Publications by authors named "Yongnan Hao"

Objectives: This study aimed to investigate the correlations between carotid intima-media thickness (IMT) and systemic immune inflammation index (SII), platelet-to-lymphocyte ratio (PLR), and neutrophil-to-lymphocyte (NLR) ratio.

Materials And Methods: This was a cross-sectional study enrolling a total of 582 middle-aged and elderly patients. The correlations between SII, PLR, and NLR with IMT were assessed using logistic regression models, which were subsequently incorporated into the underlying models with traditional risk factors and their predictive values for IMT.

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In order to explore the epigenetic characteristics of hemorrhagic transformation (HT) after acute ischemic stroke, we used transcriptome sequencing technology to analyze the global transcriptome expression profile of patients with and without HT after acute ischemic stroke and to study the differential expression of messenger RNA (mRNA), long noncoding RNA (lncRNA), circular RNA (circRNA) and mircoRNA (miRNA) between the two groups. To further explore the role of differentially expressed genes in HT, we annotated the function of differentially expressed genes by using gene ontology (GO) and pathway analysis on the results and showed that there were 1,051 differential expressions of lncRNAs, 2,575 differential expressions of mRNAs, 447 differential expressions of circRNAs and 47 miRNAs in patients with HT compared with non-HT patients. Pathway analysis showed that ubiquitin-mediated proteolysis, MAPK signal pathway, axon guidance, HIF-1 signal pathway, NOD-like receptor signal pathway, beta-alanine metabolism, Wnt signal pathway, sphingolipid signal pathway, neuroactive ligand-receptor interaction, and intestinal immune network used in IgA production play an important role in HT.

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Long non-coding RNA MALAT1 was previously revealed to express abnormally in animal and cellular models of stroke, suggesting its indispensable role in stroke. The aims of the present study were to further investigate the functions of MALAT1 and to elucidate the underlying molecular mechanisms. Oxygen glucose deprivation/re-oxygenation (OGD/R) challenge was used in human brain microvascular endothelial cells (HBMECs) to mimic stroke injury in vitro.

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Delayed diagnosis of insulinoma remains an intractable clinical challenge because the symptoms are in most cases misattributed to other disorders. In this study, a 64-year-old man presented with intermittent seizure episodes after being misdiagnosed with epilepsy and receiving anti-epileptic drugs for 4 years. During this period, the patient continued to suffer from repeated seizures.

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BACKGROUND This study investigated the clinical effect of interventional therapy in ischemic cerebrovascular disease (ICD). MATERIAL AND METHODS A retrospective analysis was performed on 260 ICD patients who were divided into a control group (122 patients, conventional drug treatment) and an observation group (138 patients, interventional therapy plus conventional drug treatment). Enzyme-linked immunosorbent assay was used to examine the expression of IL-1β, IL-6, and NLR.

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Stroke is one of the leading causes of death and disability worldwide, and the majority of the cases are ischemic stroke. However, it still lacks effective treatment except for thrombolytic therapy in an extremely narrow time window. Increased evidence suggests that histone deacetylase 4 (HDAC4) was dysregulated in ischemic stroke, which plays a key role in the pathogenesis of ischemic stroke and post-stroke recovery by affecting neuronal death, angiogenesis, and neurogenesis.

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In this study, we investigated the protective effect of l-homocarnosine, l-carnosine, and anserine (HCA) on seizure-induced brain injuries. We evaluated the protective effect of HCA on brain oxidative damage in a pentylenetetrazole (PTZ)-induced epilepsy model using ovariectomized (OVX) rats. The experimental groups were as follows: group I, sham; group II, sham + PTZ; group III, sham + HCA + PTZ; group IV, OVX; group V, OVZ + PTZ; and group VI, OVX + HCA + PTZ.

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The aim of this study was to determine the effects of VEGF treatment on focal cerebral ischemia in rats. Rats were administered PBS or VEGF at concentrations of 10, 20 or 30 µg/ml. The effects of VEGF on the rat infarct volume and neurological deficits were investigated.

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