Discovery of Orally Active Phenylquinoline-Based Soluble Epoxide Hydrolase Inhibitors with Anti-Inflammatory and Analgesic Activity.

Currently, there are no specific drugs for treating acute pancreatitis. Soluble epoxide hydrolase (sEH) inhibitors show promise, but face challenges like low blood drug concentrations and potential adverse effects on CYP enzymes and the human ether-a-go-go-related gene (hERG). In this study, an approach involving scaffold hopping and structure-activity guided optimization was employed to design a series of phenylquinoline-based sEH inhibitors. Among these compounds, DJ-53 exhibited potent in vitro and in vivo effects in alleviating pain and reducing inflammation. The in vivo mechanism of action involved inhibiting sEH enzyme activity, thereby increasing levels of anti-inflammatory epoxyeicosatrienoic acids (EETs) and decreasing levels of proinflammatory dihydroxyeicosatrienoic acids (DHETs). Importantly, DJ-53 showed exceptional oral bioavailability and pharmacokinetics, while avoiding inhibition of CYP enzymes or the hERG channel. These results highlight DJ-53's potential as a new lead compound for anti-inflammatory and analgesic applications and provide a safe and effective scaffold for developing sEH inhibitors.

Total Synthesis of Ryanodane Diterpenoids Garajonone and 3-epi-Garajonone.

Ryanodane diterpenes are structurally complex natural products that are well-known for their high degree of oxidation and the challenges associated with synthesizing them within the terpene class. Herein, we present a two-stage synthetic strategy that draws inspiration from the broad biosynthesis of terpenes, allowing us to successfully achieve the first chemical synthesis of garajonone, a ryanodane diterpenoid that occurs naturally at low abundance, as well as its epimer, 3-epi-garajonone. The key to this success lies in the rapid construction of the carbon framework of target molecule by employing an early-stage palladium-catalyzed Heck/carbonylative esterification cascade annulation, followed by successive late-stage selective redox manipulation to establish the desired oxidation state of the molecule. This research not only showcases the synthesis of garajonone and its epimer but also provides a platform for the chemical synthesis of other members and analogs within this complex diterpenoid family.

Screening for early Alzheimer's disease: enhancing diagnosis with linguistic features and biomarkers.

Introduction: Research has shown that speech analysis demonstrates sensitivity in detecting early Alzheimer's disease (AD), but the relation between linguistic features and cognitive tests or biomarkers remains unclear. This study aimed to investigate how linguistic features help identify cognitive impairments in patients in the early stages of AD. Method: This study analyzed connected speech from 80 participants and categorized the participants into early-AD and normal control (NC) groups. The participants underwent amyloid-ß positron emission tomography scans, brain magnetic resonance imaging, and comprehensive neuropsychological testing. Participants' speech data from a picture description task were examined. A total of 15 linguistic features were analyzed to classify groups and predict cognitive performance. Results: We found notable linguistic differences between the early-AD and NC groups in lexical diversity, syntactic complexity, and language disfluency. Using machine learning classifiers (SVM, KNN, and RF), we achieved up to 88% accuracy in distinguishing early-AD patients from normal controls, with mean length of utterance (MLU) and long pauses ratio (LPR) serving as core linguistic indicators. Moreover, the integration of linguistic indicators with biomarkers significantly improved predictive accuracy for AD. Regression analysis also highlighted crucial linguistic features, such as MLU, LPR, Type-to-Token ratio (TTR), and passive construction ratio (PCR), which were sensitive to changes in cognitive function. Conclusion: Findings support the efficacy of linguistic analysis as a screening tool for the early detection of AD and the assessment of subtle cognitive decline. Integrating linguistic features with biomarkers significantly improved diagnostic accuracy.

Lymphatic absorption characteristics of eicosapentaenoic acid -enriched phosphoethanolamine plasmalogen and its gastric and intestinal hydrolysates.

The aim of this work was to study the lymphatic absorption characteristics of gastric hydrolysates and intestinal hydrolysates of eicosapentaenoic acid-enriched phosphoethanolamine plasmalogen (EPA-pPE) with focusing on the fate of EPA and vinyl ether bonds in the lymph fluid using lymphatic intubation and lipidomics. The results showed that the EPA peak occurred earlier in the gastric (1.5 h) and intestinal (1 h) hydrolysates than in the EPA-pPE group (3 h) with EPA peak content being 2.03 and 1.46 times higher, suggesting pre-hydrolysis contributed to lymphatic absorption. Further, duodenal injection of gastric hydrolysates sn2 EPA-lysoPE produced higher levels of EPA-LPC, PC, PE, and PG. Meanwhile, intestinal hydrolysates free EPA and sn1 lyso-pPE enriched the sn1 + 2 + 3 TG (20:5_20:5_20:5) and increased the vinyl ether bond-containing lipids, such as PE (18:0p_18:0) and PE (18:0p_20:4). This study provides insight into dietary molecular structures of EPA and plasmalogen.

Caenorhabditis elegans CYP33 Family in Eicosanoid Regulation, Xenobiotic Metabolism, Nanotoxicity and Spermatogenesis.

The CYP33 family in Caenorhabditis elegans is integral to processes like xenobiotic detoxification, eicosanoid regulation, nanotoxicity response and spermatogenesis. Limited research on C. elegans CYP33 suggests its functions are similar to human CYP33, indicating conserved roles in metabolism and disease. This review examines C. elegans CYP33 enzymes, especially CYP-33E1 and CYP-33E2, and their human homologues, focusing on their roles in eicosanoid biosynthesis, xenobiotic metabolism, nanotoxicity and spermatogenesis. Understanding these enzymes enhances insights into cytochrome P450 biology, metabolism and cyp-associated diseases.

ATP-binding cassette transporter TaABCG2 contributes to Fusarium head blight resistance by mediating salicylic acid transport in wheat.

ATP-binding cassette (ABC) transporters hydrolyse ATP to transport various substrates. Previous studies have shown that ABC transporters are responsible for transporting plant hormones and heavy metals, thus contributing to plant immunity. Herein, we identified a wheat G-type ABC transporter, TaABCG2-5B, that responds to salicylic acid (SA) treatment and is induced by Fusarium graminearum, the primary pathogen causing Fusarium head blight (FHB). The loss-of-function mutation of TaABCG2-5B (ΔTaabcg2-5B) reduced SA accumulation and increased susceptibility to F. graminearum. Conversely, overexpression of TaABCG2-5B (OE-TaABCG2-5B) exerted the opposite effect. Quantification of intracellular SA in ΔTaabcg2-5B and OE-TaABCG2-5B protoplasts revealed that TaABCG2-5B acts as an importer, facilitating the transport of SA into the cytoplasm. This role was further confirmed by Cd2+ absorption experiments in wheat roots, indicating that TaABCG2-5B also participates in Cd2+ transport. Thus, TaABCG2-5B acts as an importer and is crucial for transporting multiple substrates. Notably, the homologous gene TaABCG2-5A also facilitated Cd2+ uptake in wheat roots but did not significantly influence SA accumulation or FHB resistance. Therefore, TaABCG2 could be a valuable target for enhancing wheat tolerance to Cd2+ and improving FHB resistance.

Colorectal cancer-associated bacteria are broadly distributed in global microbiomes and drivers of precancerous change.

The gut microbiome is implicated in the pathogenesis of colorectal cancer (CRC), but the full scope of this dialogue is unknown. Here we aimed to define the scale and membership of the body of CRC- and health-associated gut bacteria in global populations. We performed a microbiome-CRC correlation analysis of published ultra-deep shotgun metagenomic sequencing data from global microbiome surveys, utilizing a de novo (reference-agnostic) gene-level clustering approach to identify protein-coding co-abundant gene (CAGs) clusters. We link an unprecedented ~ 23-40% of gut bacteria to CRC or health, split nearly evenly as CRC- or health-associated. These microbes encode 2319 CAGs encompassing 427,261 bacterial genes significantly enriched or depleted in CRC. We identified many microbes that had not previously been linked to CRC, thus expanding the scope of "known unknowns" of CRC-associated microbes. We performed an agnostic CAG-based screen of bacterial isolates and validated predicted effects of previously unimplicated bacteria in preclinical models, in which we observed differential induction of precancerous adenomas and field effects. Single-cell RNA sequencing disclosed microbiome-induced senescence-associated gene expression signatures in discrete colonic populations including fibroblasts. In organoid co-cultures, primary colon fibroblasts from mice with microbiomes promoted significantly greater growth than fibroblasts from microbiome-depleted mice. These results offer proof-of-principle for gene-level metagenomic analysis enabling discovery of microbiome links to health and demonstrate that the microbiome can drive precancer states, thereby potentially revealing novel cancer prevention opportunities.

Regulatory Effects of SLC7A2-CPB2 on Lymphangiogenesis: A New Approach to Suppress Lymphatic Metastasis in HNSCC.

BACKGROUND: Lymph node metastasis (LNM) is a critical factor affecting the outcomes of head and neck squamous cell carcinoma (HNSCC) and the main reason for treatment failure. This study was designed to examine the effects of the key genes involved in the LNM of HNSCC. METHODS: Tissue samples (HNSCC) were examined by transcriptome sequencing, and the core genes associated with LNM were detected via bioinformatics analysis. The functions of these core genes were then validated using the TCGA biological database and their effects on the propagation, invasion, and metastasis of HNSCC cells were evaluated through cell culture experiments. Moreover, the effect of core gene expression on the LNM capability of HNSCC was confirmed via a footpad xenograft mice model. RESULTS: In the findings, a key gene involved in the LNM of HNSCC was identified as SLC7A2. It was correlated with adverse clinical prognosis and expressed with low expression in HNSCC tissues. As shown in cell culture experiments, FaDu and SCC15 cell growth, invasion, and migration were inhibited when SLC7A2 was overexpressed. Further, cell apoptosis was stimulated, and lymphangiogenesis was suppressed through the downregulation of CPB2 expression. Animal studies demonstrated that the growth and LNM of HNSCC cells were inhibited by SLC7A2 overexpression. CONCLUSION: It is concluded that SLC7A2 is involved in HNSCC lymphatic metastasis by controlling CPB2 function. The results are anticipated to offer new directions for the effective treatment of HNSCC.

Overlapping group between non-alcoholic fatty liver disease and metabolic associated fatty liver disease better for liver research.

Aims: Metabolic associated fatty liver disease (MAFLD) was proposed to replace "non-alcoholic fatty liver disease (NAFLD) with new diagnostic criteria." The group meeting these two diagnostic criteria is called "Overlapping Fatty Liver Disease (FLD)." Its clinical characteristics remain unknown. Methods: This study included participants from the Taiwan Bio-Bank database, where NAFLD was defined as hepatic steatosis in liver ultrasound, with exclusion of other known chronic liver diseases. MAFLD was defined as the presence of hepatic steatosis plus metabolic dysfunction, defined as having any of following three criteria: overweight/obesity, type 2 diabetes mellitus (DM), or ≥2 metabolic risk abnormalities in lean/normal weight subjects. According to these two diagnostic criteria, three groups were identified: "overlapping FLD", "NAFLD alone", and "MAFLD alone." NAFLD fibrosis score (NFS) >0.675 was defined as advanced liver fibrosis. Results: Eight thousand thirty-eight NAFLD participants (age 55.86 ± 10.12; males 41.07%) were included in the final analysis. Of them, "overlapping FLD" was diagnosed in 7377 (91.8%) and "NAFLD alone" in 661 (8.2%) participants. "Overlapping FLD" patients were older and had a higher percentage of male, worse metabolic profiles, higher NFS, and the percentage of carotid plaques was higher than those with "NAFLD alone." Multivariate analysis showed age, hypertension, DM, and BMI were positively associated with advanced liver fibrosis in "overlapping FLD" patients. Conclusions: "Overlapping FLD" is better for liver research due to identifying a high-risk population among NAFLD patients. NAFLD definition introduces the heterogeneity through "NAFLD alone" group and MAFLD criteria overcome this limitation.

Absence of Survival Impact from Hepatitis During Immunotherapy in 193 Patients with Advanced Hepatocellular Carcinoma - An Observational Study from Taiwan.

Background: Hepatitis often occurs after initiating immune checkpoint inhibitor (ICI) treatment. The time and grade of hepatitis after ICI starts and the prognostic role of immune-related hepatitis in patients with advanced hepatocellular carcinoma (aHCC) remain unclear. Methods: In this real-world analysis, we enrolled aHCC patients receiving ICIs, documented the highest level of liver enzymes during/after ICIs, and analyzed the survival impact of different hepatitis patterns. Results: One hundred and ninety-three aHCC patients receiving ICIs were recruited. During ICIs, 88.6% of patients experienced aspartate transaminase (AST) elevations (Grade III/IV: 7.8%). For alanine transaminase (ALT), 81.3% had elevated levels (Grade III/IV: 3.6%), and 41.5% of patients had elevated bilirubin levels (Grade 3/4: 6.7%). The median AST, ALT, and total bilirubin values significantly increased after ICI treatment initiated (all p < 0.001) and, similarly, after excluding progressive disease (p = 0.014, p = 0.002, p < 0.001). The median time of hepatitis occurrence is from the 4.0th to 15.9th weeks. Multivariable analysis showed that patterns of liver enzyme change of AST and total bilirubin in patients receiving ICIs significantly correlate to overall survival (OS, p = 0.009 and 0.001, respectively). After ICI termination, patients with elevated bilirubin (p = 0.003) and AST (p = 0.005) would indicate poor survival, with adjustment of viral hepatitis and ICI responses. Conclusion: Hepatitis emerges between the 4th and 20th weeks post-ICI initiation. Changes in liver enzymes during ICI therapy do not directly affect OS, implying the safety of ICI use when corticosteroids are promptly administered if clinically indicated.

Quality of life in disease-free survived patients with early-stage extranodal nasal-type NK/T-cell lymphoma after definitive intensity-modulated radiotherapy: a cross-sectional study of 310 cases.

PURPOSE: Radiotherapy is a critical treatment for early-stage extranodal nasal-type NK/T-cell lymphoma (ENKTL) and has yielded favorable survival outcomes. However, their postradiotherapy quality of life (QOL) has not been investigated. Here, we conducted a cross-sectional study to assess the QOL of ENKTL patients with disease-free survival after definitive radiotherapy and to identify factors associated with QOL and treatment optimization. METHODS: This cross-sectional study included 310 patients with stage I-II ENKTL of the upper aerodigestive tract (UADT) who had received simultaneous integrated boost intensity-modulated radiotherapy (SIB-IMRT) with a consistent design and achieved disease-free survival. The median postradiotherapy time was 47.2 months (range, 3.1-115.7). The EORTC QLQ-H&N35 questionnaire was used to assess symptom-related QOL, and nine additional items were added to incorporate nasal, optical, and aural-related symptoms. The scores indicate the severity of the symptoms. RESULTS: The most common postradiotherapy symptoms among patients with ENKTL were nose problems (49.7%), dry mouth (44.8%), tooth problems (41.3%), sensory problems (32.6%), and less sexuality (25.8%). Tooth problems had the highest average score of 18.6, which is still acceptable. The severity of these symptoms decreased over time and reached a plateau in the second year after radiotherapy. Multivariable regression analysis showed that whole-neck irradiation was an independent predictive factor for xerostomia (P = 0.013, OR = 1.114), while age > 60 years was a predictive factor for lower sexuality (P < 0.001, OR = 1.32). CONCLUSION: The QOL of patients with early-stage ENKTL after radiotherapy was favorable, and most symptoms improved over time. Radiotherapy was correlated with specific symptoms, which may suggest a direction for further improvement in SIB-IMRT.

Trillium tschonoskii rhizome saponin improves spatial learning and memory by enhancing neurovascular restorative in ischemic rats.

BACKGROUND: Trillium tschonoskii rhizome saponins (TSTT) has been significantly effective in treating traumatic injury, neurasthenia, cancer and inflammatory diseases as a folk medicine. However, the mechanism regarding to TSTT induced the neurovascular restorative after ischemia is without fully elucidated. PURPOSE: This research was constructed to study the value of TSTT in promoting endogenous repair of neurovascular and augmenting the ability of spatial study and memory retention in ischaemic rats. STUDY DESIGN: The improvement of TSTT on cerebral infraction and perfusion was observed by magnetic resonance imaging (MRI) experiments and the molecular mechanisms were further explored. METHODS: First, rats were ligated the middle cerebral artery to construct a permanent ischaemia model, subsequently intragastric injection administrated with TSTT (120, 60, 30 mg kg-1) at 6 h after operation, then once a day during next 30 days. Morris water maze was applied to observe the neurobehavioral changes. Multimodal MRI sequences were performed to monitoring brain injuries as well as cerebral blood flow. Histopathological staining was employed to evaluate the morphological changes of neurons. Transmission electron microscopy (TEM) was employed to detect the neurons, vascular structure, and synapse. Immunofluorescent staining was utilized to evaluate the endogenous repair progress. The axonal growth-inhibitors and axonal guidance cues were analyzed using western blotting. RESULTS: Contrast to the model group, TSTT declined the infarction and elevated the parenchymal volume. Notably, treated with TSTT significantly decreased the ADC (ipsilateral/contralateral). In histopathologic examination, TSTT prominently boosted amounts of cortical and striatal nerve cells and protected ultrastructure of neurovascular unit. According with results of nuclear magnetic imaging, TSTT enhanced endogenous repair progress. Especially, TSTT treatments obviously inhibited protein levels of NogoA/NgR/RhoA/ROCK2, accompanied by increased expression of Netrin/DCC and Slit2/Robo1. CONCLUSION: To sum up, our data illustrated that TSTT promoted cerebral reestablishment. The above result was in line with improving cerebral blood flow, elevated integrity of neurovascular structure, accelerating endogenous restoration and impairing the axonal growth inhibitors NogoA/NgR/RhoA/ROCK2 signaling, thereby improving poststroke learning and memory.

ZNF521 promotes acute myeloid leukemogenesis by suppressing the expression and acetylation of SMC3.

Zinc finger protein 521 (ZNF521) participates in the self-renewal of hematopoietic stem cells, and its abnormal expression has been implicated to promote leukemia. However, the specific role of ZNF521 in leukemia has not been fully understood. In this study, we aimed to further elucidate its role. Using acute leukemia cell line THP-1, we demonstrated that knocking down ZNF521 inhibited leukemia cell proliferation, promoted apoptosis, and induced cell arrest in G2/M phase. Interestingly, we also observed the upregulation of SMC3 expression and acetylation, as well as the downregulation of histone deacetylases 8 (HDAC8), CDK2, and CDK6. The proliferation inhibition was reversed by knocking down SMC3, suggesting the key role of SMC3 reduction in ZNF521 elevated proliferation. Conversely, ZNF521 overexpression in HL-60 cells resulted in enhanced proliferation and inhibited apoptosis. Furthermore, we discovered that ZNF521 can interact with HDAC8, which deacetylates SMC3, and the interaction promotes proliferation and suppresses apoptosis. Notably, when HDAC8 was knocked down or its activity was inhibited by a HDAC8 inhibitor, the previous observed trend was reversed. Consequently, ZNF521 plays a critical role in acute myeloid leukemogenesis by reducing the expression and acetylation of SMC3. Overall, this study sheds light on the potential for targeted treatment in highly ZNF521 expressed acute myeloid leukemia, providing a valuable clue for precise and effective therapeutic approaches.

Unraveling the rapid progression of non-target lesions: risk factors and the therapeutic potential of PCSK9 inhibitors in post-PCI patients.

BACKGROUND: Rapid progression of non-target lesions (NTLs) leads to a high incidence of NTL related cardiac events post-PCI, which accounting half of the recurrent cardiac events. It is important to identify the risk factors and establish an accurate clinical prediction model for the rapid progression of NTLs post-PCI. PCSK9 inhibitors lower LDL-c levels significantly, also show the anti-inflammation effect, and may have the potential to reduce the rapid progression of NTLs post-PCI. We tried to test this hypothesis and explore the potential mechanisms. METHODS: This retrospective study included 1250 patients who underwent the first PCI and underwent repeat coronary angiography for recurrence of chest pain within 24 months. General characteristics, laboratory tests and inflammatory factors(IL-10, IL-6, IL-8, IL-1ß, sIL-2R, and TNF-α) were collected. Machine learning (LASSO regression) was mainly employed to select the important characteristic risk factors for the rapid progression of NTLs post-PCI and build prediction models. Finally, mediator analysis was employed to explore the potential mechanisms by which PCSK9 inhibitors reduce the rapid progression of NTLs post-PCI. RESULTS: There were more diabetes, less beta-blockers and PCSK9 inhibitors application, higher HbA1c, LDL-c, ApoB, TG, TC, uric acid, hs-CRP, TNF-α, IL-6, IL-8, and sIL-2R in NTL progressed group. LDL-c, hs-CRP, IL-8, and sIL-2R were characteristic risk factors for the rapid progression of NTLs post-PCI, combining LDL-c, hs-CRP, IL-8, and sIL-2R builds the optimal model for predicting the rapid progression of NTLs post-PCI (AUC = 0.632). LDL-c had a clear and incomplete mediating effect (95% CI, mediating effect: 51.56%) in the reduction of the progression of NTLs by PCSK9 inhibitors, and there was a possible mediating effect of IL-8 (90% CI), and sIL-2R (90% CI). CONCLUSIONS: LDL-c, hs-CRP, IL-8, and sIL-2R may be the key characteristic risk factors for the rapid progression of NTLs post-PCI, and combining these parameters might predict the rapid progression of NTLs post-PCI. The application of PCSK9 inhibitors had a negative correlation with the rapid progression of NTLs. In addition to the significant LDL-c-lowering, PCSK9 inhibitors may reduce the rapid progression of NTLs by reducing local inflammation of plaque. TRIAL REGISTRATION: ChiCTR2200058529; Date of registration: 2022-04-10.

Anemia, blood cell indices, genetic correlations, and brain structures: A comprehensive analysis of roles in Parkinson's disease risk.

INTRODUCTION: Anemia may contribute significantly to the onset of Parkinson's disease (PD). Current research on the association between anemia and PD risk is inconclusive, and the relationships between anemia-related blood cell indices and PD incidence require further clarification. This study aims to investigate the relationships between anemia, blood cell indicators, and PD risk using a thorough prospective cohort study. METHODS: We used data from the UK Biobank, a prospective cohort study of 502,649 participants, and ultimately, 365,982 participants were included in the analysis. Cox proportional hazards models were utilized to adjust for confounding factors, aiming to thoroughly explore the associations between anemia and blood cell indices with the risk of incident PD. The interaction between anemia and Polygenic Risk Score (PRS) for PD was also examined. Linear regression and mediation analyses assessed potential mechanisms driven by brain structures, including grey matter volume. RESULTS: During a median follow-up of 14.24 years, 2513 participants were diagnosed with PD. Anemia considerably increased PD risk (hazard ratio [HR] 1.98, 95 % confidence interval [CI]: 1.81-2.18, P < 0.001) after adjustments. Those with high PRS for anemia had an 83 % higher PD incidence compared to low PRS participants. Sensitivity analyses confirmed result robustness. Linear regression showed that anemia correlated with grey matter volumes and most white matter tracts. Furthermore, mediation analyses identified that the volume of grey matter in Thalamus mediates the relationship between anemia and PD risk. CONCLUSION: In summary, we consider there to be a substantial correlation between anemia and increased PD risk.

Taraxasterol attenuates zearalenone-induced kidney damage in mice by modulating oxidative stress and endoplasmic reticulum stress.

Taraxasterol is one of the bioactive ingredients from traditional Chinese herb Taraxacum, which exhibits multiple pharmacological activities and protective effects. However, the underlying influence and mechanism of its use against kidney damage caused from zearalenone (ZEA) remain unexplored. The ZEA-induced kidney damage model of mice was established by feeding diets containing ZEA (2 mg/kg), and taraxasterol (5 and 10 mg/kg) was administered by gavage for 28 days. Results demonstrated taraxasterol increased average daily gain (ADG) and average daily feed intake (ADFI), reduced feed-to-gain ratio (F/G) and kidney index of mice induced by ZEA. Taraxasterol alleviated histopathological changes of kidney, reduced ZEA residue and the levels of blood urea nitrogen (BUN), uric acid (UA), and creatinine (CRE). Concurrently, taraxasterol reduced the contents of oxidative stress indicator reactive oxygen species (ROS) and malondialdehyde (MDA), and increased the activities of antioxidant enzymes catalase (CAT), total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px). Further, taraxasterol up-regulated the mRNA and protein expression of nuclear factor erythroid-2-related factor 2 (Nrf2), GSH-Px, NAD(P)H quinone oxidoreductase 1 (NQO1), and heme oxygenase-1 (HO-1), and down-regulated the mRNA and protein expression of KELCH like ECH associated protein (Keap1) in Nrf2/Keap1 pathway. Taraxasterol down-regulated the mRNA and protein expression of immunoglobulin binding protein (Bip), C/EBP homologous protein (CHOP), Bcl-2 associated X (Bax), cysteine protease (Caspase)-12, and Caspase-3, and up-regulated B-cell lymphoma 2 (Bcl-2) expression in endoplasmic reticulum stress pathway. This study suggests that taraxasterol attenuates ZEA-induced mouse kidney damage through the modulation of Nrf2/Keapl pathway to play antioxidant role and endoplasmic reticulum stress pathway to enhance anti-apoptotic ability. It will provide a basis for taraxasterol as a potential drug to prevent and treat ZEA-induced kidney damage.

Adsorption and C-C bond cleavage of benzene on hematite α-Fe2O3 surfaces: a DFT mechanistic study.

Reforming tar molecules into smaller gaseous molecules has been a critical challenge for biomass energy utilization. Hematite (α-Fe2O3) has been demonstrated as an effective catalyst for the catalytic reforming of tar, nevertheless, the detailed mechanism of α-Fe2O3 catalyzed tar reforming remains unclear. In this work, we apply the density functional theory method to investigate this problem. Specifically, we study both (0001) and (01[Formula: see text]2) surface structures of α-Fe2O3 and then use the structures to investigate the adsorption and C-C bond cleavage of benzene on these surfaces. Our results show that the dominant interactions between benzene and a single Fe-terminated (0001) surface are van der Waals forces, yet benzene could be chemisorbed on the Fe and O co-exposed (01[Formula: see text]2) surface via strong C-O interactions. As a result, the (0001) surface is not active towards benzene cleavage, whereas the (01[Formula: see text]2) surface can promote the aromatic C-C bond breaking. Furthermore, our calculations indicate that chain-like alkene species and carbonyl species are the two types of potential products that form after the C-C bond cleavage of benzene on the α-Fe2O3 (01[Formula: see text]2) surface, with the activation energy of 1.78 eV and 2.62 eV, respectively. In summary, we reveal the importance of co-adsorption on both Fe and O centers and oxidative addition on C-C bond cleavage of aromatic compounds on the α-Fe2O3 surface, which provides novel insights into the mechanisms of tar cracking on oxide catalysts.

Spectrum aided vision enhancer enhances mucosal visualization by hyperspectral imaging in capsule endoscopy.

Narrow-band imaging (NBI) is more efficient in detecting early gastrointestinal cancer than white light imaging (WLI). NBI technology is available only in conventional endoscopy, but unavailable in magnetic-assisted capsule endoscopy (MACE) systems due to MACE's small size and obstacles in image processing issues. MACE is an easy, safe, and convenient tool for both patients and physicians to avoid the disadvantages of conventional endoscopy. Enabling NBI technology in MACE is mandatory. We developed a novel method to improve mucosal visualization using hyperspectral imaging (HSI) known as Spectrum Aided Visual Enhancer (SAVE, Transfer N, Hitspectra Intelligent Technology Co., Kaohsiung, Taiwan). The technique was developed by converting the WLI image captured by MACE to enhance SAVE images. The structural similarity index metric (SSIM) between the WLI MACE images and the enhanced SAVE images was 91%, while the entropy difference between the WLI MACE images and the enhanced SAVE images was only 0.47%. SAVE algorithm can identify the mucosal break on the esophagogastric junction in patients with gastroesophageal reflux disorder. We successfully developed a novel image-enhancing technique, SAVE, in the MACE system, showing close similarity to the NBI from the conventional endoscopy system. The future application of this novel technology in the MACE system can be promising.