Ultrathin Rh Nanosheets with Rich Grain Boundaries for Efficient Hydrogen Oxidation Electrocatalysis.

Two-dimensional (2D) Pt-group ultrathin nanosheets (NSs) are promising advanced electrocatalysts for energy-related catalytic reactions. However, improving the electrocatalytic activity of 2D Pt-group NSs through the addition of abundant grain boundaries (GBs) and understanding the underlying formation mechanism remain significant challenges. Herein, we report the controllable synthesis of a series of Rh-based nanocrystals (e.g., Rh nanoparticles, Rh NSs, and Rh NSs with GBs) through a CO-mediated kinetic control synthesis route. In light of the 2D NSs' structural advantages and GB modification, the Rh NSs with rich GBs exhibit an enhanced electrocatalytic activity compared to pure Rh NSs and commercial Pt/C toward the hydrogen oxidation reaction (HOR) in alkaline media. Both experimental results and theoretical computations corroborate that the GBs in the Rh NSs have the capacity to ameliorate the adsorption free energy of reaction intermediates during the HOR, thus resulting in outstanding HOR catalytic performance. Our work offers novel perspectives in the realm of developing sophisticated 2D Pt-group metal electrocatalysts with rich GBs for the energy conversion field.

Interfacial Reaction-Directed Green Synthesis of CeO2-MnO2 Catalysts for Imine Production through Oxidative Coupling of Alcohols and Amines.

Direct oxidative coupling of alcohols with amines over cheap but efficient catalysts is a promising choice for imine formation. In this study, porous CeO2-MnO2 binary oxides were prepared via an interfacial reaction between Ce2(SO4)3 and KMnO4 at room temperature without any additives. The as-prepared porous CeO2-MnO2 catalyst has a higher fraction of Ce3+, Mn3+, and Mn4+ and contains larger surface area and more oxygen vacancies. During the oxidative coupling reaction of alcohol with amine to imine, the as-obtained CeO2-MnO2 catalyst is motivated by the above encouraging characteristics and exhibits superior catalytic activity (98% conversion and 97% selectivity) and can also work effectively under a wide scope of temperatures and substrates. The in-depth in situ DRIFTS and density functional theory (DFT) results demonstrate that there is a strong interaction between CeO2 and MnO2 in the CeO2-MnO2 catalyst, exhibiting especially a positive synergistic effect in the direct coupling of alcohol and amine reaction.

FKBP12 mediates necroptosis by initiating RIPK1-RIPK3-MLKL signal transduction in response to TNF receptor 1 ligation.

Necroptosis is a regulated form of necrotic cell death that is mediated by receptor-interacting serine/threonine-protein kinase 1 (RIPK1), RIPK3 and mixed-lineage kinase domain-like protein (MLKL), which mediates necroptotic signal transduction induced by tumor necrosis factor (TNF). Although many target proteins for necroptosis have been identified, no report had indicated that FK506-binding protein 12 (FKBP12, also known as FKBP1A), an endogenous protein that regulates protein folding and conformation alteration, is involved in mediating necroptosis. In this study, we found that FKBP12 acts as a novel target protein in mediating necroptosis and the related systemic inflammatory response syndrome triggered by TNF. The mechanistic study discovered that FKBP12 is essential for initiating necrosome formation and RIPK1-RIPK3-MLKL signaling pathway activation in response to TNF receptor 1 ligation. In addition, FKBP12 is indispensable for RIPK1 and RIPK3 expression and subsequent spontaneous phosphorylation, which are essential processes for initial necrosome formation and necroptotic signal transduction; therefore, FKBP12 may target RIPK1 and RIPK3 to mediate necroptosis in vitro and in vivo Collectively, our data demonstrate that FKBP12 could be a potential therapeutic target for the clinical treatment of necroptosis-associated diseases.

Efficacy and Safety of Sacubitril/Valsartan Therapy for Acute Decompensated Heart Failure with Reduced Ejection Fraction during the Vulnerable Phase: A Multicenter, Assessor-Blinded, Prospective, Observational, Cohort Study.

BACKGROUND: The 3-month period after hospitalization for acute cardiac failure is a vulnerable phase with the highest risk of mortality and rehospitalization. Safety and efficacy of early initiation of sacubitril/valsartan during the index hospitalization for acute decompensated heart failure (ADHF) is unclear. Therefore, we tested whether sacubitril/valsartan could result in a lower rate of a composite outcome of first hospitalization for heart failure and death from cardiovascular causes compared to inhibition of the renin-angiotensin system alone. METHODS: We enrolled patients hospitalized for ADHF and reduced ejection fraction at 4 sites; patients were divided into a sacubitril/valsartan group or an angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) group. All patients were followed up for 3 months after discharge. The primary endpoint was outcomes as a composite of death from cardiovascular causes and rehospitalization for heart failure. RESULTS: In total, 251 patients who received sacubitril/valsartan and 251 patients who received ACEIs/ARBs had similar propensity scores and were included and compared. The primary endpoint was reached in 40 patients (15.9%) treated with sacubitril/valsartan and in 59 patients (23.5%) managed by ACEI/ARB (HR, 0.650; 95% CI: 0.435-0.971; p = 0.035). The NYHA class improved in 72.1% of patients in the sacubitril/valsartan group and in 59.8% of patients in the ACEI/ARB group (HR, 1.303; 95% CI: 1.097-1.548, p = 0.004). The key safety outcomes endpoints did not significantly differ. CONCLUSIONS: Among patients hospitalized with ADHF and reduced left ventricular ejection fraction, we observed that sacubitril/valsartan therapy led to reduction in death from cardiovascular causes and rehospitalizations for heart failure when compared to ACEI/ARB therapy alone during the vulnerable phase. Our results support that sacubitril/valsartan may be administered early in the vulnerable phase after ADHF and improves NYHA class.

Nitrogen-Doped Cobalt Diselenide with Cubic Phase Maintained for Enhanced Alkaline Hydrogen Evolution.

The introduction of heteroatoms is one of the most important ways to modulate the intrinsic electronic structure of electrocatalysts to improve their catalytic activity. However, for transition metal chalcogenides with highly symmetric crystal structure (HS-TMC), the introduction of heteroatoms, especially those with large atomic radius, often induces large lattice distortion and vacancy defects, which may lead to structural phase transition of doped materials or structural phase reconstruction during the catalytic reaction. Such unpredictable situations will make it difficult to explore the connection between the intrinsic electronic structure of doped catalysts and catalytic activity. Herein, taking thermodynamically stable cubic CoSe2 phase as an example, we demonstrate that nitrogen incorporation can effectively regulate the intrinsic electronic structure of HS-TMC with structural phase stability and thus promote its electrocatalytic activity for the hydrogen evolution activity (HER). In contrast, the introduction of phosphorus can lead to structural phase transition from cubic CoSe2 to orthorhombic phase, and the structural phase of phosphorus-doped CoSe2 is unstable for HER.

PI3K mediates tumor necrosis factor induced-necroptosis through initiating RIP1-RIP3-MLKL signaling pathway activation.

Necroptosis is a recently identified programmed cell death, which is initiated by receptor-interacting serine/threonine-protein kinase 1 (RIP1), RIP3 and mixed-lineage kinase domain-like protein (MLKL). It has been reported that necroptosis induced by tumor necrosis factor (TNF) was inhibited by the inhibitor of phosphatidylinositol-3-kinase (PI3K) and its substrate protein AKT, indicating that PI3K-AKT signaling pathway was involved in mediating TNF-induced necroptosis, whereas it is unclear how PI3K initiates necroptosis. In this study, we found that TNF-induced necroptosis was inhibited by chemical inhibition or genetic deletion of PI3K. Moreover, knockdown of p110α, the catalytic subunit of PI3K, significantly suppressed the phosphorylation of PI3K substrate protein AKT, and TNF-induced necroptosis was blocked by AKT inhibitors. Furthermore, we found that p110α knockdown also suppressed the phosphorylation and oligomerization of RIP1, RIP3 and MLKL in response to TNF stimulation. In addition to the critical role in mediating TNF-induced necrosome formation, p110α was also essential for the spontaneous phosphorylation of RIP1 and RIP3. Finally, we found that p110α bound to RIP3, but not RIP1, to form protein complex in the process of TNF-induced necroptosis, and mediated TNF-induced necroptosis in the absence of RIP1. Our results demonstrate that PI3K is essential for TNF-induced necroptosis, which may act as the partner of RIP3 to initiate the activation of RIP1-RIP3-MLKL signal pathway and the subsequent necroptosis.

Implanting Atomic Dispersed Ru in PtNi Colloidal Nanocrystal Clusters for Efficient Catalytic Performance in Electro-oxidation of Liquid Fuels.

Although PtRu alloy nanocatalysts have been certified to possess excellent electrocatalytic performance and CO-poisoning tolerance toward formic acid and methanol electro-oxidation, the unaffordable usages of ruthenium (Ru) and platinum (Pt) have greatly limited their widespread adoption. Here, a facile one-pot method is reported for implanting atomic dispersed Ru in PtNi colloidal nanocrystal clusters with different Ru/Pt/Ni molar ratios, greatly reducing the dosages of Pt and Ru, and further improving the catalytic performances for the electro-oxidation of formic acid and methanol. Through simple control of the amount of Ni(acac)2 precursor, trimetallic Ru0.3 Pt70.5 Ni29.2 , Ru0.6 Pt55.9 Ni43.5 , Ru0.2 Pt77.3 Ni22.5 , and Ru0.9 Pt27.3 Ni71.8 colloidal nanocrystal clusters (CNCs) are obtained. In particular, the Ru0.3 Pt70.5 Ni29.2 CNCs exhibit excellent specific activities for formic acid and methanol electro-oxidation, that is, 14.2 and 15.3 times higher, respectively, than those of the Pt/C catalyst. Moreover, the Ru0.3 Pt70.5 Ni29.2 CNCs also possess better anti-CO-poisoning properties and diffusion ability than the other RuPtNi CNCs. The excellent formic acid and methanol electro-oxidation activities of RuPtNi CNCs are ascribed to the optimal ligand effects derived from the Pt, Ni, and atomic dispersed Ru atoms, which can improve the OH adsorption ability and further the anti-CO-poisoning capability. This research opens a new door for increasing the electro-oxidation properties of liquid fuels by using lower dosages of noble metals in Pt-based catalysts.

Tandem Catalysis of Ammonia Borane Dehydrogenation and Phenylacetylene Hydrogenation Catalyzed by CeO2 Nanotube/Pd@MIL-53(Al).

Heterogeneously catalyzed, selective hydrogenation in the liquid phase is widely used in industry for the synthesis of chemicals. However, it can be a challenge to prevent active nanoparticles (e.g., palladium) from aggregation/leaching and meanwhile achieve high conversion as well as selectivity, especially under mild conditions. To address these issues, a CeO2 nanotube/Pd@MIL-53(Al) sandwich-structured catalyst has been prepared in which the MIL-53(Al) porous shell can efficiently stabilize the palladium nanoparticles. When this catalyst was used in a tandem catalytic reaction involving the dehydrogenation of ammonia borane and the hydrogenation of phenylacetylene, remarkably, the hydrogen released from the dehydrogenation of ammonia borane boosted the catalytic process, with 100 % conversion of phenylacetylene and a selectivity of 96.2 % for styrene, even at room temperature and atmospheric pressure, within 1 min. This work therefore provides an alternative strategy for balancing the conversion and selectivity of liquid-phase hydrogenation reactions.

JS-K induces reactive oxygen species-dependent anti-cancer effects by targeting mitochondria respiratory chain complexes in gastric cancer.

As a nitric oxide (NO) donor prodrug, JS-K inhibits cancer cell proliferation, induces the differentiation of human leukaemia cells, and triggers apoptotic cell death in various cancer models. However, the anti-cancer effect of JS-K in gastric cancer has not been reported. In this study, we found that JS-K inhibited the proliferation of gastric cancer cells in vitro and in vivo and triggered mitochondrial apoptosis. Moreover, JS-K induced a significant accumulation of reactive oxygen species (ROS), and the clearance of ROS by antioxidant reagents reversed JS-K-induced toxicity in gastric cancer cells and subcutaneous xenografts. Although JS-K triggered significant NO release, NO scavenging had no effect on JS-K-induced toxicity in vivo and in vitro. Therefore, ROS, but not NO, mediated the anti-cancer effects of JS-K in gastric cancer. We also explored the potential mechanism of JS-K-induced ROS accumulation and found that JS-K significantly down-regulated the core proteins of mitochondria respiratory chain (MRC) complex I and IV, resulting in the reduction of MRC complex I and IV activity and the subsequent ROS production. Moreover, JS-K inhibited the expression of antioxidant enzymes, including copper-zinc-containing superoxide dismutase (SOD1) and catalase, which contributed to the decrease of antioxidant enzymes activity and the subsequent inhibition of ROS clearance. Therefore, JS-K may target MRC complex I and IV and antioxidant enzymes to exert ROS-dependent anti-cancer function, leading to the potential usage of JS-K in the prevention and treatment of gastric cancer.

Metal-Organic Framework (MOF)-Derived Carbon-Mediated Interfacial Reaction for the Synthesis of CeO2 -MnO2 Catalysts.

CeO2 -based catalysts are widely studied in catalysis fields. Developing one novel synthetic approach to increase the intimate contact between CeO2 and secondary species is of particular importance for enhancing catalytic activities. Herein, an interfacial reaction between metal-organic framework (MOF)-derived carbon and KMnO4 to synthesize CeO2 -MnO2 , in which carbon is derived from the pyrolysis of Ce-MOFs under an inert atmosphere, is described. The MOF-derived carbon is found to restrain the growth of CeO2 crystallites under a high calcination temperature and, more importantly, intimate contact within CeO2 /C is conveyed to CeO2 /MnO2 after the interfacial reaction; this is responsible for the high catalytic activity of CeO2 -MnO2 towards CO oxidation.

Design and Biosynthesis of Dimeric Alboflavusins with Biaryl Linkages via Regiospecific C-C Bond Coupling.

Alboflavusins (AFNs) are a group of cyclohexapeptides with moderate antibacterial and antitumor activities from Streptomyces alboflavus sp. 313. In vivo and in vitro studies proposed that AFNs are biosynthesized by a nonribosomal peptide synthetase machinery, and the 6-Cl-L-Trp precursor is supplied by a tryptophan halogenase gene located outside the afn gene cluster. Guided by the structure-activity relationship knowledge about the AFN-like cyclohexapeptides, two dimeric AFNs (di-AFNs) with regiospecific biaryl linkages were designed and generated biotechnologically by expressing the P450 gene hmtS or clpS in S. alboflavus wild-type and mutant strains. The di-AFNs displayed much better antibacterial and antitumor activities than their monomers as anticipated, exemplifying a rational strategy to generate natural product congeners with improved bioactivities.

PPARγ suppresses the proliferation of cardiac myxoma cells through downregulation of MEF2D in a miR-122-dependent manner.

Peroxisome proliferator-activated receptor gamma (PPARγ), a multiple functional transcription factor, has been reported to have anti-tumor effects through inhibition of cells proliferation. However, its effects on cardiac myxoma (CM) cells and the underlying signaling mechanism is unclear. In the present study, we demonstrated that the level of PPARγ is inversely correlated with that of myocyte enhancer factor 2D (MEF2D), a biomarker of CM. We found that activation of PPARγ inhibit MEF2D expression via upregulation of miR-122, which can target the 3'-UTR of MEF2D and inhibit MEF2D expression, by directly binding to the PPRE in the miR-122 promoter region. Functional experiments further showed that miR-122-dependent downregulation of MEF2D by PPARγ suppress the proliferation of CM cells. These results suggest that PPARγ may exert its antiproliferative effects by negatively regulating the MEF2D in CM cells, which through upregulation of miR-122, and PPARγ/miR-122/MEF2D signaling pathway may be a novel target for treatment of CM.

RIP1-dependent Bid cleavage mediates TNFα-induced but Caspase-3-independent cell death in L929 fibroblastoma cells.

L929 fibroblastoma cells (L929-A) and L929 fibrosarcoma cells (L929-N) are different cell lines that are commonly used to study the cytotoxicity of tumor necrosis factor alpha (TNFα). TNFα has been reported to induce necrosis in both of these cell lines. However, comparing the TNFα-induced cell death in these two cell lines, we found that, unlike the L929-N cells that show typical RIP3-dependent necrosis, TNFα-induced cell death in L929-A cells is pan-caspase inhibitor Z-VAD-FMK (Z-VAD)-sensitive, which does not depend on RIP3. We also confirmed that the cell death signal in the L929-A cells was initiated through cytosol-preassembled ripoptosome and that the knockdown of either Caspase-8 or RIP1 protein blocked cell death. Compared with the L929-N cells, the L929-A cell line had lower levels of constitutive and inducible TNFα autocrine production, and the pan-caspase inhibitors Z-VAD or Q-VD did not kill the L929-A cells as they affect the L929-N cells. Moreover, the L929-A cells expressed less RIP3 protein than the L929-N cells; therefore, TNFα failed to induce RIP3-dependent necroptosis. In addition, the ripoptosome-mediated cell death signal was transduced to the mitochondria through Caspase-8-mediated and RIP1 kinase activity-dependent Bid cleavage. The RIP1 kinase inhibitor Necrostatin-1 (Nec-1) or Caspase-8 knockdown completely blocked Bid cleavage, and the knockdown of Bid or Bax/Bak prevented TNFα-induced cell death in the L929-A cells. Although the activation of Bax/Bak decreased the mitochondrial membrane potential, the levels of mitochondrial intermembrane space proteins, including cytochrome-c (cyt-C) and Smac, declined, and western blotting and immunofluorescence staining analysis did not determine whether these proteins were redistributed to the cytosol. In addition, the mitochondrial outer membrane protein Tom20 was also reduced, indicating that the reduced mitochondria proteins may be induced by the reduced mitochondria numbers. No efficient cyt-C release was observed; therefore, the limited activation and cleavage of downstream caspases, including Caspase-9, Caspase-7, Caspase-6 and Caspase-3, was insufficient to kill the cells. The Caspase-9, Caspase-6 and Caspase-3/7 inhibitors or Caspase-9 and -3 knockdown also failed to block cell death, and the overexpression of Bcl-2 also did not abrogate cell death. Moreover, the dead cells showed necrotic-like but not apoptotic characteristics under transmission electronmicroscopy, and these features were significantly different from mitochondrial apoptosis, indicating that the effector caspases were not the executioners of cell death. These new discoveries show that TNFα-induced cell death in L929-A cells is different than typical RIP3-dependent necrosis and Caspase-8/Caspase-3-mediated apoptosis. These results highlight that caution is necessary when using different L929 cells as a model to investigate TNFα-induced cell death.

Inhaled budesonide prevents acute mountain sickness in young Chinese men.

BACKGROUND: Oral glucocorticoids can prevent acute mountain sickness (AMS). Whether inhaled budesonide (BUD) can prevent AMS remains unknown. OBJECTIVE: Our aim was to investigate the effectiveness of BUD in AMS prevention. METHODS: Eighty subjects were randomly assigned to receive budesonide (BUD, inhaled), procaterol tablet (PT), budesonide/formoterol (BUD/FM, inhaled), or placebo tablet (n = 20 in each group). Subjects were treated for 3 days before ascending from 500 m to 3700 m within 2.5 h by air. Lake Louis AMS questionnaire, blood pressure, heart rate, and oxygen saturation (SpO2) were examined at 20, 72, and 120 h after high-altitude exposure. Pulmonary function was measured at 20 h after exposure. RESULTS: Compared with placebo, BUD significantly reduced the incidence of AMS (70% vs. 25% at 20 h, p < 0.05; both 10% vs. 5% at 72 and 120 h, both p > 0.05) without side effects. The relative risk was 0.357, and the risk difference was 0.45. Mean SpO2 was higher in BUD, BUD/FM, and PT groups than in the placebo group at 20 h (p < 0.05). SpO2 in all 80 subjects dropped after ascent (98.1% to 88.12%, p < 0.01) and increased gradually, but it was still lower at 120 h than at baseline (92.04% vs. 98.1%, p < 0.01). Pulmonary function did not differ among the four groups at 20 h. CONCLUSION: BUD can prevent AMS without side effects. The alleviation of AMS may be related to increased blood oxygen levels rather than pulmonary function.

Semiconductor and metallic core-shell nanostructures: synthesis and applications in solar cells and catalysis.

Nano-heterostructures have attracted great attention due to their extraordinary properties beyond those of their single-component counterparts. This review focuses on a specific type of hybrid structures: core-shell structures. In particular, we present and discuss the recent wet-chemical synthesis approaches for semiconductor and metallic core-shell nanostructures, and their relevant properties and potential applications in photovoltaics and catalysis, respectively.

A high-quality chromosome-level genome assembly of the Chinese medaka Oryzias sinensis.

Oryzias sinensis, also known as Chinese medaka or Chinese ricefish, is a commonly used animal model for aquatic environmental assessment in the wild as well as gene function validation or toxicology research in the lab. Here, a high-quality chromosome-level genome assembly of O. sinensis was generated using single-tube long fragment read (stLFR) reads, Nanopore long-reads, and Hi-C sequencing data. The genome is 796.58 Mb, and a total of 712.17 Mb of the assembled sequences were anchored to 23 pseudo-chromosomes. A final set of 22,461 genes were annotated, with 98.67% being functionally annotated. The Benchmarking Universal Single-Copy Orthologs (BUSCO) benchmark of genome assembly and gene annotation reached 95.1% (93.3% single-copy) and 94.6% (91.7% single-copy), respectively. Furthermore, we also use ATAC-seq to uncover chromosome transposase-accessibility as well as related genome area function enrichment for Oryzias sinensis. This study offers a new improved foundation for future genomics research in Chinese medaka.

A bimodal feature fusion convolutional neural network for detecting obstructive sleep apnea/hypopnea from nasal airflow and oximetry signals.

The most prevalent sleep-disordered breathing condition is Obstructive Sleep Apnea (OSA), which has been linked to various health consequences, including cardiovascular disease (CVD) and even sudden death. Therefore, early detection of OSA can effectively help patients prevent the diseases induced by it. However, many existing methods have low accuracy in detecting hypopnea events or even ignore them altogether. According to the guidelines provided by the American Academy of Sleep Medicine (AASM), two modal signals, namely nasal pressure airflow and pulse oxygen saturation (SpO2), offer significant advantages in detecting OSA, particularly hypopnea events. Inspired by this notion, we propose a bimodal feature fusion CNN model that primarily comprises of a dual-branch CNN module and a feature fusion module for the classification of 10-second-long segments of nasal pressure airflow and SpO2. Additionally, an Efficient Channel Attention mechanism (ECA) is incorporated into the second module to adaptively weight feature map of each channel for improving classification accuracy. Furthermore, we design an OSA Severity Assessment Framework (OSAF) to aid physicians in effectively diagnosing OSA severity. The performance of both the bimodal feature fusion CNN model and OSAF is demonstrated to be excellent through per-segment and per-patient experimental results, based on the evaluation of our method using two real-world datasets consisting of polysomnography (PSG) recordings from 450 subjects.

Effects of microhabitat features on the intraspecific variability of the distribution and functional traits in a highest elevational distributed lizard.

Exploring the microhabitat determinants of organisms distribution and functional traits differences can help us better understand the importance of intraspecific variations in ecological niches. Investigations on animals functional niche primarily focused on differences among species and tended to neglect the potential variability within species, despite the fact that the ecological and evolutionary importance of intraspecific variations was widely recognized. In this study, we examined the influence of microhabitat features on the intraspecific variability of the distribution and functional traits of a highest elevational distributed lizard species Phrynocephalus erythrurus. To do so, field work was conducted between July and August, 2020 and August and September, 2021 in Namtso watershed in central Xizang, China. Specifically, 11 transects were sampled for P. erythrurus individuals, which were measured for a set of 10 morphological traits. Moreover, 11 microhabitat variables that potentially affect the distribution of lizards were also measured for each transect. Our results indicated that juveniles, males, and females exhibited different functional traits, allowing them to occupy distinct functional space. The distribution of juveniles, males, and females was determined by different microhabitat variables such as illuminance and air temperature. More importantly, these variables also determined the intraspecific functional traits variability in this lizard species. All of these results supported previous claims that intraspecific traits variation should be incorporated into functional ecological studies, and diverse microhabitat features should be conserved to maintain high intraspecific diversity. Future studies can focus on the food analysis to explore the linkage between functional traits and resources utilization within animal populations.

Surface hydrophobization of zeolite enables mass transfer matching in gas-liquid-solid three-phase hydrogenation under ambient pressure.

Attaining high hydrogenation performance under mild conditions, especially at ambient pressure, remains a considerable challenge due to the difficulty in achieving efficient mass transfer at the gas-liquid-solid three-phase interface. Here, we present a zeolite nanoreactor with joint gas-solid-liquid interfaces for boosting H2 gas and substrates to involve reactions. Specifically, the Pt active sites are encapsulated within zeolite crystals, followed by modifying the external zeolite surface with organosilanes. The silane sheath with aerophilic/hydrophobic properties can promote the diffusion of H2 and the mass transfer of reactant/product molecules. In aqueous solutions, the gaseous H2 molecules can rapidly diffuse into the zeolite channels, thereby augmenting H2 concentration surround Pt sites. Simultaneously, the silane sheath with lipophilicity nature promotes the enrichment of the aldehydes/ketones on the catalyst and facilitates the hydrophilia products of alcohol rediffusion back to the aqueous phase. By modifying the wettability of the catalyst, the hydrogenation of aldehydes/ketones can be operated in water at ambient H2 pressure, resulting in a noteworthy turnover frequency up to 92.3 h-1 and a 4.3-fold increase in reaction rate compared to the unmodified catalyst.

The histone deacetylase inhibitor vorinostat prevents TNFα-induced necroptosis by regulating multiple signaling pathways.

Histone deacetylase (HDAC) inhibitors are novel anticancer reagents that have recently been reported to have anti-inflammatory and neuroprotective effects; however, the mechanisms underlying their activities are largely undefined. The data from this study show that the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) can protect L929 cells from TNFα-induced necroptosis. This effect involves multiple mechanisms, including the upregulation of cFLIPL expression, the enhanced activation of NFκB and p38 MAPK, and the inactivation of JNK. In addition, SAHA could initiate cell autophagy by inhibiting Akt and mTOR, which also play important roles in protecting cells from necroptosis. Because cell necroptosis is important for inflammation-related deterioration and neurodegenerative disease, our results indicate that preventing cell necrosis may be an important mechanism through which HDAC inhibitor compounds exert their anti-inflammatory or neuroprotective effects.