Search

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is the most serious sequel of acute CO poisoning, with structure or function injury of the brain. LncRNA colorectal neoplasia differentially expressed (CRNDE) aberrant expression was involved in nerve cell injury; however, the mechanism of CRNDE in DEACMP remains elusive. CO poisoning model of Sprague-Dawley rats was established. Neurological function was measured by Morris water maze (MWM) testing. Histopathological condition of brain and hippocampus tissues was observed by hematoxylin and eosin (HE), Nissl, and TUNEL staining. Pro-inflammatory cytokine levels were evaluated by enzyme-linked immunosorbent assay (ELISA). Oxidative damage and apoptosis markers were determined by related detection assays. Cell apoptosis were evaluated by flow cytometry analysis. Luciferase report and RNA immunoprecipitation (RIP) assays were employed to identify the binding relationship of CRNDE and miR-212-5p. CRNDE was significantly increased in CO poisoning animal model and oxygen-glucose deprivation (OGD) group, while that of miR-212-5p was decreased. CRNDE knockdown repressed the histopathological damage and apoptosis of brain and hippocampus tissues. Besides, CRNDE suppressed the AKT/GSK3β/β-catenin signaling pathway via targeting miR-212-5p. Furthermore, the protective effects of CRNDE silencing on brain tissue injury and apoptosis and AKT/GSK3β/β-catenin signaling pathway were reversed by inhibition of miR-212-5p in CO poisoning model. Collectively, CRNDE, serving as a sponge of miR-212-5p, aggravated the injury and apoptosis of brain and hippocampus tissues through regulating AKT/GSK3β/β-catenin signaling pathway under the CO-poisoning and OGD-treated model, suggesting a selected therapeutic target of DEACMP.

Objective Ubiquitin C-terminal hydrolase-L1 (UCH-L1) has been established as a reliable and potential biomarker of neuronal damage after acute neurologic insults, such as ischemic stroke, subarachnoid hemorrhage, and traumatic brain injury. However, the effect of serum UCH-L1 levels has not been investigated in carbon monoxide (CO)-poisoned patients. The aim of the present study was to evaluate whether serum UCH-L1 levels are a reliable marker of brain damage and the association of UCH-L1 with outcome. Design and methods This case–control study enrolled 46 CO-poisoned subjects and 30 controls. Using an enzyme-linked immunosorbent assay (ELISA) kit, we studied the temporal profile of serum UCH-L1 levels at 6, 12, 24 and 48 h after acute CO poisoning. Poisoning severity was assessed using the Glasgow Coma Scale (GCS) score. Long-term outcome was assessed using the Glasgow Outcome Scale (GOS) at 6 months after poisoning. Results Compared with controls, CO-poisoned patients had significantly elevated serum levels of UCH-L1 at each time point after poisoning. There were significantly higher levels of UCH-L1 in CO-poisoned patients with a lower GCS score as well as in those with a poor 6-month outcome dichotomized GOS. Conclusions Serum levels of UCH-L1 appear to have potential clinical utility in providing valuable information about poisoning severity and outcome after CO poisoning.

Acid soil/aluminium toxicity is one of the major constraints on barley production around the world. Genetic improvement is the best solution and molecular-marker-assisted selection has proved to be an efficient tool for developing barley cultivars with acid soil/aluminium tolerance. In this study, barley variety Svanhals—introduced from CYMMIT (International Maize and Wheat Improvement Center)—was identified as acid soil/aluminium tolerant and the tolerance was mapped to chromosome 4H in 119 doubled haploid (DH) lines from a cross of Hamelin/Svanhals. The HvMATE gene, encoding an aluminium-activated citrate transporter, was selected as a candidate gene and gene-specific molecular markers were developed to detect acid soil/aluminium tolerance based on the polymerase chain reaction. Sequence analysis of the HvMATE gene identified a 21-bp indel (insertion–deletion) between the tolerant and sensitive cultivars. The new marker was further mapped to the QTL (quantitative trait loci) region on chromosome 4H for acid soil tolerance and accounted for 66.9 % of phenotypic variation in the DH population. Furthermore, the polymorphism was confirmed in other tolerant varieties which have been widely used as a source of acid soil tolerance in Australian barley breeding programs. The new gene-specific molecular marker provides an effective and simple molecular tool for selecting the acid soil tolerance gene from multiple tolerance sources.

The purpose of this study was to evaluate the efficacy of erythropoietin (EPO) for treating patients with carbon monoxide (CO) poisoning. We conducted a randomized, prospective study of 103 patients with CO poisoning in two groups: an EPO group (n = 54; patients received EPO) and a placebo group (n = 49; patients received normal saline). The study endpoints were the functional outcome at day 30 (the Barthel index and neurologic sequelae), National Institutes of Health Stroke Scale (NIHSS) score, and the levels of S-100β. At 18 days, the NIHSS score improved significantly and S-100β levels significantly decreased in patients in the EPO group. At 30 days, patients in the EPO group had a superior Barthel index and fewer patients had delayed neurologic sequelae (DNS). This study demonstrated that early administration of EPO to patients with CO poisoning improved neurological outcomes and reduced the incidence of DNS.

Background Acid soil is a serious limitation to crop production all over the world. Toxic aluminium (Al) cations in acid soil inhibit root growth and reduce yield. Although a gene tolerant to acid soil has been identified, it has not been used in malting barley breeding, which is partly due to the acid soil tolerance gene being linked to unfavorable malting quality traits. Results A Brazilian malting barley variety Br2 was identified as tolerant to acid soil. A doubled haploid (DH) population was developed from a cross between Br2 and the Australian acid-sensitive cultivar Hamelin. The DH population was tested for acid soil tolerance in native acid soil and a hydroponic system with pH 4.2, pH 4.2 + Al or pH 6.5, and genotyped using SSR, DArT and gene-specific markers. A single QTL was detected for all parameters related to acid soil tolerance. The QTL was mapped to the known HvMATE location on chromosome 4H. Sequence alignment of the HvMATE gene identified 13 INDELs and 87 SNPs, where one SNP coded for a single amino acid difference between the two varieties. A gene-specific marker was developed to detect the single nucleotide polymorphism between Hamelin and Br2. This marker co-segregated with aluminium tolerance and accounted for 79 % of phenotypic variation for acid soil tolerance. Conclusion The present study identified a novel source of acid soil/Al tolerance from a Brazilian malting barley cultivar Br2. This variety tolerated Al toxicity but was sensitive to low pH which is similar to most other Al-tolerant varieties. A gene-specific marker Cit7 was developed based on the HvMATE gene sequence. Cit7 will improve the efficiency of molecular-assisted selection of new barley varieties with tolerance to acid soil. Multiple alleles exist for the acid soil tolerance gene on chromosome 4H, so a malting barley variety that tolerates acid soil could be developed by selecting suitable tolerant alleles. Tolerance to low pH may play an important role for barley to adapt to acid soils. Electronic supplementary material The online version of this article (doi:10.1186/s12863-015-0254-4) contains supplementary material, which is available to authorized users.

The purpose of this study was to evaluate the efficacy of erythropoietin (EPO) for treating patients with carbon monoxide (CO) poisoning. We conducted a randomized, prospective study of 103 patients with CO poisoning in two groups: an EPO group (n = 54; patients received EPO) and a placebo group (n = 49; patients received normal saline). The study endpoints were the functional outcome at day 30 (the Barthel index and neurologic sequelae), National Institutes of Health Stroke Scale (NIHSS) score, and the levels of S-100β. At 18 days, the NIHSS score improved significantly and S-100β levels significantly decreased in patients in the EPO group. At 30 days, patients in the EPO group had a superior Barthel index and fewer patients had delayed neurologic sequelae (DNS). This study demonstrated that early administration of EPO to patients with CO poisoning improved neurological outcomes and reduced the incidence of DNS.