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Significance: Ferroptosis is featured by the accumulation of polyunsaturated-lipid peroxidation on cellular membranes in an iron-dependent manner. Ferroptosis has been implicated in various pathophysiological processes, including cancer, neurodegeneration, and ischemia-reperfusion tissue injury. However, our understanding about the dynamic and context-specific regulation of ferroptosis remains incomplete. Recent Advances: As the major substrate for peroxidation, the cellular lipidome regulates ferroptosis sensitivity and execution by controlling the abundance and availability of polyunsaturated-lipids for peroxidative modifications. In turn, the cellular lipidome is regulated by a complex network of enzymes and transporters, as well as upstream layers of receptors, kinases, and transcription factors. A number of research has shed light on the link between lipid metabolism and ferroptosis. Here, we summarize our current knowledge on the role of the lipidome and associated protein regulators in various stages of ferroptosis, ranging from initiation, execution to cell death evasion by cells experiencing ferroptotic stress. Critical Issues: This review provides an overview of the mechanisms underlying lipid peroxidation and ferroptosis by discussing the lipid species that directly contribute to lipid peroxidation and ferroptosis, how cells regulate the abundances of these pro-ferroptosis lipids, how lipid peroxidation causes cell death, and how cells prevent and repair membrane lipid damage under ferroptotic conditions. Future Directions: Cell fate regulation in vivo could be different from in vitro culture settings. We envision that a comprehensive and detailed understanding about these important questions in the dynamic regulation of ferroptosis in vivo will accelerate our development of ferroptosis-targeted therapies to improve human health. [ABSTRACT FROM AUTHOR]

Abstract The number of biosafety evaluation studies of nanoparticles (NPs) using different biological models is increasing with the rapid development of nanotechnology. Thus far, nematode Caenorhabditis elegans (C. elegans), as a complete model organism, has become an important in vivo alternative assay system to assess the risk of NPs, especially at the environmental level. According to results of qualitative and quantitative analyses, it can be concluded that studies of nanoscientific research using C. elegans is persistently growing. However, the comprehensive conclusion and analysis of toxic effects of NPs in C. elegans are limited and chaotic. This review focused on the effects, especially sublethal ones, induced by NPs in C. elegans , including the development, intestinal function, immune response, neuronal function, and reproduction, as well as the underlying mechanisms of NPs causing these effects, including oxidative stress and alterations of several signaling pathways. Furthermore, we presented some factors that influence the toxic effects of NPs in C. elegans. The advantages and limitations of using nematodes in the nanotoxicology study were also discussed. Finally, we predicted that the application of C. elegans to assess long-term impacts of metal oxide NPs in the ecosystem would become a vital part of the nanoscientific research field, which provided an insight for further study. Graphical abstract Image 1 Highlights • The publication related to the nanoscientific research using C. elegans is increasing in recent years. • The toxicity of NPs can be assessed in C. elegans through endpoints of biological functions and molecular markers. • Factors of both NPs physicochemical properties and C. elegans cultivation environment can influence the toxicity of NPs. • There are several advantages and drawbacks of C. elegans in nanotoxicology studies. [ABSTRACT FROM AUTHOR]

Abstract Recently, the use of silica nanoparticles (SiO 2 -NPs) and mesoporous silica nanoparticles (mSiO 2 -NPs) in the biomedical field, such as biosensors, drug deliveries and bioactivator carriers, is increasing due to their special physiochemical properties. However, the biosafety assessment of them is far lagging behind their rapid application. In this study, we observed that both SiO 2 -NPs and mSiO 2 -NPs with certain exposed doses decreased the cell viability while increased the apoptosis rates in the human pulmonary alveolar epithelial cells (HPAEpiC). Generally, mSiO 2 -NPs presented less toxic effects than SiO 2 -NPs with same treated dose, which assures the positive application prospect of mSiO 2 -NPs in the area of biomedicine. Since both SiO 2 -NPs could be taken into cells and accumulated in the endoplasmic reticulum (ER), which resulted in pathologically morphological changes and subcellular organelle damages, we hypothesized that the ER stress response could be involved in the NPs-induced apoptosis. The findings suggested that SiO 2 -NPs and mSiO 2 -NPs exposure increased the expression levels of two ER stress markers, e.g. BiP and CHOP, which could be inhibited by the ER stress inhibitor 4-PBA, following with decreased apoptosis rates in HPAEpiC. Even though it is still unclear of the direct target of NPs causing ER stress response following with cell apoptosis, our findings provide a novel insight for researchers to explore the toxic mechanisms of SiO 2 -NPs and mSiO 2 -NPs in order to reduce the adverse effects of them. Highlights • SiO 2 -NPs and mSiO 2 -NPs both have value in the biomedical applications. • SiO 2 -NPs and mSiO 2 -NPs exposure induced cell death and apoptosis. • SiO 2 -NPs and mSiO 2 -NPs activated endoplasmic reticulum stress response to cause apoptosis. • mSiO 2 -NPs generally presented less toxicity than SiO 2 -NPs. [ABSTRACT FROM AUTHOR]

Abstract Epidemiological studies and experimental research have illustrated that PM2.5 has an association with cardiovascular adverse events. However, the underlying mechanisms are still unknown. Long non-coding RNAs (lncRNAs) have been proposed to take part in diverse diseases. To comprehensively gain insight into the molecular toxicity of PM2.5, expression patterns are analyzed in EA.hy926 cell line through RNAs microarray. A total of 356 lncRNA transcripts are dysregulated in 2.5 μg/cm2 group, and there are 1283 lncRNAs differentially expressed in 10 μg/cm2 group. From functional analysis, several lncRNAs may be implicated in the bio-pathways of phagosome, TNF signaling pathway, chemokine signaling pathway and gap junction. Moreover, certain lncRNAs participate in the toxicity of PM2.5 through cis- and/or trans-regulation of their co-expressed genes. Therefore, lncRNAs may be used as new candidate biomarkers and potentially preventive targets in cardiotoxicity of PM2.5. Our study indicates that not limited to transcriptional regulation, post-transcriptional regulation plays a pivotal role in PM2.5-caused toxicity. Highlights • A cluster of RNA transcripts are dysregulated in EA.hy926 cells after exposure of PM2.5. • The pivotal bio-pathways induced by PM2.5 are phagosome, gap junction, TNF and chemokine signaling pathway. • Several lncRNAs are implicated in cell processes through their cis- and/or trans-regulation of co-expressed genes. [ABSTRACT FROM AUTHOR]

Abstract The excellent optical properties of CdTe quantum dots (QDs) make researchers realize their value on the application of biomedicine, especially neuroscience, as an advanced fluorescent probe. Thus, it is important to evaluate the biosafety of CdTe QDs on the central nervous system (CNS). Our previous studies have conducted a systematic biosafety evaluation of CdTe QDs on the CNS and found several toxic endpoints, one of which is the inflammation on the rat hippocampus, but their underlying mechanism remains unclear. In this study, when BV2 microglial cells were exposed to CdTe QDs with doses <20 nM, there was no obviously adverse effect. However, 40 nM CdTe QDs exposure could significantly activate the BV2 cells and increase the pro-inflammatory cytokine IL-1ß secretion. Molecular biology analyses suggested that both TLR2/MyD88/NF-κB pathway and NLRP3 inflammasome participated in the CdTe QD-induced IL-1ß secretion. The former served as the first signal for pro-IL-1ß expression, while the later played a role on the maturation of pro-IL-1ß into IL-1ß. The results, taken together, demonstrated that MPA-modified CdTe QDs exposure with a high concentration was capable of activating microglial cells and promoting IL-1ß secretion, which was highly correlated with the activations of both TLR2/MyD88/NF-κB pathway and ROS-induced NLRP3 inflammasome. These findings provide some mechanistic insights regarding the neuroinflammatory responses to cadmium-based QDs. Graphical abstract Unlabelled Image Highlights • Cadmium-based quantum dots (QDs) have value in the biomedical applications. • CdTe QDs activated microglial cells and increased interleukin-1ß (IL-1ß) secretion. • The expression of pro-IL-1ß increased in CdTe QD-treated cells because of the nuclear factor κB (NF-κB) activation. • CdTe QDs caused excessive ROS generation to trigger NLRP3 inflammasome activation. [ABSTRACT FROM AUTHOR]

Quantum dots (QDs) could be used in the field of biology and medicine as excellent nano-scale fluorescent probes due to their unique optical properties, but the adverse effects of QDs are always the obstruction for its usage in living organisms. In this study, we observed that CdTe QDs exposure decreased the cell viability while increased the apoptosis rates in the L929 cells. Apart from QD-induced oxidative stress indicated by excessive ROS generation, three signal transductions, including Akt, p38 and JNK, played important roles on the regulation of cell apoptosis by CdTe QDs exposure as well. In order to reduce the toxicity of CdTe QDs, we explored the protective effects of three treatments, i.e. resveratrol, H 2 S and thermotherapy at 43 °C, against the cell apoptosis elicited by CdTe QDs. The results showed that resveratrol, H 2 S and thermotherapy at 43 °C were capable of attenuating cell apoptosis and intercellular ROS production through inhibiting signal pathways of Akt, p38 and JNK, respectively. As there is only limited number of exogenous treatments reported to diminish the toxicity of QDs, our findings will provide a novel insight for researchers who try to reduce or even eliminate the adverse health effects of QDs. [ABSTRACT FROM AUTHOR]

Graphene quantum dots (GQDs), as a novel graphene-based nanoparticle, presented a bright prospect in fields of biomedicine due to their excellent optical property. However, the biosafety assessment of GQDs is far behind their rapid development, which could restrict their wilder applications. This study focused on the potential adverse effects of two kinds of promising GQDs, i.e. nitrogen-doping graphene quantum dots (N-GQDs) and amino-modified graphene quantum dot (A-GQDs) on primary target organs of GNMs, including lung, liver and kidney. The intranasal instillation used here was to imitate the respiratory exposure of GQDs that is a commonly exposure route of GQDs in the environment. Although no severe damages associated with general health occurred in mice treated with GQDs, the fibrosis evidenced by statistically significant increases in the area of collagen I and TGF-ß1 and p-Smad3 expressions were observed in the lung, liver and kidney tissues. Interestingly, the fibrotic effect induced by GQDs could be effectively alleviated by a ferroptosis-specific inhibitor, which demonstrated a close relationship of fibrosis and ferroptosis. This study not only provides new insights on the toxicity mechanisms of GQDs, but also offers some efficient ways to control toxicity of GQDs, like dosage threshold and small molecular drugs. [Display omitted] [ABSTRACT FROM AUTHOR]

• Face-specific depth enhancement to refine the low-quality depth. • Iterative inter-modal feature interaction to fully exploit complementary information. • Feature re-calibration and weighted complementary feature aggregation to strengthen intra-modal representation. • Masked RGB-depth modeling mechanism to improve robustness towards missing-modality data. Existing RGB-based 2D face recognition approaches are sensitive to facial variations, posture, occlusions, and illumination. Current depth-based methods have been proved to alleviate the above sensitivity by introducing geometric information but rely heavily on high-quality depth from high-cost RGB-D cameras. To this end, we propose a Progressive Multi-modal Fusion framework to exploit enhanced and robust face representation for RGB-D facial recognition based on low-cost RGB-D cameras, which also deals with incomplete RGB-D modal data. Due to the defects such as holes caused by low-cost cameras, we first design a depth enhancement module to refine the low-quality depth and correct depth inaccuracies. Then, we extract and aggregate augmented feature maps of RGB and depth modality step-by-step. Subsequently, the masked modeling scheme and iterative inter-modal feature interaction module aim to fully exploit the implicit relations among these two modalities. We perform comprehensive experiments to verify the superior performance and robustness of the proposed solution over other FR approaches on four challenging benchmark databases. [ABSTRACT FROM AUTHOR]

Quantum dots (QDs), as advanced nanotechnology products, are widely used in the bio-medical field for diagnostic and therapeutic purposes due to their unique properties. Therefore, it becomes important for researchers to elucidate the adverse effects of QDs on human beings. This essay provides an overview of the toxic effects of QDs on respiratory system, which are summarized into two main parts: in vitro toxicity, including reduction of cell viability, genetic material damage and disordered immune cell reactions; as well as in vivo toxicity, involving accumulation of QDs, lung injury and inflammation, and potential long-term adverse effects. As the toxic severity of a QD type depends on its composition, dose, size, surface chemistry and structure, it is a big challenge to determine a benchmark of QDs. Thus, we have to remember that each QD type is a unique nanocrystal, which needs to be assessed individually. However, there are still some feasible recommendations for minimizing the toxicity provided in this review. Overall, more and more large-scale well-organized toxicity studies of different QD types on different species need to be conducted in order to provide guidelines of QDs' safety application. [ABSTRACT FROM AUTHOR]

Abstract: Growth and structural evolution of La0.5Sr0.5CoO3 thin films fabricated directly on SiO2/Si substrate by pulsed laser deposition were investigated. Films deposited at 780 °C and oxygen partial pressure of 2 Pa showed highly c-axis orientation. Films with low electrical resistivity of 2×10−3 Ω cm were obtained by annealing at 650 °C for 40 min. C-axis oriented Ba0.5Sr0.5TiO3 thin film was then grown on the La0.5Sr0.5CoO3 film, and large dielectric tuning (>50%) was achieved. This method may have good prospect for the integration of ferroelectric materials with conventional Si process technology. [Copyright &y& Elsevier]

Identity-independent factors, such as variations of pose, expression, illumination, etc., are the key challenges in face recognition. To avoid the effects of these factors, existing face recognition methods usually adopt two approaches: pose-invariant face feature extracting and face normalization before feature extraction. Contrary to these, we propose a single deep model jointly performing face normalization and representation learning tasks for face recognition, named normalization and reconstruction general adversarial network (NRGAN). First, the unified NRGAN model can boost the performance of the two tasks for each other. Second, NRGAN can synthesize normalized face images without the requirement of paired data, which makes our method have better generalization ability to the uncontrolled environment. Third, a factor-invariant identity disentanglement training strategy is introduced to decouple the identity feature representation from other factors without using any of these factors’ labels. Extensive experiment results on four currently popular face datasets demonstrate the effectiveness of NRGAN on both normalized face synthesis and face recognition tasks. [ABSTRACT FROM AUTHOR]

Graphene quantum dots (GQDs) have been broadly applied in biomedicine in recent years. So far, researches have reported that GQDs might contribute to the injury of the central nervous system (CNS), yet the latent toxicological mechanism is not clear. This study aims to investigate the underlying biological mechanism responsible for the neurotoxicity of nitrogen-doped GQDs (N-GQDs) and amino-functionalized GQDs (A-GQDs) by use of genome-wide transcription microarray. The findings showed that 174 and 1341 genes were altered significantly in the BV2 cells treated by 25 μg/mL N-GQDs and 100 μg/mL N-GQDs compared with the control, respectively. As for the BV2 cells exposed to 100 μg/mL A-GQDs, 1396 diversely expressed genes were detected. By comparing the 100 μg/mL N-GQDs exposed group with 100 μg/mL A-GQDs exposed group, the expression of 256 genes was extensively altered, including 58 upregulated genes and 198 downregulated genes. From Gene Ontology (GO) analysis, the altered genes were mainly enriched in functions of ion channel activation and cellular processes. Based on the KEGG pathway and signal-net analysis, the toxicity of GQDs in BV2 cells was closely related to calcium signaling pathway, cell cycle and endocytosis. And the pathways that the shared mRNAs involved all served as the crucial roles in the neurotoxicity of GQDs despite the chemical functionalization (N-GQDs or A-GQDs). In addition, the consequences from qRT-PCR, Western blot, intracellular calcium level measurements and comet assay further confirmed that calcium dyshomeostasis, DNA damage and cell cycle arrest were the key factors responsible for the GQDs-induced neurotoxicity through affecting several classical signaling pathways. In conclusion, our research will supply essential data for further studies on mechanisms of GQDs-induced neurotoxicity by use of genome-wide screening. Unlabelled Image • The altered genes were mainly involved in ion channel activity and cellular processes. • GABAergic synapse, calcium signaling pathway, tyrosine metabolism and cell cycle might be the toxic pathways of GQDs. • The severer neurotoxicity of N-GQDs than A-GQDs on BV2 cells might be from the maladjustment of Ubiquinone pathway. [ABSTRACT FROM AUTHOR]

• PM SRM1648a induces ER stress and mitochondrial dysfunction in endothelial cells. • Oxidative stress and calcium overload are involved in organelle damage and endothelial apoptosis by PM SRM1648a. • The effect of calcium modulators on PM SRM1648a-caused endothelial apoptosis is independent of mitochondrial pathways. • It is crucial to explore target toxicity at both cellular and subcellular levels. Ambient particulate matter (APM) is becoming a global environmental problem that seriously jeopardizes public health. Previous evidence hinted that APM correlates to cardiovascular diseases. As a potential target, equilibrium of endothelial cell is a prerequisite for vascular health which could be vulnerably attacked by particles, but the specific mechanisms whereby APM damages endothelial cells have not been fully elucidated. In the current study, based on two classical mechanisms of oxidative stress and intracellular calcium overload, we aimed to explore their roles in APM-induced endothelial cell apoptosis from the perspective of subcellular levels, including endoplasmic reticulum (ER) stress and mitochondrial dysfunction. As a result, PM SRM1648a results in oxidative stress and calcium overload in EA.hy926 cells. Additionally, ERs and mitochondria could be severely disturbed by particles in morphology and function, characterized by swelling ERs, mitochondrial fission and disappearance of cristae, coupled with ER damage, mtROS overproduction and significant reduction in mitochondrial membrane potential (MMP). Adverse effects on these organelles are the prime culprits of following apoptosis in endothelial cells. Fortunately, additional antioxidants and calcium inhibitors could mitigate cellular lesion through improvement of subcellular function. Intriguingly, antioxidants relieve cell stress via both mitochondrial and ER stress-mediated pathways, whereas the role of calcium modulators in cell apoptosis is independent of the mitochondrial pathway but could be explained by amelioration of ER stress. In conclusion, our data basically revealed that internalized PM SRM1648a triggers oxidative stress and calcium influx in EA.hy926 endothelial cells, followed by multiple subcellular damage and eventually contributes to cell death, during which antioxidants and calcium inhibitors confer protective effects. [ABSTRACT FROM AUTHOR]

CdTe quantum dots (QDs) are still widely considered as excellent fluorescent probes because of their far more superior optical performance and fluorescence efficiency than non‑cadmium QDs. Thus, it is important to find ways to control their toxicity. In this study, CdTe QDs and CdTe@ZnS QDs both could cause IL-1ß-mediated inflammation following with pyroptosis in BV2 cells, but the toxic effects caused by CdTe@ZnS QDs was weaker than CdTe QDs, which demonstrated the partial protection of ZnS shell. When investigating the molecular mechanisms of QDs causing the inflammatory injury, the findings suggested that cadmium-containing QDs exposure activated NF-κB that participated in the NLRP3 inflammasome priming and pro-IL-1ß expression. After that, QDs-induced excessive ROS generation triggered the NLRP3 inflammasome activation and resulted in active caspase-1 to process pro-IL-1ß into mature IL-1ß release and inflammatory cell death, i.e. pyroptosis. Fortunately, the inhibitions of caspase-1, NF-κB and ROS or knocking down of NLRP3 all effectively attenuated the increases in the IL-1ß secretion and cell death caused by QDs in BV2 cells. This study provided two methods to alleviate the toxicity of cadmium-containing QDs, in which one is to encapsulate bare-core QDs with a shell and the other is to inhibit their toxic pathways. Since the latter way is more effective than the former one, it is significant to evaluate QDs through a mechanism-based risk assessment to identify controllable toxic targets. • Cadmium-containing QDs exposure caused IL-1ß secretion and pyroptosis in BV2 cells. • The ZnS shell could alleviate inflammatory injury caused by CdTe QDs to some extent. • NLRP3 activation was involved in QDs causing IL-1ß-mediated inflammatory injury. • QDs-induced NF-κB and ROS generation resulted in NLRP3 priming and activation. • Inhibitions of caspase-1, NF-κB, ROS and NLRP3 all attenuated inflammatory injury. [ABSTRACT FROM AUTHOR]

Hot data identification plays a very important role in NAND flash memory because it can improve the efficiency of garbage collection and decrease the degree of wear leveling. Existing hot data identification mechanisms have drawbacks in terms of their memory-space overhead and the true identification of hot data. To address these problems, this paper proposes a novel hot data identification mechanism. This mechanism mainly consists of kernel density estimation and a hot degree function. The kernel density estimation is used to build the kernel density function of the read and write operations by monitoring them in the NAND flash memory. That is, the kernel density function can be used for preliminary estimation of the probability distribution of the hot and cold data in NAND flash memory. After preliminary estimation of the kernel density function, the hot degree function is introduced to accurately identify the hot data in the NAND flash memory. Experimental results show that the proposed mechanism performs better than existing hot data identification mechanisms in terms of the false identification ratio between hot data and memory-space overheads. [ABSTRACT FROM AUTHOR]

Silver nanoparticles (AgNPs) have been widely used in biomedicine and cosmetics, increasing their potential risks in neurotoxicity. But the involved molecular mechanism remains unclear. This study aims to explore molecular events related to AgNPs-induced neuronal damage by RNA-seq, and elucidate the role of Ca2+/CaMKII signal and Drp1-dependent mitochondrial disorder in HT22 cells synaptic degeneration induced by AgNPs. This study found that cell viabilities were decreased by AgNPs in a dose/time-dependent manner. AgNPs also increased protein expression of PINK1, Parkin, synaptophysin, and inhibited PGC-1 α , MAP2 and APP protein expression, indicating AgNPs-induced synaptic degeneration involved in disturbance of mitophagy and mitochondrial biogenesis in HT22 cells. Moreover, inhibition of AgNPs-induced Ca2+/CaMKII activation and Drp1/ROS rescued mitophagy disturbance and synaptic degeneration in HT22 cells by reserving aforementioned protein express changes except for PGC-1 α and APP protein. Thus, AgNPs-induced synaptic degeneration was mediated by Ca2+/CaMKII signal and Drp1-dependent mitochondrial disorder in HT22 cells, and mitophagy is the sensitive to the mechanism. Our study will provide in-depth molecular mechanism data for neurotoxic evaluation and biomedical application of AgNPs. [Display omitted] • Ca2+/CaMKII signal promotes AgNPs-induced mitophagy and synaptic degeneration in HT22 cells. • Drp1/ROS triggers AgNPs-induced mitochondrial disorder and synaptic degeneration. • Mitophagy is the sensitive to AgNPs-induced synaptic degeneration via Ca2+/CaMKII and Drp1/ROS signal. [ABSTRACT FROM AUTHOR]

[Display omitted] • Molecular networking was used to identify TPs of antidepressants in wastewater. • 22 TPs were tentatively identified and 19 ones were new TPs of antidepressants. • N-acylation and N-hydroxylation were characteristics reactions for antidepressants. • The high electrophilic activity of the amino caused characteristics reactions. The extensive detection of antidepressants in wastewater has raised increasing concerns for human beings. During biological wastewater treatment processes, antidepressants cannot be completely removed and mineralized, which caused the formation of transformation products (TPs). To date, knowledges on TPs that participated in the transformation processes of antidepressants were scarce. To fill this gap, molecular networking nontarget screening based on lab-scale batch assays were employed to explore the removal and transformation of five antidepressants (amitriptyline (AMI), clomipramine (CLO), duloxetine (DUL), nortriptyline (NOR) and paroxetine (PAR)). The removal rate constants per unit of biomass (k bio) of the five antidepressants were found to range from 0.29 to 0.56 L/(gMLSS*d). Comparatively, clomipramine was removed more slowly than other antidepressants, which attributed to its lower electrophilic properties. Subsequently, 22 TPs were tentatively identified, among which 19 ones were newly found in the present study. The proposed transformation pathways indicated that demethylation, N-formylation, N-acetylation, N-succinylation, N-hydroxylation, dealkylation, hydrolysis and nitrosation participated in the transformation of antidepressants in wastewater. Particularly, N-acylation and N-hydroxylation were found as characteristics reactions for antidepressants in wastewater and these reactions consistently occurred at the site of amino functional group, where high electrophilic activity was the dominant causes for the observed characteristics reactions. In silico results revealed that TPs formed during biological wastewater treatment generally had lower toxicity, lower bioaccumulation and higher bioavailability than their parent compounds. Collectively, the present study provides insights into the transformation processes of antidepressants in wastewater, indicating that characteristic transformation reactions occur across different antidepressants, which is theoretically useful to effectively remove pharmaceuticals from wastewater. [ABSTRACT FROM AUTHOR]

The split-radix fast Fourier transform (SRFFT) is attractive for low-power FFT processors as it has the lowest numbers of multiplication operations among all FFT algorithms. FFT algorithms differ from one another by the location of the twiddle factor. The irregular locations of the twiddle factors in the SRFFT lead to complex address generators for the memory containing the twiddle factors. This paper proposes a novel twiddle factor addressing architecture for the split-radix FFT processor, which can effectively reduce its power consumption. This is then used to design a simple memory address generator and a low-power pipelined SRFFT. The proposed algorithm is used to implement a 1024-point pipelined circuit. Post-layout simulation shows that the proposed 1024-point design achieves over 24% and 14.7% lower power consumption for the multiplications and ROM, respectively, compared to a traditional radix-2 single delay feedback (SDF) FFT architecture. • In this paper, a novel twiddle factor addressing architecture is proposed, which can reduce the power consumption of the SRFFT processor. • Under the TSMC 65 nm process, we compared the newly proposed SRFFT processor with the traditional radix-2 FFT processor. • SRFFT processor can reduce the power consumption of the multiplier by 24% and the power consumption of the ROM by 14.7%. [ABSTRACT FROM AUTHOR]

Generated from plastics, microplastics (MPs) and nanoplastics (NPs) are difficult to completely degrade in the natural environment, which can accumulate in almost all lives. Liver is one of the main target organs. In this study, HepG2 and L02 cells were exposed to 0–50 μg/mL polystyrene (PS)-NPs to investigate the mechanism of mitochondrial damage and inflammation. The results showed mitochondria damage and inflammatory caused by NPs, and it can be inhibited by N-acetyl-L-cysteine (NAC). In addition, reactive oxygen species (ROS) activated nuclear factor erythroid-derived factor 2-related factor (Nrf2) pathway. Nrf2 siRNA exacerbated the injury, suggesting Nrf2 plays a protective role. Moreover, p62 siRNA increased ROS and mitochondrial damage by inhibiting Nrf2, but didn't affect the inflammation. In conclusion, Nrf2 was activated by ROS and played a protective role in PS-NPs-mediated hepatotoxicity. This study supplemented the data of liver injury caused by PS-NPs, providing a basis for the safe disposal of plastics. [Display omitted] • Polystyrene nanoplastics (PS-NPs) decreased in the viability of HepG2 and L02 cells in a dose and time-dependent manner. • PS-NPs induced oxidative, mitochondria damage and inflammation in HepG2 and L02 cells. • N-acetylcysteine (NAC) alleviated PS-NPs-induced oxidative and inflammation in HepG2. • Nrf2 protected HepG2 from PS-NPs-induced oxidative, mitochondria damage and inflammation. • p62 siRNA aggravated PS-NPs-induced oxidative and mitochondria damage in HepG2. [ABSTRACT FROM AUTHOR]

Along with the rapid development of nanotechnology, the biosafety assessment of nanotechnology products, including nanomaterials (NMs), has become more and more important. The nematode Caenorhabditis elegans is a valuable model organism that has been widely used in the field of biology because of its excellent advantages, including low cost, small size, short life span, and highly conservative genomes with vertebral animals. In recent years, the number of nanotoxicological researchers using C. elegans has been growing. According to these available studies, the present review classified the adverse effects of NMs in C. elegans into systematic, cellular, and molecular toxicity, and focused on summarizing and analyzing the underlying mechanisms of metal, metal oxide, and nonmetallic NMs causing toxic effects in C. elegans. Our findings provide insights into what further studies are needed to assess the biosafety of NMs in the ecosystem using C. elegans. Environ Toxicol Chem 2021;40:2406–2424. © 2021 SETAC [ABSTRACT FROM AUTHOR]

Daunorubicin is a common antineoplastic agent used for the treatment of lymphoma and acute leukemia. Here, we report an 808 nm-excited, citric acid coated, core–shell upconversion fluorescent sensor for daunorubicin (DAU) detection in aqueous solutions. The designed Nd3+ doped core–shell structure significantly raises the upconversion fluorescence intensity, while the presence of citric acid ligands helps to reduce the surface quenching effect exerted by water and improve the dispersibility. The upconversion fluorescence of nanoparticles is efficiently quenched in the presence of DAU via a fluorescence resonance energy transfer mechanism. The dynamic quenching constant was 1.58 × 104 M−1. The fluorescence intensity ratio showed a good linear response to DAU concentration in the range of 0.1 μM to 70 μM with a detection limit of 0.06 μM. The sensing method was simple, rapid, and low-cost and was further applied to determine the levels of DAU in urine with spike recoveries from 97.3% to 101.5%. The proposed fluorescent sensor holds great potential for in vivo imaging and detection of DAU. [ABSTRACT FROM AUTHOR]

Self-Organizing Map (SOM) algorithm as an unsupervised learning method has been applied in anomaly detection due to its capabilities of self-organizing and automatic anomaly prediction. However, because of the algorithm is initialized in random, it takes a long time to train a detection model. Besides, the Cloud platforms with large scale virtual machines are prone to performance anomalies due to their high dynamic and resource sharing characters, which makes the algorithm present a low accuracy and a low scalability. To address these problems, an Improved Incremental Self-Organizing Map (IISOM) model is proposed for anomaly detection of virtual machines. In this model, a heuristic-based initialization algorithm and a Weighted Euclidean Distance (WED) algorithm are introduced into SOM to speed up the training process and improve model quality. Meanwhile, a neighborhood-based searching algorithm is presented to accelerate the detection time by taking into account the large scale and high dynamic features of virtual machines on cloud platform. To demonstrate the effectiveness, experiments on a common benchmark KDD Cup dataset and a real dataset have been performed. Results suggest that IISOM has advantages in accuracy and convergence velocity of anomaly detection for virtual machines on cloud platform. [ABSTRACT FROM AUTHOR]

Silver nanoparticles (AgNPs) are widely used in various fields such as industry, agriculture, and medical care because of their excellent broad-spectrum antibacterial activity. However, their extensive use has raised concerns about their health risks. Liver is one of the main target organs for the accumulation and action of AgNPs. Therefore, evaluating the toxic effects of AgNPs on liver cells and its mechanisms of action is crucial for the safe application of AgNPs. In the study, polyvinylpyrrolidone (PVP)-coated AgNPs were characterized. The human hepatoma cell line (HepG2) and the normal hepatic cell line (L02) were exposed to different concentrations of AgNPs (20–160 μg/mL) and pretreated with the addition of N -acetylcysteine (NAC) or by Nrf2 siRNA transfection. NAC was able to inhibit the concentration-dependent increase in the level of apoptosis induced by AgNPs in HepG2 cells and L02 cells. Interestingly, HepG2 cells were more sensitive to AgNPs than L02 cells, and this may be related to the different ROS generation and responses to AgNPs by cancer cells and normal cells. In addition, NAC also alleviated the imbalance of antioxidant system and cell cycle arrest, which may be related to AgNPs-induced DNA damage and autophagy. The knockdown of nuclear factor erythroid-derived factor 2-related factor (Nrf2) found that AgNPs-induced ROS and apoptosis levels were further upregulated, but the cell cycle arrest was alleviated. On the whole, Nrf2 exerts a protective role in AgNPs-induced hepatotoxicity. This study complements the hepatotoxicity mechanisms of AgNPs and provides data for a future exploration of AgNPs-related anti-hepatocellular carcinoma drugs. [Display omitted] • AgNPs induced a concentration-dependent decline in HepG2 and L02 cells viability. • AgNPs induced ROS increase and apoptosis in HepG2 and L02 cells. • AgNPs induced DNA damage, autophagy and cell cycle arrest in HepG2 and L02 cells. • N -acetylcysteine alleviated AgNPs-induced cytotoxicity in HepG2 and L02 cells. • Nrf2 siRNA aggravated AgNPs-induced cytotoxicity in HepG2 and L02 cells. [ABSTRACT FROM AUTHOR]

Silver nanoparticles (AgNPs) have been incorporated in many consumer and biomedical products. Serious concerns have been expressed about the environmental and public health risks caused by nanoparticles. In previous studies, we found that AgNPs induced microglia polarization of the inflammatory phenotype. Autophagy was a critical for AgNPs-induced neuroinflammation. In the present study, we evaluated in detail the effects of AgNPs in different stages of the autophagy process, and we found that AgNPs induced neuroinflammatory responses and autophagic flux blockage both in the mouse brain and BV2 cells. AgNPs inhibited autophagosome-lysosome fusion and impaired the lysosomal functions by reducing the levels of lysosomal-associated membrane proteins, promoting lysosome membrane permeability and altering the lysosomal acidic microenvironment. These changes resulted in the defects in autophagic substrate clearance and subsequently led neuroinflammation. In addition, the elevation of autophagy could prevent the neuroinflammation induced by AgNPs. As a result, AgNPs hindered autophagic flux by inhibiting autophagosome fusion with lysosomes, thus aggravating the AgNPs-induced neurotoxicity. These findings will provide new insights to investigate the molecular mechanisms of neurotoxicity caused by AgNPs. [Display omitted] • AgNPs induced neuroinflammation and autophagic flux blockage in vivo & in vitro. • AgNPs inhibited autophagosome-lysosome fusion and impaired the lysosomal functions. • AgNPs hindered autophagic flux thus aggravating the AgNPs-induced neurotoxicity. • Autophagy might play a protective role in AgNPs-induced neuroinflammation. [ABSTRACT FROM AUTHOR]

Silver nanoparticles (AgNPs) could accumulate in the central nervous system (CNS) and induce neurotoxicity for their widespread use in industry and medicine. Mitochondria are vulnerable to toxicity of AgNPs, however, their role in the neurotoxicity remains unclear. This study aimed to evaluate AgNPs-induced synaptic degeneration in mouse hippocampal neurons (at a dose of 12–120 mg/kg BW via intravenous injection), and to further investigate mechanism of mitophagy, mitochondrial biogenesis process in the neurotoxicity. The results indicated that AgNPs accumulated in mouse hippocampal neurons and induced neurological deficits of learning and memory, which involved in synaptic degeneration accompanied with mitochondrial damage. Mechanistically, AgNPs exposure increased protein expression of PTEN-induced kinase 1 (PINK1), Parkin and inhibited peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1 α) protein expression, caused disturbed mitophagy and mitochondrial biogenesis. AgNPs also induced synaptic damage by increasing the protein expression of synaptophysin and decreasing PSD95, MAP2 protein expression. AgNPs exposure even promoted protein expression of amyloid precursor protein (APP) using in amyloid- β (A β) cleavage. Furthermore, AgNPs induced hippocampal neuronal synaptic degeneration, mitophagy and mitochondrial biogenesis is dependent on particle-specific AgNPs rather than released silver ions. Our research could provide insights into the regulatory mechanisms of AgNPs-induced neurotoxicity. This study will shed the light of neurotoxicological evaluation of nanoparticles and possible early warning of biomedical applications. [Display omitted] [ABSTRACT FROM AUTHOR]

Virtual machines (VM) on a Cloud platform can be influenced by a variety of factors which can lead to decreased performance and downtime, affecting the reliability of the Cloud platform. Traditional anomaly detection algorithms and strategies for Cloud platforms have some flaws in their accuracy of detection, detection speed, and adaptability. In this paper, a dynamic and adaptive anomaly detection algorithm based on Self-Organizing Maps (SOM) for virtual machines is proposed. A unified modeling method based on SOM to detect the machine performance within the detection region is presented, which avoids the cost of modeling a single virtual machine and enhances the detection speed and reliability of large-scale virtual machines in Cloud platform. The important parameters that affect the modeling speed are optimized in the SOM process to significantly improve the accuracy of the SOM modeling and therefore the anomaly detection accuracy of the virtual machine. [ABSTRACT FROM AUTHOR]

In this paper, a page replacement algorithm based on counting bloom filter for NAND flash memory is proposed. This algorithm mainly consists of two schemes: the data separation scheme based on counting bloom filter and the free block management scheme. The former is used for classifying the dirty subpages within the victim pages as hot or cold and the latter is used for classifying the free blocks within the free block list into young or old. Moreover, in order to improve the performance of NAND flash memory, the hot dirty subpages are written back to the young free block, and the cold subpages are distributed to the old free block. Experimental results show that the proposed algorithm performs better than the existing page replacement algorithms in terms of the number of write operations, the total runtime, the buffer hit ratio and the degree of wear leveling. [ABSTRACT FROM PUBLISHER]

[Display omitted] • PANI nanorod modification enables 45% higher Cr(VI) removal than CFF cathode. • CFF-PANI cathode had 35% lower energy consumption (48.5 Wh/mol) than CFF cathode. • The morphology of PANI nanorod forests significantly affected the Cr(VI) reduction. • Cr(VI) reduction on cathode was the main mechanism for Cr(VI) removal in FES. • Energy efficiency for Cr(VI) reduction on CFF-PANI cathode were kept ~95% at 0.8 V. Cr(VI) reduction to Cr(III) has been demonstrated to be an effective method for Cr(VI) detoxification. Herein, we fabricated polyaniline (PANI) nanorod forests-modified Carbon fiber felt (CFF) as CFF-PANI cathode in a Flow-through electrode system (FES) with the counter CFF anode for enhancing Cr(VI) reduction. The CFF-PANI was synthetized via in-situ polymerization under different aniline concentration to investigate the effect of PANI nano-structures on Cr(VI) reduction. It was revealed that BET and electrochemical surface area of PANI nanorods significantly affected the Cr(VI) reduction, and CFF-PANI cathode with the largest BET and electrochemical surface area exhibited ∼ 45% higher Cr(VI) removal and ∼ 35% lower specific energy consumption than the CFF cathode. A decrease-then-stable Cr(VI) removal was observed within 120 min operation time, which was attributed to the electro-adsorption of Cr(VI) species on CFF anode. In-situ sampling experiments revealed that the electrochemical oxidation on CFF anode inhibited the Cr(VI) electro-adsorption, and at applied voltage above 0.7 V, the Cr(VI) reduction on cathode was the main mechanism for Cr(VI) removal. The operation of FES at 0.8 V had the lowest specific energy consumption (48.5 Wh/mol) and maintained ∼ 95% energy efficiency for Cr(VI) reduction with minor competitive reduction of H 2 O or O 2 species. The results suggested that CFF-PANI can be a promising cathode for Cr(VI) reduction from aqueous solutions. [ABSTRACT FROM AUTHOR]

Abstract: This paper proposes an adaptive buffer replacement algorithm for NAND flash memory-based databases, which is called HDC. HDC introduces an efficient replacing index for selecting pages to be evicted. This replacing index considers two factors: the hot degree of each page and the cost of writing the victim page back to NAND flash memory. It can adaptively change the weight of each factor according to the cost ratio of NAND flash memory. HDC also introduces an efficient partial update scheme, which only writes the dirty data within the dirty victim page back to NAND flash memory for further reducing the number of write operations and writes the dirty data to the free block with the lowest erase count for improving the wear-leveling degree of NAND flash memory. We conduct trace-driven simulations on two kinds of NAND flash memories the cost ratios of which are 118:1 and 2:1. The experimental results show that HDC outperforms the state-of-the-art algorithms on both these kinds of NAND flash memories. [Copyright &y& Elsevier]

Along with the rapidly increasing applications of nitrogen-doped graphene quantum dots (N-GQDs) in the field of biomedicine, the exposure of N-GQDs undoubtedly pose a risk to the health of human beings, especially in the nervous system. In view of the lack of data from in vivo studies, this study used the nematode Caenorhabditis elegans (C. elegans), which has become a valuable animal model in nanotoxicological studies due to its multiple advantages, to undertake a bio-safety assessment of N-GQDs in the nervous system with the assistance of a deep learning model. The findings suggested that accumulated N-GQDs in the nematodes' bodies damaged their normal behavior in a dose- and time-dependent manner, and the impairments of the nervous system were obviously severe when the exposure dosages were above 100 μg/mL. When assessing the morphological changes of neurons caused by N-GQDs, a quantitative image-based analysis based on a deep neural network algorithm (YOLACT) was used because traditional image-based analysis is labor-intensive and limited to qualitative evaluation. The quantitative results indicated that N-GQDs damaged dopaminergic and glutamatergic neurons, which are involved in the neurotoxic effects of N-GQDs in the nematode C. elegans. This study not only suggests a fast and economic C. elegans model to undertake the risk assessment of nanomaterials in the nervous system, but also provides a valuable deep learning approach to quantitatively track subtle morphological changes of neurons at an unbiased level in a nanotoxicological study using C. elegans. [ABSTRACT FROM AUTHOR]

[Display omitted] • FES with a sequential Ox-Red process achieved Cr(VI) removal at near neutral pHs. • In FES with a sequential Ox-Red process, anode-treated effluent is strong acidic. • Subsequently, Cr(VI) reduction to Cr(III) occur easily on the subsequent cathode. • Regenerating passivated CFF electrodes is enhanced with reversed applied voltage. • The FES can be a feasible approach for Cr(VI) remediation of drinking water. Cr(VI) reduction to Cr(III) and subsequent Cr(III) precipitation is an extensively employed strategy to treat Cr(VI)-contaminated wastewater, which generally generates large volumes of sludge that need expensive disposal, and requires high chemical cost for pH adjustment. Herein, flow-through electrode system (FES) with a sequential oxidation-reduction process was employed to simultaneously reduce Cr(VI) and in-situ precipitate Cr(III), thereby simplifying the treatment processes and providing potentials to recollect Cr resource. The influent (10 mg/L Cr(VI)) with near neutral pHs (6–8) was first oxidized by the anode with H+ ions generation via H 2 O oxidation, leading to the anode-treated effluent turned into strong acidic with pH below 3.5. Subsequently, under acidic condition, the Cr(VI) species were prone to reduce to Cr(III) on the cathode. The multi-cathode FESs (1A + n C) equipped with one counter anode (1A) and multiple cathodes (n C) were constructed to enhance the Cr(VI) reduction by providing more cathode reactive sites and in-situ Cr(III) precipitation by maintaining near neutral effluent pHs. The flow-through flux and applied voltage were optimized to be 500 L/h/m2 and 2.6 V, under which Cr species were undetectable in effluent of 1A + 4C FES within continuous operation time of 30 min. Regenerating the Cr(OH) 3 -passivated CFF electrodes and recollecting the Cr waste resource were easily accomplished by using a small volume of acidic solution with reversed applied voltage. This study suggested that carbon fiber-based FES with a sequential oxidation-reduction process can be a feasible approach for remediation and recovery of Cr(VI) contamination. [ABSTRACT FROM AUTHOR]

As the release of silver nanoparticles (AgNPs) in the environment continues to increase, great concerns have been raised about their potential toxicity to humans. It is urgent to assess the possible toxicity of AgNPs to the immune cells of the central nervous system due to the continuous accumulation of AgNPs in the brain. This study aimed to evaluate the neurotoxicity of AgNPs and the regulatory mechanism of autophagy in AgNPs-induced inflammation by using mouse microglia BV2 cell lines. AgNPs decreased the microglia cell activity in a concentration and time-dependent manner. The exposure of BV2 cells to AgNPs at a non-cytotoxic level of 5 μg/mL resulted in increase of pro-inflammatory cytokines and decrease of mRNA expression of anti-inflammatory cytokines. AgNPs exposure increased M1 markers of iNOS expression and decreased the expression of M2 markers of CD206 in a time-dependent manner. Meanwhile, the expression of inflammatory proteins IL-1β and NF-κB increased significantly. Additionally, AgNPs induced an increase in autophagosome and upregulation of LC3II, Beclin1, and p62 expression levels. Pretreatment by an autophagy inhibitor, 3-Methyladenine, caused more AgNPs-treated microglia to polarized into pro-inflammatory phenotypes. Inhibition of autophagy also increased the expression of inflammation-associated mRNA and proteins in BV2 cells. These results indicated that AgNPs could induce pro-inflammatory phenotypic polarization of microglia and the autophagy could play a key regulatory role in the pro-inflammatory phenotypic polarization of microglia induced by AgNPs. [Display omitted] [ABSTRACT FROM AUTHOR]

In this study, a metabolomic analysis was used to reveal the neurotoxicity of the CdTe/ZnS QDs via microglia polarization. A gas chromatography-mass spectrometer (GC-MS) was applied to uncover the metabonomic changes in microglia (BV-2 cell line) after exposure to 1.25 μM CdTe/ZnS QDs. 11 annotated metabolic pathways (KEGG database) were significantly changed in all exposed groups (3 h, 6 h, 12 h), 3 of them were related to glucose metabolism. The results of the Seahorse XFe96 Analyzer indicated that the CdTe/ZnS QDs increased the glycolysis level of microglia by 86% and inhibited the aerobic respiration level by 54% in a non-hypoxic environment. In vivo study, 3 h after the injection of CdTe/ZnS QDs (2.5 mM) through the tail vein in mice, the concentration of the CdTe/ZnS QDs in hippocampus reached the peak (1.25 μM). The polarization level of microglia (Iba-1 immunofluorescence) increased 2.7 times. In vitro study, the levels of the extracellular TNF-α, IL-1β and NO of BV-2 cells were all increased significantly after a 6 h or 12 h exposure. According to the results of the Cell Counting Kit-8, after a 6 h or 12 h exposure to the CdTe/ZnS QDs, the exposed microglia could significantly decrease the number of neurons (HT-22 cell line). This study proved that CdTe/ZnS QDs could polarize microglia in the brain and cause secondary inflammatory damage to neurons. There are potential risks in the application of the CdTe/ZnS QDs in brain tissue imaging. Image 1 • CdTe/ZnS QDs could enter into the mouse brain through tail vein injection. • CdTe/ZnS QDs could inhibit aerobic respiration in microglia after exposure. • We first found that CdTe/ZnS QDs could polarize the microglia. • CdTe/ZnS QDs could induce inflammatory damage to the neurons. • The inflammatory damage is dependent on the cytotoxicity of the CdTe/ZnS QDs. [ABSTRACT FROM AUTHOR]