We report measurements of the thermal conductivity of isotopically modulated silicon that consists of alternating layers of highly enriched silicon-28 and silicon-29. A reduced thermal conductivity of the isotopically modulated silicon compared to natural silicon was measured by means of time-resolved x-ray scattering. Comparison of the experimental results to numerical solutions of the corresponding heat diffusion equations reveals a factor of three lower thermal conductivity of the isotope structure compared to natural Si. Our results demonstrate that the thermal conductivity of silicon can be effectively reduced with isotopically modulated structures. This offers a promising approach to optimize silicon for thermoelectric applications.
Introduction: Recent findings indicate that metabolic disturbances are involved in multiple sclerosis (MS) pathology and influence the susceptibility to treatment, directing attention toward anti-diabetic drugs such as metformin and pioglitazone. Liraglutide, a drug of the glucagon-like peptide-1 (GLP-1) family, is also anti-diabetic and weight-reducing and is, moreover, directly neuroprotective and anti-inflammatory in a broad spectrum of experimental models of brain disease. In this study we investigate the potential for this FDA-approved drug, liraglutide, as a treatment for MS by utilizing the experimental model, experimental autoimmune encephalitis (EAE). Methods: EAE was induced in 30 female Lewis rats that subsequently received twice-daily liraglutide (200 μg/kg s.c.) or saline. Healthy controls were included (saline, n = 6, liraglutide, n = 7). Clinical score and weight were assessed daily by blinded observers. Animals were killed at peak disease severity (day 11) or if exceeding humane endpoint (clinical score ≥4). Protein levels of manganese superoxide dismutase (MnSOD), amyloid precursor protein (APP), and glial fibrillary acidic protein (GFAP) were determined. Results: Liraglutide treatment delayed disease onset (group clinical score significantly >0) by 2 days and markedly reduced disease severity (median clinical score 2 vs. 5; p = 0.0003). Fourteen of 15 (93%) of vehicle-treated rats reached the humane endpoint (clinical score ≥4) by day 11 compared to 5 of 15 (33%) of liraglutide-treated rats (p = 0.0004). Liraglutide substantially increased the mitochondrial antioxidant MnSOD (p < 0.01) and reduced the neurodegenerative marker APP (p = 0.036) in the brain. GFAP levels were not significantly changed with drug treatment (p = 0.09). Conclusion: We demonstrate, for the first time, that liraglutide treatment delays onset of EAE in Lewis rats and is associated with improved protective capacity against oxidative stress. These data suggest GLP-1 receptor agonists should be investigated further as a potential therapy for MS.
Background:In obesity, the distribution and metabolic function of adipose tissue are of vast importance for the risk of type 2 diabetes development.The homeostasis of zinc and iron is believed to be disturbed in diabetic patients.Zinc dyshomeostasis could affect the metabolic function of adipose tissue as zinc is known to facilitate the functions of insulin within adipose tissue as well as take part in cell proliferation and apoptosis.Further, altered iron levels have been shown to affect insulin sensitivity.This study investigates the intracellular zinc regulation and total zinc and iron status in adipose tissues in obesity-linked, type 2 diabetes in the Psammomys obesus model.Methods: Subcutaneous and visceral adipose tissue were collected from diabetic (n=6) and non-diabetic animals (n=6).Total zinc and iron levels were analyzed by induced-coupled plasma mass spectrometry.Gene expressions of zinc transporters of the SLC30A and SLC39A family, regulating the intracellular zinc distribution, as well as several metabolic markers were investigated by RealTime-PCR.Results: Diabetic animals exhibited signs of an altered zinc homeostasis i.e. a re-distribution of total zinc within visceral adipose tissues and altered transcription of zinc regulatory proteins ZIP6, ZIP8, ZIP9, and ZnT9.Further, diabetic animals displayed an iron accumulation in visceral adipose tissue that was positively correlated with insulin degrading enzyme and peroxisome proliferator-activated receptor gamma. Conclusion:Psammomys obesus, a complex animal model of diet-induced type 2 diabetes, exhibits changes in the mineral status of zinc and iron in visceral adipose tissue.These changes might be related to the altered insulin sensitivity and metabolic function of visceral adipose tissue seen in type 2 diabetes.This study warrants further investigations into the role minerals, especially zinc and iron, play in the pathophysiology of type 2 diabetes.
Bismuth compounds have been used in medicine for more than 200 years. In recent years, bismuth has gained renewed interest as a remedy for eradication of gastrointestinal pathogens, especially Helicobacter pylori. In this study we describe the anatomical distribution of bismuth in the gastrointestinal tract and other organs after oral exposure in a mouse model. After exposure of the experimental animals to ranitidine bismuth citrate or bismuth citrate, we used the autometallographic silver enhancement technique to demonstrate the presence of bismuth in tissue samples from the gastrointestinal tract, liver, spleen, thymus, kidney and lymph nodes. We exposed cultured murine peritoneal macrophages to bismuth citrate and examined the bismuth accumulation over time. We found that in the mouse bismuth is absorbed systemically after a single dose of either compound, ranitidine bismuth more easily than bismuth citrate. Uptake could be shown in the stomach, duodenum, ileum and kidney for hours after exposure. Weeks after the exposure, deposits of bismuth were found in lymph nodes, liver, spleen and kidney as well as in macrophages in the gastrointestinal lamina propria. At the subcellular level, bismuth was found exclusively in lysosomes, primarily in macrophages and dendritic cells. Subsequent analyses of macrophage cultures showed lysosomal accumulations to be time and dose dependent.
Experimental studies of Ge nanocrystals embedded in SiO2 films doped with Er and Yb deposited by rf-magnetron sputtering are presented. Although inter-band photoluminescence (PL) from the Ge nanocrystals is not observed, it is nevertheless found that the presence of Ge nanocrystals is crucial for obtaining light emission from Er3+ and Yb3+. For both kinds of rare earth ions, the intensity of the related PL line has a maximum after heat treatment at 800 °C, and the PL excitation spectra for the two cases are very similar. This suggests that the presence and the structure of the nanocrystals are important for the efficiency of PL from Er3+ and Yb3+. Experiments performed with multilayer structures of Ge nanocrystals and SiO2 show that the optically active rare earth ions are located in the SiO2 layers, and not inside the Ge nanocrystals. The mechanism of energy transfer from Ge nanocrystals to the rare earth ions is found to be non-optical.
