Publications by authors named "Xue-Feng Shen"

Article Synopsis
  • The experiment aimed to study how foliar sprays of 5-aminolevulinic acid (5-ALA) and 2-Diethylaminoethyl hexanoate (DTA-6) affect rice seedlings' growth and salt tolerance under saline conditions.
  • The rice seedlings experienced salt stress which significantly hindered their growth and disrupted their antioxidant system, leading to increased harmful compounds in the plants.
  • Both 5-ALA and DTA-6 treatments improved the rice plants' stress response by enhancing antioxidant enzyme activity and reducing oxidative damage, ultimately allowing better growth and adaptation under salt stress.
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Brain volume decrease in the anterior cingulate cortex (ACC) after lead (Pb) exposure has been linked to persistent impairment of attention behavior. However, the precise structural change and molecular mechanism for the Pb-induced ACC alteration and its contribution to inattention have yet to be fully characterized. The present study determined the role of miRNA regulated synaptic structural and functional impairment in the ACC and its relationship to attention deficit disorder in Pb exposed mice.

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Abnormal tau accumulation in the brain has a positively correlation with neurodegeneration and memory deterioration, but the mechanism underlying tau-associated synaptic and cognitive impairments remains unclear. Our previous work has found that human full length tau (hTau) accumulation activated signal transducer and activator of transcription-1 (STAT1) to suppress N-methyl-D-aspartate receptors (NMDARs) expression, followed by memory deficits. STAT3 also belongs to STAT protein family and is reported to involve in regulation of synaptic plasticity and cognition.

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Lead (Pb) can cause a significant neurotoxicity in both adults and children, leading to the impairment to brain function. Pb exposure plays a key role in the impairment of learning and memory through synaptic neurotoxicity, resulting in the cognitive function. Researches have demonstrated that Pb exposure plays an important role in the etiology and pathogenesis of neurodegenerative diseases, such as Alzheimer's disease.

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An association between artery tortuosity and neuroimaging of cerebral small vessel disease (SVD) has been reported, especially in the posterior circulation. However, few studies involved the whole magnetic resonance imaging (MRI) spectrum of SVD in association with anterior circulation arterial tortuosity. This study aimed to investigate the relationship between internal carotid artery (ICA) tortuosity and the neuroimaging of SVD.

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Understanding the precise intracellular localization of lead (Pb) is a key in deciphering processes in Pb-induced toxicology. However, it is a great challenge to trace Pb , especially in cultured cells. We aimed to find an innovative and efficient approach to investigate distribution of Pb in cells and to validate it through determining the subcellular Pb content.

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Hypoperfusion plays an important role in the pathophysiology of cerebral small vessel disease (SVD). Lenticulostriate arteries (LSAs) are some of the most important cerebral arterial small vessels. This study aimed to investigate whether the number of LSAs was associated with the cerebral perfusion in SVD patients and determine the correlation between the number of LSAs and SVD severity.

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Vascular calcification is part of the atherosclerotic process. Intracranial artery calcification is closely associated with cerebral small vessel disease (SVD). The present study aimed to investigate the distribution pattern of intracranial arterial calcification and its association with magnetic resonance imaging (MRI) markers of SVD in patients with acute ischemic cerebrovascular disease.

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Lead (Pb) is known to impair children's cognitive function. It has been previously shown that developmental Pb exposure alters dendritic spine formation in hippocampal pyramidal neurons. However, the underlying mechanism has not yet been defined.

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Article Synopsis
  • Macrophages and microglia are crucial for the body's response to spinal cord injuries, and modifying their behavior could aid recovery.
  • Low-level laser therapy (LLLT) is a promising noninvasive treatment for neurotrauma, though its effects on macrophage/microglia polarization after spinal cord injury were previously unknown.
  • The study found that LLLT shifted macrophage/microglia towards a protective state, improved neuron survival, enhanced recovery scores, and increased levels of beneficial cytokines like IL-4 and IL-13, suggesting its potential as a treatment for spinal cord injuries.
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Low-to-moderate level developmental and adult lead exposure produces retinal dysfunction and/or degeneration in humans and experimental animals. Although high level in vivo or in vitro lead disrupts blood-brain-barrier tight junctions and increases its permeability, the blood-retinal-barrier (BRB) has not been examined. There were four overall goals.

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As the structural basis of blood-cerebrospinal fluid barrier (BCB), epithelial cells in the choroid plexus (CP) are targets for lead (Pb). Pb is known to accumulate in the CP; however, the mechanism of Pb uptake in the choroidal epithelial cells remains unknown. Recently, hemichannels of Connexin 43 (Cx43), the most ubiquitously expressed gap junction proteins in the CP, were found to be important pathways for many substances.

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Lead (Pb) is an environmental neurotoxic metal. Pb exposure may cause neurobehavioral changes, such as learning and memory impairment, and adolescence violence among children. Previous animal models have largely focused on the effects of Pb exposure during early development (from gestation to lactation period) on neurobehavior.

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Ropivacaine (Ropi), one of the newest and safest amino amide local anesthetics, is linked to toxicity, including the potential for seizures, changes in behavior, and even cardiovascular collapse. Dexmedetomidine (Dex), an α2-adrenergic receptor agonist, has been widely used in anesthesia and critical care practice. To date, the underlying mechanisms of the effects of Dex premedication on Ropi-induced toxicity have not been clearly identified.

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Lead (Pb) has long been recognized as a neurodevelopmental toxin. Developing blood-brain barrier (BBB) is known to be a target of Pb neurotoxicity; however, the underlying mechanisms are still unclear. Recent evidence suggests that intracellular nonreceptor protein tyrosine kinase Src regulates tight junctional proteins (TJPs).

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Exposure of Lead (Pb), a known neurotoxicant, can impair spatial learning and memory probably via impairing the hippocampal long-term potentiation (LTP) as well as hippocampal neuronal injury. Activation of hippocampal microglia also impairs spatial learning and memory. Thus, we raised the hypothesis that activation of microglia is involved in the Pb exposure induced hippocampal LTP impairment and neuronal injury.

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Objective: To investigate the intra-retinal expression of neuroglobin (Ngb) and death of retinal ganglion cells (RGCs) in acute retina ischemia rats.

Methods: It was an experimental study. The acute retina ischemia model was established by specific hypothesised left retina artery of Sprague-Dawley rats.

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Shu-Xue-Tong (SXT) is a traditional Chinese drug widely used to ameliorate stagnation of blood flow, such as brain or myocardial infarction. Whether SXT may have therapeutic value for spinal cord injury (SCI), during which ischemia plays an important role in its pathology, remains to be elucidated. We hypothesized that SXT may promote SCI healing by improving spinal cord blood flow (SCBF), and a study was thus designed to explore this possibility.

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Background: The incidence of spinal injury with spinal cord contusion is high in developed countries and is now growing in China. Furthermore, spinal cord injury happens mostly in young people who have a long life expectance. A large number of patients thus are wheelchair bound for the rest of their lives.

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Age-related macular degeneration (AMD) remains high incidence and accounts for a main cause of blindness in ageing people, but its mechanism is still poorly understood. Ageing and associated dysfunction of retinal pigment epithelial (RPE) cells were believed to be the pathological onset of AMD. 20S proteasome has been tightly correlated with cell ageing due to its fundamental role in maintaining cellular homeostasis, but its implication in the ageing process of human RPE cells was seldom concerned.

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Objective: This study aimed at investigating the effects of vitamin D analogue EB1089 on the proliferation and apoptosis of hepatic carcinoma cells.

Methods: Hepatic carcinoma cell strain G(2) (Hep-G(2)) in which prominent vitamin D receptor (VDR) mRNA could be expressed and the cell strain T (HCC-T) negative in VDR gene expression were incubated in culture media with 100 nmol/L, 10 nmol/L and 1 nmol/L EB1089 for 2 d, 4 d and 6 d, respectively. Survival and proliferation of the cells were detected by blue tetrazolium colorimetric test and plate clone-forming test, the VDR mRNA expression was determined by reverse transcription-polymerase chain reaction (RT-PCR) and apoptosis of the cells was detected by flow cytometry (FCM) and electron microscopy.

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