Special Computed Tomography Imaging Features of Thymic Cyst.

Objective: To explore the features and diagnostic value of computed tomography (CT) imaging in cases of thymic cysts. Methods: A total of 24 cases of the thymic cysts (confirmed by postoperative pathology) were retrospectively analyzed. The location, morphology, and density of the thymic cysts were summarized, and the changes in CT value of the region of interest (ROI) in the thymic cysts between noncontrast enhanced and enhanced chest scans were compared and classified. Results: The average long-axis dimension was 17.50 ± 6.00 mm, the CT value range across the 24 cases was 5-81 HU, and the average CT value of the noncontrast enhanced scans was 39.75 ± 20.66 HU. The CT value in the noncontrast enhanced scan was >20 HU in 79% of the sample cases. The CT value in the ROI of the thymic cysts under enhanced scan showed a significant decrease in 15 cases, a significant increase in 5 cases, and an insignificant change in 4 cases. Conclusion: The CT values of the thymic cysts in the enhanced scans were generally lower than in the noncontrast enhanced scans, which might be a valuable finding for thymic cysts diagnosis.

Abnormal expression of MAPK, EGFR, CK17 and TGk in the skin lesions of chloracne patients exposed to dioxins.

OBJECTIVE: Chloracne is one of the most sensitive and specific hallmark of dioxin intoxication. Although its clinical features are clearly described, poor understanding of the molecular pathways of dioxin-induced chloracne hampers a rational approach to therapy. The aim of the present study was to investigate the role of EGFR, MAPK, CK17, and TGk in the pathogenesis of chloracne related to dioxin exposures. METHODS: Epidermal tissues of twelve chloracne patients exposed to dioxins were compared with tissues from 12 healthy controls. These skin tissues were obtained by punch biopsies. p-EGFR and p-MAPK were examined by immunofluorescence. The mRNA and protein levels of CK17 and TGk were examined by fluorescence in situ hybridization and immunohistochemistry, respectively. RESULTS: p-EGFR and p-MAPK were found in all chloracne tissues, whereas no expression was found in the controls. CK17 mRNA and protein were also found in all chloracne lesions, but none in controls (P=0.000). TGk mRNA and protein were detected in both groups, but the distribution was distinct. The positive signals in the controls were mainly in the stratum granulosum, while in the chloracne tissues, the positive signals were found more significantly in the stratum granulosum and stratum spinosum. CONCLUSIONS: The results demonstrate that in the human skin the activation of mitogen-activated protein kinase pathway and up-regulation of CK17 and TGK may play roles in the pathogenesis of chloracne related to dioxin exposures.

[Association of the glycophorin A gene mutation in peripheral erythrocytes and chronic benzene poisoning].

OBJECTIVE: To explore the association of the glycophorin A(GPA) gene mutation in peripheral erythrocytes and chronic benzene poisoning. METHODS: Sixty-three patients with chronic benzene poisonings and 45 benzene-exposed workers who were engaged in the same job title were investigated. Fluorescence immunolabeling technique and flow cytometry were used to detect GPA mutation frequency in peripheral read blood cell. RESULTS: A significant decrease in WBC count and neutrophil count was found in patients with chronic benzene poisoning compared with control individuals (P<0.01). The WBC count and neutrophil count both decreased along with the GPA-NN frequency, and the trends were significant(P<0.05).Both WBC counts and neutrophil counts decreased as the frequency, and trends were significant(P<0.05). GPA-NN frequency increased along with the accumulative exposure score, and the trend was significant (P = 0.0026). There was no significant trend between the GPA-Nphi frequency and the accumulative exposure score (P = 0.2037). CONCLUSION: A decrease in WBC count and neutrophil count is found in patients with chronic benzene poisoning, which can arise from genetic damage in bone marrow stem cells, namely gene-duplicating mutations (NN) at the GPA locus in bone marrow cells of MN-heterozygous subjects, GPA-NN mutagens contributed to the pathogenesis of chronic benzene poisoning.

[Study on repair capacity of DNA damage associated with chronic benzene poisoning].

OBJECTIVE: To explore the repair capacity of DNA damage associated with chronic benzene poisonings. METHODS: 63 workers suffered from chronic benzene poisonings and 45 workers exposed to benzene, who were engaged in the same job title, were investigated. Comet assay and cytokinesis-block micronucleus (CBMN) detection were used to evaluate gamma-radiation-induced DNA and chromosomal damage and repair capacity in peripheral blood lymphocyte. RESULTS: The comet tail length difference of the benzene poisoning group (4.64 +/- 1.57 microm) was significantly higher than that of the control group (3.77 +/- 1.30 microm) (P = 0.0029). There was no significant difference of the 3AB index between the poisoning group and the control group. The relative risk of benzene poisoning in the subject with comet tail length difference > 3.81 was significantly higher than that in the subject with comet tail length difference < or = 3.81 microm (OR = 2.490, 95% CI:1.068 - 5.806, P = 0.0346). The relative risk increased along with the comet tail length difference, and the trend was significant (P = 0.0024). There was no significant difference between the relative risk of benzene poisoning in the subject with 3AB index < 0.20 and that in the subject with 3AB index > or = 0.20. CONCLUSION: DNA repair capacity on DNA-strand level might tightly associate with chronic benzene poisoning. The DNA repair capacity on DNA-strand level would be worse, and the benzene poisoning risk could be higher. There was no clear relation between the DNA repair capacity on chromosome level and the benzene poisoning risk.

[Detection of DNA damages of peripheral white blood cells in benzene-exposed workers].

OBJECTIVE: To investigate the effect of benzene exposure on DNA damage of the peripheral white blood cells and to assess the possible dose-response relationship between benzene and DNA damage. METHODS: Personal benzene exposure was sampled with 3M organic vapor monitors. The time weighted average concentration (8h-TWA) and the cumulative dose were calculated. Single cell gel electrophoresis assay was used to detect DNA damage in white blood cells of benzene-exposed workers. The Olive tail moment and the grade of DNA breakage were used to measure DNA damage. RESULTS: The Olive tail moment and the grade of DNA breakage in benzene exposure groups were significantly increased in comparison with those in the control group (F = 30.03, P < 0.0001, chi2 = 239.9, P < 0.0001, respectively) and showed a dose-response relationship with benzene concentration. Correlation analysis showed that Olive tail moment was correlated with benzene exposure concentration. CONCLUSIONS: Benzene exposure resulted in an increase of DNA damage of the peripheral white blood cell, which was in a dose-response relationship manner; cumulative dose was better than simply concentration to reflect benzene exposure.

[Genetic polymorphisms of NQO1, GSTT1, GSTM1 and susceptibility to chronic benzene poisoning].

OBJECTIVE: To explore the relationship between genetic polymorphism of quinone oxidoreductase 1 (NQO1), glutathione S-transferase theta 1 (GSTT1), glutathiones S-transferase mu 1 (GSTM1) and susceptibility to chronic benzene poisoning (BP). METHODS: The genotypes of NQO1, GSTT1, GSTM1 for 100 patients with benzene poisoning and 90 workers exposed to benzene who were engaged in the same working time and job title as patients with benzene poisoning were detected by PCR-RFLP and multi-PCR. RESULTS: There was a 2.82-fold (95% CI: 1.42 approximately 5.58, P < 0.05) increased risk of BP in the subjects with NQO1 C609T mutation genotype (T/T) compared with those carrying heterozygous (C/T) and wild type (C/C), and there was a 2.94-fold (95% CI: 1.25 approximately 6.90, P < 0.05) increased risk of BP in the subjects with NQO1 C609T T/T genotype compared with those carrying C/C genotype. The subjects with GSTT1 null genotype had a 1.91-fold (95% CI: 1.05 approximately 3.45, P < 0.05) increased risk of BP compared with those with GSTT1 non-null genotype. The interaction of two genes showed that there was a increased risk of BP in subjects with any two genotypes of NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype, compared to the individual with any two genotypes of NQO1 C609T C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype. The interaction of three genes showed that there was a 20.41-fold (95% CI: 3.79 approximately 111.11, P < 0.01) increased risk of BP in subjects with NQO1 C609T T/T genotype and GSTT1 null genotype and GSTM1 null genotype compared with those carrying NQO1 C609T C/T genotype and C/C genotype and GSTT1 non-null genotype and GSTM1 non-null genotype. CONCLUSIONS: The interaction of multi-genes may be an important role to BP. The genetic polymorphisms of 3 genes (NQO1, GSTT1 and GSTM1) led to declining of detoxifying ability in benzene metabolism, so the individual with NQO1 C609T T/T genotype, GSTT1 null genotype and GSTM1 null genotype is most susceptive to benzene. The results were consistent with that of the theoretic presumption. It could be suggested as a biomarker to assess the risk of benzene poisoning for individuals.

[Effects of pyrethroids on the activity of gamma-aminobutyric acid transferase in rat brain].

OBJECTIVE: To study the effects of pyrethroids on the activity of gamma-aminobutyric acid transferase (GABAT) in rat brain. METHOD: The coupled enzyme ultraviolet spectrophotography was applied to observe the effects of deltamethrin (DM) and permethrin (PM) on the activities of GABAT in rat cerebral cortex, hippocampus, corpus striatum and cerebellum in vitro and in vivo. RESULTS: In vitro, DM and PM had no significant effects on the activities of GABAT in rat cerebral cortex, hippocampus, corpus striatum and cerebellum at the final concentration of 10(-9) - 10(-4) mol/L. When 37.5 mg/kg DM and 600 mg/kg PM were orally administrated to the rats at one time, the activities of GABAT in rat cerebral cortex, hippocampus and cerebellum in the DM group [(2.96 +/- 0.43), (2.13 +/-0.44), (5.12 +/- 1.36) nmol x mg pro(-1) x min(-1), respectively] were lower than those in the control group [(3.43 +/- 0.41), (2.68 +/- 0.47), (6.74 +/- 1.64) nmol x mg pro(-1) x min(-1)] (P < 0.05), and the activities of GABAT in rat cerebral cortex and hippocampus in the PM group [(4.57 +/- 0.30), (4.18 +/- 0.63) nmol.mg pro(-1) x min(-1), respectively] were higher than those in the control group (P < 0.05). When 12.5 mg/kg DM and 200 mg/kg PM were orally administrated to the rats once a day for consecutive five days, the two pesticides had no significant effects on the activities of GABAT in rat cerebral cortex, hippocampus, corpus striatum and cerebellum (P > 0.05). CONCLUSIONS: In vitro, DM and PM had no significant effects on the activity of GABAT in rat brain; in vivo, DM and PM may have different effects on the activity of GABAT in rat brain, which deserve further study.