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ABSTRACT: Deep hypothermic circulatory arrest induce cerebral injury

PROVIDER: PRJNA739516 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14868874_1.fastq.gz	Fastqsanger.gz
	SRR14868874_2.fastq.gz	Fastqsanger.gz
	SRR14868875_1.fastq.gz	Fastqsanger.gz
	SRR14868875_2.fastq.gz	Fastqsanger.gz
	SRR14868876_1.fastq.gz	Fastqsanger.gz

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Project description:deep hypothermic circulatory arrest rats

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Differential expression profiles and functional prediction of tRNA-derived small RNAs in plasma of patients with aortic dissection during deep hypothermic circulatory arrest

Project description:The purpose of this study was to detect the expression profile of tsRNA during deep hypothermia circulatory arrest, and to find possible regulatory factors according to the changes in its expression level, in the hope of providing an effective organ protection strategy for this process.Three blood samples were collected from a central veins line into ethylenediaminetetraacetic acid (EDTA) tubes as follows: T1 (before starting circulatory arrest), T2 (15 min after initiation of DHCA), T3 (after declamping the left common carotid artery and before rewarming). A total of 286 commonly expressed tsRNAs were identified in the T1 and T2 groups, 68 tsRNAs specifically expressed in the T1 group, and 44 tsRNAs specifically expressed in the T2 group. A total of 290 commonly expressed tsRNAs were identified in the T2 and T3 groups, 64 tsRNAs specifically expressed in the T2 group, and 43 tsRNAs specifically expressed in the T3 group. Next, four tsRNAs were selected to be verified by qRT-PCR. In summary, this study innovatively proposed the correlation between the deep hypothermic circulatory arrest process and the expression profile of tsRNA, and evaluated the expression level and regulation mode of tsRNA. A preliminary exploration of its potential biological role in the process of deep hypothermic circulatory arrest has been carried out, which can provide a better basis and a more comprehensive explanation for the organ protection mechanism of deep hypothermic circulatory arrest. And in further research, we are expected to achieve targeted protection of organs by overexpressing or inhibiting the corresponding tsRNA.

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Deletion of LOX-1 has protective effects on ischemic brain damage in the genetic background of stroke-prone spontaneously hypertensive rat

Project description:To explore the impact of oxidized low density lipoprotein receptor 1 (Olr1 aka LOX-1) gene on stroke, we newly generate a LOX-1 deficient strain of the genetic background of stroke-prone spontaneously hypertensive rat (SHRSP). We explored circulatory miRNAs as diagnostic biomarkers for cerebral ischemic injury by microarray analysis in related rat strains.

2020-05-19 | E-MTAB-8389 | biostudies-arrayexpress

Deletion of LOX-1 has protective effects on ischemic brain damage in the genetic background of stroke-prone spontaneously hypertensive rat

2020-05-19 | E-MTAB-8388 | biostudies-arrayexpress

Transcriptional profiling of pig striatum after deep hypothermic cardiac arrest

Project description:Transcriptional profiling of pig striatum after deep hypothermic cardiac arrest

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Transcriptional profiling of pig striatum after deep hypothermic cardiac arrest

Project description:The goal of the study was to identify the gene changes that occur in the striatum of neonatal piglets exposed to cardiopulmonary bypass (CPB) with deep hypothermic cardiac arrest (DHCA) then recovered for 6h. To accomplish our goal, mRNA-seq was performed on RNA isolated from neonatal pigs exposed to either DHCA or sham conditions.

2019-01-15 | GSE120863 | GEO

Differential expression profiles and functional prediction of tRNA-derived small RNAs in plasma of patients with aortic dissection during deep hypothermic circulatory arrest

Project description:Differential expression profiles and functional prediction of tRNA-derived small RNAs in plasma of patients with aortic dissection during deep hypothermic circulatory arrest

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Hypothermic oxygenated machine perfusion promotes mitophagy flux against hypoxia ischemic injury in donation after circulatory death liver

Project description:Hypothermic oxygenated machine perfusion promotes mitophagy flux against hypoxia ischemic injury in donation after circulatory death liver

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Doxycycline alters porcine renal proteome and degradome during hypothermic machine perfusion

Project description:Ischemia/reperfusion injury (IRI) is a hallmark of tissue injury in donation after circulatory death (DCD) kidneys. The implementation of hypothermic machine perfusion (HMP) provides a platform for repair of DCD kidneys. Doxycycline administration has shown protective effects during IRI. Here, we explore the impact of doxycycline on proteolytic degradation mechanisms and the urinary proteome of perfused kidney grafts. Porcine kidneys underwent 30 min of warm ischemia, 24 h of oxygenated HMP (control/doxycycline) and 240 min of ex-vivo reperfusion. A high-efficiency undecanal-based N-termini enrichment workflow (HUNTER) was performed to identify the tissue degradome. In addition, a proteomic analysis was applied on urine samples collected during reperfusion using label-free quantitation (LFQ) mass spectrometry. Hierarchical clustering showed distinctive clustering profiles between urine samples collected at T15 min (metabolism) and T240 min (complement and coagulation). At T10, significantly more degraded proteins were observed in perfusates of the control group. At T240, significantly more degraded proteins were observed in the doxycycline group, indicating that doxycycline alters protein degradation during HMP. In conclusion, doxycycline administration during HMP led to significant proteomic differences including protective effects by attenuating urinary NGAL levels. Ultimately, we unravelled multiple pathways that undergo alterations during machine perfusion that can be targeted to attenuate IRI induced injury.

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Project description:Severe cerebral ischemia caused by events such as ischemic stroke or cardiac arrest is a relatively common and life-threating condition. Those who survive frequently suffer from significant cerebral dysfunction, often with poor outcome. To date the treatment options are limited. Concomitant hyperglycemia is frequently perceived both in focal and global transient ischemia, augmenting the ischemic brain injury as revealed by experimental and clinical studies. The aim with the current study was to improve the understanding of the pathogenesis behind how concomitant hyperglycemia can augment the cerebral injury seen after cerebral ischemia. To that end we performed a global transcriptome analysis of brains from hyperglycemic and normoglycemic pigs after transient global ischemia.

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