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Background: Patients with dementia often present agitated behaviors. The Cohen–Mansfield Agitation Inventory-short form (CMAI-SF) is one of the most widely used instruments to evaluate agitated behaviors that affect patients’ quality of life and impose burden on caregivers. However, there is no simplified Chinese version of the CMAI-SF (C-CMAI-SF) in clinical settings. Purpose: This study aimed to develop a Chinese version of the C-CMAI-SF and examine its validity and reliability. Methods: This cross-sectional study included three phases. In Phase I, the original CMAI-SF was translated to Chinese. In Phase II, experts were invited to examine the content validity index (CVI). Phase III was conducted to test the validity and reliability of the C-CMAI-SF. Results: The scale showed good validity and reliability with a scale-level CVI of 0.89, Cronbach’s alpha (measure of internal consistency) of 0.874, and test–retest correlation coefficient of 0.902 (for 257 individuals). Using factor analysis, three factors were identified. Regarding concurrent validity, the C-CMAI-SF score was correlated with the Neuropsychiatric Inventory (agitation aggression subscale) and the Cornell Scale for Depression in Dementia (agitation subscale). Conclusions: The study demonstrated that the C-CMAI-SF is a valid and reliable instrument for evaluating agitated behaviors in people with dementia. Relevance to clinical practice: The C-CMAI-SF is an easy and quick tool used to identify and evaluate agitated behaviors in busy clinical settings.

Background: The frail elderly are prone to falls and fractures, which can result in dependency, disability, admission to institutions, and even death. They are at increased risk of frailty due to decreased physical activity, cognitive decline, and depression. Some evidence suggests that music therapy with physical activities may be particularly beneficial. Objective: This study aimed to investigate the intervention effect of music therapy with physical activities (MTPA) on frail elderly in the community. Methods: A quasi-experimental design was adopted. We selected 10 community care centers in southern Taiwan, in which elderly people over the age of 65 were assigned to a MTPA group and a comparison group after obtaining their informed consent. The MTPA group performed group music activities once a week for 120 min for 12 weeks, while the comparison group only continued with their daily activities. Instruments in this study included the Kihon Checklist, Senior Fitness Test (with Body Mass Index (BMI) and seven physical fitness items), Mini-Mental Status Examination (MMSE), and Geriatric Depression Scale Short Form (GDS-SF). Results: A total of 132 community elders agreed to participate in this study, and 122 completed both the pretest and posttest, with 62 in the music therapy group and 60 in the comparison group. The results of ANCOVA showed that after intervention, except for BMI, the Kihon frailty assessment, seven fitness scores individually and in total, MMSE, and depression showed significant improvements in the music therapy group relative to the comparison group (all p < 0.05). Conclusion: MTPA can improve the frailty index, cognitive function, depression, and physical fitness index in the community elderly. The results of this study can be used as a reference for the design of activities for the community elderly, to provide them with appropriate activities, improve their physical functions, and improve or delay their disability.

Objective The work of firefighters involves the risk of exposure to the harmful effects of toxic substances as well as the possibility of enormous emotional shock from disasters, which may result in psychiatric impairments and a lower quality of life. Therefore, we examined quality of life, prevalence of posttraumatic stress disorder (PTSD) and major depression, and the related risk factors for firefighters in Kaohsiung, Taiwan. Methods This is a two-stage survey study. During the first stage, we used the 36-item Short-Form Health Survey (SF-36) and the Disaster-Related Psychological Screening Test (DRPST) to assess quality of life, probable PTSD, probable major depression, and the related risk factors for 410 firefighters. During the second stage, psychiatrists categorized these probable cases according to self-reported questionnaires against DSM-IV into PTSD or major depression group, subclinical group, and health group. All the data were analyzed with SPSS 10.0 Chinese version. Results The estimated current prevalence rates for major depression and PTSD were 5.4% (22/410) and 10.5% (43/410), respectively. The firefighters with estimated PTSD or major depression scored significantly lower on quality of life measures than subclinical PTSD/major depression and mentally healthy groups, which was evident in eight concepts and two domains of the SF-36. The major predictors of poor quality of life and PTSD/major depression were mental status, psychosocial stressors, or perceived physical condition. Conclusion Firefighters have a higher estimated rate of PTSD, and the risk factors that affect quality of life and PTSD/major depression should encourage intervention from mental health professionals.

This study tested a structural model and examined the relationships between age, suicidal ideation, and scores on the 5-item Brief Symptom Rating Scale (BSRS-5), the 15-item Geriatric Depression Scale (GDS-15), and the Medical Outcome Study Short Form-12 (MOS SF-12) in a sample of veterans' home residents. Of the 266 individuals recruited, 226 completed the questionnaires, resulting in a response rate of 84.9%. Participants completed the BSRS-5, GDS-15, MOS SF-12, and a demographic survey. Analysis of Moment Structures, Version 7.0, was used to test the structural relationships of the model with a structural equation modeling analysis and a maximum likelihood ratio estimation. Patient subitem scores, which ranked their feelings of depression, hostility, and inferiority, were summed to determine their 3-BSRS-subitem sum scores. The measures of model fitness were as follows: goodness-of-fit (χ2 = 12.03, df = 7, p = 0.1), goodness-of-fit index (0.98), adjusted goodness-of-fit index (0.95), comparative fit index (0.99), parsimony ratio (0.47), and root mean square error of approximation (0.06). All indices suggested that the final model fit the data well. Age was inversely related to physical component summary, which was inversely related to the 3-BSRS-subitem sum score. Mental component summary was inversely related to the 3-BSRS-subitem sum score and the GDS-15. Physical component summary was inversely related to the GDS-15. The 3-BSRS-subitem sum score correlated with suicidal ideation. The data reveal a significant relationship between quality of life and suicidal ideation, which may be affected more by the 3-BSRS-subitem sum score than by the GDS-15. The proposed model has the potential to help healthcare professionals effectively design and implement their suicide prevention programs.

Psychological stress is widely acknowledged as a major contributor to immunosuppression, rendering individuals more susceptible to various diseases. The complex interplay between the nervous, endocrine, and immune systems underlies stress-induced immunosuppression. However, the underlying mechanisms of psychological-stress-induced immunosuppression remain unclear. In this study, we utilized a restraint stress mouse model known for its suitability in investigating physiological regulations during psychological stress. Comparing it with cold exposure, we observed markedly elevated levels of stress hormones corticosterone and cortisol in the plasma of mice subjected to restraint stress. Furthermore, restraint-stress-induced immunosuppression differed from the intravenous immunoglobulin-like immunosuppression observed in cold exposure, with restraint stress leading to increased macrophage cell death in the spleen. Suppression of pyroptosis through treatments of inflammasome inhibitors markedly ameliorated restraint-stress-induced spleen infiltration and pyroptosis cell death of macrophages in mice. These findings suggest that the macrophage pyroptosis associated with restraint stress may contribute to its immunosuppressive effects. These insights have implications for the development of treatments targeting stress-induced immunosuppression, emphasizing the need for further investigation into the underlying mechanisms.

Metformin is one of the most commonly used drugs for type 2 diabetes mellitus. In addition to its anti-diabetic property, evidence suggests more potential applications for metformin, such as antiaging, cellular protection, and anti-inflammation. Studies have reported that metformin activates pathways with anti-inflammatory effects, enhances the integrity of gut epithelial tight junctions, and promotes a healthy gut microbiome. These actions contribute to the protective effect of metformin against gastrointestinal (GI) tract injury. However, whether metformin plays a protective role in psychological-stress-associated GI tract injury remains elusive. We aim to elucidate the potential protective effect of metformin on the GI system and develop an effective intervention strategy to counteract GI injury induced by acute psychological stress. By monitoring the levels of GI-nonabsorbable Evans blue dye in the bloodstream, we assessed the progression of GI injury in live mice. Our findings demonstrate that the administration of metformin effectively mitigated GI leakage caused by psychological stress. The GI protective effect of metformin is more potent when used on wild-type mice than on activating-transcription-factor 3 (ATF3)-deficient (ATF3−/−) mice. As such, metformin-mediated rescue was conducted in an ATF3-dependent manner. In addition, metformin-mediated protection is associated with the induction of stress-induced GI mRNA expressions of the stress-induced genes ATF3 and AMP-activated protein kinase. Furthermore, metformin treatment-mediated protection of CD326+ GI epithelial cells against stress-induced apoptotic cell death was observed in wild-type but not in ATF3−/− mice. These results suggest that metformin plays a protective role in stress-induced GI injury and that ATF3 is an essential regulator for metformin-mediated rescue of stress-induced GI tract injury.

Hepatocellular carcinoma (HCC) is a lethal human malignancy and a leading cause of cancer‐related death worldwide. Patients with HCC are often diagnosed at an advanced stage, and the prognosis is usually poor. The multikinase inhibitor sorafenib is the first‐line treatment for patients with advanced HCC. However, cases of primary or acquired resistance to sorafenib have gradually increased, leading to a predicament in HCC therapy. Thus, it is critical to investigate the mechanism underlying sorafenib resistance. Transactivation response element RNA‐binding protein 2 (TARBP2) is a multifaceted miRNA biogenesis factor that regulates cancer stem cell (CSC) properties. The tumorigenicity and drug resistance of cancer cells are often enhanced due to the acquisition of CSC features. However, the role of TARBP2 in sorafenib resistance in HCC remains unknown. Our results demonstrate that TARBP2 is significantly downregulated in sorafenib‐resistant HCC cells. The TARBP2 protein was destabilized through autophagic–lysosomal proteolysis, thereby stabilizing the expression of the CSC marker protein Nanog, which facilitates sorafenib resistance in HCC cells. In summary, here we reveal a novel miRNA‐independent role of TARBP2 in regulating sorafenib resistance in HCC cells. Sorafenib is the first‐line treatment for patients with advanced hepatocellular carcinoma (HCC). The cases of sorafenib resistance have gradually increased, leading to a predicament HCC therapy. Our results demonstrate that transactivation response element RNA‐binding protein 2 (TARBP2) is downregulated in sorafenib‐resistant HCC cells. TARBP2 protein was destabilized through autophagic–lysosomal proteolysis, thereby stabilizing Nanog, which facilitates sorafenib resistance in HCC cells.

The interaction between environmental stressors, such as cold exposure, and immune function significantly impacts human health. Research on effective therapeutic strategies to combat cold-induced immunosuppression is limited, despite its importance. In this study, we aim to investigate whether traditional herbal medicine can counteract cold-induced immunosuppression. We previously demonstrated that cold exposure elevated immunoglobulin G (IgG) levels in mice, similar to the effects of intravenous immunoglobulin (IVIg) treatments. This cold-induced rise in circulating IgG was mediated by the renin–angiotensin–aldosterone system and linked to vascular constriction. In our mouse model, the cold-exposed groups (4 °C) showed significantly elevated plasma IgG levels and reduced bacterial clearance compared with the control groups maintained at room temperature (25 °C), both indicative of immunosuppression. Using this model, with 234 mice divided into groups of 6, we investigated the potential of tanshinone IIA, an active compound in Salvia miltiorrhiza ethanolic root extract (SMERE), in alleviating cold-induced immunosuppression. Tanshinone IIA and SMERE treatments effectively normalized elevated plasma IgG levels and significantly improved bacterial clearance impaired by cold exposure compared with control groups injected with a vehicle control, dimethyl sulfoxide. Notably, bacterial clearance, which was impaired by cold exposure, showed an approximately 50% improvement following treatment, restoring immune function to levels comparable to those observed under normal temperature conditions (25 °C, p < 0.05). These findings highlight the therapeutic potential of traditional herbal medicine in counteracting cold-induced immune dysregulation, offering valuable insights for future strategies aimed at modulating immune function in cold environments. Further research could focus on isolating tanshinone IIA and compounds present in SMERE to evaluate their specific roles in mitigating cold-induced immunosuppression.

Psychological stress increases risk of gastrointestinal tract diseases. However, the mechanism behind stress-induced gastrointestinal injury is not well understood. The objective of our study is to elucidate the putative mechanism of stress-induced gastrointestinal injury and develop an intervention strategy. To achieve this, we employed the restraint stress mouse model, a well-established method to study the pathophysiological changes associated with psychological stress in mice. By orally administering gut-nonabsorbable Evans blue dye and monitoring its plasma levels, we were able to track the progression of gastrointestinal injury in live mice. Additionally, flow cytometry was utilized to assess the viability, death, and inflammatory status of splenic leukocytes, providing insights into the stress-induced impact on the innate immune system associated with stress-induced gastrointestinal injury. Our findings reveal that neutrophils represent the primary innate immune leukocyte lineage responsible for stress-induced inflammation. Splenic neutrophils exhibited elevated expression levels of the pro-inflammatory cytokine IL-1, cellular reactive oxygen species, mitochondrial burden, and cell death following stress challenge compared to other innate immune cells such as macrophages, monocytes, and dendritic cells. Regulated cell death analysis indicated that NETosis is the predominant stress-induced cell death response among other analyzed regulated cell death pathways. NETosis culminates in the formation and release of neutrophil extracellular traps, which play a crucial role in modulating inflammation by binding to pathogens. Treatment with the NETosis inhibitor GSK484 rescued stress-induced neutrophil extracellular trap release and gastrointestinal injury, highlighting the involvement of neutrophil extracellular traps in stress-induced gastrointestinal inflammation. Our results suggest that neutrophil NETosis could serve as a promising drug target for managing psychological stress-induced gastrointestinal injuries.

HIF-1α, one of the most extensively studied oncogenes, is activated by a variety of microenvironmental factors. The resulting biological effects are thought to depend on its transcriptional activity. The RNAse enzyme Dicer is frequently downregulated in human cancers, which has been functionally linked to enhanced metastatic properties; however, current knowledge of the upstream mechanisms regulating Dicer is limited. In the present study, we identified Dicer as a HIF-1α-interacting protein in multiple types of cancer cell lines and different human tumors. HIF-1α downregulated Dicer expression by facilitating its ubiquitination by the E3 ligase Parkin, thereby enhancing autophagy-mediated degradation of Dicer, which further suppressed the maturation of known tumor suppressors, such as the microRNA let-7 and microRNA-200b. Consequently, expression of HIF-1α facilitated epithelial-mesenchymal transition (EMT) and metastasis in tumor-bearing mice. Thus, this study uncovered a connection between oncogenic HIF-1α and the tumor-suppressive Dicer. This function of HIF-1α is transcription independent and occurs through previously unrecognized protein interaction-mediated ubiquitination and autophagic proteolysis.