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Questions to compare localized and globalized distribution transformer supply has contributed to debate around the ‘Transformer Miles’ concept, i.e., ‘the distance a distribution transformer (raw materials and the finished unit) travels, from the supplier/factory to factory/installation site”. A relatively new question related to this issue seeks to answer the question of carbon footprint due to the transportation of raw materials to the factory and delivery of the finished transformer to the end user. Within this framework, this article investigates the question - What is the carbon footprint due to transportation: distribution transformers made in New Zealand (as an example), in comparison with importing distribution transformers from overseas into New Zealand? Are there advantages or otherwise from a carbon footprint point of view?

The design of transformers with a low carbon footprint is a topic that is gaining significant traction in the electricity industry. In this article, an investigation is conducted for a 50/62.5 MVA, 154/33.6 kV transformer to evaluate the effect of the No Load Capitalization Factor (A) and Load Capitalization Factor (B) on the carbon footprint of the transformer. The benefit of including the cost of CO2 in the Total Cost of Ownership (TCO) formula, i.e., the extended TCO concept, is highlighted, which results in a similar carbon footprint but with reduced material usage.

To find a possible association between the Mouse Double Minute 2(MDM2) 344TA, alone and in combination with p53 72 Arg/Pro polymorphism, and resistance to anthracycline-based chemotherapy of breast cancer in Tunisia.This study enrolled 542 patients with invasive ductal carcinoma (IDC) treated with anthracycline-based chemotherapy. Genomic DNA was isolated from whole blood, using the phenol chloroform method. Anthracycline response was scored according to the World Health Organization (WHO). MDM2 344TA polymorphism was genotyped using real time polymerase chain reaction (RT-PCR) with the TaqMan method. Data was statistically analyzed using the x2 test.Response was evaluated in 400 patients, of whom a quarter was found to be resistant to chemotherapy. Genetic data revealed that resistance to anthracycline-based chemotherapy did not seem to be correlated with 344TA polymorphism in the studied population. Also, no significant association was found between the single nucleotide polymorphism (SNP) 344TA status and clinicopathologic parameters (p0.05 for all comparisons). Moreover, analysis of p53 rs1042522 and MDM2 rs1196333 combination showed no significant association between these two genetic variants and anthracycline resistance (p=0.2).Our findings provide no evidence indicating that SNP 344 TA may affect response to anthracycline-based chemotherapy. However, the results obtained from the combination of SNPs 344TA of MDM2 and 72 Arg/Pro of p53, do not support the hypothesis of the prominent role of common p53 and MDM2 variations in the genetic mechanisms of chemotherapy resistance in breast cancer.

We undertook a case-control and a case-case study to examine the possible association of p53 codon72 polymorphism with the breast cancer risk and resistance to anthracycline-based chemotherapy.Case-control study: This study enrolled 175 patients with breast cancer treated at the Salah Aziez Institute and 159 healthy Tunisian women (matched for age, ethnicity and origin), used as a control, with no clinical evidence of any neoplastic disorder. Case-Case study: 400 breast cancer patients, with invasive ductal carcinoma (IDC) treated with anthracycline based-chemotherapy. Genomic DNA was isolated from whole-blood leucocytes using the phenol-chloroform method. Anthracycline response was scored according to the World Health Organization (WHO) criteria. P53 codon72 polymorphism was genotyped using real-time polymerase chain reaction (RT-PCR) with the TaqMan method. Data were statistically analyzed using the Chi-square test.Clinical data revealed that among the 400 patients, one quarter was resistant to chemotherapy treatment. Genetic data revealed that the p53 Arg72Pro genotype was found to be greatly associated with breast cancer risk (p0.001), as well as tumor site (p=0.046). However, resistance to anthracycline-based chemotherapy does not seem to be correlated with p53 codon72 polymorphism in our population. Also, the distribution of tumor size, lymph node involvement and tumor grade was not significantly different among the polymorphic variants.We conclude that p53 codon72 polymorphism is involved in susceptibility to developing breast cancer. It may be a factor of progression when breast sites are taken into account. However, there is no evidence indicating that Arg72Pro SNP may influence response to anthracycline-based chemotherapy.