作者机构：
[Li, Li] The First Affiliated Hospital, Department of Gastrointestinal Surgery, Hengyang Medical School, University of South China, Hengyang, China
摘要：
Small bowel adenocarcinoma (SBA) is a rare tumor entity with a relatively poor prognosis. Diagnosis and management of SBA are still challenging despite recent advancement of diagnostic methods and publication of guidelines. This study aimed to analyze and visualize the trending of SBA research in the past 22 years in the 21st century through bibliometric analysis. Our study collected 1270 publication records of SBA from 2000 Jan 1st to 2022 December 31 from Web of Science and used VOSviewer and CiteSpace to analyze countries, institutions, journals, authors, references and keywords to present the latest trends in SBA research. The USA was the most productive country in terms of the total number of publications (n = 418). The Mayo Clinic (n = 22) and University of Texas MD Cancer Center (n = 22) were the institutions with top publications. The "World Journal Of Gastroenterology" (n = 30) had the largest publications. Overman Michael J (n = 17) was the most active and prolific author. The "small bowel adenocarcinoma" was the most frequent keyword. Our bibliometric analysis provides a comprehensive overview of the trends and gaps in the research of SBA. Despite the challenges faced, researchers from USA, Japan and China have made significant contributions to the field of SBA research, and further research is necessary to develop evidence-based guidelines, and advance the understanding and management of SBA.
摘要：
To explore the influence of lithology on the failure behavior of layered tunnel, true triaxial compression experiments were undertaken on cubical phyllite and yellow sandstone samples containing a "D" shaped hole. The failure progress of the hole sidewalls was monitored and captured using a miniature camera. The results reveal that the initial vertical failure stress of the phyllite samples presents a "U" shaped change as the bedding angle increases. At the bedding angle of 45 degrees, compared with the initial vertical failure stress of the yellow sandstone tunnel, that of the phyllite tunnel is lower, resulting in larger rock fragments and deeper V-shaped grooves. The failure pattern of the phyllite tunnel is primarily manifested as extensive shear sliding failure, and the failure is more severe. The failure of the yellow sandstone tunnel is primarily characterized by the sequential laminar fracturing along the maximum principal stress direction, predominantly manifesting as tensile failure. The primary factors influencing the failure of two types of layered rocks are the significant variations in the clay mineral content within the rocks. For the phyllite, it contains nearly one-third of montmorillonite (a clay mineral). This results in the formation of weak bedding planes within surrounding rocks, which induces shear slip failures along these bedding planes. In contrast, the yellow sandstone has a lower clay mineral content, leading to the absence of distinct weak bedding planes within the surrounding rock. In this case, bedding planes present ignorable effect on the surrounding rock.
摘要：
In order to improve the reliability and maintainability of rod control power cabinets in nuclear power plants, this paper uses insulated gate bipolar transistors (IGBTs), the key power device of rod control power cabinets, as the object of research on cross-working-condition fault prediction. An improved transfer learning (TL) model based on a temporal convolutional network (TCN) is proposed to solve the problem of low fault prediction accuracy across operating conditions. First, the peak emitter voltage of an IGBT aging dataset is selected as the source domain failure characteristic, and the TCN model is trained after the removal of outliers and noise reduction. Then, the time–frequency features are extracted according to the characteristics of the target domain data, and the target domain representation data are obtained using kernel principal component analysis (KPCA) for dimensionality reduction. Finally, the TCN model trained on the source domain is transferred; the model is fine-tuned according to the target domain data, and the learning rate, the number of hidden layer nodes, and the number of training times in the network model are optimized using the dung beetle optimization (DBO) algorithm to obtain the optimal network, making it more suitable for target sample fault prediction. The prediction results of this TCN model, the long short-term memory (LSTM) model, the gated recurrent unit (GRU) model, and the recursive neural network (RNN) model are compared and analyzed by selecting prediction performance evaluation indexes. The results show that the TCN model has a better predictive effect. Comparing the prediction results of the TCN-based optimized transfer learning model with those of the directly trained TCN model, the mean square error, root mean square error, and mean absolute error are reduced by a factor of two to three, which provides an effective solution for fault prediction across operating conditions.
摘要：
ATP-binding cassette protein A1 (ABCA1) is a key protein in the transport of intracellular cholesterol to the extracellular and plays an important role in reduc-ing cholesterol accumulation in surrounding tissues. Bibliometric analysis refers to the cross-science of quan-titative analysis of a variety of documents by mathemati-cal and statistical methods. It combines an analysis of structural and temporal patterns in scholarly publica-tions with a description of topic concentration and types of uncertainty. This paper analyzes the history, hotspot, and development trend of ABCA1 through bibliometrics. It will provide readers with the research status and development trend of ABCA1 and help the hot research in this field explore new research directions. After screening, the research on ABCA1 is still in a hot phase in the past 20 years. ABCA1 is emerging in previously unrelated disciplines such as cancer. There were 551 key-words and 6888 breakout citations counted by CiteSpace. The relationship between cancer and cardiovascular dis-ease has been linked by ABCA1. This review will guide readers who are not familiar with ABCA1 research to quickly understand the development process of ABCA1 and provide researchers with a possible future research focus on ABCA1. (Curr Probl Cardiol 2024;49:102036.)
摘要：
Objectives: This study aimed to evaluate the therapeutic effects and mechanism of genistein on dextran sulfate sodium-induced mouse model of ulcerative colitis (UC).Materials and Methods: A DSS-induced mouse model for UC was used in this study. Mice were then treated with genistein or a combination of genistein and the G protein-coupled estrogen receptor (GPER) antagonist G15. Colon length, disease activity index (DAI), spleen index (SI), histopathological alterations, and integrity of the colonic barrier were evaluated. The expression of inflammatory cytokines and antioxidant capacity were detected. Populations of T helper 17 cells (Th17) and Regulatory T cells (Treg) in the mesenteric lymph nodes (MLN) were analyzed. The expression of a transcription factor for Th17 and Treg in the colonic tissues was detected.Results: Genistein treatment significantly alleviated DSS-induced colitis, summarized as increased colonic length, decreased DAI, SI, improved histopathological alterations, and colonic barrier integrity. Genistein treatment restrained pro-inflammatory cytokines and oxidative enzyme release while promoting anti-inflammatory and anti-oxidative enzyme release. Flow cytometry indicated that genistein significantly reduced the Th17 population while boosting Treg populations. Furthermore, genistein inhibited the expression of transcription factors associated with Th17 and promoted the expression of transcription factors associated with Treg in the colonic tissue. Intriguingly, these observed effects of genistein were abolished when UC mice were treated with a combination of genistein and GPER antagonist G15.Conclusion: This study suggests that genistein is potent in protecting against DSS-induced colonic injuries by rebalancing Th17/Treg and that GPER may be a vital target for genistein-mediated immunomodulatory effects in UC.
摘要：
Neutralizing antibodies are a key component in protective humoral immunity against SARS-CoV-2. Currently, available technologies cannot track epitope-specific antibodies in global antibody repertoires. Thus, the comprehensive repertoire of spike-specific neutralizing antibodies elicited by SARS-CoV-2 infection is not fully understood. We therefore combined high-throughput immunoglobulin heavy chain (IgH) repertoire sequencing, and structural and bioinformatics analysis to establish an antibodyomics pipeline, which enables tracking spike-specific antibody lineages that target certain neutralizing epitopes. We mapped the neutralizing epitopes on the spike and determined the epitope-preferential antibody lineages. This analysis also revealed numerous overlaps between immunodominant neutralizing antibody-binding sites and mutation hotspots on spikes as observed so far in SARS-CoV-2 variants. By clustering 2677 spike-specific antibodies with 360 million IgH sequences that we sequenced, a total of 329 shared spike-specific antibody clonotypes were identified from 33 COVID-19 convalescents and 24 SARS-CoV-2-naïve individuals. Epitope mapping showed that the shared antibody responses target not only neutralizing epitopes on RBD and NTD but also non-neutralizing epitopes on S2. The immunodominance of neutralizing antibody response is determined by the occurrence of specific precursors in human naïve B-cell repertoires. We identified that only 28 out of the 329 shared spike-specific antibody clonotypes persisted for at least 12 months. Among them, long-lived IGHV3-53 antibodies are likely to evolve cross-reactivity to Omicron variants through accumulating somatic hypermutations. Altogether, we created a comprehensive atlas of spike-targeting antibody lineages in COVID-19 convalescents and antibody precursors in human naïve B cell repertoires, providing a valuable reference for future vaccine design and evaluation.
期刊：
JOURNAL OF CELLULAR PHYSIOLOGY,2024年 ISSN：0021-9541
通讯作者：
Li, Lanfang;Lu, RR
作者机构：
[Liu, Huimei; Li, Lanfang] Univ South China, Hengyang Med Sch, Dept Pharmacol, Hengyang, Peoples R China.;[Lu, Ruirui; Li, Lanfang] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Sch Pharmaceut Sci, Hengyang Med Sch, Hengyang, Peoples R China.;[Lu, Ruirui; Li, Lanfang; Li, LF; Lu, RR] Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Sch Pharmaceut Sci, Hengyang Med Sch, Hengyang 421001, Peoples R China.
通讯机构：
[Li, LF; Lu, RR ] U;Univ South China, Hunan Prov Cooperat Innovat Ctr Mol Target New Dru, Sch Pharmaceut Sci, Hengyang Med Sch, Hengyang 421001, Peoples R China.
关键词：
ZIP transporters;cancers;cardiovascular diseases;neurological diseases;zinc
摘要：
As an essential trace element for organisms, zinc participates in various physiological processes, such as RNA transcription, DNA replication, cell proliferation, and cell differentiation. The destruction of zinc homeostasis is associated with various diseases. Zinc homeostasis is controlled by the cooperative action of zinc transporter proteins that are responsible for the influx and efflux of zinc. Zinc transporter proteins are mainly categorized into two families: Zrt/Irt-like protein (SLC39A/ZIP)family and zinc transporter (SLC30A/ZNT)family. ZIP transporters contain 14 members, namely ZIP1-14, which can be further divided into four subfamilies. Currently, ZIP transporters-regulated zinc homeostasis is one of the research hotspots. Cumulative evidence suggests that ZIP transporters-regulated zinc homeostasis may cause physiological dysfunction and contribute to the onset and progression of diverse diseases, such as cancers, neurological diseases, and cardiovascular diseases. In this review, we initially discuss the structure and distribution of ZIP transporters. Furthermore, we comprehensively review the latest research progress of ZIP transporters-regulated zinc homeostasis in diseases, providing a new perspective into new therapeutic targets for treating related diseases.
摘要：
HNRNPA2B1 and HNRNPR stabilize ASCL1 mRNA in neuroblastoma, but whether their regulatory effects depend on m6A modification and whether their function involves ASCL1 remain unknown. This study investigated the m6A-dependent binding of HNRNPA2B1 and HNRNPR to ASCL1 and subsequent regulation, as well as the expression, clinical significance, and function of HNRNPA2B1 and HNRNPR in neuroblastoma. We revealed that METTL14 mediated ASCL1 m6A modification to stabilize ASCL1. HNRNPA2B1 and HNRNPR significantly enriched ASCL1 mRNA by binding to the 5' and 3' untranslated regions, respectively, and METTL14 knockdown reduced this enrichment. Mutations in m6A sites in the untranslated regions of ASCL1 mRNA considerably decreased probe capacity to engage HNRNPA2B1 and HNRNPR. HNRNPR interacts with IGF2BP1, and knocking down either impaired binding to ASCL1 mRNA. HNRNPA2B1 and HNRNPR knockdown suppressed neuroblastoma cell growth and invasion, while ASCL1 overexpression restored these effects. The high HNRNPA2B1 and HNRNPR expression in neuroblastoma correlated with ASCL1 expression. Thus, HNRNPA2B1 and HNRNPR bind and stabilize ASCL1 mRNA in an m6A-dependent manner to promote neuroblastoma progression. This study not only discovered a new mechanism underlying the high ASCL1 expression in neuroblastoma but also identified the HNRNPA2B1/HNRNPR/ASCL1 axis as a promising target for inhibiting neuroblastoma progression.
摘要：
Multiple pesticides are often used in combination for plant protection and public health. Therefore, it is important to analyze the physiological changes induced by multiple pesticides exposure. The objective of this study was to investigate the combined toxicity of the widely-used organophosphorus and pyrethroid pesticides diazinon, dimethoate, and cypermethrin. Male Wistar rats were administrated by gavage once daily with the three pesticides individual or in combination for consecutive 28 days. The metabolic components of serum and urine samples were detected by using 1H nuclear magnetic resonance (NMR)-based metabolomics method. Histopathological examination of liver and kidneys and serum biochemical determination were also carried out. The results showed that after the 28-day subacute exposure, serum glutamic transaminase and albumin were significantly increased and blood urea nitrogen was significantly decreased in the rats exposed to the mixture of the pesticides compared with the control rats, suggesting that the co-exposure impaired liver and kidney function. Metabolomics analysis indicated that the indicators 14 metabolites were statistically significant altered in the rats after the exposure of the pesticides. The increase in 3-hydroxybutyric acid in urine or decrease of lactate and N-acetyl-L-cysteine in serum could be a potentially sensitive biomarker of the subchronic combined effects of the three insecticides. The reduction level of 2-oxoglutarate and creatinine in urine may be indicative of dysfunction of liver and kidneys. In summary, the exposure of rats to pesticides diazinon, dimethoate, and cypermethrin could cause disorder of lipid and amino acid metabolism, induction of oxidative stress, and dysfunction of liver and kidneys, which contributes to the understanding of combined toxic effects of the pesticides revealed by using the metabolomics analysis of the urine and serum profiles.
通讯机构：
[Zhu, HM ] U;Univ South China, Sch Mech Engn, Hengyang 421001, Hunan, Peoples R China.;Hunan Prov Key Lab Adv Laser Mfg Technol, Hengyang 421001, Hunan, Peoples R China.
关键词：
distortion;laser repairing;microstructure;properties;scanning strategy;temperature distribution
摘要：
In order to explore the effects of scanning strategies on the distortion and properties of laser-repaired thin-plate components, four commonly used strategies, including continuous raster scanning strategy, continuous orthogonal scanning strategy (COS), subarea W-type scanning strategy and subarea leap-type scanning strategy, were applied for laser-repairing thin-plate 2Cr13 steel. The finite element simulation and experimental results show that the temperature field of the laser-repaired layer prepared by COS exhibits symmetrical elliptical characteristic, with homogeneous temperature gradient along all directions. Consequently, the outermost of COS sample exhibits the smallest deformation of 2.86 mm, by avoiding both the unidirectional shrinkage of molten pool and the cumulative effect of longitudinal stress. In contrast, much larger distortion was produced by the other three scanning strategies due to the uneven temperature gradient. Dense martensite without defects was achieved by continuous scanning, while the coarsen martensite occurred by using subarea scanning. The repaired layer by using subarea scanning exhibits lower microhardness of 585-590 HV0.2 and poor wear resistance of 1.45 x 10-5-1.48 x 10-5 mm3/N m, in comparison to 613-618 HV0.2 and 0.9 x 10-5-0.92 x 10-5 mm3/N m obtained by using continuous strategy. COS is the most ideal strategy in laser-repairing thin-plate 2Cr13 steel in this work, exhibiting the lowest distortion as well as the highest microhardness and wear resistance.
摘要：
The formation of the BCR-ABL fusion gene drives human chronic myeloid leukemia (CML). The last 2 decades have witnessed that specific tyrosine kinase inhibitors (TKIs, e.g., imatinib mesylate, IM) against ABL1 improve disease treatment, although some patients still suffer from relapse and TKI resistance. Therefore, a better understanding of the molecular pathology of CML is still urgently needed. miR-181a-5p (miR-181a) acts as a tumor suppressor in CML; however, the molecular mechanism of miR-181a in CML stem/progenitor cells remains elusive. Herein, we showed that miR-181a inhibited the growth of CML CD34(+) cells, including the quiescent subset, and sensitized them to IM treatment, while miR-181a inhibition by a sponge sequence collaborated with BCR-ABL to enhance the growth of normal CD34(+) cells. Transcriptome data and biochemical analysis revealed that SERPINE1 was a bona fide and critical target of miR-181a, which deepened the understanding of the regulatory mechanism of SERPINE1. Genetic and pharmacological inhibition of SERPINE1 led to apoptosis mainly mediated by caspase-9 activation. The dual inhibition of SERPINE1 and BCR-ABL exhibited a significantly stronger inhibitory effect than a single agent. Taken together, this study demonstrates that a novel miR-181a/SERPINE1 axis modulates CML stem/progenitor cells, which likely provides an important approach to override TKI resistance.
摘要：
BACKGROUND: Pulmonary sclerosing pneumocytoma (PSP) and pulmonary carcinoid (PC) are difficult to distinguish based on conventional imaging examinations. In recent years, radiomics has been used to discriminate benign from malignant pulmonary lesions. However, the value of radiomics based on computed tomography (CT) images to differentiate PSP from PC has not been well explored. PURPOSE: We aimed to investigate the feasibility of radiomics in the differentiation between PSP and PC. METHODS: Fifty-three PSP and fifty-five PC were retrospectively enrolled and then were randomly divided into the training and test sets. Univariate and multivariable logistic analyses were carried to select clinical predictor related to differential diagnosis of PSP and PC. A total of 1316 radiomics features were extracted from the unenhanced CT (UECT) and contrast-enhanced CT (CECT) images, respectively. The minimum redundancy maximum relevance and the least absolute shrinkage and selection operator were used to select the most significant radiomics features to construct radiomics models. The clinical predictor and radiomics features were integrated to develop combined models. Two senior radiologists independently categorized each patient into PSP or PC group based on traditional CT method. The performances of clinical, radiomics, and combined models in differentiating PSP from PC were investigated by the receiver operating characteristic (ROC) curve. The diagnostic performance was also compared between the combined models and radiologists. RESULTS: In regard to differentiating PSP from PC, the area under the curves (AUCs) of the clinical, radiomics, and combined models were 0.87, 0.96, and 0.99 in the training set UECT, and were 0.87, 0.97, and 0.98 in the training set CECT, respectively. The AUCs of the clinical, radiomics, and combined models were 0.84, 0.92, and 0.97 in the test set UECT, and were 0.84, 0.93, and 0.98 in the test set CECT, respectively. In regard to the differentiation between PSP and PC, the combined model was comparable to the radiomics model, but outperformed the clinical model and the two radiologists, whether in the test set UECT or CECT. CONCLUSIONS: Radiomics approaches show promise in distinguishing between PSP and PC. Moreover, the integration of clinical predictor (gender) has the potential to enhance the diagnostic performance even further.
摘要：
Narrative Medicine (NM), a contemporary medical concept proposed in the 21st century, emphasizes the use of narrative as a literary form in medicine. This study aims to explore the understanding about NM and willingness to learn NM among medical students in our hospital. A questionnaire survey was conducted among 130 students at Xiangya Medical College of Central South University. The findings revealed that a small percentage of students (3.1%) were familiar with narrative medicine and its training methods. Knowledge about the treatment skills (77.7%) and core content (55.4%) of narrative medicine was limited among the students. Despite this, a majority (63.1%) expressed a lack of interest in further understanding and learning about narrative medicine. Surprisingly, the survey indicated that students possessed a high level of narrative literacy, even without formal training in narrative medicine. Additionally, over half of the surveyed students (61.5%) believed that narrative medicine could benefit their clinical practice. This study serves as a preliminary basis for the future development of narrative medicine education in China. It highlights the need to prioritize medical humanities education and provide medical students with more opportunities to access information on narrative medicine. By doing so, we can strive to enhance the visibility and promote the integration of narrative medicine into medical humanities education in China.
摘要：
Neuronal ferroptosis plays a critical role in the pathogenesis of cognitive deficits. The present study explored whether artemisinin protected type 2 diabetes mellitus (T2DM) mice from cognitive impairments by attenuating neuronal ferroptosis in the hippocampal CA1 region. STZ-induced T2DM mice were treated with artemisinin (40 mg/kg, i.p.), or cotreated with artemisinin and Nrf2 inhibitor MEL385 or ferroptosis inducer erastin for 4 weeks. Cognitive performance was determined by the Morris water maze and Y maze tests. Hippocampal ROS, MDA, GSH, and Fe2+ contents were detected by assay kits. Nrf2, p-Nrf2, HO-1, and GPX4 proteins in hippocampal CA1 were assessed by Western blotting. Hippocampal neuron injury and mitochondrial morphology were observed using H&E staining and a transmission electron microscope, respectively. Artemisinin reversed diabetic cognitive impairments, decreased the concentrations of ROS, MDA and Fe2+, and increased the levels of p-Nr2, HO-1, GPX4 and GSH. Moreover, artemisinin alleviated neuronal loss and ferroptosis in the hippocampal CA1 region. However, these neuroprotective effects of artemisinin were abolished by Nrf2 inhibitor ML385 and ferroptosis inducer erastin. Artemisinin effectively ameliorates neuropathological changes and learning and memory decline in T2DM mice; the underlying mechanism involves the activation of Nrf2 to inhibit neuronal ferroptosis in the hippocampus.
期刊：
AMERICAN JOURNAL OF PATHOLOGY,2024年 ISSN：0002-9440
通讯作者：
Jiang, Yongliang;Wu, Xu
作者机构：
[Huang, Li] Department of Pediatrics, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Henan, China;[Huang, Li] Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Henan, China;[Xie, Li; Li, Rong; Li, Li; Tan, Xiaowu; Li, Feifan; Xi, Yunzhu; Luo, Qing; Zhao, Meiyun] Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Henan, China;[Xuan, Weixia] Department of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, China;[Jiang, Yongliang] Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Henan, China. Electronic address: yvfei316@163.com
通讯机构：
[Yongliang Jiang; Xu Wu] H;Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Henan, China<&wdkj&>Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, Henan, China Pulmonary and Critical Care Medicine, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Henan, China
摘要：
Neutrophil extracellular traps (NETs) and pyroptosis are critical events in lung injury. This study investigated whether ficolin-A influences NET formation through pyroptosis to exacerbate lipopolysaccharide (LPS)-induced lung injury. The expression of ficolin-A/2, NETs, and pyroptosis-related molecules was investigated in animal and cell models. Knockout and knockdown (recombinant protein) methods were used to elucidate regulatory mechanisms. The Pearson correlation coefficient was used to analyze the correlation between ficolins and pyroptosis- and NET-related markers in clinical samples. In this study, ficolin-2 (similar to ficolin-A) showed significant overexpression in patients with acute respiratory distress syndrome. Invivo, knockout of ficolin-A, but not ficolin-B, attenuated lung inflammation and inhibited NET formation in the LPS-induced mouse model. DNase I further alleviated lung inflammation and NET formation in ficolin-A knockout mice. Invitro, neutrophils derived from Fcna(-/-)mice showed less pyroptosis and necroptosis than those from the control group after LPS stimulation. Additionally, gasdermin D knockdown or Nod-like receptor protein 3 inhibitor reduced NET formation. Addition of recombinant ficolin-2 protein to human peripheral blood neutrophils promoted NET formation and pyroptosis after LPS stimulation, whereas ficolin-2 knockdown had the opposite effect. Acute respiratory distress syndrome patients showed increased levels of pyroptosis- and NET-related markers, which were correlated positively with ficolin-2 levels. In conclusion, these results suggested that ficolin-A/2 exacerbated NET formation and LPS-induced lung injury via gasdermin D-mediated pyroptosis.
作者机构：
[Lu, Jibu; Song, Cailu; Xie, Xiaoming; Liu, Lingrui; Tang, HL; Tang, Hailin; Mo, Yunxian; Wu, Song] Sun Yat Sen Univ, Canc Ctr, Guangdong Prov Clin Res Ctr Canc, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.;[Li, YH; Zhu, Hongbo; Li, Yuehua; Xie, Liming] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Hengyang, Peoples R China.;[Wu, Feiyue] Guizhou Prov Peoples Hosp, Guiyang, Peoples R China.;[Lin, Huan; Tang, Hailin] Guangzhou Med Univ, Affiliated TCM Hosp, Guangzhou, Peoples R China.
通讯机构：
[Tang, HL ] S;[Li, YH ] U;[Lin, H ] G;Sun Yat Sen Univ, Canc Ctr, Guangdong Prov Clin Res Ctr Canc, State Key Lab Oncol South China, Guangzhou 510060, Peoples R China.;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Hengyang, Peoples R China.
关键词：
Autophagy;Circular RNAs;Competitive endogenous RNAs;Triple-negative breast cancer;circKIF4A
摘要：
Among patients with triple-negative breast cancer (TNBC), distant metastasis is the leading cause of death. Our previous studies have shown that TNBC progression is greatly facilitated by circKIF4A, but uncertainty remains regarding its role in TNBC brain metastasis and the molecular mechanism. In this study, we found notable upregulation of circKIF4A in TNBC cell lines and brain metastases. Inhibition of circKIF4A impaired the ability of TNBC to proliferate, migrate, and cause brain metastasis. Luciferase reporter assays confirmed that circKIF4A competed for binding to miR-637 with STAT3 3' UTR. Western blot analysis revealed that inhibition of circKIF4A decreased STAT3 and p62 expression, while increased the LC3B-II/LC3B-I ratio and the expression of Beclin, indicating that downregulation of circKIF4A induced autophagy by competing with STAT3 for binding to miR-637. By employing a competitive endogenous RNA (ceRNA) mechanism, the circKIF4A-miR-637-STAT3 axis coordinates brain metastasis in TNBC. circKIF4A can therefore be used as a prognostic biomarker for brain metastasis in TNBC and as a therapeutic target.
期刊：
Fuzzy Sets and Systems,2024年479:108856 ISSN：0165-0114
通讯作者：
Liu, HL
作者机构：
[Xiao, Qizhen; Liu, Hongliang; Liu, HL; Luo, Zhiyong] Univ South China, Sch Math & Phys, Hengyang 421001, Peoples R China.;[Xiao, Qizhen; Liu, Hongliang; Liu, HL] Univ South China, Hunan Key Lab Math Modeling & Sci Comp, Hengyang 421001, Peoples R China.
通讯机构：
[Liu, HL ] U;Univ South China, Sch Math & Phys, Hengyang 421001, Peoples R China.;Univ South China, Hunan Key Lab Math Modeling & Sci Comp, Hengyang 421001, Peoples R China.
关键词：
Aperiodic DoS attacks;Resilient synchronization;Fixed-time stability;Fuzzy neural networks;Reaction-diffusion terms
摘要：
This work focuses on the resilient fixed -time synchronization of delayed fuzzy memristive reaction -diffusion neural networks under denial -of -service (DoS) attacks. To efficaciously tolerate the aperiodic DoS attacks, a new appropriate controller is designed to ensure the fixed -time resilient synchronization of the systems. Moreover, two mild sufficient conditions are first proposed and the constrained techniques of attacking intervals are employed to overcome the challenge of estimating the upper bound of the settling time under aperiodic DoS attacks. Lastly, an example is utilized to illustrate the effectiveness and feasibility of the theoretical result.
摘要：
Conceptual diagram illustrating shielding in polymer composite materials. Abstract Development of shielding materials for 222Rn and γ radiation has crucial implications for ensuring the safety of individuals. This paper reports the synthesis of modified graphene nanosheets (MGNPs) via the reaction of KH560 with graphene nanosheets (GNPs), while melt blending and hot‐press molding technique were used to fabricate a multifunctional polymer composite shielding material, MGNP/WB/PMMA (polymethyl methacrylate). Successful synthesis of MGNP was confirmed by Fourier transform infrared spectroscopy, and scanning electron microscope (SEM) analysis was utilized to assess the distribution of functional fillers within the cross‐section of the polymer composite. Additionally, thermogravimetric analysis (TGA) demonstrated that MGNP and WB particles enhance the thermal stability of the polymer composite materials. Compared to pure PMMA, 98.7% decrease in the radon diffusion coefficient was observed for MGNP1.5 wt%/PMMA composite material. In addition to enhance the radon‐blocking characteristics of the polymer composites, inclusion of WB particles also boosts their shielding capacity against gamma radiation. The 222Rn diffusion coefficient of MGNP1.5 wt%/WB25wt%/PMMA polymer composite material decreased by 99.6% and at energies of 60 KeV, 80 KeV, 122 KeV, 365 KeV, the mass attenuation coefficient (MAC) for the composite material increased by 0.79, 1.97, 0.57, and 0.05 cm2/g, respectively, compared to pure PMMA. Highlights The PMMA composite materials doped with graphene nanosheets demonstrate outstanding resistance to 222Rn. Graphene nanosheets modified by KH560 exhibit favorable dispersion within PMMA. WB can further enhance the radon resistance of MGNP/WB/PMMA composite materials. The polymer composites exhibit excellent 222Rn and gamma ray shielding properties.
