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Fatty acids from cooking fumes and hypochlorous acid (HOCl) released from indoor cleaning adversely affect respiratory health, but the molecular-level mechanism remains unclear. Here, the effect of cooking oil fumes [palmitic acid (PA), oleic acid (OA), and linoleic acid (LA)] on lung model phospholipid (POPG) hydrochlorination mediated by HOCl at the air–water interface of the hanged droplets was investigated. Interfacial hydrochlorination of POPG was impeded by OA and LA, while that of POPG was facilitated by PA. The effect on POPG hydrochlorination increased with the decrease in oil fume concentration. A potential mechanism with respect to the chain length of these oil fumes, regardless of their saturation, was proposed. PA with a short carbon chain looses the POPG packing and leads to the exposure of the C=C double bonds of POPG, whereas OA and LA with a long carbon chain hinder HOCl from reaching the C=C bonds of POPG. These results for short chain and low concentration dependence suggest that the decay of oil fumes or the conversion of short-chain species by indoor interfacial chemistry might be adverse to lung health. These results provide insights into the relationship between indoor multicomponent pollutants and the respiratory system. [ABSTRACT FROM AUTHOR]

In this paper, the influencing factors of environmental population capacity are categorized into three types: strict constraints, elastic constraints and non-constraints, and the systematic relationship among the three types of factors is explored, from single-factor environmental population capacity model to multifactor environmental population capacity model, and finally to obtain the regional environmental population capacity model. In this paper, we choose to take Hainan Island in China and the island of Ireland, which have similar natural conditions (area, population, etc.), as examples to measure the environmental population capacity based on the island. From the perspective of environmental capacity, this paper explores how to make the global distribution of population settlements more in line with the distribution of environment and resources, and then puts forward more effective and reliable suggestions for the coordinated development of population and economic and social resources and environment.

The primary tumor ("root") and circulating tumor cells (CTCs; "seeds") are vital factors in tumor progression. However, current treatment strategies mainly focus on inhibiting the tumor while ignoring CTCs, resulting in tumor metastasis. Here, we design a multifunctional 3D scaffold with interconnected macropores, excellent photothermal ability and perfect bioaffinity as a blood vessel implantable device. When implanted upstream of the primary tumor, the scaffold intercepts CTCs fleeing back to the primary tumor and then forms "micro-thrombi" to block the supply of nutrients and oxygen to the tumor for embolization therapy. The scaffold implanted downstream of the tumor efficiently captures and photothermally kills the CTCs that escape from the tumor, thereby preventing metastasis. Experiments using rabbits demonstrated excellent biosafety of this scaffold with 86% of the CTC scavenging rate, 99% of the tumor inhibition rate and 100% of CTC killing efficiency. The multifunctional 3D scaffold synergistically inhibits the "root" and eliminates the "seeds" of the tumor, demonstrating its potential for localized cancer therapy with few side effects and high antitumor efficacy. [ABSTRACT FROM AUTHOR]

INTRODUCTION: More robust non‐human primate models of Alzheimer's disease (AD) will provide new opportunities to better understand the pathogenesis and progression of AD. METHODS: We designed a CRISPR/Cas9 system to achieve precise genomic deletion of exon 9 in cynomolgus monkeys using two guide RNAs targeting the 3′ and 5′ intron sequences of PSEN1 exon 9. We performed biochemical, transcriptome, proteome, and biomarker analyses to characterize the cellular and molecular dysregulations of this non‐human primate model. RESULTS: We observed early changes of AD‐related pathological proteins (cerebrospinal fluid Aβ42 and phosphorylated tau) in PSEN1 mutant (ie, PSEN1‐ΔE9) monkeys. Blood transcriptome and proteome profiling revealed early changes in inflammatory and immune molecules in juvenile PSEN1‐ΔE9 cynomolgus monkeys. DISCUSSION: PSEN1 mutant cynomolgus monkeys recapitulate AD‐related pathological protein changes, and reveal early alterations in blood immune signaling. Thus, this model might mimic AD‐associated pathogenesis and has potential utility for developing early diagnostic and therapeutic interventions. Highlights: A dual‐guide CRISPR/Cas9 system successfully mimics AD PSEN1‐ΔE9 mutation by genomic excision of exon 9.PSEN1 mutant cynomolgus monkey‐derived fibroblasts exhibit disrupted PSEN1 endoproteolysis and increased Aβ secretion.Blood transcriptome and proteome profiling implicate early inflammatory and immune molecular dysregulation in juvenile PSEN1 mutant cynomolgus monkeys.Cerebrospinal fluid from juvenile PSEN1 mutant monkeys recapitulates early changes of AD‐related pathological proteins (increased Aβ42 and phosphorylated tau). [ABSTRACT FROM AUTHOR]