OBJECTIVETo study the relationship between polymorphisms of MnSOD and the susceptibility of chronic poisoning exposed to manganism occupationally.

METHODSIn a study of case-control, genotypes were determined by PCR-RFLP in 164 patients with chronic occupational mangamism poisoning and 328 controls with age- and sex-matched for MnSOD 9Ala-Val.

RESULTSThere was a significant difference in the frequency of MnSOD 9Ala-Val at V locus mutant allele between cases and controls (χ(2) = 15.225, P < 0.01, 95%CI = 1.43 ∼ 3.00). Individuals with the genotype VV had a 1.30 of risk increase of occupational chronic manganism poisoning compared with the the genotype AV or AA (OR = 2.30, 95%CI = 1.52 ∼ 3.49, P < 0.05).

CONCLUSIONThe MnSOD polymorphisms may be related with the susceptibility to chronic occupational manganism poisoning, the risk of chronic occupational manganism poisoning increases in carriers with genotype VV at MnSOD 9Ala-Val locus.

Adult ; Case-Control Studies ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; Male ; Manganese Poisoning ; genetics ; Middle Aged ; Occupational Diseases ; genetics ; Occupational Exposure ; Polymorphism, Single Nucleotide ; Superoxide Dismutase ; genetics

OBJECTIVETo study therapeutic effects by using different oxygen therapies in rats with acute carbon dioxide poisoning, to select the best oxygen therapy technology for patients with acute carbon dioxide poisoning on the spot.

METHODSSixty healthy male Sprague-Dawley rats were randomized into normal control group, carbon dioxide exposure group, hyperbaric oxygen treatment group (pressure 2 ATA, FiO(2)100%), high concentration of atmospheric oxygen treatment group (FiO(2)50%), low concentration of atmospheric oxygen treatment group (FiO(2)33%). After treated with different oxygen in rats with acute carbon dioxide poisoning, arterial pH, PO2 and PCO2 of rats were detected, in addition observe pathological changes of lung tissue and brain tissue.

RESULTSThe arterial pH (7.31 ± 0.06) and PO2 [(68.50 ± 15.02) mm Hg] of carbon dioxide exposure group were lower than those of control group [pH (7.42 ± 0.02) and PO2 (92.83 ± 8.27) mm Hg], PCO2 [(71.66 ± 12.10) mm Hg] was higher than that of control group [(48.25 ± 2.59) mm Hg] (P < 0.05); the arterial pH (hyperbaric oxygen treatment group 7.37 ± 0.02, high concentration of atmospheric oxygen treatment group 7.39 ± 0.03, low concentration of atmospheric oxygen treatment group 7.38 ± 0.02) and PO2 of oxygen treatment groups [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (82.25 ± 12.98), (84.75 ± 11.24), (83.75 ± 16.77) mm Hg, respectively] were higher than that of carbon dioxide exposure group, PCO2 [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (52.25 ± 4.95), (51.75 ± 4.82), (52.66 ± 5.61) mm Hg, respectively] was lower than that of carbon dioxide exposure group (P < 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 between oxygen treatment groups and control group (P > 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 among oxygen treatment groups (P > 0.05). There was large area of bleeding of lungs in rats with carbon dioxide poisoning, the bleeding of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment was better than the rats with carbon dioxide poisoning, there was no abnormal appearance of lungs in rats with hyperbaric oxygen treatment. The light microscope observation showed that there were diffuse bleeding and exudation of lungs in rats with carbon dioxide poisoning, the bleeding and exudation of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment were better than the rats with carbon dioxide poisoning, there were only minor bleeding and exudation of lungs in rats with hyperbaric oxygen treatment. There was no difference of brain in anatomy and microscopy among all groups, there were no significant bleeding, edema, cell degeneration and necrosis.

CONCLUSIONSLung pathology in acute carbon dioxide poisoning rats with hyperbaric oxygen treatment is better than the rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment, there is no significant difference of effect between high concentration of atmospheric oxygen treatment group and low concentration of atmospheric oxygen treatment group, however, the results of blood gas analysis and lung pathology than the exposure group improved, so qualified medical unit for hyperbaric oxygen therapy as soon as possible, hyperbaric oxygen treatment facilities in the absence of circumstances, the emergency treatment of early oxygen is also a good measure.

Animals ; Carbon Dioxide ; poisoning ; Hyperbaric Oxygenation ; Lung ; pathology ; Male ; Oxygen Inhalation Therapy ; methods ; Rats ; Rats, Sprague-Dawley ; Treatment Outcome

OBJECTIVETo investigate the effects of aluminum on learning and memory and the expression of N-methyl-D-aspartic acid receptor (NMDAR) of hippocampus in offspring from female rats exposed to Al in the pregnancy or lactation, and to explore the mechanism of toxic effects of Al on central nervous system (CNS) during development.

METHODSThe pregnant Wistar rats were randomly divided into 3 groups based on their body weight, i.e. control group was exposed to distilled water, low exposure group (0.2%AlCl3) and high exposure group (0.4%AlCl3) were exposed orally to AlCl3 in pregnancy and lactation for 6 weeks, 10 rats each group. Aluminum content in blood and brains was determined by atomic absorption spectrophotometry (AAS). Platform experiment was used to detect the abilities of learning and memory. The expression levels of NMDARs were detected by western blot assay.

RESULTSThe Al content in blood and brains of rats in exposure groups increased significantly with Al dose, as compared with the control group (P < 0.05). In platform experiment, the incubation periods of rats in low and high exposure groups were (202.71 ± 81.99) and (19.67 ± 8.44) s respectively, which were significantly lower than that [(300.00 ± 0.00) s] in control group (P < 0.01), but the mistake times of rats in low and high exposure groups were 1.43 ± 0.85 and 2.47 ± 0.99 respectively, which were significantly higher than that (0.00 ± 0.00) in control group (P < 0.01). The Al exposure could change the proportion of NMDAR subtypes, the expression levels of NR1 and NR2B in hippocampus of newborn rats in low and high exposure groups were 25.22 ± 0.68, 81.23 ± 15.37 and 24.75 ± 0.71, 56.63 ± 7.82, respectively, which were significantly lower than those (31.69 ± 3.44, 107.61 ± 9.05) in control group (P < 0.05).

CONCLUSIONAluminum exposure in pregnancy and lactation could reduce the abilities of learning and memory in newborn rats, and change the proportion of NMDAR subtypes. The reduced NR1 and NR2B expression levels may be one of important mechanisms to influence the abilities of learning and memory in offspring.

Aluminum ; toxicity ; Animals ; Female ; Hippocampus ; drug effects ; metabolism ; Male ; Maze Learning ; Pregnancy ; Prenatal Exposure Delayed Effects ; metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate ; metabolism

OBJECTIVETo construct DNA methyltransferase 1 (DNMT1) low expression 16HBE cell line and observe the variation of cell cycle and global genomic DNA methylation.

METHODSThe method of Lenti-virus induced RNA interference was applied to introduce four different shRNA fragment into 16HBE cells. Flow cytometry and 5-mC immunofluorescence methods were used to observe the cell cycle and global DNA methylation status of DNMT1 low expression 16HBE cells.

RESULTSThe DNMT1 protein relative expression level of 16HBE-shDNMT1-4 cell line was down regulated about 44% (P < 0.05) compared with the control. No obvious differences of cell cycle and global genome DNA methylation status were observed between the 16HBE and 16HBE-shDNMT1.

CONCLUSIONThe DNMT1 gene low expression cell is successfully constructed, and there are no obvious changes happened on the cell cycle and global genomic DNA methylation.

Cell Cycle ; Cell Line ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases ; genetics ; metabolism ; DNA Methylation ; Down-Regulation ; Epithelial Cells ; metabolism ; Humans ; RNA Interference ; RNA, Small Interfering ; genetics

Humans ; Lung ; cytology ; Macrophages, Alveolar ; Pulmonary Fibrosis ; pathology ; Silicosis ; pathology

Humans ; Male ; Middle Aged ; Pneumoconiosis ; diagnosis

Azabicyclo Compounds ; blood ; Chromatography, Gas ; Humans ; Piperazines ; blood ; Serum ; chemistry

Acute Lung Injury ; etiology ; surgery ; Burns, Inhalation ; surgery ; Humans ; Lung Transplantation ; Male ; Middle Aged ; Respiratory Aspiration ; complications ; Sulfuric Acids ; poisoning

OBJECTIVETo explore the effect of hemoperfusion (HP) on tylenol poisoned patients.

METHODSUrgently established the blood access by transfemoral catheterization of femoral vein, we used charcoal hemoperfusion by blood pump and dynamically monitored the plasma concentration of tylenol active ingredients for the 2 patients and the content of tylenol active ingredients in the charcoal was determined.

RESULTSPlasma concentration of tylenol active ingredients of the 2 patients was declined gradually during and after the HP management. The acetaminophen serum concentration of the case 1 was declined from the 13.4 µg/L at the start of HP to the 5.81 µg/L at the end of HP; and the case 2 was declined from 51.1 µg/L to 22.3 µg/L. The adsorption amount of acetaminophen in the blood perfusion device are respectively 119 542 µg of case 1 and 33 2154 µg of case 2.

CONCLUSIONEarly hemoperfusion should be carried out for acute tylenol poisoning patients if there were indications, hemoperfusion can clear the tylenol active ingredients and this is an effective measure to eliminate tylenol active ingredients.

Acetaminophen ; blood ; pharmacokinetics ; poisoning ; Adult ; Anti-Inflammatory Agents, Non-Steroidal ; blood ; pharmacokinetics ; poisoning ; Drug Overdose ; therapy ; Drug-Related Side Effects and Adverse Reactions ; blood ; Female ; Hemoperfusion ; Humans ; Metabolic Clearance Rate ; Young Adult

OBJECTIVETo summarise the clinical features of 18 cases with acute trichloropropane (TCP) poisoning for improving the diagnosis and treatment of the disease.

METHODSExposure history, clinical manifestations, laboratorial examinations, poisoning causes and treatment were retrospectively reviewed in 18 cases with acute TCP poisoning. The results of peripheral lymphocyte micronucleus tests were compared with the healthy control group (n = 33).

RESULTSThe common clinical symptoms were as following: respiratory symptoms were the earlier one set, such as chest tightness in 13, dry and sore throat in 7, cough and runny nose in 2. Gastrointestinal symptoms were more common, such as abdominal pain in 18, nausea and vomit in 14. Only 1 out of 18 patients was found with liver injury. The major manifestation was the increase in ALT and AST, which was returned to normal after treatment. ALL of the 18 patients were found TCP in their serum which concentration was from 39.0 to 310.0 ng/ml, and the average was (68.9 ± 42.1) ng/ml. The symptoms of toxic peripheral neuropathy were typical in all the patients, such as fatigue and numb limb in 18, burning pain of the distal lower limbs in 14, the symmetrical sock-like sensory dysfunction of pain, touch and vibration of the lower limbs in 13, muscle strength reduced in 7, hyporeflexia knee-jerks in 4, hyporeflexia ankle-jerks in 3. The peripheral nerve conduction velocity (NCV) examinations were as followed: the (sensore-nerve conduction velocity) SCV of peroneus super nerve in 18 and the (motor-nerve conduction velocity) MCV of tibial nerve in 8 was slowed down and the distal latency in 18 was prolonged. Micronucleus were found in all 18 cases. The micronucleus rate was 10.06‰ ± 2.80‰ and 8.24‰ ± 2.67‰ in acute TCP poisoning group and healthy control group, respectively. The difference was significant (P < 0.05).

CONCLUSIONThe common clinical manifestations of respiratory exposure of TCP poisoning patients were respiratory symptoms, gastrointestinal symptoms and the symptoms of toxic peripheral neuropathy. Liver injury in those 18 cases was not obvious. Lymphocyte micronucleus of peripheral blood were found in all 18 cases.

Adolescent ; Adult ; Case-Control Studies ; Female ; Gastrointestinal Diseases ; chemically induced ; diagnosis ; therapy ; Humans ; Male ; Neural Conduction ; Peripheral Nervous System Diseases ; chemically induced ; diagnosis ; therapy ; Respiratory Tract Diseases ; chemically induced ; diagnosis ; therapy ; Retrospective Studies ; Trichloroepoxypropane ; poisoning ; Young Adult