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Background This study sampled Chinese families of children with acute leukemia to assess their levels of anxiety and explore whether those levels were associated with social support levels and coping style. The study also aimed to identify demographic factors influencing anxiety, social support and coping style. Methods A purposive sample of 223 families whose children were being treated for acute leukemia at West China Second University Hospital, Sichuan University completed a questionnaire to provide basic demographic information as well as the Self-Rating Anxiety Scale, Social Support Rating Scale, and Simplified Coping Style Questionnaire. Categorical data were reported as n (%), while continuous data were reported as mean ± standard deviation if normally distributed or as median (interquartile range) if skewed. the Kruskal-Wallis or Wilcoxon rank sum test, Bonferroni correction for multiple comparisons, Pearson correlation analysis or Spearman correlation analysis were used for data analysis. Results The score of anxiety in our sample was 36.80 ± 9.05 points and 33.6% of family members exhibited clinically significant symptoms of anxiety; anxiety level was significantly higher in family members whose affected children had no siblings ( P  < 0.05). The score of social support was 42.86 ± 7.80 points. Objective social support level was significantly higher for families living in urban areas than rural areas ( P  < 0.05), and it correlated positively with monthly household income (B = 2.176, P  = 0.009). The score of coping style was 50.23 ± 10.04 points. Coping style score was significantly higher for family members in urban areas, with more education, or with higher monthly household income. It also correlated positively with overall social support score. Conclusions Our results suggest that many families of children with acute leukemia suffer clinically significant anxiety. Families from rural areas and those with lower income have relatively poor social support and coping abilities. Additionally, levels of education is related to their coping abilities, and they can benefit from education and psychological support.

Accurate monitoring of atmospheric carbon dioxide (CO2) is critical for addressing climate change, as CO2 is one of the dominant greenhouse gases. Satellite remote sensing remains the primary method for monitoring column-averaged CO2 (XCO2), yet different satellite missions and retrieval algorithms generate distinct XCO2 products. Thus, recommendations for selecting appropriate XCO2 products remain unclear due to a lack of systematic evaluation of XCO2 products. Here, we present a comprehensive evaluation of eleven XCO2 products from major satellite missions—including the Environmental Satellite (Envisat), Greenhouse Gases Observing Satellite (GOSAT/GOSAT-2), Orbiting Carbon Observatories (OCO-2/OCO-3), and TanSat—alongside one ensemble product based on the ensemble median algorithm (EMMA). We assess their spatiotemporal coverage and performance using Total Carbon Column Observing Network (TCCON) measurements as reference, evaluating both at global and regional scales across seasons. Our results reveal distinct latitudinal and seasonal variations in the evaluation results. Most products show the highest accuracy at 60–80°N in summer (optimal root mean square error < 1.0 ppm), while the largest uncertainties appear in the tropics (20°S–20°N; root mean square error > 2 ppm). Furthermore, systematic biases are most pronounced during winter, with mean absolute error increasing by 0.3–1.0 ppm compared to other seasons. Among the twelve satellite XCO2 products, the Atmospheric CO2 Observations from Space-Orbiting Carbon Observatory-2 (ACOS-OCO-2) product shows the best overall performance globally. These results provide practical guidelines for the informed selection and application of satellite-derived XCO2 products in climate research.

PurposeMicroRNAs (miRNAs) participate in a variety of biological processes, including tumorigenesis, progression, invasion, and drug resistance to multiple cancers. Phosphatase and tensin homolog (PTEN) is a cancer suppressor gene that has been certified to be regulated by miRNAs in various tumors, including colorectal cancer (CRC). In this review, we screened articles focusing on low PTEN expression in CRC, observed the expression of related miRNAs, analyzed their correlation and relationship with clinicopathological features, and discussed the possibility of these miRNAs as prognostic molecules.MethodsWe conducted a systematic search for articles published in the Web of Science, PubMed and EBSCO databases between January 1, 2002, and July 18, 2019. We identified these studies by using combinations of the following index entries and key words: ‘colorectal tumor OR colorectal neoplasm OR colorectal carcinoma OR colorectal cancer OR CRC’, ‘protein tyrosine phosphatase OR PTEN’, and ‘microRNA OR MiRNA OR miRNA OR MicroRNA’. Moreover, we evaluated the underlying association between alterations in PTEN and CRC prognosis.ResultsPTEN expression was obviously lower in CRC tissues than in normal mucosa. However, PTEN expression did not differ significantly between adenoma and normal tissues. PTEN tends to be negatively associated with tumor size and metastasis. MiR-21, miR-200a, miR-543, miR-32, miR-92a, miR-26a, miR-106a and miR-181a were correlated with the downregulation of PTEN. MiR-26a, miR-106a and miR-181a were obviously higher in CRC tissues than in normal tissues, while PTEN was downregulated in CRC tissues. Additionally, miRNAs were mainly positively correlated with distant metastasis, followed by TNM stage. The relationship between miRNAs and tumor differentiation is controversial. However, there were no significant differences between miRNAs and either sex or age.ConclusionsThe loss of PTEN may be a diagnostic factor for CRC patients. The above-mentioned miRNAs may function as oncogenes in CRC and represent potential targets for CRC therapy. However, further prospective clinical studies are necessary.

Ozone pollution in densely populated urban regions poses a great threat to public health, due to the intensive anthropogenic emissions of ozone precursors and is further aggravated by global warming and the urban heat island phenomenon. Air quality models have been utilized to formulate and evaluate air pollution control strategies. This study presents a comprehensive modeling assessment of ozone mitigation strategies during an ozone pollution episode in Changzhou, an industrial city in the Yangtze River Delta region. Utilizing the Community Multiscale Air Quality Modeling System (CMAQ), we quantified the contribution of ozone from different emission sectors and counties within Changzhou using the integrated source apportionment method (ISAM). During the pollution period, local emissions within Changzhou account for an average of 41.5% of MDA8 ozone, with particularly notable contributions from Jingkai (11.2%), Wujin (9.5%), and Liyang (7.8%). Upon these findings, we evaluated three sets of emission reduction scenarios: uniform, sector-specific, and county-specific reductions. Results show that industry and transportation are responsible for over 20% of ozone concentrations, and targeted reductions in these sources yielded the most significant decreases in ozone levels. Notably, reducing industrial emissions alone decreased ozone concentrations by 3.2 μg m−3 during the pollution episode. County-specific reductions revealed the importance of targeted strategies, with certain counties showing more pronounced responses to emission controls. On a daily basis, emission reductions in Xinbei contributed to a maximum ozone decrease of 4.4 μg m−3. This study provides valuable insights into the efficacy of different mitigation measures in Changzhou and offers a practical and useful framework for policymakers to implement strategies while addressing the complexities of urban air quality management.

Background Some natural compounds inhibit cancer cell growth in various cancer cell lines with fewer side effects than traditional chemotherapy. Here, we explore the pharmacological effects and mechanisms of worenine (isolated from Coptis chinensis ) against colorectal cancer. Methods The effects of worenine on colorectal cancer cell proliferation, colony formation and cell cycle distribution were measured. Glycolysis was investigated by examining glucose uptake and consumption, lactate production, and the activities and expressions of glycolysis enzymes (PFK-L, HK2 and PKM2). HIF-1α was knocked down and stimulated in vitro to investigate the underlying mechanisms. Results Worenine somewhat altered the glucose metabolism and glycolysis (Warburg effect) of cancer cells. Its anti-cancer effects and capability to reverse the Warburg effect were similar to those of HIF-1α siRNA and weakened by deferoxamine (an HIF-1α agonist). Conclusion It is suggested that worenine targets HIF-1α to inhibit colorectal cancer cell growth, proliferation, cell cycle progression and the Warburg effect.

In order to clarify the causes of variability among the model outputs for surface ozone in the Model Intercomparison Study Asia Phase III (MICS-Asia III), three regional models, CMAQ v.5.0.2, CMAQ v.4.7.1, and NAQPMS (abbreviated as NAQM in this paper), have been selected. Detailed analyses of monthly averaged diurnal variation have been performed for selected grids covering the metropolitan areas of Beijing and Tokyo and at a remote oceanic site, Oki. The chemical reaction mechanism, SAPRC99, used in the CMAQ models tended to give a higher net chemical ozone production than CBM-Z used in NAQM, agreeing with previous studies. Inclusion of the heterogeneous “renoxification” reaction of HNO3 (on soot surface)→NO+NO2 only in NAQM would give a higher NO concentration resulting in a better agreement with observational data for NO and nighttime O3 mixing ratios. In addition to chemical processes, the difference in the vertical transport of O3 was found to affect the simulated results significantly. Particularly, the increase in downward O3 flux from the upper layer to the surface after dawn was found to be substantially different among the models. Larger early morning vertical transport of O3 simulated by CMAQ 5.0.2 is thought to be the reason for higher daytime O3 in July in this model. All three models overestimated the daytime ozone by ca. 20 ppbv at the remote site Oki in July, where in situ photochemical activity is minimal.

This study uses multi-model ensemble results of 11 models from the second phase of Task Force Hemispheric Transport of Air Pollution (HTAP II) to calculate the global sulfur (S) and nitrogen (N) deposition in 2010. Modeled wet deposition is evaluated with observation networks in North America, Europe and East Asia. The modeled results agree well with observations, with 76–83 % of stations being predicted within ±50 % of observations. The models underestimate SO42-, NO3- and NH4+ wet depositions in some European and East Asian stations but overestimate NO3- wet deposition in the eastern United States. Intercomparison with previous projects (PhotoComp, ACCMIP and HTAP I) shows that HTPA II has considerably improved the estimation of deposition at European and East Asian stations. Modeled dry deposition is generally higher than the “inferential” data calculated by observed concentration and modeled velocity in North America, but the inferential data have high uncertainty, too. The global S deposition is 84 Tg(S) in 2010, with 49 % in continental regions and 51 % in the ocean (19 % of which coastal). The global N deposition consists of 59 Tg(N) oxidized nitrogen (NOy) deposition and 64 Tg(N) reduced nitrogen (NHx) deposition in 2010. About 65 % of N is deposited in continental regions, and 35 % in the ocean (15 % of which coastal). The estimated outflow of pollution from land to ocean is about 4 Tg(S) for S deposition and 18 Tg(N) for N deposition. Comparing our results to the results in 2001 from HTAP I, we find that the global distributions of S and N deposition have changed considerably during the last 10 years. The global S deposition decreases 2 Tg(S) (3 %) from 2001 to 2010, with significant decreases in Europe (5 Tg(S) and 55 %), North America (3 Tg(S) and 29 %) and Russia (2 Tg(S) and 26 %), and increases in South Asia (2 Tg(S) and 42 %) and the Middle East (1 Tg(S) and 44 %). The global N deposition increases by 7 Tg(N) (6 %), mainly contributed by South Asia (5 Tg(N) and 39 %), East Asia (4 Tg(N) and 21 %) and Southeast Asia (2 Tg(N) and 21 %). The NHx deposition increases with no control policy on NH3 emission in North America. On the other hand, NOy deposition has started to dominate in East Asia (especially China) due to boosted NOx emission.

Background Shen-Bai-Jie-Du decoction (SBJDD), a traditional Chinese herb formula developed based on evidence-based medicine, is efficacy to reduce the recurrence and carcinogenesis of colorectal adenoma. However, the mechanism of SBJDD to treat colorectal adenoma remains unclear. The present study aims to investigate the efficacy and mechanism of SBJDD on colorectal adenoma carcinogenesis from the aspects of regulating gut microbiota and short-chain fatty acids (SCFAs). Methods Twenty-one patients diagnosed with colorectal adenoma were recruited in the study and required to take SBJDD for four consecutive weeks. Analysis of gut microbiota was conducted using 16S rRNA gene amplicon sequencing, while levels of SCFAs in fecal and serum samples were determined through HPLC–MS/MS. Additionally, twenty-four Apc min/+ mice were randomly assigned to normal diet (ND), high-fat diet (HFD), and SBJDD groups. The pharmacological effects and mechanism of SBJDD on colorectal adenoma carcinogenesis were assessed using RT-qPCR, HE staining, IHC staining, Western blot, IF staining, and Flow cytometry assays. Results Our clinical study has shown that SBJDD can regulate the gut microbiota composition and enhance SCFAs production in patients with colorectal adenoma. SBJDD alleviated colorectal adenoma formation and carcinogenesis, as well as protected the integrity of the intestinal barrier in the Apc min/+ mice model compared to the HFD group. Additionally, SBJDD was found to regulate gut microbiota capable of producing SCFAs. G protein-coupled receptors GPR43, GPR41, and GPR109a were effectively activated in the SBJDD group, while HDAC1 and HDAC3 were inhibited. Furthermore, decreased expression levels of interleukin 1 beta (IL-1β) and interleukin 6 (IL-6), along with elevated expression level of interleukin 10 (IL-10), were observed in the colorectal tissue of the SBJDD group. Finally, SBJDD exhibited the ability to reduce the proportion of M1-type macrophages while increasing the proportion of M2-type macrophages. Conclusions Our study objectively demonstrated the pharmacological effects of SBJDD in inhibiting the progression of colorectal adenoma and investigated its mechanisms in terms of regulating gut microbiota, increasing SCFAs, and reducing colorectal inflammation.

Colorectal cancer (CRC) is the third most common malignancy in terms of global tumor incidence, and the rates of morbidity and mortality due to CRC are rising. Experimental models of CRC play a vital role in CRC research. Clinical studies aimed at investigating the evolution and mechanism underlying the formation of CRC are based on cellular and animal models with broad applications. The present review classifies the different experimental models used in CRC research, and describes the characteristics and limitations of these models by comparing the research models with the clinical symptoms. The review also discusses the future prospects of developing new experimental models of CRC.