定時定量自動餵食器

[[abstract]]現代人生活腳步極快，凡事希望自動化或來便利自己的生活，連飼養寵物也不例外，若是能從每天早晚各餵食一次變成一段時間補充飼料到餵食器裡，那就很令人動心了，而且餵食器又能定時定量，可以保護寵物的健康這會是許多飼主所樂意見到。 本組所製作的定時定量餵食器，其製作動機是來自於家中有養殖觀賞魚，然而在飼養的過程中因工作繁忙或出遠門無法將自己所養的寵物按時的餵食，如果寄放在朋友或寵物店裡委託人照顧，多少一定會有金錢上的負擔，如長期累積下來帳單也是一筆龐大的費用。我們以這為出發點想出一個是否可以解決無人照顧寵物時讓牠們不至於挨餓的方法，因此啟發了我們想製作一個定時又定量的器具來滿足寵物的口腹之慾

Phenethyl isothiocyanate triggers apoptosis in human malignant melanoma A375.S103 cells through reactive oxygen species and the mitochondria-dependent pathways

[[abstract]]We have reported previously that phenethyl isothiocyanate (PEITC) induces apoptosis in human osteosarcoma U-2 OS cells. Cytotoxic activity of PEITC towards other cancer cells such as human malignant melanoma and skin cancer cells has not been reported. In this study, the anticancer activity of PEITC towards human malignant melanoma cancer A375.S2 cells was investigated. To determine the mechanisms of PEITC inhibition of cell growth, the following end points were determined in A375.S2 cells: cell morphological changes, cell cycle arrest, DNA damage and fragmentation assays and morphological assessment of nuclear change, reactive oxygen species (ROS) and Ca(2+) generations, mitochondrial membrane potential disruption, and nitric oxide and 10-N-nonyl acridine orange productions, expression and activation of caspase-3 and -9, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, poly (adenosine diphosphate-ribose) polymerase, and cytochrome c release, apoptosis-inducing factor and endonuclease G. PEITC induced morphological changes in time- and dose-dependent manner. PEITC induced G2/M phase arrest and induced apoptosis via endoplasmic reticulum stress-mediated mitochondria-dependent pathway. Western blot analysis showed that PEITC promoted Bax expression and inhibited Bcl-2 expression associated with the disintegration of the outer mitochondrial membrane causing cytochrome c release, and activation of caspase-9 and -3 cascade leading to apoptosis. We conclude that PEITC-triggered apoptotic death in A375.S2 cells occurs through ROS-mediated mitochondria-dependent pathways