Analysis of a novel waste heat recovery mechanism for an I.C. engine

Typical internal combustion engines lose about 75% of the fuel energy through the engine coolant, exhaust and surface radiation. Most of the heat generated comes from converting the chemical energy in the fuel to mechanical energy and in turn thermal energy is produced. In general, the thermal energy is unutilized and thus wasted. This report describes the analysis of a novel waste heat recovery (WHR) system that operates on a Rankine cycle. This novel WHR system consists of a second piston within the existing piston to reduce losses associated with compression and exhaust strokes in a four-cycle engine. The wasted thermal energy recovered from the coolant and exhaust systems generate a high temperature and high pressure working fluid which is used to power the modified piston assembly. Cycle simulation shows that a large, stationary natural gas spark ignition engine produces enough waste heat to operate the novel WHR system. With the use of this system, the stationary gas compression ignition engine running at 900 RPM and full load had a net increase of 177.03 kW (240.7 HP). This increase in power improved the brake fuel conversion efficiency by 4.53%.

Nuclear Factor I-C acts as a regulator of hepatocyte proliferation at the onset of liver regeneration

BACKGROUND & AIMS: Knockout studies of the murine Nuclear Factor I-C (NFI-C) transcription factor revealed abnormal skin wound healing and growth of its appendages, suggesting a role in controlling cell proliferation in adult regenerative processes. Liver regeneration following partial hepatectomy (PH) is a well-established regenerative model whereby changes elicited in hepatocytes lead to their rapid and phased proliferation. Although NFI-C is highly expressed in the liver, no hepatic function was yet established for this transcription factor. This study aimed to determine whether NFI-C may play a role in hepatocyte proliferation and liver regeneration. METHODS: Liver regeneration and cell proliferation pathways following two-thirds PH were investigated in NFI-C knockout (ko) and wild-type (wt) mice. RESULTS: We show that the absence of NFI-C impaired hepatocyte proliferation because of plasminogen activator I (PAI-1) overexpression and the subsequent suppression of urokinase plasminogen activator (uPA) activity and hepatocyte growth factor (HGF) signalling, a potent hepatocyte mitogen. This indicated that NFI-C first acts to promote hepatocyte proliferation at the onset of liver regeneration in wt mice. The subsequent transient down regulation of NFI-C, as can be explained by a self-regulatory feedback loop with transforming growth factor beta 1 (TGF-ß1), may limit the number of hepatocytes entering the first wave of cell division and/or prevent late initiations of mitosis. CONCLUSION: NFI-C acts as a regulator of the phased hepatocyte proliferation during liver regeneration.

Die Jewish Colonization Assaciation (I.C.A.)

Margarete Goldstein

In Die Parasceves De Meditatione Passionis Mortis D. N. I. C. Carmen

A. E. D.

Jorge H. Evans Civit (ed.), Antología del Index Aristotelicus de H. Bonitz, Buenos Aires, Santiago Arcos, 2010. Colaboradores del área de Lenguas Clásicas: L. Sardi de Estrella, E. Driban, E. Cecco, M.E. Guevara de Álvarez, C. Silventi, M.G. Barandica. Colaboradores del área de Filosofía: J.H. Evans Civit, D. Lema Sarmento, T. Squizzato, I. Anton Mlinar; ISBN 978-987-1240-53-1; 640 pág.

Fil: Bieda, Esteban.

Jorge H. Evans Civit (ed.), Antología del Index Aristotelicus de H. Bonitz, Buenos Aires, Santiago Arcos, 2010. Colaboradores del área de Lenguas Clásicas: L. Sardi de Estrella, E. Driban, E. Cecco, M.E. Guevara de Álvarez, C. Silventi, M.G. Barandica. Colaboradores del área de Filosofía: J.H. Evans Civit, D. Lema Sarmento, T. Squizzato, I. Anton Mlinar

Fil: Bieda, Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas