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The aim in this study was to explore protein expression profiles in the rat hippocampus after induction of focal ischemia injury. Forty male Sprague Dawley rats were randomly divided into four equal groups after ischemia injury surgery: Control, Day 3, Day 7, and Day 14. Focal cortical ischemia was induced in thirty rats by photothrombosis of cortical microvessels. After surgery, the induction of ischemia was confirmed by infarct size measurement using staining by 2, 3, 5-triphenyltetrazolium chloride. To identify the differential expression of proteins between the diseased and control sides of the hippocampus, a comparative proteome analysis was performed using isobaric tags for relative or absolute quantification coupled with 2D liquid chromatography-tandem mass spectrometry analysis. 4,081 proteins were identified, 260 of which were non-redundant and showed differential expression between the three surgery groups and the control. Hierarchical cluster analysis indicated that the three surgical groups had markedly different expression patterns of these 260 proteins, including 160 upregulated and 80 downregulated proteins. A gene ontology analysis revealed 4,944 terms, among which myelin sheath and cell junction were the two most enriched items. In kyoto encyclopedia of genes and genomes database pathway analysis, ribosome was the most abundant item. A Venn diagram showing the overlap of 25 of the differentially expressed proteins quantified from the four groups and results from the kyoto encyclopedia of genes and genomes pathway analysis suggested that Epstein-Barr virus infection was the most abundant item. From the protein-protein interaction network, a total of 223 interactive proteins were predicted and used to construct a network. In conclusion, myelin sheath, cell junction, and Epstein-Barr virus infection were implicated in focal ischemia injury. Vimentin and albumin may be important proteins involved in focal ischemia injury.

A high‐fat diet (HFD) leads to long‐term exposure to gut microbial metabolite secondary bile acids, such as deoxycholic acid (DCA), in the intestine, which is closely linked to colorectal cancer (CRC). Evidence reveals that vasculogenic mimicry (VM) is a critical event for the malignant transformation of cancer. Therefore, this study investigated the crucial roles of DCA in the regulation of VM and the progression of intestinal carcinogenesis. The effects of an HFD on VM formation and epithelial‐mesenchymal transition (EMT) in human CRC tissues were investigated. The fecal DCA level was detected in HFD‐treated Apcmin/+ mice. Then the effects of DCA on VM formation, EMT, and vascular endothelial growth factor receptor 2 (VEGFR2) signaling were evaluated in vitro and in vivo. Here we demonstrated that compared with a normal diet, an HFD exacerbated VM formation and EMT in CRC patients. An HFD could alter the composition of the gut microbiota and significantly increase the fecal DCA level in Apcmin/+ mice. More importantly, DCA promoted tumor cell proliferation, induced EMT, increased VM formation, and activated VEGFR2, which led to intestinal carcinogenesis. In addition, DCA enhanced the proliferation and migration of HCT‐116 cells, and induced EMT process and vitro tube formation. Furthermore, the silence of VEGFR2 reduced DCA‐induced EMT, VM formation, and migration. Collectively, our results indicated that microbial metabolite DCA promoted VM formation and EMT through VEGFR2 activation, which further exacerbated intestinal carcinogenesis. [ABSTRACT FROM AUTHOR]

Introduction: Turns‐amplitude, number of small segments (NSS)‐activity, and envelope‐activity clouds are three methods of electromyography (EMG) interference pattern analysis. Our objective was to evaluate the sensitivity and specificity of each individual cloud analysis and combined clouds analysis to compare with that of quantitative motor unit potential (QMUP) analysis. Methods: A total of 379 muscles from 100 patients were analyzed by both QMUP and clouds analyses. Calculation of sensitivity and specificity was based on the clinical diagnosis as the "gold standard." Results: For discrimination of abnormal vs normal and neuropathic vs non‐neuropathic, combined clouds analysis had greater sensitivity than QMUP analysis and any single cloud analysis, but there were no differences in specificity. For discrimination of myopathic vs non‐myopathic, combined clouds analysis and single cloud analysis had greater sensitivity than QMUP analysis, but there were no differences in specificity. Discussion Combined clouds analysis was superior to QMUP and each single cloud analysis for distinguishing normal, myopathic, and neuropathic muscles. [ABSTRACT FROM AUTHOR]

Background: Number of small segments (NSS) and activity analysis is a mature method for electromyographic automatic interference pattern analysis (IPA), but there are few reports on the application of this technique. Our objective was to establish normal reference values of NSS-activity clouds.Methods: The NSS and activity data of the sternocleidomastoid, deltoid, biceps brachii (long head), extensor digitorum communis, abductor digiti minimi, vastus medialis, tibialis anterior, and gastrocnemius (lateral head) muscles were obtained from 34 men and 25 women, aged 15-80 years, using concentric needle electrodes. A linear regression of log(NSS) vs log(activity) was performed and the slope, intercept and standard deviation were calculated for each muscle. These variables were transformed back to the original parameters to yield clouds.Results: Normal NSS-activity clouds for the above eight muscles were obtained.Conclusions: Normal reference values of NSS-activity may facilitate detection of early and mild neurogenic and myogenic abnormalities. [ABSTRACT FROM AUTHOR]

The prevalence of colorectal cancer (CRC) has markedly increased worldwide in the last decade. Alterations of bile acid metabolism and gut microbiota have been reported to play vital roles in intestinal carcinogenesis. About trillions of bacteria have inhabited in the human gut and maintained the balance of host metabolism. Bile acids are one of numerous metabolites that are synthesized in the liver and further metabolized by the gut microbiota, and are essential in maintaining the normal gut microbiota and lipid digestion. Multiple receptors such as FXR, GPBAR1, PXR, CAR and VDR act as sensors of bile acids have been reported. In this review, we mainly discussed interplay between bile acid metabolism and gut microbiota in intestinal carcinogenesis. We then summarized the critical role of bile acids receptors involving in CRC, and also addressed the rationale of multiple interventions for CRC management by regulating bile acids–microbiota axis such as probiotics, metformin, ursodeoxycholic acid and fecal microbiota transplantation. Thus, by targeting the bile acids–microbiota axis may provide novel therapeutic modalities in CRC prevention and treatment. [ABSTRACT FROM AUTHOR]

Ralstonia solanacearum species complex (RSSC) contains a group of destructive plant pathogenic bacteria, causing bacterial wilt of >200 species of crops and trees, such as Casuarina equisetifolia , worldwide. RSSC can survive in the soil environment for a long time and start infection after activation by host plants. This study conducted a transcriptome analysis on the expression pattern of the pathogenicity-related genes of a new isolated RSSC strain YQ ( Ralstonia pseudosolanacearum phylotype I-16) in response to C. equisetifolia cladophyll (a branch of a stem that resembles and functions as a leaf) and root debris under in vitro culture. The cladophyll debris induced more genes up-regulated than the root debris, including pathogenicity-related genes involved in motility, effectors, type III secretion systems, quorum sensing, and plant cell wall degradation. Besides, many differentially expressed genes were related to transcriptional regulator such as cyclic dimeric guanosine monophosphate. Moreover, the cultures with cladophyll debris induced a faster wilting in bioassays, and the cell swimming was enhanced by cladophyll exudate. C. equisetifolia cladophylls could activate the expression of pathogenicity-related genes of strain YQ and accelerate infection. Our findings suggest that litterfall management in C. equisetifolia forests, or even other plantations, should receive attention to prevent the induction of bacterial wilt disease caused by RSSC.

Circular RNAs (circRNAs), formed from pre-messenger RNAs by back-splicing, are a novel class of evolutionarily-conserved endogenous non-coding RNAs. While circRNAs are involved in various diseases, the role of circRNAs in intracerebral hemorrhage (ICH) remains unknown. In the present study, we performed high-throughput sequencing to profile the expression of circRNAs in the rat brain at 24 and 48 hours after ICH onset, and utilized bioinformatics methods to make predictions about the function of dysregulated circRNAs. Compared with the sham group, 346 and 389 circRNAs changed significantly (|log2 (fold change)| > 1 and P < 0.05) at 24 and 48 hours after ICH, respectively. Bioinformatics analyses indicated that parent genes of dysregulated circRNAs were involved in biological processes, cellular component, and molecular function following ICH, and that they were enriched in the dopaminergic synapses, glutamatergic synapses, endocytosis, regulation of actin cytoskeleton, the mitogen-activated protein kinase signaling pathway, and the retrograde endocannabinoid signaling pathway. Enrichment analyses of target mRNAs showed that these mRNAs were enriched in synaptic plasticity, ion channel activity, and pathways including the phospholipase D signaling and the cGMP-PKG signaling. Our study indicates that the expression profile of circRNAs changes significantly after ICH in rat brains, and suggests that circRNAs may be crucial for the pathophysiological process following ICH., Competing Interests: None., (AJTR Copyright © 2020.)

Focal cerebral infarction leads to secondary changes in non-ischemic areas remote from but connected to the infarct site. Circular RNAs (circRNAs) are involved in the pathophysiological processes of many diseases. However, the expression and roles of circRNAs in non-ischemic remote regions after ischemic stroke remain unknown. In this study, adult male C57BL/6J mice were subjected to permanent distal middle cerebral artery occlusion (MCAO) to establish focal cortical infarction. High-throughput sequencing was used to profile the circRNA expression in the mouse ipsilateral thalamus at 7 and 14 d after MCAO. Bioinformatics analyses were conducted to predict the function of the differential expressed circRNAs' host and target genes. Compared with sham group, a total of 2659 circRNAs were significantly altered in the ipsilateral thalamus at 7 or 14 d after MCAO in mice. Among them, 73 circRNAs were significantly altered at both two time points after stroke. GO and KEGG analyses indicated that circRNAs plays important roles in secondary thalamic neurodegeneration and remodeling after focal cortical infarction. This is the first study to profile the circRNA expression in non-ischemic region of ischemic stroke, suggesting that circRNAs may be therapeutic targets for reducing post-stroke secondary remote neurodegeneration.

Angiogenesis plays a critical role in neural repair following ischemic stroke. Therapeutic angiogenesis contributes to neurological functional recovery after cerebral infarction. Nerve growth factor (NGF) has been reported as a neurotrophic factor. However, the angiogenic efficacy of NGF in cerebral ischemia remains unclear. In this study, we investigated the effect of NGF on angiogenesis in the ischemic penumbra and neurological outcome in a rat model of middle cerebral artery occlusion (MCAO). Our results demonstrate that the intranasal administration of NGF improves neurological outcome and reduces infarct volume on day 7 after MCAO in rats. Treatment with NGF promoted angiogenesis in the peri-infarct region, increased the serum levels of VEGF and SDF-1 protein, and elevated the number of circulating endothelial progenitor cells (EPCs) on day 4 after MCAO. In addition, NGF enhanced capillary-like tube formation of rat brain microvascular endothelial cells in vitro, further confirming its angiogenic effect. Furthermore, the neuroprotective and angiogenic effects of NGF can be significantly attenuated by the phosphatidylinositide 3-kinase (PI3K)/Akt pathway antagonist LY294002. Our results indicate that NGF-enhanced angiogenesis contributes to neurological functional recovery after ischemic stroke, which may occur partly via activation of the PI3K/Akt signaling pathway. This study provides novel experimental evidence for the angiogenic role of NGF in treating ischemic stroke., Competing Interests: None.

The aim in this study was to explore protein expression profiles in the rat hippocampus after induction of focal ischemia injury. Forty male Sprague Dawley rats were randomly divided into four equal groups after ischemia injury surgery: Control, Day 3, Day 7, and Day 14. Focal cortical ischemia was induced in thirty rats by photothrombosis of cortical microvessels. After surgery, the induction of ischemia was confirmed by infarct size measurement using staining by 2, 3, 5-triphenyltetrazolium chloride. To identify the differential expression of proteins between the diseased and control sides of the hippocampus, a comparative proteome analysis was performed using isobaric tags for relative or absolute quantitation coupled with 2D liquid chromatographytandem mass spectrometry analysis. 4,081 proteins were identified, 260 of which were non-redundant and showed differential expression between the three surgery groups and the control. Hierarchical cluster analysis indicated that the three surgical groups had markedly different expression patterns of these 260 proteins, including 160 upregulated and 80 downregulated proteins. A gene ontology analysis revealed 4,944 terms, among which myelin sheath and cell junction were the two most enriched items. In KEGG database pathway analysis, ribosome was the most abundant item. A Venn diagram showing the overlap of 25 of the differentially expressed proteins quantified from the four groups and results from the KEGG pathway analysis suggested that Epstein-Barr virus infection was the most abundant item. From the protein-protein interaction network, a total of 223 interactive proteins were predicted and used to construct a network. In conclusion, myelin sheath, cell junction, and Epstein–Barr virus infection were implicated in focal ischemia injury. Vimentin and albumin may be important proteins involved in focal ischemia injury.