Photoluminescence and excitation spectra are observed for Ca(S, Se):Eu2+ and Sr(S, Se):Eu2+ powder phosphors at various temperatures between 4.2 and 300 K. The emission band of Ca(S1- x Se x ):Eu2+ at 300 K shifts almost linearly with an increase in x, from 652 nm (x=0) to 597 nm (x=1). In Sr(S1- x Se x ):Eu2+, the emission band shifts also linearly from 620 nm (x=0) to 571 nm (x=1). At low temperatures, vibronic structures on emission bands are observed for CaS:Eu2+, CaSe:Eu2+, SrS:Eu2+ and SrSe:Eu2+. The excitation processes are attributed to two transitions; the intraionic 4f 7→4f 65d transition within Eu2+ and the fundamental absorption by host crystal, followed by the transfer of the excitation energy to an unexcited Eu2+ ion.

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We focused on heat shock protein 70 (HSP70) as a marker of viability in hepatic warm ischemiareperfusion. Segmental hepatic warm ischemia was produced in rats for 15, 30, 60, 90, 120, or 180 min. Liver sections were evaluated at 30, 60, and 120 min of reperfusion. Expression of HSP70 and messenger RNA (mRNA), apoptosis, and apoptosis-associated genes such as Bcl-2 and Bax were studied. Expression of HSP70 and mRNA was augmented as warm ischemia was prolonged, but was markedly suppressed in livers with more than 120 min of ischemia. The highest accumulation of HSP70 was observed in the nucleus. In livers subjected to longer duration of warm ischemia, necrosis and apoptosis were evident and Bcl-2 mRNA expression and Bcl-2/Bax protein ratio were markedly diminished. Apoptosis may be related to the process of cellular injury induced by warm ischemiareperfusion. Expression of HSP70 and the Bcl-2 family can be effective markers of viability in hepatic warm ischemia-reperfusion.

The advantages of this procedure are: the free tracheal graft has as much strength as a prosthesis to support the respiratory tract; the autologous graft is biologically compatible; and the procedure can be completed in one surgical field and adopted for primary and secondary repair of the tracheal defect.

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