Objective This study examines the factors influencing oral frailty in the elderly community,develops a risk prediction model,and validates its efficacy,so as to provide references for identifying and preventing oral weakness in the elderly.Methods 556 elderly individuals from 4 communities were selected by convenience sampling from June to August 2024 in Zigong City Sichuan Province.They were randomly divided into a training group(383 cases)and a validation group(165 cases).Data were collected by a general information questionnaire,Social Frailty Scale,Geriatric Depression Scale,and the Oral Frailty Index-8 screening tool.Logistic regression was used to determine the influencing factors,and R software was used to establish a nomogram model for predicting the risk of oral frailty.Bootstrap method and the validation group were used for internally validation of the model.Calibration curve was used to evaluate the prediction performance of the model.Results 548 valid questionnaires were collected.The final model variables included whether the age ≥80 years,wearing removable dentures,reduced frequency of going out,brushing teeth less than twice a day,frequent dry mouth,increased difficulty in eating hard foods,and choking.The area under the receiver operating characteristic curve of the training group was 0.95(95％CI:0.93～0.97),and the best cutoff value was 0.687.The model achieved an accuracy of 87％,sensitivity of 91％,specificity of 85％,positive predictive value of 0.75,and negative predictive value of 0.95.The Hosmer-Lemeshow fitting test show that x2=3.036,P=0.932,indicating a good model fit.Conclusion The oral frailty prediction model demonstrated a good discrimination,calibration,and clinical utility,which can provide a scientific basis for the prevention and early screening of oral frailty in the elderly.

Aim To investigate the effect and mechanism of angiotensin Ⅱ(Ang Ⅱ)on ferroptosis in white adi-pocytes.Methods The 3T3-L1 preadipocytes were differentiated into white adipocytes by inducer stimulation.The experiment was divided into control group,Ang Ⅱ group,Ang Ⅱ+Fer-1(ferroptosis inhibitor)group and Ang Ⅱ+PFT-α(p53 inhibitor)group.Ang Ⅱ was used to treat cells.RT-qPCR and Western blot were used to detect the expression levels of ferroptosis factors and adipokines.JC-1 kit was used to detect mitochondrial membrane potential(MMP)level.Iron ion kit was used to detect intracellular iron content.Glutathione(GSH)kit was used to detect GSH content.Fer-1 and Ang Ⅱ were added to treat cells to detect the the changes of ferroptosis level.The expression of p53 and spermidine/spermine N1-acetyltransferase 1(SAT1)protein was detected.Subsequently,PFT-α and Ang Ⅱ were added to co-treat cells to detect the changes of p53 and SAT1 protein expression,and to observe the effect of inhibiting p53 expression on the expression levels of ferroptosis factors and adipokines.Results 3T3-L1 cells were successfully differentiated into white adipocytes by stimulator-induced differentiation.Ang Ⅱ induced ferroptosis in white adipocytes.RT-qPCR results showed that compared with control group,the mRNA expression of anti-ferroptosis factor glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11)and iron regulatory protein 1(IRP-1)was down-regulated in Ang Ⅱ group,and the mRNA expression of pro-ferroptosis factor acyl-CoA synthetase of long-chain family member 4(ACSL4)was up-regulated.Western blot results showed that compared with control group,the protein expression of SLC7A11 and GPX4 was down-regulated in Ang Ⅱ group,and the protein expression of ACSL4 was up-regulated.Ang Ⅱ treatment increased the content of intracellular iron ions and decreased the levels of GSH and MMP.Compared with Ang Ⅱ group,the mRNA expression of IRP-1 and SLC7A11 was up-regulated in Ang Ⅱ+Fer-1 group.Ang Ⅱ induced changes in the expression profile of adipokines in white adipocytes.Western blot results showed that compared with control group,the protein ex-pression of pro-inflammatory adipokine leptin(LEP),resistin(RETN),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)was up-regulated in Ang Ⅱ group,and the protein expression of anti-inflammatory adipokine adiponectin(AD-PN)and omentin 1(ITLN1)was down-regulated.In addition,Ang Ⅱ increased the protein expression of p53 and SAT1.Inhibition of p53 expression can improve the level of ferroptosis and adipokine expression in white adipocytes trea-ted with Ang Ⅱ.Western blot results showed that compared with Ang Ⅱ group,the protein expression of p53 and SAT1 was down-regulated in Ang Ⅱ+PFT-α group,the protein expression of SLC7A11 and GPX4 was up-regulated,and the protein expression of ACSL4 was down-regulated.The protein expression of ADPN was up-regulated in Ang Ⅱ+PFT-αgroup,and the protein expression of TNF-α,LEP and RETN was down-regulated.Conclusion Ang Ⅱ induces fer-roptosis in white adipocytes through activating the p53/SAT1 signaling pathway.

Aim To investigate the effect and mechanism of angiotensin Ⅱ(Ang Ⅱ)on ferroptosis in white adi-pocytes.Methods The 3T3-L1 preadipocytes were differentiated into white adipocytes by inducer stimulation.The experiment was divided into control group,Ang Ⅱ group,Ang Ⅱ+Fer-1(ferroptosis inhibitor)group and Ang Ⅱ+PFT-α(p53 inhibitor)group.Ang Ⅱ was used to treat cells.RT-qPCR and Western blot were used to detect the expression levels of ferroptosis factors and adipokines.JC-1 kit was used to detect mitochondrial membrane potential(MMP)level.Iron ion kit was used to detect intracellular iron content.Glutathione(GSH)kit was used to detect GSH content.Fer-1 and Ang Ⅱ were added to treat cells to detect the the changes of ferroptosis level.The expression of p53 and spermidine/spermine N1-acetyltransferase 1(SAT1)protein was detected.Subsequently,PFT-α and Ang Ⅱ were added to co-treat cells to detect the changes of p53 and SAT1 protein expression,and to observe the effect of inhibiting p53 expression on the expression levels of ferroptosis factors and adipokines.Results 3T3-L1 cells were successfully differentiated into white adipocytes by stimulator-induced differentiation.Ang Ⅱ induced ferroptosis in white adipocytes.RT-qPCR results showed that compared with control group,the mRNA expression of anti-ferroptosis factor glutathione peroxidase 4(GPX4),solute carrier family 7 member 11(SLC7A11)and iron regulatory protein 1(IRP-1)was down-regulated in Ang Ⅱ group,and the mRNA expression of pro-ferroptosis factor acyl-CoA synthetase of long-chain family member 4(ACSL4)was up-regulated.Western blot results showed that compared with control group,the protein expression of SLC7A11 and GPX4 was down-regulated in Ang Ⅱ group,and the protein expression of ACSL4 was up-regulated.Ang Ⅱ treatment increased the content of intracellular iron ions and decreased the levels of GSH and MMP.Compared with Ang Ⅱ group,the mRNA expression of IRP-1 and SLC7A11 was up-regulated in Ang Ⅱ+Fer-1 group.Ang Ⅱ induced changes in the expression profile of adipokines in white adipocytes.Western blot results showed that compared with control group,the protein ex-pression of pro-inflammatory adipokine leptin(LEP),resistin(RETN),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α)was up-regulated in Ang Ⅱ group,and the protein expression of anti-inflammatory adipokine adiponectin(AD-PN)and omentin 1(ITLN1)was down-regulated.In addition,Ang Ⅱ increased the protein expression of p53 and SAT1.Inhibition of p53 expression can improve the level of ferroptosis and adipokine expression in white adipocytes trea-ted with Ang Ⅱ.Western blot results showed that compared with Ang Ⅱ group,the protein expression of p53 and SAT1 was down-regulated in Ang Ⅱ+PFT-α group,the protein expression of SLC7A11 and GPX4 was up-regulated,and the protein expression of ACSL4 was down-regulated.The protein expression of ADPN was up-regulated in Ang Ⅱ+PFT-αgroup,and the protein expression of TNF-α,LEP and RETN was down-regulated.Conclusion Ang Ⅱ induces fer-roptosis in white adipocytes through activating the p53/SAT1 signaling pathway.

Objective This study examines the factors influencing oral frailty in the elderly community,develops a risk prediction model,and validates its efficacy,so as to provide references for identifying and preventing oral weakness in the elderly.Methods 556 elderly individuals from 4 communities were selected by convenience sampling from June to August 2024 in Zigong City Sichuan Province.They were randomly divided into a training group(383 cases)and a validation group(165 cases).Data were collected by a general information questionnaire,Social Frailty Scale,Geriatric Depression Scale,and the Oral Frailty Index-8 screening tool.Logistic regression was used to determine the influencing factors,and R software was used to establish a nomogram model for predicting the risk of oral frailty.Bootstrap method and the validation group were used for internally validation of the model.Calibration curve was used to evaluate the prediction performance of the model.Results 548 valid questionnaires were collected.The final model variables included whether the age ≥80 years,wearing removable dentures,reduced frequency of going out,brushing teeth less than twice a day,frequent dry mouth,increased difficulty in eating hard foods,and choking.The area under the receiver operating characteristic curve of the training group was 0.95(95％CI:0.93～0.97),and the best cutoff value was 0.687.The model achieved an accuracy of 87％,sensitivity of 91％,specificity of 85％,positive predictive value of 0.75,and negative predictive value of 0.95.The Hosmer-Lemeshow fitting test show that x2=3.036,P=0.932,indicating a good model fit.Conclusion The oral frailty prediction model demonstrated a good discrimination,calibration,and clinical utility,which can provide a scientific basis for the prevention and early screening of oral frailty in the elderly.

Objective To analyze the research status,hotspots and trends of TCM in the treatment of attention deficit hyperactivity disorder(ADHD).Methods The literature on the treatment of ADHD by TCM were was retrieved from CNKI,VIP,Wanfang Data,and CBM from the establishment of the databases to 7th,Sep.2023.NoteExpress 3.9 was used to manage and remove weight;Excel 2019 was used to draw a line trend chart for the number of published literature.CiteSpace 6.1R.6 software was used to perform co-occurrence and clustering analysis on authors,institutions and keywords,and a visual graph was drawn.Results A total of 1215 articles were included after screening.800 authors were involved,forming research teams with Han Xinmin,Wang Junhong,Ma Rong and Li Yirui as the cores respectively;Nanjing University of Chinese Medicine,Guangzhou University of Chinese Medicine,Beijing University of Chinese Medicine and so on published more papers.High-frequency keywords included clinical efficacy,acupuncture and moxibustion treatment,clinical experience,Chinese materia medica and so on;research frontiers included clinical efficacy,acupuncture and moxibustion treatment,clinical experience,data mining and attention.Conclusion The main research on the treatment of ADHD by TCM includes clinical efficacy,clinical experience,animal experiments and data mining,and relatively stable research teams have been formed,but there is less cooperation between teams and institutions.

OBJECTIVE: To compare the effect of 7 antipsychotic drugs on the life quality of schizophrenia patients including chlorpromazine, sulpiride, clozapine, risperidone, olanzapine, quetiapine, and aripiprazole. METHODS: A total of 1,227 stable schizophrenic patients within 5 years onset who took 1 of the 7 study medications as maintenance treatment were followed up for 1 year at 10 China sites. Patients were evaluated by the short form-36 health survey (SF-36) at the baseline and at the end of 1 year. RESULTS: The life quality was improved obviously at the end of the follow-up. There was significant difference in body pain, vitality, and mental health (P<0.05) among these antipsychotic drugs. CONCLUSION All 7 antipsychotic drugs can improve the life quality of schizophrenia patients. Atypical antipsychotic drugs, especially olazapine and quetiapine, are superior to typical antipsychotic drugs in improving life quality.
Adolescent ; Adult ; Antipsychotic Agents ; therapeutic use ; Benzodiazepines ; therapeutic use ; Dibenzothiazepines ; therapeutic use ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Olanzapine ; Quality of Life ; Quetiapine Fumarate ; Schizophrenia ; drug therapy ; Surveys and Questionnaires ; Young Adult

BACKGROUND: LIM Mineralization protein 1 (LMP-1), an intracellular non-secretory protein, plays roles in bone calcification. Presently, it is found that LMP-1 can promote an increase in bone morphogenetic protein 2 and transforming growth factor ? 1. This indicates that LMP-1 may recruit a mass of ossified factors to participate in the differentiation of osteoblasts. OBJECTIVE: To construct human LMP-1 gene adenovirus recombinant with AdEasy adenovirus vector system, and to detect LMP-1 expression in infected rabbit bone marrow mesenchymal stem cells (BMSCs). DESIGN, TIME AND SETTING: An opening experiment was performed at the Central Laboratory of South West Hospital, Third Military Medical University of Chinese PLA from March 2006 to February 2007. MATERIALS: Three New Zealand rabbits were used to isolate bone marrow mesenchymal stem cells. Plasmid pIRES2-EGFP-LMP-1 carrying human LMP-1 gene was kept in Department of Orthopedics, Second Hospital Affiliated to Chongqing Medical University. AdEasy was presented by Dr. Tong-Chuan He from USA. Human embryo kidney 293 cells were gifted by Wang from Department of Clinical Laboratory of Chongqing Medical University. METHODS: LMP-1 gene with a sequence encoding His-tag was amplified by using pIRES2-EGFP-LMP-1 plasmid as a template for polymerase chain reaction (PCR) with a specially designed downstream primer. The target gene was cloned to the pMD18-T vector for sequencing. Once verified, the gene was cut out by double endonucleases, connected to the shuttle vector pAdTrack-CMV. The newly constructed vector was linearized by PmeⅠ following efficient homologous recombination with the backbone vector pAdEasy-1 in BJ5183. The correct recombinant pAd-LMP-1 was linearized with Pac I and transfected to HEK293 cell by means of mediated Lipofectamine. The titer of virus was measured after amplification and purification. The mRNA and protein expression of LMP-1 was detected in BMSCs, which were infected with Ad-LMP-1 at the most appropriate MOI, were detected by reverse transcription (RT)-PCR and Western blot, respectively. MAIN OUTCOME MEASURES: Plasmid pAd-LMP-1 identification, its titre and efficiency of infection. mRNA and protein expression of LMP-1 were detected by RT-PCR and Western blot, respectively. RESULTS: The recombinant plasmid pMD18-T-LMP-1 carrying LMP-1 gene with His-tag was successfully constructed. After packaging and amplification of the recombinant adenovirus, the 3.5?109 efu/ml titer of Ad-LMP-1 was obtained by CsCl gradient purification. The optimal efficiency infection was 50%-70%, which was get after Ad-LMP-1 infected BMSCs for 3 days at the most appropriate MOI 150. The mRNA and protein expression of LMP-1 in infected BMSCs had been proved. CONCLUSION: The recombinant adenovirus containing human LMP-1 gene with His-tag is successfully constructed. The BMSCs infected with recombinant adenovirus Ad-LMP-1 can effectively express LMP-1.

Objective To study the causes and protection of intracranial aneurysms uncompletely embolized with micro-coils. Methods 47 cases of intracranial aneurysms were treated with micro-coils to embolize the aneurysaml sac via femoral artery approach to endovascular embolization.The aneurysms were located on AcoA in 19,on MCA in 7,on PcoA in 16 and on ICA in 5,2 aneurysms were foundin each of 2 cases. Results The uncompletely occuluded in 12 of them,aneurysms were completely occluded in 35,9 aneurysms wereoccluded to 95%,2 aneurysms were occluded to 90%,1 neurysms were occluded to 80%. Conclusion The wide neck intracranialaneurysms,hugeness intracranial aneurysms and ophidian,irregular intracranial aneurysms are of high rate of uncompletely occluded.Usingbasket-technique,remodel technique,vein rebuild technique and nibble subdivision endovascular embolization can decrease the rate ofuncompletely embolize intracranial aneurysm.