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Ozone pollution is increasingly recognized as a serious environmental threat that exacerbates dementia risks, including Alzheimer's Disease (AD) and Mild Cognitive Impairment (MCI). Amid rapid industrialization, China faces significant air quality challenges. However, there has been a scarcity of detailed studies assessing the health and economic impacts of ozone pollution on these conditions. This study aims to address this gap by utilizing the BenMap-CE tool and incorporating parameters obtained from systematic reviews of epidemiological studies, official statistics, and weighted averages, to accurately quantify the effects of ozone exposure in China. This research evaluated the health and economic burdens at both national and provincial levels, focusing on the additional impacts attributed to increased ozone levels. The results reveal that in 2023, compared to 2015, ozone pollution contributed to approximately 110,000 new cases (5.6 per 10,000) of AD and 1.6 million new cases (81.7 per 10,000) of MCI, imposing significant economic costs of about US $1200 million for AD and US $18,000 million for MCI, based on 2015 dollar values. Additionally, our projections indicate that reducing the 2023 ozone concentrations to 70 µg/m3 could significantly curb these conditions, potentially preventing over 210,000 new AD cases (10.7 per 10,000) and 2.9 million (148.1 per 10,000) MCI cases. Such reductions are projected to yield substantial economic benefits, estimated at US $2200 million for AD and US $34,000 million for MCI (2015 dollar values). These findings underscore the profound implications of ozone pollution on public health and the economy in China, highlighting the urgent need for effective ozone management strategies to mitigate these impacts.
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To amplify the displacement of the radiation shell, a double-shell type-IV curved hydroacoustic transducer was proposed. Through Ansys finite element simulation, the vibration modes of the transducer in different stages and the harmonic response characteristics in air and water were studied, and the bandwidth emission of the hydroacoustic transducer was achieved. By optimizing the size of each component, the resonant frequency of the transducer is 740 Hz, the maximum conductivity was 0.66 mS, and the maximum transmitting voltage response was 130 dB. According to the optimized parameters, a longitudinal acoustic transducer prototype was manufactured, and a physical test was conducted in an anechoic pool. The obtained resonant frequency was 750 Hz, the maximum conductivity was 0.44 mS, the maximum transmitting voltage response was 129.25 dB, and the maximum linear dimension was 250 mm, which match the simulated value of the virtual prototype and meet the expected requirements.
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OBJECTIVES: Oral lichen planus (OLP) is a chronic inflammatory condition with an unclear pathological mechanism. IκB kinase α (IKKα)-regulated mammary serine protease inhibitor (MASPIN) has been shown to mediate inflammation, particularly in cancers. Here, we explored the expression of MASPIN in OLP and its role in the inflammatory response. MATERIALS AND METHODS: Immunohistochemistry staining and reverse transcription-polymerase chain reaction assays were used to detect the subcellular localization and expression of MASPIN and IKKα in OLP and healthy control tissues. Levels of the inflammatory factors were compared with enzyme-linked immunosorbent assays. MASPIN and IKKα were overexpressed and silenced, respectively, in an inflammation model of human oral keratinocytes (HOKs) stimulated with lipopolysaccharide (LPS). RESULTS: Mammary serine protease inhibitor expression was down-regulated, whereas IKKα expression was up-regulated in OLP tissues (p < 0.01). The levels of tumour necrosis factor-alpha and interleukin-6 in OLP tissues were increased compared to those of healthy controls (p < 0.01). MASPIN overexpression in LPS-stimulated HOK cells inhibited the levels of IKKα and the secretion of inflammatory cytokines. By contrast, IKKα silencing promoted the expression of MASPIN and inhibited the secretion of inflammatory cytokines. CONCLUSION: Both MASPIN and IKKα are involved in the inflammatory process of OLP, suggesting potential therapeutic targets.
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Citocinas/metabolismo , Líquen Plano Bucal/metabolismo , Inibidores de Serina Proteinase/metabolismo , Adulto , Idoso , Citocinas/genética , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Queratinócitos , Lipopolissacarídeos , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Inibidores de Serina Proteinase/genética , SerpinasAssuntos
Doenças Cardiovasculares , Osteoporose Pós-Menopausa , Feminino , Humanos , Osteoporose Pós-Menopausa/tratamento farmacológico , Ligante RANK , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/prevenção & controle , Ligantes , Fatores de Risco , Hormônio Paratireóideo , Densidade Óssea , Fatores de Risco de Doenças CardíacasRESUMO
Cancer drug resistance has always been a serious issue regarding cancer research and therapy. Different cancers undergo different mutations, which may cause suppression of tumor suppressor genes, inhibition of apoptosis, stimulation of drug resistance mediators, and exhaustion of the immune system. The modulation of pro-death and survival-related mediators is an intriguing strategy for cancer therapy. Several nature-derived molecules, e.g., quercetin, have shown interesting properties against cancer through the modulation of apoptosis and autophagy mediators. Such molecules, e.g., quercetin, have been shown to stimulate apoptosis and other types of cell death pathways in cancers via the modulation of ROS metabolism. Quercetin may affect immune system function and trigger the expression and activity of tumor suppressor genes. Furthermore, it may suppress certain multidrug resistance mechanisms in cancer cells. This paper aims to review the effects of quercetin on various cell death mechanisms such as apoptosis, autophagic cell death, senescence, ferroptosis, and others.
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Neoplasias , Quercetina , Humanos , Quercetina/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Morte Celular , Neoplasias/tratamento farmacológico , Apoptose , Autofagia , Linhagem Celular TumoralRESUMO
OBJECTIVE: To observe the predictive value of 25-hydroxyvitamin D3 (25(OH)D3), C-reactive protein (CRP), and tumor necrosis factor-α (TNF-α) levels for osteoporosis in elderly men. METHODS: A retrospective analysis was conducted in 122 elderly male patients that were tested in The Affiliated Hospital of Xinyang Vocational and Technical College between January 2020 and May 2022. The patients were divided into an osteoporosis group (OG, n = 77) and a control group (CG, n = 45) according to the results of bone mineral density. The formula N = Z^2*(P*(1-P))/E^2 was used to calculate the required sample size (N) for a given confidence interval (Z), total error (E), and proportion (P) of the target population. The proportion (P) is often assumed to be 0.5 and not randomly distributed across the population. The levels of cross-linked C-terminal telopeptide of type I collagen (CTX-I), procollagen type I N-terminal propeptide (PINP), intact parathyroid hormone (iPTH), osteocalcin (OC), and serum levels of 25(OH)D3, CRP, and TNF-α were measured and compared between the two groups. Pearson correlation was used to analyze the relationship between the parameters. The predictive value of 25(OH)D3, CRP and TNF-α for osteoporosis was also analyzed using receiver operating characteristic (ROC) curves. Logistic multivariate analysis was performed to analyze the risk factors for osteoporosis in elderly men. RESULTS: Compared with the CG, the OG exhibited evidently lower serum 25(OH)D3, but significantly higher CRP and TNF-α (P < 0.05). Pearson correlation demonstrated that the bone mineral density was negatively correlated with CTX-I, PINP, serum CRP and TNF-α, whereas it was positively correlated with OC and 25(OH)D3 in elderly men. The areas under the ROC curve (AUCs) of serum 25(OH)D3, CRP and TNF-α were identified as 0.931, 0.878 and 0.846, respectively, and the AUC of the combined detection of the three was 0.991. Furthermore, age, CTX-I, PINP, OC, 25(OH)D3, as well as serum CRP and TNF-α were identified as risk factors for osteoporosis among elderly men. CONCLUSION: Serum 25(OH)D3, CRP, and TNF-α are associated with osteoporosis in elderly men, and can serve as predictors for osteoporosis.
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Advanced age is one of the leading risk factors for vision loss and eye disease. Photoreceptors are the primary sensory neurons of the eye. The extended photoreceptor cell lifespan, in addition to its high metabolic needs due to phototransduction, makes it critical for these neurons to continually respond to the stresses associated with aging by mounting an appropriate gene expression response. Here, we sought to untangle the more general neuronal age-dependent transcriptional signature of photoreceptors with that induced by light stress. To do this, we aged flies or exposed them to various durations of blue light, followed by photoreceptor nuclei-specific transcriptome profiling. Using this approach, we identified genes that are both common and uniquely regulated by aging and light induced stress. Whereas both age and blue light induce expression of DNA repair genes and a neuronal-specific signature of death, both conditions result in downregulation of phototransduction. Interestingly, blue light uniquely induced genes that directly counteract the overactivation of the phototransduction signaling cascade. Lastly, unique gene expression changes in aging photoreceptors included the downregulation of genes involved in membrane potential homeostasis and mitochondrial function, as well as the upregulation of immune response genes. We propose that light stress contributes to the aging transcriptome of photoreceptors, but that there are also other environmental or intrinsic factors involved in age-associated photoreceptor gene expression signatures.
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Transdução de Sinal Luminoso , Células Fotorreceptoras , Perfilação da Expressão Gênica , Transdução de Sinal Luminoso/genética , Células Fotorreceptoras/metabolismo , TranscriptomaRESUMO
Bioelectricity is defined as endogenous electrical signaling mediated by the dynamic distribution of charged molecules. Recently, increasing evidence has revealed that cellular bioelectric signaling is critical for regulating embryonic development, regeneration, and congenital diseases. However, systematic real-time in vivo dynamic electrical activity monitoring of whole organisms has been limited, mainly due to the lack of a suitable model system and voltage measurement tools for in vivo biology. Here, we addressed this gap by utilizing a genetically stable zebrafish line, Tg (ubiquitin: ASAP1), and ASAP1 (Accelerated sensor of action potentials 1), a genetically encoded voltage indicator (GEVI). With light-sheet microscopy, we systematically investigated cell membrane potential (Vm) signals during different embryonic stages. We found cells of zebrafish embryos showed local membrane hyperpolarization at the cleavage furrows during the cleavage period of embryogenesis. This signal appeared before cytokinesis and fluctuated as it progressed. In contrast, whole-cell transient hyperpolarization was observed during the blastula and gastrula stages. These signals were generally limited to the superficial blastomere, but they could be detected within the deeper cells during the gastrulation period. Moreover, the zebrafish embryos exhibit tissue-level cell Vm signals during the segmentation period. Middle-aged somites had strong and dynamic Vm fluctuations starting at about the 12-somite stage. These embryonic stage-specific characteristic cellular bioelectric signals suggest that they might play a diverse role in zebrafish embryogenesis that could underlie human congenital diseases.
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Fenômenos Eletrofisiológicos , Peixe-Zebra , Animais , Humanos , Pessoa de Meia-Idade , Peixe-Zebra/metabolismo , Gástrula/metabolismo , Desenvolvimento Embrionário , BlastômerosRESUMO
Here, we report the development of a class of bifunctional monoprotected amino-imidazoline (MPAI) ligands and their applications in Pd-catalyzed C(sp3)-H arylation of free aliphatic acids. The newly developed MPAI ligand allows the use of 1.0 equiv of aliphatic acids containing an alpha hydrogen for the first time.
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Imidazolinas , Paládio , Ligantes , Ácidos Graxos , CatáliseRESUMO
At present, the concentration of PM2.5 in the Fenwei Plain has become the second highest in China, ranking second to the Beijing-Tianjin-Hebei region. At the same time, China began to monitor and control the PM2.5 concentration in the Fenwei Plain, but the data indicated that the concentration of PM2.5 in the Fenwei Plain rose instead of falling. PM2.5 concentrations in 6 cities from the Fenwei Plain ranked highest among the 20 cities in 2018 in China, and PM2.5 pollution can cause some health economic loss. Based on this background, the exposure-response model is used to estimate the impact of PM2.5 pollution on the health economic loss in the Fenwei Plain, and PM2.5 concentration in 2020, 2025, and 2030 is also predicted based on the setting of three scenarios: baseline scenario, emission reduction scenario, and enhanced emission reduction scenario. Then, according to the estimated results, the paper provides suggestions for reducing public health loss in the Fenwei Plain in the future.
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Poluentes Atmosféricos , Poluição do Ar , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Pequim , China , Cidades , Monitoramento Ambiental , Material Particulado/análise , Saúde PúblicaRESUMO
China's energy structure is based on coal resource and it accounts for main proportion in the primary energy consumption. Coal consumption produces PM2.5 pollution, which seriously affects public health. Considering that there are few studies on the effect PM2.5 pollution produced by coal consumption, this paper uses the Poisson Regression model to estimate the impacts on public health and the economic loss of PM2.5 pollution produced by coal consumption using the data in 2015. Based on these results, the paper also predicts the impacts on public health effect and its economic loss caused by PM2.5 pollution from coal consumption under the baseline scenario and total coal consumption control scenario in 2020 and 2030. Finally, based on the research conclusions, suggestions are proposed to reduce the public health economic loss from PM2.5 pollution caused by coal consumption.