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1.
Journal of Breast Cancer ; : 157-161, 2012.
Artigo em Inglês | WPRIM | ID: wpr-210072

RESUMO

PURPOSE: Although the etiology of breast cancer is multifactorial, oxidative stress plays an important role in carcinogenesis. In this study, manganese superoxide dismutase (MnSOD) gene polymorphism and activity were evaluated in benign and breast cancer tissue. METHODS: One hundred and one females were enrolled in this study, 65 who were histopathologically diagnosed with breast cancer and 46 who were benign patients. MnSOD enzyme activity was determined using an indirect competitive inhibition assay and MnSOD gene polymorphism using poly merase chain reaction and agarose gel electrophoresis. RESULTS: MnSOD enzymatic activity (79.83+/-42.14) was lower in breast cancer tissue compared to benign tumors (236.18+/-46.37). At the same time, MnSOD enzymatic activity among Ala/Val patients was significantly lower in breast cancer tissue (39.19+/-7.33) than in Val/Val malignant breast tumors tissue (96.9+/-22.9). MnSOD enzymatic activity was significantly lower in Val/Val cancer tissue (96.9+/-22.9) than in benign tissue (255.44+/-42.7). CONCLUSION: Breast cancer tumors contain less MnSOD than benign breast samples. Patients with Ala/Val polymorphism had reduced MnSOD activity compared to patients with Val/Val breast cancer. Ala/Val gene polymorphism may be a risk factor associated with more advanced breast cancer stage. MnSOD gene polymorphism Ala/Val may be a risk factor associated with more advanced breast cancer stage, and reduction of MnSOD activity may be a mechanism of the progression of benign to malignant tumors. Further investigations are needed to evaluate the role of MnSOD in breast cancer progression.


Assuntos
Feminino , Humanos , Mama , Neoplasias da Mama , Manganês , Estresse Oxidativo , Fatores de Risco , Sefarose , Superóxido Dismutase
2.
Journal of the Royal Medical Services. 2008; 15 (3): 17-21
em Inglês | IMEMR | ID: emr-116873

RESUMO

To detect and evaluate the role of the newly recognized human coronavirus [HCoV]-NL63 and HCoV-HKUl as aetiologic agents of acute respiratory tract infections in hospitalized Jordanian children younger than 5 years of age. Between December 2003 and May 2004, a total of 326 nasopharyngeal aspirates were collected from Jordanian children hospitalized with acute respiratory tract infections. Total DNA and RNA were extracted using Qiagen commercial kits. HCoV-NL63 and HCoV-HKUl were detected by random reverse transcription-polymerase chain reaction using random hexamer primer for the reverse transcription step, and specific primers that target the replicase and polymerase genes to produce 215-bp and 392-bp amplicons respectively. Other potential respiratory pathogens w7ere detected according to previously published protocols. HCoV-NL63 was detected in 4 [1.2%] out of 325 examined nasopharyngeal aspirates. HCoV-NL63 was detected in two children with severe, and in two with mild to moderate acute respiratory tract infections. HCoV-NL63 was the only pathogen detected in three patients, and mixed with adenovirus in one patient. HCoV-HKUl was not detected in the 325 nasopharyngeal aspirates examined. HCoV-NL63 is a significant causative agent of acute respiratory tract infections in hospitalized Jordanian children. HCoV-NL-63 can cause the respiratory disease either alone or in combination with other potential respiratory pathogens. Further studies are required to further characterize the clinical and epidemiological features of these newly recognized HCoVs in Jordan

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