A model for phonon heat conduction in a semiconductor nanowire with dimensions comparable to the phonon mean free path is developed. It is based on the solution of Boltzmann's equation, which takes into account ͑i͒ modification of the acoustic phonon dispersion due to spatial confinement, and ͑ii͒ change in the nonequilibrium phonon distribution due to partially diffuse boundary scattering. Numerical simulation is performed for a silicon nanowire with boundaries characterized by different interface roughness. Phonon confinement and boundary scattering lead to a significant decrease of the lattice thermal conductivity. The value of this decrease and its interface roughness and temperature dependence are different from the predictions of the early models. The observed change in thermal resistance has to be taken into account in simulation of deep-submicron and nanometer-scale devices.

We report details of the calculation of the lattice thermal conductivity in wurtzite GaN. Numerical simulations are performed for n-type wurtzite GaN with different density of silicon dopants, point defects and threading dislocations. Using the material specific model we verified the experimentally observed linear decrease of the room-temperature thermal conductivity with the logarithm of the carrier density n. The decrease was attributed mostly to the increased phonon relaxation on dopants. Our calculations show that the increase in the doping density from 10 17 to 10 18 cm Ϫ3 leads to about a factor of 2 decrease in thermal conductivity from 1.77 W/cm K to 0.86 W/cm K. We have also established that the room-temperature thermal conductivity in GaN can be limited by dislocations when their density is high, e.g., N D Ͼ10 10 cm Ϫ2. The obtained results are in good agreement with experimental data. The developed calculation procedure can be used for accurate simulation of self-heating effects in GaN-based devices.

We report calculation of the lattice thermal conductivity in wurtzite GaN. The proposed model is material specific and explicitly includes phonon relaxation on threading dislocations and impurities typical for GaN. We have found that a decrease of the dislocation density by two orders of magnitude in GaN leads to a corresponding increase of the thermal conductivity from 1.31 to 1.97 W/cm K. This theoretical prediction is in very good agreement with experimental data obtained from scanning thermal microscopy. The developed model can be used for thermal budget calculations in high-power density GaN devices.

Human dihydroorotate dehydrogenase (DHODH) is a flavin-dependent mitochondrial enzyme catalyzing the fourth step in the de novo pyrimidine synthesis pathway. It is originally a target for the treatment of the non-neoplastic diseases involving in rheumatoid arthritis and multiple sclerosis, and is re-emerging as a validated therapeutic target for cancer therapy. In this review, we mainly unravel the biological function of DHODH in tumor progression, including its crucial role in de novo pyrimidine synthesis and mitochondrial respiratory chain in cancer cells. Moreover, various DHODH inhibitors developing in the past decades are also been displayed, and the specific mechanism between DHODH and its additional effects are illustrated. Collectively, we detailly discuss the association between DHODH and tumors in recent years here, and believe it will provide significant evidences and potential strategies for utilizing DHODH as a potential target in preclinical and clinical cancer therapies.

Flap endonuclease 1 (FEN1) overexpression promotes breast cancer. We investigated the role of FEN1 in cisplatin resistance and the chemosensitizing effects of curcumin in breast cancer cells. We demonstrated that FEN1 overexpression promotes cisplatin resistance in breast cancer cells, and that FEN1 knockdown enhances cisplatin sensitivity. Curcumin down-regulated FEN1 expression in a dose-dependent manner. A combination of cisplatin and curcumin enhanced breast cancer cell sensitivity to cisplatin by down-regulating FEN1 expression in vitro and in vivo. Increased ERK phosphorylation contributed to cisplatin resistance and cisplatin-induced FEN1 overexpression in breast cancer cells. Inhibiting ERK phosphorylation stimulated the chemosensitizing effect of curcumin to cisplatin by targeting FEN1. These data reveal that FEN1 overexpression promotes cisplatin resistance, and suggest FEN1 could be a potential therapeutic target to relieve cisplatin resistance in breast cancer. We also demonstrated that curcumin sensitizes breast cancer cells to cisplatin through FEN1 down-regulation.