Resistive transport in a mesoscopic proximity superconductor

We review transport measurements in a normal metal (N) in contact with one or two superconducting (S) islands. From the experiment, we distinguish the Josephson coupling, the mesoscopic fluctuations and the proximity effect. In a loop-shaped N conductor, we observe large h/2e-periodic magnetoresistance oscillations that decay with temperature T with a 1/T power-law. This behaviour is the signature of the long-range coherence of the low-energy electron pairs induced by the Andreev reflection at the S interface. At temperature and voltage below the Thouless energy $\hbar D / L^2$, we observe the re-entrance of the metallic resistance. Experimental results agree with the linearized quasiclassical theory.Comment: 8 pages, 6 included epsf figures, Invited paper at the LT21 Conference, Praha, August 1996. To appear in Czech. J. of Phys. 46, Part S6 (1996

Re-entrance of the metallic conductance in a mesoscopic proximity superconductor

We present an experimental study of the diffusive transport in a normal metal near a superconducting interface, showing the re-entrance of the metallic conductance at very low temperature. This new mesoscopic regime comes in when the thermal coherence length of the electron pairs exceeds the sample size. This re-entrance is suppressed by a bias voltage given by the Thouless energy and can be strongly enhanced by an Aharonov Bohm flux. Experimental results are well described by the linearized quasiclassical theory.Comment: improved version submitted to Phys. Rev. lett., 4 pages, 5 included epsf figure

Cold atoms in a high-Q ring-cavity

We report the confinement of large clouds of ultra-cold 85-Rb atoms in a standing-wave dipole trap formed by the two counter-propagating modes of a high-Q ring-cavity. Studying the properties of this trap we demonstrate loading of higher-order transverse cavity modes and excite recoil-induced resonances.Comment: 4 pages, 4 figure

Influence of a hypoiodite mouth-wash on dental plaque formation in vivo

This study describes an in vivo inhibition of dental plaque growth after peroxidase-generated hypoiodite (OI-) mouth-washes. After giving up ail other usual hygiene procedures nine healthy volunteers washed their mouth using 10 ml of the mouth-wash [H2O2 (0.005%), Kl (50 mM) and lactoperoxidase (0.04%)] three times a day for 1 minute for 3 days. The initial oxidation power of this mixture represented 430 ±11 µM oxidised cysteine (n=6), dropping down to 87 ± 6 µM after the solution was spat out (n=5). A saline solution served as a negative control, and a 0.2% chlorhexidine digluconate solution as a positive control. Proximal dental plaque between mandibular canine and lateral incisor (left and right) was collected after 3 days using standardized sterile toothpicks, then analysed for ATP and protein content. ATP concentrations dropped to 49% of the control values after OI- rinsing, and to 9% after chlorhexidine rinsing while the protein content dropped to 48% for OI- versus 31 % for chlorhexidine. However, when considering the ATP content per protein µg, only the decrease to 6% of the initial value in the chlorhexidine testing was significant while the drop to 81% for the OI- testings was not significant. This study points out a negative effect of OI- on plaque growth in vivo.Cette étude décrit l’inhibition de la croissance in vivo de la plaque dentaire après traitement à l’aide d’un bain de bouche contenant de la peroxydase et produisant de l’hypoiodite (OI-). Neuf personnes ont utilisé ce rinçage pendant une minute, 3 fois par jour pendant 3 jours, cependant qu’elles cessaient toute autre pratique d’hygiène bucco-dentaire; une solution saline servant de contrôle négatif et une solution de chlorhexidine de contrôle positif. Des échantillons de plaque interproximale furent prélevés de manière standardisée à l’aide de cure-dents stériles et leur contenu en ATP et en protéines furent mesurés. Les concentrations en ATP après traitement à l’OI- ne représentaient plus que 49% des valeurs des contrôles négatifs; le traitement à la chlorhexidine 31%. Le rapport ATP/masse protéique est fortement abaissé après traitement à la chlorhexidine (6%) mais se maintient à 85% de la valeur témoin après traitement à l’OI-

Laser-induced resonance shifts of single molecules self-coupled by a metallic surface

The spectral properties of single molecules placed near a metallic surface are investigated at low temperatures. Because of the high quality factor of the optical resonance, a laser-induced shift of the molecular lines is evidenced for the first time. The shift dependence on the laser excitation intensity and on the dephasing rate of the transition dipole is studied. A simple theoretical model of a laser-driven molecule self-coupled by a mirror is developed to qualitatively interpret the observations.Peer reviewedPhysic

Optineurin Is Required for CYLD-Dependent Inhibition of TNFα-Induced NF-κB Activation

The nuclear factor kappa B (NF-κB) regulates genes that function in diverse cellular processes like inflammation, immunity and cell survival. The activation of NF-κB is tightly controlled and the deubiquitinase CYLD has emerged as a key negative regulator of NF-κB signalling. Optineurin, mutated in certain glaucomas and amyotrophic lateral sclerosis, is also a negative regulator of NF-κB activation. It competes with NEMO (NF-κB essential modulator) for binding to ubiquitinated RIP (receptor interacting protein) to prevent NF-κB activation. Recently we identified CYLD as optineurin-interacting protein. Here we have analysed the functional significance of interaction of optineurin with CYLD. Our results show that a glaucoma-associated mutant of optineurin, H486R, is altered in its interaction with CYLD. Unlike wild-type optineurin, the H486R mutant did not inhibit tumour necrosis factor α (TNFα)-induced NF-κB activation. CYLD mediated inhibition of TNFα-induced NF-κB activation was abrogated by expression of the H486R mutant. Upon knockdown of optineurin, CYLD was unable to inhibit TNFα-induced NF-κB activation and showed drastically reduced interaction with ubiquitinated RIP. The level of ubiquitinated RIP was increased in optineurin knockdown cells. Deubiquitination of RIP by over-expressed CYLD was abrogated in optineurin knockdown cells. These results suggest that optineurin regulates NF-κB activation by mediating interaction of CYLD with ubiquitinated RIP thus facilitating deubiquitination of RIP

p53 Amino-Terminus Region (1–125) Stabilizes and Restores Heat Denatured p53 Wild Phenotype

BACKGROUND:The intrinsically disordered N-ter domain (NTD) of p53 encompasses approximately hundred amino acids that contain a transactivation domain (1-73) and a proline-rich domain (64-92) and is responsible for transactivation function and apoptosis. It also possesses an auto-inhibitory function as its removal results in remarkable reduction in dissociation of p53 from DNA. PRINCIPAL FINDINGS/METHODOLOGY:In this report, we have discovered that p53-NTD spanning amino acid residues 1-125 (NTD125) interacted with WT p53 and stabilized its wild type conformation under physiological and elevated temperatures, both in vitro and in cellular systems. NTD125 prevented irreversible thermal aggregation of heat denatured p53, enhanced p21-5'-DBS binding and further restored DBS binding activity of heat-denatured p53, in vitro, in a dose-dependent manner. In vivo ELISA and immunoprecipitation analysis of NTD125-transfected cells revealed that NTD125 shifted equilibrium from p53 mutant to wild type under heat stress conditions. Further, NTD125 initiated nuclear translocation of cytoplasmic p53 in transcriptionally active state in order to activate p53 downstream genes such as p21, Bax, PUMA, Noxa and SUMO. CONCLUSION/SIGNIFICANCE:Here, we showed that a novel chaperone-like activity resides in p53-N-ter region. This study might have significance in understanding the role of p53-NTD in p53 stabilization, conformational activation and apoptosis under heat-stress conditions

Finding the Needles in the Metagenome Haystack

In the collective genomes (the metagenome) of the microorganisms inhabiting the Earth’s diverse environments is written the history of life on this planet. New molecular tools developed and used for the past 15 years by microbial ecologists are facilitating the extraction, cloning, screening, and sequencing of these genomes. This approach allows microbial ecologists to access and study the full range of microbial diversity, regardless of our ability to culture organisms, and provides an unprecedented access to the breadth of natural products that these genomes encode. However, there is no way that the mere collection of sequences, no matter how expansive, can provide full coverage of the complex world of microbial metagenomes within the foreseeable future. Furthermore, although it is possible to fish out highly informative and useful genes from the sea of gene diversity in the environment, this can be a highly tedious and inefficient procedure. Microbial ecologists must be clever in their pursuit of ecologically relevant, valuable, and niche-defining genomic information within the vast haystack of microbial diversity. In this report, we seek to describe advances and prospects that will help microbial ecologists glean more knowledge from investigations into metagenomes. These include technological advances in sequencing and cloning methodologies, as well as improvements in annotation and comparative sequence analysis. More significant, however, will be ways to focus in on various subsets of the metagenome that may be of particular relevance, either by limiting the target community under study or improving the focus or speed of screening procedures. Lastly, given the cost and infrastructure necessary for large metagenome projects, and the almost inexhaustible amount of data they can produce, trends toward broader use of metagenome data across the research community coupled with the needed investment in bioinformatics infrastructure devoted to metagenomics will no doubt further increase the value of metagenomic studies in various environments

Protection from ultraviolet damage and photocarcinogenesis by vitamin d compounds

© Springer Nature Switzerland AG 2020. Exposure of skin cells to UV radiation results in DNA damage, which if inadequately repaired, may cause mutations. UV-induced DNA damage and reactive oxygen and nitrogen species also cause local and systemic suppression of the adaptive immune system. Together, these changes underpin the development of skin tumours. The hormone derived from vitamin D, calcitriol (1,25-dihydroxyvitamin D3) and other related compounds, working via the vitamin D receptor and at least in part through endoplasmic reticulum protein 57 (ERp57), reduce cyclobutane pyrimidine dimers and oxidative DNA damage in keratinocytes and other skin cell types after UV. Calcitriol and related compounds enhance DNA repair in keratinocytes, in part through decreased reactive oxygen species, increased p53 expression and/or activation, increased repair proteins and increased energy availability in the cell when calcitriol is present after UV exposure. There is mitochondrial damage in keratinocytes after UV. In the presence of calcitriol, but not vehicle, glycolysis is increased after UV, along with increased energy-conserving autophagy and changes consistent with enhanced mitophagy. Reduced DNA damage and reduced ROS/RNS should help reduce UV-induced immune suppression. Reduced UV immune suppression is observed after topical treatment with calcitriol and related compounds in hairless mice. These protective effects of calcitriol and related compounds presumably contribute to the observed reduction in skin tumour formation in mice after chronic exposure to UV followed by topical post-irradiation treatment with calcitriol and some, though not all, related compounds