This paper presents a distributed implementation of RAND, a randomized time slot scheduling algorithm, called DRAND. DRAND runs in OðÞ time and message complexity where is the maximum size of a two-hop neighborhood in a wireless network while message complexity remains OðÞ, assuming that message delays can be bounded by an unknown constant. DRAND is the first fully distributed version of RAND. The algorithm is suitable for a wireless network where most nodes do not move, such as wireless mesh networks and wireless sensor networks. We implement the algorithm in TinyOS and demonstrate its performance in a real testbed of Mica2 nodes. The algorithm does not require any time synchronization and is shown to be effective in adapting to local topology changes without incurring global overhead in the scheduling. Because of these features, it can also be used even for other scheduling problems such as frequency or code scheduling (for FDMA or CDMA) or local identifier assignment for wireless networks where time synchronization is not enforced. We further evaluate the effect of the time-varying nature of wireless links on the conflictfree property of DRAND-assigned time slots. This experiment is conducted on a 55-node testbed consisting of the more recent MicaZ sensor nodes.

No abstract

Short-chain fatty acids (SCFAs; butyrate, propionate and acetate) are metabolites derived from the gut microbiota via dietary fiber fermentation. In colon cancer, treatment with SCFAs, mainly butyrate and propionate, suppresses cell proliferation, migration and invasion. Furthermore, although sodium butyrate is known to induce cell apoptosis in lung cancer, the anticancer effects of sodium propionate (SP) on lung cancer are not well understood. In the present study, SP treatment induced cell cycle arrest, especially in the G2/M phase, and cell apoptosis in the H1299 and H1703 lung cancer cell lines. As determined by reverse transcription-quantitative PCR and western blotting, Survivin and p21 expression levels were significantly affected by SP treatment, suggesting that SP treatment suppressed cell proliferation in these lung cancer cell lines. Thus, it was proposed that the SP-mediated regulation of Survivin and p21 in lung cancer may be applicable to lung cancer therapy.

No abstract