This paper reports measurements of the effective thermal conductivity and thermal diffusivity of various nanofluids using the transient short-hot-wire technique. To remove the influences of the static charge and electrical conductance of the nanoparticles on measurement accuracy, the short-hot-wire probes are carefully coated with a pure Al 2 O 3 thin film. Using distilled water and toluene as standard liquids of known thermal conductivity and thermal diffusivity, the length and radius of the hot wire and the thickness of the Al 2 O 3 film are calibrated before and after application of the coating. The electrical leakage of the short-hot-wire probes is frequently checked, and only those probes that are coated well are used for measurements. In the present study, the effective thermal conductivities and thermal diffusivities of Al 2 O 3 /water, ZrO 2 /water, TiO 2 /water, and CuO/water nanofluids are measured and the effects of the volume fractions and thermal conductivities of nanoparticles and temperature are clarified. The average diameters of Al 2 O 3 , ZrO 2 , TiO 2 , and CuO particles are 20, 20, 40, and 33 nm, respectively. The uncertainty of the present measurements is estimated to be within 1% for the thermal conductivity and 5% for the thermal diffusivity. The measured results demonstrate that the effective thermal conductivities of the nanofluids show no anomalous enhancement and can be predicted accurately by the model equation of Hamilton and Crosser, when the spherical nanoparticles are dispersed into fluids.

No abstract

No abstract

No abstract

Opioids are the most widely used analgesics in the treatment of severe acute and chronic pain. However, opioids have many adverse side effects, including the development of antinociceptive tolerance after long-term use. The antinociceptive tolerance of opioids has limited their clinical use. A recent study has reported that autophagy is responsible for morphine-induced neuronal injury. However, little is known about the role of autophagy in morphine antinociceptive tolerance. In the present study, chronic morphine administration was found to induce the expression of autophagy-related proteins, including Beclin1 and microtubule-associated protein light chain 3 (LC3)-II, in GABAergic interneurons in the superficial layer (lamina I-II) of the spinal cord. A single intrathecal administration of autophagy inhibitors, 3-methyladenine (3MA) or wortmannin, inhibited the development of antinociceptive tolerance in a dose-dependent manner. Autophagy in the lamina I-II neurons was associated with increased level of cathepsin B (CatB), a lysosomal cysteine protease. The pharmacological blockade or gene deletion of CatB markedly prevented the development of morphine antinociceptive tolerance. Furthermore, the intrathecal administration of 3MA suppressed the upregulation of CatB 5 days after morphine administration. Finally, CatB deficiency inhibited the increased release probability of glutamate in the lamina I neurons after chronic morphine treatment. These observations suggest that the dysfunction of the spinal GABAergic system induced by CatB-dependent excessive autophagy is partly responsible for morphine antinociceptive tolerance following chronic treatment.