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Climate change literacy (CCL) is recognized as a critical component in formulating and implementing effective climate change policies and actions. However, the degree of CCL among those entrusted with these very responsibilities – public officials, remains relatively unexplored. This study pioneers an investigation into the CCL of public officials in Taiwan through a national survey. Our findings indicate that while a majority of these officials are cognizant of climate change issues, their personal commitment to climate action leaves considerable room for growth. Furthermore, their general understanding of climate change, its impacts, and the necessary adaptation strategies is found wanting. A similar deficit is observed in their comprehension of the relevance of the United Nations’ Sustainable Development Goals (SDGs) to climate change. Our study, by establishing a framework for assessing CCL among public officials and providing preliminary data on the CCL of Taiwanese officials, not only fills a significant knowledge gap but also lays the groundwork for comparative studies across nations. Moreover, our findings underscore the need for governments to invest in enhancing the CCL of their personnel, thereby equipping them with the requisite knowledge and motivation to contribute effectively to global climate change mitigation and adaptation efforts. [ABSTRACT FROM AUTHOR]

Tight junctions (TJs) are the most apical components of junctional complexes in epithelial and endothelial cells. Barrier function is one of the major functions of TJ, which restricts the ions and small water-soluble molecules from passing through the paracellular pathway. Adherens junctions (AJs) play an important role in cell–cell adhesion and cell signaling. Gap junctions (GJs) are intercellular channels regulating electrical and metabolic signals between cells. It is well known that TJ integral membrane proteins, such as claudins and occludins, are the molecular building blocks responsible for TJ barrier function. However, recent studies demonstrate that proteins of other junctional complexes can influence and regulate TJ barrier function. Therefore, the crosstalk between different cell junctions represents a common means to modulate cellular activities. In this review, we will discuss the interactions among TJ, AJ, and GJ by focusing on how AJ and GJ proteins regulate TJ barrier function in different biological systems. [ABSTRACT FROM AUTHOR]

Background: Research has shown that epigenetic modification are involved the regulation of diapause in bivoltine silkworms (Bombyx mori), but it remains unclear how epigenetic modification in response to environmental signals precisely to regulate the diapause processing of bivoltine B. mori. Methods and results: In this study, the diapause terminated eggs of bivoltine B. mori, Qiufeng (QF) were divided into two groups: a QFHT group incubated at 25 °C with a natural day/night cycle to produce diapause eggs, and a QFLT group incubated at 16.5 °C in darkness to produce non-diapause eggs. On the 3rd day of the pupal stage, the total RNAs of the eggs were extracted and their N6-adenosine methylation (m6A) abundances were analyzed to explore the effects of m6A methylation on diapause in the silkworm. The results showed that 1984 m6A peaks are shared, 1563 in QFLT and 659 in QFHT. The m6A methylation level of the QFLT group was higher than that of the QFHT one in various signaling pathways. The m6A methylation rate of mevalonate kinase (MK) in the insect hormone synthesis pathway was significantly different between the two groups. The knockdown of MK by RNA interference in the pupae of QFLT resulted in females laying diapause eggs rather than non-diapause eggs after mating. Conclusions: m6A methylation involves in the diapause regulation of bivoltine B. mori by changing the expression levels of MK. This result provides a clearer image of the environmental signals on the regulation of diapause in bivoltine silkworms. [ABSTRACT FROM AUTHOR]

A total of 3 607 surface soil samples in the cultivated land of Quanzhou City were collected and analyzed. The spatial distribution of available boron content in the cultivated soil and its influencing factors were studied by u- sing the statistical analysis method. The results showed that: the content of available boron in the cultivated soil of Quanzhou City was relatively deficient on the whole. The content of available boron ranged from 0.01 to 1.90 mg ⋅ kg-1, and the average content of available boron in the soil was 0.33 mg ⋅ kg-1. The content of available boron in 79.5% of cultivated soil was at a low or very low level. The land use types, soil types, altitude, soil physical and chemical properties had different effects on the content of available boron in soil. The content of available boron in soil varied greatly, and the content of available boron in the high altitude area was significantly lower than that in the low altitude area. Boron was generally deficient in the cultivated soil in Quanzhou City, so it was necessary to apply boron fertilizer. [ABSTRACT FROM AUTHOR]

The high frequency of chemotherapy resistance is ultimately responsible for clinical relapse in acute lymphoblastic leukemia (ALL). Nevertheless, the molecular mechanism relevant to glucocorticoid (GC) resistance remains ambiguous. Quantitative real-time polymerase chain reaction and Western blot were performed to detect the expressions of paraoxonase 2 (PON2), Bcl-2 and Bax. shRNA was used to knockdown PON2 expression in SUP-B15 and REH cell. CCK-8 and flow cytometry assay were conducted to monitor the changes of proliferation and apoptosis in ALL cells. The growth of ALL REH cells in vivo was determined using transplanted tumor model. This study was designed to identify GC resistance-associated genes by means of the transcriptome chip from the public Gene Expression Omnibus database, and preliminarily investigation of dexamethasone (DEX)-resistance mechanism in ALL. We disclosed that PON2 expression was elevated in ALL patients and especially higher in DEX-resistance ALL patients. Then, cell apoptosis assay suggested that silencing of PON2 dramatically promoted in DEX-resistant ALL cells apoptosis and the activity of Caspase 3 induced by DEX administration. In xenograft tumor model, PON2 knockdown significantly reduced DEX-resistant ALL cells growth in immunodeficient mice. Collectively, inhibition of PON2 may represent a novel method to restore the sensitivity of treatment-resistant ALL to GC-induced cell death. [ABSTRACT FROM AUTHOR]