TiN as Radical Scavenger in Fe─N─C Aerogel Oxygen Reduction Catalyst for Durable Fuel Cell.

Fe─N─C is the most promising alternative to platinum-based catalysts to lower the cost of proton-exchange-membrane fuel cell (PEMFC). However, the deficient durability of Fe─N─C has hindered their application. Herein, a TiN-doped Fe─N─C (Fe─N─C/TiN) is elaborately synthesized via the sol-gel method for the oxygen-reduction reaction (ORR) in PEMFC. The interpenetrating network composed by Fe─N─C and TiN can simultaneously eliminate the free radical intermediates while maintaining the high ORR activity. As a result, the H2 O2 yields of Fe─N─C/TiN are suppressed below 4%, ≈4 times lower than the Fe─N─C, and the half-wave potential only lost 15 mV after 30 kilo-cycle accelerated durability test (ADT). In a H2 ─O2 fuel cell assembled with Fe─N─C/TiN, it presents 980 mA cm-2 current density at 0.6 V, 880 mW cm-2 peak power density, and only 17 mV voltage loss at 0.80 A cm-2 after 10 kilo-cycle ADT. The experiment and calculation results prove that the TiN has a strong adsorption interaction for the free radical intermediates (such as *OH, *OOH, etc.), and the radicals are scavenged subsequently. The rational integration of Fe single-atom, TiN radical scavenger, and highly porous network adequately utilize the intrinsic advantages of composite structure, enabling a durable and active Pt-metal-free catalyst for PEMFC.

Rich Sulfur Vacancies and Reduced Schottky Barrier Height Synergistically Enable Au/ZnIn2S4 with Enhanced Photocatalytic CO2 Reduction into CO.

Constructing the plasmonic metal/semiconductor heterostructure with a suitable Schottky barrier height (SBH) and the sufficiently reliable active sites is of importance to achieve highly efficient and selective photocatalytic CO2 reduction into hydrocarbon fuels. Herein, we report Au/sulfur vacancy-rich ZnIn2S4 (Au/VSR-ZIS) hierarchical photocatalysts, fabricated via in situ photodepositing Au nanoparticles (NPs) onto the nanosheet self-assembled ZnIn2S4 (ZIS) micrometer flowers (MFs) with rich sulfur vacancies (VS). Density functional theory (DFT) calculations confirm that for the Au/VSR-ZIS system, the Au NPs serve as the reaction sites for H2O oxidation, and the VSR-ZIS MFs serve as those for CO2 reduction. The rich VS in the Au/VSR-ZIS hybrid can reduce its SBH so as to boost more hot electrons in the Au NPs across its Schottky barrier and then inject into the conduction band (CB) of the VSR-ZIS MFs. In addition, VS can also act as the electron sink to trap the photogenerated electrons, retarding the recombination of photogenerated carriers. The two merits effectively enhance the photogenerated electron density in the surface of VSR-ZIS MFs, availing CO2 photoreduction. In addition, the introduction of rich VS in the Au/VSR-ZIS hybrid can offer more active sites, benefiting the CO2 adsorption and accelerating the desorption of CO* from the surface of the photocatalyst. Therefore, under visible light illumination with no sacrificial reagent, the optimum photocatalyst (Au/VSR-ZIS-0.4) presents the enhanced and selective CO2 photoreduction into CO (8.15 µmol g-1h-1 and near 100%), which are superior to those of most of ZIS-based and plasmon-based photocatalysts. The photocatalytic activity is about 40.0-fold as high as that of the Vs-poor-ZIS (VSP-ZIS) MFs. This work contributes a viable strategy for designing highly efficient plasmonic photocatalysts by using the synergism of the anion vacancies and the optimized SBH induced by them.

Constructing an Ultra-Rapid Nanoconfinement-Enhanced Fluorescence Clinical Detection Platform by Using Machine Learning and Tunable DNA Xerogel "Probe".

Low mass transfer efficiency and unavoidable matrix effects seriously limit the development of rapid and accurate determination of biosensing systems. Herein, we have successfully constructed an ultra-rapid nanoconfinement-enhanced fluorescence clinical detection platform based on machine learning (ML) and DNA xerogel "probe", which was performed by detecting neutrophil gelatinase-associated lipocalin (NGAL, protein biomarker of acute kidney injury). By regulating pore sizes of the xerogels, the transfer of NGAL in xerogels can approximate that in homogeneous solution. Due to electrostatic attraction of the pore entrances, NGAL rapidly enriches on the surface and inside the xerogels. The reaction rate of NGAL and aptamer cross-linked in xerogels is also accelerated because of the nanoconfinement effect-induced increasing reactant concentration and the enhanced affinity constant KD between reactants, which can be promoted by ∼667-fold than that in bulk solution, thus achieving ultra-rapid detection (ca. 5 min) of human urine. The platform could realize one-step detection without sample pretreatments due to the antiligand exchange effect on the surface of N-doped carbon quantum dots (N-CQDs) in xerogels, in which ligand exchange between -COOH and underlying interfering ions in urine will be inhibited due to higher adsorption energy of -COOH on the N-CQD surface relative to the interfering ions. Based on the ML-extended program, the real-time analysis of the urine fluorescence spectra can be completed within 2 s. Interestingly, by changing DNA, aptamer sequences, or xerogel fluorescence intensities, the detection platform can be customized for targeted diseases.

Accelerating Ethanol Complete Electrooxidation via Introducing Ethylene as the Precursor for the C-C Bond Splitting.

The crucial issue restricting the application of direct ethanol fuel cells (DEFCs) is the incomplete and sluggish electrooxidation of ethanol due to the chemically stable C-C bond thereof. Herein, a unique ethylene-mediated pathway with a 100 % C1-selectivity for ethanol oxidation reaction (EOR) is proposed for the first time based on a well-structured Pt/Al2 O3 @TiAl catalyst with cascade active sites. The electrochemical in situ Fourier transform infrared spectroscopy (FTIR) and differential electrochemical mass spectrometry (DEMS) analysis disclose that ethanol is primarily dehydrated on the surface of Al2 O3 @TiAl and the derived ethylene is further oxidized completely on nanostructured Pt. X-ray absorption and density functional theory (DFT) studies disclose the Al component doped in Pt nanocrystals can promote the EOR kinetics by lowering the reaction energy barriers and eliminating the poisonous species. Strikingly, Pt/Al2 O3 @TiAl exhibits a specific activity of 3.83 mA cm-2 Pt , 7.4 times higher than that of commercial Pt/C and superior long-term durability.

Improved urine DNA methylation panel for early bladder cancer detection.

BACKGROUND: Bladder cancer is one of the most common malignancies but the corresponding diagnostic methods are either invasive or limited in specificity and/or sensitivity. This study aimed to develop a urine-based methylation panel for bladder cancer detection by improving published panels and validate performance of the new panel with clinical samples. METHODS: Related researches were reviewed and 19 potential panels were selected. RRBS was performed on a cohort with 45 samples to reassess these panels and a new panel inherited best markers was developed. The new panel was applied with qMSP platform to 33 samples from the RRBS cohort and the results were compared to those of RRBS. Lastly, another larger cohort with 207 samples was used to validate new panel performance with qMSP. RESULTS: Three biomarkers (PCDH17, POU4F2 and PENK) were selected to construct a new panel P3. P3 panel achieved 100% specificity and 71% sensitivity with RRBS in corresponding cohort and then showed a better performance of 100% specificity and 84% sensitivity with qMSP platforms in a balanced cohort. When validated with 207-sample cohort, P3 with qMSP showed a performance of 97% specificity and 87% sensitivity which was modestly improved compared to the panels it derided from. CONCLUSIONS: Overall, the P3 panel achieved relatively high sensitivity and accuracy in bladder cancer detection.

Hierarchical S-Scheme Heterostructure of CdIn2S4@UiO-66-NH2 toward Synchronously Boosting Photocatalytic Removal of Cr(VI) and Tetracycline.

Developing highly efficient photocatalysts toward synchronously removing heavy metals and organic pollutants is still a serious challenge. Herein, we depict hierarchical S-scheme heterostructured photocatalysts prepared via in situ anchoring UiO-66-NH2 nanoparticles onto the CdIn2S4 porous microsphere structures assembled with numerous nanosheets. In the mixed system of Cr(VI) and tetracycline (TC), the optimal photocatalyst (CIS@U66N-30) shows remarkable photocatalytic activities toward the synchronous removal of Cr(VI) (97.26%) and TC (close to 100% of) under visible-light irradiation for 60 min, being the best removal rates among those of the reported photocatalysts, and sustains the outstanding stability and reusability. Its reaction rate constants of Cr(VI) reduction and TC degradation are about 2.06 and 1.58 folds that in the single Cr(VI) and TC systems, respectively. The enhanced photocatalytic activities of CIS@U66N-30 mainly result from the following synergism: (1) its hierarchical structure offers abundant active sites, and the S-scheme migration mechanism of charge carriers in the heterostructure accelerates the separation and migration of the useful photoinduced electrons and holes with the high redox capability; (2) Cr(VI) and TC can serve as the electron scavenger for TC oxidation degradation and the hole and •OH scavenger for Cr(VI) reduction, respectively, further enhancing the separation and utilization efficiency of photoinduced electrons and holes. Besides, the possible TC degradation pathway and plausible S-scheme photocatalytic mechanism over CIS@U66N-30 for the concurrent elimination of Cr(VI) and TC are proposed.

Leonurine inhibits the TXNIP/NLRP3 and NF-κB pathways via Nrf2 activation to alleviate carrageenan-induced pleurisy in mice.

Oxidative stress and inflammation play important roles in pleurisy. Leonurine (Leo) has been confirmed to exert antioxidative and antiinflammatory effects in many preclinical experiments, but these effects have not been studied in pleurisy. The aim of this study was to explore the therapeutic effect and mechanism of Leo in a carrageenan (CAR)-induced pleurisy model. In this study, we found that the increase of reactive oxygen species (ROS), myeloperoxidase (MPO), and malondialdehyde (MDA) and decrease of glutathione (GSH) induced by CAR could be reversed by the treatment of Leo. Leo effectively reduced the levels of proinflammatory cytokines interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), and the percentages of mature macrophages and increased the levels of antiinflammatory cytokines (IL-10). Furthermore, Western blotting revealed that Leo significantly activated the Nrf2 pathway to restrain the thioredoxin-interacting protein/NOD-like receptor protein 3 (TXNIP/NLRP3) and nuclear factor kappa-B (NF-κB) pathways. However, the protective effect of Leo was significantly weakened in Nrf2-deficient mice. These results indicate that Leo confers potent protection against CAR-induced pleurisy by inhibiting the TXNIP/NLRP3 and NF-κB pathways dependent on Nrf2, which may serve as a promising agent for attenuating pleurisy.

Visual Inspection System for Uncoupling Status of Control-Rod Drive Rod in Nuclear Reactor.

Under some unexpected conditions, drive rods and control-rod assemblies may not be disconnected. If this situation is not detected, the control rod will be lifted out of the reactor core together with the upper reactor internals. This situation will seriously affect the follow-up work and reduce the economy and safety protection of the nuclear power plant. To ensure safety, the tripping status must be checked after tripping. Follow-up work can be carried out after checking and confirming that all drive rods are in the tripping status. There are many problems for traditional inspection methods, such as misjudgment, low accuracy, and labor consumption. This paper proposes a visual inspection system for the uncoupling state of the control-rod drive rod of the nuclear reactor. The proposed method is based on the fitting model of the ellipse parameter of the drive-rod head and the height of the drive rod. The ellipse of the drive-rod head is firstly accurately detected. Then, a mathematical model between the ellipse parameter and the height of the drive rod is established. The measurement error caused by the swing of the head of the drive rod is eliminated. The accurate measurement of the height difference before and after the tripping of the drive rod is computed. Finally, the status of the uncoupling of the drive rod is judged according to the difference. Many experiments are carried out with our developed system. The experimental results show that the proposed system realizes remote operation, ensures the quality of trip-status inspection, improves work efficiency, and reduces the workload of staff.

Instantly Detecting Catalysts' Hot Spots Temperature In Situ during Photocatalysis by Operando Raman Spectroscopy.

Precisely detecting the catalysts' hot spots temperature in situ instantly during photocatalysis is a great challenge but extremely important for chemical reactions. However, no efficient method has been developed to instantly detect the hot spots temperature in situ during photocatalysis. Herein, we designed a simple and convenient method to measure the instant hot spots temperature in situ on the nanostructure surface during photocatalysis by operando Raman spectroscopy using 4-methoxyphenyl isocyanide (MI) as the probe molecule. The νN≡C frequency of MI varied linearly with temperature, which is caused by the orientation change of the MI induced by temperature, leading to the change in the frequency of the νN≡C bond that directly interacts with the nanostructure surface. Using in situ surface-enhanced Raman spectroscopy (SERS), the surface temperature of the catalysts illuminating for each time can be measured instantly. Interestingly, the catalytic activity of the hydrogen evolution reaction (HER) for the Au-Ag/Ag2S heterojunction nanorods (HJNRs) are higher than that for the Ag-Au-Ag HJNRs, although they have a lower surface temperature during photocatalysis; therefore, hot carriers and electronic structure contributed more to the catalytic activity of the Au-Ag/Ag2S HJNRs than that of the Ag-Au-Ag HJNRs. Such an instant hot spots temperature detecting method of catalysts can greatly facilitate the analysis of the mechanism of catalytic processes.

The impact of payer status on hospital admissions: evidence from an academic medical center.

BACKGROUND: There are plenty of studies investigating the disparity of payer status in accessing to care. However, most studies are either disease-specific or cohort-specific. Quantifying the disparity from the level of facility through a large controlled study are rare. This study aims to examine how the payer status affects patient hospitalization from the perspective of a facility. METHODS: We extracted all patients with visiting record in a medical center between 5/1/2009-4/30/2014, and then linked the outpatient and inpatient records three year before target admission time to patients. We conduct a retrospective observational study using a conditional logistic regression methodology. To control the illness of patients with different diseases in training the model, we construct a three-dimension variable with data stratification technology. The model is validated on a dataset distinct from the one used for training. RESULTS: Patients covered by private insurance or uninsured are less likely to be hospitalized than patients insured by government. For uninsured patients, inequity in access to hospitalization is observed. The value of standardized coefficients indicates that government-sponsored insurance has the greatest impact on improving patients' hospitalization. CONCLUSION: Attention is needed on improving the access to care for uninsured patients. Also, basic preventive care services should be enhanced, especially for people insured by government. The findings can serve as a baseline from which to measure the anticipated effect of measures to reduce disparity of payer status in hospitalization.

Recent advances on the roles of LncRNAs in cardiovascular disease.

Cardiovascular diseases are a main cause of mortality whose prevalence continues to increase worldwide. Long non-coding RNAs (lncRNAs) regulate a variety of biological processes by modifying and regulating transcription of coding genes, directly binding to proteins and even coding proteins themselves. LncRNAs play key roles in the occurrence and development of myocardial infarction, heart failure, myocardial hypertrophy, arrhythmias and other pathological processes that significantly affect the prognosis and survival of patients with cardiovascular diseases. We here review the latest research on lncRNAs in cardiovascular diseases as a basis to formulate future research on prevention and treatment of cardiovascular diseases.

Cardiac-specific Mst1 deficiency inhibits ROS-mediated JNK signalling to alleviate Ang II-induced cardiomyocyte apoptosis.

Apoptosis is associated with various myocardial diseases. Angiotensin II (Ang II) plays a central role in the pathogenesis of RAAS-triggered cardiac apoptosis. Our previous studies showed that mammalian Ste20-like kinase 1 (Mst1) aggravates cardiac dysfunction in cardiomyocyte under pathological conditions, but its role in Ang II-mediated cardiomyocyte apoptosis is not known. We addressed this in the present study by investigating whether cardiac-specific Mst1 knockout can alleviate Ang II-induced cardiomyocyte apoptosis along with the underlying mechanisms. In vitro and in vivo experiments showed that Ang II increased intracellular reactive oxygen species (ROS) production and cardiomyocyte apoptosis; these were reversed by administration of the ROS scavenger N-acetylcysteine and by Mst1 deficiency, which suppressed c-Jun N-terminal kinase (JNK) phosphorylation and downstream signaling. Interestingly, Mst1 knockout failed to alleviate Ang II-induced phosphorylation of extracellular signal-regulated kinase 1/2, and inactivated apoptosis signal-regulating kinase1 (ASK1) by promoting its association with thioredoxin (Trx), which reversed the Ang II-induced activation of the ASK1-JNK pathway and suppressed Ang II-induced cardiomyocyte apoptosis. Thus, cardiac-specific Mst1 knockout inhibits ROS-mediated JNK signalling to block Ang II-induced cardiomyocyte apoptosis, suggesting Mst1 as a potential therapeutic target for treatment of RAAS-activated heart failure.

Convincing Synthesis of Atomically Thin, Single-Crystalline InVO4 Sheets toward Promoting Highly Selective and Efficient Solar Conversion of CO2 into CO.

Atomically thin, single-crystalline InVO4 sheets with the uniform thickness of ∼1.5 nm were convincingly synthesized, which was identified with strong, low-angle X-ray diffraction peaks. The InVO4 atomic layer corresponding to 3 unit cells along [110] orientation exhibits highly selective and efficient photocatalytic conversion of CO2 into CO in the presence of water vapor. Surface potential change measurement and liquid photoluminescence decay spectra confirm that the atomically ultrathin structure can shorten the transfer distance of charge carriers from the interior onto the surface and decrease the recombination in body. It thus allows more electrons to survive and accumulate on the surface, which is beneficial for activation and reduction of CO2. In addition, exclusively exposed {110} facet of the InVO4 atomic layer was found to bind the generating CO weakly, facilitating quick desorption from the catalyst surface to form free CO molecules, which provides an ideal platform to catalytically selective CO product.

Minocycline promotes cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy to prevent sepsis-induced cardiac dysfunction by Akt/mTOR signaling.

Myocardial damage is responsible for the high mortality of sepsis. However, the underlying mechanism is not well understood. Cardiomyocyte autophagy alleviates the cardiac injury caused by myocardial infarction. Enhanced cardiomyocyte autophagy also has protective effects against cardiomyocyte mitochondrial injury. Minocycline enhances autophagy in many types of cells under different types of pathological stress and can be easily taken up by cardiomyocytes. The present study investigated whether minocycline prevented myocardial injury caused by sepsis and whether cardiomyocyte autophagy participated in this process. The results indicated that minocycline enhanced cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy and improved myocardial mitochondrial and cardiac function. Minocycline upregulated protein kinase B (Akt) phosphorylation, inhibited mTORC1 expression and enhanced mTORC2 expression. In conclusion, minocycline enhanced cardiomyocyte mitochondrial autophagy and cardiomyocyte autophagy and improved cardiac function. The underlying mechanisms were associated with mTORC1 inhibition and mTORC2 activation. Thus, our findings suggest that minocycline may represent a potential approach for treating myocardial injury and provide novel insights into the underlying mechanisms of myocardial injury and dysfunction after sepsis.

Mst1 knockout enhances cardiomyocyte autophagic flux to alleviate angiotensin II-induced cardiac injury independent of angiotensin II receptors.

AIMS: Angiotension II (Ang II) plays a central role in the pathogenesis of renin-angiotensin-aldosterone system (RAAS)-induced heart failure. Mst1 exerts its function in cardiomyocytes subjected to pathological stimuli via inhibiting autophagy and aggravating apoptosis, but its role in RAAS-mediated cardiac injury is still unknown. Here, we aimed to determine whether cardiomyocyte-specific Mst1 knockout can alleviate Ang II-induced cardiac injury by improving cardiomyocyte autophagy and whether these functions depend on Ang II receptors. RESULTS: Mst1 knockout alleviated Ang II-induced heart failure, without affecting blood pressure and compensatory concentric hypertrophy. Mst1 specific knockout improved the effects of Ang II on cardiomyocyte autophagy, as evidenced by further increased LC3-II expression and decreased P62 expression. More typical autophagosomes accompanied by less damaged mitochondria were also observed by electron microscopy in Ang II-treated Mst1Δ/Δ mice. In vitro, Mst1 knockdown promoted cardiomyocyte autophagic flux, as demonstrated by more GFP-mRFP-LC3 puncta per cell. Increased LC3-II and decreased P62 expression both in the presence and absence of chloroquine were observed in Mst1 knockdown cardiomyocytes administered with Ang II. Treatment with 3-MA, an inhibitor of autophagy, abolished the beneficial effects of Mst1 knockout against Ang II-induced cardiac dysfunction. The compensatory effects of Ang II on upregulated autophagy were associated with Mst1 inhibition. Interestingly, the knockdown or antagonization of AT1R inhibited cardiomyocyte autophagy, which may represent a threat to cardiac function. Importantly, Mst1 knockout consistently enhanced cardiomyocyte autophagy following the knockdown or blocking of AT1R and AT2R. CONCLUSION: Cardiomyocyte-specific Mst1 knockout alleviates Ang II-induced cardiac injury by enhancing cardiomyocyte autophagy. Mst1 inhibition may counteract the undesirable effects of Ang II receptors blockage on cardiomyocyte autophagy and represent a promising complementary treatment strategy against Ang II-induced cardiac injury.

Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition.

Mitophagy eliminates dysfunctional mitochondria and thus plays a cardinal role in diabetic cardiomyopathy (DCM). We observed the favourable effects of melatonin on cardiomyocyte mitophagy in mice with DCM and elucidated their underlying mechanisms. Electron microscopy and flow cytometric analysis revealed that melatonin reduced the number of impaired mitochondria in the diabetic heart. Other than decreasing mitochondrial biogenesis, melatonin increased the clearance of dysfunctional mitochondria in mice with DCM. Melatonin increased LC3 II expression as well as the colocalization of mitochondria and lysosomes in HG-treated cardiomyocytes and the number of typical autophagosomes engulfing mitochondria in the DCM heart. These results indicated that melatonin promoted mitophagy. When probing the mechanism, increased Parkin translocation to the mitochondria may be responsible for the up-regulated mitophagy exerted by melatonin. Parkin knockout counteracted the beneficial effects of melatonin on the cardiac mitochondrial morphology and bioenergetic disorders, thus abolishing the substantial effects of melatonin on cardiac remodelling with DCM. Furthermore, melatonin inhibited Mammalian sterile 20-like kinase 1 (Mst1) phosphorylation, thus enhancing Parkin-mediated mitophagy, which contributed to mitochondrial quality control. In summary, this study confirms that melatonin rescues the impaired mitophagy activity of DCM. The underlying mechanism may be attributed to activation of Parkin translocation via inhibition of Mst1.

Controlling Shape and Plasmon Resonance of Pt-Etched Au@Ag Nanorods.

Pt-based catalysts with novel structure have attracted great attention due to their outstanding performance. In this work, H2PtCl6 was used as both precursor and etching agent to realize the shape-controlled synthesis of Pt-modified Au@Ag nanorods (NRs). During the synthesis, the as-prepared Ag shell played a crucial role in both protecting the Au NRs from being etched away by PtCl62- and leading to an unusual growth mode of Pt component. The site-specified etching and/or growth depended on the concentration of H2PtCl6, where high-yield core-shell structure or dumbbell-like structure could be obtained. The shape-controlled synthesis also led to a tunable longitudinal surface plasmon resonance from ca. 649 to 900 nm. Meanwhile, the core-shell Pt-modified Au@Ag NRs showed approximately 4-fold enhancement in catalytic reduction reaction of p-nitrophenol than that of the Au NRs, suggesting the great potential for photocatalytic reaction.

I2-Mediated Iodobenzannulation of Yne-Allenones toward 1-Naphthols and Their Synthetic Application.

A new I2-mediated iodobenzannulation of yne-allenones has been established, enabling breaking/rearranging of C≡C bonds to selectively access 4-iodonaphthalen-1-ols with generally good yields. The resulting 4-iodonaphthalen-1-ols could serve as a new and reliable coupling reagent, which further reacted with H2O under the oxygen conditions to generate unexpected 1,2-carbonyls with good yields through Pd-catalyzed deiodinated carbonylation, whereas employment of benzene-1,2-diamine as the nucleophile rendered 3-(quinoxalin-2-yl)naphthalen-1-ols through Pd-catalyzed [4 + 2] heterocyclization. On the basis of the controlled experiments, the mechanism for forming 1,2-carbonyls was proposed, including an oxidative addition, 1,3-palladium migration, reductive elimination, and oxidative dehydrogenation sequence.

Atom-economic synthesis of cyclobuta[a]naphthalen-4-ols via a base-promoted [2 + 2] cycloaddition/1,6-nucleophilic addition cascade.

A first atom-economic [2 + 2] cycloaddition/1,6-conjugate addition cascade of yne-allenones with C-nucleophiles including 1,3-dicarbonyls and α,α-dicyanoolefins under base-promoted conditions has been established, enabling the direct construction of C(sp3)-C(sp3) bonds to generate cyclobuta[a]naphthalen-1-ols with generally good yields. These resulting products have a cyclobutene unit that contains both an aryl and alkyl group.

Understanding Mechanisms of Synergy between Acidification and Ultrasound Treatments for Activated Sludge Dewatering: From Bench to Pilot-Scale Investigation.

Enhancing activated sludge dewaterability is of scientific and engineering importance in the face of accelerated urbanization and stringent environmental regulations. In this study, we investigated the integration of acidification and ultrasound (A/US) treatment for improving sludge dewaterability at both bench- and pilot-scales. Our results showed that the A/US process exhibited significantly improved sludge dewatering performance, characterized by capillary suction time, cake moisture, and water/solid content of sludge cake. Synergistic dewatering mechanisms were elucidated with a suite of macro and spectroscopic evidence. Characterization of treated sludge revealed that US-induced thermal, mechanical shearing force, and radical oxidation effects disrupts floc cells and accelerates the decomposition of extracellular polymeric substances (EPS), releasing bound water into the bulk phase. In addition to enhancing hydrolysis of EPS, the acidic pH environment caused the protonation of functional groups on EPS, facilitating the reflocculation of US decomposed sludge for improved filterability. Our bench-scale and pilot-scale investigations provide a mechanistic basis for better understanding of the A/US process, and enable development of a viable and economical dewatering technology.