Silencing of LINC00707 Alleviates Brain Injury by Targeting miR-30a-5p to Regulate Microglia Inflammation and Apoptosis.

The role of microglia in traumatic brain injury (TBI) has gained considerable attention. The present study aims to elucidate the potential mechanisms of Long intergenic non-protein coding RNA 707 (LINC00707) in TBI-induced microglia activation and inflammatory factor release. An in vivo model of rat TBI and in vitro microglia model was established using Controlled cortex injury (CCI) and lipopolysaccharide (LPS) stimulation. RT-qPCR to detect LINC00707 levels in rat cerebral cortex or cells. Modified Neurological Impairment Score (mNSS) and Morris Water Maze test was conducted to assess the neurological deficits and cognitive impairment. ELISA analysis of pro-inflammatory factors levels. CCK-8 and flow cytometry for cell viability and apoptosis levels. Dual-luciferase report and RIP assay to validate the targeting relationship between LINC00707 and miR-30a-5p. LINC00707 was elevated in the TBI rat cerebral cortex and LPS-induced microglia, while miR-30a-5p was noticeably decreased (P < 0.05). Increased mNSS, cognitive dysfunction, and brain edema in TBI rats were all prominently reversed by silencing of LINC00707, but this reversal was partially abrogated by decreasing miR-30a-5p (P < 0.05). Inhibition of LINC00707 suppressed the overproduction of inflammatory factors in TBI rats (P < 0.05). LPS decreased microglial cell viability, increased apoptosis, and promoted inflammatory overproduction than control, but the silencing of LINC00707 reversed its effect. Suppression of miR-30a-5p attenuated this reversal (P < 0.05). miR-30a-5p was the target miRNA of LINC00707. All in all, the results suggested that inhibiting LINC00707/miR-30a-5p axis could alleviate the progression of TBI by suppressing the inflammation and apoptosis of microglia cells.

Novel Mechanisms and Therapeutic Targets for Ischemic Stroke: A Focus on Gut Microbiota.

Ischemic stroke is the most common type of stroke with limited treatment options. Although the pathological mechanisms and potential therapeutic targets of ischemic stroke have been comprehensively studied, no effective therapies were translated into clinical practice. Gut microbiota is a complex and diverse dynamic metabolic ecological balance network in the body, including a large number of bacteria, archaea, and eukaryotes. The composition, quantity and distribution in gut microbiota are found to be associated with the pathogenesis of many diseases, such as individual immune abnormalities, metabolic disorders, and neurodegeneration. New insight suggests that ischemic stroke may lead to changes in the gut microbiota and the alterations of gut microbiota may determine stroke outcomes in turn. The link between gut microbiota and stroke is expected to provide new perspectives for ischemic stroke treatment. In this review, we discuss the gut microbiota alterations during ischemic stroke and gut microbiota-related stroke pathophysiology and complications. Finally, we highlight the role of the gut microbiota as a potential therapeutic target for ischemic stroke and summarize the microbiome-based treatment options that can improve the recovery of stroke patients.

Laser ranging at few-photon level by photon-number-resolving detection.

Sensitive laser ranging was demonstrated at few-photon level using photon-number-resolving (PNR) detectors. The reflected photon pulses from a non-cooperation remote target were distinguished in a sunlight environment of 2.5×103 lx by setting the discrimination threshold at 5-photon level. By comparing the detected photon numbers, two remote targets with different reflection coefficients were well recognized. PNR detection facilitated remote laser ranging of few-photon sensitivity with similar capabilities of linear optical detectors. This technique avoids photon-counting saturation and is important for ultra-long distance LIDAR and 3D imaging at a few photon level.