[Association analysis of polymorphisms of metabolizing enzyme genes with chronic benzene poisoning based on logistic regression and multifactor dimensionality reduction].

Objective: To explore the association of polymorphisms of metabolizing enzyme genes with chronic benzene poisoning (CBP) comprehensively by case-control design.

Methods: 152 CBP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. 30 single nucleotide polymorphisms (SNPs) in 13 genes such as CYP2E1 were tested by PCR-RFLP, sequencing approaches.

Polymorphisms in phase I and phase II metabolism genes and risk of chronic benzene poisoning in a Chinese occupational population.

It is widely accepted that the cytotoxicity and genotoxicity of benzene results from the action of reactive metabolites. Therefore, genetic variation in metabolic enzyme genes may contribute to susceptibility to chronic benzene poisoning (CBP) in the exposed population. Using a case-control study that included 268 benzene-poisoned patients and 268 workers occupationally exposed to benzene in South China, we aimed to investigate the association between single-nucleotide polymorphisms in genes with phase I and II of metabolism and risk of CBP.

[In vitro evaluation of cutaneous allergic reaction induced by chemicals using dendritic cells].

Objective: To investigate the use of dendritic cells derived from mice bone marrow to evaluate the cutaneous allergic reaction induced by chemical sensitizers.

Methods: Dendritic cells derived from mice bone marrow were cultured and administrated with 2, 4-dinitrochlorobenzene (DNCB), nickel sulfate (NiSO4), sodium dodecyl sulfate (SDS) and hexyl cinnamic aldehyde (HCA), respectively. Cell membrane molecule CD86 and extracellular IL-1 beta, IL-6 and IL-12 were detected after 0, 1, 6, 12, 24, 36, 48 hour's administration, respectively.

[Intervention of nicotinamide on skin melanin genesis after UVA exposed].

Objective: To investigate the interference effect of nicotinamide on UVA-induced melanin genesis and melanin transport in human skin melanocyte.

Methods: The optimum UVA dose expected to cause cell proliferation: 0.2 J/cm(2), nicotinamide was added immediately after the 0.

Genetic polymorphisms in CYP1A1, CYP2D6, UGT1A6, UGT1A7, and SULT1A1 genes and correlation with benzene exposure in a Chinese occupational population.

Metabolic enzymes involved in benzene activation or detoxification, including cytochrome P-450 1A1 (CYP1A1), cytochrome P-450 2D6 (CYP2D6), UDP-glucuronosyltransferase 1A6 (UGT1A6), UDP-glucuronosyltransferase1A7 (UGT1A7), and sulfotransferase 1A1 (SULT1A1), were studied for their roles in human susceptibility to benzene poisoning. All 304 subjects were investigated with a unitary questionnaire and their DNA was isolated from blood samples by a routine phenol-chloroform extraction. The study included 152 benzene poisoning patients, and 152 control workers occupationally exposed to benzene in South China.

[Relationship of genetic polymorphism in APE1 and ADPRT to risks of chronic benzene poisoning].

Objective: To explore the relationship between genetic polymorphisms in apurinic/apyrimidinic endonuclease (APE1) and ADP ribosyltransferase (ADPRT) and individuals' susceptibility to chronic benzene poison ing (BP).

Methods: A case-control study was conducted. One hundred and fifty-two B P patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated.

[Genetic polymorphism of CYP-1A1, CYP2D6 and risks of chronic benzene poisoning].

Objective: To explore the relationship between genetic polymorphisms of CYP-1A1 and CYP2D6 and risks of chronic benzene poisoning (BP).

Methods: A case control study was conducted. 152 BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were involved.

[Relationship between genetic polymorphism in hMTH1c.83, hOGG1c.326 and hMYHc.335 and risks of chronic benzene poisoning].

Objective: To explore the relationship between genetic polymorphisms in hMTH1, hOGG1 and hMYH and risks of chronic benzene poisoning (CBP).

Methods: A case control study was conducted. One hundred and fifty-two BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated.

[The intervention of nicotinamide on skin melanocyte's cell proliferation after UVA (365 nm) exposed.].

Objective: To investigate the interference effect of nicotinamide on UVA-induced cell proliferation in human skin melanocyte.

Methods: To apply the optimum UVA dose expected to cause cell proliferation: 0.2 cm2, nicotinamide was added after the 0.

[Relationship of genetic polymorphism of microsomal epoxide hydrolase with susceptibility of chronic benzene poisoning].

Objective: To explore the relationship between genetic polymorphisms of microsomal epoxide hydrolase (mEH) and susceptibility of chronic benzene poisoning (BP).

Method: A case-control study was conducted. 152 BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated.

[Assessment of exposure to extremely low frequency magnetic field emitted from monitors].

Objectives: To investigate intensity of extremely low frequency magnetic field (ELFMF) emitted from cathode-ray tubes (CRT) of monitors in various directions and to find ways to avoid its influence.

Methods: Two hundred CRT monitors and 10 monitors with liquid-crystal display (LCD) were selected. Their ELFMF was detected for three times in front of the monitor at an interval of every 5 cm from 0 cm to 50 cm, as well as at various directions from the monitor.

Restorative effects of zinc and selenium on cadmium-induced kidney oxidative damage in rats.

Objective: To investigate whether cadmium-induced oxidative stress in the kidney is influenced by zinc and selenium.

Methods: Five groups of rats were maintained: (A) Cd (CdCl2, 400 micrograms.kg-1.