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In order to optimize the design of high-altitude sprinkling system of fire-fighting aircraft, it is necessary to establish a model reflecting the high-altitude spraying and distribution mechanism of mass fire extinguishing bags during the flight. Based on the discrete element method and the computational fluid dynamics method, a high-altitude spraying and distributing model of aircraft mass fire extinguishing bags is established, and the spraying characteristics and landing area distribution at different flight speeds and altitudes are obtained. The model is verified by experiments. The deviations between simulated landing distribution and experimental data are less than 20.0%. The research results provide a theoretical model for the development of aircraft high altitude fire extinguishing system, so as to significantly improve the fire extinguishing performance of aircraft spraying system.

ABSTRACT Root System Architecture (RSA) is a crucial plant trait that governs a plant's ability to absorb water and nutrients. In this study, we describe a mutant with nutrient‐dependent defects in root development, affecting both the primary root and lateral roots (LRs). This mutant, identified through a screen for defects in LR development, has been designated dlr1‐1. The dlr1‐1 mutant exhibits impaired LR emergence rather than defects in the LR primordium (LRP) formation, particularly under potassium (K+)‐deprivation conditions. This impairment likely stems from inhibited cell proliferation caused by the dlr1‐1 mutation. K+ deprivation specifically leads to the accumulation of salicylic acid (SA) in the dlr1‐1 mutant, consistent with the upregulation of SA biosynthesis genes. Moreover, exogenous application of SA to wild‐type plants (B73) mimics the dlr1‐1 phenotype. Conversely, treatment of the dlr1‐1 mutant with 2‐aminoindane‐2‐phosphonic acid, an SA biosynthesis inhibitor, partially restores LR emergence, indicating that elevated SA levels may be responsible for the mutant's developmental defects. MutMap analysis and allelism tests confirmed that the phenotypes of the dlr1‐1 mutant results from the loss of the Na+/H+ antiporter, ZmNHX7. Additionally, the application of NaCl exacerbates the dlr1‐1 mutant phenotype, suggesting that the root defects in dlr1‐1 mutant depend on ion homoeostasis. In conclusion, our findings demonstrate that maize DLR1/NHX7 is essential for root development under potassium deprivation. [ABSTRACT FROM AUTHOR]

In Arabidopsis, RNA editing alters more than 500 cytidines (C) to uridines (U) in mitochondrial transcripts, a process involving the family of pentatricopeptide repeat (PPR) proteins. Here, we report a previously uncharacterized mitochondrial PLS-type PPR protein, GEND2, which functions in the mitochondrial RNA editing. The T-DNA insertion in the 5'-untranslated region of GEND2, referred to as gend2-1, results in defective root development compared to wild-type (WT) plants. A comprehensive examination of mitochondrial RNA editing sites revealed a significant reduction in the gend2-1 mutant compared to WT plants, affecting six specific mitochondrial RNA editing sites, notably within the mitochondrial genes CcmFn-1, RPSL2 and ORFX. These genes encode critical components of cytochrome protein maturation pathway, mitochondrial ribosomal subunit, and twin arginine translocation subunits, respectively. Further analysis of the transcriptional profile of the gend2-1 mutant and wild type revealed a striking induction of expression in a cluster of genes associated with mitochondrial dysfunction and regulated by ANAC017, a key regulator coordinating organelle functions and stress responses. Intriguingly, the gend2-1 mutation activated an ANAC017-dependent signaling aimed at countering cell wall damage induced by cellulose synthase inhibitors, as well as an ANAC017-independent pathway that retarded root growth under normal condition. Collectively, our findings identify a novel mitochondrial PLS-type PPR protein GEND2, which participates in the editing of six specific mitochondrial RNA editing sites. Furthermore, the gend2-1 mutation triggers two distinct pathways in plants: an ANAC017-dependent pathway and ANAC017-independent pathway., (© The Author(s) 2024. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site–for further information please contact journals.permissions@oup.com.)

Objective: To explore the electrophysiological properties and mechanism of aging for the susceptibility of left atrium (LA) to arrhythmogenesis in rabbits., Methods: A total of 50 male New Zealand rabbits were divided into young (6 months, n = 25) and aged (26 months, n = 25) groups. According to comparisons before and after isoproterenol (ISO) dosing, young rabbits were further divided into young control and medication groups while aged ones into aged control and medication groups. Electrophysiological study was performed on perfused isolated left atrium and conventional microelectrodes were used for recording transmenbrane action potentials (tAP), resting membrane potential (RMP), amplitude of APs (APA), maximum upstroke velocity (Vmax), APs duration at 20%, at 50% or at 90% repolarization (APD20, APD50, APD90), atrial effective refractory periods (AERP) and atrial arrhythmia inducibility before and after ISO dosing. L-type calcium current (ICa-L) was measured via whole-cell patch clamp technique. And fluorescent intensity of intracellular Ca²⁺ was detected with Flup-3/AM loading by laser scanning confocal microscope in enzymatically dissociated single LA myocytes before and after dosing., Results: Compared with major parameters of tAP in young control group, APDs and AERP significantly increased and APA, Vmax, RMP and AERP/APD90 obviously decreased in aged control group (all P < 0.05). Otherwise, the conduction of tAP was rapid and delayed afterdepolarizations (DADs) were induced in both young and aged medication groups after ISO dosing. However, as compared with major parameters of young medication group, APDs dramatically declined while APA, Vmax, RMP and DAD amplitude significantly increased. And triggered activity was induced in aged medication group (all P < 0.05). With voltage clamp model, ICa-L significantly declined in aged control group versus young control group. The peak current density of ICa-L dramatically decreased ((6.3 ± 0.8) pA/pF in aged control group vs (9.5 ± 1.3) pA/pF in young control group, P < 0.01) under 10 mV clamp voltage. And current-voltage (I-V) curve of ICa-L was greatly upgraded in aged control group on the top of all I-V curves without changing direction. The current density of ICa-L increased much more in aged medication group than that in young medication group ((15.9 ± 3.1) vs (11.3 ± 2.6) pA/pF, P < 0.01). And I-V curve of ICa-L shifted the bottom of all I-V curves in aged medication group. Fluorescent intensities of intracellular free Ca²⁺ became completely attenuated ((437.9 ± 21.7) µmol/L in aged control group vs (778.3 ± 19.5) µmol/L in young control group, P < 0.01). Under the effect of ISO administration, fluorescent intensities of intracellular free Ca²⁺ significantly increased in both young and aged medication groups. But [Ca²⁺]i were altered more in aged medication group than that in young medication group ((1 635.6 ± 51.6) vs (1 008.7 ± 34.5) µmol/L, P < 0.05)., Conclusions: The electrophysiological characteristics are significantly altered with electrical remodeling before and after ISO dosing in aging LA in rabbits. And it may contribute to the vulnerability and pathophysiological basis for reentry and atrial arrhythmogenesis. The electrophysiological mechanism is probably attributed to the alterations of ICa-L and [Ca²⁺]i before and after ISO perfusion in aging LA myocytes.

Objective: To explore the regulatory effects of luteolin on airway inflammation in asthmatic rats., Methods: A total of 48 male Sprague-Dawley (SD) rats were randomly divided into 3 groups of control, asthmatic and luteolin(n = 16 each). The rat model of bronchial asthma was established in asthmatic and luteolin groups. The model was induced by intraperitoneally injecting a mixture of ovalbumin and aluminum hydroxide at Day 1 and 8. After two weeks, aomization excitation of normal saline (containing 1% ovalbumin) was induced thrice weekly. The treatment lasted 8 weeks. In control group, the mixture of ovalbumin, aluminum hydroxide and normal saline containing 1% ovalbumin was replaced by normal saline. At 30 min after aomization excitation, normal saline was given to rats in control and asthmatic groups, while 1 mg/kg luteolin was given intraperitoneally to luteolin group. The inflammatory cell number and level of interleukin-4 (IL-4) were measured in bronchoalveolar lavage fluid (BALF). The histopathological changes were observed under light microscope. The activities of peroxisome proliferator-activated receptors (PPARγ) and p38 mitogen-activated protein kinases (p38MAPK) in pulmonary tissues were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR)., Results: The bronchial wall thickness of asthma group, along with smooth muscle thickness ((93.3 ± 7.4), (34.9 ± 2.3) µm) was more than that of control ((61.9 ± 8.2), (19.3 ± 1.5) µm) and luteolin ((76.6 ± 6.7), (25.4 ± 4.6) µm) groups (all P < 0.05). The total cell count ((5.61 ± 0.63)×10(9)/L), neutrophil count ((1.83 ± 0.09)×10(9)/L), eosinophil count ((0.59 ± 0.09)×10(9)/L) and level of IL-4 ((78.23 ± 12.73) pg/ml) in BALF of asthmatic group were markedly higher than those of control ((1.53 ± 0.31)×10(9)/L, (0.45 ± 0.21)×10(9)/L, (0.07 ± 0.03) ×10(9)/L and (21.21 ± 2.53) pg/ml) and luteolin ((3.24 ± 0.25)×10(9)/L, (1.54 ± 0.10)×10(9)/L, (0.33 ± 0.05)×10(9)/L and (43.24 ± 8.65) pg/ml) groups (all P < 0.05). The results of semi-quantitative immunohistochemical analysis showed that the p38 protein level in control group (0.143 ± 0.017) and luteolin group (0.251 ± 0.021) was significantly less than that in asthmatic group (0.362 ± 0.008) (both P < 0.01). As compared with asthmatic group, the expression of PPARγ protein markedly increased (0.247 ± 0.034) in control (0.331 ± 0.056) and luteolin (0.442 ± 0.031) groups (all P < 0.05). The level of p38 mRNA in asthmatic group (0.718 ± 0.064) was significantly higher than that of control (0.312 ± 0.052) and luteolin (0.426 ± 0.067) groups (all P < 0.01). However, the PPARγ mRNA level in asthmatic group (0.266 ± 0.036) was much less than that in control (0.573 ± 0.042) and luteolin (0.687 ± 0.054) groups (all P < 0.01)., Conclusion: The anti-inflammatory effects of luteolin may be associated with the regulation of PPARγ expression and p38MAPK signaling pathway in asthmatic rats.