China ; epidemiology ; Humans ; Occupational Diseases ; epidemiology ; prevention & control ; Surveys and Questionnaires ; Trimethyltin Compounds ; analysis ; poisoning

Chromatography, Gas ; Humans

Chlorine ; Computer Simulation ; Computers, Analog ; Diffusion ; Software

Adult ; Dimethylformamide ; analysis ; toxicity ; Dose-Response Relationship, Drug ; Humans ; Liver ; drug effects ; Male ; Middle Aged ; Occupational Exposure ; statistics & numerical data ; Physical Examination ; statistics & numerical data

Acetamides ; metabolism ; toxicity

Noise, Occupational ; prevention & control ; Occupational Health Services ; standards ; Threshold Limit Values

Female ; Humans ; Infant, Newborn ; Maple Syrup Urine Disease ; diagnosis ; therapy

OBJECTIVETo evaluate the effects of prenatal stress on neurological functions after middle cerebral artery occlusion (MCAO) in adult offspring rats.

METHODSPregnant rats were randomly assigned to prenatal stress treatment, which was exposed to restraint three times daily in the last week of pregnancy, and no prenatal stress treatment. Adult male offspring rats were subjected to transient focal cerebral ischemia by MCAO. They were randomly divided into four groups: sham group, prenatal stress + sham group, MCAO group and prenatal stress + MCAO group (n = 10). After 24 hours of reperfusion, the neurological deficits were evaluated. The infarct size, cell apoptosis and expression of Caspase 3, cleaved Caspase 3 and Bcl-2 were detected.

RESULTSCompared with MCAO group, the neurological deficits, infarct size and apoptotic cells in prenatal stress + MCAO group were increased significantly (all P < 0.05). The expressions of Caspase 3 and cleaved Caspase 3 were much greater in prenatal stress + MCAO group than those of MCAO group, while the expression of Bcl-2 was significantly decreased in prenatal stress + MCAO group compared with MCAO group (all P < 0.05).

CONCLUSIONPrenatal stress might exacerbate neuroloeical deficits in the offspring rats after MCAO by increasing cell apoptosis.

Animals ; Apoptosis ; Caspase 3 ; metabolism ; Female ; Infarction, Middle Cerebral Artery ; physiopathology ; Ischemic Attack, Transient ; physiopathology ; Male ; Pregnancy ; Prenatal Exposure Delayed Effects ; physiopathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological

Objective To explore the influence of the lactation exposure to fluoxetine on offspring's behavior and serotonin transporter (SERT) and tryptophan hydroxylase (TPH). Methods Six SD pregnant rats were randomly divided into 2 groups (n=3 each group). Experimental maternal rats were intraperitoneally injected with fluoxetine at a dose of 12 mg/kg from postnatal day 5 to 21. The control group were injected with the same amount of normal saline. In infancy, the offspring's weight, hair length, eye opening and auditory development were measured. The free suspension test and bur?ied food pellets test were applied to evaluate the offspring's behaviors. After postnatal day 21, all the offspring were wean. At early childhood (P35d) and adulthood (P75d), 6 offspring rats from each group were executed to examine SERT and TPH in the prefrontal cortex by immunohistochemistry. Results The offspring's weight of experimental group was significantly lower than control group (P<0.05). The sensitivity of auditory in experimental group was significantly higher than control group (P<0.01). The time of free suspension in experimental group significantly was decreased comparing to control group (P<0.01). The SERT and TPH in prefrontal cortex was significantly lower in experimental group than those in control group either at childhood (P35d) or at adulthood (P75d) (P<0.05). Conclusion Lactation exposure to fluoxetine re?sults in offspring's abnormal development and behaviors through down-regulation of SERT and TPH in the prefrontal cor?tex.

Air ; analysis ; Chromatography, Gas ; methods ; Ethylene Oxide ; analysis ; Furans ; analysis ; Methylene Chloride ; analysis ; Workplace