Optimization of a Low Surface Energy Coating for Enhanced Water Resistance and Condensation Suppression.

This study focuses on formulating a low-surface-energy, water-resistant, and anti-condensation coating utilizing a fluorocarbon and acrylic resins composite (FAC), enhanced by six functional additives: antistatic agents, water-repellent agents, nanofillers, anti-mold and anti-algae agent, leveling agents, and wetting and dispersing agents. An orthogonal experimental design was implemented to systematically investigate the effects of varying concentrations of these additives on the surface tension of the coating. The results show that the optimized combination of fluorocarbon and acrylic resins composite (OFAC)with functional additives significantly reduces the surface tension, thereby improving both water resistance and anti-condensation properties.

Fabrication of a Fluorocarbon Low Surface Energy Coating for Anti-Stain Applications.

In the long-term working state, stains such as dust, oil, and charged particles in the environment are prone to deposit on the surface of the power equipment, which has great security risks. To achieve anti-stain performance, fluorocarbon composite coating with a low surface energy was prepared and studied. In this paper, SiO nanoparticles were used as inorganic fillers and fluorocarbon resin was used as the substrate to form anti-stain coatings.

Design and Synthesis of Low Surface Energy Coating with Functionalized AlO Nanoparticles.

In a high-moisture environment where dust and coastal saltwater are prevalent, the stability of power equipment can be adversely affected. This issue can result in equipment downtime, particularly for transformers, severely disrupting the continuous operation of DC transmission systems. To address this challenge, a superhydrophobic modified fluorosilicone coating was developed, incorporating anti-stain properties.

High level of ANO1 promotes pancreatic cancer growth in concert with oncogenic KRAS.

Background: Anoctamin-1 (ANO1) was identified as an unfavorable prognostic marker in pancreatic cancer. However, the exact implication of ANO1 in pancreatic cancer is still poorly understood. Here we investigated the effect of ANO1 in pancreatic cancer progression under the context of oncogenic KRAS, aiming at finding a new therapeutic target.

Research trend of microbiota-gut-brain axis in Alzheimer's disease based on CiteSpace (2012-2021): A bibliometrics analysis of 608 articles.

Background: Recently, research on the microbiota-gut-brain axis (MGBA) has received increasing attention, and the number of studies related to Alzheimer's disease (AD) has increased rapidly, but there is currently a lack of summary of MGBA in AD.

Objective: To capture research hotspots, grasp the context of disciplinary research, and explore future research development directions.

Methods: In the core dataset of Web of Science, documents are searched according to specific subject words.

Tβ4 ameliorates oxidative damage and apoptosis through ERK/MAPK and 5-HT1A signaling pathway in Aβ insulted SH-SY5Y cells.

Aims: Alzheimer's disease (AD) is the most common progressive neurodegenerative disorder seriously endangering the physical and mental health of the elderly, while no effective treatments and drugs in clinical practice are available. Thymosin β4 (Tβ4) is a multifunctional polypeptide involved in many physiological and pathological processes including AD. This study aims to understand the function and molecular mechanism of Tβ4 in the development of AD.

Inhibited HDAC3 promotes microRNA-376c-3p to suppress malignant phenotypes of gastric cancer cells by reducing WNT2b.

Objective: Our study aims to identify the impact of histone deacetylase 3 (HDAC3) and microRNA-376c-3p (miR-376c-3p) on gastric cancer (GC) by targeting wingless-type MMTV integration site family member 2b (WNT2b).

Methods: Levels of miR-376c-3p, HDAC3 and WNT2b were assessed. GC cells were treated with altered HDAC3 or miR-376c-3p to evaluate their biological functions, and rescue experiment was performed to assess the effect of WNT2b on GC cells.

Thymosin β4 reverses phenotypic polarization of glial cells and cognitive impairment via negative regulation of NF-κB signaling axis in APP/PS1 mice.

Background: Thymosin β4 (Tβ4) is the most abundant member of the β-thymosins and plays an important role in the control of actin polymerization in eukaryotic cells. While its effects in multiple organs and diseases are being widely investigated, the safety profile has been established in animals and humans, currently, little is known about its influence on Alzheimer's disease (AD) and the possible mechanisms. Thus, we aimed to evaluate the effects and mechanisms of Tβ4 on glial polarization and cognitive performance in APP/PS1 transgenic mice.

TREM2 overexpression rescues cognitive deficits in APP/PS1 transgenic mice by reducing neuroinflammation via the JAK/STAT/SOCS signaling pathway.

Overactivated microglia and neuroinflammation are considered to play a crucial role in the progression of Alzheimer's disease (AD). Triggering receptor expressed on myeloid cells-2 (TREM2), a type I transmembrane receptor, expressed uniquely by microglia in the brain, is involved in the neuroinflammatory responses of AD. In this study, to further explore the precise effects of TREM2 on neuroinflammation and the underlying mechanisms in AD, we employed a lentiviral-mediated strategy to overexpress TREM2 in the brain of APPswe/PS1dE9 (APP/PS1) transgenic mice and cultured BV2 cells.

PNU282987 alleviates Aβ-induced anxiety and depressive-like behaviors through upregulation of α7nAChR by ERK-serotonin receptors pathway.

Patients with Alzheimer's disease often undergo anxiety and depression. Our previous studies have shown that α7nAChR protects against Aβ-induced neurotoxicity via downregulation of p38 and JNK MAPKs, but the role of α7nAChR on Aβ-induced anxiety and depressive-like behaviors and the effect of α7nAChR on the regulation of MAPKs pathways remain unknown. To examine the effects of α7nAChR and MAPKs pathways on Aβ-induced anxiety and depression-like behaviors and to explore their relationships between them, elevated plus maze, open field and forced swim tests were performed.

5-HTR alleviates Aβ-induced cognitive decline and neuroinflammation through crosstalk with NF-κB pathway in mice.

The 5-hydroxytryptamine (5-HT) receptor is significant for the regulation of mood and memory. However, the role of 5-HTR in β-Amyloid protein (Aβ)-induced cognitive decline, neuroinflammation and the possible mechanism remains elusive. Thus, we aimed to evaluate the effects of 5-HTR on Aβ-induced learning and memory decline and neuroinflammation in mice.

Modulation of the MAPKs pathways affects Aβ-induced cognitive deficits in Alzheimer's disease via activation of α7nAChR.

Cognitive impairment in Alzheimer's disease (AD) is characterized by being deficient at learning and memory. Aβ oligomers have been shown to impair rodent cognitive function. We previously demonstrated that activation of α7nAChR, inhibition of p38 or JNK could alleviate Aβ-induced memory deficits in Y maze test.

Tanshinone IIA ameliorates cognitive deficits by inhibiting endoplasmic reticulum stress-induced apoptosis in APP/PS1 transgenic mice.

Our previous data indicated that tanshinone IIA (tan IIA) improves learning and memory in a mouse model of Alzheimer's disease (AD) induced by streptozotocin via restoring cholinergic function, attenuating oxidative stress and blocking p38 MAPK signal pathway activation. This study aims to estimate whether tan IIA inhibits endoplasmic reticulum (ER) stress-induced apoptosis to prevent cognitive decline in APP/PS1 transgenic mice. Tan IIA (10 mg/kg and 30 mg/kg) was intraperitoneally administered to the six-month-old APP/PS1 mice for 30 consecutive days.

Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis.

Objective: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).

Results: Highly expressed FOXD2-AS1 was found in glioma. There was more powerful chemotherapeutic resistance of TMZ resistant cell lines than that of the parent cell lines.

Single housing-induced effects on cognitive impairment and depression-like behavior in male and female mice involve neuroplasticity-related signaling.

Single-housed stress elicits a range of social isolation-related behavioral and neurobiological abnormalities. To investigate single housing-induced behavioral changes and sex differences on stress outcomes, we examined single-housed stress-induced learning and memory impairment, depression-like behaviors, neuroplasticity abnormalities and underlying mechanism. The results showed that male and female mice socially isolated for 8 weeks had significantly decreased memory acquisition, as demonstrated in the learning curve of the Morris water maze task.

CDK5 Participates in Amyloid-β Production by Regulating PPARγ Phosphorylation in Primary Rat Hippocampal Neurons.

Cyclin-dependent kinase 5 (CDK5) in adipose tissue mediates peroxisome proliferator-activated receptor γ (PPARγ) phosphorylation at Ser273 to inhibit its activity, causing PPARγ target gene expression changes. Among these, insulin-degrading enzyme (IDE) degrades amyloid-β peptide (Aβ), the core pathological product of Alzheimer's disease (AD), whereas β-amyloid cleavage enzyme 1 (BACE1) hydrolyzes amyloid-β protein precursor (AβPP). Therefore, we speculated that CDK5 activity in the brain might participate in Aβ production, thereby functioning as a key molecule in AD pathogenesis.

Pioglitazone Reduces β Amyloid Levels Inhibition of PPARγ Phosphorylation in a Neuronal Model of Alzheimer's Disease.

It has been demonstrated that peroxisome proliferator-activated receptor γ (PPARγ) can regulate the transcription of its target gene, insulin-degrading enzyme (), and thus enhance the expression of the IDE protein. The protein can degrade β amyloid (Aβ), a core pathological product of Alzheimer's disease (AD). PPARγ can also regulate the transcription of other target gene, β-amyloid cleavage enzyme 1 (), and thus inhibit the expression of the BACE1 protein.

The Effects of Intelectin-1 on Antioxidant and Angiogenesis in HUVECs Exposed to Oxygen Glucose Deprivation.

Ischemic stroke leads to cellular death and tissue damage by depriving the areas of glucose and oxygen supplies. The effective treatment of stroke remains a challenge for modern medicine. This study used an oxygen-glucose deprivation (OGD) model of human umbilical vein endothelial cells (HUVECs) to mimic ischemic injuries and explored the role and mechanism of intelectin-1.

Alpha 7 nicotinic acetylcholine receptor and its effects on Alzheimer's disease.

Alzheimer's disease (AD) is one of the major disabling and lethal diseases for aged individuals worldwide. To date, there are more than 10 hypotheses proposed for AD pathology. The beta-amyloid (Aβ) cascade hypothesis is the most widely accepted and proposes that the accumulation of Aβ in the brain is one potential mechanism for AD pathogenesis.

Protective effects of tanshinone IIA on SH-SY5Y cells against oAβ-induced apoptosis due to prevention of endoplasmic reticulum stress.

Endoplasmic reticulum (ER) stress caused by β-amyloid protein (Aβ) may play an important role in the pathogenesis of Alzheimer disease (AD). Our previous data have indicated that tanshinone IIA (tan IIA) protected primary neurons from Aβ induced neurotoxicity. To further explore the neuroprotection of tan IIA, here we study the effects of tan IIA on the ER stress response in oligomeric Aβ (oAβ)-induced SH-SY5Y cell injury.

Activation of α7 nicotinic acetylcholine receptor alleviates Aβ-induced neurotoxicity via downregulation of p38 and JNK MAPK signaling pathways.

Amyloid β peptide 1-42 (Aβ) could induce cognitive deficits through oxidative stress, inflammation, and neuron death in Alzheimer's disease (AD). MAPK pathways have been thought to mediate Aβ-induced neuroinflammation responses, neuron death and cognitive decline in AD. The α7 nicotinic acetylcholine receptor (α7nAChR) exerts a neuroprotective effect.

The p38 mitogen activated protein kinase regulates β-amyloid protein internalization through the α7 nicotinic acetylcholine receptor in mouse brain.

Alzheimer's disease (AD) is one of the most devastating neurodegenerative disorders. Intracellular β-amyloid protein (Aβ) is an early event in AD. It induces the formation of amyloid plaques and neuron damage.

Inhibition of CCR7 promotes NF-κB-dependent apoptosis and suppresses epithelial-mesenchymal transition in non-small cell lung cancer.

Activation of C-C chemokine receptor type 7 (CCR7) has been demonstrated to mediate the occurrence and progression of non-small cell lung cancer (NSCLC). However, the potential therapeutic role of CCR7 inhibition in NSCLC is still obscure. Thus, the present study was conducted to investigate the molecular mechanism underlying the inhibition of CCR7 on cell apoptosis and epithelial-mesenchymal transition (EMT) in NSCLC A549 cells.

Tongxinluo improves cognition by decreasing β-amyloid in spontaneous hypertensive rats.

β-Amyloid (Aβ) accumulation in the brain is the major pathophysiology of Alzheimer disease (AD). Hypertension is a risk factor for AD by promoting Aβ deposition. Traditional Chinese medicinal compound tongxinluo (TXL) can improve blood circulation and endothelium-dependent vasodilation.