The Transition from Acute to Chronic Pain

Chronic pain is not merely a prolonged form of acute pain but rather results from plastic changes that occur along sensory transduction pathways from the peripheral to the central nervous system. Recent studies have revealed that “hyperalgesic priming,” the plastic changes of nociceptors, is essential for the transition from acute to chronic pain. Once challenged, nociceptors may elicit a signal switch to favor pain chronicity in response to future noxious stimuli. This article summarizes the recent progress in research into hyperalgesic priming in different chronic pain models and highlight how the plastic changes of the signal switch varies in different nociceptors. Also discussed is the involvement of proton-sensing receptors in pain chronicity associated with rheumatoid arthritis and fibromyalgia.

Long-term transient radiation effects in high-speed signal switches implemented in 0.1 um E/D pHEMT process

The transient radiation effects in 0.1 μm E/D pHEMT high-speed signal switches have been investigated. It was shown that a signal switch transient recovery time caused by pulsed irradiation can exceed 100 ms due to a switch control driver’s functional upset.

Regulation of the porcine corpus luteum during pregnancy

The new corpora lutea (CLs) in pigs are formed from the preovulatory follicles after the luteinizing hormone (LH) surge. However, total autonomy and independence of CLs from LH up to Day 12 of cycle has recently been questioned. Transformation of estrous cycle CL to CL of pregnancy initiated by embryonic signals requires not only the cessation of prostaglandin F2 (PGF2α) supply to the luteal tissue but also needs the CL to overcome luteolytic acquisition and/or changing its sensitivity to PGF2αduring Days 12–14 of pregnancy. The luteolytic cascade is prevented by inhibition of lymphocyte infiltration and leucocyte recruitment, limitation of cell apoptosis, upregulation of pregnancy-associated genes and an enhanced antiluteolytic role of PGE2. Our ‘two-signal switch hypothesis’ highlights the importance ofpostPGF2αand PGE2receptor signaling pathways activation in CLs during luteolysis and rescue. The ‘luteolytic switch’ involves increased expression of many regression mediators and activation of thepostPTGFR signaling pathway. The ‘rescue switch’ initiated by embryonic signals – estradiol 17β and PGE2– inducespostPTGER2/4 pathway, turning the ‘luteolytic switch’ off and triggering activity of genes responsible for CL maintenance. In mid and late pregnancy, CLs are maintained by LH and the synergistic action of metabolic hormones. This paper provides an outline of recent views on CL regression, rescue and maintenance during pregnancy in pigs that conflict with previous paradigms and highlights new findings regarding the actions of prostaglandins, role of microRNAs (miRNA) and immune system and signaling pathways governing the life cycle of porcine CL.