Underwater shock wave induced lung and brain injuries in canines / 第二军医大学学报

[Abstract] Objective To explore underwater shock wave-induced injuries of the lung and brain in canines. Methods Eighteen Beagle dogs were randomly divided into six groups according to the distances to the explosion source: control group and 5 experimental groups (5 m, 7 m, 9 m, 11 m and 13 m groups). The animals were exposed to underwater shock wave via a self-designed underwater explosive instrument. The dynamic explosive process was recorded by the underwater high-speed camera. Computed tomography (CT) scans of brain and chest were performed 6 h after injury. Pathological examination and H-E staining for hippocampus and lung were conducted 24 h after injury. The expression levels of interleukin (IL)-6, IL-1β, IL-10, tumor necrosis factor α (TNF-α) and transforming growth factor β (TGF-β) in the hippocampus were measured by immunohistochemical staining. Results The underwater high-speed camera showed that the injury process included blast wave and bubble pulsation. The total mortality of the animals was 40.0% (6/15) in the experimental groups. CT examination revealed no major alterations in the brain of the animals, while there were pleural effusion and pneumothorax in the chest of animals in the experimental groups. H-E staining showed inflammatory cells infiltration in the hippocampal tissue and erythrocyte deposition in the alveoli of animals in the experimental groups. The expression levels of IL-6, IL-1β, IL-10, TNF-α, and TGF-β in the hippocampus of animals in the experimental groups were significantly elevated compared with those in control group (all P0.05). Conclusion Brain and chest are damaged significantly after underwater explosion, which may be the main causes for the death of animals. It is important to elucidate the underlying mechanisms of brain injury caused by underwater explosive wave for the protection of underwater blast injuries.

Expression of protein p53 in workers occupationally exposed to benzidine and bladder cancer patients / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study expression of mutant p53 protein in workers occupationally exposed to benzidine and bladder cancer patients.</p><p><b>METHODS</b>Mutant p53 protein in serum from the workers occupationally exposed to benzidine and bladder cancer patients were determined with Immuno-PCR, while exfoliated urothelial cells in the urine samples were classified with Papanicolau grading.</p><p><b>RESULTS</b>Positive rate of mutant p53 protein increased with the exposed intensity index in workers occupationally exposed to benzidine. The positive rate of mutant p53 protein in bladder cancer patients (83.3%) was significantly higher than that in the group 1 of exposed intensity index. The average scanning integrals of PCR amplified band in the group of bladder cancer patients and group 2 of exposed intensity index were both higher than that in the group 1 significantly. Workers in the groups of different exposed intensity indices were further stratified according to Papanicolau grades. In the group 2 of exposed intensity index, the average scanning integrals of PCR amplified band in the stratum of Papanicolau grade II and III were significantly higher than that in the strata of Papanicolau grade I. And in the group 3 of exposed intensity index, the positive rate of mutant p53 protein in the strata of Papanicolau grade III was higher than that in the strata of Papanicolau grade I significantly.</p><p><b>CONCLUSION</b>The increase of exposed intensity may not only result in the positive rate of mutant p53 protein, but also the quantity of mutant p53 protein in serum within the low range of benzidine exposure. Once the exposed intensity was beyond that spectrum, the positive rate of mutant p53 protein in serum and the average scanning integrals of PCR amplified band were no longer enhanced with the increase of exposed intensity. There was tight correlation between Papanicolau grade of exfoliated urothelial cells and the positive rate or the quantity of mutant p53 protein for the higher benzidine exposure intensity.</p>

Polymorphism of N-acetyltransferase 2 (NAT2) gene polymorphism in shanghai population: occupational and non-occupational bladder cancer patient groups / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Arylamine N-acetyltransferases (NATs) are involved in the detoxification of aromatic amines and hydrazine. In order to explore the possible association of NAT2 polymorphism with bladder cancer risk in benzidine exposed or non-exposed Chinese individuals, healthy subjects, subjects with bladder cancer of a former benzidine exposed cohort in Shanghai dyestuff industry and a group of bladder cancer patients without known occupational exposure to aromatic amines were genotyped for NAT2 gene polymorphism.</p><p><b>METHODS</b>NAT2 genotyping was performed with a set of RFLP procedures at seven major polymorphic loci of gene coding area: G191A, C282T, T341C, C481T, G590A, A803G and G857A.</p><p><b>RESULTS</b>The wild allele NAT2 *4 was the most prevalent allele (59%) in healthy individuals. The alleles NAT2*6A and NAT2*7B were also frequently observed (21% and 17%, respectively). In contrast to Caucasians, the percentage of slow acetylators was lower (12% in Chinese vs. 58% in Caucasians, P < 0.001). No relevant differences were observed for homogenous rapid, heterogeneous rapid/slow and homogeneous slow acetylation genotypes between the healthy subjects and both groups of bladder cancer patients.</p><p><b>CONCLUSION</b>The present work did not support the association of slow acetylating genotypes of NAT2 gene with elevated risk of bladder cancer in Chinese whereas it was documented as an important genetically determined risk factor in Caucasians. Different mechanisms might play a role in individual susceptibility to bladder cancer related with aromatic amine exposure in various races or ethnic groups.</p>

Polymorphism of glutathione S-transferase T1, M1 and P1 genes in a Shanghai population: patients with occupational or non-occupational bladder cancer / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>Glutathione S-transferases are involved in the conjugation of xenobiotics. To explore whether GSTs polymorphisms are involved in the development of occupational or non-occupational bladder cancer, polymorphism frequencies of GSTT1, M1 and P1 were investigated in a normal population, which had been settled in a rural area in Shanghai suburb for at least 5 generations as well as in a group of patients with benzidine exposure related occupational bladder cancer in Shanghai dyestuff industry and a group of patients with non-occupational bladder cancer.</p><p><b>METHODS</b>PCR based procedures were performed in the study populations to confirm the genotypes of GSTT1, M1 and P1.</p><p><b>RESULTS</b>The polymorphisms at locus of GSTP1-A1578G in the normal population differed significantly from those in Caucasians or African Americans. All the subjects genotyped so far (n = 118) bore only homogenous wild genotype (C2293/C2293) at GSTP1-C2293T locus. This locus seemed to be a monomorphic in Shanghai population. No significant difference in GSTT1 and GSTM1 polymorphic form frequencies could be confirmed among three groups of subjects. An overrepresentation of GSTP1 AG or GG genotype corresponding a less stable and less effective isozyme protein was detected in patients with benzidine related occupational bladder cancer, compared with that in the normal population though a statistical significance was not yet reached (P = 0.09, OR = 1.96, 95% CI 0.89-4.32).</p><p><b>CONCLUSION</b>This study suggests that GSTM1 or GSTT1 homozygous deficiency genotypes and their combination do not have a clear impact on bladder cancer incidence in a Shanghai population. It seems that GSTP1 polymorphism is not associated with non-occupational bladder cancer. GSTP1 AG or GG genotype has a higher frequency in the patients with benzidine related occupational bladder cancer, and further work is needed to confirm if GSTP1 AG or GG genotype plays a role in the development of occupational bladder cancer.</p>