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The goal of this study was to demonstrate the functions and specific mechanism of long non-coding RNA (lncRNA) GNAS-AS1 in lung adenocarcinoma. Levels of lncRNA GNAS-AS1, microRNA (miR)-433-3p, and Rab3A were assessed by quantitative real-time PCR (qRT-PCR). The target-binding sites of lncRNA GNAS-AS1, miR-433-3p, and Rab3A were predicted and confirmed by bioinformatics tool (StarBase) and a dual-luciferase reporter system. Cell proliferation and apoptosis were checked using MTT and flow cytometry, respectively. Additionally, the levels of apoptosis-related and epithelial–mesenchymal transition (EMT)-associated genes in A549 cells were analyzed by qRT-PCR and western blot. We found that lncRNA GNAS-AS1 was upregulated, miR-433-3p was low-expressed, and Rab3A was overexpressed in lung adenocarcinoma tissues and cell lines. LncRNA GNAS-AS1 interacted with miR-433-3p and negatively regulated miR-433-3p levels. Rab3A was a direct target of miR-433-3p. Downregulation of lncRNA GNAS-AS1 remarkably suppressed cell proliferation, promoted cell apoptosis, decreased B-cell lymphoma-2 (Bcl-2) expression, enhanced the Bcl-2-Associated X (Bax) level, promoted E-cadherin expression, and reduced N-cadherin and Rab3A levels. However, the miR-433-3p inhibitor reversed all these findings. Similarly, the inhibitory effects of miR-433-3p mimic on A549 cells were reversed by the Rab3A-plasmid. In conclusion, lncRNA GNAS-AS1 downregulation suppressed lung adenocarcinoma cell proliferation and EMT through the miR-433-3p/Rab3A axis.

Hydrogenation of biomass-derived levulinic acid (LA) could produce a high value-added compound, gamma-valerolactone (GVL). However, metal leaching is a major issue in the efficient production of GVL from LA due to the acidity of LA. Some endeavors have tended to focus on the external factors of the catalysts for preventing metal leaching, such as reaction at high temperature and H2 pressure or the esterification of LA with alcohols. Focusing on the catalyst itself, in this work, metal leaching was overcome by the selection of suitable catalyst compositions and preparation methods. The CuAgZrGO catalyst was synthesized by regulating the pH of the precipitation system to achieve a one-pot layered assembly of Zr4+, Cu2+, and Ag+ components on the graphene oxide (GO) surface at the atomic level. The catalyst without reduction pretreatment resulted in the complete conversion of LA and achieved approximately 100% yield of GVL, and metal leaching in the LA aqueous phase could be substantially prevented. Under mild reaction conditions, the catalyst exhibited good stability after four times of recycling in the aqueous phase. The positive-titration co-precipitation method controls the Ag more scattered on the surface of Cu and Zr precipitates, which makes CuAgZrGO a metal-leaching-resistant catalyst for aqueous-phase hydrogenation of LA. [ABSTRACT FROM AUTHOR]

Background and Aims: Sleep is predicted as a key modulator of cognition, but the underlying mechanisms are poorly understood. In this study, we investigated the effects of melatonin on chronic rapid eye movement sleep deprivation (CRSD)‐induced cognitive impairment and circadian dysfunction in rat models. Methods: Thirty‐six Sprague‐Dawley male rats were divided into three groups: CRSD with saline treatment, CRSD with chronic melatonin injection (20 mg/kg/day), and non‐sleep‐deprived control. The cognitive behavioral tests as well as the expression of clocks and HDAC3 were evaluated in all groups. Results: CRSD significantly reduced recognition index in novel object location, increased escape latency and distance traveling in Morris water maze while melatonin treatment attenuated CRSD‐induced hippocampal‐dependent spatial learning and memory deficits. Furthermore, the mRNAs of brain and muscle aryl hydrocarbon receptor nuclear translocator‐like 1(Bmal1) and circadian locomotor output cycles kaput (Clock) were globally down‐regulated by CRSD with constant intrinsic oscillation in both hippocampus and peripheral blood. The protein levels of hippocampal Bmal1, Clock, and HDAC3 were also remarkably down‐regulated following CRSD. Melatonin treatment reversed CRSD‐induced alterations of Bmal1/Clock and HDAC3 on both mRNA levels and protein levels. Conclusions: Our data indicate that melatonin treatment attenuates CRSD‐induced cognitive impairment via regulating HDAC3‐Bmal1/Clock interaction. These findings explore a broader understanding of the relationship between sleep and cognition and provide a potential new therapeutic target for cognitive impairment. [ABSTRACT FROM AUTHOR]

Objective: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease involving both upper and lower motor neurons. The motor phenotypes of ALS are highly clinically heterogeneous, and the underlying mechanisms are poorly understood. Methods: A comparative proteomic analysis was performed in the cerebrospinal fluid (CSF) of bulbar‐onset (BO) and spinal‐onset (SO) ALS patients and controls (n = 14). Five biomarker candidates were selected from a differentially regulated protein pool, and further validation was performed in a larger independent cohort (n = 92) using enzyme‐linked immunosorbent assay (ELISA). Results: A total of 1732 CSF proteins were identified, and 78 differentially expressed proteins were found among BO‐ALS patients, SO‐ALS patients, and controls. Five promising biomarker candidates were selected for further validation, and lipopolysaccharide‐binding protein (LBP) and HLA class II histocompatibility antigen, DR alpha chain (HLA‐DRA) were validated. CSF LBP levels were increased in ALS patients compared with controls and higher in BO‐ALS versus SO‐ALS. The increased CSF LBP levels were correlated with the revised ALS Functional Scale (ALSFRS‐R) score. CSF HLA‐DRA levels were specifically elevated in BO‐ALS patients, and there was no significant difference between SO‐ALS patients and controls. Increased HLA‐DRA expression was correlated with decreased survival. Interpretation: Our data shows that elevated CSF LBP is a good biomarker for ALS and correlates with clinical severity, and increased HLA‐DRA is a specific biomarker for BO‐ALS and may predict short survival. It also suggests that the microglial pathway and HLA‐II‐related adaptive immunity may be differentially involved in ALS phenotypes and may be new therapeutic targets for ALS. [ABSTRACT FROM AUTHOR]

In order to increase molecular weight of PLGA, BuOH was introduced as a co-initiator to Sn[(Oct).sub.2] in ring-opening precipitation polymerization of L-lactide and glycolide in supercritical carbon dioxide (Sc[CO.sub.2]). The polymerization mechanism of the reaction processes on Sn[(Oct).sub.2] with BuOH was explored. The positive effect of BuOH on polymer molecular weight was studied. PLGA with higher [M.sub.w] (of 19,500 g/mol) and narrower PDI (of 1.12) was successfully prepared by ring-opening precipitation polymerization in ScC02 using Sn[(Oct).sub.2]/BuOH as an efficient catalytic system.Influence of reaction conditions, such as monomer feed concentration, reaction temperature, pressure, and time, were also investigated in detail. POLYM. ENG. SCI., 54:704-710, 2014. © 2013 Society of Plastics Engineers, INTRODUCTION Poly (L-lactide-co-glycolide) (PLGA), due to its advantages of biocompatibility, degradability, processability, and mechanical strength, has been widely used for medical applications including the controlled release of drugs, absorbable sutures, [...]

As a result of antibiotic overuse, bacterial antibiotic resistance has become a severe threat to worldwide public health. The development of more effective antimicrobial therapies and alternative antibiotic strategies is urgently required. The role played by bacterial membrane vesicles (BMVs) in antibiotic resistance has become a current focus of research. BMVs are nanoparticles derived from the membrane components of Gram-negative and Gram-positive bacteria and contain diverse components originating from the cell envelope and cytoplasm. Antibiotic stress stimulates the secretion of BMVs. BMVs promote and mediate antibiotic resistance by multiple mechanisms. BMVs have been investigated as conceptually new antibiotics and drug-delivery vehicles. In this article, we outline the research related to BMVs and antibiotic resistance as a reference for the intentional use of BMVs to combat antibiotic resistance. [ABSTRACT FROM AUTHOR]

Herein, cobalt-reduced graphene oxide (rGO) catalyst was synthesized with a practical impregnation–calcination approach for the selective hydrodeoxygenation (HDO) of guaiacol to cyclohexanol. The synthesized Co/rGO was characterized by transmission electron microscopy (TEM), high-angle annular dark-field scanning TEM (HAADF-STEM), X-ray photoelectron spectroscopy (XPS), Raman spectroscopy, X-ray diffraction (XRD), and H2 temperature-programmed reduction (H2-TPR) analysis. According to the comprehensive characterization results, the catalyst contains single Co atoms in the graphene matrix and Co oxide nanoparticles (CoOx) on the graphene surface. The isolated Co atoms embedded in the rGO matrix form stable metal carbides (CoCx), which constitute catalytically active sites for hydrogenation. The rGO material with proper amounts of N heteroatoms and lattice defects becomes a suitable graphene material for fabricating the catalyst. The Co/rGO catalyst without prereduction treatment leads to the complete conversion of guaiacol with 93.2% selectivity to cyclohexanol under mild conditions. The remarkable HDO capability of the Co/rGO catalyst is attributed to the unique metal–acid synergy between the CoCx sites and the acid sites of the CoOx nanoparticles. The CoCx sites provide H while the acid sites of CoOx nanoparticles bind the C-O group of reactants to the surface, allowing easier C-O scission. The reaction pathways were characterized based on the observed reaction–product distributions. The effects of the process parameters on catalyst preparation and the HDO reaction, as well as the reusability of the catalyst, were systematically investigated. [ABSTRACT FROM AUTHOR]

Objective: p75 neurotrophin receptor (p75NTR) is associated with the pathogenesis of amyotrophic lateral sclerosis (ALS). However, its role is not fully understood. The aim of this study was to evaluate the association between ALS and the extracellular domain of p75NTR(p75ECD) in urine. Methods: We conducted a comprehensive literature search using keywords in the PubMed, Embase, Science, and the Cochrane Library, and identified five case control studies, with the latest date of search being 18 April 2021. Results: The results showed that urinary p75ECD levels were significantly higher in patients with ALS compared to non-neurological control (weighted mean difference (WMD) = 4.18, 95% CI [2.525, 6.990], p < 0.001), and other neurological diseases (WMD = 6.005, 95% CI [1.596, 10.414], p = 0.008). Increased urinary p75ECD levels were inversely associated with ALSFRS-R in ALS patients (r = −0.32, 95% CI [−0.43, −0.21], p < 0.001). Conclusions: Given the associations between p75ECD and ALS found in this meta-analysis, urinary p75ECD levels have potential to be used as a diagnostic biomarker and a progression indicator in the future. [ABSTRACT FROM AUTHOR]

Keywords: actinomycosis israelii; CNS actinomycosis; microbiological next-generation sequencing; moyamoya syndrome EN actinomycosis israelii CNS actinomycosis microbiological next-generation sequencing moyamoya syndrome 1139 1142 4 06/06/22 20220701 NES 220701 ACKNOWLEDGMENTS We are grateful to staff at Hugo biotech Co., Ltd., (Beijing, China) for sequencing. Central nervous system (CNS) actinomycosis is a rare infectious disease associated with several types of lesions, including abscesses, meningitis/meningoencephalitis, and actinomycetoma.1 Here, we report a case of moyamoya syndrome caused by CNS actinomycosis in a woman who had just undergone a cesarean section a month ago and was probably immunocompromised. [Extracted from the article]

The aim of this study was to investigate the effect of vestibular disruption on autophagy-related proteins and the tumour-associated pathway P13K/Akt in rat sleep and its hypothalamus tissue and to examine whether catechins trigger tumour autophagy. Healthy adult male rats were randomly selected and divided into the vestibular damage group, the sham operation group, and the control group, with 8 rats in each group. A vestibular damage model was established through penetrating the tympanic membrane of the external auditory canal by injecting sodium p-aminophenylarsonate. The electroencephalogram (EGG) activity was used to record the sleep-wakefulness cycle of rats, and the expression levels of hypothalamic orexin (orexin) mRNA and autophagy proteins were detected. Primary hippocampal neurons were intervened with orexin at different concentrations and at different times to detect cell viability and the expression of autophagy protein and P13K/Akt signal pathway protein. The results showed that compared with the control group and the sham operation group, NREM duration in the vestibular damage group decreased significantly (P < 0.05), while its W time increased significantly (P < 0.05). The expression level of orexin mRNA in the hypothalamus of the vestibular damage group was significantly higher than that of the other two groups (P < 0.05), the expression of autophagy microtubule-related proteins LC3B and Beclin-1 increased significantly (P < 0.05), and the protein expression level of p62 decreased significantly (P < 0.05). After orexin intervention, compared with the control group, the expression of Beclin-1 protein that positively correlated with autophagy decreased significantly (P < 0.05) and the expression of mTOR, PDK1, and Akt protein increased significantly (P < 0.05). Compared with the orexin intervention group, the expression of Beclin-1 and LC3B proteins in cells of the orexin receptor inhibitor (Almorexant) group, the autophagy activator (Rapamycin) group, the orexin + Almorexant group, and the orexin + Rapamycin group increased significantly (P < 0.05), and the expression of mTOR, PDK1, and Akt proteins decreased significantly (P < 0.05). Catechins trigger autophagy in part by regulating the p-Akt/p-mTOR and P13K pathways and by stimulating the MAPK pathway. Catechins initiate apoptosis in common tumour types of hepatocellular carcinoma cells by activating autophagy-related pathways. The conclusion is that vestibular damage can affect the sleep-wakefulness cycle of rats; the level of autophagy in hypothalamic tissue is upregulated and may affect cell proliferation and activity through mTOR-P13K/Akt, which has a certain reference value for tumor formation and provides a basis for the research of insomnia or sleep disorders caused by tumors. Autophagy activation is a key process by which catechins promote apoptosis in tumour cells, providing an avenue for more research on the use of catechins-rich diets for cardiovascular protection in the treatment of tumours. [ABSTRACT FROM AUTHOR]

Cellulose-derived levulinic acid (LA) can be converted into gamma-valerolactone (GVL), a sustainable platform chemical for the production of bio-based chemicals. However, LA as an organic acid causes severe metal leaching during the heterogeneous hydrogenation of LA to GVL, especially in the presence of water. Various endeavors for preventing metal leaching have focused more on the process and less on the intrinsic nature of catalysts. The aim of this work is to derive a novel metal-leaching-resistant catalyst for the aqueous-phase hydrogenation of LA into GVL by using a nanocomposite containing three components, Ag, ZrO2, and graphene oxide (GO). The AgZrO2GO catalyst without pre-reduction treatment resulted in complete conversion of LA and approximately 100 mol% selectivity to GVL in the aqueous reaction, and metal leaching from the catalyst was completely eliminated. The relationship between the catalytic performance and the distinct physicochemical properties of the catalyst was extensively discussed. [ABSTRACT FROM AUTHOR]