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• The types and challenges of PVC waste management are discussed. • Dehydrochlorination and dechlorination of PVC are reviewed. • Recent progress in the chemical recycling technologies of PVC is summarized. • The dechlorination principles of different technologies are explained. • Chemical recycling treatments of PVC-containing plastic waste are summarized. The extensive production and consumption of plastics has resulted in significant plastic waste and plastic pollution. Polyvinyl chloride (PVC) waste has a high chlorine content and is the primary source of chlorine in the plastic waste stream, potentially generating hazardous chlorinated organic pollutants if treated improperly. This review discusses PVC synthesis, applications, and the current types and challenges of PVC waste management. Dechlorination is vital for the chemical recycling of PVC waste and PVC-containing plastic waste. We review dehydrochlorination and dechlorination mechanisms of PVC using thermal degradation and wet treatments, and summarize the recent progress in chemical treatments and dechlorination principles. This review provides readers with a comprehensive analysis of chemical recycling technologies for PVC waste and PVC-containing plastic waste to transform them into chemicals, fuels, feedstock, and value-added polymers. [ABSTRACT FROM AUTHOR]

This article investigates the problem of adaptive event‐triggered resilient stabilization for nonlinear semi‐Markov jump systems with DoS attacks. In this article, both DoS attacks and event‐triggered transmission strategy (ETTS) are considered. The DoS attacks may disturb the event‐triggered strategy, which implies that the original inequality condition of ETTS will no longer be satisfied. Different from the traditional ETTS, the adaptive ETTS is designed to reduce bandwidth usage. Based on the adaptive ETTS and resilient controller, the sufficient condition for stochastic stability of the closed‐loop system is proposed. Then, the calculation method of controller and observer parameters is given in the form of linear matrix inequality. Finally, the proposed adaptive event‐triggered resilient controller is applied to a single‐link robot arm model, which can show effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

[Display omitted] • H 2 production of seaweed hydrolysate was studied with C. tyrobutyricum. • Acetate assimilation significantly promotes mannitol digestion and H 2 evolution. • Mannitol generates more reducing power for hydrogen evolution pathway. • Mannitol evolves 42.02% higher H 2 and 40.82% higher butyrate than glucose. • High H 2 yield (2.33 mol/mol) and energy recovery (41.20 %) were obtained from seaweed. In this study, mannitol and mannitol-rich seaweed were fermented to investigate the relationship between substrate reduction degree and hydrogen production performance. The results showed that acetate was required in mannitol fermentation with an optimum acetate/mannitol mass ratio of 1:5. Hydrogen production and yield of mannitol fermentation reached 123.76 mL and 2.12 mol/mol-mannitol, respectively, 42.02 % and 26.95 % higher than that of glucose, respectively. The acetate was fully assimilated and the butyrate selectivity reached 100 % in the effluent. Redox potential and electron distribution showed that mannitol increased the overall electron input from mannitol and acetate, leading to the increase in hydrogen and butyrate generation. Hydrogen yield reached 2.33 mol/mol-mannitol with brown algae hydrolysate, which was the highest ever reported. This study demonstrated that substrate with a higher reduction degree could yield higher hydrogen and showed the great application potential of brown algae fermentation for the co-production of hydrogen and butyrate. [ABSTRACT FROM AUTHOR]

Effective detection of pollutant gases is vital for protection of natural environment and human health. There is an increasing demand for sensing devices that are equipped with high sensitivity, fast response/recovery speed, and remarkable selectivity. Particularly, attention is given to the designability of sensing materials with porous structures. Among diverse kinds of porous materials, metal-organic frameworks (MOFs) exhibit high porosity, high degree of crystallinity and exceptional chemical activity. Their strong host-guest interactions with guest molecules facilitate the application of MOFs in adsorption, catalysis and sensing systems. In particular, the tailorable framework/composition and potential for post-synthetic modification of MOFs endow them with widely promising application in gas sensing devices. In this review, we outlined the fundamental aspects and applications of MOFs for gas sensors, and discussed various techniques of monitoring gases based on MOFs as functional materials. Insights and perspectives for further challenges faced by MOFs are discussed in the end. [Display omitted] • The classifications and functions of MOFs in gas monitoring are provided. • This review emphasizes the techniques of MOFs for monitoring gas interactions. • Roles of MOFs in gas sensors are classified into three items. [ABSTRACT FROM AUTHOR]

B-cell acute lymphoblastic leukemia (B-ALL) is the most prevalent malignant tumor affecting children. While the majority of B-ALL patients (90%) experience successful recovery, early relapse cases of B-ALL continue to exhibit high mortality rates. MZ1, a novel inhibitor of Bromodomains and extra-terminal (BET) proteins, has demonstrated potent antitumor activity against hematological malignancies. The objective of this study was to examine the role and therapeutic potential of MZ1 in the treatment of B-ALL. In order to ascertain the fundamental mechanism of MZ1, a sequence of in vitro assays was conducted on B-ALL cell lines, encompassing Cell Counting Kit 8 (CCK8) assay, Propidium iodide (PI) staining, and Annexin V/PI staining. Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to examine protein and mRNA expression levels. Transcriptomic RNA sequencing (RNA-seq) was utilized to screen the target genes of MZ1, and lentiviral transfection was employed to establish stably-expressing/knockdown cell lines. MZ1 has been observed to induce the degradation of Bromodomain Containing 4 (BRD4), Bromodomain Containing 3 (BRD3), and Bromodomain Containing 2 (BRD2) in B-ALL cell strains, leading to inhibited cell growth and induction of cell apoptosis and cycle arrest in vitro. These findings suggest that MZ1 exhibits cytotoxic effects on two distinct molecular subtypes of B-ALL, namely 697 (TCF3/PBX1) and RS4;11 (MLL-AF4) B-ALL cell lines. Additionally, RNA-sequencing analysis revealed that MZ1 significantly downregulated the expression of Cyclin D3 (CCND3) gene in B-ALL cell lines, which in turn promoted cell apoptosis, blocked cell cycle, and caused cell proliferation inhibition. Our results suggest that MZ1 has potential anti-B-ALL effects and might be a novel therapeutic target. [ABSTRACT FROM AUTHOR]

Background. Arising from T progenitor cells, T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignant tumor, accounting for 15% of childhood ALL and 25% of adult ALL. Composing of putative enhancers in close genomic proximity, super enhancer (SE) is critical for cell identity and the pathogenesis of multiple cancers. Belonging to the cytosolute linker protein group, FYB1 is essential for TCR signaling and extensively studied in terms of tumor pathogenesis and metastasis. Dissecting the role of FYN binding protein 1 (FYB1) in T-ALL holds the potential to improve the treatment outcome and prognosis of T-ALL. Methods. In this study, SEs were explored using public H3K27ac ChIP-seq data derived from T-ALL cell lines, AML cell lines and hematopoietic stem and progenitor cells (HSPCs). Downstream target of FYB1 gene was identified by RNA-seq. Effects of shRNA-mediated downregulation of FYB1 and immunoglobulin lambda-like polypeptide 1 (IGLL1) on self-renewal of T-ALL cells were evaluated in vitro and/or in vivo. Results. As an SE-driven gene, overexpression of FYB1 was observed in T-ALL, according to the Cancer Cell Line Encyclopedia database. In vitro, knocking down FYB1 led to comprised growth and enhanced apoptosis of T-ALL cells. In vivo, downregulation of FYB1 significantly decreased the disease burden by suppressing tumor growth and improved survival rate. Knocking down FYB1 resulted in significantly decreased expression of IGLL1 that was also an SE-driven gene in T-ALL. As a downstream target of FYB1, IGLL1 exerted similar role as FYB1 in inhibiting growth of T-ALL cells. Conclusion. Our results suggested that FYB1 gene played important role in regulating self-renewal of T-ALL cells by activating IGLL1, representing a promising therapeutic target for T-ALL patients. [ABSTRACT FROM AUTHOR]

Background: AML (acute myeloid leukemia) is a common hematological malignancy in children with poor treatment effects and poor prognosis. Recent studies have shown that as a novel BRD4 (bromodomain containing 4) PROTACs (proteolysis targeting chimeras) degrader, GNE-987 can slow down the growth of various tumors and increase apoptosis, with promising clinical prospects. However, the function and molecular mechanism of GNE-987 in AML remain unclear. This study is aimed at investigating the therapeutic effect of GNE-987 on AML and its underlying mechanism.Methods: The association between BRD4 and AML was assessed by studying public databases. After GNE-987 was added to AML cells, cell proliferation slowed down, the cycle was disturbed, and apoptosis increased. Western blotting was used to detect BRD2 (bromodomain containing 2), BRD3 (bromodomain containing 3), BRD4, and PARP (poly ADP-ribose polymerase) proteins. The effect of GNE-987 on AML cells was analyzed in vivo. RNA-seq (RNA sequencing) and ChIP-seq (chromatin immunoprecipitation sequencing) validated the function and molecular pathways of GNE-987 in processing AML.Results: BRD4 expression was significantly elevated in pediatric AML samples compared with healthy donors. GNE-987 inhibited AML cell proliferation by inhibiting the cell cycle and inducing apoptosis. BRD2, BRD3, and BRD4 were consistent with decreased VHL (Von Hippel Lindau) expression in AML cells. In an AML xenograft model, GNE-987 significantly reduced the hepatosplenic infiltration of leukemia cells and increased the mouse survival time. Based on analysis of RNA-seq and ChIP-seq analyses, GNE-987 could target multiple SE- (super-enhancer-) related genes, including LYL1 (lymphoblastic leukemia 1), to inhibit AML.Conclusions: GNE-987 had strong antitumor activity in AML. GNE-987 could effectively inhibit the expression of SE-related oncogenes including LYL1 in AML. Our results suggested that GNE-987 had broad prospects in the treatment of AML. [ABSTRACT FROM AUTHOR]

Acute myeloid leukemia (AML) is a highly cancerous and aggressive hematologic disease with elevated levels of drug resistance and relapse resulting in high mortality. Recently, bromodomains and extra-terminal (BET) protein inhibitors have been extensively researched in hematological tumors as potential anticancer agents. MZ1 is a novel BET inhibitor that mediates selective proteins degradation and suppression of tumor growth through proteolysis-targeting chimeras (PROTAC) technology. Accordingly, this study aimed to investigate the role and therapeutic potential of MZ1 in AML. In this study, we first identified that AML patients with high BRD4 expression had poor overall survival than those with low expression group. MZ1 inhibited AML cell growth and induced apoptosis and cycle arrest in vitro. MZ1 induced degradation of BRD4, BRD3 and BRD2 in AML cell strains. Additionally, MZ1 also initiated the cleavage of poly-ADP-ribose polymerase (PARP), which showed cytotoxic effects on NB4 (PML-RARa), K562 (BCR-ABL), Kasumi-1 (AML1-ETO), and MV4-11 (MLL-AF4) cell lines representing different molecular subtypes of AML. In AML mouse leukemia model, MZ1 significantly decreased leukemia cell growth and increased the mouse survival time. According to the RNA-sequencing analysis, MZ1 led to c-Myc and ANP32B genes significant downregulation in AML cell lines. Knockdown of ANP32B promoted AML cell apoptosis and inhibited cell growth. Overall, our data indicated that MZ1 had broad anti-cancer effects on AML cell lines with different molecular lesions, which might be exploited as a novel therapeutic strategy for AML patients. [ABSTRACT FROM AUTHOR]

Conscious perception is greatly diminished during sleep, but the underlying circuit mechanism is poorly understood. We show that cortical ignition—a brain process shown to be associated with conscious awareness in humans and non-human primates—is strongly suppressed during non-rapid-eye-movement (NREM) sleep in mice due to reduced cholinergic modulation and rapid inhibition of cortical responses. Brain-wide functional ultrasound imaging and cell-type-specific calcium imaging combined with optogenetics showed that activity propagation from visual to frontal cortex is markedly reduced during NREM sleep due to strong inhibition of frontal pyramidal neurons. Chemogenetic activation and inactivation of basal forebrain cholinergic neurons powerfully increased and decreased visual-to-frontal activity propagation, respectively. Furthermore, although multiple subtypes of dendrite-targeting GABAergic interneurons in the frontal cortex are more active during wakefulness, soma-targeting parvalbumin-expressing interneurons are more active during sleep. Chemogenetic manipulation of parvalbumin interneurons showed that sleep/wake-dependent cortical ignition is strongly modulated by perisomatic inhibition of pyramidal neurons. [Display omitted] • Visual-to-frontal cortex activity propagation is strongly reduced during NREM sleep • Responses of frontal pyramidal neurons are strongly inhibited during NREM sleep • Basal forebrain cholinergic neurons powerfully modulate frontal cortical ignition • Increased perisomatic inhibition during NREM sleep suppresses cortical ignition Investigation into the circuit mechanisms that diminish awareness during sleep shows that frontal cortical ignition is suppressed during NREM sleep due to reduced cholinergic modulation and a shift from dendritic to perisomatic inhibition of frontal cortical pyramidal neurons. [ABSTRACT FROM AUTHOR]

Most animals require sleep, and sleep loss induces serious pathophysiological consequences, including death. Previous experimental approaches for investigating sleep impacts in mice have been unable to persistently deprive animals of both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS). Here, we report a "curling prevention by water" paradigm wherein mice remain awake 96% of the time. After 4 days of exposure, mice exhibit severe inflammation, and approximately 80% die. Sleep deprivation increases levels of prostaglandin D 2 (PGD 2) in the brain, and we found that elevated PGD 2 efflux across the blood-brain-barrier—mediated by ATP-binding cassette subfamily C4 transporter—induces both accumulation of circulating neutrophils and a cytokine-storm-like syndrome. Experimental disruption of the PGD 2 /DP1 axis dramatically reduced sleep-deprivation-induced inflammation. Thus, our study reveals that sleep-related changes in PGD 2 in the central nervous system drive profound pathological consequences in the peripheral immune system. [Display omitted] • A highly efficient paradigm is introduced for depriving mice of sleep • PGD 2 efflux across the BBB is enhanced by sleep deprivation • Sleep deprivation triggers increases in both cytokines and circulating neutrophils • The sleep-deprived brain affects the peripheral immune system via the PGD 2 /DP1 axis Enhanced efflux of PGD 2 across the BBB during prolonged sleep deprivation induces a cytokine-storm-like syndrome via the PGD 2 /DP1 axis. Sleep deprivation in mice that involves disruption of REMS and NREMS leads to lethality due to brain prostaglandin D 2 -mediated cytokine-storm-like systemic inflammation. [ABSTRACT FROM AUTHOR]