Strain TSBY 67(T) was isolated during a study on the phylogenetic diversity of culturable bacteria from alpine permafrost in Tianshan Mountains, China. On the basis of 16S rRNA gene sequence ...analysis, strain TSBY 67(T) was closely related to members of the genus Chryseobacterium and exhibited 96.8 % 16S rRNA gene sequence similarity to Chryseobacterium aquaticum 10-46(T) and Chryseobacterium soldanellicola PSD 1-4(T). Strain TSBY 67(T) grew aerobically, at 4-37 °C, with 0-2 % NaCl and at pH 6-8. Cells were Gram-staining negative, non-motile and non-spore-forming rods. The dominant cellular fatty acids were iso-C(15 : 0) (26.9 %), iso-C(17 : 0) 3-OH (16.1 %) and iso-C(17 : 1)ω9c (15.4 %). The G+C content of the DNA was 33.5 mol%. Strain TSBY 67(T) was distinguishable from its closest phylogenetic neighbours by a combination of phenotypic characteristics. Therefore, strain TSBY 67(T) represents a novel species of the genus Chryseobacterium, for which the name Chryseobacterium xinjiangense sp. nov. is proposed. The type strain is TSBY 67(T) ( = NRRL B-51308(T) = CCTCC AB 207183(T)).
In 340 Chinese patients with basilar-artery occlusion, endovascular treatment resulted in better neurologic outcomes than medical care. Approximately one third of patients underwent intravenous ...thrombolysis.
In this study, for the first time, DISS was used in APP/PS1 transgenic mice to explore its neuroprotective effect. After gavage DISS for 1 mo, the impairment of learning and spatial memory ability ...and the loss of neurons in APP/PS1 mice were alleviated. DISS reduced a neuroprotective effect in AD mice via decreasing neuronal apoptosis, enhancing the expressions of CREB phosphorylation and BDNF, pointing to DISS as a new therapeutic target for AD.
Alzheimer’s disease (AD) is a neurodegenerative disorder with insidious onset and progressive development. There is an urgent need to find drugs that prevent and slow AD progression. We focus our attention on 3,6′-disinapoyl sucrose (DISS), an oligosaccharide with antidepressant and antioxidant activities. In this work, APP/PS1 transgenic mice were used to explore the neuroprotective impact of DISS to provide new applications for prevention and therapy of AD. This study aims to assess DISS’s neuroprotective impact on learning and memory deficits in APP/PS1 transgenic mice using behavioral tests (Morris water maze, novel object recognition test, and passive avoidance test). Morphological alterations of hippocampus neurons were observed by Nissl staining and neuronal apoptosis was assessed by TUNEL assay. By using ELISA, the expressions of inflammatory factors were evaluated, and Western blotting was used to measure the protein expressions of neuron-related regulators in the hippocampus. DISS significantly ameliorated the cognitive disorder in APP/PS1 transgenic mice, reduced apoptosis by decreasing the ratio of Bax/B-cell lymphoma/leukemia-2 (Bcl-2) in hippocampal neurons, and restored the abnormal secretion of inflammatory factors (IL-2, TNF-α, IL-1β, and IL-6). Moreover, the gavage of high-dose DISS can boost the expressions of CREB/brain-derived neurotrophic factor (BDNF). Overall, our results indicate that DISS improves cognitive function in APP/PS1 transgenic mice by inhibiting neural apoptosis and activating the CREB/BDNF signal pathway.
NEW & NOTEWORTHY In this study, for the first time, DISS was used in APP/PS1 transgenic mice to explore its neuroprotective effect. After gavage DISS for 1 mo, the impairment of learning and spatial memory ability and the loss of neurons in APP/PS1 mice were alleviated. DISS reduced a neuroprotective effect in AD mice via decreasing neuronal apoptosis, enhancing the expressions of CREB phosphorylation and BDNF, pointing to DISS as a new therapeutic target for AD.
Alzheimer's disease (AD) is characterized by the abnormal aggregation of amyloid-β peptide (Aβ) in extracellular deposits known as senile plaques. The tyrosine residue (Tyr-10) is believed to be ...important in Aβ-induced neurotoxicity due to the formation of tyrosyl radicals. To reduce the likelihood of cross-linking, here we designed an Aβ-40 analogue (Aβ-40 Y10F) in which the tyrosine residue was substituted by a structurally similar residue, phenylalanine. The aggregation rate was determined by the Thioflavin T (ThT) assay, in which Aβ-40 Y10F populated an ensemble of folded conformations much quicker and stronger than the wild type Aβ. Biophysical tests subsequently confirmed the results of the ThT assay, suggesting the measured increase of β-aggregation may arise predominantly from enhancement of hydrophobicity upon substitution and thus the propensity of intrinsic β-sheet formation. Nevertheless, Aβ-40 Y10F exhibited remarkably decreased neurotoxicity compared to Aβ-40 which could be partly due to the reduced generation of hydrogen peroxide. These findings may lead to further understanding of the structural perturbation of Aβ to its fibrillation.
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•EGR3 shows poor expression in CIRI and upregulated EGR3 mitigates CIRI in rats.•EGR3 overexpression attenuates oxidative stress and mitochondrial injury in vitro.•EGR3 facilitates ...miR-146 transcription.•Overexpression of miR-146 relieves oxidative stress and mitochondrial injury.•Upregulated SORT1 abrogates the protection of overexpressed miR-146 against OGD/R.
EGR3 is implicated in angiogenesis in rats with cerebral ischemia/reperfusion injury (CIRI). This research aimed to explore the effect and in vivo and ex vivo mechanisms of EGR3 in CIRI.
CIRI rat models were established via middle cerebral artery occlusion. Cell models were established via oxygen-glucose deprivation/reoxygenation (OGD/R). Brain injury was assessed by neurological scoring, HE, and TTC staining. Inflammatory factors and oxidative stress markers were measured using corresponding kits. Mitochondrial membrane potential and mitochondrial respiration were examined by flow cytometry and respirometry. EGR3-miR-146 network was predicted on TransmiR v2.0 database. Target genes of miR-146 were screened on Starbase, Targetscan, and miRDB databases. miR-146 expression was determined by RT-qPCR. Levels of EGR3 and SORT1 were determined by Western blot. Binding relationships among EGR3, miR-146, and SORT1 were validated by dual-luciferase assay. EGR3, miR-146, and SORT1 levels were altered by injection or cell transfection to observe their functions.
EGR3 was poorly-expressed in CIRI rats and OGD/R-induced neurons. EGR3 overexpression reduced inflammatory factor levels and attenuated oxidative stress and mitochondrial injury in CIRI rats and OGD/R-induced neurons. EGR3 bound to miR-146b promoter region. EGR3 promoted pri-miR-146a/146b processing and stimulated miR-146 transcription. miR-146 overexpression ameliorated oxidative stress and mitochondrial injury and miR-146 downregulation abolished the effect of EGR3 overexpression in vitro. miR-146 targeted SORT1. SORT1 overexpression invalidated the protective function of miR-146 overexpression on oxidative stress and mitochondrial injury in vitro.
EGR3 protected against CIRI by mitigating oxidative stress and mitochondrial injury via the miR-146/SORT1 axis.
•COS dose-dependently decreased the cell apoptosis mediated by APPswe overexpression.•COS repressed the secretion of both Aβ40 and Aβ42 in HEK293 APPswe cells.•COS significantly reduced both BACE1 ...expression and enzymatic activity.•eIF2α phosphorylation was involved in COS-mediated BACE1 reduction.
Amyloid precursor protein (APP) proteolysis is essential for the production of β-amyloid peptides (Aβ) that form senile plaques in Alzheimer’s disease (AD) brains. The β-site amyloid protein precursor cleaving enzyme 1 (BACE1) is the rate limiting enzyme in the generation of Aβ from APP, inhibition of BACE1 is thereby considered as an attractive strategy for anti-AD drug discovery. Chitosan oligosaccharides (COS) has been shown to possess various biological activities. Here we investigated the potential inhibitory effect of COS on both BACE1 expression in HEK293 APPswe cells and BACE1 enzymatic activity in vitro. The results showed that COS (100–500μg/ml) dose-dependently decreased the cell apoptosis, and potently repressed the secretion of both Aβ40 and Aβ42 as determined by ELISA. Moreover, treatment with COS resulted in a dramatic reduction in BACE1 mRNA and protein expression level, eIF2α phosphorylation as well as BACE1 enzymatic activity. Taken together, our findings indicate that COS can ameliorate Aβ-associated neurotoxicity, which may be, at least in part, attributable to reductions in BACE1 enzymatic activity and expression.
•MiR-532-5p is downregulated while BACH1 is upregulated in IS.•Restoring miR-532-5p or inhibiting BACH1 attenuates IS.•MiR-532-5p targets BACH1.•BACH1 overexpression reverses the role of miR-532-5p ...elevation in IS.•This study may provide novel targets for IS treatment.
MicroRNA (miR)-532-5p has been reported to protect against ischemic stroke (IS), while the underlying mechanism of miR-532-5p targeting BTB and CNC homology 1 (BACH1) in IS remains unknown. Thus, we aim to detect the role of miR-532-5p in IS via targeting BACH1.
Blood samples were collected from IS patients and healthy controls. Rat middle cerebral artery occlusion (MCAO) models were established and intracerebrally injected with altered miR-532-5p or BACH1 plasmid vectors to reveal their roles in neurological function, brain tissue pathology and inflammation in MCAO. Expression of miR-532-5p and BACH1 in patients’ blood samples and rat brain tissues was assessed, and the targeting relationship between miR-532-5p and BACH1 was confirmed.
MiR-532-5p was downregulated and BACH1 was upregulated in IS. BACH1 was targeted by miR-532-5p. Restored miR-532-5p or inhibited BACH1 improved neurological function and inhibited inflammation and apoptosis in MCAO rats. On the contrary, miR-532-5p reduction or BACH1 overexpression had totally opposite effects on MCAO rats. The protective role of miR-532-5p for MCAO rats was reversed by upregulated BACH1.
MiR-532-5p upregulation protects against neurological deficits after IS through inhibition of BACH1.
We performed a longitudinal field study in a swine breeding herd that presented with an outbreak of vesicular disease (VD) that was associated with an increase in neonatal mortality. Initially, a ...USDA Foreign Animal Disease (FAD) investigation confirmed the presence of Senecavirus A (SVA) and ruled out the presence of exotic agents that produce vesicular lesions, e.g., foot-and-mouth disease virus and others. Subsequently, serum samples, tonsil swabs, and feces were collected from sows (n = 22) and their piglets (n = 33) beginning 1 week after the onset of the clinical outbreak and weekly for 6 weeks. The presence of SVA RNA was evaluated in all specimens collected by reverse transcriptase quantitative PCR (RT-qPCR) targeting a conserved region of the 5' untranslated region (5'-UTR). The serological response (IgG) to SVA was evaluated by the weekly testing of sow and piglet serum samples on a SVA VP1 recombinant protein (rVP1) indirect enzyme-linked immunosorbent assay (ELISA). The rVP1 ELISA detected seroconversion against SVA in clinically affected and non-clinically affected sows at early stages of the outbreak as well as maternal SVA antibodies in offspring. Overall, the absence of vesicles (gross lesions) in SVA-infected animals and the variability of RT-qPCR results among specimen type demonstrated that a diagnostic algorithm based on the combination of clinical observations, RT-qPCR in multiple diagnostic specimens, and serology are essential to ensure an accurate diagnosis of SVA.
To assess the relationship between LRG1 and CD4
T cells, cognitive impairment and neurological function in acute ischemic stroke (AIS).
Plasma LRG1 was detected by ELISA in 175 patients with AIS at ...baseline, day (D) 1, D7, month (M) 1 and M3.
LRG1 was negatively related to Th2 and Treg cells and positively linked to Th17 (all p < 0.05). LRG1 increased from baseline to D1, then decreased until M3 (p < 0.001). LRG1 at each assessment point was increased in patients with cognitive impairment or poor neurological function at M3 versus those without (all p < 0.05).
LRG1 is linked to decreased Th2 and Tregs, increased Th17, cognitive impairment and nonideal neurological function recovery in patients with AIS.
Abstract
Deep learning has been widely used in image, speech, natural language, and robot and so on. However, how to use these technologies in radar detection is still very few. There are a lot of ...artificial design elements in the traditional radar processing, its application range must be considered practically, while the intelligent radar relies more on the self-learning and improvement ability of the algorithm itself. In this paper, a method of target detection based on convolution neural network is proposed. By matching the received signal with the transmitted waveform, the matching feature of the sliding window is extracted. Moreover, the feature information processed by convolution network is connected into a network, and the anti-jamming target detection under any transmitted waveform and given form of interference is completed. As a creative way, this paper compares the signal anti-interference detection and processing ability of convolution network and full connection network on independent distance unit, and finds that convolution network has the best effect.
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