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A system of ultrasound radiation coupled with Zn 0 was applied to degrade diclofenac. The effects of initial pH, dosage of Zn 0 and ultrasound density were investigated. To further explore the mechanism of the microcosmic reaction, the fresh and used Zn 0 powders were characterized by SEM, XRD and XPS. Radical scavengers were used to determine the oxidation performance of strong oxidizing free radicals on diclofenac, including hydroxyl radicals and superoxide radicals. The results showed that the optimum removal of diclofenac reached to over 85% at pH of 2.0 in 15 min, with Zn 0 dosage of 0.1 g/L and ultrasound density of 0.6 W/cm 3 . TOC removal of 72.6% in 15 min and dechlorination efficiency of diclofenac reached 70% in 30 min. Characterization results showed that a ZnO membrane was generated on the surface of Zn particles after use. According to the mass spectrometry results, several possible pathways of diclofenac degradation were proposed, and most diclofenac was turned into micro-molecules or CO 2 finally. The synergistic effect of US/Zn 0 in the reactions led to a proposed degradation mechanism in which zinc could directly attack the target contaminant diclofenac because of its good reducibility with the auxiliary functions of ultrasonic irradiation, mechanical shearing and free radical oxidation.

The degradation of diclofenac in a like Fenton system, FeCeOx-H2O2, was studied in details. The influencing factors, reaction kinetics, reaction mechanism and degradation pathways of diclofenac were investigated. The optimum conditions were at a solution pH of 5.0, H2O2 concentration of 3.0 mmol/L, diclofenac initial concentration of 0.07 mmol/L, FeCeOx dosage of 0.5 g/L, and 84% degradation of diclofenac was achieved within 40 min. The kinetics of FeCeOx catalyzed H2O2 process involved adsorption-dominating and degradation-dominating stages and fitted pseudo-second order model and pseudo-first order model, respectively. Singlet oxygen 1O2 was the primary intermediate oxidative species in the degradation process; superoxide radical anion O2 − also participated in the reaction. The surface cerium and iron sites and the oxygen vacancies in the FeCeOx catalyst were proposed to play an important role in H2O2 decomposition and active species generation. The detected intermediates were identified as hydroxylated derivatives (m/z of 310, 326 and 298), quinone imine compounds (m/z of 308, 278 and 264) and hydroxyl phenylamine (m/z of 178). The majority intermediates were hydroxylated derivatives and the minority was hydroxyl phenylamine. The degradation pathways were proposed to involve hydroxylation, decarboxylation, dehydrogenation and C N bond cleavage.

This paper studies the sonocatalytic degradation of diclofenac in water using FeCeOx-catalyzed ultrasound. The effects of pre-adsorption and gas addition were investigated. Nitrogen adsorption/desorption, SEM, XRD, Raman and XPS analyses of FeCeOx before and after sonication were characterized. The proposed mechanism was based on the microstructure changes of FeCeOx and reactive-species-scavenging performances. The results show that FeCeOx has excellent performance in catalyzing an ultrasonic system in water, and 80% of diclofenac was removed in 30min ([Diclofenac]=20mg/L, FeCeOx amount=0.5g/L, pH=6, ultrasonic density=3.0W/cm3, ultrasonic frequency=20kHz, temperature=298K). The Fe, Ce, and O elements remained highly dispersed in the structure of FeCeOx, and the solid solution structure of FeCeOx remained stable after the reaction. Ce (III) was gradually oxidized to Ce (IV) and Fe (III) was gradually reduced to Fe (II) after the reaction, which indicates that Fe and Ce ions with different valences coexisted in dynamic equilibrium. The amount of oxygen vacancies in FeCeOx significantly decreased after the reaction, which indicates that oxygen vacancy participated in the ultrasonic process. Singlet oxygen 1O2 was the primary reactive species in the degradation process, and the hydroxyl radicals OH and superoxide radical anion O2- also participated in the reaction. FeCeOx had excellent chemical stability with negligible leaching ions in the ultrasonic process.

Introduction Transplant-associated thrombotic microangiopathy (TA-TMA) is a potentially life-threatening complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT), which can result in multiorgan injury and increased risk for mortality. Renewed interest has emerged in the prognostication of TA-TMA with the development of novel diagnostic and management algorithms. Our previous study reported an adverse outcome in patients with TA-TMA and concomitant acute graft-versus-host disease (Eur J Haematol, 2018). However, information on markers for the early identification of severe cases remains limited. Therefore, this study is concentrated on the development and validation of a prognostic model for TA-TMA, which might facilitate risk stratification and contribute to individualized management. Methods Patients receiving allo-HSCT in Peking University People's Hospital with 1) a diagnosis of microangiopathic hemolytic anemia (MAHA) or 2) evidence of microangiopathy were retrospectively identified from 2010 to 2018. The diagnosis of TA-TMA was reviewed according to the Overall-TMA criteria (Transplantation, 2010). Patients without fulfillment of the diagnostic criteria or complicated with other causes of MAHA were excluded from analysis. Prognostic factors for TA-TMA were determined among patients receiving HSCT between 2010 and 2014 (derivation cohort). Candidate predictors (univariate P < 0.1) were included in the multivariate analysis using a backward stepwise logistic regression model. A risk score model was then established according to the regression coefficient of each independent prognostic factor. The performance of this predictive model was evaluated through internal validation (bootstrap method with 1000 repetitions) and external temporal validation performed on data from those who received HSCT between 2015 and 2018 (validation cohort). Results 5337 patients underwent allo-HSCT at Peking University Institute of Hematology from 2010 to 2018. A total of 1255 patients with a diagnosis of MAHA and/or evidence of microangiopathy were retrospectively identified, among whom 493 patients met the inclusion criteria for this analysis (269 in the derivation cohort and 224 in the validation cohort). The median age at the time of TA-TMA diagnosis was 28 (IQR: 17-41) years. The median duration from the time of transplantation to the diagnosis of TA-TMA was 63 (IQR: 38-121) days. The 6-month overall survival rate was 42.2% (208/493), and the 1-year overall survival rate was 45.0% (222/493). In the derivation cohort, patient age (≥35 years), anemia (hemoglobin 800 U/L) and elevated total bilirubin (TBIL >1.5*ULN) were identified by multivariate analysis as independent prognostic factors for the 6-month outcome of TA-TMA. A risk score model was constructed according to the regression coefficients (Table 1), and patients were stratified into a low-risk group (0-1 points), an intermediate-risk group (2-4 points) and a high-risk group (5-6 points). The Kaplan-Meier estimations of overall survival separated well between these risk groups (Figure 1). The prognostic model showed significant discriminatory capacity, with a cross-validated c-index of 0.770 (95%CI, 0.714-0.826) in the internal validation and 0.768 (95%CI, 0.707-0.829) in the external validation cohort. The calibration plots also indicated a good correlation between model-predicted and observed probabilities. Conclusions A prognostic model for TA-TMA incorporating several baseline laboratory factors was developed and evaluated, which demonstrated significant predictive capacity through internal and external validation. This predictive model might facilitate prognostication of TA-TMA and contribute to early identification of patients at higher risk for adverse outcomes. Further study may focus on whether these high-risk patients could benefit from early application of specific management. Disclosures No relevant conflicts of interest to declare.

Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although several studies have demonstrated the neuroprotective effects of Hericium erinaceus (H.E.), its mechanisms in cerebellar ataxia remain largely unknown. Here, we investigated the neuroprotective effects of H.E. treatment in an animal model of 3-acetylpyridine (3-AP)-induced cerebellar ataxia. Animals administered 3-AP injection exhibited remarkable impairments in motor coordination and balance. There were no significant effects of 25 mg/kg H.E. on the 3-AP treatment group compared to the 3-AP saline group. Interestingly, there was also no significant difference in the 3-AP treatment group compared to the non-3-AP control, indicating a potential rescue of motor deficits. Our results revealed that 25 mg/kg H.E. normalised the neuroplasticity-related gene expression to the level of non-3-AP control. These findings were further supported by increased protein expressions of pERK1/2-pCREB-PSD95 as well as neuroprotective effects on cerebellar Purkinje cells in the 3-AP treatment group compared to the 3-AP saline group. In conclusion, our findings suggest that H.E. potentially rescued behavioural motor deficits through the neuroprotective mechanisms of ERK-CREB-PSD95 in an animal model of 3-AP-induced cerebellar ataxia.

Neuronal NOS (nNOS) accounts for most of the NO production in the nervous system that modulates synaptic transmission and neuroplasticity. Although previous studies have selectively described the localisation of nNOS in specific brain regions, a comprehensive distribution profile of nNOS in the brain is lacking. Here we provided a detailed morphological characterization on the rostro-caudal distribution of neurons and fibres exhibiting positive nNOS-immunoreactivity in adult Sprague-Dawley rat brain. Our results demonstrated that neurons and fibres in the brain regions that exhibited high nNOS immunoreactivity include the olfactory-related areas, intermediate endopiriform nucleus, Islands of Calleja, subfornical organ, ventral lateral geniculate nucleus, parafascicular thalamic nucleus, superior colliculus, lateral terminal nucleus, pedunculopontine tegmental nucleus, periaqueductal gray, dorsal raphe nucleus, supragenual nucleus, nucleus of the trapezoid body, and the cerebellum. Moderate nNOS immunoreactivity was detected in the cerebral cortex, caudate putamen, hippocampus, thalamus, hypothalamus, amygdala, and the spinal cord. Finally, low NOS immunoreactivity were found in the corpus callosum, fornix, globus pallidus, anterior commissure, and the dorsal hippocampal commissure. In conclusion, this study provides a comprehensive view of the morphology and localisation of nNOS immunoreactivity in the brain that would contribute to a better understanding of the role played by nNOS in the brain.

Depression is a common and severe neuropsychiatric disorder that is one of the leading causes of global disease burden. Although various anti-depressants are currently available, their efficacies are barely adequate and many have side effects. Hericium erinaceus, also known as Lion’s mane mushroom, has been shown to have various health benefits, including antioxidative, antidiabetic, anticancer, anti-inflammatory, antimicrobial, antihyperglycemic, and hypolipidemic effects. It has been used to treat cognitive impairment, Parkinson’s disease, and Alzheimer’s disease. Bioactive compounds extracted from the mycelia and fruiting bodies of H. erinaceus have been found to promote the expression of neurotrophic factors that are associated with cell proliferation such as nerve growth factors. Although antidepressant effects of H. erinaceus have not been validated and compared to the conventional antidepressants, based on the neurotrophic and neurogenic pathophysiology of depression, H. erinaceus may be a potential alternative medicine for the treatment of depression. This article critically reviews the current literature on the potential benefits of H. erinaceus as a treatment for depressive disorder as well as its mechanisms underlying the antidepressant-like activities.

Significance Retroviruses can integrate their DNA into the host-cell genome. Inherited retroviral DNA and other transposable elements account for more than half of the human genome. Transposable elements must be tightly regulated to restrict their proliferation and prevent toxic gene expression. KAP1/TRIM28 is an essential regulator of transposable element transcription. We determined the crystal structure of the KAP1 TRIM. The structure identifies a protein–protein interaction site required for recruitment of KAP1 to transposable elements. An epigenetic gene silencing assay confirms the importance of this site for KAP1-dependent silencing. We also show that KAP1 self-assembles in solution, but this self-assembly is not required for silencing. Our work provides insights into KAP1-dependent silencing and tools for expanding our mechanistic understanding of this process., Transcription of transposable elements is tightly regulated to prevent genome damage. KRAB domain-containing zinc finger proteins (KRAB-ZFPs) and KRAB-associated protein 1 (KAP1/TRIM28) play a key role in regulating retrotransposons. KRAB-ZFPs recognize specific retrotransposon sequences and recruit KAP1, inducing the assembly of an epigenetic silencing complex, with chromatin remodeling activities that repress transcription of the targeted retrotransposon and adjacent genes. Our biophysical and structural data show that the tripartite motif (TRIM) of KAP1 forms antiparallel dimers, which further assemble into tetramers and higher-order oligomers in a concentration-dependent manner. Structure-based mutations in the B-box 1 domain prevent higher-order oligomerization without significant loss of retrotransposon silencing activity, indicating that, in contrast to other TRIM-family proteins, self-assembly is not essential for KAP1 function. The crystal structure of the KAP1 TRIM dimer identifies the KRAB domain binding site in the coiled-coil domain near the dyad. Mutations at this site abolished KRAB binding and transcriptional silencing activity of KAP1. This work identifies the interaction interfaces in the KAP1 TRIM responsible for self-association and KRAB binding and establishes their role in retrotransposon silencing.

Four phenylfuropyridone racemates, (±)-tersones A-C and E (1–3, 5), one phenylpyridone racemate, (±)-tersone D (4), one new pyridine alkaloid, tersone F (6), single new phenylfuropyridone, tersone G (7) and two known analogs 8 and 9 were isolated from the deep-sea fungus Phomopsis tersa. Their structures and absolute configurations were characterized on the basis of comprehensive spectroscopic analyses, single-crystal X-ray diffraction experiments, and electronic circular dichroism (ECD) calculations. Moreover, compounds 1–9 were evaluated for in vitro antimicrobial and cytotoxic activity. Compounds 5b and 8b exhibited antibacterial activity against S. aureus with the MIC value of 31.5 μg/mL, while compound 5b showed cytoxic activities against SF-268, MCF-7, HepG-2 and A549 cell lines with IC50 values of 32.0, 29.5, 39.5 and 33.2 μM, respectively.

A Ni-Fe oxalate complex catalyst was synthesized and characterized by means of Brunauer-Emmet-Teller (BET) method, scanning electron microscope (SEM) and X-ray photo-electron spectroscopy (XPS). The catalyst showed good catalytic activity for aniline degradation by heterogeneous Fenton's reaction, in which the synergetic index was 9.3. The effects of reaction temperature, catalyst dosage, hydrogen peroxide concentration and initial pH were investigated. Under the optimum conditions (T = 293 K, catalyst dosage = 0.2 g/L, H2O2 concentration = 4 mmol/L and initial pH = 5.4), 100% aniline could be removed within 35 min, and approximately 88% deamination efficiency was achieved in 60 min. The aniline degradation process followed the pseudo-first-order kinetic (k = 0.177 min(-1)) with activation energy (Ea) of 49.4 kJ mol(-1). Aniline could be removed in a broad initial pH (3-8) due to the excellent pH-tolerance property of the catalyst. The detected ammonium ion indicated that deamination occurred during aniline degradation. It was proposed that deamination synchronized with aniline removal, and aniline was attacked by free radicals to generate benzoquinonimine and phenol. This system is promising for the removal of aniline from water.

4-Nitrobenzoic acid is stable, toxic, and non-biodegradable. Conventional methods for wastewater treatment are ineffective for the treatment of 4-nitrobenzoic acid. In this study, the degradation efficiency of 4-nitrobenzoic acid by ultrasound in the presence of zero-valence zinc (Zn) was reported. The operating parameters were optimized, and the potential mechanisms were investigated. The results showed that there was a significant synergetic effect between ultrasound and Zn, and the synergetic factor was 2.26. The optimized treatment conditions were as follows: Initial pH 7.0 and Zn dosage of 0.4 g/L, under which the 4-nitrobenzoic acid degradation efficiency reached more than 85% after 30 min. The potential mechanisms included hydroxylation and the mechanical effect of ultrasound and the reduction and particle effects of Zn, which enhanced each other. The determination of intermediate products indicated that the catalytic degradation of 4-nitrobenzoic acid started with the destruction of the ni...

The use of low-coherence light is expected to be one of the effective ways to suppress or even eliminate the laser–plasma instabilities that arise in attempts to achieve inertial confinement fusion. In this paper, a review of low-coherence high-power laser drivers and related key techniques is first presented. Work at typical low-coherence laser facilities, including Gekko XII, PHEBUS, Pharos III, and Kanal-2 is described. The many key techniques that are used in the research and development of low-coherence laser drivers are described and analyzed, including low-coherence source generation, amplification, harmonic conversion, and beam smoothing of low-coherence light. Then, recent progress achieved by our group in research on a broadband low-coherence laser driver is presented. During the development of our low-coherence high-power laser facility, we have proposed and implemented many key techniques for working with low-coherence light, including source generation, efficient amplification and propagation, harmonic conversion, beam smoothing, and precise beam control. Based on a series of technological breakthroughs, a kilojoule low-coherence laser driver named Kunwu with a coherence time of only 300 fs has been built, and the first round of physical experiments has been completed. This high-power laser facility provides not only a demonstration and verification platform for key techniques and system integration of a low-coherence laser driver, but also a new type of experimental platform for research into, for example, high-energy-density physics and, in particular, laser–plasma interactions.

In this paper, we propose a three-dimensional spatially and temporally resolved method for measuring laser-induced damage fluence by identifying the time onset of defect damage and the damage location in the three-dimensional coordinate system of a Gaussian beam. When considering a second-harmonic beam splitter as an example, the defect fluence of fundamental wave (1064 nm) and second harmonic wave (532 nm) simultaneous irradiation is captured accurately by the proposed method. The defect damage threshold of a second-harmonic beam splitter and the coupling effect between multi-wavelength lasers during defect damage initiation are investigated. Our test method can not only identify complex multi-wavelength laser coupling damage mechanisms that traditional test methods cannot observe, but also provides a new method for obtaining accurate defect information for optical films, which is helpful for improving the laser resistance ability of optical films.

TOUGHREACT has been widely used as a chemical reaction simulation program for non-isothermal multiphase flow in pore and fracture media. By analyzing the comprehensive research results, the application status of TOUGHREACT in CO2 geological storage, geothermal energy development, nuclear waste disposal, mineral recovery and silica fouling and environmental pollution remediation are summarized. Finally, the future development trend of TOUGHREACT is also analyzed. It can be used as a reference for the future application of TOUGHREACT in the field of energy and environment.

In this Letter, we study the second-harmonic (SH) generation of temporally low-coherence light using the statistical optics method. By introducing the statistical characteristics of low-coherence light into the nonlinear coupled wave equation, we predict the self-convolution relationship between the power spectral density of the second-harmonic and that of the fundamental wave and demonstrate it in experiments. The effects of phase matching and group velocity matching on the second-harmonic bandwidth and conversion efficiency are analyzed, which is beneficial to improve the efficiency of low-coherent SH light. Combining the statistics optics and nonlinear optics, our research provides a suitable mathematical model for the study of nonlinear frequency conversion processes of temporally low-coherence light. Due to its statistical characteristics and temporal incoherence, low-coherence SH light would have further applications in uniform illumination, quantum optics, metrology, and so on.

A μJ-level low-coherent pulse with dynamic and precise temporal shaping and spectral control is demonstrated. Low-coherent light delivered by a superluminescent diode is precisely shaped through a wave guide amplitude modulator driven by an arbitrary waveform generator. Utilizing a three-stage axial-alternating polarization-maintaining single-mode fiber amplifier, μJ-level low-coherent pulses with 3 ns durations and 20 nm instantaneous bandwidths at a 1 kHz repetition rate are obtained. In addition, a spectral control unit is used to adjust the spectrum shape. As a result, near flat-top, saddle-type, or other required special spectra can be produced. The low temporal coherence characteristics and output stability are characterized experimentally.

Transcription of transposable elements is tightly regulated to prevent genome damage. KRAB domain-containing zinc finger proteins (KRAB-ZFPs) and KRAB-associated protein 1 (KAP1/TRIM28) play a key role in regulating retrotransposons. KRAB-ZFPs recognize specific retrotransposon sequences and recruit KAP1, inducing the assembly of an epigenetic silencing complex, with chromatin remodeling activities that repress transcription of the targeted retrotransposon and adjacent genes. Our biophysical and structural data show that the tripartite motif (TRIM) of KAP1 forms antiparallel dimers, which further assemble into tetramers and higher-order oligomers in a concentration-dependent manner. Structure-based mutations in the B-box 1 domain prevent higher-order oligomerization without significant loss of retrotransposon silencing activity, indicating that, in contrast to other TRIM-family proteins, self-assembly is not essential for KAP1 function. The crystal structure of the KAP1 TRIM dimer identifies the KRAB domain binding site, in the coiled-coil domain near the dyad. Mutations at this site abolished KRAB binding and transcriptional silencing activity of KAP1. This work identifies the interaction interfaces in the KAP1 TRIM responsible for self-association and KRAB binding and establishes their role in retrotransposon silencing. Significance Retroviruses can integrate their DNA into the host-cell genome. Inherited retroviral DNA and other transposable elements account for over half of the human genome. T ransposable elements must be tightly regulated to restrict their proliferation and prevent toxic gene expression. KAP1/TRIM28 is an essential regulator of transposable element transcription. We determined the crystal structure of the KAP1 TRIM. The structure identifies a protein-protein interaction site required for recruitment of KAP1 to transposable elements. An epigenetic gene silencing assay confirms the importance of this site for KAP1-dependent silencing. We also show that KAP1 self-assembles in solution, but this self-assembly is not required for silencing. Our work provides insights into KAP1-dependent silencing, and tools for expanding our mechanistic understanding of this process.