[This corrects the article DOI: 10.1016/j.apsb.2021.10.012.].

Objective:To analyze the effects of shared decision-making in patients with type 2 diabetic mellitus.Methods:Databases including PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang Datebase, COVIP and SinoMed, for randomized controlled trials (RCTs) on the application of shared decision-making in patients with type 2 diabetic mellitus from inception to July 22, 2023, used R Studio software for meta-analysis.Results:A total of 14 RCTs and 2 606 patients with type 2 diabetic mellitus were included. The results of meta-analysis showed that the shared decision-making can alleviate the decision-making conflict of type 2 diabetic mellitus patients ( MD=-3.18, 95% CI -5.36 to -0.99, P<0.05), improve the decision-making self-efficacy ( MD=5.82, 95% CI 2.34 to 9.30, P<0.05), medication compliance ( RR=1.08, 95% CI 1.01 to 1.16, P<0.05), and diabetes-related knowledge ( SMD=0.46, 95% CI 0.16 to 0.75, P<0.05), reduce BMI ( MD=-0.75, 95% CI-1.33 to -0.17, P<0.05) and the HbA1c level ( MD=-0.45, 95% CI -0.65 to -0.24, P<0.05) in the 3-month follow-up. Conclusions:The shared decision-making improves the self-management in patients with type 2 diabetic mellitus. However, the long-term effect and potential risks of this model still need to be further studied. It is suggested that the application of shared decision-making in type 2 diabetic mellitus patients should be optimized in the future, and research on the long-term effects and potential risks of this model should be increased.

Objective To investigate the effect of tissue-resident memory T cells(TRM)on imiquimod-induced psoriatic-like skin lesions in mice,and to elucidate the underlying mechanisms of TRM involvement in this process.Methods Forty female BALB/c mice were procured and randomly allocated into four groups:ten in the blank control group,and thirty for the establishment of a psoriasis mouse model.Following successful modeling,the thirty mice were further randomized into three groups:the model control group,the methotrexate-treated group,and the imiquimod-treated group,with ten mice in each group.Mice in the blank control group and model control group were uniformly treated with Vaseline for intervention.The methotrexate group and the imiquimod group were treated with 62.5mg of 5％imiquimod cream.The methotrexate group was administered by gavage at a dose of 1 mg/kg,and the gavage volume of each group was 10 mL/kg.The model control group,blank group and imiquimod group were gavaged with the same volume of normal saline.Treatment was conducted over six consecutive days.Subsequently,comparisons were made across groups regarding the psoriasis area and severity index(PASI),histopathological findings,inflammatory cytokine levels,and TRM cell levels.Results(1)The imiquimod group exhibited signifi-cantly lower scores for erythema(2.54±0.32),skin thickening(2.59±0.25),and scaling(2.52±0.29)compared to the methotrexate group,model control group,and blank control group(P<0.05).Additionally,the methotrexate group demonstrated reduced scores for erythema,skin thickening,and scaling compared to the model control group(P<0.05).(2)Hematoxylin-eosin(HE)staining revealed that the epidermis in the methotrexate group became thin-ner,with fewer parakeratotic cells and increased hair follicles.Conversely,the imiquimod group displayed abnor-mal cell morphology and relatively thicker white skin after modeling.(3)The imiquimod group showed significantly lower levels of TNF-α(51.63±4.39 pg/mL),IL-1β(35.53±4.15 pg/mL),IFN-γ(23.43±3.41 pg/mL),and IL-23(15.24±2.95 pg/mL)compared to the methotrexate and model control groups(P<0.05).Similarly,the methotrexate group exhibited reduced levels of TNF-α,IL-1β,IFN-γ,and IL-23 compared to the model control group(P<0.05).(4)The imiquimod group had significantly lower levels of CD8+CD103+cells(15.39±2.31)than the methotrexate and model control groups(P<0.05).Furthermore,the methotrexate group demonstrated lower levels of CD8+CD103+cells compared to the model control group(P<0.05).Conclusion Miquimod induces heavier skin lesions,faster response,and more epidermal thickening in psoriasis like mice.CD8+CD103+TRM cells and inflammatory factors may be involved in the recurrence of psoriasis.

Objective To investigate the effect of tissue-resident memory T cells(TRM)on imiquimod-induced psoriatic-like skin lesions in mice,and to elucidate the underlying mechanisms of TRM involvement in this process.Methods Forty female BALB/c mice were procured and randomly allocated into four groups:ten in the blank control group,and thirty for the establishment of a psoriasis mouse model.Following successful modeling,the thirty mice were further randomized into three groups:the model control group,the methotrexate-treated group,and the imiquimod-treated group,with ten mice in each group.Mice in the blank control group and model control group were uniformly treated with Vaseline for intervention.The methotrexate group and the imiquimod group were treated with 62.5mg of 5％imiquimod cream.The methotrexate group was administered by gavage at a dose of 1 mg/kg,and the gavage volume of each group was 10 mL/kg.The model control group,blank group and imiquimod group were gavaged with the same volume of normal saline.Treatment was conducted over six consecutive days.Subsequently,comparisons were made across groups regarding the psoriasis area and severity index(PASI),histopathological findings,inflammatory cytokine levels,and TRM cell levels.Results(1)The imiquimod group exhibited signifi-cantly lower scores for erythema(2.54±0.32),skin thickening(2.59±0.25),and scaling(2.52±0.29)compared to the methotrexate group,model control group,and blank control group(P<0.05).Additionally,the methotrexate group demonstrated reduced scores for erythema,skin thickening,and scaling compared to the model control group(P<0.05).(2)Hematoxylin-eosin(HE)staining revealed that the epidermis in the methotrexate group became thin-ner,with fewer parakeratotic cells and increased hair follicles.Conversely,the imiquimod group displayed abnor-mal cell morphology and relatively thicker white skin after modeling.(3)The imiquimod group showed significantly lower levels of TNF-α(51.63±4.39 pg/mL),IL-1β(35.53±4.15 pg/mL),IFN-γ(23.43±3.41 pg/mL),and IL-23(15.24±2.95 pg/mL)compared to the methotrexate and model control groups(P<0.05).Similarly,the methotrexate group exhibited reduced levels of TNF-α,IL-1β,IFN-γ,and IL-23 compared to the model control group(P<0.05).(4)The imiquimod group had significantly lower levels of CD8+CD103+cells(15.39±2.31)than the methotrexate and model control groups(P<0.05).Furthermore,the methotrexate group demonstrated lower levels of CD8+CD103+cells compared to the model control group(P<0.05).Conclusion Miquimod induces heavier skin lesions,faster response,and more epidermal thickening in psoriasis like mice.CD8+CD103+TRM cells and inflammatory factors may be involved in the recurrence of psoriasis.

With the intensification of population aging, type 2 diabetes has emerged as a significant global public health concern, particularly in developing countries.Epidemiological data indicate that the elderly population faces a higher risk of diabetes, accompanied by an increasing incidence rate.Due to the unique pathological characteristics and comorbid chronic diseases prevalent among elderly diabetes patients, polypharmacy is both common and often unavoidable.Inappropriate polypharmacy poses heightened health risks for patients and complicates clinical management, underscoring the urgent need to optimize intervention strategies.Effective approaches include regular medication reviews, adjustments to blood glucose control targets, and the development of personalized deprescribing plans informed by comprehensive geriatric assessments.While some interventions have demonstrated positive effects in reducing potentially inappropriate medications, addressing prescription omissions, and enhancing medication adherence, their capacity to yield significant clinical improvements requires further validation.Future research should prioritize the identification of the most effective interventions for high-risk populations.

Objective:To analyze the effects of shared decision-making in patients with type 2 diabetic mellitus.Methods:Databases including PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang Datebase, COVIP and SinoMed, for randomized controlled trials (RCTs) on the application of shared decision-making in patients with type 2 diabetic mellitus from inception to July 22, 2023, used R Studio software for meta-analysis.Results:A total of 14 RCTs and 2 606 patients with type 2 diabetic mellitus were included. The results of meta-analysis showed that the shared decision-making can alleviate the decision-making conflict of type 2 diabetic mellitus patients ( MD=-3.18, 95% CI -5.36 to -0.99, P<0.05), improve the decision-making self-efficacy ( MD=5.82, 95% CI 2.34 to 9.30, P<0.05), medication compliance ( RR=1.08, 95% CI 1.01 to 1.16, P<0.05), and diabetes-related knowledge ( SMD=0.46, 95% CI 0.16 to 0.75, P<0.05), reduce BMI ( MD=-0.75, 95% CI-1.33 to -0.17, P<0.05) and the HbA1c level ( MD=-0.45, 95% CI -0.65 to -0.24, P<0.05) in the 3-month follow-up. Conclusions:The shared decision-making improves the self-management in patients with type 2 diabetic mellitus. However, the long-term effect and potential risks of this model still need to be further studied. It is suggested that the application of shared decision-making in type 2 diabetic mellitus patients should be optimized in the future, and research on the long-term effects and potential risks of this model should be increased.

With the intensification of population aging, type 2 diabetes has emerged as a significant global public health concern, particularly in developing countries.Epidemiological data indicate that the elderly population faces a higher risk of diabetes, accompanied by an increasing incidence rate.Due to the unique pathological characteristics and comorbid chronic diseases prevalent among elderly diabetes patients, polypharmacy is both common and often unavoidable.Inappropriate polypharmacy poses heightened health risks for patients and complicates clinical management, underscoring the urgent need to optimize intervention strategies.Effective approaches include regular medication reviews, adjustments to blood glucose control targets, and the development of personalized deprescribing plans informed by comprehensive geriatric assessments.While some interventions have demonstrated positive effects in reducing potentially inappropriate medications, addressing prescription omissions, and enhancing medication adherence, their capacity to yield significant clinical improvements requires further validation.Future research should prioritize the identification of the most effective interventions for high-risk populations.

Purpose: The junctional epithelium (JE) covers the cervical areas of developing or existing teeth. It can re-establish itself even after being removed during periodontal therapies, followed by wound healing. However, the mechanisms that can maintain this universally conserved structure are still unclear. Methods: The molecular mechanisms of JE homeostasis were investigated by altering levels of JE-specific genes in a telomerase immortalized human gingival epithelial cell line (TIGKs) by exposing TIGKs to conditioned medium (C-CM) from cultivated human cementoblasts.The mRNA and protein levels of JE-associated genes in TIGKs were examined using realtime polymerase chain reaction (PCR) and immunocytochemistry (ICC) after treatment with C-CM. The candidate pathways related to differential mRNA and protein expression were analyzed with a DNA microarray and identified using Kyoto Encyclopedia of Genes and Genomes and WikiPathways. Real-time PCR and ICC were conducted to confirm the changes in the expressions of candidate genes. Results: mRNA levels and protein expressions of amelotin (Amtn) were upregulated after treatment with C-CM for 48 hours. DNA microarray analyses identified 595 genes that were upregulated >2-fold, and 820 genes that were downregulated >2-fold. C-CM promoted the expression of suppressor of cytokine signaling 3 and reduced the expression of an inactivator of Janus kinase 2. Both signaling molecules were found, using siRNA technology, to mediate the increase of Amtn mRNA and protein expression levels. Conclusions The upregulation of Amtn in gingival epithelial cells by C-CM suggests that this regulatory pathway is associated with the homeostasis of JE structures by the cementum.

Purpose: Odontogenic ameloblast-associated protein (ODAM) is a small secretory protein produced by the junctional epithelium (JE) and mature ameloblasts. It plays a role in odontogenesis and mediates the adhesion of JE to enamel. We used human gingival epithelial cells to evaluate the mechanism of ODAM gene expression regulation in the JE by interleukin (IL)-6. Methods: Ca9-22, Sa3, and HSY cells were stimulated with IL-6 (10 ng/mL), after which total RNA and proteins were extracted. Real-time polymerase chain reaction and Western blot analyses were performed to assess the expression levels of ODAM mRNA and protein.Luciferase (LUC) assays were employed using LUC constructs with varying lengths of the ODAM gene promoter sequence. Gel mobility shift and chromatin immunoprecipitation (ChIP) analyses were conducted to investigate the binding of transcription factors to response elements within the gene promoter. Results: Treatment with IL-6 increased the expressions of ODAM mRNA and protein.Additionally, it induced promoter activity of the ODAM gene, while LUC activity was suppressed by inhibitors of protein kinase A, tyrosine kinase, MEK1/2, phosphatidylinositol 3-kinase, nuclear factor-κB, signal transducer and activator of transcription (STAT) 3, and glycoprotein 130. Gel mobility shift and ChIP analyses revealed that IL-6 induced the binding of yin yang 1 (YY1), CCAAT/enhancer-binding protein (C/EBP) β, GATA binding protein (GATA), and phospho-STAT3 to the YY1, C/EBP, GATA, and interferon-γ activated transcriptional element (GATE) 1-3 elements. Conclusions These findings indicate that IL-6 upregulates ODAM gene expression by targeting the YY1, C/EBP, GATA, and GATE1-3 elements in the promoter region of the human ODAM gene.

The aim of this study is to establish a simple and accurate method for vaccine immune e-valuation of porcine pseudorabies virus.In this research,PRV-gD recombinant protein was ex-pressed from mammalian cell HEK-293F as coating antigen,and then the reaction conditions of gD-iELISA were optimized according to checkerboard titration method.The gD-iELISA was used to detect the antibody levels of 211 clinical pig serum samples and the consistency with the neu-tralizing antibody levels wasanalyzed.The results showed that the antigen coating concentration was 0.90 mg/L;the serum to be detected was diluted 1∶100 and incubated at 37 ℃ for 30 min;goat anti-pig IgG-HRP antibody was diluted 1∶55 000 and incubated at 37 ℃ for 30 min;TMB sub-strate was developed at 37 ℃ for 20 min.The method could detect 1∶6 400 diluted PRV positive serum.The results of CSFV,PRRSV,PCV-2,PEDV and FMDV positive sera were all negative by gD-iELISA,and there was no cross-reaction between the method and the above positive sera.The coincidence rate of gD-iELISA and commercial kits was 95.26％,and the intra-and inter-batch co-efficients of variation were both less than 10％.Correlation analysis showed that the correlation coefficient(r)between gD antibody level and neutralizing antibody level was significantly greater than that of gB antibody level,and the gD antibody level had a good linear relationship with the neutralizing antibody level.The results indicated that gD-iELISA was more suitable for vaccine im-mune evaluation of PRV than gB-iELISA.Therefore,the method will have a good prospect of ap-plication in the immunization control of the PRV.