Programmed cell death (PCD), referring to apoptosis, autophagy and programmed necrosis, is proposed to be death of a cell in any pathological format, when mediated by an intracellular program. These three forms of PCD may jointly decide the fate of cells of malignant neoplasms; apoptosis and programmed necrosis invariably contribute to cell death, whereas autophagy can play either pro-survival or pro-death roles. Recent bulk of accumulating evidence has contributed to a wealth of knowledge facilitating better understanding of cancer initiation and progression with the three distinctive types of cell death. To be able to decipher PCD signalling pathways may aid development of new targeted anti-cancer therapeutic strategies. Thus in this review, we present a brief outline of apoptosis, autophagy and programmed necrosis pathways and apoptosis-related microRNA regulation, in cancer. Taken together, understanding PCD and the complex interplay between apoptosis, autophagy and programmed necrosis may ultimately allow scientists and clinicians to harness the three types of PCD for discovery of further novel drug targets, in the future cancer treatment.

The caspase family is well characterized as playing a crucial role in modulation of programmed cell death (PCD), which is a genetically regulated, evolutionarily conserved process with numerous links to many human diseases, most notably cancer. In this review, we focus on summarizing the intricate relationships between some members of the caspase family and their key apoptotic mediators, involving tumour necrosis factor receptors, the Bcl-2 family, cytochrome c, Apaf-1 and IAPs in cancer initiation and progression. We elucidate new emerging types of cross-talk between several caspases and autophagy-related genes (Atgs) in cancer. Moreover, we focus on presenting several PCD-modulating agents that may target caspases-3, -8 and -9, and their substrates PARP-1 and Beclin-1, which may help us harness caspase-modulated PCD pathways for future drug discovery.

SummaryThis study was designed to evaluate the effect of diluting fentanyl 50 lg.ml )1 to 25 or 10 lg.mlwith 0.9% saline and prolonged injection time on fentanyl-induced cough. Two hundred patients requiring general anaesthesia were randomly allocated into four groups: 50 lg.ml

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Combustion and emission characteristics of a direct-injection diesel engine fuelled with diesel—ethanol blends were investigated. The results show that the ignition delay and the premixed combustion duration increase, while the diffusive combustion duration and the total combustion duration decrease with increase in the oxygen mass fraction in the blends. The addition of 0.2 per cent volume fraction of cetane number improver (isoamyl nitrite) could mean that the ignition delay and the premixed combustion duration of the fuel blends with 10vol% ethanol fraction recover to those of diesel fuel. Meanwhile, with the increase in the ethanol fraction in the fuel blends, the centre of the heat release curve moves closer to the top dead centre. The brake specific fuel consumption increases, while the diesel equivalent brake specific fuel consumption decreases with increase in the ethanol fraction. The exhaust smoke concentration increases and exhaust nitrogen oxide (NO x) concentration decreases on prolonging the fuel delivery advance angle for both diesel fuel and the blended fuels. For a specific fuel injection advance angle, the exhaust smoke concentration shows a large decrease and the exhaust NO x concentration a small decrease on ethanol addition.