Electronic properties and phase transitions in low-dimensional semiconductors

We present the first review of the current state of the literature on electronic properties and phase transitions in TlX and TlMX2 (M = Ga, In; X = Se, S, Te) compounds. These chalcogenides belong to a family of the low-dimensional semiconductors possessing chain or layered structure. They are of significant interest because of their highly anisotropic properties, semi- and photoconductivity, non-linear effects in their I-V characteristics (including a region of negative differential resistance), switching and memory effects, second harmonic optical generation, relaxor behavior and potential applications for optoelectronic devices. We review the crystal structure of TlX and TlMX2 compounds, their transport properties under ambient conditions, experimental and theoretical studies of the electronic structure, transport properties and semiconductor-metal phase transitions under high pressure, and sequences of temperature-induced structural phase transitions with intermediate incommensurate states. Electronic nature of the ferroelectric phase transitions in the above-mentioned compounds, as well as relaxor behavior, nanodomains and possible occurrence of quantum dots in doped and irradiated crystals is discussed.Comment: 70 pages, 38 figure

Cyclin d1 depletion interferes with cancer oxidative balance and sensitizes cancer cells to senescence

Expression of cyclin D1 is required for cancer cell survival and proliferation. This is presumably due to the role of cyclin D1 in RB inactivation. Here we investigated the prosurvival function of cyclin D1 in a number of cancer cell lines. We found that cyclin D1 depletion facilitated cellular senescence in several cancer cell lines tested. Senescence triggered by cyclin D1 depletion was more extensive than that caused by the prolonged CDK4 inhibition. Intriguingly, the senescence caused by cyclin D1 depletion was independent of RB status of the cancer cell. We identified a buildup of intracellular reactive oxygen species, in the cancer cells that underwent senescence upon cyclin D1 depletion, but not in CDK4 inhibition, and that ROS buildup was responsible for the senescence. Lastly, the senescence was found to be instigated by the p38/JNK-FOXO3a-p27 pathway. Therefore, expression of cyclin D1 prevents cancer cells from undergoing senescence, at least partially, by keeping the level of intracellular oxidative stress at a tolerable sub-lethal level. Depletion of cyclin D1 promotes the RB-independent pro-senescence pathway, and cancer cell succumbing to the endogenous oxidative stress

Mitochondria-targeted hydrogen sulfide delivery molecules protect against uva-induced photoaging in dermal fibroblasts, and in mouse skin in vivo

Aims Oxidative stress and mitochondrial dysfunction play a role in the process of skin photoaging via activation of matrix metalloproteases (MMPs) and the subsequent degradation of collagen. The activation of nuclear factor E2-related factor 2 (Nrf2), a transcription factor controlling antioxidant and cytoprotective defense systems, might offer a pharmacological approach to prevent skin photoaging. We therefore investigated might offer a pharmacological approach to prevent skin photoaging. We therefore investigated protective effect of the novel mitochondria-targeted hydrogen sulfide (H(2)S) delivery molecules AP39 and AP123, and non-targeted control molecules on UVA-induced photoaging in normal human dermal fibroblasts (NDHFs) in vitro and the skin of BALB/c mice in vivo. Results In NDHFs AP39 and AP123 (50-200 nM) but not non-targeted controls suppressed UVA (8 J/cm2)-mediated cytotoxicity and induction of MMP-1 activity, preserved cellular bioenergetics and increased the expression of collagen and nuclear levels of Nrf2. In in vivo experiments, topical application of AP39 or AP123 (0.3-1 µM/cm(2); but not non-targeted control molecules) to mouse skin prior to UVA (60 J/cm(2)) irradiation prevented skin thickening, MMP induction, collagen loss oxidative stress markers 8-hydroxy-2'-deoxyguanosine (8-OHdG), increased Nrf2-dependent signaling as well as increased manganese superoxide dismutase (MnSOD) levels and levels of the mitochondrial biogenesis marker peroxisome proliferator-activated receptor-gamma coactivator (PGC-1?). Innovation and Conclusion Targeting H(2)S delivery to mitochondria may represent a novel approach for the prevention and treatment of skin photoaging, as well as being useful tools for determining the role of mitochondrial H(2)S in skin disorders and aging.Not heldPublished version, accepted version (12 month embargo