Effects of Pregnancy-Onset Asthma on Perinatal Outcomes: A Retrospective Cohort Study.

BACKGROUND: It is unknown whether women with pregnancy-onset asthma are predisposed to worse pregnancy outcomes compared with women with pre-pregnancy asthma. OBJECTIVE: To explore whether pregnancy-onset asthma leads to worse perinatal outcomes compared with pre-pregnancy asthma. METHODS: Women who were discharged with a diagnosis of asthma and gave birth to a live singleton were included in this retrospective cohort analysis. Women were separated into groups based on whether the asthma was diagnosed during or before pregnancy. We compared clinical characteristics, perinatal outcomes, and asthma exacerbations (AEs) between groups. RESULTS: A total of 335 women were included in this study, 39 of whom (11.6%) had pregnancy-onset asthma and 296 had pre-pregnancy asthma. All pregnant women in the pregnancy-onset group experienced AEs during pregnancy. The proportion of chronic hypertension, chronic hypertension with superimposed preeclampsia, and spontaneous preterm births in the pregnancy-onset group was significantly higher than that in the pre-pregnancy asthma group. After adjusting for age, body mass index, onset of asthma during pregnancy, and severity of AEs through multivariate analysis, pregnancy-onset asthma was an independent risk factor for spontaneous preterm birth (adjusted odds ratio = 7.71; 95% CI, 1.30-46.12) and severe AE was an independent risk factor for gestational hypertension and preeclampsia (adjusted odds ratio = 3.58; 95% CI, 1.30-9.87). CONCLUSIONS: During pregnancy, pregnancy-onset asthma in women is associated with an exacerbation of the condition. Obstetricians should be vigilant for signs of asthma onset during pregnancy. Other health care providers should watch for symptoms of gestational hypertension and preeclampsia in pregnant women with preexisting or new-onset asthma.

Metabolic Recoding of NSUN2-Mediated m5C Modification Promotes the Progression of Colorectal Cancer via the NSUN2/YBX1/m5C-ENO1 Positive Feedback Loop.

The RNA modification, 5-methylcytosine (m5C), has recently gained prominence as a pivotal post-transcriptional regulator of gene expression, intricately intertwined with various tumorigenic processes. However, the exact mechanisms governing m5C modifications during the onset and progression of colorectal cancer (CRC) remain unclear. Here, it is determined that the m5C methyltransferase NSUN2 exhibits significantly elevated expression and exerts an oncogenic function in CRC. Mechanistically, NSUN2 and YBX1 are identified as the "writer" and "reader" of ENO1, culminating in the reprogramming of the glucose metabolism and increased production of lactic acid in an m5C-dependent manner. The accumulation of lactic acid derived from CRC cells, in turn, activates the transcription of NSUN2 through histone H3K18 lactylation (H3K18la), and induces the lactylation of NSUN2 at the Lys356 residue (K356), which is crucial for capturing target RNAs. Together, these findings reveal an intriguing positive feedback loop involving the NSUN2/YBX1/m5C-ENO1 signaling axis, thereby bridging the connection between metabolic reprogramming and epigenetic remodeling, which may shed light on the therapeutic potential of combining an NSUN2 inhibitor with immunotherapy for CRC.

Research progress on and molecular mechanism of vacuum sealing drainage in the treatment of diabetic foot ulcers.

Diabetic foot ulcers (DFUs) are common chronic wounds and a common complication of diabetes. The foot is the main site of diabetic ulcers, which involve small and medium-sized arteries, peripheral nerves, and microcirculation, among others. DFUs are prone to coinfections and affect many diabetic patients. In recent years, interdisciplinary research combining medicine and material science has been increasing and has achieved significant clinical therapeutic effects, and the application of vacuum sealing drainage (VSD) in the treatment of DFUs is a typical representative of this progress, but the mechanism of action remains unclear. In this review, we integrated bioinformatics and literature and found that ferroptosis is an important signaling pathway through which VSD promotes the healing of DFUs and that System Xc-GSH-GPX4 and NAD(P)H-CoQ10-FSP1 are important axes in this signaling pathway, and we speculate that VSD is most likely to inhibit ferroptosis to promote DFU healing through the above axes. In addition, we found that some classical pathways, such as the TNF, NF-κB, and Wnt/ß-catenin pathways, are also involved in the VSD-mediated promotion of DFU healing. We also compiled and reviewed the progress from clinical studies on VSD, and this information provides a reference for the study of VSD in the treatment of DFUs.

Constructing Efficient CuO-Based CO Oxidation Catalysts with Large Specific Surface Area Mesoporous CeO2 Nanosphere Support.

CeO2 is an outstanding support commonly used for the CuO-based CO oxidation catalysts due to its excellent redox property and oxygen storage-release property. However, the inherently small specific surface area of CeO2 support restricts the further enhancement of its catalytic performance. In this work, the novel mesoporous CeO2 nanosphere with a large specific surface area (~190.4 m2/g) was facilely synthesized by the improved hydrothermal method. The large specific surface area of mesoporous CeO2 nanosphere could be successfully maintained even at high temperatures up to 500 °C, exhibiting excellent thermal stability. Then, a series of CuO-based CO oxidation catalysts were prepared with the mesoporous CeO2 nanosphere as the support. The large surface area of the mesoporous CeO2 nanosphere support could greatly promote the dispersion of CuO active sites. The effects of the CuO loading amount, the calcination temperature, mesostructure, and redox property on the performances of CO oxidation were systematically investigated. It was found that high Cu+ concentration and lattice oxygen content in mesoporous CuO/CeO2 nanosphere catalysts greatly contributed to enhancing the performances of CO oxidation. Therefore, the present mesoporous CeO2 nanosphere with its large specific surface area was considered a promising support for advanced CO oxidation and even other industrial catalysts.

YAP promotes the healing of ischemic wounds by reducing ferroptosis in skin fibroblasts through inhibition of ferritinophagy.

The impaired healing of chronic wounds is often attributed to the ischemic and hypoxic microenvironment, leading to increased cell death. Ferroptosis, a novel form of cell death unveiled in recent years, could potentially be linked with the process of wound healing. In this study, we explored the significance and mechanism of ferroptosis in ischemic wounds. Using transmission electron microscopy, Western blot, flow cytometry, immunofluorescence, and glutathione (GSH) assay, we observed that the death of primary mouse skin fibroblasts induced by oxygen and glucose deprivation (OGD) was associated with ferroptosis. Specifically, we observed elevated intracellular Fe2+ and lipid peroxidation levels and decreased GSH levels in vitro, indicative of ferroptosis. Importantly, we found that ferroptosis in OGD-treated skin fibroblasts was dependent on autophagy, as the autophagy inhibitor chloroquine phosphate (CHQ) significantly reduced ferroptosis induced by OGD. Moreover, our study revealed that NCOA4-mediated ferritinophagy significantly contributed to the occurrence of ferroptosis induced by OGD in skin fibroblasts. Additionally, we identified the involvement of YAP in the regulation of ferritinophagy, with YAP suppressing NCOA4 expression in OGD-treated skin fibroblasts, thereby reducing ferroptosis. Furthermore, in ischemic wound models in mice, both inhibitors of ferroptosis and autophagy promoted wound healing, while a YAP inhibitor, verteporfin, delayed wound healing. In conclusion, these findings indicate that ferroptosis, regulated by YAP through ferritinophagy inhibition, presents a novel mechanism responsible for the delayed healing of ischemic wounds. Understanding this process could offer promising therapeutic targets to improve wound healing in ischemic conditions.

Baroreflex activation therapy for heart failure with reduced ejection fraction: A comprehensive systematic review and meta-analysis.

Background: In recent years, baroreflex activation therapy (BAT) has been utilized to treat heart failure with reduced ejection fraction (HFrEF). However, the supporting literature on its efficacy and safety is still limited. This investigation elucidates the effects of BAT in HFrEF patients to provide a reference for future clinical applications. Methods: This investigation follows Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) 2020 guidelines. Relevant investigations on the use of BAT in HFrEF patients were searched and selected from 5 databases, including Web of Science, MEDLINE, PubMed, Embase, and Cochrane Library, from inception to December 2022. The methodological quality of eligible articles was assessed via the Cochrane risk of bias tool, and for meta-analysis, RevMan (5.3) was used. Results: Randomized controlled trials comprising 343 participants were selected for the meta-analysis, which revealed that in HFrEF patients, BAT enhanced the levels of LVEF (MD: 2.97, 95 % CI: 0.53 to 5.41), MLHFQ (MD: -14.81, 95 % CI: -19.57 to -10.06) and 6MWT (MD: 68.18, 95 % CI: 51.62 to 84.74), whereas reduced the levels of LVEDV (MD: -15.79, 95 % CI: -32.96 to 1.37) and DBP (MD: -2.43, 95 % CI: -4.18 to -0.68). Conclusion: It was concluded that BAT is an efficient treatment option for HFrEF patients. However, to validate this investigation, further randomized clinical trials with multiple centers and large sample sizes are needed.

How and when does a used (vs. unused) account affect consumption behavior?

How does spending from a used (vs. unused) account affect consumption behavior? An account is used when some resources of that account have been used (e.g., $90 has been used on a gift card that originally had $100). An account is unused when no resources of that account have been used (e.g., no money has been used on a gift card that has $10). Across seven studies (N = 8,667), we find that people are more likely to spend resources from a used account than otherwise equivalent resources from an unused account. This is because people engage in within-account comparisons, comparing the remaining resources in the account with what the account originally had, leading them to value the remaining resources less in a used account. We demonstrate the robustness of the effect of a used (vs. unused) account across several domains, including gift cards, checking accounts, and credit card reward points. Further, we demonstrate a boundary condition of the effect, revealing that the proportion of the account remaining moderates the subsequent consumption. Lastly, we generalize this effect from consumption to charitable giving. The findings provide insights into how policymakers, companies, and individuals may consider leveraging the perception of an account being used or unused to curb expenses and encourage charitable giving. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

P75NTR regulates autophagy through the YAP-mTOR pathway to increase the proliferation of interfollicular epidermal cells and promote wound healing in diabetic mice.

Wound healing is delayed in diabetic patients. Increased autophagy and dysfunction of interfollicular epidermal (IFE) cells are closely associated with delayed healing of diabetic wounds. Autophagy plays an important role in all stages of wound healing, but its role in diabetic wound healing and the underlying molecular mechanisms are not clear. Here, we found that diabetic mice had delayed wound healing and increased autophagy in wounds compared with normal mice and that chloroquine, an inhibitor of autophagy, decreased the level of autophagy, improved the function of IFE cells, and accelerated wound healing in diabetic mice. Treatment of IFE cells with advanced glycosylation end products (AGEs) resulted in increased microtubule-associated protein chain (LC3) expression and decreased prostacyclin-62 (P62) expression, indicating increased autophagy in AGE-treated IFE cells. Moreover, P75NTR reduced autophagy in IFE cells in the presence of AGEs and significantly increased the proliferation of IFE cells. In addition, P75NTR participated in regulating autophagy in IFE cells and in wounds in diabetic mice through the YAP-mTOR signalling pathway, which increased the functional activity of the cells and the healing rate of wounds in diabetic mice. Thus, our study suggests that P75NTR protects IFE cells against AGEs by affecting autophagy and accelerating wound healing in diabetic mice, providing a basis for understanding the role of autophagy in diabetic wound healing.

Propolis alleviates ulcerative colitis injury by inhibiting the protein kinase C - transient receptor potential cation channel subfamily V member 1 - calcitonin gene-related peptide/substance P (PKC-TRPV1-CGRP/SP) signaling axis.

This study investigated the protective effect of water-soluble propolis (WSP) on colonic tissues in ulcerative colitis (UC) and the role of the protein kinase C - transient receptor potential cation channel subfamily V member 1 - calcitonin gene-related peptide/substance P (PKC-TRPV1-CGRP/SP) signaling pathway. Male SD rats were divided into a control group, a UC model group, various WSP groups (Low-WSP, Medium-WSP, and High-WSP) with UC, and a salazosulfapyridine (SASP) positive control group with UC. After UC was established, the WSP and SASP groups were treated with WSP or SASP, respectively, for 7 d. Each day, body weight measurements were obtained, and the disease activity index (DAI) was recorded by observing fecal characteristics and blood in the stool. After the experiment, hematoxylin and eosin (HE) colonic tissue staining was performed to observe pathological changes, western blotting and immunohistochemistry were performed to detect PKC, TRPV1, CGRP, and SP expression in colonic tissues, and laser confocal microscopy was performed to observe the fluorescence colocalization of PKC/TRPV1, TRPV1/CGRP, and TRPV1/SP. HE staining showed significant colonic tissue structure disruption and inflammatory infiltration in the UC group. Western blotting and immunohistochemistry showed that the expression of PKC, TRPV1, CGRP, and SP in the colonic tissues of the UC group increased significantly compared with that of the control group. Compared with the UC group, the expression of PKC, TRPV1, CGRP, and SP in colonic tissues was significantly reduced in the High-WSP, Medium-WSP, and SASP groups. Immunofluorescence showed the colocalized expression of PKC/TRPV1, TRPV1/CGRP, and TRPV1/SP proteins in the colon tissue of the UC group was significantly reduced after WSP and SASP interventions compared with that of the control group. The results suggest that the mechanism of UC alleviation by propolis may inhibit the PKC-TRPV1-CGRP/SP signaling pathway and the release of inflammatory mediators, thus alleviating inflammation.

Coronary computed tomography angiography analysis using artificial intelligence for stenosis quantification and stent segmentation: a multicenter study.

Background: Accurate interpretation of coronary computed tomography angiography (CCTA) is a labor-intensive and expertise-driven endeavor, as inexperienced readers may inadvertently overestimate stenosis severity. Recent artificial intelligence (AI) advances in medical imaging present compelling prospects for auxiliary diagnostic tools in CCTA. This study aimed to externally validate an AI-assisted analysis system capable of rapidly evaluating stenosis severity, exploring its potential integration into routine clinical workflows. Methods: This multicenter study consisted of an internal and external cohort of patients who underwent CCTA scans between April 2017 and February 2023. CCTA scans were evaluated using Coronary Artery Disease Reporting and Data System (CAD-RADS) scores to determine stenosis severity, while ground-truth stents were manually annotated by expert readers. The InferRead CT Heart (version 1.6; Infervision Medical Technology Co., Ltd., Beijing, China), which incorporates AI-assisted coronary artery stenosis quantification and automatic stent segmentation, was employed for CCTA scan analysis. AI-based stenosis assessment performance was determined using sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), while the AI-based stent segmentation overlap was assessed using the Dice similarity coefficient (DSC). Results: For ≥50% stenosis diagnoses, the AI system attained per-patient sensitivity, specificity, PPV, and NPV surpassing 90.0% for the internal dataset; for the external dataset, the per-patient values were 88.0% [95% confidence interval (CI): 81.0-94.4%], 94.5% (95% CI: 90.7-97.6%), 90.0% (95% CI: 83.3-95.6%), and 93.4% (95% CI: 89.2-96.8%), respectively. For ≥70% stenosis diagnoses, the per-patient values on the internal dataset were 94.2% (95% CI: 89.2-98.1%), 95.8% (95% CI: 94.1-97.4%), 80.8% (95% CI: 73.5-87.7%), and 98.9% (95% CI: 97.9-99.6%), respectively; for the external dataset, the per-patient values were 91.9% (95% CI: 82.6-100.0%), 97.3% (95% CI: 94.9-99.1%), 85.0% (95% CI: 72.5-94.6%), and 98.6% (95% CI: 96.8-100.0%), respectively. Regarding CAD-RADS categorization, the Cohen kappa was 0.75 and 0.81 for the internal per-patient and per-vessel basis, respectively, and 0.72 and 0.76 for the external per-patient and per-vessel basis, respectively. The DSC for stent segmentation was 0.96±0.06. Conclusions: The AI-assisted analysis system for CCTA interpretation exhibited exceptional proficiency in stenosis quantification and stent segmentation, indicating that AI holds considerable potential in advancing CCTA postprocessing techniques.

Reference-Point Theory: An Account of Individual Differences in Risk Preferences.

We propose an account of individual differences in risk preferences called "reference-point theory" for choices between sure things and gambles. Like most descriptive theories of risky choice, preferences depend on two drivers-hedonic sensitivities to change and beliefs about risk. But unlike most theories, these drivers are estimated from judged feelings about choice options and gamble outcomes. Furthermore, the reference point is assumed to be the less risky option (i.e., sure thing). Loss aversion (greater impact of negative change than positive change) and pessimism (belief the worst outcome is likelier) predict risk aversion. Gain seeking (greater impact of positive change than negative change and optimism (belief the best outcome is likelier) predict risk seeking. But other combinations of hedonic sensitivities and beliefs are possible, and they also predict risk preferences. Finally, feelings about the reference point predict hedonic sensitivities. When decision makers feel good about the reference point, they are frequently loss averse. When they feel bad about it, they are often gain seeking. Three studies show that feelings about reference points, feelings about options and feelings about outcomes predict risky choice and help explain why individuals differ in their risk preferences.

O2 plasma-modified carbon nanotube for sulfamethoxazole degradation via peroxymonosulfate activation: Synergism of radical and non-radical pathways boosting water decontamination and detoxification.

Sulfamethoxazole (SMX), a widely used antibiotic, has triggered increasing attention due to its extensive detection in wastewater effluent, causing serious ecological threats. Herein, a carbon-based heterogeneous catalyst was developed by the O2 plasma-etching process, regulating oxygen-containing functional groups (OFGs) and defects of carbon nanotubes (O-CNT) to activate peroxymonosulfate (PMS) for highly efficient SMX abatement. Through adjusting the etching time, the desired active sites (i.e., C=O and defects) could be rationally created. Experiments collectively suggested that the degradation of SMX was owing to the contribution of synergism by radical (•OH (17.3%) and SO4•- (39.3%)) and non-radical pathways (1O2, 43.4%), which originated from PMS catalyzed by C=O and defects. In addition, the possible degradation products and transformation pathways of SMX in the system were inferred by combining the Fukui function calculations and the LC-MS/MS analysis. And the possible degradation pathway was effective in reducing the environmental toxicity of SMX, as evidenced by the T.E.S.T. software and the micronucleus experiment on Vicia faba root tip. Also, the catalytic system exhibited excellent performance for different antibiotics removal, such as amoxicillin (AMX), carbamazepine (CBZ) and isopropylphenazone (PRP). This study is expected to provide an alternative strategy for antibiotics removal in water decontamination and detoxification.

Deep learning-enhanced radiomics for histologic classification and grade stratification of stage IA lung adenocarcinoma: a multicenter study.

Background: Preoperative prediction models for histologic subtype and grade of stage IA lung adenocarcinoma (LUAD) according to the update of the WHO Classification of Tumors of the Lung in 2021 and the 2020 new grade system are yet to be explored. We aim to develop the noninvasive pathology and grade evaluation approach for patients with stage IA LUAD via CT-based radiomics approach and evaluate their performance in clinical practice. Methods: Chest CT scans were retrospectively collected from patients who were diagnosed with stage IA LUAD and underwent complete resection at two hospitals. A deep learning segmentation algorithm was first applied to assist lesion delineation. Expansion strategies such as bounding-box annotations were further applied. Radiomics features were then extracted and selected followed by radiomics modeling based on four classic machine learning algorithms for histologic subtype classification and grade stratification. The area under the receiver operating characteristic curve (AUC) was used to evaluate model performance. Results: The study included 294 and 145 patients with stage IA LUAD from two hospitals for radiomics analysis, respectively. For classification of four histological subtypes, multilayer perceptron (MLP) algorithm presented no annotation strategy preference and achieved the average AUC of 0.855, 0.922, and 0.720 on internal, independent, and external test sets with 1-pixel expansion annotation. Bounding-box annotation strategy also enabled MLP an acceptable and stable accuracy among test sets. Meanwhile, logistic regression was selected for grade stratification and achieved the average AUC of 0.928, 0.837, and 0.748 on internal, independent, and external test sets with optimal annotation strategies. Conclusions: DL-enhanced radiomics models had great potential to predict the fine histological subtypes and grades of early-stage LUADs based on CT images, which might serve as a promising noninvasive approach for the diagnosis and management of early LUADs.

Integrated network pharmacology and experimental validation to explore the mechanisms underlying naringenin treatment of chronic wounds.

Naringenin is a citrus flavonoid with various biological functions and a potential therapeutic agent for skin diseases, such as UV radiation and atopic dermatitis. The present study investigates the therapeutic effect and pharmacological mechanism of naringenin on chronic wounds. Using network pharmacology, we identified 163 potential targets and 12 key targets of naringenin. Oxidative stress was confirmed to be the main biological process modulated by naringenin. The transcription factor p65 (RELA), alpha serine/threonine-protein kinase (AKT1), mitogen-activated protein kinase 1 (MAPK1) and mitogen-activated protein kinase 3 (MAPK3) were identified as common targets of multiple pathways involved in treating chronic wounds. Molecular docking verified that these four targets stably bound naringenin. Naringenin promoted wound healing in mice in vivo by inhibiting wound inflammation. Furthermore, in vitro experiments showed that a low naringenin concentration did not significantly affect normal skin cell viability and cell apoptosis; a high naringenin concentration was cytotoxic and reduced cell survival by promoting apoptosis. Meanwhile, comprehensive network pharmacology, molecular docking and in vivo and in vitro experiments revealed that naringenin could treat chronic wounds by alleviating oxidative stress and reducing the inflammatory response. The underlying mechanism of naringenin in chronic wound therapy involved modulating the RELA, AKT1 and MAPK1/3 signalling pathways to inhibit ROS production and inflammatory cytokine expression.

Chitosan based smart polymer composites: Fabrication and pH-Responsive behavior for bio-medical applications.

This research aimed to synthesize Chitosan/PVA-blank and a series of Cs/PVA/Sepolite based pH-sensitive membranes using a solution casting process. The synthesized Cs/PVA-blank and Cs/PVA/Sep based membranes were investigated via SEM, FTIR, XRD, and TGA techniques. The SEM results of Cs/PVA/Sep based membrane reveal that the hydrolytic stability and strength were improved in acidic and basic media owing to the incorporation of sepiolite content into chitosan. The characteristic band at 3741 cm-1 in the FTIR spectra of the Cs/PVA/Sep membrane confirmed the successful synthesis. The obtained XRD results showed higher d-spacing for Cs/PVA/Sep membranes as compared to the Cs/PVA-blank membranes owing to the intercalation of chitosan in the interlayer spacing of the sepiolite. The obtained TGA results show higher thermally stability for Cs/PVA/Sep membrane as compared to the Cs/PVA-blank sample due to the interaction of sepiolite content with the chitosan matrix. The obtained hydrolytic and swelling studies revealed that the Cs/PVA/Sep membrane displayed enhanced stability in basic and neutral media while showing minimum swelling in an acidic medium. The water uptake ability was checked for Cs/PVA/-blank and Cs/PVA/Sep-60% membrane and the results exhibited that the Cs/PVA/-blank membrane had maximum water uptake value as compared to the Cs/PVA/Sep-60% membrane. While those with a considerable amount of filler had the lowest water uptake values. As Sepolite content increased, the water uptake % values decreases because of weakness in H-bonding (of hydrophilic groups) and due to intercalation in Sepolite layers during polymer formation.

Single-cell RNA-Seq analysis of diabetic wound macrophages in STZ-induced mice.

The crucial role of macrophages in the healing of chronic diabetic wounds is widely known, but previous in vitro classification and marker genes of macrophages may not be fully applicable to cells in the microenvironment of chronic wounds. The heterogeneity of macrophages was studied and classified at the single-cell level in a chronic wound model. We performed single-cell sequencing of CD45 + immune cells within the wound edge and obtained 17 clusters of cells, including 4 clusters of macrophages. One of these clusters is a previously undescribed population of macrophages possessing osteoclast gene expression, for which analysis of differential genes revealed possible functions. We also analysed the differences in gene expression between groups of macrophages in the control and diabetic wound groups at different sampling times. We described the differentiation profile of mononuclear macrophages, which has provided an important reference for the study of immune-related mechanisms in diabetic chronic wounds.

Regulation of defects and nitrogen species on carbon nanotube by plasma-etching for peroxymonosulfate activation: Inducing non-radical/radical oxidation of organic contaminants.

The structural defects and heteroatom dopants of carbonaceous materials play critical roles in their activation of peroxymonosulfate (PMS) for organic pollutants' removal. This study uses plasma-etching technology to control the levels of structural defects and nitrogen species in nitrogen-doped carbon nanotubes (N-CNTs) for excellent PMS activation. The vacancy defects, CO, pyrrolic N and graphitic N could be rationally designed by controlling the plasma-etching time. Obviously, the ID/IG (from 0.56 to 0.94) and CO contents (from 0.07 to 0.44 at%) of N-CNTs increase with rising etching time, exhibiting good linear positive correlations with phenol oxidation rates. Furthermore, through active species identification, quantitative structure-activity relationships analysis and theoretical calculations, vacancy defects (adsorbing PMS O1 site) and CO are confirmed to be the active sites for the generation of 1O2, which is major pathway (82%) for phenol degradation. While radicals induced by pyrrolic N and graphitic N adsorbing PMS O2 site are the minor pathway (18%). Overall, this study sheds new light on the crucial roles of defects and N species in inducing PMS non-radical/radical activation by carbocatalyst via efficiently controlled plasma-etching technology.

Gongying-Jiedu-Xiji recipe promotes the healing of venous ulcers by inhibiting ferroptosis via the CoQ-FSP1 axis.

Objective: Gongying-Jiedu-Xiji recipe (DDL, batch number Z01080175) reduces body temperature, detoxifies, activates the blood circulation, reduces swelling, and dispels decay and pus. The aim of this study was to investigate the mechanism of action by which DDL functions in the treatment of venous ulcers (VUs). Methods: Normal tissues as well as VU tissues before and after DDL treatment were collected from nine VU patients in the hospital with ethical approval. These three tissues were subjected to Prussian blue iron staining, immunoblotting, immunohistochemistry, immunofluorescence, and quantitative real-time PCR to detect the expression of ferroptosis suppressor protein 1 (FSP1), coenzyme Q (CoQ), 4-hydroxynonenal (4-HNE), and glutathione peroxidase 4 (GPX4). After successful validation of the heme-induced human foreskin fibroblast (HFF) ferroptosis model, lyophilized DDL powder was added to the cells, and the cells were subjected to viability assays, immunoblotting, flow cytometry, glutathione (GSH) and malonaldehyde (MDA) assays, electron microscopy and qPCR assays. Results: Ferroptosis in VU tissues was stronger than that in normal tissues, and ferroptosis in VU tissues after DDL treatment was weaker than that before treatment. Inhibition of CoQ and FSP1 and transfection of FSP1 influenced the effects of DDL. Conclusion: Our results suggest that DDL may promote healing by attenuating ferroptosis in VUs and that DDL may promote VU healing by modulating the CoQ-FSP1 axis.

ALDH3B1 protects interfollicular epidermal cells against lipid peroxidation via the NRF2 pathway.

Reactive oxygen species (ROS) production is critical for the initiation of wound repair; however, persistently high levels of ROS can lead to lipid peroxidation in cells and thus affect wound healing. Iron is a transition metal that is an essential component of almost all living cells and organisms. When present in excess in cells and tissues, iron disrupts redox homeostasis and catalyzes the generation of ROS, leading to increased lipid peroxidation. In this study, we found that after treating interfollicular epidermal (IFE) cells with different concentrations of holotransferrin (0 µg/ml, 1 µg/ml, 10 µg/ml, 100 µg/ml, and 1 mg/ml), the intracellular iron content increased, and cell viability and function did not differ significantly among the treatment groups of cells. In addition, the level of lipid peroxidation in IFE cells did not increase following holotransferrin treatment. We speculated that there is a protective mechanism within IFE cells that reduces the occurrence of intracellular lipid peroxidation. We also found that the elevated intracellular iron content of IFE cells was accompanied by elevated ALDH3B1 expression. We investigated the effect of ALDH3B1 on the level of lipid peroxidation in IFE cells and found that elevated ALDH3B1 expression decreased the damage to IFE cells induced by lipid peroxidation. In addition, the NRF2 pathway was found to affect the expression of ALDH3B1, which in turn affected lipid peroxidation in IFE cells. These findings suggest that in IFE cells, activation of the NRF2 pathway can increase the expression of ALDH3B1 and thus reduce the production of intracellular ROS and the occurrence of intracellular lipid peroxidation. Therefore, ALDH3B1 may be a potential target for the treatment of chronic wounds.