Under the trend of increasing aging， integrated elderly care and medical services is an important measure to optimize the supply of elderly care services and promote the good death of the elderly. Using the cooperative production theory and the classical grounded theory， a qualitative analysis was conducted on 38 cases of elderly palliative care and 25 cases of hospital-based palliative care under the integrated elderly care and medical services model from a hospital in Nanning City using Nvivo 20.0 software. This paper found that the integrated elderly care and medical services mode emphasized the deep integration of medical and elderly care services by integrating resources and improving service efficiency， to achieve the basic experience of comprehensive health care for the elderly. The promotion of these experiences has a positive significance for building a multi-agent cooperative production system， strengthening personnel training， perfecting the performance distribution mechanism， and further promoting the development of the national palliative care pilot.

OBJECTIVE To explore the potential mechanisms of astragalin （AG） in allevating ulcerative colitis （UC） in mice through modulation of the intestinal flora. METHODS Male C57BL/6 mice were randomly divided into normal group （CON group）， model group [dextran sodium sulfate （DSS） group]， 5-aminosalicylic acid group （5-ASA group）， AG low-dose group and high-dose group （AGL and AGH groups）， with 8 mice in each group. The mice UC model was established by drinking 3% DSS solution continuously for 7 days in all groups except the CON group. After that， 3% DSS solution was replaced by water， and the mice of each drug group were gavaged with the corresponding drug solution. Mice in the CON and DSS groups were gavaged with an equal volume of normal saline， once a day， for 7 days. After the last gavage， the body weight change index， disease activity index （DAI） score， colon length and spleen index， and levels of inflammatory factors （tumor necrosis factor-α， interleukin-1β， interleukin-6） were compared among the mice in each group； pathological changes in colonic tissues of the mice were observed in each group， and the pathological score and the percentage of goblet cells were compared； mRNA expressions of barrier-related factors [occludin and ZO-1] and inflammation-related factors [silencing information regulatory factor 1 （SIRT1）， c-Jun N-terminal kinase （JNK） and p38 mitogen-activated protein kinase （p38 MAPK）] were detected in each group of mice； the changes in the intestinal flora of mice in each group were analyzed and the contents of intestinal metabolites short-chain fatty acids （SCFAs） was determined. Using DSS and AG-treated fecal bacterial liquid as an intervention， the mechanism of anti-UC effect of AG was further verified by a fecal microbiota transplant experiment. RESULTS Compared with the CON group， the intestinal mucosal structure of mice in the DSS group was severely damaged， with obvious infiltration of inflammatory cells collapsing the wall； their body weight change index， colon length， the percentage of goblet cells， mRNA expressions of occludin， ZO-1 and SIRT1， Chao1 and Shannon indexes， and contents of acetic acid and butyric acid were significantly reduced， shortened or down-regulated （P＜0.05）； however， DAI score， spleen index， levels of inflammatory factors， pathological score， as well as mRNA expressions of p38 MAPK and JNK， were all significantly increased or up-regulated （P＜0.05）. Compared with the DSS group， colon tissue lesions of AG mice in all dose groups showed different degrees of improvement， and the above quantitative indexes were generally regressed （P＜0.05）， and the intervention effect of AG-treated fecal bacterial fluid was basically the same as that of AG. CONCLUSIONS AG can improve relevant symptoms in UC mice and reduce their inflammatory response and colonic histopathological changes. The above effects may be related to regulating the diversity of intestinal flora in mice， increasing the contents of butyric acid and propionic acid， and promoting the repair of the colonic mucosal barrier， thus regulating the expressions of genes related to the SIRT1/p38 MAPK inflammatory pathway.

Objective: To explore the individual and joint effects of outdoor activities and different types of sedentary behavior on adolescent internalizing behaviors, so as to provide a basis for the prevention and intervention of such behaviors. Methods: From July to December 2023, a stratified cluster random sampling method was used to select 1 691 primary and secondary school students in grades 5-12 from four primary and secondary schools in Baise City. Anonymous surveys were conducted by using the Outdoor Activities Questionnaire,Adolescent Sedentary Activity Questionnaire, and Youth Self Report. The Chi square test and Logistic regression analyses were used for statistical analysis. Results: The detection rate of internalizing behavior among adolescents was 13.13%, and the detection rate of internalizing behaviors in girls (15.53%) was significantly higher than that in boys ( 10.77 %) ( χ 2=8.39, P <0.01). Logistic regression analysis showed that outdoor activities ≥1 h/d ( OR =0.56), screen based entertainment sedentary behavior < 2 h/d ( OR =0.58), and cultural sedentary behavior < 2 h/d ( OR =0.55) significantly reduced the risk of internalizing behaviors (all P <0.05). Logistic regression analysis of interaction effects revealed that the risks of internalizing behaviors were lower in the groups with "outdoor activities ≥1 h/d + screen based entertainment sedentary behavior <2 h/d" ( OR = 0.27) and "outdoor activities ≥1 h/d + cultural sedentary behavior <2 h/d" ( OR =0.30)(both P <0.01). Conclusions Outdoor activities can mitigate the adverse effects of sedentary behaviors on adolescents internalizing behaviors. Reducing screen time and leveraging the synergistic effects of "outdoor + cultural" activities may help reduce the risk of internalizing behaviors among primary and secondary school students.

Alzheimer's disease (AD), a prototypical neurodegenerative disorder, encompasses multifaceted pathological processes. As pivotal cellular structures within the central nervous system, ion channels play critical roles in regulating neuronal excitability, synaptic transmission, and neurotransmitter release. Extensive research has revealed significant alterations in the expression and function of ion channels in AD, implicating an important role of ion channels in the pathogenesis of abnormal Aβ deposition, neuroinflammation, oxidative stress, and disruptions in calcium homeostasis and neural network functionality. This review systematically summarizes the crucial roles and underlying mechanisms of ion channels in the onset and progression of AD, highlighting how these channel abnormalities contribute to AD pathophysiology. We also discuss the therapeutic potential of ion channel modulation in AD treatment, emphasizing the importance of addressing multifactorial nature and heterogeneity of AD. The development of multi-target drugs and precision therapies is proposed as a future direction of scientific research.
Alzheimer Disease/therapy* ; Humans ; Ion Channels/physiology* ; Oxidative Stress ; Animals ; Amyloid beta-Peptides/metabolism* ; Synaptic Transmission ; Calcium/metabolism*

Objective The tissue motion mitral annular displacement(TMAD)technique was used to evaluate left ventricular longitudinal systolic function in patients with hyperthyroidism,and its correlation with myocardial damage was analyzed.Methods Sixty-nine cases of hyperthyroidism diagnosed in Affiliated Hospital of Youjiang Medical University for Nationalities from July 2021 to November 2022 were selected as the study objects.According to whether the patients were combined with hyperthyroidism heart disease,they were divided into simple hyperthyroidism group(n=43)and thyrotoxic heart group(n=26).35 healthy people who underwent physical examination in our hospital during the same period were selected as normal control group.Three-dimensional echocardiography was used to obtain the left ventricular end diastolic volume(LVEDV),left ventricular end systolic volume(LVESV),left ventricular ejection fraction(LVEF)and TMAD parameters.The differences of above parameters among all groups were compared,and the correlations of TMAD parameters with creatine kinase isoenzymes(CK-MB)and high-sensitivity cardiac troponin T(hs-cTnT)were analyzed.Results The LVEDV,LVESV,LVEF,TMAD parameters,CK-MB and hs-cTnT of three groups were statistically significant(P<0.001),and LVEDV,LVESV,CK-MB and hs-cTnT of normal control groupsimple hyperthyroidism group>thyrotoxic heart group.All parameters of TMAD were positively correlated with LVEF(P<0.001),and some parameters of TMAD were negatively correlated with CK-MB(P<0.05).Conclusion TMAD technology can early evaluate left ventricular longitudinal systolic function in patients with hyperthyroidism,and is related to CK-MB and hs-cTnT.

Objective: To explore the mechanism by which icariin alleviates viral myocarditis. Methods: CVB3-induced cardiomyocytes were used as an in vitro model of viral myocarditis to assess the effects of icariin treatment on cell viability, inflammation, and apoptosis. Moreover, the effects of icariin on ferroptosis and TLR4 signaling were assessed. After AC16 cells were transfected with TLR4 overexpression plasmids, the role of TLR4 in mediating the regulatory effect of icariin in viral myocarditis was investigated. Results: Icariin significantly elevated cell viability and reduced inflammatory factors TNF-α, IL-1β, IL-6, and IL-18. Flow cytometry revealed that icariin decreased apoptosis rate, and the protein expression of Bax and cleaved caspase 3 and 9 in CVB3-induced cardiomyocytes. Additionally, it suppressed ferroptosis including lipid peroxidation and ferrous ion, as well as the TLR4 signaling. However, TLR4 overexpression abrogated the modulatory effects of icariin. Conclusions: Icariin mitigates CVB3-induced myocardial injury by inhibiting TLR4-mediated ferroptosis. Further animal study is needed to verify its efficacy.

Objective : To investigate the effects of immunoglobulin gene superfamily 10 (IGSF10) on prolifera- tion，migration and invasion of lung adenocarcinoma cells． Methods : ioinformatics was applied to study the ex- pression levels of IGSF10 in tumor tissues and normal tissues． Western blot and quantitative real-time PCR ( qPCR) were used to detect the expression level of IGSF10 in lung adenocarcinoma cell lines and normal lung epi- thelial cells．Knockdown of IGSF10，the effect of knockdown of IGSF10 on proliferation，migration and invasion of lung adenocarcinoma A549 cells was examined using cell counting kit-8 ( CCK-8) ，Transwell migration and inva- sion assay，scratch assay and plate cloning assay．The effects of knockdown of IGSF10 on the expression of invasion and migration-related genes in A549 cells were examined by Western blot and qPCR assays. Results : IGSF10 ex- pression in lung adenocarcinoma tissues was lower than that in normal tissues (P ＜0. 05) ．IGSF10 expression in lung adenocarcinoma cell lines was lower than that in lung epithelial cells (P＜0. 05) ．Knockdown of IGSF10 pro- moted the ability of lung adenocarcinoma A549 cells to proliferate ，proliferation ，migration and invasion ( P < 0. 05) ．Knockdown of IGSF10 promoted the expression of regulatory epithelial-mesenchymal transition marker Neu- ral-cadherin (N-cadherin) and key transcription factors Snail family transcriptional repressor 1 (Snail) and Snail family transcriptional repressor 2 (Slug) (P＜0. 05) and inhibited the expression of Epithelial-cadherin (E-cad- herin) (P＜0. 05) ． Conclusion Knockdown of IGSF10 may promote proliferation，migration and invasion of lung adenocarcinoma cells through activation of Snail，Slug / E-cadherin signaling axis，and this result may provide a po- tential new target for clinical diagnosis and treatment of lung adenocarcinoma.

Acute B-lymphoblastic leukemia (B-ALL) is the most common type of acute lymphoblastic leukemia. Chemotherapy is the main treatment for most patients, but there are serious side effects. CD19 is generally highly expressed in B-lineage malignancies and plays a key role in B cell signal transduction, activation and development. Therefore, it has become one of the effective targets for treatment of B-cell malignancies. At present, a variety of therapies targeting CD19 have been developed, including antibody drug conjugates, monoclonal antibodies, bispecific antibodies and chimeric antigen receptors cell therapies. This paper reviews the clinical trial progress of CD19-targeted therapy for B-ALL.

Objective To analyze the expressions of receptor-interacting protein kinase 3 (RIPK3) and mixed lineage kinase domain-like protein (MLKL) in peripheral blood of neonates with necrotizing enterocolitis (NEC) and their relationships with the severity of the disease. Methods Ninety-two children with NEC were selected and divided into NEC group, and further divided into mild group (grade Ⅰ, n=60) and severe group (gradeⅡ to Ⅲ, n=32) according to the severity of the disease. Another 60 children with inguinal hernia were selected as control group. Real-time fluorescence quantitative polymerase chain reaction was used to detect the expressions of RIPK3 mRNA and MLKL mRNA in peripheral blood. Pearson correlation analysis was used to determine the correlation between RIPK3 mRNA and MLKL mRNA expression in peripheral blood of the NEC group. Western blot was used to detect the expression of RIPK3 and MLKL proteins in ileal tissues of NEC and normal ileal tissues. Multivariate Logistic regression analysis was used to identify independent risk factors for severe NEC. The receiver operating characteristic curve was plotted to analyze the value of peripheral blood RIPK3 mRNA and MLKL mRNA alone and their combination for predicting severe NEC. Results The relative expression levels of RIPK3 mRNA and MLKL mRNA in peripheral blood of the NEC group were significantly higher than those in the control group[(2.41±0.52) versus (1.02±0.21), (3.03±0.64) versus (0.93±0.20), P < 0.001]. The relative gray values of RIPK3 and MLKL proteins in ileal tissues of NEC were significantly higher than those in normal ileal tissues[(1.20±0.21) versus (0.34±0.12), (1.13±0.24) versus (0.32±0.11), P < 0.05]. There was a positive correlation between the relative expression level of RIPK3 mRNA and MLKL mRNA in peripheral blood of children with NEC (r=0.623, P < 0.001). The proportion of children with severe NEC complicated by pneumoperitoneum, multiple organ dysfunction syndrome, and sepsis, as well as the relative expression levels of RIPK3 mRNA and MLKL mRNA were significantly higher in the severe NEC group than in the mild NEC group (P < 0.05). The relative expression levels of RIPK3 mRNA and MLKL mRNA were independent risk factors for severe NEC (P < 0.05). The area under the curve for combined prediction of severe NEC by RIPK3 mRNA and MLKL mRNA in peripheral blood was larger than that for individual prediction (Z=4.127, 4.261, P < 0.05). Conclusion The expression levels of RIPK3 mRNA and MLKL mRNA in peripheral blood are elevated in neonates with NEC, and both are associated with the severity of NEC. The combined detection of RIPK3 mRNA and MLKL mRNA has a higher predictive value for severe NEC.

Objective To establish a fluorescent assay for rapid detection of Plasmodium falciparum based on recombinaseaided amplification (RAA) and CRISPR-Cas12a system,and to preliminarily evaluate the diagnostic efficiency of this system.. Methods The 18S ribosomal RNA (rRNA) gene of P. falciparum was selected as the target sequence, and three pairs of RAA primers and CRISPR-derived RNA (crRNA) were designed and synthesized. The optimal combination of RAA primers and crRNA was screened and the reaction conditions of the system were optimized to create a fluorescent RAA/CRISPR-Cas12a system. The plasmid containing 18S rRNA gene of the P. falciparum strain 3D7 was generated, and diluted into concentrations of 1 000, 100, 10, 1 copy/μL for the fluorescent RAA/CRISPR-Cas12a assay, and its sensitivity was evaluated. The genomic DNA from P. vivax, P. malariae, P. ovum, hepatitis B virus, human immunodeficiency virus and Treponema pallidum was employed as templates for the fluorescent RAA/CRISPR-Cas12a assay, and its specificity was evaluated. Fifty malaria clinical samples were subjected to the fluorescent RAA/CRISPR-Cas12a assay and nested PCR assay, and the consistency between two assays was compared. In addition, P. falciparum strain 3D7 was cultured in vitro. Then, the culture was diluted into blood samples with parasite densities of 1 000, 500, 200, 50, 10 parasites/μL with healthy volunteers’ O-positive red blood cells for the RAA/CRISPR-Cas12a assay, and the detection efficiency was tested. Results The Pf-F3/Pf-R3/crRNA2 combination, 2.5 μL as the addition amount of B buffer, 40 min as the RAA reaction time, 37 °C as the reaction temperature of the CRISPR-Cas12a system were employed to establish the fluorescent RAA/CRISPR-Cas12a system. Such a system was effective to detect the plasmid containing 18S rRNA gene of the P. falciparum strain 3D7 at a concentration of 1 copy/μL, and presented fluorescent signals for detection of P. falciparum, but failed to detect P. ovum, P. malariae, P. vivax, T. pallidum, hepatitis B virus or human immunodeficiency virus. The fluorescent RAA/CRISPR-Cas12a system and nested PCR assay showed completely consistent results for detection of 50 malaria clinical samples (kappa = 1.0, P < 0.001). Following 6-day in vitro culture of the P. falciparum strain 3D7, 10 mL cultures were generated and the fluorescent RAA/CRISPR-Cas12a system showed the minimal detection limit of 50 parasites/μL. Conclusion The fluorescent RAA/CRISPR-Cas12a system is rapid, sensitive and specific for detection of P. falciparum, which shows promising value for rapid detection and risk monitoring of P. falciparum.