With the rapid advancement of artificial intelligence technology, chatbots have shown great potential in the healthcare sector. From personalized health advice to chronic disease management and psychological support, chatbots have demonstrated significant advantages in improving the efficiency and quality of healthcare services. As the scope of their applications expands, the relationship between technological complexity and practical application scenarios has become increasingly intertwined, necessitating a more comprehensive evaluation of both aspects. This paper, from the perspective of he althcare applications, systematically reviews the technological pathways and development of chatbots in the medical field, providing an in-depth analysis of their performance across various medical scenarios. It thoroughly examines the advantages and limitations of chatbots, aiming to offer theoretical support for future research and propose feasible recommendations for the broader adoption of chatbot technologies in healthcare.

This study aimed to explore the mechanisms and molecular targets of total flavones of Abelmoschus manihot(TFA) plus empagliflozin(EM) in attenuating diabetic tubulopathy(DT) by targeting mitochondrial homeostasis and pyroptosis-apoptosis-necroptosis(PANoptosis). In the in vivo study, the authors established the DT rat models through a combination of uninephrectomy, administration of streptozotocin via intraperitoneal injections, and exposure to a high-fat diet. Following modeling successfully, the DT rat models received either TFA, EM, TFA+EM, or saline(as a vehicle) by gavage for eight weeks, respectively. In the in vitro study, the authors subjected the NRK52E cells with or without knock-down Z-DNA binding protein 1(ZBP1) to a high-glucose(HG) environment and various treatments including TFA, EM, and TFA+EM. In the in vivo and in vitro studies, The authors investigated the relative characteristics of renal tubular injury and renal tubular epithelial cells damage induced by reactive oxygen species(ROS), analyzed the relative characteristics of renal tubular PANoptosis and ZBP1-mediatted PANoptosis in renal tubular epithelial cells, and compared the relative characteristics of the protein expression levels of marked molecules of mitochondrial fission in the kidneys and mitochondrial homeostasis in renal tubular epithelial cells, respectively. Furthermore, in the network pharmacology study, the authors predicted and screened targets of TFA and EM using HERB and SwissTargetPrediction databases; The screened chemical constituents and targets of TFA and EM were constructed the relative network using Cytoscape 3.7.2 network graphics software; The relative targets of DT were integrated using OMIM and GeneCards databases; The intersecting targets of TFA, EM, and DT were enriched and analyzed signaling pathways by Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG) software using DAVID database. In vivo study results showed that TFA+EM could improve renal tubular injury, the protein expression levels and characteristics of key signaling molecules in PANoptosis pathway in the kidneys, and the protein expression levels of marked molecules of mitochondrial fission in the kidneys. And that, the ameliorative effects in vivo of TFA+EM were both superior to TFA or EM. Network pharmacology study results showed that TFA+EM treated DT by regulating the PANoptosis signaling pathway. In vitro study results showed that TFA+EM could improve ROS-induced cell injury, ZBP1-mediatted PANoptosis, and mitochondrial homeostasis in renal tubular epithelial cells under a state of HG, including the protein expression levels of marked molecules of mitochondrial fission, mitochondrial ultrastructure, and membrane potential level. And that, the ameliorative effects in vitro of TFA+EM were both superior to TFA or EM. More importantly, using the NRK52E cells with knock-down ZBP1, the authors found that, indeed, ZBP1 was mediated PANoptosis in renal tubular epithelial cells as an upstream factor. In addition, TFA+EM could regulate the protein expression levels of marked signaling molecules of PANoptosis by targeting ZBP1. In summary, this study clarified that TFA+EM, different from TFA or EM, could attenuate DT with multiple targets by ameliorating mitochondrial homeostasis and inhibiting ZBP1-mediated PANoptosis. These findings provide the clear pharmacological evidence for the clinical treatment of DT with a novel strategy of TFA+EM, which is named "coordinated traditional Chinese and western medicine".
Animals ; Rats ; Mitochondria/metabolism* ; Benzhydryl Compounds/administration & dosage* ; Glucosides/administration & dosage* ; Abelmoschus/chemistry* ; Male ; Homeostasis/drug effects* ; Flavones/administration & dosage* ; Rats, Sprague-Dawley ; Diabetic Nephropathies/physiopathology* ; Drugs, Chinese Herbal/administration & dosage* ; DNA-Binding Proteins/genetics* ; Humans ; Apoptosis/drug effects*

OBJECTIVE: To explore the neuroprotective effects of Xuefu Zhuyu Decoction (XFZYD) based on in vivo and metabolomics experiments. METHODS: Traumatic brain injury (TBI) was induced via a controlled cortical impact (CCI) method. Thirty rats were randomly divided into 3 groups (10 for each): sham, CCI and XFZYD groups (9 g/kg). The administration was performed by intragastric administration for 3 days. Neurological functions tests, histology staining, coagulation and haemorheology assays, and Western blot were examined. Untargeted metabolomics was employed to identify metabolites. The key metabolite was validated by enzyme-linked immunosorbent assay and immunofluorescence. RESULTS: XFZYD significantly alleviated neurological dysfunction in CCI model rats (P<0.01) but had no impact on coagulation function. As evidenced by Evans blue and IgG staining, XFZYD effectively prevented blood-brain barrier (BBB) disruption (P<0.05, P<0.01). Moreover, XFZYD not only increased the expression of collagen IV, occludin and zona occludens 1 but also decreased matrix metalloproteinase-9 (MMP-9) and cyclooxygenase-2 (COX-2), which protected BBB integrity (all P<0.05). Nine potential metabolites were identified, and all of them were reversed by XFZYD. Adenosine was the most significantly altered metabolite related to BBB repair. XFZYD significantly reduced the level of equilibrative nucleoside transporter 2 (ENT2) and increased adenosine (P<0.01), which may improve BBB integrity. CONCLUSIONS XFZYD ameliorates BBB disruption after TBI by decreasing the levels of MMP-9 and COX-2. Through further exploration via metabolomics, we found that XFZYD may exert a protective effect on BBB by regulating adenosine metabolism via ENT2.
Animals ; Drugs, Chinese Herbal/therapeutic use* ; Blood-Brain Barrier/metabolism* ; Brain Injuries, Traumatic/metabolism* ; Adenosine/metabolism* ; Male ; Rats, Sprague-Dawley ; Rats

Apical microsurgery is accurate and minimally invasive, produces few complications, and has a success rate of more than 90%. However, due to the lack of awareness and understanding of apical microsurgery by dental general practitioners and even endodontists, many clinical problems remain to be overcome. The consensus has gathered well-known domestic experts to hold a series of special discussions and reached the consensus. This document specifies the indications, contraindications, preoperative preparations, operational procedures, complication prevention measures, and efficacy evaluation of apical microsurgery and is applicable to dentists who perform apical microsurgery after systematic training.
Microsurgery/standards* ; Humans ; Apicoectomy ; Contraindications, Procedure ; Tooth Apex/diagnostic imaging* ; Postoperative Complications/prevention & control* ; Consensus ; Treatment Outcome

Intentional tooth replantation (ITR) is an advanced treatment modality and the procedure of last resort for preserving teeth with inaccessible endodontic or resorptive lesions. ITR is defined as the deliberate extraction of a tooth; evaluation of the root surface, endodontic manipulation, and repair; and placement of the tooth back into its original socket. Case reports, case series, cohort studies, and randomized controlled trials have demonstrated the efficacy of ITR in the retention of natural teeth that are untreatable or difficult to manage with root canal treatment or endodontic microsurgery. However, variations in clinical protocols for ITR exist due to the empirical nature of the original protocols and rapid advancements in the field of oral biology and dental materials. This heterogeneity in protocols may cause confusion among dental practitioners; therefore, guidelines and considerations for ITR should be explicated. This expert consensus discusses the biological foundation of ITR, the available clinical protocols and current status of ITR in treating teeth with refractory apical periodontitis or anatomical aberration, and the main complications of this treatment, aiming to refine the clinical management of ITR in accordance with the progress of basic research and clinical studies; the findings suggest that ITR may become a more consistent evidence-based option in dental treatment.
Humans ; Tooth Replantation/methods* ; Consensus ; Periapical Periodontitis/surgery*

The rapid development of artificial intelligence (AI), especially generative AI (GenAI), has already brought, and will continue to bring, revolutionary changes to our daily production and life, as well as create new opportunities and challenges for diagnostic and therapeutic practices in the medical field. Haihe Hospital of Tianjin University collaborates with the National Supercomputer Center in Tianjin, Tianjin University, and other institutions to carry out research in areas such as smart healthcare, smart services, and smart management. We have conducted research and development of a full-process disease diagnosis and treatment assistance system based on GenAI in the field of smart healthcare. The development of this project is of great significance. The first goal is to upgrade and transform the hospital's information center, organically integrate it with existing information systems, and provide the necessary computing power storage support for intelligent services within the hospital. We have implemented the localized deployment of three models: Tianhe "Tianyuan", WiNGPT, and DeepSeek. The second is to create a digital avatar of the chief physician/chief physician's voice and image by integrating multimodal intelligent interaction technology. With generative intelligence as the core, this solution provides patients with a visual medical interaction solution. The third is to achieve deep adaptation between generative intelligence and the entire process of patient medical treatment. In this project, we have developed assistant tools such as intelligent inquiry, intelligent diagnosis and recognition, intelligent treatment plan generation, and intelligent assisted medical record generation to improve the safety, quality, and efficiency of the diagnosis and treatment process. This study introduces the content of a full-process disease diagnosis and treatment assistance system, aiming to provide references and insights for the digital transformation of the healthcare industry.
Artificial Intelligence ; Humans ; Delivery of Health Care ; Generative Artificial Intelligence

Objective To investigate the influences and mechanism of X chromosome inactivation specific transcript(XIST)on the proliferation and extracellular matrix synthesis of nucleus pulposus cells in rats with intervertebral disc degeneration(IDD).Methods SD rat intervertebral disc nucleus pulposus cells were isolated and cultured in vitro,and then randomly divided cells into control group,model group,XIST knockdown group,empty plasmid group,and XIST knockdown+miR-132-3p knockdown group.Except for control group,the cells in other groups were induced by interleukin(IL)-1β to establish IDD models.After nucleus pulposus cells were grouped and treated,the expressions of XIST and miR-132-3p in the nucleus pulposus cells of rats were detected by qRT-PCR;the proliferation of intervertebral disc nucleus pulposus cells was detected by MTS method and EdU staining;ELISA was used to measure the levels of inflammatory factors IL-6 and IL-18 in the intervertebral disc nucleus pulposus cells;Immunoblotting was used to detect the expression of extracellular matrix labeled proteins Collagen Ⅱ and Aggrecan in rat nucleus pulposus cells.The targeted regulation of miR-132-3p by XIST in rat nucleus pulposus cells was detected by dual-luciferase reporter gene assay.IDD rat models were established by intramuscular injection of IL-1β and divided into sham operation group,model group,XIST knockdown group,no-load plasmid group,XIST knockdown+miR-132-3p knockdown group,with 12 rats in each group.After treatment in each group,the expressions of XIST and miR-132-3p in intervertebral disc tissues were detected by qRT-PCR;TUNEL staining was used to detect apoptosis of nucleus pulposus cells in intervertebral disc tissue of rats;the morphology of intervertebral disc cartilage was observed by saffron O staining;serum levels of inflammatory factors IL-6 and IL-18 were determined by ELISA;the expressions of Collagen Ⅱ and Aggrecan in intervertebral disc tissues were detected by Western blotting.Results Compared with control group(cells)/sham operation group(rats),XIST expression in intervertebral disc tissue and nucleus pulposus cells,apoptosis rate of intervertebral disc nucleus pulposus cells,levels of inflammatory factors IL-6 and IL-18 in intervertebral disc nucleus pulposus cells culture medium and serum were increased in model group(P＜0.05),the activity and proliferation rate of nucleus pulposus cells and the expressions of miR-132-3p,Collagen Ⅱ and Aggrecan protein in nucleus pulposus cells and intervertebral disc tissues decreased(P＜0.05);compared with model group,the apoptosis rate of nucleus pulposus cells,the levels of inflammatory factors IL-6 and IL-18 in intervertebral disc nucleus pulposus cells culture medium and serum,and the expression of XIST in nucleus pulposus cells and intervertebral disc tissues of rats in XIST knockdown group decreased(P＜0.05),the activity and proliferation rate of nucleus pulposus cells and the expressions of miR-132-3p,Collagen Ⅱ and Aggrecan protein in nucleus pulposus cells and intervertebral disc tissues increased(P＜0.05).Down-regulation of miR-132-3p attenuates the ameliorative effect of knockdown XIST on IL-1β-induced intervertebral disc injury and cartilage matrix loss.XIST was able to target and down-regulate the expression of miR-132-3p in rat nucleus pulposus cells.Conclusion Knockdown of XIST can inhibit inflammation by up-regulating miR-132-3p,thereby inhibiting the apoptosis of IDD nucleus pulposus cells and promoting their proliferation and extracellular matrix synthesis.

Objective To investigate the formation and mechanism of dipeptidylpeptidase-4 inhibitor anagliptin inhibiting lung metastasis of colorectal cancer.Methods Twenty-four male BALB/c mice were randomly divided into normal group,model group,anagliptin group.The control group did not undergo any treatment.The model group was injected with 0.1 ml CT-26 cells of 109 cells/L.once through the tail vein of the mouse to construct a lung metastasis model,while the anagliptin group was injected intraperitoneally 20 mg/(kg d)0 day after constructing a lung metastasis model.The mice were sacrificed after 14 days.HE staining was used to detect the morphological alteration.Determination of CT-26 cell viability through MTT assay and CT-26 cell apoptosis was detected by flow cytometry and live/dead cell staining.Reactive oxygen species(ROS)production was measured by ROS kit.Western blotting was conducted to measure the expression level of Bcl-2,Bax,cleaved-caspase-3,superoxide dismutase(SOD-1)and SOD-2.Results HE staining showed that the administration of anagliptin could significantly inhibit the abnormal changes in the model group.Anagliptin inhibited the viability of CT-26 cells above 2 mmol/L.Anagliptin promoted the apoptosis of CT-26 cells.Incubation of anagliptin in CT-26 cells significant promoted the production of ROS.Incubation of anagliptin stimulated the expressions of Bax and cleaved-Caspase-3,while down-regulated the expression of Bcl-2 in CT-26 cells.Administration of anagliptin decreased the expression of SOD-1,but not SOD-2.Conclusion Anagliptin promotes apoptosis of colorectal cancer cells and inhibits the formation of lung metastatic tumors through the SOD-1/ROS pathway.

Purpose::Acute kidney injury (AKI) is one of the most common functional injuries observed in trauma patients. However, certain trauma medications may exacerbate renal injury. Therefore, the early detection of trauma-related AKI holds paramount importance in improving trauma prognosis.Methods::Qualified datasets were selected from public databases, and common differentially expressed genes related to trauma-induced AKI and hub genes were identified through enrichment analysis and the establishment of protein-protein interaction (PPI) networks. Additionally, the specificity of these hub genes was investigated using the sepsis dataset and conducted a comprehensive literature review to assess their plausibility. The raw data from both datasets were downloaded using R software (version 4.2.1) and processed with the "affy" package19 for correction and normalization.Results::Our analysis revealed 585 upregulated and 629 downregulated differentially expressed genes in the AKI dataset, along with 586 upregulated and 948 downregulated differentially expressed genes in the trauma dataset. Concurrently, the establishment of the PPI network and subsequent topological analysis highlighted key hub genes, including CD44, CD163, TIMP metallopeptidase inhibitor 1, cytochrome b-245 beta chain, versican, membrane spanning 4-domains A4A, mitogen-activated protein kinase 14, and early growth response 1. Notably, their receiver operating characteristic curves displayed areas exceeding 75%, indicating good diagnostic performance. Moreover, our findings postulated a unique molecular mechanism underlying trauma-related AKI. Conclusion::This study presents an alternative strategy for the early diagnosis and treatment of trauma-related AKI, based on the identification of potential biomarkers and therapeutic targets. Additionally, this study provides theoretical references for elucidating the mechanisms of trauma-related AKI.

Objective To investigate the molecular genetic characteristics and clinical characteristics of severe combined immunodeficiency(SCID)in children caused by a novel mutation of interleukin 2 receptor gamma IL-2RG gene.Methods The clinical data,laboratory results and genetic testing data of a child with SCID admitted to the Department of Children's Hematology of Northwest Women and Children's Hospital were analyzed.Results A two-month-old male infant was admitted to the hospital for treatment due to recurrent infections after birth.The child's blood routine results showed that the total number of white blood cells was normal,but lymphocytes were decreased.The lymphocyte subpopulation results showed a significant decrease in the proportion of total T(CD3+),helper T(CD3+CD4+),killer T(CD3+CD8+),and NK(CD3-CD16+CD56+)lymphocytes,while the proportion of B(CD3-CD19+)lymphocytes were increased.The immunoglobulin levels showed a significant decrease in IgG,and IgM and IgA were below the lower detection limit.The patient's cytokine levels did not significantly increase during infection.In the last three generations of the mother's family,9 males died of infection within one year after birth.The whole exome sequencing results of the core family revealed a semi zygous new missense mutation[c.675 C＞A,p.S225R(p.Ser225Arg)]in the IL-2RG gene on the X chromosome(chrX:70329160)of the patient,and the mother was a carrier.Based on the above evidence,the child was diagnosed with X-SCID.Subsequently,intravenous immunoglobulin was injected monthly,and routine antibiotics and antiviral drugs were taken to prevent infection,preparing for hematopoietic stem cell transplantation.Because the child was vaccinated with BCG after birth,the child developed disseminated BCG disease at the age of 6 months.After treatment,hematopoietic stem cell transplantation was performed.Conclusion The immune function of the X-SCID patient was severely compromised,which endangered the patient's life,and vaccination with live vaccines may lead to severe infections.This study found that the c.675 C＞A mutation of the IL-2RG gene was a novel pathogenic variation of the genetic cause of X-SCID,expanding the mutation spectrum of the X-SCID pathogenic gene IL-2RG.