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China is currently entering a stage of high-quality development, with urban development and governance facing systematic reconstruction of internal and external conditions, showing clear differences and the complex superposition of multi-stage development. The steady progress of urbanization has facilitated significant changes in the population structure of Chinese cities. It is expected that the population and industries will further converge to urban agglomerations and big cities, indicating basic multicenter and network patterns. Therefore, analyzing the negative population growth risks of urban agglomerations at different development stages is crucial. This study examined the cities of 19 urban agglomerations in China by adopting the data of the seventh population census, employing the optimized fuzzy logic method, building a complex network of population flow with ArcGIS and MATLAB platforms, and using the intensity of population flow and the registered population fertility rate to represent exogenous and endogenous growth, respectively. The negative population growth evaluation index system was constructed with five indicators: child ratio, aging rate, average family size, population density, and sex ratio. The risk index of negative population growth was measured using the fuzzy logic method, and the growth mechanism of negative population growth risk in urban agglomerations in China was analyzed using the spatial measurement method. (1) The negative population growth risk of growing urban agglomerations was influenced by both exogenous and endogenous growth, with exogenous growth having a greater impact. (2) The dynamic mechanism of negative population growth risk in large urban agglomerations is exogenous growth, whereas that of nurturing urban agglomerations is endogenous growth. (3) According to the risk of negative population growth in China's urban agglomerations and its influencing factors, negative population growth in 19 urban agglomerations can be divided into eight types. 1) The state of population growth of expanding urban agglomerations can be divided into two types, with the middle reaches of the Yangtze River and Chengdu-Chongqing urban agglomerations as one type; the capital city has a low risk of negative population growth, while other cities have a high risk of negative population growth. The Yangtze River Delta, Pearl River Delta, and Beijing-Tianjin-Hebei city clusters are the same, with the capital and other cities having a relatively low risk of negative population growth. 2) The status of large urban agglomerations can be divided into two types: Shandong Peninsula, Central Plains, Guanzhong Plain, and Beibu Gulf urban agglomerations. The capital city has a low risk of negative population growth, whereas other cities have a high risk of negative population growth. The risk of negative population growth in capital cities and other cities is relatively low. 3) The state of population growth of cultivated urban agglomerations can be divided into four types: the Harbin and Changsha urban agglomerations and the central and southern Liaoning urban agglomerations, which have a high risk of negative population growth. Meanwhile, the northern slope of the Tianshan Mountain City cluster and the Hubao Eyu City cluster have low risk of negative population growth. The risk of negative population growth is low in the provincial capital city and high in the other cities, while endogenous growth is positive in the provincial capital city and negative in the other cities. In the Jinzhong City, Central Guizhou City, and Central Yunnan City groups, the risk of negative population growth is low in provincial cities and high in other cities. Endogenous growth shows that the capital city and other cities have positive growth. In conclusion, this study posits that upgrading urban agglomerations should consider the spatial balance of population distribution, large urban agglomerations should fulfill their role in "blocking the flow" of big cities, and nurturing urban agglomerations should "consolidate human capital." This study presents a comprehensive and in-depth analysis of the negative population growth risk and its impact mechanisms in different development stages of urban agglomerations. This can provide a decision-making reference for the formulation of scientific and reasonable population and economic policies in various urban agglomerations and plays a significant role for maintaining a long-term stable population, economy, and social growth in the region.

Understanding the near-ground vertical and temporal photochemical O 3 formation mechanism is important to mitigate O 3 pollution. Here, we measured the vertical profiles of O 3 and its precursors at six different heights, ranging from 5 to 335 m, using a newly built vertical observation system in the Pearl River Delta (PRD) region of China. The net photochemical ozone production rate (P (O 3) net) and O 3 formation sensitivities at various heights were diagnosed using an observation-based model coupled with the Master Chemical Mechanism (MCM v3.3.1). Moreover, to assess model performance and identify the causative factors behind O 3 pollution episodes, the P (O 3) net was measured at 5 m above ground level with a custom-built detection system. In total, three O 3 pollution episodes and two non-episodes were captured. The identified O 3 pollution episodes were found to be jointly influenced by both photochemical production and physical transport, with local photochemical reactions playing a major role. The high index of agreement (IOA) calculated by comparing the modelled and measured P (O 3) net values indicated the rationality of investigating the vertical and temporal variability in O 3 formation mechanisms using model results. However, the measured P (O 3) net values were generally higher than the modelled P (O 3) net values, particularly under high-NO x conditions, which may indicate a potential underestimation of total RO 2 by the model. Throughout the measurement period, the contribution of different reaction pathways to O 3 production remained consistent across various heights, with HO 2 + NO as the major O 3 production pathway, followed by RO 2 + NO. We observed that P (O 3) net decreased with an increase in measurement height, which was primarily attributed to the reduction in O 3 precursors, such as oxygenated volatile organic compounds (OVOCs) and non-methane hydrocarbons (NMHCs). The O 3 formation regimes were similar at different heights during both episodes and non-episodes, either being located in the VOC-sensitive regime or in the transition regime that is more sensitive to VOCs. Diurnally, photochemical O 3 formation typically remained in the VOC-sensitive regime during the morning and noon, but it transitioned to the transition regime and was more sensitive to VOCs in the afternoon at around 16:00 LT (local time). Vertical and temporal photochemical O 3 formation is most sensitive to OVOCs, suggesting that targeting specific VOCs for control measures is more practical and feasible at the observation site. The vertical temporal analysis of O 3 formation mechanisms near the ground surface in this study provides critical foundational knowledge that can be used to formulate effective short-term emergency and long-term control strategies to combat O 3 pollution in the PRD region of China. [ABSTRACT FROM AUTHOR]

Activated carbon filter is the main equipment used to remove pollutants in the ventilation system in a nuclear power plant. Its main function is to remove radioactive iodine to minimize radioactive hazards against workers in the ventilation area. Periodic evaluation is a key step for verifying its operation effectiveness, further to ensure the safety and long-term operation. In this paper, by changing the micropore structure and surface chemical properties of activated carbon, its physicochemical properties and adsorption performance against methyl iodide under the high humidity working environment are studied. The results show that the adsorption performance of activated carbon on organic compound decreases significantly under the high humidity conditions; however, the combination of potassium iodide, triethylene diamine and functional groups on the activated carbon surface form stable chemical bonds and a new surface structure, which enhances the adsorption performance and stability of activated carbon against pollutants and makes it difficult to remove pollutants. The adsorption capacity of nuclear activated carbon can be restored to 80.7% of the initial capacity, and the adsorption performance can be obviously improved.

Objective: To investigate the therapeutic effect and mechanism of sivelestat sodium on acute lung injury (AIL). Methods: A rat model for ALI/acute respiratory distress syndrome (ALI/ARDS) was established. Pathological examination of lung tissue was conducted to assess lung injury. Blood gas in the arteries was measured using a blood analyzer. Changes in PaO2, PaO2/FiO2, and lung wet/dry (W/D) weight ratio were carefully compared. ELISA assay was conducted to estimate cell adhesion and inflammation response. Finally, real-time reverse transcription polymerase chain reaction and western blotting assay was used to determine the activation of PI3K/AKT/mTOR pathway. Results: ARDS in vivo model was successfully constructed by LPS injection. Compared with the sham group, PaO2 and PaO2/FiO2 were significantly lower in the vehicle group, while the lung W/D ratio, the lung injury score, NE, VCAM-1, IL-8 andTNF-αwere significantly increased. After treatment with different doses of sivelestat sodium, we found PaO2, PaO2/FiO2 were prominently increased, while the lung W/D ratio, the lung injury score, NE, VCAM-1, IL-8, TNF-α levels were decreased in the dose-dependent manner. Meanwhile, compared with the vehicle group, the expression levels of Bax, PI3K, Akt and mTOR were significantly lower, and the expression of Bcl-2 was significantly higher after injection with sivelestat sodium. Conclusion: Sivelestat sodium has an interventional effect on ALI in sepsis by inhibiting the PI3K/AKT/mTOR signalling pathway. [ABSTRACT FROM AUTHOR]

Current process-based research mainly uses box models to evaluate photochemical ozone production and destruction rates, and it is unclear to what extent the photochemical reaction mechanisms are elucidated. Here, we modified and improved a net photochemical ozone production rate (NPOPR, P (O 3) net) detection system based on the current dual-channel reaction chamber technique, which makes the instrument applicable to different ambient environments, and its various operating indicators were characterized, i.e., "airtightness", light transmittance, wall losses of the reaction and reference chambers, conversion rate of O 3 to NO 2 , air residence time, and performance of the reaction and reference chambers. The limits of detection of the NPOPR detection system were determined to be 0.07, 1.4, and 2.3 ppbv h -1 at sampling flow rates of 1.3, 3, and 5 L min -1 , respectively. We further applied the NPOPR detection system to field observations at an urban site in the Pearl River Delta (China). During the observation period, the maximum value of P (O 3) net was 34.1 ppbv h -1 , which was ∼ 0 ppbv h -1 at night within the system detection error and peaked at approximately noon local time. The daytime (from 06:00–18:00 LT) average value of P (O 3) net was 12.8 (± 5.5) ppbv h -1. We investigated the detailed photochemical O 3 formation mechanism in the reaction and reference chambers of the NPOPR detection system using a zero-dimensional box model. We found that the photochemical reactions in the reaction chamber were very close to those in ambient air, but there was not zero chemistry in the reference chamber because the reaction related to the production and destruction of RO 2 (= HO 2 + RO 2) continued in the reference chamber, which led to a small amount of P (O 3) net. Therefore, the P (O 3) net measured here can be regarded as the lower limit of the real P (O 3) net in the atmosphere; however, the measured P (O 3) net was still ∼ 7.5 to 9.3 ppbv h -1 higher than the modeled P (O 3) net value depending on different modeling methods, which may be due to the inaccurate estimation of HO 2 / RO 2 radicals in the modeling study. Short-lived intermediate measurements coupled with direct P (O 3) net measurements are needed in the future to better understand O 3 photochemistry. Our results show that the NPOPR detection system can achieve high temporal resolution and continuous field observations, which helps us to better understand photochemical O 3 formation and provides a key scientific basis for continuous improvement of air quality in China. [ABSTRACT FROM AUTHOR]

Background/aims: Dexamethasone (DEX) is a widely used exogenous therapeutic glucocorticoid in clinical settings. Its long-term use leads to many side effects. However, its effect on metabolic disorders in individuals on a high-fat diet (HFD) remains poorly understood., Methods: In this study, HFD-fed mice were intraperitoneally injected with DEX 2.5 mg/kg/day for 30 days. Lipid metabolism, adipocyte proliferation, and inflammation were assayed using typical approaches., Results: DEX increased the epididymal fat index and epididymal adipocyte size in HFD-fed mice. The number of epididymal adipocytes with diameters > 70 μm accounted for 0.5% of the cells in the control group, 30% of the cells in the DEX group, 19% of the cells in the HFD group, and 38% of all the cells in the D+H group. Adipocyte proliferation in the D+H group was inhibited by DEX treatment. Adipocyte enlargement in the D+H group was associated with increased the lipid accumulation but not the adipocyte proliferation. In contrast, the liver triglyceride and total cholesterol levels and their metabolism were downregulated by the same treatment, indicating the therapeutic potential of DEX for nonalcoholic fatty liver disease., Conclusion: DEX synergizes with HFD to promote lipid deposition in adipose tissues. A high risk of obesity development in patients receiving HFD and DEX treatment is suggested.

Background/aim: Depression is associated with metabolic disorders, including non-alcoholic fatty liver disease (NAFLD). However, the mechanisms underlying the interaction between them are still poorly known., Materials and Methods: In this study, mice on a choline deficiency, L-amino acid-defined, high-fat diet (CDAHFD) developing steatosis were challenged with chronic restraint stress (CRS), a protocol widely used to induce depression. The development of depression and steatosis was evaluated using histopathology analysis, ELISA, q-PCR and Western Blot., Results: The contribution of the activated HPA axis to hepatic steatosis progress was fully established, which was validated using a hepatocyte model. Histopathological and biochemical analysis indicated that steatosis was exacerbated by CRS challenge, and behavioral tests indicated that the mice developed depression. Among the screened endocrinal pathways, the hypothalamic-pituitary-adrenal (HPA) axis was significantly activated and the synergistic effect of CDAHFD and CRS in activating the HPA axis was observed. In the hypothalamus, expression of corticotropin-releasing hormone (CRH) was increased by 86% and the protein levels of hypothalamic CRH were upregulated by 25% to 33% by CRS treatment. Plasma CRH levels were elevated by 45-56% and plasma adrenocorticotropic hormone (ACTH) levels were elevated by 29-58% by CRS treatment. In the liver, target genes of the HPA axis were activated, accompanied by disruption of the lipid metabolism and progression of steatohepatitis. The lipid metabolism in the Hepa1-6 cell line treated with endogenous corticosterone (CORT) was in accordance with the aforementioned in vivo responses., Conclusion: Depression aggravated hepatic steatosis in CDAHFD-fed mice by activating the HPA axis. The risk of NAFLD development should be fully considered in depressive patients and improvement of psychotic disorders could be an etiological treatment strategy for them., (Copyright © 2024, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Objective: To analyze the clinical effect of high-flow nasal cannula (HFNC) oxygen therapy combined with naloxone on severe respiratory failure (SRF) in older adult patients., Methods: We enrolled 96 older adult patients with SRF who were admitted to Hai'an People's Hospital between February 2019 and March 2022. The patients were divided into two groups: the control group (treated with non-invasive positive pressure ventilation combined with naloxone) and the observation group (treated with HFNC oxygen therapy combined with naloxone). The blood gas measurement, respiratory rate (RR), St. George's Respiratory Questionnaire (SGRQ) score, Clara cell secreted protein (CC16) level, tumor necrosis factor-alpha (TNF-α) level, interleukin-1 (IL-1) level, length of intensive care unit (ICU) stay, tracheal intubation rate, and 28-day mortality rate were compared between the groups., Results: Blood gas measurement or RR did not differ significantly between the groups ( P >0.05). The observation group showed improved outcome, including reduced partial pressure of CO 2 , RR, and pH, and increased partial pressure of O 2 (PaO 2 ), PaO 2 /fraction of inspired O 2 ratio, and O 2 saturation after treatment ( P <0.05). Additionally, the observation group exhibited lower TNF-α level, IL-1 level, and SGRQ score, and higher CC16 level ( P <0.05). The length of ICU stay, tracheal intubation rate, and 28-day mortality rate were lower in the observation group ( P <0.05)., Conclusions: HFNC oxygen therapy combined with naloxone in older adult patients with SRF could improve blood gas results, disease duration, tracheal intubation rate, and 28-day mortality rate. This may occur through regulation of TNF-α, IL-1, and CC16 expression., Competing Interests: None., (AJTR Copyright © 2023.)

Platelet hyperreactivity and increased atherothrombotic risk are specifically associated with dyslipidemia. Peroxisome proliferator-activated receptor alpha (PPARα) is an important regulator of lipid metabolism. It has been suggested to affect both thrombosis and hemostasis, yet the underlying mechanisms are not well understood. In this study, the role and mechanism of PPARα in platelet activation and thrombosis related to dyslipidemia were examined. Employing mice with deletion of PPARα (Pparα-/-), we demonstrated that PPARa is required for platelet activation and thrombus formation. The effect of PPARα is critically dependent on platelet dense granule secretion, and is contributed by p38MAPK/Akt, fatty acid b-oxidation, and NAD(P)H oxidase pathways. Importantly, PPARα and the associated pathways mediated a prothrombotic state induced by a high-fat diet and platelet hyperactivity provoked by oxidized low density lipoproteins. Platelet reactivity was positively correlated with the levels of expression of PPARα, as revealed by data from wild-type, chimeric (Pparα+/-), and Pparα-/- mice. This positive correlation was recapitulated in platelets from hyperlipidemic patients. In a lipid-treated megakaryocytic cell line, the lipid-induced reactive oxygen species-NF-kB pathway was revealed to upregulate platelet PPARα in hyperlipidemia. These data suggest that platelet PPARα critically mediates platelet activation and contributes to the prothrombotic status under hyperlipidemia.

Background: VGF (nonacryonimic) and phosphatidylinositol 3-kinase (PI3K)/AKT (also known as protein kinase B, PKB)/mammalian target of rapamycin (mTOR) signaling play pivotal roles in depression. However, whether phosphatidylinositol 3-kinase/AKT/mTOR signaling-mediated VGF participates in rapid-acting antidepressant-like actions of GLYX-13 is unclear., Methods: Herein, we evaluated the effects of acute treatment of GLYX-13 (0.5, 5, and 10mg/kg, i.p.) in the forced swim test. In addition, we assessed whether the acute treatment with GLYX-13 reverses the depressive-like behaviors induced by chronic unpredictable mild stress. Furthermore, we determined whether the Vgf knockdown in hippocampus of mice blocks the effects of GLYX-13. Moreover, we also demonstrated the effects of intra-hippocampus infusion of LY294002 (10 nmol/side), a specific phosphatidylinositol 3-kinase inhibitor prior to the treatment of GLYX-13 in the forced swim test. Lastly, whether alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor and mTOR activation involves in the antidepressant-like effects of GLYX-13 was examined., Results: Our results shown that GLYX-13 dose-dependently reversed the depressive-like behaviors in forced swim test. Additionally, GLYX-13 significantly reversed the downregulation of phosphorylation of AKT, mTOR, and eukaryotic elongation factor 2 as well as VGF induced by chronic unpredictable mild stress in hippocampus. Further, Vgf knockdown in hippocampus of mice significantly blocked the rapid-acting antidepressant-like effects and upregulation on phosphatidylinositol 3-kinase/AKT/mTOR/VGF signaling of GLYX-13. Moreover, intra-hippocampus infusion of LY294002 significantly abolished the antidepressant-like effects and upregulation on phosphatidylinositol 3-kinase/AKT/mTOR/VGF signaling of GLYX-13. Finally, antidepressant-like effects of GLYX-13 required AMPA receptor and mTOR activation, as evidenced by the ability of NBQX and rapamycin to block the effects of GLYX-13, respectively., Conclusions: Our results suggest that phosphatidylinositol 3-kinase/AKT/mTOR signaling-mediated VGF in hippocampus may be involved in the antidepressant-like effects of GLYX-13., (© The Author 2015. Published by Oxford University Press on behalf of CINP.)