Rapid and efficient isolation platform for plasma extracellular vesicles: EV-FISHER.

Extracellular vesicles (EVs) have found diverse applications in clinical theranostics. However, the current techniques to isolate plasma EVs suffer from burdensome procedures and limited yield. Herein, we report a rapid and efficient EV isolation platform, namely, EV-FISHER, constructed from the metal-organic framework featuring cleavable lipid probes (PO -spacer-DNA-cholesterol, PSDC).

Rheological Properties of Graphene/Polyethylene Composite Modified Asphalt Binder.

Aiming to improve the comprehensive road performance of asphalt binders, especially the high-temperature performance, a novel asphalt binder was prepared by compounding high-quality and low-cost polyethylene (PE) with graphene (GNPs) using a high-speed shearing machine. The rheological properties and interaction mechanism of PE/GNPs composite modified asphalt were investigated using temperature sweep (TeS), multiple stress creep recovery (MSCR), linear amplitude sweep (LAS) and Fourier transform infrared spectroscopy (FT-IR) and field emission scanning electron microscopy (FESEM). The experimental results demonstrated that GNPs and PE can synergistically improve the high-temperature performance of asphalt binders and enhance the rutting resistance of pavements; the pre-blended PE/GNPs masterbatch has good medium-temperature fatigue and low-temperature cracking resistance.

Smoothing process of conformal vibration polishing for mid-spatial frequency errors: characteristics research and guiding prediction.

By combining the conformal polishing method with short stroke vibration, a novel, to the best of our knowledge, conformal vibration polishing (CVP) method is proposed. The CVP method is expected to be an efficient means of optical processing by its high material removal rate and smoothing characteristics of mid-spatial frequency (MSF) errors. A quantitative time-domain smoothing model and a convergence factor (${\rm CF}_C$) are presented based on the research of smoothing characteristics.

Chemical constituents from and their anti-inflammatory and antioxidant activities.

A new flavonoid named (2)-7,4'-dimethoxyl-6-(2″,3″-epoxy-3″-methylbutyl)flavanone (), along with five known compounds (), were isolated from the EtOAc-soluble extract of the stem bark of Their structures were elucidated on the basis of spectroscopic methods. All compounds were evaluated for anti-inflammatory and antioxidant activities . Among them, compound showed the highest inhibitory activity on NO production in RAW264.

Decreased cpg15 augments oxidative stress in sleep deprived mouse brain.

Sleep deprivation (SD) has detrimental effects on the physiological function of the brain. However, the underlying mechanism remains elusive. In the present study, we investigated the expression of candidate plasticity-related gene 15 (cpg15), a neurotrophic gene, and its potential role in SD using a REM-SD mouse model.

Decreased IL-17RB expression impairs CD11bCD11c myeloid cell accumulation in gastric mucosa and host defense during the early-phase of Helicobacter pylori infection.

Interleukin-17 receptor B (IL-17RB), a member of the IL-17 receptor family activated by IL-17B/IL-17E, has been shown to be involved in inflammatory diseases. However, the regulation and function of IL-17RB in Helicobacter pylori (H. pylori) infection, especially in the early-phase is still unknown.

MicroRNA-365 modulates astrocyte conversion into neuron in adult rat brain after stroke by targeting Pax6.

Reactive astrocytes induced by ischemia can transdifferentiate into mature neurons. This neurogenic potential of astrocytes may have therapeutic value for brain injury. Epigenetic modifications are widely known to involve in developmental and adult neurogenesis.

The spatial-temporal interaction in the LTP induction between layer IV to layer II/III and layer II/III to layer II/III connections in rats' visual cortex during the development.

During the early developmental period, long-term potentiation (LTP) can be induced in both vertical and horizontal connections in the rat visual cortex. However, the temporal difference in LTP change between the two pathways during animal development remains unclear. In this study, LTP in vertical (from layer IV to layer II/III) and horizontal (from layer II/III to layer II/III) synaptic connections were recorded in brain slices from the same rats, and the developmental changes of LTP in both directions were compared within the animals' eye-opening period.

Soluble cpg15 from Astrocytes Ameliorates Neurite Outgrowth Recovery of Hippocampal Neurons after Mouse Cerebral Ischemia.

The present study focuses on the function of cpg15, a neurotrophic factor, in ischemic neuronal recovery using transient global cerebral ischemic (TGI) mouse model and oxygen-glucose deprivation (OGD)-treated primary cultured cells. The results showed that expression of cpg15 proteins in astrocytes, predominantly the soluble form, was significantly increased in mouse hippocampus after TGI and in the cultured astrocytes after OGD. Addition of the medium from the cpg15-overexpressed astrocytic culture into the OGD-treated hippocampal neuronal cultures reduces the neuronal injury, whereas the recovery of neurite outgrowths of OGD-injured neurons was prevented when cpg15 in the OGD-treated astrocytes was knocked down, or the OGD-treated-astrocytic medium was immunoadsorbed by cpg15 antibody.

Transcriptome profiling and pathway analysis of hepatotoxicity induced by tris (2-ethylhexyl) trimellitate (TOTM) in mice.

Tris (2-ethylhexyl) trimellitate (TOTM) is commonly used as an alternative plasticizer for medical devices. But very little information was available on its biological effects. In this study, we investigated toxicity effects of TOTM on hepatic differential gene expression analyzed by using high-throughput sequencing analysis for over-represented functions and phenotypically anchored to complementary histopathologic, and biochemical data in the liver of mice.

Neurogenic effect of VEGF is related to increase of astrocytes transdifferentiation into new mature neurons in rat brains after stroke.

To study the cellular mechanism of vascular endothelial growth factor (VEGF)-enhanced neurogenesis in ischemic brain injury, we used middle cerebral artery occlusion (MCAO) model to induce transient focal ischemic brain injury. The results showed that ischemic injury significantly increased glial fibrillary acidic protein immunopositive (GFAP(+)) and nestin(+) cells in ipsilateral striatum 3 days following MCAO. Most GFAP(+) cells colocalized with nestin (GFAP(+)-nestin(+)), Pax6 (GFAP(+)-Pax6(+)), or Olig2 (GFAP(+)-Olig2(+)).

Striatal astrocytes transdifferentiate into functional mature neurons following ischemic brain injury.

To determine whether reactive astrocytes stimulated by brain injury can transdifferentiate into functional new neurons, we labeled these cells by injecting a glial fibrillary acidic protein (GFAP) targeted enhanced green fluorescence protein plasmid (pGfa2-eGFP plasmid) into the striatum of adult rats immediately following a transient middle cerebral artery occlusion (MCAO) and performed immunolabeling with specific neuronal markers to trace the neural fates of eGFP-expressing (GFP(+)) reactive astrocytes. The results showed that a portion of striatal GFP(+) astrocytes could transdifferentiate into immature neurons at 1 week after MCAO and mature neurons at 2 weeks as determined by double staining GFP-expressing cells with βIII-tubulin (GFP(+)-Tuj-1(+)) and microtubule associated protein-2 (GFP(+)-MAP-2(+)), respectively. GFP(+) neurons further expressed choline acetyltransferase, glutamic acid decarboxylase, dopamine receptor D2-like family proteins, and the N-methyl-D-aspartate receptor subunit R2, indicating that astrocyte-derived neurons could develop into cholinergic or GABAergic neurons and express dopamine and glutamate receptors on their membranes.

Regulation of RAGE splicing by hnRNP A1 and Tra2β-1 and its potential role in AD pathogenesis.

The receptor for advanced glycation end products (RAGE) gene expresses two major alternative splicing isoforms, full-length membrane-bound RAGE (mRAGE) and secretory RAGE (esRAGE). Both isoforms play important roles in Alzheimer's disease (AD) pathogenesis, either via interaction of mRAGE with β-amyloid peptide (Aβ) or inhibition of the mRAGE-activated signaling pathway. In the present study, we showed that heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and Transformer2β-1 (Tra2β-1) were involved in the alternative splicing of mRAGE and esRAGE.

Splicing factor NSSR1 reduces neuronal injury after mouse transient global cerebral ischemia.

This study focuses on the function of NSSR1, a splicing factor, in neuronal injury in the ischemic mouse brain using the transient global cerebral ischemic mouse model and the cultured cells treated with oxygen-glucose deprivation (OGD). The results showed that the cerebral ischemia triggers the expression of NSSR1 in hippocampal astrocytes, predominantly the dephosphorylated NSSR1 proteins, and the Exon3 inclusive NCAM-L1 variant and the Exon4 inclusive CREB variant. While in the hippocampus of astrocyte-specific NSSR1 conditional knockdown (cKD) mice, where cerebral ischemia no longer triggers NSSR1 expression in astrocytes, the expression of Exon3 inclusive NCAM-L1 variant and Exon4 inclusive CREB variant were no longer triggered as well.

Splicing factor transformer-2β (Tra2β) regulates the expression of regulator of G protein signaling 4 (RGS4) gene and is induced by morphine.

Regulator of G protein signaling 4 (RGS4) is a critical modulator of G protein-coupled receptor (GPCR)-mediated signaling and plays important roles in many neural process and diseases. Particularly, drug-induced alteration in RGS4 protein levels is associated with acute and chronic effects of drugs of abuse. However, the precise mechanism underlying the regulation of RGS4 expression is largely unknown.

Characterization of nuclear localization signals (NLSs) and function of NLSs and phosphorylation of serine residues in subcellular and subnuclear localization of transformer-2β (Tra2β).

The serine/arginine-rich (SR) proteins are one type of major actors in regulation of pre-mRNA splicing. Their functions are closely related to the intracellular spatial organization. The RS domain and phosphorylation status of SR proteins are two critical factors in determining the subcellular distribution.

Dephosphorylated NSSR1 is induced by androgen in mouse epididymis and phosphorylated NSSR1 is increased during sperm maturation.

NSSR1 (Neural salient serine/arginine rich protein 1, alternatively SRp38) is a newly identified RNA splicing factor and predominantly expressed in neural tissues. Here, by Western blot analysis and immunofluorescent staining, we showed that the expression of dephosphorylated NSSR1 increased significantly during development of the caput epididymis. In adult mice, phosphorylated NSSR1 was mainly expressed in the apical side of epithelial cells, and dephosphorylated NSSR1 in caput epididymis was upregulated in a testosterone dependent manner.

HuD regulates the cpg15 expression via the 3'-UTR and AU-rich element.

The candidate plasticity related gene 15 (cpg15) plays important roles in neural development and plasticity. In the present study, we studied the role of the cpg15 3'-untranslated region (UTR) in regulating the expression of the gene. The results showed that the presence of the 3'-UTR significantly decreases, while loss of a putative AU-rich element (ARE) in the 3'-UTR increases the cpg15 expression, indicating that the 3'-UTR and ARE may be essential for regulation of cpg15 expression.

NSSR1 is regulated by testosterone in the mouse uterus and extensively expressed in endometrial carcinoma.

Neural salient serine/arginine-rich protein 1 (NSSR1) has been found to play important roles in inhibiting alternative splicing during heat shock and mitosis and is predominantly expressed in neural tissues such as cerebral neurons, cerebellar Purkinje cells and bipolar cells of the retina. Recently, NSSR1 has also been shown to be highly expressed in the testes, suggesting its potential roles in reproductive system. In this report, the expression of NSSR1 in the columnar epithelium of the endometrium and gland epithelium during the development of the mouse uterus, the regulation of NSSR1 level by testosterone in the adult mouse uterus, and expression level of NSSR1 in both human endometrial carcinomas and ovarian cancers were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemistry.

The expression pattern of heterogeneous nuclear ribonucleoprotein R in rat retina.

The heterogeneous nuclear ribonucleoproteins (hnRNPs) play important roles in DNA repairing, cell signaling, telomere biogenesis, and in regulating gene expression at both transcriptional and translational levels. In the present study, we demonstrated that the expression of hnRNP-R1 and hnRNP-R2 is developmentally regulated in rat retina. The neural specific isoform hnRNP-R2 is expressed in 7-day postnatal rat retina, but not in the adult retina.

hnRNP-R regulates the PMA-induced c-fos expression in retinal cells.

This study focused on the function of hnRNP-R in the regulation of c-fos expression. We demonstrated that hnRNP-R accelerated the rise and decline phases of c-fos mRNAs and Fos proteins, allowing PMA to induce an augmented pulse response of c-fos expression. Then, we examined the role of the c-fos-derived AU-rich element (ARE) in hnRNP-R-regulated mRNA degradation.

The expression and distribution of neural salient serine/arginine-rich protein 1 in rat retina.

Neural salient serine/arginine-rich protein 1 (NSSR1) expression has been found in mouse cerebral neurons, cerebellar Purkinje cells, pyramidal neurons and granule cells of dentate gyrus and regulates the pre-mRNA splicing of genes important for neural functions. In this study, we demonstrated that NSSR1 is expressed in rat retina and extensively distributed in the outer and inner plexiform layers. Double staining experiments showed that NSSR1 distributed mainly in ON-type bipolar cells and localized in the dendrites, somata and axon terminals.