Metabolic reprogramming and astrocytes polarization following ischemic stroke.

Astrocytes are critical for maintaining neuronal activity. Activation of astrocytes, occurs within minutes from ischemic stroke onset due to ischemic causes and subsequent inflammatory damage. Activated astrocytes, also known as reactive astrocytes, are divided into two different phenotypes: A1 (pro-inflammatory) and A2 (anti-inflammatory) astrocytes.

Anti-Inflammatory Effects of Hydrogen Sulfide in Axes Between Gut and Other Organs.

Hydrogen sulfide (HS), a ubiquitous small gaseous signaling molecule, plays a critical role in various diseases, such as inflammatory bowel disease (IBD), rheumatoid arthritis (RA), ischemic stroke, and myocardial infarction (MI) reducing inflammation, inhibiting oxidative stress, and cell apoptosis. Uncontrolled inflammation is closely related to pathological process of ischemic stroke, RA, MI, and IBD. Solid evidence has revealed the axes between gut and other organs like joint, brain, and heart, and indicated that HS-mediated anti-inflammatory effect against IBD, RA, MI, and ischemic stroke might be related to regulating the functions of axes between gut and other organs.

The Roles of RhoA/ROCK/NF-κB Pathway in Microglia Polarization Following Ischemic Stroke.

Ischemic stroke is the leading cause of death and disability worldwide. Nevertheless, there still lacks the effective therapies for ischemic stroke. Microglia are resident macrophages of the central nervous system (CNS) and can initiate immune responses and monitor the microenvironment.

Neuroinflammation and Post-Stroke Depression: Focus on the Microglia and Astrocytes.

Post-stroke depression (PSD), a frequent and disabling complication of stroke, has a strong impact on almost thirty percent of stroke survivors. The pathogenesis of PSD is not completely clear so far. Neuroinflammation following stroke is one of underlying mechanisms that involves in the pathophysiology of PSD and plays an important function in the development of depression and is regarded as a sign of depression.

Crosstalk Among Glial Cells in the Blood-Brain Barrier Injury After Ischemic Stroke.

Blood-brain barrier (BBB) is comprised of brain microvascular endothelial cells (ECs), astrocytes, perivascular microglia, pericytes, neuronal processes, and the basal lamina. As a complex and dynamic interface between the blood and the central nervous system (CNS), BBB is responsible for transporting nutrients essential for the normal metabolism of brain cells and hinders many toxic compounds entering into the CNS. The loss of BBB integrity following stroke induces tissue damage, inflammation, edema, and neural dysfunction.

Flavonoids and ischemic stroke-induced neuroinflammation: Focus on the glial cells.

Ischemic stroke is one of the most cases worldwide, with high rate of morbidity and mortality. In the pathological process of ischemic stroke, neuroinflammation is an essential process that defines the functional prognosis. After stroke onset, microglia, astrocytes and the infiltrating immune cells contribute to a complicated neuroinflammation cascade and play the complicated roles in the pathophysiological variations of ischemic stroke.

The role of RhoA/ROCK pathway in the ischemic stroke-induced neuroinflammation.

It is widely known that ischemic stroke is the prominent cause of death and disability. To date, neuroinflammation following ischemic stroke represents a complex event, which is an essential process and affects the prognosis of both experimental stroke animals and stroke patients. Intense neuroinflammation occurring during the acute phase of stroke contributes to neuronal injury, BBB breakdown, and worse neurological outcomes.

HS-RhoA/ROCK Pathway and Glial Cells in Axonal Remyelination After Ischemic Stroke.

Ischemic stroke is one of the main reasons of disability and death. Stroke-induced functional deficits are mainly due to the secondary degeneration of the white matter characterized by axonal demyelination and injury of axon-glial integrity. Enhancement of the axonal regeneration and remyelination could promote the neural functional recovery.

HS-mediated inhibition of RhoA/ROCK pathway and noncoding RNAs in ischemic stroke.

Ischemic stroke is one of major causes of disability. In the pathological process of ischemic stroke, the up-regulation of Ras homolog gene family, member A (RhoA) and its downstream effector, Ras homolog gene family (Rho)-associated coiled coil-containing kinase (ROCK), contribute to the neuroinflammation, blood-brain barrier (BBB) dysfunction, neuronal apoptosis, axon growth inhibition and astrogliosis. Accumulating evidences have revealed that hydrogen sulphide (HS) could reduce brain injury in animal model of ischemic stroke via inhibiting the RhoA/ROCK pathway.

RhoA/ROCK signaling pathway and astrocytes in ischemic stroke.

Ischemic stroke is one of the most common and undertreated cerebral diseases with high mortality and disability rate. Various intrinsic and extrinsic factors regulate the onset, severity, and progression of ischemic stroke. As an integral part of the neuronal glia system, astrocytes provide many housekeeping functions in nervous system, and perform multiple functions both beneficial and detrimental for neuronal survival after ischemic stroke.

Neuroprotective roles of total flavones of Camellia on early brain injury andcognitive dysfunction following subarachnoid hemorrhage in rats.

The present study was undertaken to explore the role of total flavones of Camellia (TFC) on cerebral injury following subarachnoid hemorrhage (SAH) in rats. We showed that the increase of malondialdehyde (MDA) level in brain tissues, leakages of neuron-specifc enolase (NSE) and lactate dehydrogenase (LDH) from brain tissues to serum at 48 h after SAH were significantly blocked by TFC treatment. Besides, TFC treatment could reduce brain edema and the Bax/Bcl-2 ratio in hippocampal tissues at mRNA and protein levels at 48 h after SAH.

Distinct Roles of ROCK1 and ROCK2 on the Cerebral Ischemia Injury and Subsequently Neurodegenerative Changes.

Cerebral ischemic injury is one of the main causes of adult disability and death. Although significant progress has been made, cerebral ischemia continues to be a major risk to public health worldwide. The Rho kinase (ROCK) signaling pathway has been reported to be significantly involved in many mechanisms of cerebral injury.

Determining the environmental impact of material hauling with wheel loaders during earthmoving operations.

A method has been developed to estimate the environmental impact of wheel loaders used in earthmoving operations. The impact is evaluated in terms of energy use and emissions of air pollutants (CO, CO, NO, CH, VOC, and PM) based on the fuel consumption per cubic meter of hauled material. In addition, the effects of selected operational factors on emissions during earthmoving activities were investigated to provide better guidance for practitioners during the early planning stage of construction projects.

Establishment of competitive binding assay to detect and differentiate hepatitis E virus infection.

Introduction And Objectives: This study was undertaken to demonstrate a promising approach for detection and differentiation the serum immunoglobulin G (IgG) against hepatitis E virus (anti-HEV IgG) using a competitive binding assay established with known genotype-specific monoclonal antibodies (mAbs) 2B1 and 4C5.

Materials And Methods: The mAb 2B1 derived from genotype 1 hepatitis E virus (HEV) antigen and specifically reacted with genotype 1, 2 antigens; 4C5 induced by genotype 4 HEV antigen was specific to genotypes 3, 4 antigens. The 2B1 and 4C5 were labeled with Horseradish peroxidase (HRP), respectively.

Protective effect of extract of the Camellia japonica L. on cerebral ischemia-reperfusion injury in rats.

Objective: We investigated the protective effect of the extract of the Camellia japonica L. flower on cerebral ischemia-reperfusion injury in rats.

Methods: The rat ischemia-reperfusion injury was induced by middle cerebral artery occlusion for 90 minutes and reperfusion for 48 hours.

Establishment of a Competitive Binding Assay Identifying the Different Characteristics of Neutralizing Epitopes of Hepatitis E Virus.

Aims: To confirm the different characteristics of genotype-specific and common neutralizing epitopes of hepatitis E virus (HEV).

Methods: A competitive binding assay was established with known genotype-common neutralizing monoclonal antibodies (mAbs) 3G1 and 5G5 as well as genotype-specific neutralizing mAbs 2B1 and 4C5. HEV ORF2 recombinant p166W01 derived from genotype 1 and p166Chn derived from genotype 4 were used as coated antigens, to determine whether the mAbs recognize independent, similar, or overlapping epitopes.