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BACKGROUND: Jilin white goose is an excellent local breed in China, with a high annual egg production and laying eggs mainly from February to July each year. The testis, as the only organ that can produce sperm, can affect the sexual maturity and fecundity of male animals. Its growth and development are affected and regulated by a variety of factors. Proteomics is generally applied to identify and quantify proteins in cells and tissues in order to understand the physiological or pathological changes that occur in tissues or cells under specific conditions. Currently, the female poultry reproductive system has been extensively studied, while few related studies focusing on the regulatory mechanism of the reproductive system of male poultry have been conducted. RESULTS: A total of 1753 differentially expressed proteins (DEPs) were generated in which there were 594, 391 and 768 different proteins showing differential expression in three stages, Initial of Laying Cycle (ILC), Peak of Laying Cycle (PLC) and End of Laying Cycle (ELC). Furthermore, bioinformatics was used to analyze the DEPs. Gene ontology (GO) enrichment, Clusters of Orthologous Groups (COG), Kyoto Encyclopedia of Genes and Genomes (KEGG) and protein-protein interaction (PPI) network analysis were adopted. All DEPs were found to be implicated in multiple biological processes and pathways associated with testicular development, such as renin secretion, Lysosomes, SNARE interactions in vesicle trafficking, the p53 signaling pathway and pathways related to metabolism. Additionally, the reliability of transcriptome results was verified by real-time quantitative PCR by selecting the transcript abundance of 6 selected DEPs at the three stages of the laying cycle. CONCLUSIONS: The funding in this study will provide critical insight into the complex molecular mechanisms and breeding practices underlying the developmental characteristics of testicles in Jilin white goose.
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Gansos , Testículo , Animales , Masculino , Femenino , Gansos/genética , Reproducibilidad de los Resultados , Semen , Transcriptoma , Perfilación de la Expresión GénicaRESUMEN
Brown fat adipose tissue (BAT) is a therapeutic potential target to improve obesity, diabetes and cold acclimation in mammals. During the long-term cold exposure, the hyperplastic sympathetic network is crucial for BAT the maintain the highly thermogenic status. It has been proved that the sympathetic nervous drives the thermogenic activity of BAT via the release of norepinephrine. However, it is still unclear that how the thermogenic BAT affects the remodeling of the hyperplastic sympathetic network, especially during the long-term cold exposure. Here, we showed that following long-term cold exposure, SCD1-mediated monounsaturated fatty acid biosynthesis pathway was enriched, and the ratios of monounsaturated/saturated fatty acids were significantly up-regulated in BAT. And SCD1-deficiency in BAT decreased the capacity of cold acclimation, and suppressed long-term cold mediated BAT thermogenic activation. Furthermore, by using thermoneutral exposure and sympathetic nerve excision models, we disclosed that SCD1-deficiency in BAT affected the thermogenic activity, depended on sympathetic nerve. In mechanism, SCD1-deficiency resulted in the unbalanced ratio of palmitic acid (PA)/palmitoleic acid (PO), with obviously higher level of PA and lower level of PO. And PO supplement efficiently reversed the inhibitory role of SCD1-deficiency on BAT thermogenesis and the hyperplastic sympathetic network. Thus, our data provided insight into the role of SCD1-mediated monounsaturated fatty acids metabolism to the interaction between thermogenic activity BAT and hyperplastic sympathetic networks, and illustrated the critical role of monounsaturated fatty acids biosynthetic pathway in cold acclimation during the long-term cold exposure.
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Tejido Adiposo Pardo , Termogénesis , Animales , Tejido Adiposo Pardo/metabolismo , Termogénesis/fisiología , Sistema Nervioso Simpático , Obesidad/metabolismo , Ácidos Grasos Monoinsaturados/metabolismo , Frío , MamíferosRESUMEN
The quantum Hall effect is one of the exclusive properties displayed by Dirac Fermions in topological insulators, which propagates along the chiral edge state and gives rise to quantized electron transport. However, the quantum Hall effect formed by the nondegenerate Dirac surface states has been elusive so far. Here, we demonstrate the nondegenerate integer quantum Hall effect from the topological surface states in three-dimensional (3D) topological insulator ß-Ag2Te nanostructures. Surface-state dominant conductance renders quantum Hall conductance plateaus with a step of e2/h, along with typical thermopower behaviors of two-dimensional (2D) massless Dirac electrons. The 2D nature of the topological surface states is proven by the electrical and thermal transport responses under tilted magnetic fields. Moreover, the degeneracy of the surface states is removed by structure inversion asymmetry (SIA). The evidenced SIA-induced nondegenerate integer quantum Hall effect in low-symmetry ß-Ag2Te has implications for both fundamental study and the realization of topological magneto-electric effects.
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In recent years, China has focused its development on technological innovation, trying to achieve a win-win situation between environmental protection and economic growth, and it has formulated a series of policies to promote technological innovation. Taking China's national independent innovation demonstration zone (NIIDZ) policy as an example, this paper empirically investigates the impact of China's innovation policy on haze pollution by using a difference-in-differences (DID) model. The results show that the NIIDZ policy promotes the governance of urban haze pollution and confirms the applicability of the experimentalist governance model in the practice of innovation policy in developing countries. Dynamic analysis shows that the NIIDZ policy has an experience accumulation effect. This policy can continue to promote haze control for at least 6 years, and the policy effect increases year by year. Action mechanism analysis shows that the NIIDZ policy can inhibit urban haze pollution by promoting urban technological innovation and high-tech industrial agglomeration. The estimation results of the spatial DID model show that the NIIDZ policy not only inhibits haze pollution in NIIDZ cities but also has an inhibitory effect on haze pollution in the surrounding non-NIIDZ cities and the NIIDZ cities, which confirms the positive externality characteristics of policy diffusion theory and environmental governance. The conclusions of this paper have important theoretical value for understanding the ecological effect of innovation policy and provide experience for developing countries to implement an experimentalist governance model.
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Contaminación del Aire , Contaminación del Aire/análisis , Contaminación del Aire/prevención & control , China , Ciudades , Conservación de los Recursos Naturales , Desarrollo Económico , Política Ambiental , Contaminación Ambiental/análisis , PolíticasRESUMEN
In the troposphere, the knowledge about nitrous acid (HONO) sources is incomplete. The missing source of sulfate and fine particles cannot be explained during haze events. Air quality models cannot predict high levels of secondary fine-particle pollution. Despite extensive studies, one challenging issue in atmospheric chemistry is identifying the source of HONO. Here, we present direct ab initio molecular dynamics simulation evidence and typical air pollution events of the formation of gaseous HONO, nitrogen dioxide/hydrogen sulfite (HOS(O)2-NO2 or NO2-HSO3) from nitrogen dioxide (NO2), sulfur dioxide (SO2), water (H2O), and ammonia (NH3) molecules in a proportion of 2:1:3:3. The reactions show a new mechanism for the formation of HONO and NO2-HSO3 in the troposphere, especially when the concentration of NO2, SO2, H2O, and NH3 is high (e.g., 2:1:3:3 or higher) in the air. Contrary to the proportion NO2, SO2, H2O, and NH3 equaling to 1:1:3:1 and 1:1:3:2, the proportion (2:1:3:3) enables barrierless reactions and weak interactions between molecules via the formation of HONO, NO2-HSO3, and NH3/H2O. In addition, field observations are carried out, and the measured data are summarized. Correlation analysis supported the conversion of NO2 to HONO during observational studies. The weak interactions promote proton transfer, resulting in the generation of HONO, NO2-HSO3, and NH3/H2O pairs.
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We designed a simulation program that mimics the CRISPR-Cas9 editing on evolving barcode and double strand break repair procedure along with cell divisions. Emerging barcode mutations tend to build upon previously existing mutations, occurring sequentially with each generation. This process results in a unique mutation profile in each cell. We sample the barcodes in leaf cells and reconstruct the lineage, comparing it to the original lineage tree to test algorithm accuracy under different parameter settings. Our computational simulations validate the reasonable assumptions deduced from experimental observations, emphasizing that factors such as sampling size, barcode length, multiple barcodes, indel probabilities, and Cas9 activity are critical for accurate and successful lineage tracing. Among the many factors we found that sampling size and indel probabilities are two major ones that affect lineage tracing accuracy. Large segment deletions in early generations could greatly impact lineage accuracy. These simulation results offer insightful recommendations for enhancing the design and analysis of Cas9-mediated molecular barcodes in actual experiments.
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Sistemas CRISPR-Cas , Simulación por Computador , Edición Génica , Edición Génica/métodos , Algoritmos , Código de Barras del ADN Taxonómico/métodos , Linaje de la Célula/genética , Mutación INDEL , MutaciónRESUMEN
In noncentrosymmetric superconductors, superconducting and normal conductions can interchange on the basis of the current flow direction. This effect is termed a superconducting diode effect (SDE), which is a focal point of recent research. The broken inversion and time-reversal symmetry is believed to be the requirements of SDE, but their intrinsic role has remained elusive. Here, we report strain-controlled SDEs in a layered trigonal superconductor, PbTaSe2. The SDE was found exclusively in a strained device with its absence in an unstrained device despite that it is allowed in unstrained trigonal structure. Moreover, the zero-field or magnetic field-even (magnetic field-odd) SDE is observed when the strain and current are along armchair (zigzag) direction The results unambiguously demonstrate the intrinsic SDE under time-reversal symmetry and the critical role of strain-induced electric polarization.
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Tumor-associated neutrophils (TANs) have been shown to promote immunosuppression and tumor progression, and a high TAN frequency predicts poor prognosis in triple-negative breast cancer (TNBC). Dysregulation of CREB binding protein (CBP)/P300 function has been observed with multiple cancer types. The bromodomain (BRD) of CBP/P300 has been shown to regulate its activity. In this study, we found that IACS-70654, a novel and selective CBP/P300 BRD inhibitor, reduced TANs and inhibited the growth of neutrophil-enriched TNBC models. In the bone marrow, CBP/P300 BRD inhibition reduced the tumor-driven abnormal differentiation and proliferation of neutrophil progenitors. Inhibition of CBP/P300 BRD also stimulated the immune response by inducing an IFN response and MHCI expression in tumor cells and increasing tumor-infiltrated CTLs. Moreover, IACS-70654 improved the response of a neutrophil-enriched TNBC model to docetaxel and immune checkpoint blockade. This provides a rationale for combining a CBP/P300 BRD inhibitor with standard-of-care therapies in future clinical trials for neutrophil-enriched TNBC.
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Feather is an important economic trait of poultry, and growth and development state of feathers plays an important role in the economic value of poultry. Dermal fibroblasts are required for structural integrity of the skin and for feather follicle development. How FOXO3 affects feather follicle development as skin tissues change during goose embryo (Anser cygnoides) development and growth is not well understood. Here, we demonstrate that in vitro culture of single feathers and skin tissue results in changes in feather morphological structure by adding drugs to the culture medium that affect FOXO3 expression. We used feather follicles to show that during growth, the root location of feathers, the dermis layer, affects cell proliferation and apoptosis and regulates the expression of major genes in the Wingless-types/beta-catenin (Wnt/ß-catenin) signaling pathway through the activity of FOXO3 in dermal fibroblasts. Feathers and dorsal skin tissues develop the correct structure, but feather length and width and feather follicle diameter change significantly (p < 0.05) without significant changes in feather follicle density (p > 0.05). Transfected dermal fibroblasts also showed that FOXO3 affected the formation and development of feather follicles in the embryonic stage by regulating the Wnt/ß-catenin signaling pathway. Therefore, this study reveals the critical role of dermal fibroblast-FOXO3-induced Wnt/ß-catenin signaling in promoting the formation and development of embryonic feather follicles.
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Plumas , Gansos , Animales , Vía de Señalización Wnt , beta Catenina/genética , PollosRESUMEN
Renal cell carcinoma (RCC) bone metastatis progression is driven by crosstalk between tumor cells and the bone microenvironment, which includes osteoblasts, osteoclasts, and osteocytes. RCC bone metastases (RCCBM) are predominantly osteolytic and resistant to antiresorptive therapy. The molecular mechanisms underlying pathologic osteolysis and disruption of bone homeostasis remain incompletely understood. We previously reported that BIGH3/TGFBI (transforming growth factor-beta-induced protein ig-h3, shortened to BIGH3 henceforth) secreted by colonizing RCC cells drives osteolysis by inhibiting osteoblast differentiation, impairing healing of osteolytic lesions, which is reversible with osteoanabolic agents. Here, we report that BIGH3 induces osteocyte apoptosis in both human RCCBM tissue specimens and in a preclinical mouse model. We also demonstrate that BIGH3 reduces Cx43 expression, blocking gap junction (GJ) function and osteocyte network communication. BIGH3-mediated GJ inhibition is blocked by the lysosomal inhibitor hydroxychloroquine (HCQ), but not osteoanabolic agents. Our results broaden the understanding of pathologic osteolysis in RCCBM and indicate that targeting the BIGH3 mechanism could be a combinational strategy for the treatment of RCCBM-induced bone disease that overcomes the limited efficacy of antiresorptives that target osteoclasts.
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Apoptosis , Neoplasias Óseas , Carcinoma de Células Renales , Proteínas de la Matriz Extracelular , Uniones Comunicantes , Neoplasias Renales , Osteocitos , Osteocitos/metabolismo , Osteocitos/patología , Humanos , Animales , Neoplasias Óseas/secundario , Neoplasias Óseas/metabolismo , Neoplasias Óseas/patología , Neoplasias Óseas/tratamiento farmacológico , Carcinoma de Células Renales/patología , Carcinoma de Células Renales/metabolismo , Carcinoma de Células Renales/tratamiento farmacológico , Carcinoma de Células Renales/secundario , Apoptosis/efectos de los fármacos , Neoplasias Renales/patología , Neoplasias Renales/metabolismo , Neoplasias Renales/tratamiento farmacológico , Uniones Comunicantes/metabolismo , Uniones Comunicantes/patología , Proteínas de la Matriz Extracelular/metabolismo , Ratones , Progresión de la Enfermedad , Conexina 43/metabolismo , Línea Celular Tumoral , Factor de Crecimiento Transformador beta/metabolismo , Osteólisis/patología , Osteólisis/metabolismo , FemeninoRESUMEN
Microenvironment niches determine cellular fates of metastatic cancer cells. However, robust and unbiased approaches to identify niche components and their molecular profiles are lacking. We established Sortase A-Based Microenvironment Niche Tagging (SAMENT), which selectively labels cells encountered by cancer cells during metastatic colonization. SAMENT was applied to multiple cancer models colonizing the same organ and the same cancer to different organs. Common metastatic niche features include macrophage enrichment and T cell depletion. Macrophage niches are phenotypically diverse between different organs. In bone, macrophages express the estrogen receptor alpha (ERα) and exhibit active ERα signaling in male and female hosts. Conditional knockout of Esr1 in macrophages significantly retarded bone colonization by allowing T cell infiltration. ERα expression was also discovered in human bone metastases of both genders. Collectively, we identified a unique population of ERα+ macrophages in the metastatic niche and functionally tied ERα signaling in macrophages to T cell exclusion during metastatic colonization. HIGHLIGHTS: SAMENT is a robust metastatic niche-labeling approach amenable to single-cell omics.Metastatic niches are typically enriched with macrophages and depleted of T cells.Direct interaction with cancer cells induces ERα expression in niche macrophages. Knockout of Esr1 in macrophages allows T cell infiltration and retards bone colonization.
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Regional integration is an important trend of economic development worldwide, which helps to break the restrictions of administrative divisions on economic development and pollution control. According to the relevant theories of environmental economic geography, regional integration will have an important impact on regional pollution control. Based on China's urban panel data, we empirically tested the impact of regional integration on regional environmental pollution and its mechanism by using econometric analysis methods, such as the difference-in-differences model and the mediating effect model. We found that regional integration can effectively reduce urban pollutant emissions and that the emission reduction effect of regional integration is characterized by significant heterogeneity at different pollution levels. The mechanism analysis showed that the green technology innovation effect of regional integration is an important mechanism for promoting urban emission reduction. The conclusions of this paper enrich the relevant theories of environmental economic geography and provide new ideas to implement integration strategies to promote sustainable economic development in developing countries.
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Contaminantes Ambientales , Contaminación Ambiental , Contaminación Ambiental/análisis , China , Contaminantes Ambientales/análisis , Desarrollo Sostenible , Invenciones , Desarrollo Económico , CiudadesRESUMEN
Since the reform and opening up, China's urbanization level has rapidly increased. However, urban civilization construction lags behind, creating a series of problems, such as environmental pollution, further restricting the healthy and sustainable development of cities. Therefore, China has carried out top-down civilized city construction led by the government. This paper regards the "national civilized city" selection implemented by the Chinese government as a quasi-natural experiment and empirically tests the impact of government-led civilized city construction on urban green innovation and the mechanism of this impact by using the progressive difference-in-differences (DID) model based on panel data of 281 Chinese cities from 2003 to 2018. The results show that civilized city construction contributes to increasing the level of urban green innovation, which is supported by a series of robustness tests conducted through variable substitution and sample adjustment. The quantile regression results show that the higher the level of green innovation, the stronger the green innovation effect of civilized city construction. This finding indicates that the marginal effect of green innovation in civilized city construction is gradually enhanced with the gradual increase in the level of green innovation in cities. The mediating effect analysis shows that civilized city construction can provide financial support for green innovation activities by promoting the expansion of the urban investment scale, which, in turn, increases the level of urban green innovation. In addition, environmental regulation can strengthen the promoting effect of civilized city construction on green innovation. These findings hold important theoretical and practical significance for understanding the green innovation effect of government-led civilized city construction and further leveraging the important role of government in the construction of the urban business environment as a means to promote urban investment clustering, lay the factor foundation for green innovation and strengthen the synergy between environmental regulation policies and civilized city construction policies.
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Ciudades , Desarrollo Sostenible , Urbanización , China , Industria de la Construcción , Desarrollo Económico , Gobierno , Política AmbientalRESUMEN
Purpose: Older cancer patients are more likely to develop and die from chemotherapy-related toxicity. However, evidence on drug safety and optimal effective doses is relatively limited in this group. The aim of this study was to develop a tool to identify elderly patients vulnerable to chemotherapy toxicity. Patients and methods: Elderly cancer patients ≥60 years old who visited the oncology department of Peking Union Medical College Hospital between 2008 and 2012 were included. Each round of chemotherapy was regarded as a separate case. Clinical factors included age, gender, physical status, chemotherapy regimen and laboratory tests results were recorded. Severe (grade ≥3) chemotherapy-related toxicity of each case was captured according to the National Cancer Institute Common Terminology Criteria for Adverse Events, version 5.0. Univariate analysis was performed by chi-square statistics to determine which factors were significantly associated with severe chemotherapy toxicity. Logistic regression was used to build the predictive model. The prediction model was validated by calculating the area under the curve of receiver operating characteristic (ROC). Results: A total of 253 patients and 1,770 cases were included. The average age of the patients was 68.9 years. The incidence of grade 3-5 adverse events was 24.17%. Cancer type (non-GI cancers), BMI<20 kg/m2, KPS<90%, severe comorbidity, polychemotherapy, standard dose chemotherapy, low white blood cells count, anemia, low platelet cells count, low creatine level and hypoalbuminemia were associated with severe chemotherapy-related toxicity. We used these factors to construct a chemotherapy toxicity prediction model and the area under the ROC curve was 0.723 (95% CI, 0.687-0.759). Risk of toxicity increased with higher risk score (11.98% low, 31.51% medium, 70.83% high risk; p < 0.001). Conclusion: We constructed a predictive model of chemotherapy toxicity in elderly cancer patients based on a Chinese population. The model can be used to guide clinicians to identify vulnerable population and adjust treatment regimens accordingly.
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Bone loss is prevalent in clinical pathological phenomena such as osteoporosis, which is characterized by decreased osteoblast function and number, increased osteoclast activity, and imbalanced bone homeostasis. However, current treatment strategies for bone diseases are limited. Regulated cell death (RCD) is a programmed cell death pattern activated by the expression of specific genes in response to environmental changes. Various studies have shown that RCD is closely associated with bone diseases, and manipulating the death fate of osteoblasts could contribute to effective bone treatment. Recently, microRNA-targeting therapy drugs have emerged as a potential solution because of their precise targeting, powerful curative effect, and limited side effects. Nevertheless, their clinical application is limited by their inherent instability, easy enzymatic degradation, and poor membrane penetrability. To address this challenge, a self-assembling tetrahedral DNA nanostructure (TDN)-based microRNA (Tmi) delivery system has been proposed. TDN features excellent biocompatibility, cell membrane penetrability, serum stability, and modification versatility, making it an ideal nucleic acid carrier for miRNA protection and intracellular transport. Once inside cells, Tmi can dissociate and release miRNAs to manipulate key molecules in the RCD signaling pathway, thereby regulating bone homeostasis and curing diseases caused by abnormal RCD activation. In this paper, we discuss the impact of the miRNA network on the initiation and termination of four critical RCD programs in bone tissues: apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we present the Tmi delivery system as a miRNA drug vector. This provides insight into the clinical translation of miRNA nucleic acid drugs and the application of miRNA drugs in bone diseases.
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Enfermedades Óseas , MicroARNs , Humanos , MicroARNs/genética , MicroARNs/metabolismo , Preparaciones Farmacéuticas , Osteoclastos/metabolismo , Huesos , Enfermedades Óseas/metabolismoRESUMEN
The rapid advancement of tumor immunotherapies poses challenges for the tools used in cancer immunology research, highlighting the need for highly effective biomarkers and reproducible experimental models. Current immunotherapy biomarkers encompass surface protein markers such as PD-L1, genetic features such as microsatellite instability, tumor-infiltrating lymphocytes, and biomarkers in liquid biopsy such as circulating tumor DNAs. Experimental models, ranging from 3D in vitro cultures (spheroids, submerged models, air-liquid interface models, organ-on-a-chips) to advanced 3D bioprinting techniques, have emerged as valuable platforms for cancer immunology investigations and immunotherapy biomarker research. By preserving native immune components or coculturing with exogenous immune cells, these models replicate the tumor microenvironment in vitro. Animal models like syngeneic models, genetically engineered models, and patient-derived xenografts provide opportunities to study in vivo tumor-immune interactions. Humanized animal models further enable the simulation of the human-specific tumor microenvironment. Here, we provide a comprehensive overview of the advantages, limitations, and prospects of different biomarkers and experimental models, specifically focusing on the role of biomarkers in predicting immunotherapy outcomes and the ability of experimental models to replicate the tumor microenvironment. By integrating cutting-edge biomarkers and experimental models, this review serves as a valuable resource for accessing the forefront of cancer immunology investigation.
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Remote tumors disrupt the bone marrow (BM) ecosystem (BME), eliciting the overproduction of BM-derived immunosuppressive cells. However, the underlying mechanisms remain poorly understood. Herein, we characterized breast and lung cancer-induced BME shifts pre- and post-tumor removal. Remote tumors progressively lead to osteoprogenitor (OP) expansion, hematopoietic stem cell dislocation, and CD41- granulocyte-monocyte progenitor (GMP) aggregation. The tumor-entrained BME is characterized by co-localization between CD41- GMPs and OPs. OP ablation abolishes this effect and diminishes abnormal myeloid overproduction. Mechanistically, HTRA1 carried by tumor-derived small extracellular vesicles upregulates MMP-13 in OPs, which in turn induces the alterations in the hematopoietic program. Importantly, these effects persist post-surgery and continue to impair anti-tumor immunity. Conditional knockout or inhibition of MMP-13 accelerates immune reinstatement and restores the efficacies of immunotherapies. Therefore, tumor-induced systemic effects are initiated by OP-GMP crosstalk that outlasts tumor burden, and additional treatment is required to reverse these effects for optimal therapeutic efficacy.
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Ecosistema , Neoplasias , Humanos , Metaloproteinasa 13 de la Matriz/farmacología , Mielopoyesis , Células Madre Hematopoyéticas , Neoplasias/patología , Terapia de Inmunosupresión , Serina Peptidasa A1 que Requiere Temperaturas Altas/farmacologíaRESUMEN
Atmospheric reactive oxygen species (ROS) play a key role in the process of air pollution and oxidative damage to organisms. The analysis of ROS was carried out by the capture-derivative method. Therefore, it is necessary to prepare an effective molecular membrane to trap and detect ROS. Electrospinning membranes were prepared by combining the electrospinning technique with chrysin, baicalein, scutellarin, genistein, quercetin, and baicalin. By comparing the structures of the membranes before and after the reaction, the fluorescence enhancement characteristics of the reactive molecular membranes and the atmospheric radicals were studied. The ability of the active molecular membranes to trap atmospheric radicals was also studied. It was found that the genistein active molecular membrane had good trapping ability in four environments. The fluorescence enhancement rates in ROS, OH radical and O3 simulated environments were 39.32%, 7.99% and 11.92%, respectively. The fluorescence enhancement rate in atmospheric environment was 16.16%. Indeed, the sites where the atmospheric radicals react with the active molecular membranes are discussed. It is found that it is mainly related to the 5,7 phenolic hydroxyl of ring A, catechol structure and the coexistence structure of 4' phenolic hydroxyl of ring B and 7 phenolic hydroxyl of ring A. Therefore, the genistein molecular membrane has shown great potential in its trapping ability and it is also environmentally friendly.
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Localized inflammatory lesions in one area of the body may affect other distant organs through various modes of transmission thus initiating secondary inflammatory infections. Periodontal disease (PD) and inflammatory bowel disease (IBD) have been shown to coexist. Periodontitis is a multifactorial inflammatory disease, and dental plaque is considered to be the initial risk factor. Individuals with genetic susceptibility are more likely to develop periodontitis when exposed to external stimuli. IBD is affected by host genetics, immunoregulation, daily diet, and the gut microbiota, and its risk factors appear to be shared with those of PD. However, the key etiologies of both diseases remain unclear, thus hindering the exploration of possible links between IBD and PD. Recent studies and systematic reviews have focused on evidence-based statistics of the prevalence and clinical manifestations of both diseases, but discussions of the microbial etiological correlation between periodontitis and intestinal inflammation are scarce. Here, we summarize the potential common pathogenic microorganisms that may serve as bridges between the two diseases. Studies have shown that invasive microorganisms such as Porphyromonas gingivalis, Fusobacterium nucleatum, Klebsiella spp. and Campylobacter spp. play key roles in the comorbidity of PD and IBD.