Multi-Active Sites Loaded NiCu-MOF@MWCNTs as a Bifunctional Electrocatalyst for Electrochemical Water Splitting Reaction.

Water can be sustainably and ecologically converted by electrocatalysts into hydrogen and oxygen, which, in turn, can be converted into energy. However, the advancement of using water as green energy is hampered by limitations in the study of high-performance catalysts. The purpose of this study was to construct an electrocatalyst by anchoring well-dispersed multiwalled carbon nanotubes (MWCNTs) on nickel-copper (NiCu-MOF) nanoblocks through a simple solvothermal method. The synthesis of NiCu-MOF@MWCNTs demonstrated exceptional electrocatalytic performance for the hydrogen evolution reaction (HER) and oxygen evolution reaction (OER) in an alkaline medium. At 10 mA cm-2 in 1.0 M KOH, the OER and HER performance of the catalyst displays a relatively low overpotential, with only 220 and 78 mV, respectively. Furthermore, the catalytic activity remained unchanged for 24 h in 1.0 M KOH. This performance was superior to the majority of electrocatalysts that have been reported. This was achieved by utilizing the strong synergy that exists between MWCNTs and bimetallic (Ni-Cu) nano blocks present in the metal-organic framework. The enhanced electrocatalytic activity of the nanocomposite can be attributed to the synergistic impact caused by its various components.

'M' mechanics for midline diastema correction in mixed dentition.

Maxillary midline diastema is a self-correcting anomaly which in few conditions may get retained in adolescence stage due to various aetiological factors and correction of which is usually done at permanent dentition stage. The persistence of midline diastema can be predicted in mixed dentition period and necessary management could be provided at the mixed dentition period. This case report is on a novel technique using 'M' spring to correct the midline diastema in mixed dentition period.

Rational design of α-MnO2/HT-GCN nanocomposite for effective photocatalytic degradation of ciprofloxacin and pernicious activity.

The present study is mainly concerned with the development of cost-efficient composite material utilized to produce one-dimensional manganese oxide (α-MnO2) nanoparticles coated on two-dimensional graphitic carbon nitrides (HT-GCN) as nanocomposite (α-MnO2/HT-GCN) for highly efficient CIP degradation. The α-MnO2 nanoparticles (NPs) were prepared by a simple hydrothermal technique before being decorated on HT-GCN (H denotes protonation and T represents thermal-decomposition-graphitic carbon nitride). Tauc plots were used to calculate the band gap values of the photocatalysts α-MnO2 (1.74 eV), GCN (2.84 eV), HT-GCN (2.63 eV), and α-MnO2/HT-GCN (2.31 eV). The mechanism was investigated by various scavengers, particularly isopropanol (•OH) makes a significant role in the photodegradation process. The degradation percentage for ciprofloxacin was 89.2% and the rate of reaction R2 = 0.9913. This study demonstrates a unique method for developing a heterojunction-based nanocomposite of α-MnO2/HT-GCN, which exhibit better light absorption performance.

Anti-inflammatory and memory-enhancing properties of Chinese herbal extracts: The possible application in Alzheimer's disease.

Alzheimer's disease (AD) is a progressive brain disease that causes cognitive impairment in seniors. The beta-amyloid (Aß) deposition and intracellular neurofibrillary tangles are two pathological hallmarks of AD. The increase of AD hallmarks causes inflammatory response enhancement, reduction of synaptic plasticity, and impaired cognition. The percentage of the aging population is growing along with the number of AD patients; however, effective treatment of AD is still limited. Therefore, developing preventive and therapeutic drugs for AD with fewer adverse side effects is urgently needed. The crude extracts from herbs such as Centella asiatica, Dendrobium catenatum, Litsea cubeba, Nardostachys jatamansi, Convolvulus pluricaulis, Melissa officinalis, Magnolia officinalis, Withania somnifera, and Nigella sativa improved memory performance and reduced inflammation response in various diseases. In addition, herbal blends usually have minimum aversive effects and can be mixed into diet and served as nutritional supplements. Hence, it is promising to develop Chinese herbal extracts to prevent or treat early AD. This review article highlights the currently available treatments of AD and the therapeutic effects of a group of crude extracts from Chinese herbs that can prevent cognitive decline and reduce the excessive inflammatory response. The possible clinical use of these Chinese herbal extracts in AD is also discussed.

Attenuation of HECT-E3 ligase expression rescued memory deficits in 3xTg-AD mice.

Alzheimer's disease (AD) is one of the most common progressive neurodegenerative disorders that cause deterioration of cognitive functions. Recent studies suggested that the accumulation of inflammatory molecules and impaired protein degradation mechanisms might both play a critical role in the progression of AD. Autophagy is a major protein degradation pathway that can be controlled by several HECT-E3 ligases, which then regulates the expression of inflammatory molecules. E3 ubiquitin ligases are known to be upregulated in several neurodegenerative diseases. Here, we studied the expressional change of HECT-E3 ligase using M01 on autophagy and inflammasome pathways in the context of AD pathogenesis. Our results demonstrated that the M01 treatment reversed the working memory deficits in 3xTg-AD mice when examined with the T-maze and reversal learning with the Morris water maze. Additionally, the electrophysiology recordings indicated that M01 treatment enhanced the long-term potentiation in the hippocampus of 3xTg-AD mice. Together with the improved memory performance, the expression levels of the NLRP3 inflammasome protein were decreased. On the other hand, autophagy-related molecules were increased in the hippocampus of 3xTg-AD mice. Furthermore, the protein docking analysis indicated that the binding affinity of M01 to the WWP1 and NEDD4 E3 ligases was the highest among the HECT family members. The western blot analysis also confirmed the decreased expression level of NEDD4 protein in the M01-treated 3xTg-AD mice. Overall, our results demonstrate that the modulation of HECT-E3 ligase expression level can be used as a strategy to treat early memory deficits in AD by decreasing NLRP3 inflammasome molecules and increasing the autophagy pathway.

Behavioral and Synaptic Phenotypes of Female Prdx6-/- Mice.

Peroxiredoxin 6 (PRDX6) is expressed throughout the brain, including the hippocampus, where it plays a potential role in synaptic regulation and forming emotional and spatial memories. PRDX6 is predominantly detected in the female mouse's hippocampus; thus, we investigate the effect of the Prdx6 gene on behavioral phenotypes and synaptic functions using female Prdx6 knockout (Prdx6-/-) mice. Our results demonstrate that female Prdx6-/- mice exhibited anxiety-like behavior, enhanced contextual fear memory, and impaired spatial memory. We also found increased, paired-pulse facilitation ratios, and decreased long-term potentiation (LTP) in the hippocampal region of these female Prdx6-/- mice. The present study helps to understand better the PRDX6's role in emotional response and spatial memory formation in female mice.

Age and gender differences for the behavioral phenotypes of 3xTg alzheimer's disease mice.

The triple transgenic Alzheimer's disease (3xTg-AD) strain is a common mouse model used for studying the pathology and mechanism of Alzheimer's disease (AD). The 3xTg-AD strain exhibits two hallmarks of AD, amyloid beta (Aß) and neurofibrillary tangles. Several studies using different gender and age of 3xTg-AD mice to investigate their behavior phenotypes under the influence of various treatments have reported mixed results. Therefore, a comprehensive investigation on the optimal gender, age, and training paradigms used for behavioral studies of 3xTg-AD is necessary. In the present study, we investigated the behavioral phenotypes for the two genders of 3xTg-AD mice at 3, 6, 9, and 12 months old and compared the results with age-, gender-matched C57BL/6N control strain. All mice were subjected to tail flick, pinprick, open field, elevated plus maze, passive avoidance, and trace fear conditioning (TFC) tests to evaluate their sensory, locomotor, anxiety, and learning/memory functions. The results showed that TFC on male 3xTg-AD mice is optimal for studying the memory performance in AD. The sensory and locomotor functions of 3xTg-AD mice for two genders appear to be normal before 6 months, decline in fear memory afterwards. The differences between control and 3xTg-AD male mice in contextual and cued memory are robust, thus they are ideal for evaluating the effect of a treatment. Since it is costly and time consuming to obtain wildtype littermates as controls, C57BL/6N strain is suggested to be used as control mice because their baseline performance of sensorimotor functions are similar to that of 3xTg-AD mice.

The 4-(Phenylsulfanyl) butan-2-one Improves Impaired Fear Memory Retrieval and Reduces Excessive Inflammatory Response in Triple Transgenic Alzheimer's Disease Mice.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by an excessive inflammatory response and impaired memory retrieval, including spatial memory, recognition memory, and emotional memory. Acquisition and retrieval of fear memory help one avoid dangers and natural threats. Thus, it is crucial for survival. AD patients with impaired retrieval of fear memory are vulnerable to dangerous conditions. Excessive expression of inflammatory markers is known to impede synaptic transmission and reduce the efficiency of memory retrieval. In wild-type mice, reducing inflammation response can improve fear memory retrieval; however, this effect of this approach is not yet investigated in 3xTg-AD model mice. To date, no satisfactory drug or treatment can attenuate the symptoms of AD despite numerous efforts. In the past few years, the direction of therapeutic drug development for AD has been shifted to natural compounds with anti-inflammatory effect. In the present study, we demonstrate that the compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) is effective in enhancing fear memory retrieval of wild-type and 3xTg-AD mice by reducing the expression of TNF-α, COX-2, and iNOS. We also found that 4-PSB-2 helps increase dendritic spine density, postsynaptic density protein-95 (PSD-95) expression, and long-term potentiation (LTP) in the hippocampus of 3xTg-AD mice. Our study indicates that 4-PSB-2 may be developed as a promising therapeutic compound for treating fear memory impairment of AD patients.

Enhanced contextual fear memory in peroxiredoxin 6 knockout mice is associated with hyperactivation of MAPK signaling pathway.

Fear dysregulation is one of the symptoms found in post-traumatic stress disorder (PTSD) patients. The functional abnormality of the hippocampus is known to be implicated in the development of such pathology. Peroxiredoxin 6 (PRDX6) belongs to the peroxiredoxin family. This antioxidant enzyme is expressed throughout the brain, including the hippocampus. Recent evidence reveals that PRDX6 plays an important role in redox regulation and the modulation of several signaling molecules involved in fear regulation. Thus, we hypothesized that PRDX6 plays a role in the regulation of fear memory. We subjected a systemic Prdx6 knockout (Prdx6-/-) mice to trace fear conditioning and observed enhanced fear response after training. Intraventricular injection of lentivirus-carried mouse Prdx6 into the 3rd ventricle reduced the enhanced fear response in these knockout mice. Proteomic analysis followed by validation of western blot analysis revealed that several proteins in the MAPK pathway, such as NTRK2, AKT, and phospho-ERK1/2, cPLA2 were significantly upregulated in the hippocampus of Prdx6-/- mice during the retrieval stage of contextual fear memory. The distribution of PRDX6 found in the astrocytes was also observed throughout the hippocampus. This study identifies PRDX6 as a participant in the regulation of fear response. It suggests that PRDX6 and related molecules may have important implications for understanding fear-dysregulation associated disorders like PTSD.

Modulation of microglia activation and Alzheimer's disease: CX3 chemokine ligand 1/CX3CR and P2X7R signaling.

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive deficits. Two hallmarks of AD that cause chronic inflammation and lead to neuronal dysfunction and damage are tau tangles and amyloid plaques. Microglial cells, the primary immune cells of the central nervous system, maintain a homeostatic active/inactive state via a bidirectional, dynamic communication with neurons. Several studies have revealed that dysregulated microglial activation leads to AD pathology. Therefore, we reviewed the relationship between AD and two important signaling complexes, CX3 chemokine ligand 1 (CX3CL1)/CX3CR1 and ATP/P2X7R, that play critical roles in the regulation of microglial activation. CX3CL1/CX3CR1 is one important signaling which controls the microglia function. Altering this pathway can have opposite effects on amyloid and tau pathology in AD. Another important molecule is P2X7R which involves in the activation of microglia. Over activation of P2X7R is evident in AD pathogenesis. In this review, we discuss influence of the two signaling pathways at different stages of AD pathology as well as the drug candidates that can modulate CX3CL1/CX3CR1 and ATP/P2X7R.