Recent Advances in Pipeline Monitoring and Oil Leakage Detection Technologies: Principles and Approaches.

Pipelines are widely used for the transportation of hydrocarbon fluids over millions of miles all over the world. The structures of the pipelines are designed to withstand several environmental loading conditions to ensure safe and reliable distribution from point of production to the shore or distribution depot. However, leaks in pipeline networks are one of the major causes of innumerable losses in pipeline operators and nature. Incidents of pipeline failure can result in serious ecological disasters, human casualties and financial loss. In order to avoid such menace and maintain safe and reliable pipeline infrastructure, substantial research efforts have been devoted to implementing pipeline leak detection and localisation using different approaches. This paper discusses pipeline leakage detection technologies and summarises the state-of-the-art achievements. Different leakage detection and localisation in pipeline systems are reviewed and their strengths and weaknesses are highlighted. Comparative performance analysis is performed to provide a guide in determining which leak detection method is appropriate for particular operating settings. In addition, research gaps and open issues for development of reliable pipeline leakage detection systems are discussed.

Pancratistatin selectively targets cancer cell mitochondria and reduces growth of human colon tumor xenografts.

The naturally occurring Amaryllidaceae alkaloid pancratistatin exhibits potent apoptotic activity against a large panel of cancer cells lines and has an insignificant effect on noncancerous cell lines, although with an elusive cellular target. Many current chemotherapeutics induce apoptosis via genotoxic mechanisms and thus have low selectivity. The observed selectivity of pancratistatin for cancer cells promoted us to consider the hypothesis that this alkaloid targets cancer cell mitochondria rather than DNA or its replicative machinery. In this study, we report that pancratistatin decreased mitochondrial membrane potential and induced apoptotic nuclear morphology in p53-mutant (HT-29) and wild-type p53 (HCT116) colorectal carcinoma cell lines, but not in noncancerous colon fibroblast (CCD-18Co) cells. Interestingly, pancratistatin was found to be ineffective against mtDNA-depleted (ρ(0)) cancer cells. Moreover, pancratistatin induced cell death in a manner independent of Bax and caspase activation, and did not alter ß-tubulin polymerization rate nor cause double-stranded DNA breaks. For the first time we report the efficacy of pancratistatin in vivo against human colorectal adenocarcinoma xenografts. Intratumor administration of pancratistatin (3 mg/kg) caused significant reduction in the growth of subcutaneous HT-29 tumors in Nu/Nu mice (n = 6), with no apparent toxicity to the liver or kidneys as indicated by histopathologic analysis and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling. Altogether, this work suggests that pancratistatin may be a novel mitochondria-targeting compound that selectively induces apoptosis in cancer cells and significantly reduces tumor growth.