ObjectiveTo systematically evaluate the effect of art therapy on the mental health of older adults with mild cognitive impairment (MCI), based on International Classification of Functioning, Disability and Health. MethodsLiterature on art therapy for mental health of MCI older adults was retrieved from databases of CNKI, VIP, Wanfang Data, PubMed, ProQuest and Web of Science, between 2014 and 2024, and selected according to inclusion and exclusion criteria. The quality of the literature was assessed using PEDro scale, and a systematic review was conducted following the PRISMA guideline. ResultsA total of nine researches were included from China, Tanzania, Spain, Malaysia and Singapore, involving 763 individuals with MCI aged 60 or more (average 71.23). The types of art therapy interventions were visual arts therapy (painting, collage, paper-cutting, sculpture and modeling, etc.), expressive arts therapy (encompassing dance and music) and creative arts therapy (narrative creation), 30 to 120 minutes a time (majority of 60 minutes), one to four times a week (majority of two to four times), for six to 36 weeks (majority of six to twelve weeks). Health outcomes predominantly focused on mental health, such as anxiety and depression. ConclusionMost researches support that art therapy is effective on mental health of older adults with MCI, but there are disagreements in some researches, and more researches are needed.

One of the basic questions in the aging field is whether there is a fundamental difference between the aging of lower invertebrates and mammals. A major difference between the lower invertebrates and mammals is the abundancy of noncoding RNAs, most of which are not conserved. We have previously identified a noncoding RNA Terc-53 that is derived from the RNA component of telomerase Terc. To study its physiological functions, we generated two transgenic mouse models overexpressing the RNA in wild-type and early-aging Terc-/- backgrounds. Terc-53 mice showed age-related cognition decline and shortened life span, even though no developmental defects or physiological abnormality at an early age was observed, indicating its involvement in normal aging of mammals. Subsequent mechanistic study identified hyaluronan-mediated motility receptor (Hmmr) as the main effector of Terc-53. Terc-53 mediates the degradation of Hmmr, leading to an increase of inflammation in the affected tissues, accelerating organismal aging. adeno-associated virus delivered supplementation of Hmmr in the hippocampus reversed the cognition decline in Terc-53 transgenic mice. Neither Terc-53 nor Hmmr has homologs in C. elegans. Neither do arthropods express hyaluronan. These findings demonstrate the complexity of aging in mammals and open new paths for exploring noncoding RNA and Hmmr as means of treating age-related physical debilities and improving healthspan.
Animals ; Mice ; RNA, Untranslated/metabolism* ; Aging/genetics* ; Mice, Transgenic ; Telomerase/metabolism* ; RNA/genetics* ; Hippocampus/metabolism* ; Humans ; Mice, Inbred C57BL

Background Pneumoconiosis is the most serious occupational disease in China, among which silicosis accounts for more than 50%. microRNA (miRNA) plays an important role in the occurrence process of silicosis fibrosis, but the mechanism of it has not been fully clarified yet. Objective To explore the molecular mechanism by which miR-411-3p modulates the ubiquitination degradation of SMAD specific E3 ubiquitin protein ligase (SMURF) 2/Smad7, thereby suppressing epithelial-mesenchymal transition (EMT) in mouse alveolar type II epithelial cells and counteracting silica-induced pulmonary fibrosis. Methods Twenty-four 8-week-old SPF male C57BL/6J mice were randomly divided into four groups: Control group, silica group, silica +miR-411-3p agomir-NC group, and silica +miR-411-3p agomir group, with 6 mice in each group. Silicosis model was prepared by a one-time bronchial infusion of silicon dioxide (SiO₂) (200 mg·mL^-1, 50 μL). In vitro MLE-12 cells were divided into (1) control group and SiO₂ group, (2) SiO₂+negative control siRNA (siRNA-NC) group and SiO₂+Smurf2 gene silencing (si-Smurf2) group, (3) SiO₂+solvent (DMSO) group and SiO₂+protease inhibitor (MG132) group, (4) mutant sequence plasmid (Mut)+miR-411-3p mimic control (miR-NC) group, Mut+miR-411-3p mimic group, wild sequence plasmid (Wt)+miR-NC group, and Wt+miR-411-3p mimic group, (5) SiO₂+miR-NC group and SiO₂+miR-411-3p mimic group. The pathological morphology and collagen deposition of lung tissue were observed after staining. Detection of miR-411-3p and proteins was conducted by real-time fluorescent quantitative PCR and Western blot. The binding of SMURF2 to Smad7 protein and Smad7 to ubiquitin (Ub) were detected by co-immunoprecipitation (Co-IP) method. Dual-luciferase reporter gene assay was adopted to verify the regulatory effect of miR-411-3p on Smurf2. Results In the SiO₂-induced MLE-12 cells, compared to the control group, the SiO₂-treated group showed significantly upregulated expressions of N-cadherin (N-Cad), collagen I (CoL I), SMURF2, transforming growth factor-β1 (TGF-β1), and phosphorylated Smad2/3 (p-Smad2/3). In contrast, the expressions of E-cadherin (E-Cad), Smad7, and miR-411-3p were significantly downregulated (P<0.05). The dual-luciferase reporter gene assay revealed a regulatory effect of miR-411-3p on Smurf2 (P<0.05). Meanwhile, in the MLE-12 cells induced by SiO₂, the miR-411-3p mimic down-regulated the protein expressions of SMURF2, N-Cad, CoL I, TGF-β1, and p-Smad2/3, while up-regulated the protein expressions of E-Cad and Smad7 (P<0.05). The silenced Smurf2 gene inhibited the expressions of N-Cad, CoL I, and p-Smad2/3 proteins, while promoted the expressions of E-Cad and Smad7 proteins in the MLE-12 cells (P<0.05). The Co-IP results showed that the binding of SMURF2 to Smad7 was enhanced, and the ubiquitin binding ability of Smad7 was enhanced in the SiO₂ group. In the lung tissue of mice, the results of pathological observation with hematoxylin-eosin (HE) and sirius red (VG) staining showed that compared with the agomir-NC, the lesion was relieved in the lung tissue of the miR-411-3p agomir group. Meanwhile, the expressions of SMURF2, N-Cad, CoL I, TGF-β1, and p-Smad2/3 were significantly down-regulated, while the expressions of E-Cad and Smad7 were significantly up-regulated (P<0.05). Conclusion MiR-411-3p alleviates the EMT of alveolar type II epithelial cells and antagonizes silicosis fibrosis progression in mice by inhibiting SMURF2-mediated ubiquitination and degradation of Smad7.

Objective To investigate the expression changes of iron autophagy-mitochondrial ferric ion transport protein families(SFXNs)in acute kidney injury(AKI)and chronic kidney disease(CKD)mouse models induced by cisplatin(Cis)and ischemia reperfusion(IR).Methods C57BL/6 mice were randomly divided into control group(control),Cis-AKI group,Cis-CKD group,sham-operated group(sham),IR-AKI group,and IR-CKD group.Serum and kidney tissue samples were collected from mice.Serum creatinine(Cr)and blood urea nitrogen(BUN)levels were detected.Pathological changes in renal tissues were observed by HE staining.Western blot was used to detect the expression of renal SFXNs and kidney injury related proteins.Results Compared with the control or sham group,the levels of BUN and Cr in the serum of the model group were significantly increased(P＜0.05),the renal tissue showed significant pathological damage,with the kidney injury molecule-1(KIM-1),neutrophil gelatinase-associated lipocalin(NGAL),and pro-apoptotic protein Bax significantly upregulated(P＜0.05),while the anti-apoptotic protein Bcl-2 was significantly downregulated(P＜0.05).Compared to the control or sham group,the Cis-AKI group showed a significant downregulation of SFXN4(P＜0.05);The SFXN4 and SFXN5 subtypes were significantly downregulated in the IR-AKI group and Cis-CKD group(P＜0.05);All five subtypes of SFXN in the IR-CKD group were significantly downregulated(P＜0.05).Conclusions Cis or IR in-duces renal tissue damage and tubular mitochondrial injury in mice and affects the expression of SFXN family pro-teins,suggesting their potential role in renal injury of animal models.

Clinically,neuroendocrine liver metastasis(NELM)is not uncommonly seen,which seriously affects the quality of life and prognosis of patients.For unresectable NELM,hepatic intra-arterial therapy is an effective option for controlling tumor progression and relieving symptoms.This therapy mainly includes transcatheter arterial embolization(TAE),transcatheter arterial chemoembolization(TACE),and selective internal radiotherapy(SIRT),and there was no significant difference in the long-term efficacy among the three therapies.Usually,TAE is recommended for patients with low-grade NELM.Conventional TACE may be considered for NELM patients who have poorly differentiated tumor or high hepatic tumor burden(HTB),and drug-eluting beads TACE is not recommended for NELM patients because it has significant hepatobiliary toxicity.SIRT can be adopted for NELM patients having portal vein thrombosis or having a history of biliary bowel surgery.In comprehensive treatment strategies for unresectable NELM,the combination use of hepatic intra-arterial interventional therapy and systemic therapy has already shown its promising prospects.Through reviewing the relevant literature,this paper summarizes the current situation and research progress of NELM.

Iron is an essential element for living organisms that plays critical roles in the process of bacterial growth and metabolism. However, it remains to be elucidated whether piuB encoding iron-uptake factor is involved in iron uptake and pathogenicity of Xanthomonas axonopodis pv. glycines (Xag). To investigate the function of piuB, we firstly generated a piuB deletion mutant (ΔpiuB) by homologous recombination. Compared with the wild-type, the piuB mutant exhibited significantly reduced growth and virulence in host soybean. The mutant displayed markedly increased siderophore secretory volume, and its sensitivity to Fe³⁺, Cu²⁺, Zn²⁺ and Mn²⁺ was significantly enhanced. Additionally, the H₂O₂ resistance, exopolysaccharide yield, biofilm formation, and cell mobility of ΔpiuB were significantly diminished compared to that of the wild-type. The addition of exogenous Fe³⁺ cannot effectively restore the above characteristics of ΔpiuB. However, expressing piuB in trans rescued the properties lost by ΔpiuB to the levels in the wild-type. Taken together, our results demonstrated that PiuB is a potential factor for Xag to assimilate Fe³⁺, and is necessary for Xag to be pathogenic in host soybean.
Iron ; Glycine max ; Virulence ; Xanthomonas axonopodis/genetics* ; Hydrogen Peroxide

Objective:To summarize and evaluate the relevant evidence of exercise intervention for adult hemophiliacs patients at home and abroad, and to provide a reference basis for healthcare professionals to individualize exercise programs for adult hemophiliacs.Methods:A computer-based "6s" evidence resource pyramid model was used to systematically search for guidelines, evidence summaries, expert consensuses, systematic reviews and random controlled trials on exercise of adult hemophiliacsin databases such as China Biology Medicine disc, Wanfang Med Online, UpToDate, BMJ Best Practice, PubMed, etc, from the time of creation to January 31, 2023. Quality assessment, evidence extraction and evidence integration of relevant literature was performed by two researchers, with a third researcher adjudicating in case of conflicting opinions. An expert panel meeting was conducted to rate the level of evidence extracted.Results:A total of 15 literatures were included. Among them, 4 guidelines, 2 expert consensuses, 2 systematic reviews, and 7 randomized controlled trials. A total of 28 pieces of best evidence were developed, encompassing 6 aspects of exercise assessment, exercise modality, exercise duration, exercise intensity, precautions, and benefits of exercise.Conclusions:Before exercising, hemophiliacs should be assessed by a multidisciplinary team and an appropriate exercise program should be developed to maintain normal body functions and improve the quality of life of hemophiliacs.

Objective:To investigate the epidemiological characteristics of pneumonia and the related factors of the length of hospitalization of pneumonia in the elderly aged 60 years and older in Ningbo in 2019.Methods:Data on hospitalized cases of pneumonia in the elderly aged 60 years and older in Ningbo in 2019 were collected through the regional health information platform, and the population data of Ningbo in 2019 were obtained through the Zhejiang Provincial Bureau of Statistics. A descriptive epidemiological analysis was conducted on hospitalized cases of pneumonia in the elderly population, and factors related to the length of hospitalization were explored.Results:A total of 15 956 hospitalized cases of pneumonia aged 60 years and older were reported in Ningbo in 2019, and the incidence of pneumonia requiring hospitalization was 1.02% (15 956/1 571 431). The incidence was 1.13% (8 613/760 357) in males and 0.83% (6 759/811 074) in females, and the ratio of male to female cases was 1.27∶1. The highest incidence was found in the ≥80 age group (2.52%), and the lowest incidence was found in the 60-69 age group (0.58%). March, February, and January were the peak period of pneumonia hospitalization. The main types of pneumonia diagnosed were not specified (65.12%), followed by bacterial pneumonia (34.60%). The M( Q1, Q3) of hospitalized patients with pneumonia was 9 (7, 13) days. The results of multivariate logistic regression analysis showed that gender (female: OR=0.911, 95% CI: 0.849-0.978) and older age (70-79 years old: OR=1.211, 95% CI: 1.111-1.321; ≥80 years old group: OR=1.486, 95% CI: 1.365-1.617), settlement method (self-payment: OR=0.567, 95% CI: 0.464-0.691), higher level of hospitals (Grade Ⅱ: OR=1.902,95% CI:1.723-2.100; Grade Ⅲ: OR=1.546,95% CI:1.407-1.698) were associated with the length of hospitalization for pneumonia in people aged 60 years and older in Ningbo. Conclusions:Hospitalization with pneumonia in people aged 60 years and older was high in winter and spring, men and older adults were in high-risk groups in Ningbo in 2019. Gender, age, billing method, and level of hospitals may be related factors to the length of hospitalization for pneumonia.

The incidence rate of aortic dissection (AD) is low, but it is highly fatal in the acute phase. Miss diagnosis and misdiagnosis can occur occasionally, resulting the miss of the best intervention time. Research on the epidemiological characteristics and of AD and related risk factors can identify high-risk groups, make screening and diagnosis as soon as possible and effectively control the changeable risk factors to reduce the incidence of AD and improve the outcome of AD cases. This paper summarizes the progress in research of the epidemiological characteristics of AD and related risk factors in order to promote early prevention and diagnosis of AD, improve the AD case management and intervention level.

Objectives To explore the effect and mechanism of saikosaponin D on cellular autophagy of ICCs by regulating the CaMKKβ/AMPK signaling pathway.Methods Rat primary ICCs cells were isolated and stimulated with glutamate to construct an autophagy model.The Ca2+level was detected by immunofluorescence.Primary ICCs cells were divided into control group,model group,model+saikosaponin D group,model+CaMKKβ inhibitor group,and model+saikosaponin D+CaMKKβ inhibitor group.The ultrastructure of autophagosomes was observed by transmission electron microscopy.The levels of Ghrelin and SP were detected by ELISA.The expressions of Ca2+and LC-3Ⅱ were detected by immunofluorescence.The protein expression levels of LC-3Ⅱ/Ⅰ、CaMKKβ,p-AMPK,Drp1,MFN2,IP3R and RyR were detected by Western blot.Results The fluorescence expression of LC-3Ⅱ was enhanced.Saikosaponin D reduced the levels of CaMKKβ,AMPK and MFN2(P<0.01),and increased the levels of LC-3Ⅱ/Ⅰ、IP3R,RyR,Drp1,Ghrelin and SP(P<0.01).The effect of Saikosaponin D combined with CaMKKβ inhibitor STO-609 was more significant.Conclusion Saikosaponin D can mediate Ca2+outflow through the CaMKKβ/AMPK signaling pathway,and affect the expression of excessive autophagy and gastrointestinal motility-related factors in ICCs cells.