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Splash functions delineate the intricate interaction between wind‐driven particles and the bed. However, due to limitations in measurement methods, achieving a comprehensive understanding of splash functions remains challenging. In this study, we utilized a high‐speed system and particle trajectory tracking algorithm to reconstruct 857 collision events involving natural sand particles obtained from field samples and artificial glass microspheres interacting with a bed composed of analogous particles in a wind tunnel. During the experiments, the ratio of the wind shear velocity (u*) to the impact threshold (u*ti) consistently ranged between approximately 1.22 and 1.79. Our findings indicate that the impact angle remains independent of both impact velocity and particle size, maintaining an approximate value of 10.5 ± 6.5°. The evaluation of splash functions depends on the criterion used to define ejection, that is, the ratio of the centroid's height of the liftoff particles to their particle size (H/d). Additionally, at the same critical height (H/d = 1.5), our splash functions show differences of varying degrees from previous experiments and theoretical studies performed under no wind conditions. We believe that the main reason for these differences may be that the energy exchange between the bed surface and the airflow increases the looseness of the large‐particle (>0.1 mm) bed surface. These findings hold significant implications for accurately modeling sand‐bed collisions in natural environments. Plain Language Summary: The interaction mechanism between natural sand and the bed within the aeolian flow yields crucial insights into explaining the initiation of sand or dust emission. Due to the extremely low airflow velocity near the loose bed surface, previous studies have elucidated the interaction relationship between sand and the bed through experiments and theoretical studies conducted under no wind conditions. In our study, we observed a large number of particle‐bed collision processes within the saturated aeolian flow through high‐speed cameras and particle trajectory tracking algorithms and contributed previously unexplored insights into the interaction mechanism between natural sand and the bed. We derived coupling relation functions between key movement parameters (velocity, angle and number) of liftoff particles and their relative height above the bed, as well as the velocity at which incident particles reach the bed surface. Consequently, our findings will be pertinent for future modeling efforts aimed at understanding the interactions between transported particles and the bed in models of wind‐blown sand transport. Key Points: Eight hundred and fifty seven collision events in airflow were investigated through wind tunnel experiments utilizing high‐speed photography on a loose surfaceThe effect of the criterion used for defining ejection on splash functions was investigatedThe splash functions in airflow deviate to different extents from theoretical simulation and experimental results under windless conditions [ABSTRACT FROM AUTHOR]

Magnetic reconnection is a fundamental mechanism for energy conversion in the realms of space physics, astrophysics, and plasma physics. Over the past few decades, obtaining analytical solutions for three-dimensional (3D) magnetic reconnection has remained a challenging endeavor. Due to the complexity and nonlinearity of the equations, analytical solutions can only be obtained when specific spatiotemporal distributions of magnetic fields or plasma flows are provided. Particularly, the evolution of reconnection flows in time-dependent 3D reconnection has not been analytically discussed. Additionally, quasi-steady magnetic reconnection persisting for several hours can be observed in the turbulent solar wind, which raises an important question: can steady reconnection flows theoretically exist in a time-dependent 3D magnetic reconnection model? In this study, a generalized analytical model for time-dependent kinematic 3D magnetic reconnection has been constructed. In the framework of pure analytical approach, it is firstly demonstrated that steady reconnection outflows can theoretically exist within a time-varying magnetic field. We have also analytically discussed the possibility of the existence of quasi-steady reconnection flows in 3D magnetic reconnection for turbulent magnetic fields in the solar wind. These findings broaden our understanding of the stability and necessary conditions for time-dependent 3D magnetic reconnection, offering new insights into quasi-steady reconnection phenomena in real cosmic environments. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Hepatocarcinoma is a great threat to global health. MicroRNA-23a was suggested to regulate growth and apoptosis in certain cell lines. Our study was focused on growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H under the influence of microRNA-23a, and explored the mechanism of pro-apoptosis microRNA-23a. MATERIALS AND METHODS: MicroRNA-23a and control microRNA (scramble miRNA, for short as miRNA) were synthesized with the routine protocol. Lipofection transfection was performed in hepatocarcinoma cell line MHCC97H. 3-(4,5-dimethyl- 2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, caspase-3 activity detection, and flow cytometry were performed to examine growth, proliferation, and apoptosis of hepatocarcinoma cell line MHCC97H, respectively. Kidney inhibitor of apoptosis protein (KIAP) and small interfere RNA (siRNA) was synthesized for inhibition of KIAP. KIAP plasmid was established for activation of KIAP. Western blot was performed to examine the protein expression of KIAP and caspase protein family after transfection of KIAP siRNA or KIAP plasmid. RESULTS: Compared with miRNA transfection, microRNA-23a transfection significantly reduced the growth of MHCC97H cells, and decreased the expression of KIAP (p < 0.05). Enhanced translocation of phosphatidylserine and activation of caspase-3 were observed in microRNA-23a transfection cells. Moreover, inhibition of KIAP enhanced the pro-apoptosis effect of microRNA-23a, while activation of KIAP abrogated pro-apoptosis effect of microRNA- 23a. CONCLUSIONS: MicroRNA-23a inhibits growth and proliferation of MHCC97H cells, and induces apoptosis of MHCC97H cells via down-regulating KIAP. KIAP could be a potential therapeutic target for hepatocarcinoma treatment. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore whether the vascular endothelial growth factor (VEGF) level changes the biological markers of Alzheimer's disease (AD) and discover the relationship between VEGF and the brain aging. PATIENTS AND METHODS: The neuroimaging and neuropsychological results on Alzheimer's disease neuroimaging program (ADNI) were analyzed as biomarkers. Participants were all recruited from ADNI including cognitive ability (n=90), mild cognitive impairment (n=130) and AD (n=59). The relationship between VEGF level in cerebrospinal fluid (CSF) and hippocampal volume, episodic memory and executive ability was compared laterally and longitudinally, in order to evaluate whether VEGF was effective. Moreover, the correlation between VEGF levels in CSF and the results of brain aging was detected and evaluated, so as to detect the level of VEGF in CSF and the continuous determination of the relationship with AD biomarkers (Aβ-42, totalτprotein). RESULTS: The general linear model and the multiple regression research indicated that the VEGF in CSF was related to the brain aging (hippocampal volume, episodic memory and executive ability). The interaction between AD biomarkers (CSF amyloid beta (Aβ-42) and totalτ protein) and VEGF promoted AD biomarkers to enhance the effect of VEGF on the brain aging. The VEGF correlated with the baseline hippocampal volume (p = 0.009), longitudinal hippocampal atrophy (p = 0.010), longitudinal memory decline (p < 0.0001) and longitudinal executive capacity decline (p = 0.003). In the prediction of longitudinal hippocampal atrophy (p < 0.0001) memory loss (p = 0.010) and implementation capacity (p = 0.0002), the VEGF andτ protein interacted with each other. In the prediction of longitudinal memory loss (p = 0.010), the VEGF interacted with amyloid-β4. CONCLUSIONS: The elevated VEGF in CSF is associated with the brain aging. When AD biomarkers were elevated, the VEGF had the strongest neuro-protective effect. Moreover, in the positive AD biomarkers, especially the individualτprotein, the protective effect of VEGF was the strongest. In the prediction of longitudinal changes in the hippocampal volume, the memory and the executive ability, the interactions of VEGF andτ protein were observed. VEGF and Aβ-42 also interacted with each other in case of longitudinal changes in the memory performance. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The lung adenocarcinoma is a type of lung cancer. This research is to investigate the effects of miR-222 on the proliferation, migration and invasion of the lung adenocarcinoma cells. MATERIALS AND METHODS: At the beginning, MiR-222 and the controls were transfected to the lung adenocarcinoma cell line A549 for CCK-8 proliferation, transwell migration and Matrigel invasion, and then observed the effect of miR-222 on the proliferation, migration and invasion of lung adenocarcinoma cells. The miR- 222 target was regulated by ETS1 downwards to participate in the regulation of the process by using the luciferase reporter assay, the Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and the Western blotting. RESULTS: According to CCK-8 proliferation assay, the Transwell migration and the Matrigel invasion assay, it discovered that MiR-222 can promote the proliferation, migration and invasion of the lung adenocarcinoma cells. Luciferase reporter assay, RT-qPCR and Western blot assay showed that miR-222 could regulate the expression of ETS1 downwards and ETS1 participated in the regulation of the process CONCLUSIONS: ETS1 promotes proliferation, migration and invasion of lung adenocarcinoma cells by targeting the regulated miR-222 downwards. [ABSTRACT FROM AUTHOR]

Our newly-designed computer-controlled equipment for delivering volatile anesthetic agent uses the subminiature singlechip processor as the central controlling unit. The variables, such as anesthesia method, anesthetic agent, the volume of respiratory loop, age of patient, sex, height, weight, environment temperature and the grade of ASA are all input from the keyboard. The anesthetic dosage, calculated by the singlechip processor, is converted into the signals controlling the pump to accurately deliver anesthetic agent into respiratory loop. We have designed an electrocircuit for the equipment to detect the status of the pump's operation, so we can assure of the safety and the stability of the equipment. The output precision of the equipment, with a good anti-jamming capability, is 1-2% for high flow anesthesia and 1-5% for closed-circuit anesthesia and its self-detecting working is reliable.

The effect of progesterone on isolated rabbit coronary arteries and its possible mechanism was investigated by measuring changes of isometric tension. Progesterone (1, 3, 10 and 30 microM) induced significant coronary relaxation in K+ (30 mM)-, prostaglandin F2 alpha (3 microM)- or Bay K 8644 (1 microM plus 15 mM K+)- precontracted arteries. There was no difference between endothelium-intact and -denuded coronary arteries from both male and female rabbits, precontracted with these three agents. Haemoglobin, indomethacin, methylene blue, glibenclamide or barium chloride did not affect the relaxation. In endothelium-denuded rabbit coronary arteries, progesterone shifted calcium concentration-dependent constrictor-response curves to the right, the maximal contraction was also reduced. The -log ED50s were 3.6 in control, and 3.3 and 2.9 after incubation with progesterone (3 and 30 microM), respectively. Similar results were obtained in rat aorta. We conclude that progesterone induces significant endothelium-independent relaxation in rabbit coronary arteries in vitro, possibly by affecting calcium influx.

1. We assessed the relaxant effect of 17 beta-oestradiol (10(-7), 10(-6) and 10(-5) M) on rabbit isolated coronary arteries precontracted with prostaglandin F2 alpha (3 x 10(-6) M), high extracellular potassium (30 mM) and Bay K 8644 (10(-6) M) plus high extracellular potassium (15 mM) by measuring isometric tension. 17 beta-Oestradiol (10(-6) and 10(-5) M) induced significant relaxation in coronary arteries from male and female rabbits. No differences were seen between arteries with or without endothelium. There were also no differences between coronary arteries isolated from male and female rabbits. 2. Inhibitors of endothelium-derived relaxing factor and vasodilator prostanoids, namely, reduced haemoglobin, N omega-nitro-L-arginine methyl ester and indomethacin, did not affect the relaxation induced by 17 beta-oestradiol in endothelium-intact coronary arteries. 3. Methylene blue, an inhibitor of guanylate cyclase, did not affect the coronary artery relaxation induced by 17 beta-oestradiol. 4. The calcium concentration-dependent contraction curve in potassium-depolarization medium was shifted to the right by 17 beta-oestradiol (10(-6) and 10(-5) M) in the rabbit coronary artery and rat aorta. The -log EC50s of calcium in control and after incubation with 17 beta-oestradiol (10(-6) and 10(-5) M) were 3.7 +/- 0.09, 3.1 +/- 0.10 and 2.8 +/- 0.08 respectively in rabbit coronary arteries and 3.8 +/- 0.11, 3.3 +/- 0.14 and 2.9 +/- 0.15 in rat aorta. 5. The results indicate that 17 beta-oestradiol induces rabbit coronary artery relaxation by an endothelium-independent mechanism in vitro. A calcium antagonistic property may be involved in the mechanism of rabbit coronary arterial relaxation by 17beta-oestradiol.

Study Objective: The purpose was to assess the role of ATP sensitive potassium channels (KATP) in endothelium dependent vasodilatation induced by acetylcholine, or endothelium independent vasodilatation induced by lemakalim in rabbit coronary arteries., Design: The effect of glibenclamide, a specific inhibitor of KATP, on coronary artery relaxation induced by acetylcholine or lemakalim was investigated. The relaxing effectiveness of acetylcholine and lemakalim on coronary arteries precontracted with KCl (K+) or prostaglandin F2 alpha (PGF2 alpha) was compared., Experimental Materials: Left epicardial coronary arteries from male New Zealand white rabbits (2.5-3.0 kg), killed by an overdose of pentobarbitone, were dissected free of connective tissue. Rings suspended in organ baths for the measurement of isometric tension., Measurements and Main Results: K+ (30 mmol.litre-1) and PGF2 alpha (3 mumols.litre-1) caused comparable contraction (p greater than 0.05) in endothelium intact or endothelium denuded coronary arterial rings. Acetylcholine induced relaxation was greater in endothelium intact rings precontracted with PGF2 alpha than with K+ and was abolished by the removal of endothelium. Relaxations induced by acetylcholine (0.1 and 0.3 mumol.litre-1) were reduced from 82(SEM 2.7)% and 93(2.8)% to 71(2.4)% and 82(2.7)% (p less than 0.05), and to 63(3.2)% and 79(4.5)% (p less than 0.05 or less than 0.01) by glibenclamide (3 and 10 mumols.litre-1) respectively in PGF2 alpha precontracted rings; and also attenuated (p less than 0.05 or less than 0.01) in K+ precontracted rings. Lemakalim induced relaxation was greater in endothelium denuded rings precontracted with PGF2 alpha than with K+, and was markedly reduced by glibenclamide (p less than 0.01)., Conclusions: These results suggest that activation of KATP may partially be involved in endothelium dependent relaxation induced by acetylcholine in rabbit coronary arteries. Lemakalim-induced endothelium independent relaxation results mainly from activation of KATP.