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OBJECTIVES: We examined the expression of Lnc-ZFAS1 in osteosarcoma and comprehensively evaluated its effects on osteosarcoma in vitro and vivo. Moreover, we revealed the regulatory mechanism between Lnc-ZFAS1 and miR-520b/miR-520e-mediated RHOC and provided a novel clue for ameliorating osteosarcoma. METHOD: The expression of Long non-coding RNA Zinc Finger Antisense 1 (LncRNA ZFAS1) osteosarcoma tissues and normal tissues in the TCGA database was analyzed. Then, LncRNA ZFAS1 expression was further verified in clinical samples and osteosarcoma cell lines (U2OS and KHOS), as well as the human osteoblast cell line hFOB1.19 by qRT-PCR. Thereafter, LncRNA ZFAS1 was overexpressed or silenced to explore its effects on cell proliferation, apoptosis, migration, invasion, and Epithelial-Mesenchymal Transition (EMT). The fundamental mechanism through which Lnc-ZFAS1 affects osteosarcoma progression was further investigated and verified. RESULTS: We found that LncRNA ZFAS1 was upregulated in osteosarcoma, and Lnc-ZFAS1 overexpression facilitated osteosarcoma cells proliferation, migration, invasion and EMT, while Lnc-ZFAS1 silence exerted reverse influence. Mechanistically, Lnc-ZFAS1 functionally acted as a sponger of microRNA-520b (miR-520b) and microRNA-520e (miR-520e) to up-regulate Ras Homologue C (RHOC). In addition, depleted Lnc-ZFAS1 restrained osteosarcoma cells proliferation, migration, and invasion, which could be rescued by RHOC overexpression. Lnc-ZFAS1 was upregulated in osteosarcoma and Lnc-ZFAS1 could exert promoted impact upon osteosarcoma cells proliferation, migration, invasion, and EMT in vitro. CONCLUSIONS: Lnc-ZFAS1 acted sponger of miR-520b and miR-520e to promote RHOC, indicating that Lnc-ZFAS1/miR-520b/RHOC and Lnc-ZFAS1/miR-520e/RHOC axes might serve as potential therapeutic strategies against osteosarcoma.

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ABSTRACT Objectives: We examined the expression of Lnc-ZFAS1 in osteosarcoma and comprehensively evaluated its effects on osteosarcoma in vitro and vivo. Moreover, we revealed the regulatory mechanism between Lnc-ZFAS1 and miR-520b/miR-520e-mediated RHOC and provided a novel clue for ameliorating osteosarcoma. Method: The expression of Long non-coding RNA Zinc Finger Antisense 1 (LncRNA ZFAS1) osteosarcoma tissues and normal tissues in the TCGA database was analyzed. Then, LncRNA ZFAS1 expression was further verified in clinical samples and osteosarcoma cell lines (U2OS and KHOS), as well as the human osteoblast cell line hFOB1.19 by qRT-PCR. Thereafter, LncRNA ZFAS1 was overexpressed or silenced to explore its effects on cell proliferation, apoptosis, migration, invasion, and Epithelial-Mesenchymal Transition (EMT). The fundamental mechanism through which Lnc-ZFAS1 affects osteosarcoma progression was further investigated and verified. Results: We found that LncRNA ZFAS1 was upregulated in osteosarcoma, and Lnc-ZFAS1 overexpression facilitated osteosarcoma cells proliferation, migration, invasion and EMT, while Lnc-ZFAS1 silence exerted reverse influence. Mechanistically, Lnc-ZFAS1 functionally acted as a sponger of microRNA-520b (miR-520b) and micro-RNA-520e (miR-520e) to up-regulate Ras Homologue C (RHOC). In addition, depleted Lnc-ZFAS1 restrained osteosarcoma cells proliferation, migration, and invasion, which could be rescued by RHOC overexpression. Lnc-ZFAS1 was upregulated in osteosarcoma and Lnc-ZFAS1 could exert promoted impact upon osteosarcoma cells proliferation, migration, invasion, and EMT in vitro. Conclusions: Lnc-ZFAS1 acted sponger of miR-520b and miR-520e to promote RHOC, indicating that Lnc-ZFAS1/miR-520b/RHOC and Lnc-ZFAS1/miR-520e/RHOC axes might serve as potential therapeutic strategies against osteosarcoma.

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OBJECTIVE: To evaluate the relationship between ambient air pollutants and chronic obstructive pulmonary disease in relatively low-polluted areas in China. METHODS: Atmospheric pollutants levels and meteorological data were obtained from January 2016 to December 2020. The medical database including daily hospital admissions for chronic obstructive pulmonary disease (ICD10: J44) was derived from the First Affiliated Hospital of Gannan Medical University. The generalized additive model was used to analyze the percentage change with 95% confidence interval in daily hospital admissions for chronic obstructive pulmonary disease associated with a 10 µg/m3 increase in atmospheric pollutants levels. RESULTS: In total, occurred 4,980 chronic obstructive pulmonary disease hospital admissions (not including emergency department visits) during 2016-2020. The mean concentrations of daily PM2.5, PM10, SO2, NO2, O3, and CO were 37.5 µg/m3, 60.1 µg/m3, 18.7 µg/m3, 23.5 µg/m3, 70.0 µg/m3, and 1.2 mg/m3 in Ganzhou. Each 10 µg/m3 increment of PM2.5, PM10, NO2, and O3 were significantly associated with 2.8% (95%CI: 1.0-4.7), 1.3% (95%CI: 0.3-2.4), 2.8% (95%CI: 0.4-5.4), and 1.5% (95%CI: 0.2-2.7) elevation in daily chronic obstructive pulmonary disease hospital admissions. The estimates of delayed effects of PM2.5, PM10, NO2, and O3 were observed at lag6, lag6, lag8, lag1, respectively. The health effects of particulate pollutants (PM2.5 and PM10) may be independent of other pollutants. The adverse effects of air pollutants were more evident in the warm season (May-Oct) than in the cold season (Nov-Apr). CONCLUSION: Our study demonstrated that elevated concentrations of atmospheric pollutant (PM2.5, PM10, NO2, and O3), especially particulate pollutants, can be associated with increased daily count of hospital admissions for chronic obstructive pulmonary disease , which may promote further understanding of the potential hazards of relatively low levels of air pollution on chronic obstructive pulmonary disease and other respiratory disorders.

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ABSTRACT OBJECTIVE To evaluate the relationship between ambient air pollutants and chronic obstructive pulmonary disease in relatively low-polluted areas in China. METHODS Atmospheric pollutants levels and meteorological data were obtained from January 2016 to December 2020. The medical database including daily hospital admissions for chronic obstructive pulmonary disease (ICD10: J44) was derived from the First Affiliated Hospital of Gannan Medical University. The generalized additive model was used to analyze the percentage change with 95% confidence interval in daily hospital admissions for chronic obstructive pulmonary disease associated with a 10 µg/m3 increase in atmospheric pollutants levels. RESULTS In total, occurred 4,980 chronic obstructive pulmonary disease hospital admissions (not including emergency department visits) during 2016-2020. The mean concentrations of daily PM2.5, PM10, SO2, NO2, O3, and CO were 37.5 μg/m3, 60.1 μg/m3, 18.7 μg/m3, 23.5 μg/m3, 70.0 μg/m3, and 1.2 mg/m3 in Ganzhou. Each 10 µg/m3 increment of PM2.5, PM10, NO2, and O3 were significantly associated with 2.8% (95%CI: 1.0-4.7), 1.3% (95%CI: 0.3-2.4), 2.8% (95%CI: 0.4-5.4), and 1.5% (95%CI: 0.2-2.7) elevation in daily chronic obstructive pulmonary disease hospital admissions. The estimates of delayed effects of PM2.5, PM10, NO2, and O3 were observed at lag6, lag6, lag8, lag1, respectively. The health effects of particulate pollutants (PM2.5 and PM10) may be independent of other pollutants. The adverse effects of air pollutants were more evident in the warm season (May-Oct) than in the cold season (Nov-Apr). CONCLUSION Our study demonstrated that elevated concentrations of atmospheric pollutant (PM2.5, PM10, NO2, and O3), especially particulate pollutants, can be associated with increased daily count of hospital admissions for chronic obstructive pulmonary disease , which may promote further understanding of the potential hazards of relatively low levels of air pollution on chronic obstructive pulmonary disease and other respiratory disorders.

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The mitochondrion is an organelle that plays a vital role in energy production, cytoplasmic protein degradation and cell death. Mitophagy is an autophagic procedure that specifically clears damaged mitochondria and maintains its homeostasis. Emerging evidence indicates that mitophagy is involved in many physiological processes, including cellular homeostasis, cellular differentiation and nerve protection. In this review, we describe the regulatory mechanisms of mitophagy in mammals and yeasts and highlight the recent advances relevant to its function in carcinogenesis and drug resistance. Finally, a section has been dedicated to describing the role of mitophagy in anticancer therapeutics, which is a new frontier that offers a precise and promising strategy.

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Background: Protein glutaminase specifically deamidates glutamine residue in protein and therefore significantly improves protein solubility and colloidal stability of protein solution. In order to improve its preparation efficiency, we exploited the possibility for its secretory expression mediated by twin-arginine translocation (Tat) pathway in Bacillus licheniformis. Results: The B. licheniformis genome-wide twin-arginine signal peptides were analyzed. Of which, eleven candidates were cloned for construction of expression vectors to mediate the expression of Chryseobacterium proteolyticum protein glutaminase (PGA). The signal peptide of GlmU was confirmed that it significantly mediated PGA secretion into media with the maximum activity of 0.16 U/ml in Bacillus subtilis WB600. A mutant GlmU-R, being replaced the third residue aspartic acid of GlmU twin-arginine signal peptide with arginine by site-directed mutagenesis, mediated the improved secretion of PGA with about 40% increased (0.23 U/ml). In B. licheniformis CBBD302, GlmU-R mediated PGA expression in active form with the maximum yield of 6.8 U/ml in a 25-l bioreactor. Conclusions: PGA can be produced and secreted efficiently in active form via Tat pathway of B. licheniformis, an alternative expression system for the industrial-scale production of PGA.

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We have observed that the dry-season length (DSL) has increased over southern Amazonia since 1979, primarily owing to a delay of its ending dates (dry-season end, DSE), and is accompanied by a prolonged fire season. A poleward shift of the subtropical jet over South America and an increase of local convective inhibition energy in austral winter (June-August) seem to cause the delay of the DSE in austral spring (September-November). These changes cannot be simply linked to the variability of the tropical Pacific and Atlantic Oceans. Although they show some resemblance to the effects of anthropogenic forcings reported in the literature, we cannot attribute them to this cause because of inadequate representation of these processes in the global climate models that were presented in the Intergovernmental Panel on Climate Change's Fifth Assessment Report. These models significantly underestimate the variability of the DSE and DSL and their controlling processes. Such biases imply that the future change of the DSE and DSL may be underestimated by the climate projections provided by the Intergovernmental Panel on Climate Change's Fifth Assessment Report models. Although it is not clear whether the observed increase of the DSL will continue in the future, were it to continue at half the rate of that observed, the long DSL and fire season that contributed to the 2005 drought would become the new norm by the late 21st century. The large uncertainty shown in this study highlights the need for a focused effort to better understand and simulate these changes over southern Amazonia.

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BACKGROUND: Ecuador, the smallest of the Andean countries, is located in the northwest portion of South America. The nation's 14.5 million people have a tremendous need for high quality primary care. AIMS: To describe the profound advances as well as the persistent needs in medical education in Ecuador that have occurred with globalization and with the modernization of the country. METHODS: Through an extensive search of the literature; medical school data; reports from the Ecuador Ministry of Public Health and Ministry of Education; and information from the National Secretary of Higher Education, Science, and Innovation (SENESCYT), the medical education system in Ecuador has been thoroughly examined. RESULTS: The National System of Higher Education in Ecuador has experienced significant growth over the last 20 years. As of 2009 the system boasts 19 medical schools, all of which offer the required education needed to obtain the title of Physician, but only 12 of which offer postgraduate clinical training. Of these 19 universities, nine are public, five are private and self-financed, and five are private and co-financed. Post-graduate options for medical students include: (1) Clinical specialization, (2) Higher diploma, (3) Course specialization, (4) Master's degree, and (5) PhD degree. CONCLUSION: The rapid growth of Ecuador's system of medical education has led to inevitable gaps that threaten its ability to sustain itself. Chief among these is the lack of well-trained faculty to supply its medical schools. To ensure an adequate supply of faculty exists, the creation of sufficient postgraduate, sub-specialization, and PhD training positions must be created and maintained.

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