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Research on Product Systematic Innovative Design Based on TRIZ (2006)

Zhang, Fu Ying ; Xu, Yan Shen ; He, Qing Ping

s.l. ; Stafa-Zurich, Switzerland

Materials science forum Vol. 532-533 (Dec. 2006), p. 761-764

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ISSN: 1662-9752

Source: Scientific.Net: Materials Science & Technology / Trans Tech Publications Archiv 1984-2008

Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics

Notes: Many solution tools TRIZ provided, such as innovative principles, technology evolution,have been widely used for product innovative design in last decade. The key using TRIZ to improvedesign is the correct definition and solving of technical problems. However, it’s difficult forengineers to discover the inherent problems of product, especially for complex engineering systems.Therefore, this paper proposes a whole process model for product systematical innovation design,whose objective is to obtain ideal solution and whose technical method is to analyze and solveconflicts. This model integrates the definition, analysis of problems from top to bottom, with theresolving of problems from bottom to top, and will contribute to a systematic and operable processfor problems definition, analysis, resolving. A practical application of this work is also presented

Type of Medium: Electronic Resource

URL: http://www.tib-hannover.de/fulltexts/2011/0528/02/14/transtech_doi~10.4028%252Fwww.scientific.net%252FMSF.532-533.761.pdf

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Is Neuronal Injury Caused by Hypoglycemic Coma of the Necrotic or Apoptotic Type? (2000)

Ouyang, Yi-Bing ; He, Qing-Ping ; Li, Ping-An ; [et al.]

Springer

Neurochemical research 25 (2000), S. 661-667

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ISSN: 1573-6903

Keywords: Brain ; caspase ; cytochrome c ; hypoglycemia ; Bcl-2 family

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract In this study, we explored if a 30 minute period of hypoglycemic coma yields damage which shows some features associated with apoptosis. To that end, we induced insulin-hypoglycemic coma of 30 min duration, and studied brain tissues after the coma period, and after recovery period of 30 min, 3 h, and 6 h. Histopathological data confirmed neuronal damage in all of the vulnerable neuronal populations. Release of cytochrome c (cyt c), assessed by Western Blot, was observed in the neocortex and caudoputamen after 3 and 6 h of recovery. In these regions, the caspase-like activity increased above control after 6 h of recovery. By laser-scanning confocal microscopy, a clear expression of Bax was observed after 30 min of coma in the superficial layers of the neocortex, reaching a peak after 30 min of recovery. Punctuate immunolabeling surrounding nuclei in soma and dendrites in cortical pyramidal neurons likely represents mitochondria, which suggests that Bax protein assembled at the surface of mitochondria in vulnerable neocortical neurons. It is concluded that although previous morphological data have suggested that cells die by necrosis, neuronal damage after hypoglycemic coma shows some features of apoptosis.