Publications by authors named "Hai-Hua Zhao"

Matrix metalloproteinases (MMPs) cleave almost all components of the extracellular matrix (ECM) and cause acute neurovascular disruption and parenchymal destruction. Previously, MMPs inhibition was considered to be a therapeutic strategy in early stages of ischemia. This study was designed to investigate whether early MMPs inhibition could promote the recovery of cerebral ischemia.

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Background: Astrocyte activation is a hallmark of traumatic brain injury resulting in neurological dysfunction or death for an overproduction of inflammatory cytokines and glial scar formation. Both the silent mating type information (Sirt1) expression and mitogen-activated protein kinase (MAPK) signal pathway activation represent a promising therapeutic target for several models of neurodegenerative diseases. We investigated the potential effects of Sirt1 upregulation and MAPK pathway pharmacological inhibition on astrocyte activation in vitro and in vivo.

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Introduction: We describe the location, size, histopathologic aspect and immunohistochemical expression of a rhabdomyomatous mesenchymal hamartoma, with the aim of providing useful information for its correct diagnosis.

Case Presentation: A 31-year-old Chinese man first presented 2 years previously with a solitary subcutaneous mass on the left side of his neck and under his mastoid process; the mass's size was 2 × 2 cm. The mass increased in the size in the past 2 years.

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Article Synopsis
  • Aluminum, a neurotoxin linked to Alzheimer's disease (AD), was shown to cause brain changes similar to AD, including tau hyperphosphorylation in mice.
  • Ginsenoside Rb1, an active component in ginseng, demonstrated neuroprotective effects by improving cognitive function and decreasing tau hyperphosphorylation in mice previously exposed to aluminum.
  • The study suggests that Rb1's protective mechanism involves regulation of specific proteins (p-GSK3 and PP2A), positioning it as a potential preventive treatment for Alzheimer's and related neurodegenerative diseases.
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Excessive accumulation of β-amyloid (Aβ) has been proposed as a pivotal event in the pathogenesis of Alzheimer's disease. Possible mechanisms underlying Aβ-induced neuronal cytotoxicity include oxidative stress and apoptosis. Reactive oxygen species (ROS) have been proposed to be involved in the apoptotic mechanism of Aβ-induced cytotoxicity.

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Article Synopsis
  • Alzheimer's disease (AD) leads to gradual deterioration of learning and memory, and while exercise has shown cognitive benefits, its specific cellular and molecular interactions in AD are not well understood.
  • This study focused on the impact of treadmill exercise on learning and memory in APP/PS1 transgenic mice, a model for Alzheimer's, and found that exercise improved cognitive performance and long-term potentiation (LTP) in these mice, similar to wild-type mice.
  • The results highlight that while exercise enhanced learning and memory through improved LTP, the role of brain-derived neurotrophic factor (BDNF) as a synaptic regulator was significant in wild-type but not in APP/PS1 mice, indicating different underlying mechanisms in Alzheimer’s pathology.
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Recent studies have suggested that inflammation actively participates in ascending aortic aneurysm formation. The aim of the present study was to evaluate the expression changes of adhesion molecules and MMPs in an experimental model of ascending aortic aneurysm induced by ascending aorta banding in Wistar rats. Twelve rats developed aortic dilation after ascending aorta banding treatment, while nine normal animals underwent surgery without banding were used as controls.

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Objective: To investigate the mechanism of the different biological impacts of HBx3'-40, an engineered deletion mutant lacking the last 40 C-terminal amino acids.

Method: Human hepatocellular cells of the line Huh7 were transfected with HBx3'-40 or wtHBx (wild type HBx) constructs. An oligo cDNA microarray containing 21074 human genes and Ests was utilized to examine the different gene expression between HBx3'-40 and paired control wtHBx cells.

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