Simultaneous regeneration of activated carbon and removal of adsorbed atrazine by ozonation process: From laboratory scale to pilot studies.

A novel treatment technique by coupling granular activated carbon (GAC) adsorption and ozone regeneration was constructed for long-lasting water decontamination. The GAC adsorption showed high performance for atrazine (ATZ) removal (99.9 %), and the ozone regeneration ensured the recyclability of GAC for water purification. The regeneration process was evaluated via several paths to assist the efficient adsorption process. Employing ozone micro-nano bubbles (O3-MNBs) for regenerating GAC showed superior performance compared to traditional ozone. Meantime, inhibiting the formation of bromate (BrO3-). ATZ adsorption process suffered from the pore-filling, hydrogen bonding effect and π-π EDA interaction. The surface phenolic hydroxyl group, carboxyl group and pyridine nitrogen benefitted the triggering of ozone to generate reactive oxygen species, and regenerate the GAC surface. The superior performance of the adsorption and regeneration process was verified via a long-term running by a pilot study. It significantly improved the removal of organic micropollutants, UV254 and permanganate index. Additionally, the intermittent O3-MNBs regeneration process resulted in efficient decontamination within the pores structure of GAC, which also effectively preserved the pore structure from destruction. For actual application, the cost of water production can be saved around 0.63 kWh m-3. This work proposed new ideas and theoretical support for economic water production.

Serum DJ-1 Is a Biomarker of Colorectal Cancer and DJ-1 Activates Mitophagy to Promote Colorectal Cancer Progression.

Colorectal cancer is the second most common cancer and the third cancer-associated death in Taiwan. Currently used serum markers for detecting colorectal cancer lack excellent diagnostic accuracy, which results in colorectal cancer being often recognized too late for successful therapy. Mitophagy is the selective autophagic degradation of damaged or excessive mitochondria. DJ-1 is an antioxidant protein that attenuates oxidative stress and maintains mitochondrial quality through activating mitophagy. Mitophagy activation contributes to anti-cancer drug resistance. However, the role of DJ-1-induced mitophagy in colorectal cancer progression remains unclear. In the present study, we collected matched tumor and adjacent normal tissues and serum from patients and cancer cells to demonstrate the clinical value and physiological function of DJ-1 in colorectal cancer. We found that DJ-1 increased in tumor tissues and serum; it was positively correlated with TNM (tumor-node-metastasis) stages of colorectal cancer patients. Through stable knockdown DJ-1 expression in metastatic colorectal adenocarcinoma cells SW620, DJ-1 knockdown inhibited cancer cell survival, migration, and colony formation. In SW620 cells, DJ-1 knockdown induced an incomplete autophagic response that did not affect ATP production; DJ-1 knockdown enhanced intracellular reactive oxygen species generation and damaged mitochondrial accumulation and mitophagy inhibition. It suggests that DJ-1 knockdown inhibits mitophagy that causes metastatic colorectal adenocarcinoma cells to be unable to remove damaged mitochondria and further enhance cancer cell apoptosis. Our data indicate that DJ-1 might be clinically valuable as serum and tissue biomarkers for predicting the TNM stage in colorectal cancer patients. Since DJ-1-induced mitophagy promotes tumor progression, DJ-1 inhibition is a potential therapeutic strategy for colorectal cancer treatment.

Electroacupuncture Improves Motor Symptoms of Parkinson's Disease and Promotes Neuronal Autophagy Activity in Mouse Brain.

Autophagic defects are a hallmark of neurodegenerative disorders, such as Parkinson's disorder (PD). Enhancing autophagy to remove impaired mitochondria and toxic protein aggregation is an essential component of PD treatment. In particular, activation of autophagy confers neuroprotection in cellular and preclinical models of neurodegenerative diseases. In this study, we investigated the therapeutic mechanisms of electroacupuncture (EA) treatment in mice with established PD and evaluated the relationship between EA, autophagy, and different neurons in the mouse brain. We report that EA improves PD motor symptoms in mice and enhances (1) autophagy initiation (increased Beclin 1), (2) autophagosome biogenesis (increased Atg5, Atg7, Atg9A, Atg12, Atg16L, Atg3, and LC3-II), (3) autophagy flux/substrate degradation (decreased p62), and (4) mitophagy (increased PINK1 and DJ-1) in neurons of the substantia nigra, striatum, hippocampus, and cortex (affected brain areas of PD, Huntington disease, and Alzheimer's disease). EA enhances autophagy initiation, autophagosome biogenesis, mitophagy, and autophagy flux/substrate degradation in certain brain areas. Our findings are the first to show that EA regulates neuronal autophagy and suggest that this convenient, inexpensive treatment has exciting therapeutic potential in neurodegenerative disorders.

Electrochemically Stable Cobalt⁻Zinc Mixed Oxide/Hydroxide Hierarchical Porous Film Electrode for High-Performance Asymmetric Supercapacitor.

Construction of electrochemically stable positive materials is still a key challenge to accomplish high rate performance and long cycling life of asymmetric supercapacitors (ASCs). Herein, a novel cobalt⁻zinc mixed oxide/hydroxide (CoZn-MOH) hierarchical porous film electrode was facilely fabricated based on a cobalt⁻zinc-based metal⁻organic framework for excellent utilization in ASC. The as-constructed hierarchical porous film supported on conductive Ni foam possesses a rough surface and abundant macropores and mesopores, which allow fast electron transport, better exposure of electrochemically active sites, and facile electrolyte access and ion diffusion. Owing to these structural merits in collaboration, the CoZn-MOH electrode prepared with a zinc feeding ratio up to 45% at 110 min of heating time (CoZn-MOH-45-110) exhibited a high specific capacitance of 380.4 F·g-1, remarkable rate capability (83.6% retention after 20-fold current increase), and outstanding cycling performances (96.5% retention after 10,000 cycles), which exceed the performances of similar active electrodes. Moreover, an ASC based on this CoZn-MOH-45-110 electrode exhibited a high specific capacitance of 158.8 F·g-1, an impressive energy density of 45.8 Wh·kg-1, superior rate capability (83.1% retention after 50-fold current increase), and satisfactory cycling stability (87.9% capacitance retention after 12,000 cycles).

Celastrol Inhibits Dopaminergic Neuronal Death of Parkinson's Disease through Activating Mitophagy.

Parkinson's disease (PD) is a neurodegenerative disease, which is associated with mitochondrial dysfunction and abnormal protein accumulation. No treatment can stop or slow PD. Autophagy inhibits neuronal death by removing damaged mitochondria and abnormal protein aggregations. Celastrol is a triterpene with antioxidant and anti-inflammatory effects. Up until now, no reports have shown that celastrol improves PD motor symptoms. In this study, we used PD cell and mouse models to evaluate the therapeutic efficacy and mechanism of celastrol. In the substantia nigra, we found lower levels of autophagic activity in patients with sporadic PD as compared to healthy controls. In neurons, celastrol enhances autophagy, autophagosome biogenesis (Beclin 1↑, Ambra1↑, Vps34↑, Atg7↑, Atg12↑, and LC3-II↑), and mitophagy (PINK1↑, DJ-1↑, and LRRK2↓), and these might be associated with MPAK signaling pathways. In the PD cell model, celastrol reduces MPP+-induced dopaminergic neuronal death, mitochondrial membrane depolarization, and ATP reduction. In the PD mouse model, celastrol suppresses motor symptoms and neurodegeneration in the substantia nigra and striatum and enhances mitophagy (PINK1↑ and DJ-1↑) in the striatum. Using MPP+ to induce mitochondrial damage in neurons, we found celastrol controls mitochondrial quality by sequestering impaired mitochondria into autophagosomes for degradation. This is the first report to show that celastrol exerts neuroprotection in PD by activating mitophagy to degrade impaired mitochondria and further inhibit dopaminergic neuronal apoptosis. Celastrol may help to prevent and treat PD.

Electroacupuncture Promotes Recovery of Motor Function and Reduces Dopaminergic Neuron Degeneration in Rodent Models of Parkinson's Disease.

Parkinson's disease (PD) is a common neurodegenerative disease. The pathological hallmark of PD is a progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta in the brain, ultimately resulting in severe striatal dopamine deficiency and the development of primary motor symptoms (e.g., resting tremor, bradykinesia) in PD. Acupuncture has long been used in traditional Chinese medicine to treat PD for the control of tremor and pain. Accumulating evidence has shown that using electroacupuncture (EA) as a complementary therapy ameliorates motor symptoms of PD. However, the most appropriate timing for EA intervention and its effect on dopamine neuronal protection remain unclear. Thus, this study used the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model (systemic-lesioned by intraperitoneal injection) and the 1-methyl-4-phenylpyridinium (MPP⁺)-lesioned rat model (unilateral-lesioned by intra-SN infusion) of PD, to explore the therapeutic effects and mechanisms of EA at the GB34 (Yanglingquan) and LR3 (Taichong) acupoints. We found that EA increased the latency to fall from the accelerating rotarod and improved striatal dopamine levels in the MPTP studies. In the MPP⁺ studies, EA inhibited apomorphine induced rotational behavior and locomotor activity, and demonstrated neuroprotective effects via the activation of survival pathways of Akt and brain-derived neurotrophic factor (BDNF) in the SN region. In conclusion, we observed that EA treatment reduces motor symptoms of PD and dopaminergic neurodegeneration in rodent models, whether EA is given as a pretreatment or after the initiation of disease symptoms. The results indicate that EA treatment may be an effective therapy for patients with PD.