PSTPIP2 ameliorates aristolochic acid nephropathy by suppressing interleukin-19-mediated neutrophil extracellular trap formation.

Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by herbal medicines. Proline-serine-threonine phosphatase-interacting protein 2 (PSTPIP2) and neutrophil extracellular traps (NETs) play important roles in kidney injury and immune defense, respectively, but the mechanism underlying AAN regulation by PSTPIP2 and NETs remains unclear. We found that renal tubular epithelial cell (RTEC) apoptosis, neutrophil infiltration, inflammatory factor, and NET production were increased in a mouse model of AAN, while PSTPIP2 expression was low. Conditional knock-in of Pstpip2 in mouse kidneys inhibited cell apoptosis, reduced neutrophil infiltration, suppressed the production of inflammatory factors and NETs, and ameliorated renal dysfunction. Conversely, downregulation of Pstpip2 expression promoted kidney injury. In vivo, the use of Ly6G-neutralizing antibody to remove neutrophils and peptidyl arginine deiminase 4 (PAD4) inhibitors to prevent NET formation reduced apoptosis, alleviating kidney injury. In vitro, damaged RTECs released interleukin-19 (IL-19) via the PSTPIP2/nuclear factor (NF)-κB pathway and induced NET formation via the IL-20Rß receptor. Concurrently, NETs promoted apoptosis of damaged RTECs. PSTPIP2 affected NET formation by regulating IL-19 expression via inhibition of NF-κB pathway activation in RTECs, inhibiting RTEC apoptosis, and reducing kidney damage. Our findings indicated that neutrophils and NETs play a key role in AAN and therapeutic targeting of PSTPIP2/NF-κB/IL-19/IL-20Rß might extend novel strategies to minimize Aristolochic acid I-mediated acute kidney injury and apoptosis.

Aristolochic acid nephropathy (or AAN for short) is a serious condition affecting the kidneys that is caused by certain traditional Chinese medicines containing a compound called aristolochic acid. This compound is known to have harmful effects on kidney tubular epithelial cells, causing increased inflammation and a form of controlled cell death called apoptosis, which can ultimately lead to organ failure. There is currently no effective treatment for AAN, highlighting the need for a deeper understanding of the mechanisms responsible. Previous studies have shown that immune cells called neutrophils infiltrate the kidneys and damage cells in the early stages of AAN. Neutrophils produce web-like structures called neutrophil extracellular traps, which have been identified as potentially contributing to the damage. A protein called PSTPIP2, which regulates inflammation, has also been shown to contribute to other types of kidney injury. To understand how these inflammatory factors might be involved in AAN, Du, Xu et al. genetically engineered mice to produce extra PSTPIP2 protein specifically in their kidneys. When given aristolochic acid, these mice displayed less kidney damage. Further studies of mouse kidney cells showed that PSTPIP2 protects the kidney by suppressing an inflammatory mechanism that leads to the production of neutrophil extracellular traps. By contrast, in models where PSTPIP2 levels were reduced, neutrophil extracellular traps were shown to cause both apoptosis and kidney injury. The findings of Du, Xu et al. show that neutrophil extracellular traps cause cell damage and apoptosis in a mouse model of AAN and that this action can be reduced by increasing the levels of the protein PSTPIP2. This sheds light on the inflammatory mechanisms behind the kidney damage caused by herbal medicines containing aristolochic acid. Additionally, it opens new avenues for studies aiming to find ways to treat AAN, suggesting that targeting PSTPIP2 could be a promising strategy.

The effect of hepatic stellate cell derived-IL-11 on hepatocyte injury in hepatic fibrosis.

AIMS: This study aimed to elucidate the role of Interleukin-11 (IL-11) in hepatic fibrosis (HF) and its potential as a therapeutic target for HF treatment. MATERIALS AND METHODS: We investigated IL-11 expression in patients with varying degrees of liver injury through ELISA and immunohistochemistry. A CCl4-induced HF mouse model was constructed to study IL-11 expression and cell apoptosis using Western blotting (WB) and other techniques. The expression of IL-11 was silenced using rAAV8 in the mouse model. In vitro stimulation of hepatic stellate cells (LX-2) with TGF-ß1, and of LO-2 cells with exogenous IL-11, were performed. Cell supernatants of TGF-ß1-stimulated LX-2 were used to culture LO-2 cells, with apoptosis monitored via flow cytometry and WB. KEY FINDINGS: Increased IL-11 levels were observed in patients and the HF mouse model, with silencing reducing IL-11 expression. In vitro experiments revealed increased endogenous IL-11 in TGF-ß1-stimulated LX-2 cells and an increase in apoptotic index, IL11RA, and gp130 in IL-11-stimulated LO-2 cells. Cell apoptosis was reduced in the siRNA/IL11, siRNA/IL11RA, and anti-IL11 groups. WB and immunohistochemistry results showed upregulated p-JNK, p-ERK, and p-P53 expressions in the CCl4-induced HF mouse model and IL-11-treated LO-2 cells. SIGNIFICANCE: Our findings suggest IL-11 enhances LX-2 cell activation and proliferation, and promotes LO-2 cell apoptosis through JNK/ERK signaling pathways. This suggests that targeting IL-11 secretion may serve as a potential therapeutic strategy for HF, providing a foundation for its clinical application in HF treatment.

ZIF-67-derived Co/CoSe ultrafine nanocrystal Schottky heterojunction decorated hollow carbon nanospheres as new-type anodes for potassium-ion batteries.

Metal-organic frameworks (MOFs) have the advantages of controllable chemical properties, rich pore structures and reaction sites and are expected to be high-performance anode materials for the next generation of potassium-ion batteries (PIBs). However, due to the large radius of potassium ions, the pure MOF crystal structure is prone to collapse during ion insertion and processing, so its electrochemical performance is quite limited. In this work, a hollow carbon sphere-supported MOF-derived Co/CoSe heterojunction anode material for potassium-ion batteries was developed by a hydrothermal method. The anode has high potassium storage capacity (461.9 mA h/g after 200 cycles at 1 A/g), excellent cycling stability and superior rate performance. It is worth noting that the potassium ion storage capacity of the anode material shows a gradual upward trend with the charge-discharge cycle, which is 145.9 mA h/g after 3000 cycles at a current density of 10 A/g. This work demonstrates that MOF-derived CoSe anodes with high capacity and low cost may be promising candidates for the introduction of potassium ion storage.

BRD4 promotes hepatic stellate cells activation and hepatic fibrosis via mediating P300/H3K27ac/PLK1 axis.

Hepatic fibrosis (HF) is a reversible wound-healing response characterized by excessive extracellular matrix (ECM) deposition and secondary to persistent chronic injury. Bromodomain protein 4 (BRD4) commonly functions as a "reader" to regulate epigenetic modifications involved in various biological and pathological events, but the mechanism of HF remains unclear. In this study, we established a CCl4-induced HF model and spontaneous recovery model in mice and found aberrant BRD4 expression, which was consistent with the results in human hepatic stellate cells (HSCs)- LX2 cells in vitro. Subsequently, we found that distriction and inhibition of BRD4 restrained TGFß-induced trans-differentiation of LX2 cells into activated, proliferative myofibroblasts and accelerated apoptosis, and BRD4 overexpression blocked MDI-induced LX2 cells inactivation and promoted the proliferation and inhibited apoptosis of inactivated cells. Additionally, adeno-associated virus serotype 8-loaded short hairpin RNA-mediated BRD4 knockdown in mice significantly attenuated CCl4-induced fibrotic responses including HSCs activation and collagen deposition. Mechanistically, BRD4 deficiency inhibited PLK1 expression in activated LX2 cells, and ChIP and Co-IP assays revealed that BRD4 regulation of PLK1 was dependent on P300-mediated acetylation modification for H3K27 on the PLK1 promoter. In conclusion, BRD4 deficiency in the liver alleviates CCl4-induced HF in mice, and BRD4 participates in the activation and reversal of HSCs through positively regulating the P300/H3K27ac/PLK1 axis, providing a potential insight for HF therapy.

Berberine Ameliorates Abnormal Lipid Metabolism via the Adenosine Monophosphate-Activated Protein Kinase/Sirtuin 1 Pathway in Alcohol-Related Liver Disease.

Alcoholic fatty liver disease (AFLD) is an early stage of alcohol-related liver disease characterized by abnormal lipid metabolism in hepatocytes. To date, to our knowledge, there have been no effective strategies for preventing or treating alcohol-related liver disease besides alcohol abstinence. Berberine (BBR) is the main bioactive ingredient extracted from traditional Chinese medicines, such as Coptis and Scutellaria, which protect liver function and relieve liver steatosis. However, the potential role of BBR in AFLD remains unclear. Therefore, this study investigated the protective effects of BBR against Gao-binge model-induced AFLD in 6- to 8-week-old C57BL/6J male mice in vivo and ethyl alcohol (EtOH)-induced alpha mouse liver 12 (AML-12) cells in vitro. The results showed that BBR (200 mg/kg) attenuated alcoholic liver injury and suppressed lipid accumulation and metabolism disorders in vivo. Consistently, BBR effectively inhibited the expression of sterol regulatory element-binding transcription factor 1C, sterol regulatory element-binding transcription factor 2, fatty acid synthase, and 3-hydroxy-3-methylglutaryl-CoenzymeA reductase in EtOH-stimulated AML-12 cells in vitro and promoted the expression of sirtuin 1 (SIRT1) in EtOH-fed mice and EtOH-treated AML-12 cells. Furthermore, SIRT1 silencing attenuated the hepatic steatosis alleviation potential of BBR treatment. Mechanistically, molecular docking revealed the binding effect of BBR and adenosine monophosphate-activated protein kinase (AMPK). The results of further studies showed that a decrease in AMPK activity was accompanied by a significant inhibition of SIRT1 expression. SIRT1 silencing attenuated the protective effect of BBR, whereas the inhibition of its expression had no apparent effect on AMPK phosphorylation, suggesting that SIRT1 acts downstream of AMPK in AFLD. Collectively, BBR ameliorated abnormal lipid metabolism and alleviated EtOH-induced liver injury via the AMPK/SIRT1 pathway in AFLD mice.

Inhibition of circular RNA ASPH reduces the proliferation and promotes the apoptosis of hepatic stellate cells in hepatic fibrosis.

Circular RNAs (circRNAs) are a newly identified form of non-coding RNA that play a crucial role in various pathological processes. However, the expression profile and function of circRNAs in hepatic fibrosis (HF) remain largely unknown. In this study, we showed that a novel circRNA ASPH (circASPH) mediates HF by targeting the miR-139-5p/Notch1 axis. We investigated the expression profile of circRNAs in hepatocyte exosomes of mice with HF using circRNA-sequencing and found significant upregulation of circASPH. Loss- and gain-of-function analysis of circASPH was performed to assess its role in HF. Furthermore, we performed luciferase reporter assay, RNA pull-down, and fluorescence in situ hybridization analyses and confirmed that circASPH directly binds to miR-139-5p. We also found that circASPH was upregulated in liver fibrogenesis. Downregulation of circASPH expression inhibited hepatic stellate cell (HSC) activation and proliferation, induced apoptosis, and attenuated mouse liver fibrogenic injury. Mechanistically, circASPH directly targeted miR-139-5p to regulate the expression of Notch1 in HF. Thus, downregulation of circASPH may suppress the activation of HSCs and HF through the circASPH/miR-139-5p/Notch1 axis. Our findings indicated that circASPH may be a potential biomarker for HF diagnosis and therapy.

Emerging therapeutic potential of adeno-associated virus-mediated gene therapy in liver fibrosis.

Liver fibrosis is a wound-healing response that results from various chronic damages. If the causes of damage are not removed or effective treatments are not given in a timely manner, it will progress to cirrhosis, even liver cancer. Currently, there are no specific medical therapies for liver fibrosis. Adeno-associated virus (AAV)-mediated gene therapy, one of the frontiers of modern medicine, has gained more attention in many fields due to its high safety profile, low immunogenicity, long-term efficacy in mediating gene expression, and increasingly known tropism. Notably, increasing evidence suggests a promising therapeutic potential for AAV-mediated gene therapy in different liver fibrosis models, which helps to correct abnormally changed target genes in the process of fibrosis and improve liver fibrosis at the molecular level. Moreover, the addition of cell-specific promoters to the genome of recombinant AAV helps to limit gene expression in specific cells, thereby producing better therapeutic efficacy in liver fibrosis. However, animal models are considered to be powerless predictive of tissue tropism, immunogenicity, and genotoxic risks in humans. Thus, AAV-mediated gene therapy will face many challenges. This review systemically summarizes the recent advances of AAV-mediated gene therapy in liver fibrosis, especially focusing on cellular and molecular mechanisms of transferred genes, and presents prospective challenges.

A novel three-dimensional quantitative assessment method for abnormal root morphology of the maxillary premolars in vivo on cone-beam computed tomography.

BACKGROUND: Previous studies have described and recorded abnormal root morphology; however, most of these studies were based on two-dimensional periapical or panoramic radiographs, and only a few studies have quantified it. We aimed to combine two-dimensional periapical radiographs and three-dimensional cone-beam computed tomography (CBCT) to conduct qualitative judgments and quantitative analyses of normal and conical roots, and explore the clinical diagnostic method of normal and conical roots based on intraoral radiographs and CBCT. METHODS: The conical root was identified visually on periapical radiographs as the clinical gold standard. All teeth were divided into the cone-rooted teeth (CRT) or normal-rooted teeth (NRT) groups. Furthermore, differences in root length (RL), root surface area (RSA), and root volume (RV) of conical and normal roots in the maxillary premolars on CBCT were compared. Receiver operator characteristic curves were generated, and the area under the curve (AUC) and cut-off values were calculated to evaluate the diagnostic value of RV, RSA, RV/RL, and RSA/RL. RESULTS: The RSAs of NRT and CRT were 236.88 ± 27.93 mm2 and 207.98 ± 27.80 mm2, respectively (P = 0.000). The mean RV in the CRT group was lower than that in the NRT group, and the difference was statistically significant (253.40 ± 41.98 mm3 vs. 316.93 ± 49.89 mm3, P = 0.000). The RSA and RV of conical roots in single root premolars were 12.29% and 19.33% less than those of normal roots, respectively. The AUC values of RSA/RL and RV/RL were 0.87 and 0.89, respectively, and the best cut-off values were 19.61 for RSA/RL (if RSA/RL was < 19.61, the teeth were considered CRT) and 24.05 for RV/RL (if RV/RL was < 24.05, the teeth were considered CRT). CONCLUSIONS: CBCT has significant diagnostic value in the clinical evaluation of conical roots. RSA/RL and RV/RL were the best parameters with the largest AUC and high sensitivity and specificity.

O-alkyl and o-benzyl hesperetin derivative-1L attenuates inflammation and protects against alcoholic liver injury via inhibition of BRD2-NF-κB signaling pathway.

Alcoholic liver injury (ALI) is a major risk factor for alcoholic liver disease, characterized by excessive inflammatory response and abnormal liver dysfunction. Previous studies have indicated that O-alkyl and o-benzyl hesperetin derivative-1 L (HD-1 L) has anti-inflammatory and hepato-protective effects in CCl4-induced liver injury. However, its effect on ALI and underlying mechanism has not been elucidated. This study was designed to evaluate the protective effects of HD-1 L on alcoholic liver injury and reveal the underlying mechanisms. ALI model was established in male C57BL/6 J mice (aged 6-8 weeks) by Gao-Binge protocol. The mice were received different doses of HD-1 L (25 mg/kg, 50 mg/kg, 100 mg/kg) by daily intragastric administration, respectively. Liver function and inflammation were measured. Mechanism underlying the anti-inflammatory and hepato-protective effect of HD-1 L were studied in RAW264.7 cells. In alcoholic liver injury mice, HD-1 L effectively improved the liver pathology, and remarkably reduced the levels of alanine transaminase (ALT), aspartate transaminase (AST), triglyceride (TG) and total cholesterol (T-CHO) in serum. Moreover, HD-1 L markedly suppressed inflammation in vivo and inhibited the secretion of inflammatory factors in vitro. Our results showed that HD-1 L decreased the activity of Bromodomain-containing Protein 2 (BRD2) and inhibited expression of BRD2 in vivo and in vitro. Furthermore, HD-1 L further alleviated alcohol-induced inflammation after blocking BRD2 with inhibitor (JQ1) or BRD2 small interfering (si)-RNA in RAW264.7 cells. Besides, HD-1 L failed to effectively exert its anti-inflammatory effects after over expression of BRD2. In addition, HD-1 L significantly inhibited the phosphorylation and activation of NF-κB-P65 mediated by BRD2. In conclusion, HD-1 L alleviated liver injury and inflammation mainly by inhibiting BRD2-NF-κB signaling pathway, and HD-1 L may be a potential anti-inflammatory compound in treatment of alcoholic liver disease.

MicroRNA-195-3p promotes hepatic stellate cell activation and liver fibrosis by suppressing PTEN expression.

Liver fibrosis is a reversible wound healing reaction characterized by abnormal accumulation of extracellular matrix (ECM) in response to liver injury. Recent studies have shown that it can be epigenetically regulated, especially by microRNAs (miRNAs). It has been acknowledged that activation of hepatic stellate cells (HSCs) is a pivotal step in the initiation and progression of liver fibrosis. Notably, our results showed that miR-195-3p was increased in HSCs isolated from CCl4-treated mice and that the increase was more pronounced as the degree of liver fibrosis increased. Moreover, treatment of LX-2 cells, a human immortalized hepatic stellate cell line, with TGF-ß1 resulted remarkable upregulation of miR-195-3p. Gain-of-function and loss-of-function experiments have suggested that the increased levels of miR-195-3p inhibit the expression of phosphatase and tension homolog deleted on chromosome 10 (PTEN), a negative regulator of the PI3K/Akt/mTOR signaling pathway in liver fibrosis, thereby contributing to HSC activation and proliferation and promoting the expression of profibrotic genes, such as α-SMA and collagen I, in LX-2 cells, which accelerates the accumulation of fibrous extracellular matrix deposition in the liver, while knockdown of miR-195-3p induced the opposite effect. Taken together, these results provide evidence for the harmful role of miR-195-3p in CCl4-treated mouse liver fibrosis.

Hesperetin derivative-16 attenuates CCl4-induced inflammation and liver fibrosis by activating AMPK/SIRT3 pathway.

Liver fibrosis, a chronic inflammatory healing reaction, progresses to hepatocirrhosis without effective intervention. Hesperetin derivative (HD-16), a monomer compound derived from hesperitin, exerts anti-inflammatory and hepatoprotective effects against a spectrum of liver diseases. However, the anti-fibrotic potential of HD-16 in liver fibrosis and its underlying mechanism have not yet been elucidated. In this study, we investigated the anti-fibrotic effect of HD-16 on mouse liver fibrosis induced by CCl4 and on LX-2 cells (human immortalized HSCs) stimulated by TGF-ß1, in vivo and in vitro. HD-16 exerted an anti-fibrotic effect via regulation of the AMPK/SIRT3 pathway. Pharmacodynamic results showed that HD-16 alleviated the degree of injury and inflammation in CCl4-induced mouse liver fibrosis. Consistently, HD-16 also effectively inhibited the expression of α-SMA, Col1α1, Col3α1, and TIMP-1 in TGF-ß1-activated LX-2 cells. Mechanistically, HD-16 promoted SIRT3 expression and activity in fibrotic liver and activated LX-2 cells. Furthermore, SIRT3 depletion attenuated the anti-fibrotic effects of HD-16. Intriguingly, HD-16 increased AMPK phosphorylation, whereas inhibition of SIRT3 expression did not affect AMPK phosphorylation. In contrast, AMPK silencing suppressed SIRT3 expression, suggesting that SIRT3 is a downstream target of AMPK in liver fibrosis. Overall, HD-16 attenuated CCl4-induced liver inflammation and fibrosis by activating the AMPK/SIRT3 pathway, and HD-16 may be a potential anti-fibrotic compound in the treatment of liver fibrosis.

Grain Growth of MAPbI3 via Diethylammonium Bromide Induced Grain Mergence.

Various additives are used to improve the film morphology, crystal quality, and grain size for the sake of enhancing the performance of three-dimensional perovskite solar cells. Although significant enhancement in the performance of devices has been made due to the introduction of additives, an in-depth understanding of the additive-related crystallization kinetics and the growth mechanism is still lacking. Here, the grain growth mechanism of diethylammonium bromide (DABr)-doped MAPbI3 is investigated using in situ dynamic microscopy techniques. The results reveal that the alkyl chains of DABr restrain the growth of grains of MAPbI3 during spin-coating, and DABr-induced grain mergence during the annealing process, achieving large grains on the micrometer scale. Meanwhile, the crystallization of MAPbI3 with DABr is significantly improved and the number of defects is reduced. The solar cell with optimized DABr doping MAPbI3 as the active layer presents a higher power conversion efficiency (PCE) of 19.58% with a fill factor of 79.81%.

Impacts of carrier trapping and ion migration on charge transport of perovskite solar cells with TiO x electron transport layer.

The ion migration in perovskite materials has been extensively studied by researchers, but the charge dynamic distribution caused by ion migration and carrier trapping is partly unclear. To investigate the impacts of ion migration and defect induced carrier trapping on the carrier transport and the carrier collection, we measured the evolution of the photocurrent response in microseconds, milliseconds and seconds for the perovskite solar cells pretreated at different biases. Our results reveal that the photocurrent of the solar cells pretreated at negative bias decreases with time and achieves its minimum at several milliseconds, then rises and achieves its maximum at tens of seconds. For the device pretreated at positive bias beyond built-in potential, the time to reach maximum photocurrent is much shorter than that of the solar cell pretreated at negative bias. The transient photocurrent responses to the sequence of single-light-pulses also show that there is obvious carrier trapping in a positive bias treated device, which indicates that defect induced carrier trapping is the critical factor for the perovskite solar cells with an n-TiO x electron transport layer. In order to improve the performance of the perovskite solar cells with nano-TiO x ETL, it is very necessary to significantly reduce defects. Our results also demonstrate that cation accumulation at the interface between the perovskite active layer and ETL can enhance the device performance to a certain extent.

Improving ternary blend morphology by adding a conjugated molecule into non-fullerene polymer solar cells.

The use of ternary polymer solar cells (PSCs) is a promising strategy to enhance photovoltaic performance while improving the fill factor (FF) of a device, but is still a challenge due to the complicated morphology. Herein, ternary PSCs are fabricated via adding the conjugated small molecule p-DTS(FBTTh2)2 into a well-known blended film, PTB7-Th:IEICO-4F. The ternary blend morphology and device characterization reveal that the addition of p-DTS(FBTTh2)2 can improve crystallinity and optimize morphology, leading to the FF of the optimized device increasing to 73.69%. In combination with the advantages of an ultra-narrow bandgap material, IEICO-4F, with a broad optical absorption spectrum, the optimized ternary solar cell exhibits a high short-circuit current-density (J SC) of 25.22 mA cm-2. The best power conversion efficiency (PCE) is 12.84% for this optimized ternary device with 10 wt% p-DTS(FBTTh2)2 in the donors. This work indicates that incorporating a small molecule with high crystallinity into host binary non-fullerene PSCs would give an active layer with high crystallinity, thus greatly enhancing the FFs and PCEs of PSCs.

Efficient Quasi-Two-Dimensional Perovskite Light-Emitting Diodes with Improved Multiple Quantum Well Structure.

Quasi-two-dimensional (quasi-2D) perovskites with a multiple quantum well structure can enhance the exciton binding energy and controllable quantum confine effect, which are attractive materials for efficient perovskite light-emitting diodes (PeLEDs). However, the multiphase mixtures contained in these materials would cause nonradiative recombination at the perovskite film surface. Here, a facile solution surface treatment is adopted to improve the multiple quantum well structure of the quasi-2D perovskite emitting layer, which can reduce the influence of defectinduced nonradiative recombination and the electric-field-induced dissociation of excitons for the PeLEDs. The improved multiple quantum well structure is verified by UV absorption spectra and temperature-dependent photoluminescence spectra measurements. The photoluminescence quantum yield of the quasi-2D perovskite film with surface treatment has been approximately increased by 200%. Meanwhile, the electroluminescence device achieves a current efficiency of 45.9 cd/A.

Comparison of in situ cone beam computed tomography scan data with ex vivo optical scan data in the measurement of root surface area.

OBJECTIVE: The aim of this study was to compare root surface area (RSA) measurements of single-root teeth in a sheep mandible based on cone beam computed tomography (CBCT) with measurements made with an optical scanner. STUDY DESIGN: Eight anterior teeth of a sheep cadaver mandible were scanned in situ by using CBCT with 3 different exposure parameters, followed by treatment with smoothing software. The teeth were then extracted and scanned individually with an optical scanner. Three-dimensional digital models of the teeth were reconstructed on the basis of CBCT and optical scanner data. RSA data were calculated, and an equivalence test was used to statistically compare the measurements with significance of difference established at α = 0.05. RESULTS: The means of the differences between RSA measurements from CBCT and optical scanning ranged from 0.33% to 3.01%. There were no statistically significant differences between the 2 methods. The smoothing parameters for good fitness of the linear regression were determined to be 0.8 for the smooth factor, 8 for iterations, and 0 for compensate shrinkage. CONCLUSIONS: The proposed CBCT technique to measure RSA is feasible. RSA data obtained from CBCT in situ are as accurate as optical scanner measurements ex vivo.

The evaluation of potential immunotoxicity induced by environmental pollutant ammonia in broilers.

Ammonia (NH3) is a harmful gas with irritating odor, and higher NH3 concentration was found in intensive poultry houses. Although the toxicity of NH3 is well known, little attention has been given to the mechanism of NH3 poisoning in chicken immune organs. To investigate NH3-caused inflammatory damage of broiler spleens, in this study, a broiler model for NH3 poisoning was established, and 3 levels (including microRNA [miRNA], mRNA, and protein) were performed using qRT-PCR and western blot. The results indicated that NH3 exposure caused inflammatory damage using microstructure observation; decreased 2 inflammation-related miRNAs (miR-133a and miR-6615), 2 cytokines secreted by T helper cells 1 (Th1), and heme oxygenase-1 (HO-1); and increased 2 target genes (LOC101747543 and mothers against decapentaplegic homolog 7 [SMAD7]) of the 2 miRNAs, 7 inflammation-related factors, 3 cytokines secreted by Th2, and 5 heat shock proteins (HSPs) in broiler spleens. Our study suggested that Th1/Th2 imbalance, nuclear factor-κB (NF-κB) pathway, and compensatory response of HSPs were involved in NH3-caused inflammatory damage in broiler spleens; there was immunotoxic effect in excess NH3 on broilers. For the first time, we discovered miR-6615 and LOC101747543 may be involved in the mechanism of broiler spleen inflammatory damage caused by NH3 via the NF-κB pathway, and further mechanism needs to be investigated. This study provides new insights for NH3 toxicity identification and risk assessment in animal husbandry production practice.

Two-dimensional additive diethylammonium iodide promoting crystal growth for efficient and stable perovskite solar cells.

Methylammonium lead iodide perovskite photovoltaics have attracted remarkable attention due to their exceptional power conversion efficiencies (PCEs). The film morphology of organometallic halide perovskite plays a very important role in the performance of planar perovskite solar cells (PVSCs). Previous methods have been explored to control the crystal growth for getting a compact and smooth perovskite film. Here, we report an effective and reproducible approach for enhancing the stability and the efficiency of PVSCs by incorporating a small quantity of two-dimensional (2D) material diethylammonium iodide (DAI) in three-dimensional (3D) MAPbI3, which can facilitate the perovskite crystallization processes and improve the resulting film crystal quality. The fabricated (DA2PbI4)0.05MAPbI3 perovskite hybrid films exhibit good morphology with larger grains and uniform morphology. Simultaneously, reduced defects and enhanced carrier lifetime within a full device indicate enhanced crystallization effects as a result of the DAI inclusion. The photovoltaic device attains a high photocurrent of 22.95 mA cm-2 and a high fill factor of 79.04%, resulting in an overall PCE of 19.05%. Moreover, the stability of the 10% DAI doped perovskite solar cell is also improved. These results offer a promising stable and efficient light-absorbing material for solid-state photovoltaics and other applications.

Application of biodegradable plates for treating pediatric mandibular fractures.

OBJECTIVE: We assessed the clinical results of a biodegradable plate system for the internal fixation of mandibular fractures in children, and observed the imaging features of fracture healing and bone changes around the biodegradable plates and screws during follow-up. PATIENTS AND METHODS: We enrolled 39 patients (22 male, 17 female, average age 4 years 10 months) with different mandibular fractures. We used 2.0-mm resorbable plates to repair the fractures. Postoperative follow-up ranged from 6 months to 5 years; average follow-up was 1 year 2 months. The outcome measures identified and assessed included facial symmetry, mouth opening, occlusal relationship, infection, nonunion, malunion, and plate dehiscence. RESULTS: We fixed 42 fractures with 43 resorbable plates; the fracture site of one patient (aged 11 years 3 months) was fixed with two plates. Two patients developed small fistulas at the intraoral incision 2 months after surgery; the fistulas healed after 1 month without special treatment. In the other patients, the incision healed well, there was facial symmetry, mouth opening was >35 mm, and occlusion was good. Follow-up computed tomography examination data were available for 20 cases, and revealed different degrees of radiolucency indicating that osteolysis had occurred. Radiolucency was observed around the resorbable plates 1 month after the surgery. The extent and depth of the radiolucent region were obvious within 1 year of surgery. In the second year, there were obvious repairs, with the bony defect areas becoming shallower. After 2 years, the bony defect areas had almost disappeared. CONCLUSION: Biodegradable fixation devices are safe and efficient for treating pediatric mandibular fractures. Osteolysis commonly follows biodegradable fixation of pediatric mandibular fractures, and has no adverse effect on fracture healing.