Explore the vast range of titles available.

Both Alzheimer's disease (AD) and osteoporosis (OP) are common age‐associated degenerative diseases and are strongly correlated with clinical epidemiology. However, there is a lack of clear pathological relationship between the brain and bone in the current understanding. Here, it is found that young osteocyte, the most abundant cells in bone, secretes extracellular vesicles (OCYYoung‐EVs) to ameliorate cognitive impairment and the pathogenesis of AD in APP/PS1 mice and model cells. These benefits of OCYYoung‐EVs are diminished in aged osteocyte‐derived EVs (OCYAged‐EVs). Based on the self‐constructed OCY‐EVs tracer transgenic mouse models and the in vivo fluorescent imaging system, OCY‐EVs have been observed to be transported to the brain under physiological and pathological conditions. In the hippocampal administration of Aβ40 induced young AD model mice, the intramedullary injection of Rab27a‐shRNA adenovirus inhibits OCYYoung‐EVs secretion from bone and aggravates cognitive impairment. Proteomic quantitative analysis reveals that OCYYoung‐EVs, compared to OCYAged‐EVs, enrich multiple protective factors of AD pathway. The study uncovers the role of OCY‐EV as a regulator of brain health, suggesting a novel mechanism in bone‐brain communication. It is found that the osteocyte‐derived extracellular vesicles (OCY‐EVs) isolated from young osteocytes can ameliorate cognitive impairment and pathogenies of AD, but not OCY‐EVs isolated from aged osteocytes. OCY‐EV can transfer to the brain under physiological and pathological conditions. The study uncovers the role of OCY‐EVs as a regulator of brain, suggesting a novel mechanism in bone‐brain communication.

V0.5/Pt/TiO2 tandem catalysts exhibit both an outstanding low-temperature NH3 conversion rate and high N2 selectivity in NH3-SCO reactions, but the mechanism of high N2 selectivity remains unclear. In this work, Vx/Pt/TiO2 tandem catalysts were synthesized through a two-step impregnation–deposition method. The modulating effect of the V loading mount on NH3-SCO performance was evaluated, and the relevant reaction mechanism was explored systematically. The results demonstrated that the synergistic effect of tandem NH3 oxidation and NH3-SCR reactions could be regulated by changing the V loading amount, thereby modulating N2 selectivity. Compared with other Vx/Pt/TiO2 catalysts and previously reported SCO catalysts, the V0.5/Pt/TiO2 catalyst with a V loading amount of 0.5 wt.% exhibited outstanding NH3-SCO performance, which achieved complete NH3 conversion and >90% of N2 selectivity within a range of 250–450 °C. XPS, NH3-TPD, and O2-TPD results suggested that the increase in the V loading amount from 0.1 wt.% to 0.5 wt.% was conducive to increasing the relative contents of Pt0 and V5+ species, as well as the amount of acid sites, oxygen species, and oxygen vacancies. Consequently, the synergistic effect of tandem NH3 oxidation and NH3-SCR reactions was significantly enhanced, enabling the catalyst to exhibit excellent N2 selectivity. A further increase in the V loading amount from 0.5 wt.% to 0.9 wt.% would bring about the opposite effect to the above, resulting in a decline in catalytic performance. In situ DRIFTS results showed that a V loading amount of 0.5 wt.% was beneficial for -NH2 species to participate in NH3-SCO reactions, thereby boosting N2 selectivity.

Background To explore population aging and the epidemic trend of pulmonary tuberculosis (PTB) in the elderly, and provide a basis for the prevention and control of pulmonary tuberculosis among the elderly. Methods We collected clinical information of 239,707 newly active PTB patients in Shandong Province from 2005 to 2017. We analyzed and compared the clinical characteristics, reported incidence and temporal trend of PTB among the elderly group (≥60 years) and the non-elderly group (< 60 years) through logistic model and Join-point regression model. Results Among the total PTB cases, 77,192(32.2%) were elderly. Compared with non-elderly patients, newly active elderly PTB patients account for a greater proportion of male cases (OR 1.688, 95% CI 1.656–1.722), rural population cases (OR 3.411, 95% CI 3.320–3.505) and bacteriologically confirmed PTB cases (OR 1.213, 95%CI 1.193–1.234). The annual reported incidence of total, elderly, pulmonary bacteriologically confirmed cases were 35.21, 68.84, 35.63 (per 100,000), respectively. The annual reported incidence of PTB in the whole population, the elderly group and the non-elderly group has shown a slow downward trend since 2008. The joinpoint regression model showed that the overall reported incidence of PTB in the elderly significantly decreased from 2007 to 2017 (APC = -5.3, P  < 0.05). The reported incidence of bacteriologically confirmed PTB among elderly patients declined rapidly from 2005 to 2014(2005–2010 APC = -7.2%, P  < 0.05; 2010–2014 APC = -22.6%, P  < 0.05; 2014–2017 APC = -9.0%, P  = 0.1). The reported incidence of clinically diagnosed PTB among elderly patients from 2005 to 2017 (11.48–38.42/100,000) increased by about 235%. It rose significantly from 2007 to 2014 (APC = 9.4, P <0.05). Conclusions Compared with the non-elderly population, the reported incidence of PTB in the elderly population is higher. The main burden of PTB will shift to the elderly, men, rural population, and clinically diagnosed patients. With the intensification of aging, more researches on elderly PTB prevention and treatment will facilitate the realization of the global tuberculosis (TB) control targets.

Curcumin, a natural chemical compound found in Curcuma longa, has been applied in multiple medicinal areas from antibiotic to antitumor treatment. However, the chemical structure of curcumin results in poor stability, low solubility, and rapid degradation in vivo, hindering its clinical utilization. To address these issues, we have developed a novel niosome system composed of nonionic surfactants: Span 80, Tween 80, and Poloxamer 188. Curcumin was encapsulated in the niosomes with a high entrapment efficiency of 92.3 ± 0.4 %. This system provided controlled release of curcumin, thereby improving its therapeutic capability. Dynamic dialysis was conducted to evaluate the in vitro drug release of curcumin-niosomes. Curcumin-niosomes exhibited enhanced cytotoxic activity and apoptotic rate against ovarian cancer A2780 cells compared with freely dispersed curcumin. These results demonstrate that the curcumin-niosome system is a promising strategy for the delivery of curcumin and ovarian cancer therapy.

Long-term exposure to air pollution is associated with cardiometabolic diseases, but the modifying role of body shape distribution on cardiometabolic multimorbidity (CMM) remains unknown. This study investigated whether A Body Shape Index (ABSI), a measure of abdominal adiposity, modifies the relationship between air pollution and CMM in Chinese middle-aged and older adults. We included 11,838 participants aged ≥ 45 years from the China Health and Retirement Longitudinal Study (CHARLS) Wave 3 (2015). CMM was defined as the coexistence of ≥ 2 cardiometabolic diseases (diabetes, heart disease, and stroke). ABSI was calculated as waist circumference/(BMI^(2/3) × height^(1/2)). Individual exposure to air pollutants—including particulate matter with an aerodynamic diameter ≤ 2.5 μm (PM₂.₅), ≤ 10 μm (PM₁₀), and ≤ 1 μm (PM 1 ); sulfur dioxide (SO 2 ); nitrogen dioxide (NO₂); and ozone (O₃)—was assessed using satellite-based spatiotemporal models. Generalized linear models examined associations between air pollution and CMM, with interaction terms to evaluate ABSI’s modification effects. The final analysis included 10,487 participants, with 6,896 (65.8%) having cardiometabolic multimorbidity (CMM). All six air pollutants (PM2.5, PM10, SO2, NO2, O3, PM1) showed significant positive associations with CMM prevalence. In fully adjusted models, the odds ratios per interquartile range (IQR) increase ranged from 1.104 (95% CI 1.041–1.173) for O3 to 1.298 (95% CI 1.204–1.401) for PM1. ABSI was independently associated with increased CMM risk, with each IQR (0.005) increase associated with 14.2% higher odds (OR = 1.142, 95% CI 1.085–1.201). Significant interaction effects were observed between ABSI and all six examined air pollutants (P-interaction < 0.10). Stratified analyses revealed substantially stronger associations between air pollution and CMM among participants in the highest ABSI tertile compared to the lowest tertile. For example, PM1 showed an OR of 1.428 (95% CI 1.285–1.587) in the highest ABSI group versus weaker associations in lower ABSI groups. All sensitivity analyses confirmed the robustness of these findings. This study provides the first evidence that A Body Shape Index significantly modifies the association between long-term air pollution exposure and cardiometabolic multimorbidity in Chinese middle-aged and older adults. Individuals with higher ABSI values, indicating greater abdominal adiposity, experienced substantially stronger associations between air pollutant exposure and CMM risk. These findings suggest that central body fat distribution creates a metabolically vulnerable phenotype that amplifies environmental health risks. The results highlight the importance of considering body shape distribution when assessing air pollution health impacts and support targeted prevention strategies for high-risk individuals with central obesity in polluted environments. The demonstrated interaction between environmental and metabolic factors underscores the need for integrated approaches to cardiometabolic disease prevention that address both air quality improvement and obesity management.

Background Tuberculosis (TB) is one of the major infectious diseases that seriously endanger people’s health. In Shandong province, the relationship between the level of economic development and TB incidence has not been studied. This study aims to provide more research basis for the government to prevent and control TB by exploring the impact of different economic factors on TB incidence. Methods By constructing threshold regression model (TRM), we described the extent to which different economic factors contribute to TB registered incidence and differences in TB registered incidence among seventeen cities with different levels of economic development in Shandong province, China, during 2006–2017. Data were retrieved from the China Information System for Disease Control and Prevention. Results Per capita medical expenditure (regression coefficient, -0.0314462; SD, 0.0079305; P > |t|, 0.000) and per capita savings (regression coefficient, 0.0001924; SD, 0.0000566; P > |t|, 0.001) passed the significance test at the level of 1%.They are the two economic indicators that have the greatest impact on TB registered incidence. Through the threshold test, we selected the per capita savings as the threshold variable. In the three stages of per capita savings (<9772.8086 China Yuan(CNY); 9772.8086–33,835.5391 CNY; >33,835.5391 CNY), rural per capita income always has a significant negative impact on the TB registered incidence (The regression coefficients are − 0.0015682, − 0.0028132 and − 0.0022253 respectively. P is 0.007,0.000 and 0.000 respectively.).In cities with good economies, TB registered incidence was 38.30% in 2006 and dropped to 25.10% by 2017. In cities with moderate economies, TB registered incidence peaked in 2008 at 43.10% and dropped to 27.1% by 2017.In poorer cities, TB registered incidence peaked in 2008 at 56.30% and dropped to 28.9% in 2017. Conclusion We found that per capita savings and per capita medical expenditure are most closely related to the TB incidence. Therefore, relevant departments should formulate a more complete medical system and medical insurance policy to effectively solve the problem of “difficult and expensive medical treatment”. In order to further reduce the TB incidence, in addition to timely and accurate diagnosis and treatment, it is more important for governments to increase investment in medicine and health care.

Intracerebral hemorrhage (ICH) represents one of the most devastating forms of stroke, characterized by spontaneous bleeding into the brain parenchyma. This neurological emergency carries a substantial burden of mortality and long-term disability worldwide. A comprehensive understanding of ICH’s evolving global impact from 1990 to 2021 remains essential for healthcare planning and resource allocation. We conducted a systematic analysis of ICH burden utilizing data from the Global Burden of Disease (GBD) Study 2021. Key epidemiological indicators were extracted, including prevalence, incidence, mortality, and disability-adjusted life-years (DALYs). Temporal trends were quantified through estimated annual percentage changes (EAPCs) in age-standardized rates of prevalence (ASPR), incidence (ASIR), mortality (ASDR), and DALYs across the study period. The association between disease burden and socioeconomic development was examined using the sociodemographic index (SDI) as a metric of societal development. This analytical framework enabled assessment of ICH burden across global, regional, and national scales while accounting for demographic and socioeconomic variations. From 1990 to 2021, while absolute ICH cases increased globally, age-standardized incidence rates declined. Our novel geographic analysis revealed East Asia bearing the highest burden, with Eastern Europe showing the highest age-standardized rates. Gender analysis identified distinct age-specific patterns, with males above 35 showing higher risk, particularly in Eastern Europe, while South Asia demonstrated minimal gender differences. Our innovative analysis during COVID-19 revealed healthcare system strength significantly impacted ICH outcomes, with well-resourced countries maintaining better outcomes. Regional risk factor assessment showed varying impacts of high systolic blood pressure across regions, highest in Southern Sub-Saharan Africa and lowest in Oceania. Future projections through 2030 indicate improving survival rates in most regions, except in low-income areas, highlighting persistent healthcare disparities. While the absolute number of ICH cases, deaths, and DALYs increased globally from 1990 to 2021, age-standardized rates showed a decreasing trend. This suggests improvements in prevention and management strategies over time. However, the burden of ICH remains substantial and unevenly distributed across regions, with lower SDI areas facing a disproportionately higher burden. These findings highlight the need for targeted interventions and resource allocation, particularly in regions with higher ICH burden, to further reduce the global impact of this devastating condition.

The periosteum, a thin tissue that covers almost the entire bone surface, accounts for more than 80% of human bone mass and is essential for bone regeneration. Its osteogenic and bone regenerative abilities are well studied, but much is unknown about the periosteum. In this study, we found that macrophage-lineage cells recruit periosteum-derived cells (PDCs) for cortical bone formation. Knockout of colony stimulating factor-1 eliminated macrophage-lineage cells and resulted in loss of PDCs with impaired periosteal bone formation. Moreover, macrophage-lineage TRAP+ cells induced transcriptional expression of periostin and recruitment of PDCs to the periosteal surface through secretion of platelet-derived growth factor-BB (PDGF-BB), where the recruited PDCs underwent osteoblast differentiation coupled with type H vessel formation. We also found that subsets of Nestin+ and LepR+ PDCs possess multipotent and self-renewal abilities and contribute to cortical bone formation. Nestin+ PDCs are found primarily during bone development, whereas LepR+ PDCs are essential for bone homeostasis in adult mice. Importantly, conditional knockout of Pdgfrβ (platelet-derived growth factor receptor beta) in LepR+ cells impaired periosteal bone formation and regeneration. These findings uncover the essential role of periosteal macrophage-lineage cells in regulating periosteum homeostasis and regeneration.

Brain vascular calcification is a prevalent age-related condition often accompanying neurodegenerative and neuroinflammatory diseases. The pathogenesis of large-vessel calcifications in peripheral tissue is well studied, but microvascular calcification in the brain remains poorly understood. Here, we report that elevated platelet-derived growth factor BB (PDGF-BB) from bone preosteoclasts contributed to cerebrovascular calcification in male mice. Aged male mice had higher serum PDGF-BB levels and a higher incidence of brain calcification compared with young mice, mainly in the thalamus. Transgenic mice with preosteoclast-specific Pdgfb overexpression exhibited elevated serum PDGF-BB levels and recapitulated age-associated thalamic calcification. Conversely, mice with preosteoclast-specific Pdgfb deletion displayed diminished age-associated thalamic calcification. In an ex vivo cerebral microvascular culture system, PDGF-BB dose-dependently promoted vascular calcification. Analysis of osteogenic gene array and single-cell RNA-Seq (scRNA-Seq) revealed that PDGF-BB upregulated multiple osteogenic differentiation genes and the phosphate transporter Slc20a1 in cerebral microvessels. Mechanistically, PDGF-BB stimulated the phosphorylation of its receptor PDGFRβ (p-PDGFRβ) and ERK (p-ERK), leading to the activation of RUNX2. This activation, in turn, induced the transcription of osteoblast differentiation genes in PCs and upregulated Slc20a1 in astrocytes. Thus, bone-derived PDGF-BB induced brain vascular calcification by activating the p-PDGFRβ/p-ERK/RUNX2 signaling cascade in cerebrovascular cells.

Emerging insights into cellular senescence highlight the relevance of senescence in musculoskeletal disorders, which represent the leading global cause of disability. Cellular senescence was initially described by Hayflick et al. in 1961 as an irreversible nondividing state in in vitro cell culture studies. We now know that cellular senescence can occur in vivo in response to various stressors as a heterogeneous and tissue-specific cell state with a secretome phenotype acquired after the initial growth arrest. In the past two decades, compelling evidence from preclinical models and human data show an accumulation of senescent cells in many components of the musculoskeletal system. Cellular senescence is therefore a defining feature of age-related musculoskeletal disorders, and targeted elimination of these cells has emerged recently as a promising therapeutic approach to ameliorate tissue damage and promote repair and regeneration of the skeleton and skeletal muscles. In this review, we summarize evidence of the role of senescent cells in the maintenance of bone homeostasis during childhood and their contribution to the pathogenesis of chronic musculoskeletal disorders, including osteoporosis, osteoarthritis, and sarcopenia. We highlight the diversity of the senescent cells in the microenvironment of bone, joint, and skeletal muscle tissue, as well as the mechanisms by which these senescent cells are involved in musculoskeletal diseases. In addition, we discuss how identifying and targeting senescent cells might positively affect pathologic progression and musculoskeletal system regeneration.