Substitution of Re7+ into CaMnO3: an efficient free electron generation dopant for tuning of thermoelectric properties.

Highly dense CaMn1-xRexO3 (0 ≤ x ≤ 0.04) samples were prepared by solid-state synthesis. The effect of Re doping was assessed by the characterisation of crystal structure, oxygen content, and electrical and thermal transport properties. The oxidation state of the substituted Re was determined by X-ray absorption near edge spectra to be Re7+, and led to expansion of the lattice and an increase in electron carrier concentration due to the formation of Mn3+. The thermal behaviour of the electrical conductivity and the thermopower over a wide temperature range allowed identification of different conduction mechanisms: (1) below 110 K, 3D variable range hopping, (2) between 110 and 650 K, small polaron transport, and (3) above 650 K, activation of carriers over a mobility edge. Evaluation of the power factor expected for different dopant oxidation states as a function of dopant concentration shows that the doping strategy using a heavy heptavalent ion allows accessibility of the peak power factor at lower dopant concentrations, lowering the amount of non-ionised impurities, and therefore improves the electronic substitution efficiency, the ratio of activated carriers over the nominal doping concentration, compared to previously studied dopants. An increased power factor and a reduced lattice thermal conductivity are obtained with a peak figure of merit ZT = 0.16(3) at 947 K for CaMn0.98Re0.02O3. This is an approximately two-fold increase compared to undoped CaMnO3, and is comparable to the highest values reported for highly dense B-site doped CaMnO3

Remineralization of demineralized dentin using a dual analog system.

ObjectiveImproved methods are needed to remineralize dentin caries in order to promote conservation of dentin tissue and minimize the surgical interventions that are currently required for clinical treatment. Here, we test the hypothesis that bulk substrates can be effectively mineralized via a dual analog system proposed by others, using a tripolyphosphate (TPP) "templating analog" and a poly(acrylic acid) (PAA) or poly(aspartic acid) (pAsp) "sequestration analog," the latter of which generates the polymer-induced liquid-precursor (PILP) mineralization process studied in our laboratory.Material & methodsDemineralized human dentin slices were remineralized with and without pre-treatment with TPP, using either PAA or pAsp as the PILP process-directing agent. A control experiment with no polymer present was used for comparison.ResultsNo mineralization was observed in any of the PAA groups. In both the pAsp and no polymer groups, TPP inhibited mineralization on the surfaces of the specimens but promoted mineralization within the interiors. Pre-treatment with TPP enhanced overall mineralization of the pAsp group. However, when analysed via TEM, regions with little mineral were still present.ConclusionPoly(acrylic acid) was unable to remineralize demineralized dentin slices under the conditions employed, even when pre-treated with TPP. However, pre-treatment with TPP enhanced overall mineralization of specimens that were PILP-remineralized using pAsp

Thermal effects on electron-phonon interaction in silicon nanostructures

Raman spectra from silicon nanostructures, recorded using excitation laser power density of 1.0 kW/cm^2, is employed here to reveal the dominance of thermal effects at temperatures higher than the room temperature. Room temperature Raman spectrum shows only phonon confinement and Fano effects. Raman spectra recorded at higher temperatures show increase in FWHM and decrease in asymmetry ratio with respect to its room temperature counterpart. Experimental Raman scattering data are analyzed successfully using theoretical Raman line-shape generated by incorporating the temperature dependence of phonon dispersion relation. Experimental and theoretical temperature dependent Raman spectra are in good agreement. Although quantum confinement and Fano effects persists, heating effects start dominating at higher temperatures than room tempaerature.Comment: 9 Pages, 3 Figures and 1 Tabl

Anti-filarial Activity of Antibiotic Therapy Is Due to Extensive Apoptosis after Wolbachia Depletion from Filarial Nematodes

Filarial nematodes maintain a mutualistic relationship with the endosymbiont Wolbachia. Depletion of Wolbachia produces profound defects in nematode development, fertility and viability and thus has great promise as a novel approach for treating filarial diseases. However, little is known concerning the basis for this mutualistic relationship. Here we demonstrate using whole mount confocal microscopy that an immediate response to Wolbachia depletion is extensive apoptosis in the adult germline, and in the somatic cells of the embryos, microfilariae and fourth-stage larvae (L4). Surprisingly, apoptosis occurs in the majority of embryonic cells that had not been infected prior to antibiotic treatment. In addition, no apoptosis occurs in the hypodermal chords, which are populated with large numbers of Wolbachia, although disruption of the hypodermal cytoskeleton occurs following their depletion. Thus, the induction of apoptosis upon Wolbachia depletion is non-cell autonomous and suggests the involvement of factors originating from Wolbachia in the hypodermal chords. The pattern of apoptosis correlates closely with the nematode tissues and processes initially perturbed following depletion of Wolbachia, embryogenesis and long-term sterilization, which are sustained for several months until the premature death of the adult worms. Our observations provide a cellular mechanism to account for the sustained reductions in microfilarial loads and interruption of transmission that occurs prior to macrofilaricidal activity following antibiotic therapy of filarial nematodes

Retinoid X receptor promotes hematopoietic stem cell fitness and quiescence and preserves hematopoietic homeostasis.

Hematopoietic stem cells (HSCs) balance self-renewal and differentiation to maintain hematopoietic fitness throughout life. In steady-state conditions, HSC exhaustion is prevented by the maintenance of most HSCs in a quiescent state, with cells entering the cell cycle only occasionally. HSC quiescence is regulated by retinoid and fatty-acid ligands of transcriptional factors of the nuclear retinoid X receptor (RXR) family. Here, we show that dual deficiency for hematopoietic RXRa and RXRb induces HSC exhaustion, myeloid cell/megakaryocyte differentiation, and myeloproliferative-like disease. RXRa and RXRb maintain HSC quiescence, survival, and chromatin compaction; moreover, transcriptome changes in RXRa;RXRb-deficient HSCs include premature acquisition of an aging-like HSC signature, MYC pathway upregulation, and RNA intron retention. Fitness loss and associated RNA transcriptome and splicing alterations in RXRa;RXRb-deficient HSCs are prevented by Myc haploinsufficiency. Our study reveals the critical importance of RXRs for the maintenance of HSC fitness and their protection from premature aging.We thank the members of the J.A.C. and M.R. laboratories for extensive discussions and critiques of the manuscript. We thank Daniel Metzger (Université de Strasbourg, France) for Rxrbf/f 418 mice, Juan Carlos Zúñiga-Pflücker (Sunnybrook Health Sciences Centre, Canada) for OP9-NL1 cells, Daniel Jiménez-Carretero (CNIC) for t-SNE analysis, the CRG (Barcelona, Spain) Genomics Unit for ATACseq sequencing, and S. Bartlett (CNIC) for editorial assistance. We also thank the staff of the CNIC Cellomics and Animal facilities for technical support. This study was supported by grants from the Spanish Ministerio de Ciencia e Innovación (MICIN) (SAF2017-90604-REDT-NurCaMein, RTI2018- 095928-B100, and PID2021-122552OB-I00), La Marató de TV3 Foundation (201605-32), and the Comunidad de Madrid (MOIR-B2017/BMD-3684) to M.R and from the Formación de Profesorado Universitario (FPU17/01731) program (MICIN) to J.P. The project also received funding from the US National Institutes of Health (R01 DK124115, P01 HL158688, R01 HL147536, R01 CA237016 and U54 DK126108 to J.A.C). The CNIC is supported by the Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia e Innovación (MCIN), and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (grant CEX2020-001041-S funded by MICIN/AEI/10.13039/501100011033).S

The impact of point mutations in the human androgen receptor : classification of mutations on the basis of transcriptional activity

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