Publications by authors named "Qin-li Zhang"

Objective: To explore the effects of occupational aluminium(Al) exposure on workers' cognition through a longitudinal study.

Methods: The study population consisted of 276 workers in an Al factory. In 2014, we used inductively coupled plasma mass spectrometry (ICP-MS) to determine the plasma aluminium (P-Al) concentration of the workers, and a combined questionnaire to test the workers' cognitive function.

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To evaluate the different characteristics of cognitive impairment caused by occupational aluminium exposure at different ages, we surveyed 1660 workers in Shanxi Aluminium Plant, China, and assessed their cognitive function and plasma aluminium concentration. In multiple linear regression, the scores of the digit-span test (DST) and digit-span backward test (DSBT) were negatively correlated with plasma aluminium concentration when concentration reached 34.52 μg/L in younger group (<40 years), while in the middle-aged group (≥40 years) only found when concentration reached 42.

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The brain is one of organs vulnerable to aluminum insult. Aluminum toxicity is involved in neurobehavioral deficit, neuronal cell dysfunction, and death. The aim of this study are as follows: (1) to evaluate the repairing efficiency of Necrostatin-1 (Nec-1), a cell death inhibitor, and Z-VAD-FMK, a pan-caspase inhibitor, on Al-induced neurobehavioral deficit and neuronal cell death, in order to evidence the cell death inducing ability of aluminum, and (2) to primarily explore the possibility of treating neuronal cell loss-related disease, such as Alzheimer's disease, with Nec-1 and Z-VAD in Al-induced dementia animal model.

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Objective: To explore the effects of exposure to aluminum (Al) on long-term potentiation (LTP) and AMPA receptor subunits in rats in vivo.

Methods: Different dosages of aluminum-maltolate complex [Al(mal)3] were given to rats via acute intracerebroventricular (i.c.

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Objective: To observe the effects of maternal exposure to nano-alumina during pregnancy on the neurodevelopment in offspring mice.

Methods: Female ICR mice began to be exposed to nano-alumina 10 d before mating, and the nano-alumina exposure lasted till offspring mice were born. All the female mice were randomly divided into 5 groups: solvent control group (saline), nano-carbon group (11.

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Objective: To develop a method for simultaneous assay of propulsion and absorption in small intestine.

Methods: The mice were administrated through gastric tube with mixed reagents containing 0.12% phenol red, D-xylose (1.

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Objective: To investigate the brain oxidative stress injury induced by nano-alumina particles in ICR mice.

Methods: Sixty male ICR mice were randomly divided into 6 groups: control group, solvent control group, 100 mg/kg micro-alumina particles group, 3 groups exposed to nano-alumina particles at the doses of 50, 100 and 200 mg/kg. The mice were exposed by nasal drip for 30 days.

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Objective: To investigate the effects of caspase-3 siRNA on the neurobehavior of mice exposed to aluminum.

Methods: Male KunMing mice (3 months old) were randomly divided into 4 groups by weight:blank control group (4 microl normal saline), Al group (4 microl 0.5% AlCl3), Al plus empty vector group(3 microl 0.

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Babesia orientalis is the causative agent of babesiosis in water buffalo (Bubalus babalis, Linnaeus, 1758). In this study, a TaqMan real-time PCR assay was developed for quantitative detection of B. orientalis in water buffalo.

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Objective: To observe the effect of nano-alumina on nerve cell viability through different detection kits of cell viability, using micro-alumina and nano-carbon as controls.

Methods: Primary culturing nerve cells of mouse in vitro, which were exposed to 7 doses of 0 µmol/L, 62.5 µmol/L, 125.

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Objective: To study the effect of necrostatin (Nec-1) on apoptosis induced by aluminum (Al), and approach the mechanism.

Methods: Neural cell death model was made by 4 mmol/L Al treated neuroblastoma cells (SH-SY5Y). Cell viabilities were detected at different concentrations of Al and/or Nec-1.

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Objective: To investigate the changes of mitochondria membrane potential and cytoplasma cytochrome C as the mechanism of neuron apoptosis induced by B(a)P.

Methods: Primary neurons were dissociated from cerebral cortex of 1 - 3 days old SD rats and cultured with DMEM incubator at 37 degrees C. After 5 days' cultivation, the neurons were added S9 and B(a)P, and the concentrations of treated B(a)P were 0, 10, 20 and 40 micromol/L respectively.

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In adult mammals, CNS damage does not repair well spontaneously. The Nogo receptor (NgR) signaling pathway prevents axonal regrowth and promotes neuronal apoptosis. This pathway, and pathways like it, may be part of the reason why nerves do not regrow.

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Objective: To study whether necroptosis exists or not in neural cell death induced by aluminum.

Methods: SH-SY5Y cells were treated with 4 mmol/L AlCl(3) x 6H(2)O The cell viability was determined with CCK-8 kit after treated with Nec-1 at different dosages (0, 30, 60, 90 micromol/L). Mitochondria membrane potential (MMP), content of reactive oxygen species (ROS), and apoptotic rate/necrotic rates were measured with cytometry.

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Objective: To study the role of lipid peroxidation injury and endoplasmic reticulum stress in Al-induced apoptosis.

Methods: Neurons from 0-3 day rats were cultured and treated with different concentrations of AlCl3.6H2O.

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Objectives are to investigate the effects of benzo[a]pyrene (B[a]P) on the autonomic nervous system of coke oven workers. One hundred eighty-four coke oven workers were divided into 3 groups according to their working sites (coke oven bottom group, coke oven side group and coke oven top group), and 93 referents were recruited. B[a]P monitored by air sampling pumps as well as urinary 1-hydroxypyrene (1-OH-Py) was determined by high performance liquid chromatograph with a fluorescence detector (HPLC-FD).

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Objective: To find the optimal design of small interfering RNA compounds, transfection concentration and transfection time to reduce the Al-induced apoptosis in SH-SY5Y cells.

Methods: Three siRNA sequences on bak gene were designed and transfected into SH-SY5Y cells, which were treated at various concentrations of aluminum. Cell viability was detected by CCK-8 kit on different siRNA sequences, various transfection concentrations, and diverse transfection courses.

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77 men working in a university were investigated. Trait and state anxiety were determined by STAI I and STAI II; job strain (job demand/decision latitude), social support and job insecurity were analysed by a 46 item Karasek's questionnaire and subjective symptoms by a 12 item test. The employees of a library (mean age 49 years), in contact with students, showed significantly higher values of job strain, STAI I, STAI II and subjective symptoms than a control group of employees with similar age.

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Objective: To study the role of Bcl-2 and Bax protein contents and their gene expression in Al-induced neurons apoptosis.

Methods: Neurons from 0 - 3 day rats were cultured and treated with different concentrations of AlCl(3 x 6) H2O. The cell apoptosis was observed by the TUNEL method and under the scan electron microscope.

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Objective: To investigate the effect of 1, 2-dichloroethane (1, 2-DCE) on blood brain barrier.

Methods: Acute toxic encephalopathy model was copied with the consecutive static inhalation of 1, 2-DCE. The water content of brain tissue was measured, and the blood brain barrier permeability was detected with lanthanum nitrate.

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Objective: To observe and explore the effect of aluminum on mitochondria in nerve cells of rats.

Methods: Nerve cells of new born rats (1-3 days) were cultured. Ultrastructure of mitochondria, cell death rate (CDR), reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and MTF were performed to investigate the alteration of mitochondrial structure and functions in cultured nerve cells.

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