BACKGROUND:Research on carbon nanomaterials in the biomedical field is booming,and related scientific research results are increasing year by year.However,visualization analysis of the annual number of publications,the research status of countries,institutions,authors,and research hotspots and trends in this field is relatively scarce. OBJECTIVE:To present the research status of carbon nanomaterials in biomedical field,reveal the main research subjects,explore the research hotspots and development trends,and provide a reference for the future development of this field. METHODS:The core data set of Web of Science was used as the literature source to search the relevant researches on carbon nanomaterials in the biomedical field from 2012 to 2023.The knowledge map was generated by using Citespace software with countries,institutions,authors,keywords,and co-citations as nodes and for visualization analysis. RESULTS AND CONCLUSION:(1)A total of 2 932 papers were included in this study.In the medical field,carbon nanomaterials had a large number of papers and a fast growth rate.The United States has a large number of papers;China is an emerging force in this field,although the number of papers is the largest,but the level of research and influence need to be improved.The Chinese Academy of Sciences is the largest cooperative network institution,which mainly targets domestic institutions and lacks cooperation with well-known foreign institutions.(2)Keyword analysis displays that the green synthesis method and application of displaying carbon points have been the focus of research,followed by the new method of combining carbon nanomaterials with cancer phototherapy and immunotherapy,the key direction of future research.(3)The dynamic development trend of co-citations suggests that tissue engineering is a hot research topic of carbon nanomaterials in the field of biomedicine,mainly including the research of carbon nanomaterials for the repair and regeneration of heart and nerve tissue and as a bio-ink additive for 3D and 4D bioprinting.(4)In the future,with the development of the biomedical field in the direction of precision and treatment,researchers should speed up the creation of carbon-based systems formed by the combination of scientific and effective carbon nanomaterials with science and technology,new polymers or organic molecules,and new therapeutic methods,so as to give full play to the maximum effect of carbon nanomaterials.

Periodontal homeostasis is regulated by the complex interplay between the gingival epithelial barrier, the extracellular matrix of soft tissues, the bone coupling system, and immune responses within the periodontal region. Gingival epithelial cells are primarily composed of keratinocytes and a small proportion of non-keratinocytes, and they are integral to the formation of the gingival epithelial barrier. This epithelial barrier plays a fundamental role in defending against pathogens, exogenous substances, and mechanical stress. This study aims to explore the intrinsic connections between gingival epithelial cells and periodontal homeostasis. Research has shown that gingival epithelial cells participate in maintaining periodontal homeostasis through multiple pathways: ① gingival epithelial cells respond to the inflammatory environment by undergoing proliferation, migration, epithelial-mesenchymal transition, and forming apoptosis-mediated neutrophil extracellular traps; ② when gingival inflammation damages the epithelial barrier, lipopolysaccharides cannot be easily removed, and gingival epithelial cells play a defensive role by activating innate immune responses; ③ the interactions of gingival epithelial cells with oral microbiota and immune cells are essential for maintaining periodontal homeostasis. Thus, gingival epithelial cells are closely associated with periodontal homeostasis. However, the crucial role and mechanisms of gingival epithelial cells in the maintenance of periodontal homeostasis are not clear, which provides novel insights for the research of periodontal homeostatic medicine.

BackgroundModified electroconvulsive therapy （MECT） is a common front-line strategy widely used in psychiatric practice， and the optimal first stimulus dosage in MECT is usually estimated clinically based on the factors influencing the patient's initial seizure threshold （IST）. However， previous studies on the influencing factors of IST have mostly suffered from limitations such as small sample sizes and single-dimensional research perspectives. ObjectiveTo explore the factors influencing IST in MECT for patients with mental disorders， so as to provide references for stimulus dosing strategies in MECT for the patients. MethodsA retrospective study was used to include 1 446 inpatients fulfilling the diagnostic criteria for any specific mental disorder listed in the ICD-10 and receiving MECT at Shandong Daizhuang Hospital from January 1， 2021 to August 1， 2023. Their general and clinical data were collected， including IST， psychiatric diagnostic categories， gender， ethnicity， age， body weight， body mass index （BMI）， course of disease， family history of psychiatric disorders， first episode status， use of antiepileptic drugs the day before treatment， use of benzodiazepines the day before treatment， and previous MECT treatment history. Pearson correlation analysis was utilized to test the correlation of IST with age， height， body weight， BMI， and course of disease， and stepwise multivariate linear regression analysis was performed to identify the factors affecting IST. ResultsIST yielded statistical difference among patients in terms of gender， first episode status， use of antiepileptic drugs the day before treatment， and use of benzodiazepines the day before treatment （t=2.256， -3.059， -2.136， -3.006， P<0.05 or 0.01）. IST in patients of different ages and psychiatric diagnostic categories also demonstrated statistical difference （F=913.120， 6.212， P<0.01）. Within young population， IST varied significantly based on the psychiatric diagnostic categories （F=2.986， P<0.05）. Correlation analysis indicated that IST was positively correlated with age， body weight， BMI and course of disease （r=0.886， 0.055， 0.184， 0.456， P<0.05 or 0.01）， and negatively correlated with height （r=-0.183， P<0.01）. Stepwise multivariate linear regression analysis revealed that age， gender， and body weight were influencing factors of IST （β=0.888， -0.049， -0.035， P<0.01）. ConclusionsAge， gender and body weight may be factors influencing IST in MECT for patients with mental disorders. ［Funded by Key R&D Plan Projects of Jining City in 2024 (number, 2024YXNS202）］

Objective: To develop a simple digital chylous plasma device and validate its ability to accurately, standardly, and non-destructively determine chylous plasma in blood banks and clinical transfusions in hospitals. Methods: A digital chylous plasma assessment device was designed and manufactured. This device was used to measure the chylous degrees of chylous plasma samples before freezing, after freeze-thawing, before viral inactivation, and after viral inactivation. The measured chylosity index values were categorized according to the requirements specified in Appendix A of the Chinese national standard GB 18469-2001 "Quality Requirements for Whole Blood and Blood Components". This process established a digital standard for chylous plasma, enabling the identification of severe, moderate and mild chylous plasma, and non-chylous plasma. Results: The initial simple product of the digital chylous assessment device was successfully designed and manufactured. There was no significant difference in the degree of chylous plasma between pre-freezing 468.11±217.73 lux and post-thawing 538.91±273.39 lux of chylous plasma (P>0.05), or between pre-viral inactivation 858.33±387.79 lux and post-viral inactivation 928.33±166.51 lux of chylous plasma (P>0.05). The median of chylous degree values for plasma chylous index grades 0 to 6 were 45 lux, 250 lux, 620 lux, 835 lux, 1 130 lux, 1 390 lux, and 1 700 lux, respectively. The defined cutoff values/ranges for the chylous degree values corresponding to plasma chylous index grade 0 to 6 were ≤125 lux, 126-465 lux, 466-740 lux, 741-1 000 lux, 1 001-1 233 lux, 1 234-1 560 lux, and ≥1 561 lux. Conclusion: This study successfully developed the initial product of the digital chylous device and established digital standards for classifying chylous plasma. The device demonstrates the potential to meet the needs for assessment of chylous plasma in both blood banks and clinical transfusions in hospitals, thereby promoting the development and application of standardized, non-destructive chylous plasma assessment technology.

BACKGROUND: Chronic kidney disease (CKD) is associated with common pathophysiological processes, such as inflammation and fibrosis, in both the heart and the kidney. However, the underlying molecular mechanisms that drive these processes are not yet fully understood. Therefore, this study focused on the molecular mechanism of heart and kidney injury in CKD. METHODS: We generated an microRNA (miR)-26a knockout (KO) mouse model to investigate the role of miR-26a in angiotensin (Ang)-II-induced cardiac and renal injury. We performed Ang-II modeling in wild type (WT) mice and miR-26a KO mice, with six mice in each group. In addition, Ang-II-treated AC16 cells and HK2 cells were used as in vitro models of cardiac and renal injury in the context of CKD. Histological staining, immunohistochemistry, quantitative real-time polymerase chain reaction (PCR), and Western blotting were applied to study the regulation of miR-26a on Ang-II-induced cardiac and renal injury. Immunofluorescence reporter assays were used to detect downstream genes of miR-26a, and immunoprecipitation was employed to identify the interacting protein of LIM and senescent cell antigen-like domain 1 (LIMS1). We also used an adeno-associated virus (AAV) to supplement LIMS1 and explored the specific regulatory mechanism of miR-26a on Ang-II-induced cardiac and renal injury. Dunnett's multiple comparison and t -test were used to analyze the data. RESULTS: Compared with the control mice, miR-26a expression was significantly downregulated in both the kidney and the heart after Ang-II infusion. Our study identified LIMS1 as a novel target gene of miR-26a in both heart and kidney tissues. Downregulation of miR-26a activated the LIMS1/integrin-linked kinase (ILK) signaling pathway in the heart and kidney, which represents a common molecular mechanism underlying inflammation and fibrosis in heart and kidney tissues during CKD. Furthermore, knockout of miR-26a worsened inflammation and fibrosis in the heart and kidney by inhibiting the LIMS1/ILK signaling pathway; on the contrary, supplementation with exogenous miR-26a reversed all these changes. CONCLUSIONS Our findings suggest that miR-26a could be a promising therapeutic target for the treatment of cardiorenal injury in CKD. This is attributed to its ability to regulate the LIMS1/ILK signaling pathway, which represents a common molecular mechanism in both heart and kidney tissues.
Animals ; MicroRNAs/metabolism* ; Angiotensin II/toxicity* ; Mice ; Renal Insufficiency, Chronic/chemically induced* ; Mice, Knockout ; Disease Models, Animal ; Male ; Signal Transduction/genetics* ; LIM Domain Proteins/genetics* ; Mice, Inbred C57BL ; Cell Line ; Humans

Reactive astrocytes, which exhibit a correlation with the degeneration of dopaminergic neurons, are present in a considerable number during the progression of Parkinson's disease (PD). However, the underlying factors shaping astrocyte reactivity and neuroinflammation in PD remain inadequately elucidated. Here, we demonstrate that fibroblast growth factor 7 (FGF7)/FGF receptor 2 (FGFR2) autocrine signaling intensifies astrocyte reactivity and inflammation. Genetic deletion of Arrb2, β-Arrestin2 encoding gene, led to escalated astrocyte reactivity in MPTP-treated mice, which was further substantiated in astrocyte-specific Arrb2 knockdown mice. RNA sequencing profiling of Arrb2 knockout astrocytes identified Fgf7 as a critical effector of astrocyte reactivity. Subsequently, conditional knockdown of Fgf7 and its receptor Fgfr2 in astrocytes elicited advantageous effects for MPTP-treated mice by restraining the inflammatory phenotypic transition of reactive astrocytes. Furthermore, deletion of astrocytic Fgf7 mitigated MPTP-induced pathology in Arrb2 knockout mice. Mechanistically, STAT1 was distinguished as the transcription factor suppressing Fgf7 expression, while β-Arrestin2 counteracted the proteasomal degradation of STAT1 by binding to RNF220, an E3 ubiquitin ligase for STAT1. More importantly, selectively engaging dopamine D2 receptor (Drd2)/β-Arrestin2-biased signaling using the agonist UNC9995 exhibited therapeutic potential in MPTP-treated mice via moderation of astrocytic FGF7 production, thereby restoring balance in astrocyte reactivity. Collectively, our study bridges a crucial knowledge gap by elucidating the novel functions of FGF family members within the central nervous system, particularly within the context of PD. The autocrine signaling of FGF7/FGFR2 represents a novel mechanism and a potential druggable target for modulating astrocyte-derived inflammation.

Nonalcoholic steatohepatitis （NASH） is a chronic liver disease with the main pathological features of hepatic steatosis， inflammatory cell infiltration， and interstitial fibroplasia， and it is an important risk factor for liver fibrosis， liver cirrhosis， and hepatocellular carcinoma. NOD-like receptor protein 3 （NLRP3） inflammasome is the core of innate immunity， and the abnormal activation of NLRP3 inflammasome is closely associated with the development and progression of NASH， which involves multiple links such as inflammatory response and oxidative stress. A large number of studies have shown that the active ingredients of traditional Chinese medicine （TCM） and TCM compound prescriptions can improve oxidative stress， regulate lipid metabolism， and alleviate liver inflammation by regulating NLRP3 inflammasome. TCM treatment applied in clinical practice has achieved a good therapeutic effect， while inflammasome is one of the key pathways or targets for TCM in improving NASH. This article reviews the mechanism of action of NLRP3 inflammasome in NASH and the research advances in TCM intervention of NLRP3 inflammasome， in order to provide ideas for the clinical TCM treatment of NASH， as well as reference targets and research directions for the research and development of new TCM drugs.

Objective To investigate the individual and interaction effects of the estimated glomerular filtration rate(eGFR)and homocysteine(Hcy)on the neurological function of patients with ischemic cerebrovascular disease(ICVD)at admission.Methods We included 496 patients with ICVD hospitalized in the Department of Neurology of Tianjin First Central Hospital.Their basic information,disease history,and laboratory test results were recorded.Accord-ing to the modified Rankin Scale(mRS)score,the patients were grouped:good neurological function(0-1 points)and neurological dysfunction(2-5 points).The associations of Hcy and eGFR with the neurological function of patients with ICVD at admission were analyzed by using a multivariable logistic regression model and an additive interaction model.Results Among the 496 patients,236 had neurological dysfunction,while 260 showed good neurological function.After adjusting for confounding factors,eGFR and Hcy were independent influencing factors for the neurological function of the patients at admission(both P＜0.05).The risk of neurological impairment at admission in patients with a high Hcy level and a low eGFR was 4.38 times that of patients who were normal in Hcy and eGFR(OR=4.38,95%CI 2.72-7.14,P＜0.001).Hcy and eGFR had an interactive effect on the risk of neurological dysfunction at admission(RERI=2.01,95%CI 0.02-4.01;AP=0.46,95%CI 0.13-0.79).Conclusion Hcy and eGFR are factors influencing the neurological function of patients with ICVD at admission,and the two indicators have an additive interaction on the risk of neurological dysfunc-tion at admission.

AIM:This study aimed to investigate the expression and localization of ALOX12P2 in oral squa-mous cell carcinoma(OSCC),as well as its effects on cell viability,migration,and invasion.METHODS:The expres-sion of ALOX12P2 in head and neck squamous cell carcinoma(HNSCC)tissues and its correlation with clinicopathologi-cal features were analyzed using the UALCAN database(University of Alabama at Birmingham Cancer Data Analysis Por-tal).Additionally,the expression of ALOX12P2 in OSCC and its impact on survival prognosis were evaluated through the GDC and UCSC Xena databases.The expression levels of ALOX12P2 in OSCC cell lines were assessed via quantitative re-al-time PCR(RT-qPCR).The subcellular localization of ALOX12P2 was determined using nucleoplasmic RNA isola-tion.CAL-27 cells were used to establish an ALOX12P2 knockdown group(SS-ALOX12P2)and a control group(SS-NC).HN30 cells were employed to form an ALOX12P2 overexpression group(ALOX12P2)and a control group(vector).The effects of altered ALOX12P2 expression on the epithelial-mesenchymal transition(EMT)-related gene E-cadherin and the PI3K/AKT signaling pathway were assessed through Western blot analysis.RESULTS:ALOX12P2 expression was significantly higher in HNSCC and OSCC tissues compared to normal tissues,with its expression correlating with poor prog-nosis.RT-qPCR analysis indicated that the relative expression of ALOX12P2 in OSCC cells was comparable to that in nor-mal cells(P<0.05).RNA nucleoplasmic isolation confirmed that ALOX12P2 localized in the nucleus.In comparison to the SS-NC group,the SS-ALOX12P2 group exhibited a marked reduction in ALOX12P2 expression(P<0.01),alongside significant decreases in cell viability,migration,and invasion(P<0.01).Conversely,the ALOX12P2 group showed sub-stantially higher relative expression compared to the vector group(P<0.01),with enhanced cell viability,migration,and invasion abilities(P<0.01).Western blot analysis demonstrated that ALOX12P2 knockdown resulted in upregulation of E-cadherin and downregulation of N-cadherin and Vimentin(P<0.01),while overexpression of ALOX12P2 yielded the opposite effects(P<0.01).Knockdown of ALOX12P2 led to decreased protein expression of p-PI3K and p-AKT(P<0.01),whereas overexpression increased these protein levels(P<0.01).CONCLUSION:ALOX12P2 is highly ex-pressed in OSCC and promotes cell viability,migration,and invasion.This effect may be linked to the activation of the PI3K/AKT signaling pathway,which facilitates the epithelial-mesenchymal transition(EMT)process.

Construction of smart hospitals is of great significance to the substantial development of medical institutions and the reform of medical and health systems and meanwhile it serves as a crucial support for the high-quality development of pub-lic hospitals.Guangdong Second Provincial General Hospital actively responds to national policies,constantly exploring standard-ized application of new smart medical technology.It has successfully built itself into a first full-scene smart hospital.Through gradually deepening the intelligent construction of hospitals,the hospital has achieved obvious achievements in hospital manage-ment such as medical services,medical resources,medical data,hospital operation logistics,and medical environment improve-ment.Their practical experience can provide references for the intelligent construction of hospitals domestically.