Ultra-Stable Aqueous Zinc Anodes: Enabling High-Performance Zinc-Ion Batteries via a ZnSiF6-Derived Protective Interphase.

Zinc-ion batteries (ZIBs) hold immense promise as next-generation energy storage solutions, however, the practical application of zinc anodes is hindered by dendrite formation and parasitic side reactions. Engineering a stable solid- eletrolyte interphase (SEI) is crucial for addressing these issues. This study proposes a novel strategy to enhance Zn anode performance by incorporating a ZnSiF6 additive into a standard ZnSO4 (ZSO) electrolyte. The ZnSiF6 additive facilitates the formation of a stable, fluorine-rich SEI on the Zn anode surface. Characterization reveals a hierarchical SEI structure, primarily composed of porous alkali zinc sulfate (ZHS) with embedded ZnF2. This unique architecture promotes rapid zinc ion desolvation and efficient transport, enhances corrosion resistance, and mitigates hydrogen evolution. Consequently, ZnSiF6-modified cells exhibit exceptional cycling stability, exceeding 3000 hours at 0.5 mA cm-2 and 560 hours at 10 mA cm-2, significantly outperforming ZSO-based cells. The modified cells also achieve high areal capacities (10 mAh cm-2), indicating superior zinc utilization. This work provides key insights for designing stable electrode/electrolyte interfaces, contributing to the development of high-performance aqueous ZIBs.

Sequential oxygen evolution and decoupled water splitting via electrochemical redox reaction of nickel hydroxides.

Alkaline water electrolysis is a promising low-cost strategy for clean and sustainable hydrogen production but is largely limited by the sluggish anodic oxygen evolution reaction and the challenges in maintaining adequate separation between H2 and O2. Here, we reveal an anodic-cathodic sequential oxygen evolution process via electrochemical oxidation and subsequent reduction of Ni hydroxides, enabling much lower overpotentials than conventional anodic oxygen evolution. By using (isotope-labeled) differential electrochemical mass spectrometry and in situ Raman spectroscopy combined with density functional theory calculations, we evidence that the sequential oxygen evolution originates from the electrochemical oxidation of Ni hydroxides to NiOO- active species while undergoing a different, reductive step of NiOO- for the final release of O2 due to weakened Ni-O covalency. Based on this sequential process, we propose and demonstrate a hybrid water electrolysis and energy storage device, which enables time-decoupled hydrogen and oxygen evolution and electrochemical energy storage in the Ni hydroxides.

Exploring causal association between malnutrition, nutrients intake and inflammatory bowel disease: a Mendelian randomization analysis.

Background: Malnutrition has emerged as main side effects of inflammatory bowel disease (IBD) which might also affect the prognosis of IBD. However, whether these associations are causal remains unclear. We aimed to identify the causality of IBD on malnutrition and explore the causal relationship of malnutrition and nutrients intake on IBD by using Mendelian randomization (MR). Methods: Single nucleotide polymorphisms associated with IBD, malnutrition and nutrients intake were obtained from previous researches of genome-wide association studies (GWAS) (p < 0.00000005). MR analysis was conducted to evaluate the causality with different methods based on OR and their 95% CIs. Meanwhile, heterogeneity, pleiotropy and MR-PRESSO were used for instrumental variables evaluation. Results: The results of MR analysis revealed that IBD, both Crohn disease (CD) and ulcerative colitis (UC), could directly impact the incidence of malnutrition (p-value <0.01). CD is directly related to nutrients such as sugar, fat, VA, VC, VD and zinc, while UC is correlated with carbohydrate, fat, VB12, VC, VD, VE, iron, zinc and magnesium. However, our results suggested that malnutrition could not affect the risk of IBD directly (p > 0.05). Further analysis showed similar results that nutrients intake had no direct effect on IBD, neither CD or UC. Conclusion: Our results indicated that IBD increases the risk of malnutrition, however, malnutrition and nutrients intake might not directly affect the progression of IBD.

Precise healing of oral and maxillofacial wounds: tissue engineering strategies and their associated mechanisms.

Precise healing of wounds in the oral and maxillofacial regions is usually achieved by targeting the entire healing process. The rich blood circulation in the oral and maxillofacial regions promotes the rapid healing of wounds through the action of various growth factors. Correspondingly, their tissue engineering can aid in preventing wound infections, accelerate angiogenesis, and enhance the proliferation and migration of tissue cells during wound healing. Recent years, have witnessed an increase in the number of researchers focusing on tissue engineering, particularly for precise wound healing. In this context, hydrogels, which possess a soft viscoelastic nature and demonstrate exceptional biocompatibility and biodegradability, have emerged as the current research hotspot. Additionally, nanofibers, films, and foam sponges have been explored as some of the most viable materials for wound healing, with noted advantages and drawbacks. Accordingly, future research is highly likely to explore the application of these materials harboring enhanced mechanical properties, reduced susceptibility to external mechanical disturbances, and commendable water absorption and non-expansion attributes, for superior wound healing.

Identification of signaling pathways that specify a subset of migrating enteric neural crest cells at the wavefront in mouse embryos.

During enteric nervous system (ENS) development, pioneering wavefront enteric neural crest cells (ENCCs) initiate gut colonization. However, the molecular mechanisms guiding their specification and niche interaction are not fully understood. We used single-cell RNA sequencing and spatial transcriptomics to map the spatiotemporal dynamics and molecular landscape of wavefront ENCCs in mouse embryos. Our analysis shows a progressive decline in wavefront ENCC potency during migration and identifies transcription factors governing their specification and differentiation. We further delineate key signaling pathways (ephrin-Eph, Wnt-Frizzled, and Sema3a-Nrp1) utilized by wavefront ENCCs to interact with their surrounding cells. Disruptions in these pathways are observed in human Hirschsprung's disease gut tissue, linking them to ENS malformations. Additionally, we observed region-specific and cell-type-specific transcriptional changes in surrounding gut tissues upon wavefront ENCC arrival, suggesting their role in shaping the gut microenvironment. This work offers a roadmap of ENS development, with implications for understanding ENS disorders.

Mesenchymal Stem Cells Attenuates Hirschsprung diseases - Associated Enterocolitis by Reducing M1 Macrophages Infiltration via COX-2 Dependent Mechanism.

OBJECTIVE AND DESIGN: Hirschsprung disease-associated enterocolitis (HAEC) is a common life-threatening complication of Hirschsprung disease (HSCR). We aimed to investigate the effectiveness, long-term safety and the underlying mechanisms of Mesenchymal stem cells (MSCs) based therapy for HAEC. MATERIAL OR SUBJECTS: Specimens from HSCR and HAEC patients were used to assess the inflammatory condition. Ednrb knock-out mice was used as HAEC model. MSCs was intraperitoneally transplanted into HAEC mice. The therapy effects, long-term outcome, safety and toxicity and the mechanism of MSCs on the treatment of HAEC were explored in vivo and in vitro. RESULTS: Intestinal M1 macrophages infiltration and severe inflammation condition were observed in HAEC. After the injection of MSCs, HAEC mice showed significant amelioration of the inflammatory injury and inhibition of M1 macrophages infiltration. The expression levels of pro-inflammatory cytokines (TNF-α and IFN-γ) were decreased and anti-inflammatory cytokines (IL-10 and TGF-ß) were increased. In addition, we found that effective MSCs homing to the inflamed colon tissue occurred without long-term toxicity response. However, COX-2 inhibitor could diminish the therapeutic effects of MSCs. Using MSCs and macrophages co-culture system, we identified that MSCs could alleviate HAEC by inhibiting M1 macrophages activation through COX-2-dependent MAPK/ERK signaling pathway. CONCLUSIONS: MSCs ameliorate HAEC by reducing M1 macrophages polarization via COX-2 mediated MAPK/ERK signaling pathway, thus providing novel insights and potentially promising strategy for the treatment or prevention of HAEC.

Cinchophen induces RPA1 related DNA damage and apoptosis to impair ENS development of zebrafish.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have become contaminants widely distributed in the environment due to improper disposal and discharge. Previous study has found several components might involve in impairing enteric nervous system (ENS) development of zebrafish, including NSAIDs cinchophen. Deficient ENS development in fetal could lead to Hirschsprung disease (HSCR), a congenital neurocristopathy characterized by absence of enteric neurons in hindgut. However, the intrinsic mechanism of neurotoxicity of cinchophen is unclear. We confirmed that cinchophen could impair ENS development of zebrafish and transcriptome sequencing revealed that disfunction of Replication protein A1 (RPA1), which is involved in DNA replication and repairment, might be relevant to the neurotoxicity effects induced by cinchophen. Based on previous data of single cell RNA sequencing (scRNA-seq) of zebrafish gut cells, we observed that rpa1 mainly expressed in proliferating, differentiating ENS cells and neural crest progenitors. Interestingly, cinchophen induced apoptosis and impaired proliferation. Furthermore, cinchophen caused DNA damage and abnormal activation of ataxia telangiectasia mutated/ Rad3 related (ATM/ATR) and checkpoint kinase 2 (CHK2). Finally, molecular docking indicated cinchophen could bind and antagonize RPA1 more effectively. Our study might provide a better understanding and draw more attention to the role of environmental factors in the pathogenesis of HSCR. And the mechanism of cinchophen neurotoxicity would give theoretical guidance for clinical pharmacy.

Study on the mechanism of naringin in promoting bone differentiation: In vitro and in vivo study.

Objective: Osteoporosis is a common clinical bone disease that occurs most frequently in middle-aged and elderly people. Various traditional herbal medicine formulations have shown significant benefits in models of osteoporosis. In this study, we aim to investigate the osteogenic efficacy of naringin (NRG) in the osteoporotic state. Design: We treated Bone marrow stromal cells (BMSCs) with various concentrations of NRG for 3 and 7 days. BMSC proliferation was measured by the MTT assay. The effect of NRG on the osteogenic differentiation of BMSCs was detected by ALP and alizarin red staining. The effect of NRG on the BMP2/Runx2/Osterix signaling pathway was analyzed by using real-time PCR. The effect of NRG on the oestrogen receptor was measured by Enzyme-linked immunosorbent assay. In vivo animal experiments were performed by micro-computed tomography and ALP immunohistochemistry to determine the ectopic osteogenic effect of NRG sustained-release nanoparticles in a mouse model of osteoporosis. Results: NRG promoted the proliferation and osteogenic differentiation of BMSCs. Moreover, it also activated the BMP2/Runx2/Osterix signaling pathway. When NRG sustained-release nanoparticles were added in vivo in animal experiments, we found that NRG sustained-release nanoparticles had better ectopic osteogenic effects in a mouse model of osteoporosis. Conclusions: NRG induced osteoblastic differentiation of BMSCs by activating the BMP2/Runx2/Osterix signaling pathway and promoted the regulation of oestrogen receptor pathway protein expression, and NRG sustained-release nanoparticles exerted a more significant in vivo ectopic osteogenic effect in an osteoporosis mouse model. Therefore, naringin is expected to be developed as a novel treatment for inducing osteogenesis, because of its ubiquitous, cost-efficient, and biologically active characteristics. However, further research is needed on how to improve the pharmacokinetic properties of naringin and its specific mechanism.

Virulence and Molecular Characterization Reveal Signs of Sexual Genetic Recombination of Puccinia striiformis f. sp. tritici and Puccinia striiformis f. sp. hordei in Tibet.

Stripe rust of wheat and barley is caused by different formae speciales, Puccinia striiformis f. sp. tritici (Pst) and P. striiformis f. sp. hordei (Psh), respectively. To understand the relationship between the populations of the two formae speciales, a total of 260 P. striiformis isolates, including 140 from barley and 120 from wheat collected from Linzhi, Tibet, China, from 2018 to 2020, were tested on 18 barley and 13 wheat genotypes and genotyped with 26 single-nucleotide polymorphism (SNP)-based Kompetitive allele-specific PCR (KASP) markers. As a result, 260 isolates were identified as 83 virulence phenotypes (VPs), 115 of which as 9 VPs and could infect only wheat (wheat population), 111 as 54 VPs and could infect only barley (barley population), and 34 belonged to 20 VPs that could infect both wheat and barley (mixed population). Of the 149 multilocus genotypes (MLGs) that were identified, 92 were from wheat, 56 from barley, and 1 from both wheat and barley. Phenotypic and genotypic diversity was high in the populations from wheat and barley. Low linkage disequilibrium was found in most of the sampling sites of both crops, indicating strong signs of sexual reproduction (|r̄d| = 0.022 to 0.393, P = 0.004 to 0.847), whereas it was not observed in the overall population (wheat and barley sources) and the wheat, barley, and mixed populations, which may be because of the complex composition of isolates. Population structure analyses based on phenotyping and SNP-KASP genotypes supported the separation of the two formae speciales. However, MLGs and clusters containing isolates from both wheat and barley obviously indicated sexual genetic recombination between the two formae speciales. The results of the study provided an insight into evolution of Pst and Psh and showed the importance of management strategies for stripe rust of wheat and barley in regions where both crops are grown.

Association of carotid atherosclerotic plaque and intima-media thickness with the monocyte to high-density lipoprotein cholesterol ratio among low-income residents of rural China: a population-based cross-sectional study.

BACKGROUND: The monocytes to high-density lipoprotein cholesterol ratio (MHR) has been identified as a potential biomarker for cardiovascular and cerebrovascular diseases. In this population-based cross-sectional study, we explored the relationships among carotid artery disease (CAD), including the presence of carotid atherosclerotic plaque (CAP) and carotid artery intima-media thickness (CIMT), the MHR, and related parameter changes. METHODS: This cross-sectional study, Conducted from April to June 2019 in a rural area of Tianjin, involved middle-aged and elderly participants. Based on carotid ultrasound examinations, participants were divided into CAP and non-CAP groups. Logistic regression and Receiver Operating Characteristic (ROC) curve analyses were utilized to assess MHR's predictive value for CAP. Gender-specific analyses were also performed to examine predictive variations. The relationship between CIMT and MHR was evaluated using linear regression. RESULTS: Of the 2109 participants meeting the inclusion criteria, 51.6% were identified with CAP. Multivariate analysis revealed a significant association between MHR and CAP prevalence, (OR, 9.670; 95% CI, 2.359-39.631; P = 0.002), particularly in females (OR, 5.921; 95% CI, 1.823-19.231; P = 0.003), after adjusting for covariates. However, no significant correlation was found between CIMT and MHR when adjusted for other factors. The ROC analysis showed the area under the curve for MHR and CAP to be 0.569 (95% CI: 0.544-0.593; P < 0.001). CONCLUSIONS: These findings suggested that it is crucial to enhance early screening and intervention for CAD, specifically focusing on the prevention and progression of CAP, to address the unique health challenges faced by low-income groups in rural settings. Emphasizing these preventive measures could significantly contribute to improving cardiovascular health outcomes in this vulnerable population.

Novel 3D-printing bilayer GelMA-based hydrogel containing BP,ß-TCP and exosomes for cartilage-bone integrated repair.

The integrated repair of cartilage and bone involves the migration and differentiation of cells, which has always been a difficult problem to be solved. We utilize the natural biomaterial gelatin to construct gelatin methacryloyl (GelMA), a hydrogel scaffold with high cell affinity. GelMA is mixed with different components to print a bi-layer porous hydrogel scaffold with different modulus and composition in upper and lower layers through three-dimensional (3D) printing technology. The upper scaffold adds black phosphorus (BP) and human umbilical cord mesenchymal stem cells (hUMSCs) exosomes (exos) in GelMA, which has a relatively lower elastic modulus and is conducive to the differentiation of BMSCs into cartilage. In the lower scaffold, in addition to BP and hUMSCs exos,ß-tricalcium phosphate (ß-TCP), which has osteoconductive and osteoinductive effects, is added to GelMA. The addition ofß-TCP significantly enhances the elastic modulus of the hydrogel scaffold, which is conducive to the osteogenic differentiation of bone marrow mesenchymal stem cells(BMSCs).In vitroexperiments have confirmed that the bi-layer scaffolds can promote osteogenesis and chondrogenic differentiation respectively. And in the rabbit cartilage-bone injury model, MRI and micro-CT results show that the 3D printed bi-layer GelMA composite scaffold has a repair effect close to normal tissue.

Counting d-Orbital Vacancies of Transition-Metal Catalysts for the Sulfur Reduction Reaction.

The electrocatalytic sulfur reduction reaction (SRR) would allow the production of renewable high-capacity rechargeable lithium-sulfur (Li-S) batteries using sustainable and nontoxic elemental sulfur as a cathode material, but its slow reaction rate causes a serious shuttle effect and dramatically reduces the capacity. We found that a catalyst composed of Pd nanoparticles supported by ordered mesoporous carbon (Pd/OMC) had a high reaction rate in the SRR, and a Li-S battery assembled with this catalyst had a low shuttle constant of 0.031 h-1 and a high-rate performance with a specific capacity of 1527 mAh g-1 at 0.1 C which is close to the theoretical value. The high activity of Pd/OMC with a d-orbital vacancy of 0.87 e was predicted from a volcano relationship between the d charge for the metal and the adsorption activation entropy and reaction rate for the SRR by examining Pd, Au, Pt, Rh, and Ru transition-metal nanocatalysts. The strategy of using a single electronic structure descriptor to design high-efficiency SRR catalysts has suggested a way to produce practical Li-S batteries.

Microsatellite markers reveal genetic diversity and population structure of Portunus trituberculatus in the Bohai Sea, China.

The swimming crab, Portunus trituberculatus, is one of the main aquaculture species in Chinese coastal regions due to its palatability and high economic value. To obtain a better understanding of the genetic diversity of P. trituberculatus in the Bohai Sea, the present study used 40 SSR loci to investigate the genetic diversity and population structure of 420 P. trituberculatus individuals collected from seven populations in the Bohai Sea. Genetic parameters revealed a low level of genetic diversity in the cultured population (SI = 1.374, He = 0.687, and PIC = 0.643) in comparison with wild populations (SI ≥ 1.399, He ≥ 0.692, and PIC ≥ 0.651). The genetic differentiation index (Fst) and gene flow (Nm) ranged from 0.001 to 0.060 (mean: 0.022) and 3.917 to 249.750 (mean: 31.289) respectively, showing a low differentiation among the seven populations of P. trituberculatus. Population structure analysis, phylogenetic tree, and principal component analysis (PCA) demonstrated that the seven groups of P. trituberculatus were divided into four subpopulations (K = 4), but the correlation between genetic structure and geographical distribution was not obvious. These results are expected to provide useful information for the fishery management of wild swimming crabs.

Relevant mechanisms of MAIT cells involved in the pathogenesis of periodontitis.

Mucosal-associated invariant T (MAIT) cells are a group of unconventional T cells that are abundant in the human body, recognize microbial-derived vitamin B metabolites presented by MHC class I-related protein 1 (MR1), and rapidly produce proinflammatory cytokines, which are widely involved in the immune response to various infectious diseases. In the oral mucosa, MAIT cells tend to accumulate near the mucosal basal lamina and are more inclined to secrete IL-17 when activated. Periodontitis is a group of diseases that manifests mainly as inflammation of the gums and resorption of the alveolar bone due to periodontal tissue invasion by plaque bacteria on the dental surface. The course of periodontitis is often accompanied by a T-cell-mediated immune response. This paper discussed the pathogenesis of periodontitis and the potential contribution of MAIT cells to periodontitis.

Comprehensive characterization of the genetic landscape of familial Hirschsprung's disease.

BACKGROUND: Hirschsprung's disease (HSCR) is one of the most common congenital digestive tract malformations and can cause stubborn constipation or gastrointestinal obstruction after birth, causing great physical and mental pain to patients and their families. Studies have shown that more than 20 genes are involved in HSCR, and most cases of HSCR are sporadic. However, the overall rate of familial recurrence in 4331 cases of HSCR is about 7.6%. Furthermore, familial HSCR patients show incomplete dominance. We still do not know the penetrance and genetic characteristics of these known risk genes due to the rarity of HSCR families. METHODS: To find published references, we used the title/abstract terms "Hirschsprung" and "familial" in the PubMed database and the MeSH terms "Hirschsprung" and "familial" in Web of Science. Finally, we summarized 129 HSCR families over the last 40 years. RESULTS: The male-to-female ratio and the percentage of short segment-HSCR in familial HSCR are much lower than in sporadic HSCR. The primary gene factors in the syndromic families are ret proto-oncogene (RET) and endothelin B receptor gene (EDNRB). Most families show incomplete dominance and are relevant to RET, and the RET mutation has 56% penetrance in familial HSCR. When one of the parents is a RET mutation carrier in an HSCR family, the offspring's recurrence risk is 28%, and the incidence of the offspring does not depend on whether the parent suffers from HSCR. CONCLUSION: Our findings will help HSCR patients obtain better genetic counseling, calculate the risk of recurrence, and provide new insights for future pedigree studies.

The mechanism of efferocytosis in the pathogenesis of periodontitis and its possible therapeutic strategies.

Periodontitis is an inflammatory disease characterized by the destruction of periodontal tissues, and its etiology is related to several systemic factors. At present, the destruction of periodontal tissues is considered to be the result of inflammation resolution disorders. Efferocytosis plays an important role in the resolution of inflammation, and defective efferocytosis is an essential factor in the persistence of many chronic inflammatory diseases. Therefore, this review will describe the mechanisms involved in the efferocytosis of macrophages in the pathogenesis of periodontitis and highlight emerging therapeutic strategies to provide new ideas for future periodontal treatment.

Determinants of arterial elastic function in middle-aged and elderly people: A population-based cross-sectional study from a low-income population in China.

Background: Arterial stiffness is closely associated with the occurrence of many cardiovascular and cerebrovascular diseases. However, the risk factors and mechanisms related to arterial stiffness development have only been partially elucidated. We aimed to describe arterial elastic function and its influencing factors in middle-aged and elderly people in rural China. Methods: This was a cross-sectional study conducted among residents, aged ≥45 years, of Tianjin, China, between April and July 2015. Data regarding participant demographics, medical history, lifestyle, and physical examination results were collected and assessed the association with arterial elastic function using linear regression. Results: Of the 3,519 participants, 1,457 were male (41.4%). Brachial artery distensibility (BAD) decreased by 0.5%/mmHg with every 10-year increment in age. The mean BAD value was 0.864%/mmHg lower in women than in men. With each unit increase in mean arterial pressure, the BAD decreased by 0.042%/mmHg. In patients with hypertension or diabetes, the BAD decreased by 0.726 and 0.183%/mmHg, respectively, compared with those without hypertension or diabetes. For each unit increase in triglyceride (TG) level, the mean BAD increased by 0.043%/mmHg. With each increase in body mass index (BMI) category, the BAD increased by 0.113%/mmHg. Brachial artery compliance (BAC) decreased by 0.007 ml/mmHg with each 10-year increase in age, and brachial artery resistance (BAR) increased by 30.237 dyn s-1 cm-5. The mean BAC in women was 0.036 ml/mmHg lower and the mean BAR was 155.231 dyn s-1 cm-5 higher in women than in men. In individuals with hypertension, the mean BAC decreased by 0.009 ml/mmHg and the mean BAR increased by 26.169 dyn s-1 cm-5. With each increase in BMI category, the mean BAC increased by 0.005 ml/mmHg and the mean BAR decreased by 31.345 dyn s-1 cm-5. For each unit increase in TG level, the mean BAC increased by 0.001 ml/mmHg. Conclusion: These findings indicate that age, sex, mean arterial pressure, BMI, diabetes, hypertension, and TG level are independently associated with the components of peripheral arterial elasticity. Understanding the factors influencing arterial stiffness is important for developing interventions to minimize arterial aging and cardiovascular and cerebrovascular diseases caused by arterial aging.

The role of Nrf2 in periodontal disease by regulating lipid peroxidation, inflammation and apoptosis.

Nuclear factor E2-related factor 2(Nrf2) is a transcription factor that mainly regulates oxidative stress in the body. It initiates the expression of several downstream antioxidants, anti-inflammatory proteins and detoxification enzymes through the Kelch-like ECH-associating protein 1 (Keap1) -nuclear factor E2-related factor 2(Nrf2) -antioxidant response element (ARE) signaling pathway. Its anti-apoptosis, anti-oxidative stress and anti-inflammatory effects have gradually become the focus of periodontal disease research in recent years. In this paper, the structure and function of Nrf2 pathway and its mechanism of action in the treatment of periodontitis in recent years were analyzed and summarized, so as to further clarify the relationship between Nrf2 pathway and oxidative stress in the occurrence and development of periodontitis, and to provide ideas for the development of new treatment drugs targeting Nrf2 pathway.

Ferroptosis: A New Development Trend in Periodontitis.

Periodontitis is a chronic inflammatory disease associated with bacterial biofilm. It is characterized by loss of periodontal support tissue and has long been considered as a "silent disease". Because it is difficult to prevent and has a health impact that can not be ignored, researchers have been focusing on a mechanism-based treatment model. Ferroptosis is an iron-dependent regulatory form of cell death, that directly or indirectly affects glutathione peroxidase through different signaling pathways, resulting in a decrease in cell antioxidant capacity, accumulation of reactive oxygen species and lipid peroxidation, which cause oxidative cell death and tissue damage. Recently, some studies have proven that iron overload, oxidative stress, and lipid peroxidation exist in the process of periodontitis. Based on this, this article reviews the relationship between periodontitis and ferroptosis, in order to provide a theoretical reference for future research on the prevention and treatment of periodontal disease.

Identification and validation of the common pathogenesis and hub biomarkers in Hirschsprung disease complicated with Crohn's disease.

Background: Although increasing evidence has supported that Hirschsprung disease (HSCR) is the risk factor for children developing Crohn's disease (CD), the common mechanism of its co-occurrence remains unknown. The purpose of this study is to further explore the underlying mechanism and biomarkers for the co-occurrence of HSCR and CD. Methods: The Gene Expression Omnibus (GEO) database was used to obtain gene expression profiles for CD (GSE95095) and HSCR (GSE98502). Following the identification of the shared differentially expressed genes (DEGs) of CD and HSCR, functional annotation, protein-protein interaction (PPI) network creation, and module assembly were performed to discover hub genes. RT-qPCR was performed to validate the expression of the hub genes in HSCR samples. The receiver operating characteristic (ROC) curve was utilized to assess the accuracy of the hub genes as biomarkers in predicting CD in both the training dataset and test dataset. Results: A total of 103 common DEGs (50 downregulated genes and 53 upregulated genes) were chosen for further investigation. The importance of chemokines and cytokines in these two disorders is highlighted by functional analysis. MCODE plug identified three important modules, which functionally enriched the immune system process. Finally, nine hub genes were identified using cytoHubba, including IL1B, IL10, CXCL10, ICAM1, EGR1, FCGR3A, S100A12, S100A9, and FPR1. The nine hub genes were mainly enriched in immune- and inflammation-related pathways. External data profiles and RT-qPCR confirmed the expression of the nine hub genes in HSCR and CD. ROC analysis revealed that the nine hub genes had a strong diagnostic value. Conclusion: Our study reveals the common pathogenesis of HSCR and CD. These hub genes and diagnostic models may provide novel insight for the diagnosis and treatment of HSCR complicated with CD.