular filtration rate, serum creatinine, peritoneal KT/V and remnant kidney KT/V was not statistically significant (P>0.05). CONCLUSIONS: Clinical indicators of patients with CAPD can be partially improved through UC-MSC treatment.

Serum Levels of Lipopolysaccharide and 1,3-ß-D-Glucan Refer to the Severity in Patients with Crohn's Disease.

OBJECTIVES: Interactions between the host and gut microbial community contribute to the pathogenesis of Crohn's disease (CD). In this study, we aimed to detect lipopolysaccharide (LPS) and 1,3-ß-D-glucan (BG) in the sera of CD patients and clarify the potential role in the diagnosis and therapeutic approaches. MATERIALS AND METHODS: Serum samples were collected from 46 patients with active CD (A-CD), 22 CD patients at remission stage (R-CD), and 20 healthy controls, and the levels of LPS, BG, and TNF in sera were determined by ELISA. Moreover, sixteen patients with A-CD received anti-TNF monoclonal antibody therapy (infliximab, IFX) at a dose of 5 mg/kg body weight at weeks 0, 2, and 6, and the levels of LPS and BG were also tested at week 12 after the first intravenous infusion. RESULTS: Serum levels of LPS and BG were found to be markedly increased in A-CD patients compared with R-CD patients and healthy controls (P < 0.05). They were also observed to be positively correlated with CDAI, ESR, and SES-CD, respectively (P < 0.05). Furthermore, the levels of TNF in sera had a significant correlation with LPS and BG, respectively. The concentrations of LPS and BG were demonstrated to be significantly downregulated in the sera of A-CD patients 12 weeks after IFX treatment (P < 0.05), suggesting that blockade of TNF could inhibit bacterial endotoxin absorption, partially through improving intestinal mucosal barrier. CONCLUSIONS: Serum levels of LPS and BG are significantly increased in A-CD patients and positively correlated with the severity of the disease. Blockade of intestinal mucosal inflammation with IFX could reduce the levels of LPS and BG in sera. Therefore, this study has shed some light on measurement of serum LPS and BG in the diagnosis and treatment of CD patients.