Resistance to ursodeoxycholic acid-induced growth arrest can also result in resistance to deoxycholic acid-induced apoptosis and increased tumorgenicity

BACKGROUND: There is a large body of evidence which suggests that bile acids increase the risk of colon cancer and act as tumor promoters, however, the mechanism(s) of bile acids mediated tumorigenesis is not clear. Previously we showed that deoxycholic acid (DCA), a tumorogenic bile acid, and ursodeoxycholic acid (UDCA), a putative chemopreventive agent, exhibited distinct biological effects, yet appeared to act on some of the same signaling molecules. The present study was carried out to determine whether there is overlap in signaling pathways activated by tumorogenic bile acid DCA and chemopreventive bile acid UDCA. METHODS: To determine whether there was an overlap in activation of signaling pathways by DCA and UDCA, we mutagenized HCT116 cells and then isolated cell lines resistant to UDCA induced growth arrest. These lines were then tested for their response to DCA induced apoptosis. RESULTS: We found that a majority of the cell lines resistant to UDCA-induced growth arrest were also resistant to DCA-induced apoptosis, implying an overlap in DCA and UDCA mediated signaling. Moreover, the cell lines which were the most resistant to DCA-induced apoptosis also exhibited a greater capacity for anchorage independent growth. CONCLUSION: We conclude that UDCA and DCA have overlapping signaling activities and that disregulation of these pathways can lead to a more advanced neoplastic phenotype

<span style="font-size:14.0pt;line-height: 115%;font-family:"Times New Roman";mso-fareast-font-family:"Times New Roman"; color:black;mso-ansi-language:EN-IN;mso-fareast-language:EN-IN;mso-bidi-language: HI" lang="EN-IN">Cloning and sequencing of beta toxin gene of <i>Clostridium perfringens </i>type C</span>

109-110<span style="font-size:14.0pt;line-height: 115%;font-family:" times="" new="" roman";mso-fareast-font-family:"times="" roman";="" color:black;mso-ansi-language:en-in;mso-fareast-language:en-in;mso-bidi-language:="" hi"="" lang="EN-IN">A gene encoding beta toxin was amplified by polymerase chain reaction from C. perfringens type C isolate and cloned in pUC 19 vector. The nucleotide sequence was identical with C. perfringens type B beta toxin gene sequence. The Southern hybridization using labelled beta toxin gene probe revealed the presence of positive signals only in beta producing C. perfringens.</span

Is Miraa a Drug?: Categorizing Kenyan Khat

This article examines the varied perceptions of the substance miraa/khat in Kenya, from strong approval in the Nyambene Hills region where it is cultivated to the strong disapproval evident in its frequent denunciation in various segments of Kenyan society. Perceptions are colored by various local and global discourses, and it is argued that of great importance is "war on drugs" rhetoric, which allows the conflation of miraa with other substances also termed "drugs"; much of the Kenyan miraa debate revolves around just how miraa should be categorized and to whether it can be labeled a "drug." War-on-drugs rhetoric is countered by those more enamored of the substance by discourse in which its use is labeled "traditional," "cool," and an "economic miracle."</p