Increasing functional complexity and dimensional compactness of electronic devices have led to progressively higher power dissipation, mainly in the form of heat. Overheating of semiconductor-based electronics has been the primary reason for their failure. Such failures originate at the interface of the heat sink (commonly Cu and Al) and the substrate (silicon) due to the large mismatch in thermal expansion coefficients (∼300%) of metals and silicon. Therefore, the effective cooling of such electronics demands a material with both high thermal conductivity and a similar coefficient of thermal expansion (CTE) to silicon. Addressing this demand, we have developed a carbon nanotube-copper (CNT-Cu) composite with high metallic thermal conductivity (395 W m(-1) K(-1)) and a low, silicon-like CTE (5.0 ppm K(-1)). The thermal conductivity was identical to that of Cu (400 W m(-1) K(-1)) and higher than those of most metals (Ti, Al, Au). Importantly, the CTE mismatch between CNT-Cu and silicon was only ∼10%, meaning an excellent compatibility. The seamless integration of CNTs and Cu was achieved through a unique two-stage electrodeposition approach to create an extensive and continuous interface between the Cu and CNTs. This allowed for thermal contributions from both Cu and CNTs, resulting in high thermal conductivity. Simultaneously, the high volume fraction of CNTs balanced the thermal expansion of Cu, accounting for the low CTE of the CNT-Cu composite. The experimental observations were in good quantitative concurrence with the theoretically described 'matrix-bubble' model. Further, we demonstrated identical in-situ thermal strain behaviour of the CNT-Cu composite to Si-based dielectrics, thereby generating the least interfacial thermal strain. This unique combination of properties places CNT-Cu as an isolated spot in an Ashby map of thermal conductivity and CTE. Finally, the CNT-Cu composite exhibited the greatest stability to temperature as indicated by its low thermal distortion parameter (TDP). Thus, this material presents a viable and efficient alternative to existing materials for thermal management in electronics.
Purpose: Obesity and related metabolic abnormalities, including insulin resistance and activation of the insulin-like growth factor (IGF)/IGF-I receptor (IGF-IR) axis, are risk factors for colon cancer. Supplementation with branched-chain amino acids (BCAA) reduces the risk of liver cancer in cirrhotic patients who are obese, and this has been associated with an improvement of insulin resistance. The present study examined the effects of BCAA on the development of azoxymethane (AOM)-initiated colonic premalignant lesions in C57BL/KsJ-db/db (db/db) mice that were obese and had hyperinsulinemia. Experimental Design: Male db/db mice were given 4 weekly s.c. injections of AOM (15 mg/kg of body weight) and then they were fed a diet containing 3.0% BCAA or casein, a nitrogenc content^matched control diet, for 7 weeks. Results: Feeding with BCAA caused a significant reduction in the number of total aberrant crypt foci and h-catenin accumulated crypts, both of which are premalignant lesions of the colon, compared with the control diet^fed groups. BCAA supplementation caused a marked decrease in the expression of IGF-IR, the phosphorylated form of IGF-IR, phosphorylated glycogen synthase kinase 3h, phosphorylated Akt, and cyclooxygenase-2 proteins on the colonic mucosa of AOM-treated mice. The serum levels of insulin, IGF-I, IGF-II, triglyceride, total cholesterol, and leptin were also decreased by supplementation with BCAA. Conclusion: BCAA supplementation in diet improves insulin resistance and inhibits the activation of the IGF/IGF-IR axis, thereby preventing the development of colonic premalignancies in an obesity-related colon cancer model that was also associated with hyperlipidemia and hyperinsulinemia. BCAA, therefore, may be a useful chemoprevention modality for colon cancer in obese people.
Obesity and related metabolic abnormalities are risk factors for colorectal cancer. A state of chronic inflammation and adipocytokine imbalance may play a role in colorectal carcinogenesis. Statins, which are commonly used for the treatment of hyperlipidemia, are known to possess anti-inflammatory effects. Statins also exert chemopreventive properties against various cancers. The present study examined the effects of pitavastatin, a recently developed lipophilic statin, on the development of azoxymethane (AOM)-initiated colonic premalignant lesions in C57BL/KsJ-db/db (db/db) obese mice. Male db/db mice were administrated weekly subcutaneous injections of AOM (15 mg/kg body weight) for 4 weeks and then were subsequently fed a diet containing 1 ppm or 10 ppm pitavastatin for 8 weeks. Feeding with either dose of pitavastatin significantly reduced the number of colonic premalignant lesions, b-catenin accumulated crypts, by inhibiting proliferation and the surrounding inflammation. Pitavastatin increased the serum levels of adiponectin while conversely decreasing the serum levels of total cholesterol, tumor necrosis factor-a (TNF-a), interleukin (IL)-6, IL-18, and leptin. Pitavastatin also caused a significant increase in the expression of phosphorylated form of the AMP-activated kinase (AMPK) protein on the colonic mucosa of AOM-treated mice. In addition, the expression levels of TNF-a, IL-6, IL-18, and COX-2 mRNAs on the colonic mucosa of AOM-treated mice were decreased by treatment with this agent. These findings suggest that pitavastatin attenuates chronic inflammation and improves the imbalance of adipocytokines, both of which are caused by the presence of excess adipose tissues, thereby preventing the development of colonic premalignancies in an obesity-related colon cancer model. Therefore, some types of statins, including pitavastatin, may be a useful chemoprevention modality for colon cancer in obese individuals. (Cancer Sci
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