Multi-disease X-ray Image Classification of the Chest Based on Global and Local Fusion Adaptive Networks.

BACKGROUND: Chest X-ray image classification for multiple diseases is an important research direction in the field of computer vision and medical image processing. It aims to utilize advanced image processing techniques and deep learning algorithms to automatically analyze and identify X-ray images, determining whether specific pathologies or structural abnormalities exist in the images. OBJECTIVE: We present the MMPDenseNet network designed specifically for chest multi-label disease classification. METHODS: Initially, the network employs the adaptive activation function Meta-ACON to enhance feature representation. Subsequently, the network incorporates a multi-head self-attention mechanism, merging the conventional convolutional neural network with the Transformer, thereby bolstering the ability to extract both local and global features. Ultimately, the network integrates a pyramid squeeze attention module to capture spatial information and enrich the feature space. RESULTS: The concluding experiment yielded an average AUC of 0.898, marking an average accuracy improvement of 0.6% over the baseline model. When compared with the original network, the experimental results highlight that MMPDenseNet considerably elevates the classification accuracy of various chest diseases. CONCLUSION: It can be concluded that the network, thus, holds substantial value for clinical applications.

The Circadian Rhythm of Itching among 241 Adults with Atopic Dermatitis: A Cross-sectional Study.

The pattern of itching in patients with atopic dermatitis has not been systematically studied. Therefore, this study aimed to assess the pattern of itching in adults with atopic dermatitis using questionnaires to assess for a circadian rhythm of itching in participating patients at a single institution (n = 241). A self-report questionnaire was used to assess circadian rhythm and intensity of itching in patients. In addition, the patients' disease severity (Eczema Area and Severity Index [EASI]) and quality of life (Dermatology Life Quality Index [DLQI]) were assessed. Itching occurred most frequently (74.69%) and with the greatest severity (62.66%) between 20:00 and 00:00, and the least number of patients (25.31%) experienced itching between 04:00 and 08:00. The DLQI and EASI scores both correlated with the average and maximum itch intensity (r = 0.582, r = 0.533, respectively; r = 0.539, r = 0.517, respectively; p < 0.001). The DLQI and EASI scores were associated with average itch intensity (B = 0.179, B = 0.204, respectively; 95% CI: 0.112 to 0.246, 95% CI: 0.096 to 0.313, respectively; p < 0.001), and the EASI score was associated with males and family history (B = 0.285, B = 0.287, respectively; 95% CI: 0.094 to 0.476, 95% CI: 0.096 to 0.478, respectively; p = 0.003). Adult patients with atopic dermatitis exhibited a circadian rhythm of itching; these study results could positively impact treatment approaches.

PGC1-Alpha/Sirt3 Signaling Pathway Mediates the Anti-Pulmonary Fibrosis Effect of Hirudin by Inhibiting Fibroblast Senescence.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic lung disease for which there is a lack of effective pharmacological treatments. Hirudin, a natural peptide extracted from leeches, has been used for broad pharmacological purposes. In this study, we investigated the therapeutic effects of hirudin on IPF and its related mechanism of action. By constructing a mouse model of pulmonary fibrosis and treating it with hirudin in vivo, we found that hirudin exerted anti-fibrotic, anti-oxidative, and anti-fibroblast senescence effects. Moreover, using an in vitro model of stress-induced premature senescence in primary mouse lung fibroblasts and treating with hirudin, we observed inhibition of fibroblast senescence and upregulation of PGC1-alpha and Sirt3 expression. However, specific silencing of PGC1-alpha or Sirt3 suppressed the anti-fibroblast senescence effect of hirudin. Thus, the PGC1-alpha/Sirt3 pathway mediates the anti-fibroblast senescence effect of hirudin, potentially serving as a molecular mechanism underlying its anti-fibrosis and anti-oxidative stress effects exerted on the lungs.

Prevalence and risk factors of depression among elderly people in nursing homes from 2012 to 2022: a systematic review and meta-analysis.

OBJECTIVES: To determine a pooled prevalence of depression and its influencing factors among nursing home residents. METHOD: PsycINFO, PubMed, Embase, and Web of Science were searched for studies investigating the prevalence and risk factors of late-life depression among nursing home residents between January 2012 and November 2022. Two reviewers independently completed the literature screening, data extraction and quality assessment. A random-effects model was utilized to pool the prevalence of depression and summarize the influencing factors. RESULTS: This meta-analysis included 48 studies involving 28,501 participants. The pooled prevalence of depressive mood and major depressive disorder was 53% and 27%, respectively. The rate of depressive mood is higher in lower-middle-income countries (60.0%), compared with high- (53.0%) and upper-middle-income countries (44.0%). The rate of depressive mood (35.0%) is higher among females than male (19.0%). Depression was influenced by factors, including male (OR = 0.28), insufficient income (OR = 3.53), comorbidities (OR = 2.66), pain (OR = 2.67; r = 0.31), functional disability (r = 0.33), loneliness (r = 0.43), number of chronic health problems (r = 0.18), social support (r = -0.28), activities of daily living (r = -0.43), subjective health (r = -0.28), autonomy (r = -0.41), environment (r = -0.50) and physical (r = -0.57) and psychological health (r = -0.65). CONCLUSION: The prevalence of depressive mood is high among nursing home residents, especially in lower-middle-income countries. It is influenced by factors including gender, income, social support, daily activities, environment, physical and psychological health and autonomy. Understanding those factors can provide evidence-based recommendations for improved awareness, prevention and better management of late-life depression.

Senegenin Attenuates Pulmonary Fibrosis by Inhibiting Oxidative-Stress-Induced Epithelial Cell Senescence through Activation of the Sirt1/Pgc-1α Signaling Pathway.

Idiopathic pulmonary fibrosis is a fatal interstitial lung disease for which effective drug therapies are lacking. Senegenin, an effective active compound from the traditional Chinese herb Polygala tenuifolia Willd, has been shown to have a wide range of pharmacological effects. In this study, we investigated the therapeutic effects of senegenin on pulmonary fibrosis and their associated mechanisms of action. We found that senegenin inhibited the senescence of epithelial cells and thus exerted anti-pulmonary-fibrosis effects by inhibiting oxidative stress. In addition, we found that senegenin promoted the expression of Sirt1 and Pgc-1α and that the antioxidative and antisenescent effects of senegenin were suppressed by specific silencing of the Sirt1 and Pgc-1α genes, respectively. Moreover, the senegenin-induced effects of antioxidation, antisenescence of epithelial cells, and antifibrosis were inhibited by treatment with Sirt1 inhibitors in vivo. Thus, the Sirt1/Pgc-1α pathway exerts its antifibrotic effect on lung fibrosis by mediating the antioxidative and antisenescent effects of senegenin.

Nrf2 mediates the effects of shionone on silica-induced pulmonary fibrosis.

BACKGROUND: Extended contact with silica particles can lead to Silicosis, a chronic lung condition lacking established treatment protocols or clear mechanisms of development. The urgency for innovative treatments arises from the unavailability of effective treatment methodologies. The origin of silica-induced pulmonary fibrosis includes essential processes such as macrophage activation and the conversion of fibroblasts into myofibroblasts, with oxidative stress playing a pivotal role. Shionone (SHI), a triterpenoid extracted from the Aster tataricus plant, is recognized for its extensive health benefits. This study explores the capability of SHI to alleviate the effects of silica-induced lung fibrosis in mice. METHODS: This investigation explored the impact of SHI on lung inflammation and fibrosis at different stages (early and late) triggered by silica in mice, focusing specifically on the initial and more developed phases. It comprised an analysis of isolated peritoneal macrophages and fibroblasts extracted from mice to elucidate SHI's therapeutic potential and its underlying mechanism. The methodology employed encompassed quantitative PCR, immunofluorescence, flow cytometry, and western blotting to examine macrophage activity and their transition into myofibroblasts. The activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway by SHI was confirmed via immunofluorescence and western blot studies. SHI's antioxidative properties were evidenced by the measurement of reactive oxygen species (ROS) and mitochondrial ROS within both macrophages and fibroblasts, using 2', 7'-dichlorodihydrofluorescein diacetate and MitoSOX, respectively. The relevance of SHI was further underscored by applying ML385 and Nrf2 siRNA to gauge its effectiveness. RESULTS: Starting SHI treatment early countered the harmful effects of lung inflammation and fibrosis caused by silica, while initiating SHI at a later phase decelerated the advancement of fibrosis. SHI's action was linked to the activation of the Nrf2 signaling pathway, a boost in antioxidant enzyme levels, and a decrease in oxidative stress and inflammation in macrophages affected by silica. Furthermore, SHI prevented the conversion of fibroblasts into myofibroblasts prompted by TGF-ß, along with the resultant oxidative stress. The beneficial outcomes of SHI were negated when ML385 and Nrf2 siRNA were applied, highlighting the pivotal role of the Nrf2 pathway in SHI's efficacy. CONCLUSION: SHI plays a significant role in stimulating the Nrf2 pathway, thereby defending against silica-induced oxidative stress and inflammatory reactions in macrophages, and inhibiting the conversion of fibroblasts to myofibroblasts due to TGF-ß. This suggests that SHI is a viable option for treating lung inflammation and fibrosis in mice suffering from silicosis.

Psychometric validation of the Chinese versions of the quality of communication questionnaires for cancer patients and their family caregivers.

BACKGROUND: Given the lack of valid and reliable instruments for evaluating the quality of communication between physicians and cancer patients and their family caregivers in China, this study translated and culturally adapted the Quality of Communication questionnaires for cancer patients (QOC-P) and their family caregivers (QOC-F) for use in the Chinese context and evaluated their psychometric properties. METHODS: The QOC-P and QOC-F were translated following an adapted version of Brislin's translation model and culturally adapted according to a Delphi expert panel. We pretested and refined the Chinese versions of the QOC-P and QOC-F among 16 dyads of patients and their family caregivers. Subsequently, we administered the questionnaires to 228 dyads of patients and their family caregivers who were recruited from six tertiary hospitals. The content validity, construct validity, convergent validity, and reliability of the QOC-P and QOC-F were examined. RESULTS: Through exploratory factor analysis, The QOC-P and QOC-F were divided into two dimensions: general communication and end-of-life communication. The Cronbach's coefficients ranged from 0.905 to 0.907 for the two subscales of the QOC-P and from 0.908 to 0.953 for the two subscales of the QOC-F. The two-week test-retest reliability was acceptable for both the QOC-P and QOC-F, with intraclass correlation coefficients of 0.993 and 0.991, respectively. The scale content validity index (QOC-P: 0.857, QOC-F: 1.0) and split-half reliability (QOC-P: 0.833, QOC-F: 0.935) were satisfactory. There was a negative correlation with anxiety and depression for both the QOC-P (r = -0.233 & -0.241, p < 0.001) and QOC-F (r = -0.464 & -0.420, p<0.001). The QOC-P showed a negative correlation with decision regret (r = -0.445, p<0.001) and a positive correlation with shared decision-making (r = 0.525, p<0.001), as hypothesized. CONCLUSION: The QOC-P and QOC-F show acceptable psychometric properties for evaluating the quality of communication between physicians and cancer patients and their family caregivers in both clinical and research contexts. Future studies should use more diverse and inclusive samples to test the structure of the Chinese version of the QOC-P and QOC-F with confirmatory factor analysis.

Interventions to promote readiness for advance care planning: A systematic review and meta-analysis.

BACKGROUND: Advance care planning is recommended as part of standard medical services. Readiness, denoting stages of behavior change, exerts a substantial influence on its uptake. However, the characteristics and impacts of advance care planning interventions on readiness are not well-established. METHOD: We systematically reviewed and conducted a meta-analysis of randomized controlled trials assessing the effects of advance care planning interventions on readiness. Studies were appraised using Joanna Briggs Institute Critical Appraisal tools. Meta-analyses were performed using mean difference of continuous variables or risk ratios of binary variables and their 95 % confidence interval as the pooled effect sizes. RESULTS: Eight studies were included in this review and were all rated low quality. Meta-analysis showed that interventions resulted in slight improvement in overall readiness (mean difference = 0.19, 95 % confidence interval: 0.02-0.36) for advance care planning. However, statistically significant effects of interventions were not identified for readiness in relation to specific behaviors (appointment of a healthcare proxy, talking to a healthcare proxy, talking to a medical practitioner about living wills, and signing a living will). CONCLUSION: Our meta-analyses demonstrated that interventions can improve the overall readiness for advance care planning, suggesting the necessity to integrate readiness into future health policies and clinical practices. Nevertheless, the absence of significant effects on specific behavioral readiness underscores the requirement for additional refinement in intervention design, advanced technologies, and theoretical foundations. REGISTRATION: Not registered.

Taraxerone exerts antipulmonary fibrosis effect through Smad signaling pathway and antioxidant stress response in a Sirtuin1-dependent manner.

Idiopathic pulmonary fibrosis treatments are limited, often with severe side effects, highlighting the need for novel options. Taraxerone has diverse biomedical properties, but its mechanism remains unclear. This study investigates taraxerone's impact and the mechanisms involved in bleomycin-induced pulmonary fibrosis in mice. After establishing a pulmonary fibrosis mouse model, taraxerone was intraperitoneally injected continuously for 14-28 days. The in vivo antifibrotic and antioxidative stress effects of taraxerone were assessed. In vitro, the influence of taraxerone on transforming growth factor-ß1-induced myofibroblast transformation and oxidative stress was investigated. Subsequently, quantitative polymerase chain reaction screened the histone deacetylase and Sirtuin family, and taraxerone's effects on SIRT1 were assessed. After SIRT1 siRNA treatment, changes in myofibroblast transformation and antioxidant capacity in response to taraxerone were observed. Acetylation and phosphorylation levels of Smad3 were evaluated. We also examined the binding levels of SIRT1 with Pho-Smad3 and Smad3, as well as the nuclear localization of Smad2/3. EX527 confirmed SIRT1's in vivo action in response to taraxerone. In vitro experiments suggested that taraxerone inhibited myofibroblast differentiation by activating SIRT1 and reducing oxidative stress. We also observed a new interaction between SIRT1 and the Smad complex. Taraxerone activates SIRT1, enabling it to bind directly to Smad3. This leads to reduced Smad complex phosphorylation and limited nuclear translocation. As a result, the transcription of fibrotic factors is reduced. In vivo validation confirms taraxerone's SIRT1-mediated antifibrotic effectiveness. This suggests that targeting SIRT1-mediated inhibition of myofibroblast differentiation could be a key strategy in taraxerone-based therapy for pulmonary fibrosis.

Ultrafine nickel-rhodium nanoparticles anchored on two-dimensional vanadium carbide for high performance hydrous hydrazine decomposition at mild conditions.

The development of heterogeneous supported nanocatalysts with a high kinetics combined with low cost is off importance but remains still challenged for hydrazine hydrate served as a promising hydrogen storage material. Herein, by virtue of surficial functional groups, ultrafine NiRh NPs were monodispersed on the two-dimensional V2C surface via a conventional wet chemical co-reduction. The optimized NiRh/V2C system demonstrates an excellent catalytic performance toward selectively catalyzing dehydrogenation of hydrazine hydrate, affording 100% H2 selectivity with the turnover frequency (TOF) value of 987.5 h-1 at 323 K. Such an enhancement is mainly attributed to synergistic effect of nanosystem, which will optimize local surface energy and promote electron transfer in NiRh/V2C system, thereby improving the kinetic selectivity of catalytic hydrazine hydrate decomposition. This work has provided a facile strategy for developing nanocatalysts with high kinetics that could enable huge industrial applications in the future.

NBR1-p62-Nrf2 mediates the anti-pulmonary fibrosis effects of protodioscin.

BACKGROUND: Idiopathic pulmonary fibrosis is a persistent disease of the lung interstitium for which there is no efficacious pharmacological therapy. Protodioscin, a steroidal saponin, possesses diverse pharmacological properties; however, its function in pulmonary fibrosis is yet to be established. Hence, in this investigation, it was attempted to figure out the anti-pulmonary fibrosis influences of protodioscin and its pharmacological properties related to oxidative stress. METHODS: A mouse lung fibrosis model was generated using tracheal injections of bleomycin, followed by intraperitoneal injection of different concentrations of protodioscin, and the levels of oxidative stress and fibrosis were detected in the lungs. Multiple fibroblasts were treated with TGF-ß to induce their transition to myofibroblasts. It was attempted to quantify myofibroblast markers' expression levels and reactive oxygen species levels as well as Nrf2 activation after co-incubation of TGF-ß with fibroblasts and different concentrations of protodioscin. The influence of protodioscin on the expression and phosphorylation of p62, which is associated with Nrf2 activation, were detected, and p62 related genes were predicted by STRING database. The effects of Nrf2 inhibitor or silencing of the Nrf2, p62 and NBR1 genes, respectively, on the activation of Nrf2 by protodioscin were examined. The associations between p62, NBR1, and Keap1 in the activation of Nrf2 by protodioscin was demonstrated using a co-IP assay. Nrf2 inhibitor were used when protodioscin was treated in mice with pulmonary fibrosis and lung tissue fibrosis and oxidative stress levels were detected. RESULTS: In vivo, protodioscin decreased the levels of fibrosis markers and oxidative stress markers and activated Nrf2 in mice with pulmonary fibrosis, and these effects were inhibited by Nrf2 inhibitor. In vitro, protodioscin decreased the levels of myofibroblast markers and oxidative stress markers during myofibroblast transition and promoted Nrf2 downstream gene expression, with reversal of these effects after Nrf2, p62 and NBR1 genes were silenced or Nrf2 inhibitors were used, respectively. Protodioscin promoted the binding of NBR1 to p62 and Keap1, thereby reducing Keap1-Nrf2 binding. CONCLUSION: The NBR1-p62-Nrf2 axis is targeted by protodioscin to reduce oxidative stress and inhibit pulmonary fibrosis.

Academic-practice partnerships in evidence-based nursing practice: A theory-guided scoping review.

BACKGROUND: Academic-practice partnerships have the potential to solve many challenges in evidence-based nursing practice which is crucial for high-quality care. AIMS: To identify the existing knowledge on academic-practice partnerships in evidence-based nursing practice. METHODS: We conducted this review following the Joanna Briggs Institute scoping review methodology. We performed a comprehensive literature search of nine databases as well as five websites for gray literature. Two researchers independently conducted literature screening and data extraction and analysis. A third researcher was involved when needed. RESULTS: Dedicated time, dedicated resources, and compatible goals were found to be the top three inputs in academic-practice partnerships for evidence-based nursing practice. Meeting and discussion were the most popular forms of activities. Sufficient resources were the most important facilitators. Insufficient resources, insufficient time, and communication issues were the top three barriers. CONCLUSIONS: The assumption proposed in the practice-academic partnership logic model (i.e., inputs plus activities can lead to outputs and outcomes) was preliminarily verified by the results of this review in the context of evidence-based nursing practice. Academic-practice partnerships can leverage the advantages of both sides to overcome barriers and promote evidence-based nursing practice. However, it is essential to conduct a broader range of high-quality studies. Such endeavors could offer more comprehensive evidence for refining the framework of academic-practice partnerships in evidence-based nursing practice. IMPLICATIONS FOR NURSING EDUCATION, PRACTICE, POLICY AND RESEARCH: The "theoretical framework of academic-practice partnerships in evidence-based nursing practice" could theoretically guide academic and clinical nursing staff to collaborate on evidence-based nursing practice and related research and education programs. The academic-practice partnerships in evidence-based nursing practice could lead to a win-win situation for both the academic and the clinical sides. Furthermore, the results of this study provide an evidence-based foundation for policymakers to develop supportive policies for academic-practice partnerships in evidence-based nursing practice.

Curculigoside Attenuates Endoplasmic Reticulum Stress-Induced Epithelial Cell and Fibroblast Senescence by Regulating the SIRT1-P300 Signaling Pathway.

The senescence of alveolar epithelial cells (AECs) and fibroblasts plays a pivotal role in the pathogenesis of idiopathic pulmonary fibrosis (IPF), a condition lacking specific therapeutic interventions. Curculigoside (CCG), a prominent bioactive constituent of Curculigo, exhibits anti-osteoporotic and antioxidant activities. Our investigation aimed to elucidate the anti-senescence and anti-fibrotic effects of CCG in experimental pulmonary fibrosis and delineate its underlying molecular mechanisms. Our findings demonstrate that CCG attenuates bleomycin-induced pulmonary fibrosis and lung senescence in murine models, concomitantly ameliorating lung function impairment. Immunofluorescence staining for senescence marker p21, alongside SPC or α-SMA, suggested that CCG's mitigation of lung senescence correlates closely with the deceleration of senescence in AECs and fibroblasts. In vitro, CCG mitigated H2O2-induced senescence in AECs and the natural senescence of primary mouse fibroblasts. Mechanistically, CCG can upregulate SIRT1 expression, downregulating P300 expression, enhancing Trim72 expression to facilitate P300 ubiquitination and degradation, reducing the acetylation levels of antioxidant enzymes, and upregulating their expression levels. These actions collectively inhibited endoplasmic reticulum stress (ERS) and alleviated senescence. Furthermore, the anti-senescence effects and mechanisms of CCG were validated in a D-galactose (D-gal)-induced progeroid model. This study provides novel insights into the mechanisms underlying the action of CCG in cellular senescence and chronic diseases, offering potential avenues for the development of innovative drugs or therapeutic strategies.

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Advance care planning (ACP) is designed to ensure that patients lacking autonomous decision-making capacity receive medical services in accordance with their expectations and preferences. Individuals with advanced cancer are a crucial target for ACP implementation. However, the current practice of ACP in this group in China is suboptimal, demanding high-quality implementation evidence to strengthen ACP in the clinical practice of patients with advanced cancer. The existing literature can be summarized into 27 pieces of evidence across 7 dimensions, including initiation time, intervention content, intervention providers, intervention modalities, communication skills, outcome indicators, and environmental support. The aforementioned evidence could provide crucial support for improving ACP implementation for patients with advanced cancer. Subsequent research efforts should integrate patient preferences and explore the most suitable implementation strategies for ACP in the Chinese population with advanced cancer, considering diverse aspects such as traditional culture, ACP education and training, legislative support, and healthcare system refinement.

Discovery of an Ortho-Substituted N-Cyclopropylmethyl-7α-phenyl-6,14-endoethano-tetrahydronorthebaine Derivative as a Selective and Potent Kappa Opioid Receptor Agonist with Subsided Sedative Effect.

Research into kappa opioid receptor (KOR) agonists with attenuated central-nervous-system side effects is a critical focus for developing productive and safe analgesics. Herein, a series of ortho-substituted N-cyclopropylmethyl-7α-phenyl-6,14-endoethano-tetrahydronorthebaines were designed, synthesized, and subjected to bioassays. Compound 7a exhibited high subtype selectivity and potent agonistic activity toward KOR (KOR, Ki = 3.9 nM, MOR/KOR = 270, DOR/KOR = 1075; [35S]GTPγS binding, EC50 = 3.4 nM). Additionally, this compound exhibited robust and persistent antinociceptive effects in rodent models with different animal strains (hot plate test, ED50 = 0.20-0.30 mg/kg, i.p.; abdominal constriction test, ED50 = 0.20-0.60 mg/kg, i.p.), with its KOR-mediated mechanism for antinociception firmly established. Notably, compound 7a, unlike conventional KOR agonists, displayed minimal sedation and aversion at the antinociceptive ED50 dose. This feature addresses a crucial limitation in existing KOR agonists, positioning compound 7a as a promising novel therapeutic agent.

Ethanol extract of Cyathulae Radix inhibits osteoclast differentiation and bone loss.

Cyathulae Radix, a traditional Chinese medicine and a common vegetable, boasts a history spanning millennia. It enhances bone density, boosts metabolism, and effectively alleviates osteoporosis-induced pain. Despite its historical use, the molecular mechanisms behind Cyathulae Radix's impact on osteoporosis remain unexplored. In this study, we investigated the effects and mechanisms of Cyathulae Radix ethanol extract (CEE) in inhibiting osteoporosis and osteoclastogenesis. Eight-week-old female mice underwent ovariectomy and were treated with CEE for eight weeks. Micro-computed tomography (micro-CT) assessed histomorphometric parameters, bone tissue staining observed distal femur histomorphology, and three-point bending tests evaluated tibia mechanical properties. Enzyme-linked immunosorbent assay (ELISA) measured serum estradiol (E2), receptor activator for nuclear factor B ligand (RANKL), and osteoprotegerin (OPG) levels. Osteoclastogenesis-related markers were analyzed via Western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, CEE effects on RANKL-induced osteoclast formation and bone resorption were investigated in vitro using tartrate-resistant acid phosphatase (TRAP) staining, qRT-PCR, and WB assay. Compared with the ovariectomy (OVX) group, CEE treatment enhanced trabecular bone density, maximal load-bearing capacity, and various histomorphometric parameters. Serum E2 and OPG levels significantly increased, while Receptor activator of nuclear factor-κB (RANK) decreased in the CEE group. CEE downregulated matrix metallopeptidase 9 (MMP-9), Cathepsin K (CTSK), and TRAP gene and protein expression. In bone marrow macrophages (BMMs), CEE reduced mature osteoclasts, bone resorption pit areas, and MMP-9, CTSK, and TRAP expression during osteoclast differentiation. Compared with DMSO treatment, CEE markedly inhibited RANK, TNF receptor associated factor 6 (TRAF6), Proto-oncogene c-Fos (c-Fos), Nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) expressions, and Extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), NF-kappa B-p65 (p65) phosphorylation in osteoclasts. In conclusion, CEE significantly inhibits OVX-induced osteoporosis and RANKL-induced osteoclastogenesis, potentially through modulating the Estrogen Receptor (ER)/RANK/NFATc1 signaling pathway.

Extracellular vesicles from human urine-derived stem cells delay aging through the transfer of PLAU and TIMP1.

Aging increases the risks of various diseases and the vulnerability to death. Cellular senescence is a hallmark of aging that contributes greatly to aging and aging-related diseases. This study demonstrates that extracellular vesicles from human urine-derived stem cells (USC-EVs) efficiently inhibit cellular senescence in vitro and in vivo. The intravenous injection of USC-EVs improves cognitive function, increases physical fitness and bone quality, and alleviates aging-related structural changes in different organs of senescence-accelerated mice and natural aging mice. The anti-aging effects of USC-EVs are not obviously affected by the USC donors' ages, genders, or health status. Proteomic analysis reveals that USC-EVs are enriched with plasminogen activator urokinase (PLAU) and tissue inhibitor of metalloproteinases 1 (TIMP1). These two proteins contribute importantly to the anti-senescent effects of USC-EVs associated with the inhibition of matrix metalloproteinases, cyclin-dependent kinase inhibitor 2A (P16INK4a), and cyclin-dependent kinase inhibitor 1A (P21cip1). These findings suggest a great potential of autologous USC-EVs as a promising anti-aging agent by transferring PLAU and TIMP1 proteins.

Barriers and facilitators to patient education provided by nurses: A mixed-method systematic review.

AIM: To investigate the factors that facilitate or hinder nurses in providing patient education. DESIGN: A mixed-method systematic review. DATA SOURCES: Six databases (Cochrane Library, PubMed, EMBASE, Web of Science, MEDLINE and ERIC) were systematically searched for relevant publications. METHODS: The study was conducted following the JBI for mixed-method systematic reviews, and the reporting followed the PRISMA guideline. Two researchers independently performed literature screening, literature evaluation, data extraction and synthesis. PROSPERO registration number: CRD42023427451. RESULTS: Twenty-six eligible articles were included, including 15 quantitative articles, 10 qualitative articles and 2 mixed-methods articles. The resultant synthesis of key findings led to the identification of these barriers and facilitators, categorised into five distinct levels: nurse-related factors, organisational factors, patient-related factors, the nurse-patient relationship and interdisciplinary collaboration. CONCLUSIONS: The findings highlight the factors that facilitate or hinder nurses in providing patient education, suggesting that multifaceted interventions can enhance the practice of patient education in nursing and support the development of appropriate patient education guidelines or public policies. RELEVANCE TO CLINICAL PRACTICE: This review delineates the facilitators and barriers influencing nurses' provision of patient education, offering an initial framework for nursing managers to craft interventions aimed at enhancing the quality of patient education provided by nurses, consequently elevating the overall quality of nursing.

The impact of frailty on short-term prognosis in discharged adult stroke patients: A multicenter prospective cohort study.

BACKGROUND: Frailty is commonly observed in stroke patients and it is associated with adverse outcomes. However, there remains a gap in longitudinal studies investigating the causal relationship between baseline frailty and short-term prognosis in discharged adult stroke patients. OBJECTIVE: To examine the causal impact of frailty on non-elective readmission and major adverse cardiac and cerebral events, and investigate its associations with cognitive impairment and post-stroke disability. DESIGN: A multicenter prospective cohort study. SETTING: Two tertiary hospitals in Central and Northwest China. PARTICIPANTS: 667 adult stroke patients in stroke units were included from January 2022 to June 2022. METHODS: Baseline frailty was assessed by the Frailty Scale. Custom-designed questions were utilized to assess non-elective readmission and major adverse cardiac and cerebral events as primary outcomes. Cognitive impairment, assessed using the Mini-Mental State Examination Scale (MMSE), and post-stroke disability, measured with the Modified Rankin Scale (mRS), were considered secondary outcomes at a 3-month follow-up. The impact of baseline frailty on non-elective readmission and major adverse cardiac and cerebral events was examined using bivariate and multiple Cox regression analyses. Furthermore, associations between baseline frailty and cognitive impairment, or post-stroke disability, were investigated through generalized linear models. RESULTS: A total of 5 participants died, 12 had major adverse cardiac and cerebral events, and 57 had non-selective readmission among 667 adult stroke patients. Frailty was an independent risk factor for non-selective readmission (hazard ratio [HR]: 2.71, 95 % confidence interval [CI]: 1.59, 4.62) and major adverse cardiac and cerebral events (HR: 3.77, 95 % CI: 1.07, 13.22) for stroke patients. Baseline frailty was correlated with cognitive impairment (regression coefficient [ß]: -2.68, 95 % CI: -3.78, -1.58) adjusting for socio-demographic and clinical factors and follow-up interval. However, the relationship between frailty and cognitive impairment did not reach statistical significance when further adjusting for baseline MMSE (ß: -0.39, 95 % CI: -1.43, 0.64). Moreover, baseline frailty was associated with post-stroke disability (ß: 0.36, 95 % CI: 0.08, 0.65) adjusting for socio-demographic and clinical variables, follow-up interval, and baseline mRS. CONCLUSIONS: The finding highlights the importance of assessing baseline frailty in discharged adult stroke patients, as it is significantly associated with non-elective readmission, major adverse cardiac and cerebral events, and post-stroke disability at 3 months. These results highlight the crucial role of screening and evaluating frailty status in improving short-term prognosis for adult stroke patients. Interventions should be developed to address baseline frailty and mitigate the short-term prognosis of stroke. TWEETABLE ABSTRACT: Baseline frailty predicts non-elective readmission, major adverse cardiac and cerebral events, and post-stroke disability in adult stroke patients. @haiyanhexyyy.