ESTIMATION OF THE RADIATION-INDUCED DAMAGE IN PTFE BY DEPRESSION OF THE MELTING AND CRYSTALLIZATION TEMPERATURES

The radiation induced depression of the melting and crystallization temperatures of PTFE irradiated at various temperatures followed by heat treatment at 380-degrees-C, and their relationship to structural changes, were investigated. The G(-units) values obtained in this work are different from those of samples which have not undergone heat treatment and seem to be more closely associated with radiation induced branched structures.

High current density induced damage mechanisms in electronic solder joints: a state-of-the-art review

High current density induced damages such as electromigration in the on-chip interconnection /metallization of Al or Cu has been the subject of intense study over the last 40 years. Recently, because of the increasing trend of miniaturization of the electronic packaging that encloses the chip, electromigration as well as other high current density induced damages are becoming a growing concern for off-chip interconnection where low melting point solder joints are commonly used. Before long, a huge number of publications have been explored on the electromigration issue of solder joints. However, a wide spectrum of findings might confuse electronic companies/designers. Thus, a review of the high current induced damages in solder joints is timely right this moment. We have selected 6 major phenomena to review in this paper. They are (i) electromigration (mass transfer due electron bombardment), (ii) thermomigration (mass transfer due to thermal gradient), (iii) enhanced intermetallic compound growth, (iv) enhanced current crowding, (v) enhanced under bump metallisation dissolution and (vi) high Joule heating and (vii) solder melting. the damage mechanisms under high current stressing in the tiny solder joint, mentioned in the review article, are significant roadblocks to further miniaturization of electronics. Without through understanding of these failure mechanisms by experiments coupled with mathematical modeling work, further miniaturization in electronics will be jeopardized

Under the right conditions: protecting podocytes from diabetes-induced damage

Hyperglycemia-induced damage to the glomerular podocyte is thought to be a critical early event in diabetic nephropathy. Interventions that prevent podocyte damage or loss have been shown to have potential for the treatment of diabetic nephropathy. New data show that conditioned medium from adipocyte-derived mesenchymal stem cells has the potential to protect podocytes from high-glucose-induced damage. Furthermore, epidermal growth factor may be the critical ingredient mediating this effect. These data suggest that components of the conditioned medium of mesenchymal stem cells, in addition to the cells themselves, may have potential for the treatment of diseases such as diabetic nephropathy.

Damage threshold determination of bulk polymer samples using pulsed photothermal deflection technique

Photothermal deflection technique was used for determining the laser damage threshold of polymer samples of teflon (PTFE) and nylon. The experiment was conducted using a Q-switched Nd-YAG laser operating at its fundamental wavelength (1-06μm, pulse width 10 nS FWHM) as irradiation source and a He-Ne laser as the probe beam, along with a position sensitive detector. The damage threshold values determined by photothermal deflection method were in good agreement with those determined by other methods.

Zinc-histidine complex protects cultured cortical neurons against oxidative stress-induced damage

The levels of zinc in the brain are directly affected by dietary zinc and deficiency has been associated with alcohol withdrawal seizures, excitotoxicity, impaired learning and memory and an accelerated rate of dysfunction in aged brain. Although zinc is essential for a healthy nervous system, high concentrations of zinc are neurotoxic, thus it is important to identify the most effective forms of zinc for treatment of conditions of the central nervous system. Accumulating evidence suggests that zinc-histidine complex (Zn(HiS)(2)) has greater biological potency and enhanced bioavailability compared with other zinc salts and also has antioxidant potential. Therefore, in this study we investigated the ability of zinc-histidine to protect cultured cortical neurons against hydrogen peroxide-induced damage. Pre-treating neurons for 18h with subtoxic concentrations of zinc-histidine (5-25 muM) improved neuronal viability and strongly inhibited hydrogen peroxide-induced (75 muM, 30 min) cell damage as assessed by MTT turnover and morphological analysis 24 It later. Low concentrations of zinc-histidine were more neuroprotective than zinc chloride. There was evidence of an anti-apoptotic mechanism of action as zinc-histidine inhibited hydrogen peroxide-induced caspase-3 activation and c-jun-N-terminal kinase phosphorylation. In summary, zinc supplementation with zinc-histidine protects cultured neurons against oxidative insults and inhibits apoptosis which suggests that zinc-histidine may be beneficial in the treatment of diseases of the CNS associated with zinc deficiency. (C) 2004 Elsevier Ireland Ltd. All rights reserved.