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Urban agriculture (UA) has been adopted as a strategy for food security in urban areas. This study identified the conditions for development of UA through a systematic review of UA case studies. It classified the enabling and constraining conditions within the three compositional elements of UA – necessity, ability, and opportunity – and determined the primary and secondary conditions for UA design by the country income group. The following conditions are required for both high-income and low/ middle-income countries: Motivation/public awareness; labour/human resources; policy and institutional infrastructure; social capital; and arable land and resources for farming. Agricultural education/training and research and technical development are needed for low and middle-income countries as the key secondary conditions. In high-income countries, a lack of farmers’ knowledge and urban development are the main challenges to UA implementation. Therefore, the research findings could be meaningful evidence for making decisions and designing UA policies for sustainable food production.

The sonochemical oxidation activity was investigated for gas saturation and gas sparging under various liquid levels and volumes in 300 kHz sonoreactors. The liquid levels and volumes ranged from 5λ (25 mm, 0.47 L) to 50λ (250 mm, 4.30 L) and two gas mixtures, Ar:O2 (75:25) and N2:O2 (75:25), were used. Two types of reaction kinetics were observed to quantitatively analyze the sonochemical oxidation reactions: zero-order (KI dosimetry: C0 = 60.2 mM) and first-order (Bisphenol A (BPA) degradation: C0 = 0.043 mM). The masses of the sonochemical oxidation reactions were calculated and compared rather than the concentrations to more accurately compare the sonochemical oxidation activity under different liquid volume conditions. First, as the liquid level or volume increased for the zero-order reactions, the concentration of I3- ions representing the volume-averaged activity decreased substantially for gas saturation owing to the increase in liquid volume. However, gas sparging substantially enhanced sonochemical oxidation activity, and the mass of I3- ions representing the total activity remained constant as the liquid level increased from 20λ because of the improved liquid mixing and a shift in the sonochemical active zone. Second, as evidenced by the zero-order reactions, the concentration of BPA decreased considerably as the liquid level or volume increased in the first-order reactions. When gas sparging was used, higher reaction constants were obtained for both gas mixtures, ranging from 40λ to 50λ. However, a comparison of the sonochemical oxidation activity in terms of the degraded mass of BPA was inapplicable as the concentration of BPA decreased substantially and a lack of reactants occurred for the lower liquid level and volume conditions as the irradiation time elapsed. Instead, using the first-order reaction constant, a comparison of the required reaction times for a specific removal efficiency (30%, 60%, and 90%) was proposed. Gas sparging can substantially reduce the reaction time required for a liquid level of 40λ or higher.

This study examined forest policy agendas developed in international policy-making process by analyzing international forest policy documents from 2001 to 2022 with power, perception, potency, and proximity. The forest policy agendas consistently addressed in the documents were agroforestry, biodiversity, climate change, certification, desertification, deforestation, forest landscape restoration, illegal logging and trade, non-timber forest products, sustainable forest management, traditional knowledge, governance, participation, partnerships, forest tenure, forest fire, forest disease, and community-based forest management. The emerging agendas since 2011 were ecosystem services, reducing emissions from deforestation and forest degradation plus (REDD+), resilience, urban forests, green economy/bioeconomy, and COVID-19. The changes in international forest policy discourse with long-standing and emerging agendas over time showed three characteristics: policy coherence by the power of international environmental conventions; expansion of forest policy targets and areas by perception and proximity of urban forests; and innovative approaches to resilience and bioeconomy by potency and perception. Therefore, this study offers new insights into the creation and transitions of forest policy agendas in the international forest policy discourse.

TUBB3 is a structural neuronal protein important for multiple neuronal functions including axonal guidance and maturation. This study aimed to generate a human pluripotent stem cell (hPSC) line with a TUBB3-mCherry reporter using CRISPR/SpCas9 nuclease. The stop codon in the last exon of TUBB3 was replaced with a T2A-mCherry cassette using CRISPR/SpCas9-mediated homologous recombination. The established TUBB3-mCherry knock-in cell line exhibited typical pluripotent characteristics. The mCherry reporter faithfully replicated the endogenous level of TUBB3 upon induction of neuronal differentiation. The reporter cell line could contribute to the investigation of neuronal differentiation, neuronal toxicity, and neuronal tracing.

BACKGROUND:The BRAF(V600E) mutation leading to constitutive signaling of MEK-ERK pathways causes papillary thyroid cancer (PTC). Ras association domain family 1A (RASSF1A), which is an important regulator of MST1 tumor suppressor pathways, is inactivated by hypermethylation of its promoter region in 20 to 32% of PTC. However, in PTC without RASSF1A methylation, the regulatory mechanisms of RASSF1A-MST1 pathways remain to be elucidated, and the functional cooperation or cross regulation between BRAF(V600E) and MST1,which activates Foxo3,has not been investigated. METHODOLOGY/PRINCIPAL FINDINGS:The negative regulators of the cell cycle, p21 and p27, are strongly induced by transcriptional activation of FoxO3 in BRAF(V600E) positive thyroid cancer cells. The FoxO3 transactivation is augmented by RASSF1A and the MST1 signaling pathway. Interestingly, introduction of BRAF(V600E)markedly abolished FoxO3 transactivation and resulted in the suppression of p21 and p27 expression. The suppression of FoxO3 transactivation by BRAF(V600E)is strongly increased by coexpression of MST1 but it is not observed in the cells in which MST1, but not MST2,is silenced. Mechanistically, BRAF(V600E)was able to bind to the C-terminal region of MST1 and resulted in the suppression of MST1 kinase activities. The induction of the G1-checkpoint CDK inhibitors, p21 and p27,by the RASSF1A-MST1-FoxO3 pathway facilitates cellular apoptosis, whereas addition of BRAF(V600E) inhibits the apoptotic processes through the inactivation of MST1. Transgenic induction of BRAF(V600E)in the thyroid gland results in cancers resembling human papillary thyroid cancers. The development of BRAF(V600E)transgenic mice with the MST1 knockout background showed that these mice had abundant foci of poorly differentiated carcinomas and large areas without follicular architecture or colloid formation. CONCLUSIONS/SIGNIFICANCE:The results of this study revealed that the oncogenic effect of BRAF(V600E) is associated with the inhibition of MST1 tumor suppressor pathways, and that the activity of RASSF1A-MST1-FoxO3 pathways determines the phenotypes of BRAF(V600E) tumors.

Background: The BRAFV600E mutation leading to constitutive signaling of MEK-ERK pathways causes papillary thyroid cancer (PTC). Ras association domain family 1A (RASSF1A), which is an important regulator of MST1 tumor suppressor pathways, is inactivated by hypermethylation of its promoter region in 20 to 32% of PTC. However, in PTC without RASSF1A methylation, the regulatory mechanisms of RASSF1A-MST1 pathways remain to be elucidated, and the functional cooperation or cross regulation between BRAFV600E and MST1,which activates Foxo3,has not been investigated. Methodology/Principal Findings: The negative regulators of the cell cycle, p21 and p27, are strongly induced by transcriptional activation of FoxO3 in BRAFV600E positive thyroid cancer cells. The FoxO3 transactivation is augmented by RASSF1A and the MST1 signaling pathway. Interestingly, introduction of BRAFV600Emarkedly abolished FoxO3 transactivation and resulted in the suppression of p21 and p27 expression. The suppression of FoxO3 transactivation by BRAFV600Eis strongly increased by coexpression of MST1 but it is not observed in the cells in which MST1, but not MST2,is silenced. Mechanistically, BRAFV600Ewas able to bind to the C-terminal region of MST1 and resulted in the suppression of MST1 kinase activities. The induction of the G1-checkpoint CDK inhibitors, p21 and p27,by the RASSF1A-MST1-FoxO3 pathway facilitates cellular apoptosis, whereasaddition of BRAFV600E inhibits the apoptotic processes through the inactivation of MST1. Transgenic induction of BRAFV600Ein the thyroid gland results in cancers resembling human papillary thyroid cancers. The development of BRAFV600Etransgenic mice with the MST1 knockout background showed that these mice had abundant foci of poorly differentiated carcinomas and large areas without follicular architecture or colloid formation. Conclusions/Significance: The results of this study revealed that the oncogenic effect of BRAFV600E is associated with the inhibition of MST1 tumor suppressor pathways, and that the activity of RASSF1A-MST1-FoxO3 pathways determines the phenotypes of BRAFV600E tumors. [ABSTRACT FROM AUTHOR]

Camptothecin, a topoisomerase I inhibitor, is a well-known anticancer drug. However, its mechanism has not been well studied in human gastric cancer cell lines. Camptothecin induced apoptotic cell death in human gastric cancer cell line AGS. Z-VAD-fmk, pancaspase inhibitor, blocked apoptotic phenotypes induced by camptothecin suggesting that caspases are involved in camptothecin-induced cell death. An inhibitor of caspase-6 or -8 or -9 did not prevent cell death by campothecin. Various protease inhibitors failed to prevent camptothecin-induced cell death. These results suggest that only few caspases are involved in camptothecin-induced cell death. Camptothecin induced phosphorylation of ERK1/2, JNK, and p38 MAPK, in a dose and time-dependent manner in AGS. Z-VAD-fmk did not affect MAPK signaling induced by camptothecin suggesting that caspase signaling occurs downstream of MAPK signaling. Blocking of p38 MAPK, but not ERK1/2, resulted in partial inhibition of cell death and PARP cleavage by camptothecin in AGS. Taken together, MAPK signaling is associated with apoptotic cell death by camptothecin. [ABSTRACT FROM AUTHOR]

Trichostatin A (TSA) is an inhibitor of histone deacetylase. cDNA microarray analysis was used to identify genes modulated by TSA. A total of 93 genes were up-regulated and 27 genes down-regulated. The expressions of some of these genes were confirmed by RT-PCR analysis. [ABSTRACT FROM AUTHOR]