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Abstract Background Emergence agitation (EA) is a prevalent complication in children following general anesthesia. Several studies have assessed the relationship between melatonin or its analogs and the incidence of pediatric EA, yielding conflicting results. This meta-analysis aims to assess the effects of premedication with melatonin or its analogs on preventing EA in children after general anesthesia. Methods PubMed, EMBASE, the Cochrane Library, ProQuest Dissertations & Theses Global, Web of Science, CNKI, Wanfang Data, clinicaltrials.gov, and WHO International Clinical Trials Registry Platform were searched until 25 November 2022. We included randomized controlled trials that assessed EA in patients less than 18 years old who underwent general anesthesia. We excluded studies that did not use a specific evaluation to assess EA. Results Nine studies (951 participants) were included in this systematic review. Melatonin significantly reduced the incidence of EA compared with placebos (risk ratio 0.40, 95% CI 0.26 to 0.61, P

Heterogeneous structure is practical to improve the strain hardening abilities of materials due to the effect of hetero-deformation induced hardening, especially of composites. In this study, a series of TiB/TC4 composites with a pseudo core–shell structure of bimodal grain distribution were fabricated via a two-step ball-milling and spark plasma sintering. The synthesized TiB/TC4 composites have a structure of coarse lamella α-Ti grains of average 23.6 μm in diameter surrounded by fine α-Ti lamella grains of average 4.2 μm, with TiB distributed on the primary TC4 surface areas. TiB/TC4 composites with 0.4 wt% TiB2 exhibited the best comprehensive mechanical properties with an ultimate tensile strength of 1161.95 MPa (a 35.1% increase compared with that of pure TC4) and an elongation of 7.57%. In conclusion, the pseudo core–shell structure improved the strength by improving the strain-hardening abilities, achieved by the coordinated deformation between coarse grains and fine grains.

Background:In recent years, diabetic kidney disease (DKD) has emerged as a prominent factor contributing to end-stage renal disease. Tubulointerstitial inflammation and lipid accumulation have been identified as key factors in the development of DKD. Earlier research indicated that Astragaloside IV (AS-IV) reduces inflammation and oxidative stress, controls lipid accumulation, and provides protection to the kidneys. Nevertheless, the mechanisms responsible for its protective effects against DKD have not yet been completely elucidated.Purpose:The primary objective of this research was to examine the protective properties of AS-IV against DKD and investigate the underlying mechanism, which involves CD36, reactive oxygen species (ROS), NLR family pyrin domain containing 3 (NLRP3), and interleukin-1β (IL-1β).Methods:The DKD rat model was created by administering streptozotocin along with a high-fat diet. Subsequently, the DKD rats and palmitic acid (PA)-induced HK-2 cells were treated with AS-IV. Atorvastatin was used as the positive control. To assess the therapeutic effects of AS-IV on DKD, various tests including blood sugar levels, the lipid profile, renal function, and histopathological examinations were conducted. The levels of CD36, ROS, NLRP3, Caspase-1, and IL-1β were detected using western blot analysis, PCR, and flow cytometry. Furthermore, adenovirus-mediated CD36 overexpression was applied to explore the underlying mechanisms through in vitro experiments.Results:In vivo experiments demonstrated that AS-IV significantly reduced hyperglycemia, dyslipidemia, urinary albumin excretion, and serum creatinine levels in DKD rats. Additionally, it improved renal structural abnormalities and suppressed the expression of CD36, NLRP3, IL-1β, TNF-α, and MCP-1. In vitro experiments showed that AS-IV decreased CD36 expression, lipid accumulation, and lipid ROS production while inhibiting NLRP3 activation and IL-1β secretion in PA-induced HK-2 cells.Conclusion:AS-IV alleviated renal tubule interstitial inflammation and tubule epithelial cell apoptosis in DKD rats by inhibiting CD36-mediated lipid accumulation and NLRP3 inflammasome activation.

This study examines the relationship between analyst forecast dispersion or accuracy and supplier concentration of listed firms in China from 2008 to 2019. Our findings suggest that higher supplier concentration is associated with lower analyst forecast dispersion, which can be attributed to the increased attention from analysts. Moreover, this effect is more pronounced when firms have less bargaining power and higher institutional ownership, indicating a greater reliance on the supply chain. Our study highlights the importance of disclosing supply chain information, which provides insights beyond those of traditional financial information.

Abstract Biologically inspired neuromorphic sensory memory systems based on memristor have received a lot of attention in the booming artificial intelligence industry due to significant potential to effectively process multi‐sensory signals from complex external environments. However, many memristors have significant switching parameters disperse, which is a great challenge for using memristors in bionic neuromorphic sensory memory systems. Herein, a stable ferroelectric memristor based on the Pd/BaTiO3:Eu2O3/La0.67Sr0.33MnO3 grown on Silicon structure with SrTiO3 as buffer layer is presented. The device possesses low coercive field voltage (−1.3–2.1 V) and robust endurance characteristic (~1010 cycles) through optimizing the growth temperature. More importantly, an ultra‐stable artificial multimodal sensory memory system with visual and tactile functions was reported for the first time by combining a pressure sensor, a photosensitive sensor, and a robotic arm. Utilizing the above system, the sensitivity value of the system is expressed by the conductance of the memristor to realize the gradual change of external stimulus, and multi signals inputs at the same time to this system have faithfully achieved sensory adaptation to multimodal sensors. This work paves the way for future development of memristor‐based perception systems in efficient multisensory neural robots.

Abstract In vivo imaging in the deep near‐infrared (NIR) spectral region, that is, beyond 800 nm, has become popular due to its penetration depth. While imaging of the neutral medium/tissue has been repeatedly showcased, imaging of the high‐acidic medium remains challenging partly because of the high‐lying HOMO orbital and hence a high pKa of the electron‐donating group of the NIR fluorophores. We devised a novel electron‐donating group (D6) with which we further synthesized ECJ. ECJ exhibits an absorption wavelength beyond 900 nm and is fluorescent. Its pKa was found to be lower than zero, rendering it suitable for bioimaging of a highly‐acidic medium. Its potential for practical applications was showcased in proof‐of‐concept in vivo imaging with a mouse model.

Abstract Vitamin D insufficiency/deficiency has been linked to an increased risk of preeclampsia. Impaired placental amino acid transport is suggested to contribute to abnormal fetal intrauterine growth in pregnancies complicated by preeclampsia. However, if vitamin D-regulated amino acid transporter is involved in the pathophysiologic mechanism of preeclampsia has not been clarified yet. The aberrant expression of key isoform of L-type amino acid transporter LAT1 was determined by western blot and immunohistochemistry in the placenta from normotensive and preeclamptic pregnancies. The role for vitamin D on placental LAT1 expression was investigated through the exposure of HTR-8/SVneo human trophoblast cells to the biologically active 1,25(OH)2D3 and the oxidative stress-inducer cobalt chloride (CoCl2). Our results showed that placental LAT1 expression was reduced in women with preeclampsia compared to normotensive pregnancies, which was associated with decreased expression of vitamin D receptor (VDR). 1,25(OH)2D3 significantly upregulated LAT1 expression in placental trophoblasts, and also prevented the decrease of mTOR activity under CoCl2-induced oxidative stress. siRNA targeting VDR significantly attenuated 1,25(OH)2D3-stimulated LAT1 expression and mTOR signaling activity. Moreover, treatment of rapamycin specifically inhibited the activity of mTOR signaling and resulted in decrease of LAT1 expression. In conclusion, LAT1 expression was downregulated in the placenta from women with preeclampsia. 1,25(OH)2D3/VDR could stimulate LAT1 expression, which was likely mediated by mTOR signaling in placental trophoblasts. Regulation on placental amino acid transport may be one of the mechanisms by which vitamin D affects fetal growth in preeclampsia.

Abstract Vitamin D insufficiency or deficiency during pregnancy has been associated with an increased risk of preeclampsia. Increased placental cyclooxygenase-2 (COX-2) activity was proposed to contribute to the inflammatory response in preeclampsia. This study was to investigate if vitamin D can benefit preeclampsia by inhibiting placental COX-2 expression. Placenta tissues were obtained from 40 pregnant women (23 normotensive and 17 preeclampsia). miR-26b-5p expression was assessed by quantitative PCR. Vitamin D receptor (VDR) expression and COX-2 expression were determined by immunostaining and Western blot. HTR-8/SVneo trophoblastic cells were cultured in vitro to test anti-inflammatory effects of vitamin D in placental trophoblasts treated with oxidative stress inducer CoCl2. 1,25(OH)2D3 was used as bioactive vitamin D. Our results showed that reduced VDR and miR-26b-5p expression, but increased COX-2 expression, was observed in the placentas from women with preeclampsia compared to those from normotensive pregnant women. Transient overexpression of miR-26b-5p attenuated the upregulation of COX-2 expression and prostaglandin E2 (PGE2) production induced by CoCl2 in placental trophoblasts. 1,25(OH)2D3 treatment inhibited CoCl2-induced upregulation of COX-2 in placental trophoblasts. Moreover, miR-26b-5p expression were significantly upregulated in cells treated with 1,25(OH)2D3, but not in cells transfected with VDR siRNA. Conclusively, downregulation of VDR and miR-26b-5p expression was associated with upregulation of COX-2 expression in the placentas from women with preeclampsia. 1,25(OH)2D3 could promote miR-26b-5p expression which in turn inhibited COX-2 expression and PGE2 formation in placental trophoblasts. The finding of anti-inflammatory property by vitamin D through promotion of VDR/miR-26b-5p expression provides significant evidence that downregulation of vitamin D/VDR signaling could contribute to increased inflammatory response in preeclampsia.

Abstract Background Degeneration of ovarian function is an obvious feature of female aging. In addition, studies have shown that autophagy decreases with age, and DNA methylation is a hallmark epigenetic pattern during aging. However, it is not clear whether the expression and DNA methylation of autophagy genes are involved in the declines in ovarian function that occur during aging. Results Three groups of rats were used: 6-month-old (6 M) rats, 12-month-old (12 M) rats and 24-month-old (24 M) rats. Serum E2 levels and the mRNA and protein expression levels of Atg5, Atg12, Atg16L, Beclin1 and Lc3B were significantly decreased in aged rats. In addition, the methylation levels of the Atg5 gene were significantly increased in aged rats. The expression of the Dnmt1 and Dnmt2 genes decreased with aging; however, the expression of the Dnmt3A and Dnmt3B genes gradually increased with aging. Conclusions Decreased autophagic activity was involved in the declines in ovarian function in aging rats. Upregulation of the DNA methyltransferases Dnmt3A and Dnmt3B may have led to methylation of the autophagy genes Atg5 and Lc3B to ultimately cause the observed decreases in autophagic activity.

Biomass-based gasification is an attractive and promising pathway for hydrogen production. In this work, a biomass-based hydrogen production system integrated with organic Rankine cycle was designed and investigated to predict the performance of hydrogen production yield and electricity generation under various operating conditions. The modified equilibrium model presented desirable results for the produced syngas compositions compared with the experimental data. Hydrogen yields from four types of biomass (wood chips, daily manure, sorghum, and grapevine pruning wastes) were compared under the same operating condition, with wood chips exhibiting the maximum hydrogen yield of 11.59 mol/kg. The effects of gasification temperature, equivalence ratio, and steam-to-biomass ratio on the hydrogen yield and electricity generation were investigated by using the response surface method. Furthermore, the system was optimized using a genetic algorithm based on the response surface model. A preferred optimal solution with a hydrogen yield of 39.31 mol/kg and an output power of 3,558.08 kW (0.99 kW h/kg) was selected by the linear programming technique for multidimensional analysis of the preference method.

Alterations in placental transport may contribute to abnormal fetal intrauterine growth in pregnancies complicated by diabetes, but it is not clear whether the placental amino acid transport system is altered in diabetic pregnancies. We therefore studied the changes in the expressions of placental amino acid transporters in a rat model of diabetes induced by streptozotocin, and tested the effects of hyperglycemia on trophoblast amino acid transporter in vitro. Our results showed that the expressions for key isoforms of system L amino acid transporters were significantly reduced in the placentas of streptozotocin-induced diabetic pregnant rats, which was associated with the decreased birthweight in the rats. A decreased placental efficiency and decreased placental mammalian target of rapamycin (mTOR) complex 1 (mTORC1) activity were also found in the rat model. In addition, hyperglycemia in vitro could inhibit amino acid transporter expression and mTORC1 activity in human trophoblast. Inhibition of mTORC1 activity led to reduced amino acid transporter expression in placental trophoblast. We concluded that reduced placental mTORC1 activity during pregnancy resulted in decreased placental amino acid transporter expression and, subsequently, contributed to fetal intrauterine growth restriction in pregnancies complicated with diabetes.

Abstract Particulate organic nitrates (pON) significantly contribute to the mass of organic aerosol and influence the nitrogen oxides cycle in the atmosphere, but their evolution and lifetime remain uncertain. This study performed simultaneous measurements on the anthropogenically affected surface site and the mountain site on top of the polluted planetary boundary layer (PBL). After aging in the PBL, organic nitrate was converted from primary sources (decreased from 8.7% to 4.3%) to secondary sources (increased from 6.3% to 36.1%), spanning from the surface to the mountain. The evaporation of more volatile inorganic nitrate and the production of secondary organic nitrate during aging in the PBL contributed to the enhanced pON fraction over the top of PBL. The contribution of light absorption by brown carbon increased by 57% at the top of PBL compared to the surface, consistent with the higher fraction of nitrogenous organic aerosols over the mountain. The results provide field evidence that the nitrogenous organic aerosols (OA) may be preserved by adding into secondary OA and significantly contribute to the enhanced importance of brown carbon after aging during vertical transport in the PBL.

Atmospheric nitrogen (N) deposition is composed of both inorganic nitrogen (IN) and organic nitrogen (ON), and these sources of N may exhibit different impacts on ecosystems. However, our understanding of the impacts of N deposition is largely based on experimental gradients of INs or more rarely ONs. Thus, the effects of N deposition on ecosystem productivity and biodiversity may be biased. We explored the differential impacts of N addition with different IN:ON ratios (0:10, 3:7, 5:5, 7:3, and 10:0) on aboveground net primary productivity (ANPP) of plant community and plant diversity in a typical temperate grassland with a long-term N addition experiment. Soil pH, litter biomass, soil IN concentration, and light penetration were measured to examine the potential mechanisms underlying species loss with N addition. Our results showed that N addition significantly increased plant community ANPP by 68.33%–105.50% and reduced species richness by 16.20%–37.99%. The IN:ON ratios showed no significant effects on plant community ANPP. However, IN-induced species richness loss was about 2.34 times of ON-induced richness loss. Soil pH was positively related to species richness, and they exhibited very similar response patterns to IN:ON ratios. It implies that soil acidification accounts for the different magnitudes of species loss with IN and ON additions. Overall, our study suggests that it might be reasonable to evaluate the effects of N deposition on plant community ANPP with either IN or ON addition. However, the evaluation of N deposition on biodiversity might be overestimated if only IN is added or underestimated if only ON is added. [ABSTRACT FROM AUTHOR]

In recent years, golden tides caused by floating Sargassum have induced severe ecological disasters globally. Eutrophication is a significant factor contributing to the massive spread of Sargassum golden tides. Furthermore, the thalli of Sargassum that float on the ocean surface are subjected to more ultraviolet radiation (UVR). The coupled impact of eutrophication and UVR on the photosynthetic physiology of golden tide species remains unclear. In this study, the thalli of Sargassum horneri, known to cause golden tide, were cultured and acclimated to three distinct nitrogen (N) conditions (natural seawater, NSW; NH4+-N enrichment; and NO3–N enrichment) for 6 days. Subsequently, the thalli were exposed to two different radiation treatments (photosynthetically active radiation (150 W m-2), PAR, 400–700 nm; PAR (150 W m-2) + UVR (28 W m-2), 280–700 nm) for 120 min, to investigate the photosynthetic effects of UVR and N on this alga. The findings demonstrated that exposure to UVR impeded the photosynthetic capacity of S. horneri, as evidenced by a decrease in the maximum photochemical quantum yield (Fv/Fm), photosynthetic efficiency (α) and chlorophyll content. Under diverse N-enrichment conditions, the alga tended to adopt various strategies to mitigate the adverse effects of UVR. NH4+-enrichment dissipated excess UVR energy through a greater increase in non-photochemical quenching (NPQ). While NO3–enrichment protected alga by enhancing N assimilation (higher nitrate reductase activity (NRA) and soluble protein content), and maintained a stable energy captured per unit reaction center for electron transfer (ET0/RC) and a higher net photosynthetic rate. Although different N enrichments could not completely offset the damage caused by UV radiation, they secured the photoprotective ability of S. horneri in several ways.

Abstract Background Foetal renal dysplasia is still the main cause of adult renal disease. Placenta-derived exosomes are an important communication tool, and they may play an important role in placental (both foetal and maternal) function. We hypothesize that in women with preeclampsia, foetal renal dysplasia is impeded by delivering placenta-derived exosomes to glomerular endothelial cells. Methods In the present study, we established a PE trophoblast oxidative stress model to isolate exosomes from supernatants by ultracentrifugation (NO-exo and H/R-exo) and collected normal and PE umbilical cord blood plasma to isolate exosomes by ultracentrifugation combined with sucrose density gradient centrifugation (N-exo and PE-exo), then we investigated their effects on foetal kidney development by in vitro, ex vivo and in vivo models. Results The PE trophoblast oxidative stress model was established successfully. After that, in in vitro studies, we found that H/R-exo and PE-exo could adversely affect glomerular endothelial cell proliferation, tubular formation, migration, and barrier functions. In ex vivo studies, H/R-exo and PE-exo both inhibited the growth and branch formation of kidney explants, along with the decrease of VE-cadherin and Occludin. In in vivo studies, we also found that H/R-exo and PE-exo could result in renal dysplasia, reduced glomerular number, and reduced barrier function in foetal mice. Conclusions In conclusion, we demonstrated that PE placenta-derived exosomes could lead to foetal renal dysplasia by delivering placenta-derived exosomes to foetal glomerular endothelial cells, which provides a novel understanding of the pathogenesis of foetal renal dysplasia. Video Abstract

Abstract Exosomes originating from human umbilical cord mesenchymal stem cells (hucMSC-exos) have become a novel strategy for treating various diseases owing to their ability to regulate intercellular signal communication. However, the potential of hucMSC-exos to improve placental injury in obstetric antiphospholipid syndrome and its underlying mechanism remain unclear. Our objective was to explore the potential application of hucMSC-exos in the treatment of obstetric antiphospholipid syndrome and elucidate its underlying mechanism. In our study, hucMSC-exos ameliorated the functional impairment of trophoblasts caused by antiphospholipid antibodies in vitro and attenuated placental dysfunction in mice with obstetric antiphospholipid syndrome by delivering miR-146a-5p. Exosomal miR-146a-5p suppressed the expression of tumor necrosis factor receptor-associated factor 6 (TRAF6) and inhibited the activation of NF-κB signaling, leading to the down-regulation of IL-1β and IL-18 to rescue inflammation and modulation of Cleaved-CASP3, BAX, and BCL2 to inhibit apoptosis in HTR8/SVneo cells and mice placenta. This study identified the potential molecular basis of how hucMSC-exos improved antiphospholipid antibody-induced placental injury and highlighted the functional importance of the miR-146a-5p/TRAF6 axis in the progression of obstetric antiphospholipid syndrome. More importantly, this study provided a fresh outlook on the promising use of hucMSC-exos as a novel and effective treatment approach in obstetric antiphospholipid syndrome. Graphical Abstract

Residential biomass combustion emits a large amount of organic gases into ambient air, resulting in the formation of secondary organic aerosol (SOA) and various environmental and health impacts. In this study, we investigated the emission characteristics of non-methane organic compounds (NMOCs) from residential biomass fuels during vigorous combustion (flaming) and stable combustion (smoldering) conditions. We quantified NMOC emission factors based on the CO concentration for different combustion phases and found that NMOC emissions were higher during the smoldering phase and approximately two to four times greater than those during flaming. NMOCs were categorized into volatile organic compounds (VOCs) and intermediate-volatility organic compounds (IVOCs) through the modeling of the organic compound volatility distribution. The photochemical aging of NMOCs revealed furans, phenolics, and certain IVOCs as significant non-traditional SOA precursors, with over half being consumed during a short aging period. A parametric function was established, indicating that accounting for non-traditional SOA precursors and IVOC yields improves the representation of the net enhancement of measured organic aerosol (OA). This study emphasizes the importance of differentiating emissions from various phases of residential biomass combustion and recognizing non-traditional SOA precursors and IVOCs for accurate SOA assessment and prediction.