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Synthesis of poison dart frog indolizidine alkaloids (−)‐209D, (−)‐209B and (−)‐223V were accomplished, with a common tricyclic lactone skeleton as the starting compound, in overall yields of 8.8 %, 5.5 %, and 5.2 %, respectively. The construction of the C7−C8 bond in the synthesis of 209D involves simple ring closure metathesis and hydrogenation reactions. However, in the synthesis of 209B and 223V, the C7−C8 bond and the stereochemistry of C8, is achieved through radical cyclization reactions controlled by allylic 1,3‐strain. Cleavage of the excess carbon on the C5 for all the related intermediates were done by Barton decarboxylation protocol. Reduction of the corresponding indolizidin‐3‐ones by LAH completed the total synthesis of these three target molecules. The quantum mechanics calculations were performed on α‐amidyl carbon radical intermediates to account for the observed diastereomeric ratio (~9 : 1) of the key Barton decarboxylation step. Ultimately, the synthesis of 3‐epi‐(−)‐223AB was accomplished in 51.6 % through the cuprate addition to the activated lactam of a late intermediate in the synthesis of (−)‐167B. [ABSTRACT FROM AUTHOR]

Achieving fast‐charging capabilities in Li‐ion batteries (LIBs)—charging 80% of the battery capacity within 15 minutes—while maintaining an acceptable cycle life remains challenging due to various polarizations occurring at elevated charge rates. Such a goal is more tough at subzero, as temperature reduction slows the kinetics process including electrolyte mass transport and electrode charge transfer, substantially increasing the risk of lithium plating. Herein, it is found that adding LiFSI to a LiPF6 carbonate‐based electrolyte alters the Li+ solvation structure, endowing the dual‐salt electrolyte with a higher Li+ diffusion coefficient and lower desolvation energy. Benefit from the smaller structural change and the formation of a robust, conductive solid electrolyte interphase, the 12Ah‐pouch cells based on LiNi0.52Co0.2Mn0.28O2 cathodes and graphite anodes demonstrate fast‐charging capabilities and stable cycling performance across a wide temperature range of −20 to 50 ℃: charging 89% and 93% of pouch cell capacity within 4 minutes at 25 and 50 ℃ and 82% within 15 minutes at −20 ℃, maintaining capacity retention of 94% after 2000 cycles at 8C at 0 ℃ and 89% after 350 cycles at −20 ℃ at 4C. This work might offer new insights into enhancing the fast‐charging capabilities of LIBs under extreme conditions. [ABSTRACT FROM AUTHOR]

Thermally activated delayed fluorescence (TADF) materials that exhibit simultaneously high photoluminescence quantum yield (PLQY), rapid reverse intersystem crossing (RISC), and a high horizontal transition dipole ratio are highly desirable for realizing high‐performance organic light‐emitting diodes (OLEDs). However, achieving this goal remains a formidable challenge due to the stringent molecular design principles involved. Herein, three highly efficient TADF materials based on lactam‐type electron‐acceptors are reported. The inherent rigidity and planar structure of lactam units, along with the ordered molecular arrangement in solid states, contribute to the reduction of nonradiative decay and the high horizontal transition dipole ratio in the optimized TADF emitters. Moreover, through precise control of the alignment of the lowest excited states by adjusting the charge transfer strength, the rate constants for reverse intersystem crossing (kRISC) are dramatically boosted. Consequently, the two optimized emitters exhibit outstanding merits of ultra‐high PLQYs (98% and 99%), high horizontal transition dipole ratios (91% and 87%), and fast RISC (kRISC ≈ 1.7 × 106 s−1). Thanks to these merits, the doped OLEDs achieve excellent performance. The top‐performing device achieve a maximum external quantum efficiency of 34.3%, a peak luminance of 57376 cd m−2, and small efficiency roll‐off. [ABSTRACT FROM AUTHOR]

Hematological indicators of chronic systemic inflammation are significant biomarkers for gastroenteropancreatic neuroendocrine neoplasms (GEP‐NENs). We performed a systematic review and meta‐analysis to assess the impact of certain factors on the overall survival (OS), progression‐free survival (PFS), and disease‐free survival (DFS) of patients with GEP‐NENs. These factors include the neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), lymphocyte/monocyte ratio (LMR), and C‐reactive protein (CRP) levels. After searching the Medline, Embase, and Cochrane Library databases from January 1, 2000 to October 20, 2022 and the American Society of Clinical Oncology conference proceedings from January 1, 2017, hazard ratios (HRs) and 95% confidence intervals (CIs) were extracted. Subgroup analyses were conducted to identify the origins of heterogeneity and examine the impact of factor grouping. The effects of the cut‐off values and sample size were assessed by meta‐regression. The results revealed that higher NLRs, PLRs, and CRP levels were associated with shorter OS (HR = 2.09, 95% CI = 1.55–2.8; HR = 1.79, 95% CI = 1.40–2.28; and HR = 2.88, 95% CI = 2.09–3.95, respectively; all p < 0.001). Higher NLRs and lower LMRs were associated with shorter DFS (HR = 3.34, 95% CI = 2.11–5.29 and HR = 2.71, 95% CI = 2.27–3.24, respectively; both p < 0.001). Higher PLRs and CRP levels were correlated with shorter PFS (HR = 3.48, 95% CI = 1.34–9.03, p = 0.01 and HR = 3.14, 95% CI = 1.63–6.08, p = 0.001). As demonstrated in the research, hematological indicators of systemic inflammation are promising biomarkers for GEP‐NEN assessment. [ABSTRACT FROM AUTHOR]

Extended periods of bed rest and limb immobilization are required for healing post‐injury or disease, yet disuse can result in significant muscle atrophy and decreased quality of life in older adults. Physical rehabilitation is commonly prescribed to recover these deficits, yet accumulation of reactive oxygen species and sustained rates of protein degradation persist during the rehabilitation period that can significantly delay or prevent recovery. Pericytes, considered the primary mesenchymal and vascular stromal cell in skeletal muscle, secrete beneficial factors that maintain baseline muscle mass, yet minimal information exists regarding the pericyte response to disuse and recovery. In the current study, single‐cell RNA sequencing and functional assays were performed to demonstrate that pericytes in mouse skeletal muscle lose the capacity to synthesize antioxidants during disuse and recovery. This information was used to guide the design of a strategy in which healthy donor pericytes were stimulated with hydrogen peroxide (H2O2) to produce small extracellular vesicles (sEVs) that effectively restored myofibre size in adult and aged muscle after disuse. Proteomic assessment detected 11 differentially regulated proteins in primed sEVs that may account for recovery of muscle, including proteins associated with extracellular matrix composition and anti‐inflammatory and antioxidant processes. This study demonstrates that healthy H2O2‐primed pericyte‐derived sEVs effectively improve skeletal muscle recovery after immobilization, presenting a novel acellular approach to rebuild muscle mass in older adults after a period of disuse. Key points: Previous studies suggest that prolonged oxidative stress is a barrier to skeletal muscle recovery after a period of immobilization.In this study we demonstrate that muscle‐resident perivascular stromal cells (pericytes) become dysfunctional and lack the capacity to mount an antioxidant defence after disuse in mice.Hydrogen peroxide treatment of healthy pericytes in vitro simulates the release of small extracellular vesicles (sEVs) that effectively recover skeletal muscle fibre size and extracellular matrix remodelling in young adult and aged mice after disuse.Pericyte‐derived sEVs present a novel acellular strategy to recover skeletal muscle after disuse. [ABSTRACT FROM AUTHOR]

The environment-friendly components coupled with the ability to mimic the simplicity and originality of nature necessitate advanced sustainable materials with structural capabilities for energy-efficient applications. The use of feedstock deriving from plant-based, renewable organic material to produce nanofibril that embodies enhanced insulating properties and high mechanical strength constitutes an efficient development strategy. Herein, a free-standing, hierarchical superinsulation membrane by leveraging the principle of the bottom-up method is reported. The electrospun cellulose nanofibrils/aerogel-based core layer provides exceptional thermal properties with its thermal conductivity of 10.2mWm-1K-1. The lightweight, flexible, and durable paper-like membrane features a tensile strength of 11.3 MPa and a bending rigidity in the order of 4.6 cNmm-1. The hydrophobic superinsulation membrane material also exhibits a Δ T of ≈25 °C under continuous sunlight illumination and allows thermal runaway mitigation of rechargeable lithium-ion batteries. All the aforementioned properties position this hybrid superinsulation membrane as a promising material for energy-saving thermal management applications. [ABSTRACT FROM AUTHOR]

Disordered rocksalt cathodes have shown attractive electrochemical performance via oxygen redox, but are limited by a necessary Li‐excess level above the percolation threshold (x > 1.09 in LixTM2‐xO2, TM = transition metals) to obtain electrochemical activity. However, a relatively low‐Li content is essential to alleviate excessive oxygen charge compensation in rocksalt oxides. Herein, taking the homogeneous Li2MnO3 and LiMn2O4 as the starting point, disordered rocksalt‐like cathodes are prepared with initial Li‐deficient nanostructures, cation vacancies, and partial spinel‐type structures that provide a solution for the acquisition of fast Li+ percolation channels under Li‐deficient condition. As a result, the prepared sample exhibits high initial discharge capacity (363 mAh g−1) and energy density (1081 Wh kg−1). Advanced spectroscopy and in situ measurements observe highly reversible charge compensation during electrochemical process and assign coupled Mn‐ and O‐related redox contribution. Theoretical calculations also suggest the novel and chemical reversible trapped molecular O2 model in the rocksalt structure with vacancies, demonstrating a dual role of Li‐deficient structure in promoting cationic oxidation and extending reversible oxygen redox boundary. This work is expected to breakthrough the existing ideas of oxygen oxidation and opens up a higher degree of freedom in the design of disordered rocksalt structures. [ABSTRACT FROM AUTHOR]

A new amide tricholomine C was isolated from the dried fruiting bodies of Tricholoma bakamatsutake. Its structure was identified by a combination of nuclear magnetic resonance spectroscopic analysis and electronic circular dichroism (ECD) calculations. The ethyl alcohol crude extract and tricholomines A–C from T. bakamatsutake were evaluated for neuroprotective activities. Of these substances, the crude extract showed weak neurite outgrowth‐promoting activity in rat pheochromocytoma (PC12) cells, as well as weak inhibitory activities against acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). [ABSTRACT FROM AUTHOR]

Background: Atopic dermatitis (AD) is a chronic inflammatory skin disease with a genetic predisposition, and the traditional Chinese medicine Morinda officinalis and its roots are characterized with anti‐inflammatory effects and have been used for the treatment of various disease. However, it is still largely unknown whether Morinda officinalis extract (MOE) can be used for the treatment of AD. Objectives: In our study we aimed to determine whether MOE could ameliorate 2,4‐dinitrochlorobenzene (DNCB)‐induced AD and elucidate molecular mechanisms. Methods: We established an AD mouse model by using DNCB. Skin pathological analysis and ELISA assay were used to detect the effect of MOE on the inflammation of AD model mouse skin and the expression changes of inflammatory factors, and further functional verification was performed in TNF‐α/IFN‐γ‐induced HaCaT cells. Results: Our in vivo experiments confirmed that MOE remarkably reduced DNCB‐induced AD lesions and symptoms, such as epidermal and dermal thickness and mast cell infiltration and inflammatory cytokines secretion in the mice models. In addition, the underlying mechanisms by which MOE ameliorated AD had been uncovered, and we verified that MOE inhibited MALAT1 expression in AD, resulting in attenuated expression of C‐C chemokine receptor type 7 (CCR7) regulated by MALAT1‐sponge miR‐590‐5p in a competing endogenous RNA (ceRNA) mechanisms‐dependent manner, thereby inhibiting TNF‐α/IFN‐γ‐induced cellular proliferation and inflammation. [ABSTRACT FROM AUTHOR]

Aims: Muscleblind-like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models. Methods: To create Mbnl2 knockout neurons, cDNA encoding Cre-recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two-photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis. Results: We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha-II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2. Conclusion: MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis-splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Soybean 11S globulin has good functional properties, which are widely used in the field of food. However, natural soybean 11S globulin (N-11S) has low flexibility and is easy to aggregate, impacting its foaming process. Studies have shown that soybean 11S globulin in molten globule state (MG-11S) has better molecular flexibility than N-11S, and trehalose has been shown to improve the properties of proteins. Therefore, this study investigated the interaction mechanism between trehalose and MG-11S, and its impact on rheological and foaming properties of MG-11S. RESULTS: The molecular docking and intrinsic fluorescence results showed that hydrogen bonding was the main interaction force at lower than 0.5 mol L-1 trehalose added. Meanwhile, rheology and foaming showed that the MG-11S-trehalose complexes had better viscoelasticity, foaming ability (66.67-86.67%) and foaming stability (75.00-89.29%) than N-11S (16.67% foaming ability and 40.00% foaming stability); however, when the trehalose was higher than 0.5 mol L-1, molecular crowding occurred and H-bonds were weakened, resulting in reduction of foaming capacities. Microstructure determination showed that trehalose attached to the surface of foam membrane; meanwhile, the foaming structure of the complex with 0.5 mol L-1 trehalose had a thicker liquid film with decreased drainage rate, less agglomeration and disproportionation of foam, illustrating the best foaming ability and foaming stability. CONCLUSION: The results suggested that trehalose at different concentrations can interact with MG-11S through different mechanisms, and improve the foaming capacity of MS-11S. This provided a reference for the application of MS-11S in foaming food. [ABSTRACT FROM AUTHOR]

Aims: Muscleblind‐like 2 (MBNL2) plays a crucial role in regulating alternative splicing during development and mouse loss of MBNL2 recapitulates brain phenotypes in myotonic dystrophy (DM). However, the mechanisms underlying DM neuropathogenesis during brain development remain unclear. In this study, we aim to investigate the impact of MBNL2 elimination on neuronal development by Mbnl2 conditional knockout (CKO) mouse models. Methods: To create Mbnl2 knockout neurons, cDNA encoding Cre‐recombinase was delivered into neural progenitors of Mbnl2flox/flox mouse brains by in utero electroporation. The morphologies and dynamics of dendritic spines were monitored by confocal and two‐photon microscopy in brain slices and live animals from the neonatal period into adulthood. To investigate the underlying molecular mechanism, we further detected the changes in the splicing and molecular interactions of proteins associated with spinogenesis. Results: We found that Mbnl2 knockout in cortical neurons decreased dendritic spine density and dynamics in adolescent mice. Mbnl2 ablation caused the adducin 1 (ADD1) isoform to switch from adult to fetal with a frameshift, and the truncated ADD1 failed to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. In addition, expression of ADD1 adult isoform compensated for the reduced dendritic spine density in cortical neurons deprived of MBNL2. Conclusion: MBNL2 plays a critical role in maintaining the dynamics and homeostasis of dendritic spines in the developing brain. Mis‐splicing of downstream ADD1 may account for the alterations and contribute to the DM brain pathogenesis.In Mbnl2‐knockout mouse model of myotonic dystrophy (DM), the density and dynamics of dendritic spines of cortical neurons were decreased during adolescence. Meanwhile, adducin 1 (ADD1) switched from adult to fetal isoform with a frameshift, causing the truncated ADD1 failing to interact with alpha‐II spectrin (SPTAN1), a critical protein for spinogenesis. Their roles in maintaining the dynamics and homeostasis of dendritic spines in the developing brain may underlie the neurological symptoms in DM patients. [ABSTRACT FROM AUTHOR]

Constructing stable electrode/electrolyte interphase with fast interfacial kinetics is vital for fast‐charging batteries. Herein, we investigate the interphase that forms between a high‐voltage Na3V2(PO4)2F3 cathode and the electrolytes consisting of 3.0, 1.0, or 0.3 M NaClO4 in an organic carbonate solvent (47.5 : 47.5 : 5 mixture of EC: PC: FEC) during charging up to 4.5 V at 55 °C. It is found that a higher anion/solvent ratio in electrolyte solvation structure induces anion‐dominated interphase containing more inorganic species and more anion derivatives (CxClOy), which leads to a larger interfacial Na+ transport resistance and more unfavorable gas evolution. In comparison, a low anion/solvent ratio derives stable anion‐tuned interphase that enables better interfacial kinetics and cycle ability. Importantly, the performance of a failed cathode is restored by triggering the decomposition of CxClOy species. This work elucidates the role of tuning interphase in fast‐charging batteries. [ABSTRACT FROM AUTHOR]

Background: Most dyes are toxic, carcinogenic, and mutagenic, all of which cause severe harm to human health and the environment. Therefore, it is essential to find the most suitable method to treat dye wastewaters before discharge. In this study, the natural Ca‐type montmorillonite (Ca‐MMT) was activated by HNO3 (20 wt.%) solution under different temperatures to obtain acid‐activated MMT (Acid‐MMT). Fe (10 wt.%) was supported on Acid‐MMT (Fe/Acid‐MMT) via the impregnation method using Fe(NO3)3·9H2O as a precursor. Meanwhile, the removal of methylene blue (MB) by heterogeneous Fenton‐like reaction using Fe/Acid‐MMT as catalyst was evaluated. The material was characterized by Fourier transform infrared spectroscopy (FT‐IR), X‐ray diffraction (XRD), X‐ray photoeletron spectroscopy (XPS), scanning electron microscopy (SEM), N2 adsorption–desorption at low temperature, and the temperature program desorption of NH3 (NH3‐TPD) techniques. Results: The acidity and textural properties of the Acid‐MMT were adjusted by varying the acid activation temperature. Moreover, the amount of acidity and the surface area of the catalyst had a noticeable effect on the removal efficiency of MB. Fe‐supported Acid‐MMT activated by HNO3 at 100°C (Fe/Acid‐MMT‐100) catalyst exhibited the highest removal efficiency of MB. The removal efficiency of the MB was more than 97.8% under the following reaction conditions: H2O2 concentration of 0.85 mmol·L−1, Fe/Acid‐MMT‐100 dosage of 0.75 g°L−1, temperature of 50°C, and initial solution pH of 3.0–9.0. Conclusion: An efficient Fe/Acid‐MMT catalyst for a Fenton‐like reaction was obtained by optimizing the acid treatment temperature of Ca‐MMT. The synergistic effect between its excellent adsorption ability and the ∙OH generated from H2O2 activated by Fe/Acid‐MMT would enhance MB removal efficiency in a Fenton‐like system. © 2022 Society of Chemical Industry (SCI). [ABSTRACT FROM AUTHOR]

Spinel LiNi0.5Mn1.5O4 (LNMO), high‐voltage and high‐power density, is a very promising cathode candidate. Nevertheless, its lack of cycling stability has historically been long accepted as an inherent issue. Based on the above problem, a strategy is initiated to directly address Mn dissolution and unstable interface structure. A beneficial solid‐phase reaction occurs at the LNMO interface, transforming the spinel phase into two functional phases. One is the layered phase that provides electrochemical activity and supports charge transport. The other is the rock‐salt like phase induced by Li/Mn exchange that can inhibit the dissolution of Mn and provide inert protection. The Li/Mn exchange structure increases the diffusion energy barriers of Mn, which restrains the loss of Mn, proven by the bond valence sum calculation. The two phases are modulated successfully at the LNMO interface to balance the stable material structure and excellent charge transfer, obtaining a sample with excellent electrochemical performance. The capacity retention rate of modified LNMO is 15% higher than that of the pristine sample after 500 cycles. The preparation method does not utilize any dopants or coatings and can play a guiding role in addressing issues regarding structural stability and electrochemical performance for cathode materials. [ABSTRACT FROM AUTHOR]

We report the preparation and structural characterization of the first known pincer carbodicarbene (CDC) supported ruthenium complexes. The single‐crystal X‐ray diffraction experiment indicated that tridentate bis(pyridyl)‐CDC free ligand is coordinated to the six‐coordinated ruthenium (II) in meridional conformation with each of two chlorides trans to the carbone carbon and phosphine. The pincer effect of new ligand bis(pyridyl)‐CDC has shortened the Ru‐carbodicarbene bond length in comparison to monodentate CDC. The catalytic activity of the new CDC complexes was tested in hydrogen transfer reaction, revealing the efficient activity of CDC‐supported Ru complexes in catalytic transfer hydrogenation of ketone using 2‐propanol as hydrogen source. [ABSTRACT FROM AUTHOR]

Background: The prevalence of sleep‐disordered breathing (SDB) is closely related to the severity of heart failure (HF), and the severity of HF is different in patients with HF of different etiologies. Hypothesis: This study aimed to explore the prevalence of SDB in patients with HFof different etiologies. Methods: Hospitalized HF patients were consecutively enrolled. All patients underwent portable overnight cardiorespiratory polygraphy. Patients were divided into five groups according to the etiology of HF: ischemic, hypertensive, myocardial, valvular, and arrhythmic. The prevalence of SDB and clinical data was compared among the five groups. Results: In total, 248 patients were enrolled in this study. The prevalence of SDB in HF was 70.6%, with the prevalence of obstructive sleep apnea (OSA) at 47.6% and central sleep apnea (CSA) at 23.0%. Patients were divided into five groups: ischemic, hypertensive, myocardial, valvular, and arrhythmic. The prevalence of SDB among the five groups was 75.3%, 81.4%, 77.8%, 51.9%, and 58.5% (p =.014), respectively. The prevalence of OSA among the five groups was 42.7%, 72.1%, 36.1%, 37.0%, and 49.1% (p =.009), whereas the CSA was 32.6%, 9.3%, 41.7%, 14.8%, and 9.4% (p <.001), respectively. Conclusions: SDB is common in HF patients. The prevalence and types of SDB varied in HF with different etiologies, which may be related to the different severities of HF. SDB was highly prevalent in patients with ischemic, hypertensive, and myocardial HF. Hypertensive HF patients were mainly complicated with OSA, while myocardial HF patients were mainly complicated with CSA. Both conditions were highly prevalent in ischemic HF patients. The prevalence of SDB was relatively low in valvular and arrhythmic HF patients, and OSA was the main type. [ABSTRACT FROM AUTHOR]

WEE1 plays an important role in the regulation of cell cycle G2/M checkpoints and DNA damage response (DDR). Inhibition of WEE1 can increase the instability of the genome and have anti-tumor effects in some solid tumors. However, it has certain limitations for multiple cancer cells from different lineages. Therefore, we consider the use of synthetic lethal interactions to enhance the therapeutic effect. Our experiments proved that WEE1 inhibitor (WEE1i) can activate the ataxia telangiectasia and RAD3-related (ATR) pathway and that blockage of ATR dramatically sensitized the WEE1i-induced cell death. The tumor-selective synthetic lethality between bioavailable WEE1 and ATR inhibitors led to tumor remission in vivo. Mechanistically, the combination promoted the accumulation of cytosolic double-strand DNA, which subsequently activated the stimulator of the interferon gene (STING) pathway and induced the production of type I interferon and CD8+ T cells, thereby inducing anti-tumor immunity. Furthermore, our study found that immune checkpoint programmed death-ligand 1 is upregulated by the combination therapy, and blocking PD-L1 further enhances the effect of the combination therapy. In summary, as an immunomodulator, the combination of WEE1i with ATR inhibitor (ATRi) and immune checkpoint blockers provides a potential new approach for cancer treatment. [ABSTRACT FROM AUTHOR]

Background: The optimal first‐line approach for patients with symptomatic atrial fibrillation (AF) remains unclear. We compared the efficacy and safety of cryoballoon ablation (CBA) and antiarrhythmic drugs (AADs) in the initial management of symptomatic AF. Hypothesis: CBA is superior to AAD as initial therapy for symptomatic AF. Methods: We searched the EMBASE, PubMed, and Cochrane Library databases for randomized controlled trials (RCTs) that compared CBA with AAD as first‐line treatment for AF from the date of database establishment until March 18, 2021. The risk ratio (RR) with a 95% confidence interval (CI) was used as a measure of treatment effect. Results: Three RCTs that enrolled 724 patients in total were included in this meta‐analysis. Majority of the patients were relatively young and had paroxysmal AF. CBA was associated with a significant reduction in the recurrence of atrial arrhythmia compared with AAD therapy, with low heterogeneity (RR, 0.59; 95% CI, 0.49–0.71; p <.00001; I2 = 0%). There was a significant difference in the rate of symptomatic atrial arrhythmia recurrence (RR, 0.44; 95% CI, 0.29–0.65; p <.0001; I2 = 0%); however, the rate of serious adverse events was similar between the two treatment groups (RR: 1.18; 95% CI: 0.71–1.97, p =.53; I2 = 0%). Transient phrenic nerve palsy occurred in four patients after the CBA procedure. Conclusion: The current meta‐analysis suggests that CBA is more effective than AAD as initial therapy in patients with symptomatic paroxysmal AF. Serious iatrogenic adverse events are uncommon in CBAs. [ABSTRACT FROM AUTHOR]

To investigate the role of circKDM4C in acute myeloid leukemia (AML), the expression of circKDM4C, hsa‐let‐7b‐5p, and P53 was measured by qRT‐RCR. AML cell lines(K‐562 and HL‐60) were transfected correspondingly and investigated for cell proliferation, migration, and invasion abilities by CCK‐8, colony formation, transwell, and wound healing assays, respectively. The levels of P53, ACSL4, PTGS2, GPX4, and FTH1 in the K‐562, and HL‐60 cells were measured by western blotting. Also, circKDM4C mediated regulation of ferroptosis was studied. The Phen Green SK probe and confocal laser scanning microscope were used to assess the cellular iron levels. The reactive oxygen species levels were analyzed by fluorescence‐activated cell sorting using the C11‐BODIPY probe. Bioinformatics analysis predicted the putative binding sites among circKDM4C, hsa‐let‐7b‐5p, and P53. These were verified using the dual‐luciferase reporter assay, RNA pull‐down, and RNA immunoprecipitation assays. Finally, in vitro findings were also verified in vivo using the nude mice. CircKDM4C was significantly down‐regulated in AML patients. The overexpression of circKDM4C in AML cell lines inhibited the cell proliferation, migration, invasion, and promoted ferroptosis. We found that circKDM4C acts as a sponge of hsa‐let‐7b‐5p and thereby regulates p53 which is a target gene of hsa‐let‐7b‐5p. Also, the expression of circKDM4C and hsa‐let‐7b‐5p are negatively correlated, while circKDM4C and p53 are positively correlated to AML patients. Moreover, we found that circKDM4C induces ferroptosis by sponging hsa‐let‐7b‐5p which upregulates the expression of P53. This work emphasizes the role of circKDM4C in AML patients, which could be explored for the therapeutic role. [ABSTRACT FROM AUTHOR]

Two new amides tricholomines A (1) and B (2), along with nine known compounds, were isolated from the dried fruiting bodies of Tricholoma bakamatsutake. Their structures were determined on the basis of extensive spectroscopic analysis or comparison with the data in the literatures. The absolute configuration of 1 was confirmed by single crystal X‐ray diffraction analysis. [ABSTRACT FROM AUTHOR]

Cathodes in lithium‐ion batteries with anionic redox can deliver extraordinarily high specific capacities but also present many issues such as oxygen release, voltage hysteresis, and sluggish kinetics. Identifying problems and developing solutions for these materials are vital for creating high‐energy lithium‐ion batteries. Herein, the electrochemical and structural monitoring is conducted on lithium‐rich cathodes to directly probe the formation processes of larger voltage hysteresis. These results indicate that the charge‐compensation properties, structural evolution, and transition metal (TM) ions migration vary from oxidation to reduction process. This leads to huge differences in charge and discharge voltage profile. Meanwhile, the anionic redox processes display a slow kinetics process with large hysteresis (≈0.5 V), compared to fast cationic redox processes without any hysteresis. More importantly, a simple yet effective strategy has been proposed where fine‐modulating local oxygen environment by the lithium/oxygen (Li/O) ratio tunes the anionic redox chemistry. This effectively improves its electrochemical properties, including the operating voltage and kinetics. This is also verified by theoretical calculations that adjusting anionic redox chemistry by the Li/O ratio shifts the TM 3d—O 2p bands and the non‐bonding O 2p band to a lower energy level, resulting in a higher redox reaction potential. [ABSTRACT FROM AUTHOR]

A simple Ni(cod)2 and carbene mediated strategy facilitates the efficient catalytic cross‐coupling of methoxyarenes with a variety of organoboron reagents. Directing groups facilitate the activation of inert C−O bonds in under‐utilized aryl methyl ethers enabling their adaptation for C−C cross‐coupling reactions as less toxic surrogates to the ubiquitous haloarenes. The method reported enables C−C cross‐coupling with readily available and economical arylboronic acid reagents, which is unprecedented, and compares well with other organoboron reagents with similarly high reactivity. Extension to directing group assisted chemo‐selective C−O bond cleavage, and further application towards the synthesis of novel bifunctionalized biaryls is reported. Key to the success of this protocol is the use of directing groups proximal to the reaction center to facilitate the activation of the inert C−OMe bond. [ABSTRACT FROM AUTHOR]

Li‐rich layered oxides (LLRO) are promising high energy‐density cathode, but always suffer from the oxygen loss in initial activation and gradual structure transformation during cycling, which leads to capacity degradation and potential decay. Here, we employ a simple strategy to achieve the collaboration of surface protection and bulk doping for improving the performance of Li‐rich material. Scanning electron microscope and transmission electron microscopy tests demonstrate that a nanoscale protective layer of magnesium pyrophosphate is uniformly coated on the Li‐rich material surface. X‐ray diffraction test indicates Mg2+ and P2O74− are incorporated into the crystal structure, which induces the larger lattice spacing and lower cation mixing. As a result, the resultant LLRO displays extremely high Coulombic efficiency of 91.8% and discharge capacity of 288.4 mAh g−1, showing prominent cycling stability of 89.2% after 200 cycles. Furthermore, our strategy also suppresses the attenuation of average voltage during cycling and the potential drop is only 0.56 mV per cycle from 25 th to 200 th cycle. The excellent electrochemical performance can be ascribed to the combined merits of surface protection and bulk doping. This strategy may provide some new insights into the design and synthesis of high‐performance electrode materials. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S) has a significant effect on the regulation of interleukin‐6 (IL‐6) and signal transducer and activator of transcription 3 (STAT3) activities, while IL‐6 directly regulates hepcidin expression via STAT3. We therefore hypothesized that H 2S has a role in body iron homeostasis by regulating the expression of iron transport proteins via the IL‐6/STAT3/Hepcidin pathway. Here, we investigated the effects of two H 2S donors sodium hydrosulfide and GYY4137 on the expression of ferroportin‐1 (Fpn1), transferrin receptor‐1 (TfR1), hepcidin, IL‐6 and pSTAT3 in the spleen of mice in vivo and peritoneal macrophage in vitro. We also examined the effects of H 2S on serum iron, transferrin saturation, and ferritin light chain contents in the spleen, and on nitrite content, nuclear factor erythroid 2‐related factor‐2 (Nrf2) and iron regulatory protein 1 (IRP1) in the macrophages. We demonstrated that H 2S regulates the expression of TfR1 and Fpn1 in the spleen in vivo and in peritoneal macrophages in vitro predominantly via the IL‐6/pSTAT3/hepcidin pathway, under the conditions of inflammation induced by lipopolysaccharides. We also provide evidence that under uninflamed conditions, the regulation of Fpn1 and TfR1 expression by H 2S, both in vivo and in vitro, are mediated by the nitric oxide (NO)/Nrf2 and iron regulatory protein/iron responsive element pathways, respectively, which are independent of IL‐6/pSTAT3/hepcidin signals. These findings show that H 2S is a key player in iron homeostasis under not only the inflamed conditions but also uninflamed conditions. H2S regulates the expression of TfR1 and Fpn1 in the spleen in vivo and in peritoneal macrophages in vitro predominantly via the IL‐6/pSTAT3/hepcidin pathway, under the conditions of inflammation. Under uninflamed conditions, the regulation of Fpn1 and TfR1 expression by H 2S, both in vivo and in vitro, are mediated by the NO/Nrf2 and iron regulatory protein/iron responsive element pathways, respectively, which are independent of IL‐6/pSTAT3/hepcidin signals. These findings show that H 2S is a key player in iron homeostasis under not only the inflamed conditions but also uninflamed conditions. [ABSTRACT FROM AUTHOR]

Abstract: This paper develops a new theoretical model with an asymmetric informal one‐sided exchange rate target zone, with an application to the Swiss franc following the removal of the minimum exchange rate of CHF 1.20 per euro in January 2015. We extend and generalize a standard target zone model by introducing perceived uncertainty about the lower edge of the band. We find that informal soft edge target zone bands lead to weaker honeymoon effects, wider target zone ranges, and higher exchange rate volatility than formal target zone bands. These results suggest that it would be beneficial for exchange rate policy intentions to be stated clearly in order to anchor exchange rate expectations and reduce exchange rate volatility. We also study how exchange rate dynamics can be characterized in models in which financial markets are aware of occasional changes in the policy regime. We show that expected changes in the central bank's exchange rate policy may lead to exchange rate oscillations, providing an additional source of exchange rate volatility, and to capture this it is important to take into account the possibility of regime changes in exchange rate policy. [ABSTRACT FROM AUTHOR]

The significant positive correlation between ghrelin and iron and hepcidin levels in the plasma of children with iron deficiency anemia prompted us to hypothesize that ghrelin may affect iron metabolism. Here, we investigated the effects of fasting or ghrelin on the expression of hepcidin, ferroportin 1 (Fpn1), transferrin receptor 1 (TfR1), ferritin light chain (Ft-L) proteins, and ghrelin, and also hormone secretagogue receptor 1 alpha (GHSR1α) and ghrelin O-acyltransferase (GOAT) mRNAs in the spleen and/or macrophage. We demonstrated that fasting induces a significant increase in the expression of ghrelin, GHSR1α, GOAT, and hepcidin mRNAs, as well as Ft-L and Fpn1 but not TfR1 proteins in the spleens of mice in vivo. Similar to the effects of fasting on the spleen, ghrelin induced a significant increase in the expression of Ft-L and Fpn1 but not TfR1 proteins in macrophages in vitro. In addition, ghrelin was found to induce a significant enhancement in phosphorylation of ERK as well as translocation of pERK from the cytosol to nuclei. Furthermore, the increased pERK and Fpn1 induced by ghrelin was demonstrated to be preventable by pre-treatment with either GHSR1α antagonist or pERK inhibitor. Our findings support the hypothesis that fasting upregulates Fpn1 expression, probably via a ghrelin/GHSR/MAPK signaling pathway. [ABSTRACT FROM AUTHOR]

Abstract: Few systemic assessments have evaluated the success of these afforestation programs in alpine semiarid desert ecosystems in the Qinghai‐Tibet Plateau. In this study, we investigated the influences of three Salix cupularis plantation age classes (6, 18, and 34 years) on the carbon (C), nitrogen (N), and phosphorus (P) storages and stoichiometry of the soil–plant ecosystem. The consequences of S. cupularis plantation induced soil spatial heterogeneity. The soil–plant ecosystem C storage increased after the plantation. The N storage showed an increasing trend from 6 to 18 years and then slightly decreased. The P storage presented a continuously declining trend. The result indicated that the imbalance in soil N, P, C occurred with plantation age because of the imbalance of their inputs. The N and P uptakes from subsoil and redistribution to topsoil by S. cupularis may contribute to meet N and P demands for the understory plants. Leaf N:P ratios varied from 8.3 to 17.5. These results imply that N and P status are the main factors limiting plant growth in the alpine‐cold desert ecosystem. Thus, we recommend adding N and P fertilizers during plant growth. [ABSTRACT FROM AUTHOR]

In this paper, based on an adaptive nonbackstepping design algorithm, we proposed a novel variable universe of discourse fuzzy control (VUDFC) approach for a class of single-input-single-output strict-feedback nonlinear systems with unknown dead-zone inputs. Firstly, we convert the form of system into a normal form on the basis of some new state variables and coordinate transformation; at the same time, state-feedback control is changed to output-feedback control. Secondly, we design observers to estimate the new unmeasurable states. Then, different from considering the traditional backstepping-based fuzzy control scheme, we introduce a direct VUDFC scheme, which is mainly based on changing of contraction-expansion factors to modify the universe of discourse online, and fuzzy rules can automatically reproduce to develop the control performance; thus, the size of initial rule base is greatly reduced. This new algorithm can alleviate tracking error, improve the accuracy of the system, and strengthen robustness. Lastly, according to Lyapunov theorem analysis, we prove that all the signals in the closed-loop system can be guaranteed to be stable, and the output can track the reference signal very well. Simulation results illustrated the effectiveness of the proposed VUDFC approach. [ABSTRACT FROM AUTHOR]

This paper adds to the literature on wealth effects on consumption by disentangling house price effects on consumption for mainland China. In a stochastic modelling framework, the riskiness, rate of increase and persistence of house price movements have different implications for the consumption/housing ratio. We exploit the geographical variation in property prices by using a quarterly city-level panel data set for the period 1998Q1- 2009Q4 and rely on a panel error correction model. Overall, the results suggest a significant long-run impact of property prices on consumption. They also broadly confirm the predictions from the theoretical model. [ABSTRACT FROM AUTHOR]

The advancement of cancer-fighting drugs has never been a simple linear process. Those drug design professionals begin to find inspiration from the nature after failing to find the ideal products by creative drug design and high-throughput screening. To obtain new molecules for inhibiting tubulin, podophyllotoxin was adopted as the leading compound and 1,3,4-oxadiazole was brought in to the C-4 site of podophyllotoxin in this research. A series of seventeen podophyllotoxin-derived esters have been achieved and then evaluated their antitumor activities against four different cancer cell lines: A549, MCF-7, HepG2, and HeLa. Among all the compounds, compound 7c showed the best antiproliferating properties with IC50 = 2.54 ± 0.82 μ m against MCF-7 cancer cell line. It was obvious that the content of ROS grew significantly in MCF-7 in a way depending on the dosage. The time- and dose-dependent cell cycle assays revealed that compound 7c could apparently block cell cycle in the phase of G2/M along with the upregulation of cyclin A2 and CDK2 protein. According to further studies, confocal microscopy experiment has certified that compound 7c could restrain cancer from growing by blocking the polymerization of microtubule. Meanwhile, compound 7c could be ideally integrated with the colchicine site of tubulin. In future, it would be feasible to selectively design tubulin inhibitors with the help of 3D- QSAR. This means that it is hopeful to develop compound 7c as a potential agent against cancer due to its biological characteristics. [ABSTRACT FROM AUTHOR]

Rice starch (RS) and blend of rice starch with 10% w/w of stabilized rice bran (SRB) were subjected to extrusion process in a co-rotating twin-screw extruder. The effect of SRB addition and extrusion on gelatinization and retrogradation properties of RS was investigated. The results obtained from the rapid visco analyzer (RVA) showed a significant decrease (p<0.05) in viscosity of the extruded RS compared to the untreated RS. In addition, the viscosity was more decreased after enrichment of RS with SRB and extrusion. A similar decrease trend in gelatinization enthalpy (ΔHgel) of RS was also observed from data of the differential scanning calorimetry (DSC). On the other hand, the enrichment with SRB and extrusion led to significant changes in the crystalline structure of RS as observed from the X-ray diffraction (XRD). Furthermore, the enrichment with SRB and extrusion generated a fibrous and porous structured starch gel with lower retrogradation rate, higher water-holding capacity, and less syneresis during storage at 4°C for 7 days. Therefore, SRB can be recommended as functional food ingredient for enrichment and producing rice starch-based extruded snacks and ready-to-eat food products. [ABSTRACT FROM AUTHOR]

Oral cancer is one of the cancer-related diseases in human populations and its incidence rates are rising worldwide. Fisetin, a flavonoid from natural products, has been shown to exhibit anticancer activities in many human cancer cell lines but the molecular mechanism of fisetin-induced apoptosis in human oral cancer cells is still unclear; thus, in this study, we investigated fisetin-induced cell death and associated signal pathways on human oral cancer SCC-4 cells in vitro. We examined cell morphological changes, total viable cells, and cell cycle distribution by phase contrast microscopy and flow cytometry assays. Reactive oxygen species (ROS), Ca2+, mitochondria membrane potential (ΔΨm), and caspase-8, -9, and -3 activities were also measured by flow cytometer. Results indicate that fisetin induced cell death through the cell morphological changes, caused G2/M phase arrest, induction of apoptosis, promoted ROS and Ca2+ production, and decreased the level of ΔΨm and increased caspase-3, -8, and -9 activities in SCC-4 cells. DAPI staining and DNA gel electrophoresis were also used to confirm fisetin-induced cell apoptosis in SCC-4 cells. Western blotting also found out that Fisetin increased the proapoptotic proteins such as Bax and Bid and decreased the antiapoptotic proteins such as Bcl-2. Furthermore, results also showed that Fisetin increased the cytochrome c, AIF, and Endo G release from mitochondria in SCC-4 cells. We also used ATF-6α, ATF-6β, GADD153, and GRP78 which indicated that fisetin induced cell death through ER stress. Based on those observations, we suggest that fisetin induced cell apoptosis through ER stress, mitochondria-, and caspase-dependent pathways. [ABSTRACT FROM AUTHOR]

ABSTRACT Cantharidin (CTD), a potential anticancer agent of Traditional Chinese Medicine has cytotxic effects in different human cancer cell lines. The cytotoxic effects of CTD on A431 human skin cancer (epidermoid carcinoma) cells in vitro and in A431 cell xenograft mouse model were examined. In vitro, A431 human skin cell were treated with CTD for 24 and 48 h. Cell phase distribution, ROS production, Ca2+ release, Caspase activity and the level of apoptosis associated proteins were measured. In vivo, A431 cell xenograft mouse model were examined. CTD-induced cell morphological changes and decreased percentage of viable A431 cells via G0/G1 phase arrest and induced apoptosis. CTD-induced G0/G1 phase arrest through the reduction of protein levels of cyclin E, CDK6, and cyclin D in A431 cells. CTD-induced cell apoptosis of A431 cells also was confirm by DNA gel electrophoresis showed CTD-induced DNA fragmentation. CTD reduced the mitochondrial membrane potential and stimulated release of cytochrome c, AIF and Endo G in A431 cells. Flow cytometry demonstrated that CTD increased activity of caspase-8, −9 and −3. However, when cells were pretreated with specific caspase inhibitors activity was reduced and cell viability increased. CTD increased protein levels of death receptors such as DR4, DR5, TRAIL and levels of the active form of caspase-8, −9 and −3 in A431 cells. AIF and Endo G proteins levels were also enhanced by CTD. In vivo studies showed that CTD significantly inhibited A431 cell xenograft tumors in mice. Taken together, these in vitro and in vivo results provide insight into the mechanisms of CTD on cell growth and tumor production. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 723-738, 2017. [ABSTRACT FROM AUTHOR]

ABSTRACT Deguelin, a naturally occurring rotenoid of the flavonoid family, is known to be an Akt inhibitor, to have chemopreventive activities and anti-tumor effect on several cancers. In this study, investigation to elucidate the effect of deguelin on apoptotic pathways in human lung cancer cells and on the anti-tumor effect in lung cancer xenograft nu/nu mice was performed. In vitro studies, found that deguelin induced cell morphological changes, and decreased the percentage of viability through the induction of apoptosis in H460 lung cancer cells. Deguelin triggered apoptosis in H460 cells was also confirmed by DAPI staining, DNA gel electrophoresis, and Annexin V-FITC staining and these effects are dose-dependent manners. It was also found that deguelin promoted the Ca2+ production and activation of caspase-3 but decreased the level of Δ Ψm in H460 cells. Western blots indicated that the protein levels of cytochrome c, AIF, and pro-apoptotic Bax and Bak protein were increased, but the anti-apoptotic Bcl-2 and Bcl-x were decreased that may have led to apoptosis in H460 cells after exposure to deguelin. It was also confirmed by confocal laser microscope examination that deguelin promoted the release of AIF from mitochondria to cytosol. In vivo studies, found that in immunodeficient nu/nu mice bearing H460 tumor xenografts showed that the deguelin significantly suppressed tumor growth. Deguelin might be a potential therapeutic agent for the treatment of lung cancer in the future. This finding might fully support a critical event for deguelin via induction of apoptotic cell death and H460 tumor xenografts model against human lung cancer. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 84-98, 2017. [ABSTRACT FROM AUTHOR]

ABSTRACT Tetrandrine, a bisbenzylisoquinoline alkaloid, is extracted from the root of the Chinese herb Radix Stephania tetrandra S Moore. This compound has antitumor activity in different cancer cell types. In this study, the effects of tetrandrine on human oral cancer CAL 27 cells were examined. Results indicated that tetrandrine induced cytotoxic activity in CAL 27 cells. Effects were due to cell death by the induction of apoptosis and accompany with autophagy and these effects were concentration- and time-dependent manners. Tetrandrine induced apoptosis was accompanied by alterations in cell morphology, chromatin fragmentation, and caspase activation in CAL 27 cells. Tetrandrine treatment also induced intracellular accumulation of reactive oxygen species (ROS). The generation of ROS may play an important role in tetrandrine-induced apoptosis. Tetrandrine triggered LC3B expression and induced autophagy in CAL 27 cells. Tetrandrine induced apoptosis and autophagy were significantly attenuated by N-acetylcysteine pretreatment that supports the involvement of ROS production. Tetrandrine induced cell death may act through caspase-dependent apoptosis with Beclin-1-induced autophagy in human oral cancer cells. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 329-343, 2017. [ABSTRACT FROM AUTHOR]

ABSTRACT Melanoma cancer is one of the major causes of death in humans worldwide. Triptolide is one of the active components of Tripterygium wilfordii Hook F, and has biological activities including induced cell cycle arrest and induction of apoptosis but its antimetastatic effects on murine melanoma cells have not yet been elucidated. Herein, we investigated the effect of triptolide on the inhibition of migration and invasion and possible associated signal pathways in B16F10 murine melanoma cancer cells. Wound healing assay and Matrigel Cell Migration Assay and Invasion System demonstrated that triptolide marked inhibiting the migration and invasion of B16F10 cells. Gelatin zymography assay demonstrated that triptolide significantly inhibited the activities of matrix metalloproteinases-2 (MMP-2). Western blotting showed that triptolide markedly reduced CXCR4, SOS1, GRB2, p-ERK, FAK, p-AKT, Rho A, p-JNK, NF-κB, MMP-9, and MMP-2 but increased PI3K and p-p38 and COX2 after compared to the untreated (control) cells. Real time PCR indicated that triptolide inhibited the gene expression of MMP-2, FAK, ROCK-1, and NF-κB but did not significantly affect TIMP-1 and -2 gene expression in B16F10 cells in vitro. EMSA assay also showed that triptolide inhibited NF-κB DNA binding in a dose-dependent manner. Confocal laser microscopy examination also confirmed that triptolide inhibited the expression of NF-κB in B16F10 cells. Taken together, we suggest that triptolide inhibited B16F10 cell migration and invasion via the inhibition of NF-κB expression then led to suppress MMP-2 and -9 expressions. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1974-1984, 2016. [ABSTRACT FROM AUTHOR]

The cover image is based on the Original Article Muscleblind‐Like 2 knockout shifts adducin 1 isoform expression and alters dendritic spine dynamics of cortical neurons during brain development by Chia‐Wei Huang et al., https://doi.org/10.1111/nan.12890. [ABSTRACT FROM AUTHOR]

Soil aggregate breakdown and detachment due to raindrop splash cause crusting and interrill erosion. Although raindrop splash can cause the aggregate breakdown, this fundamental processes associated with the size of splashed raindrops and their distance interval remain unresolved. To determine the relations between splash raindrop size/distance and the soil aggregate detachment/transport in the Loess Plateau of China, simulated rainfalls were created by a self-designed raindrop generation device for six raindrop sizes (raindrop diameter, 2.67-5.45 mm) and five splash distances (range, 0-10 cm to 40-50 cm). The results showed that the relationship between the amount of splash detachment and the raindrop size increased in a positive linear trend (P < 0.05) and that the relationship between the amount of splash detachment and raindrop size was a significantly decreased exponential function (P < 0.05). A model was obtained to predict the amounts of splash detachment (M) for the raindrop sizes (D) and distance of splash detachment (S): M = 0.741D4.846 S-1.820 (P < 0.05; r2=0.916). The size of the raindrop in a rainfall event was the direct driving force for the aggregate breakdown and dispersion: the greater the diameter of raindrops, the higher was the degree of aggregate breakdown and dispersion. The splash erosion for the aggregate fragment <0.053 mm was at a maximum with increases in raindrop diameter, which accounted for 33.46 to 72.02% of the total splash amount. The contents of microaggregate fragments of <0.25 mm were highest at each splash distance and accounted for 50.49 to 94.04% of the total splash amount. This showed that microaggregate dispersion and breakdown is important in soil surface sealing and pore clogging. [ABSTRACT FROM AUTHOR]

ABSTRACT Tetrandrine is a bisbenzylisoquinoline alkaloid that was found in the Radix Stephania tetrandra S Moore. It had been reported to induce cytotoxic effects on many human cancer cells. In this study, we investigated the cytotoxic effects of tetrandrine on human oral cancer HSC-3 cells in vitro. Treatments of HSC-3 cells with tetrandrine significantly decreased the percentage of viable cells through the induction of autophagy and apoptosis and these effects are in concentration-dependent manner. To define the mechanism underlying the cytotoxic effects of tetrandrine, we investigated the critical molecular events known to regulate the apoptotic and autophagic machinery. Tetrandrine induced chromatin condensation, internucleosomal DNA fragmentation, activation of caspases-3, -8, and -9, and cleavage of poly (ADP ribose) polymerase (PARP) that were associated with apoptosis, and it also enhanced the expression of LC3-I and -II that were associated with the induction of autophagy in human squamous carcinoma cell line (HSC-3) cells. Tetrandrine induced autophagy in HSC-3 cells was significantly attenuated by bafilomycin A1 (inhibitor of autophagy) pre-treatment that confirmed tetrandrine induced cell death may be associated with the autophagy. In conclusion, we suggest that tetrandrine induced cell death may be through the induction of apoptosis as well as autophagy in human oral cancer HSC-3 cells via PARP, caspases/Becline I/LC3-I/II signaling pathways. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 395-406, 2016. [ABSTRACT FROM AUTHOR]

Human immunodeficiency virus type 1 nucleocapsid (NC) basic residues presumably contribute to virus assembly via RNA, which serves as a scaffold for Gag–Gag interaction during particle assembly. To determine whether NC basic residues play a role in Gag cleavage (thereby impacting virus assembly), Gag processing efficiency and virus particle production were analyzed for an HIV-1 mutant NC15A, with alanine serving as a substitute for all NC basic residues. Results indicate that NC15A significantly impaired virus maturation in addition to significantly affecting Gag membrane binding and assembly. Interestingly, removal of the matrix (MA) central globular domain ameliorated the NC15A assembly and processing defects, likely through enhancement of Gag multimerization and membrane binding capacities. [ABSTRACT FROM AUTHOR]