On the protection of the isolation at the fabrication of all niobium josepshson-junctions

The protection mechanism of thin gold layer for preparation of all-niobium devices is discussed. A suggestion on the electronic origin of protection is presented

Topologically associating domain boundaries are required for normal genome function

Topologically associating domain (TAD) boundaries partition the genome into distinct regulatory territories. Anecdotal evidence suggests that their disruption may interfere with normal gene expression and cause disease phenotypes1,2,3, but the overall extent to which this occurs remains unknown. Here we demonstrate that targeted deletions of TAD boundaries cause a range of disruptions to normal in vivo genome function and organismal development. We used CRISPR genome editing in mice to individually delete eight TAD boundaries (11–80 kb in size) from the genome. All deletions examined resulted in detectable molecular or organismal phenotypes, which included altered chromatin interactions or gene expression, reduced viability, and anatomical phenotypes. We observed changes in local 3D chromatin architecture in 7 of 8 (88%) cases, including the merging of TADs and altered contact frequencies within TADs adjacent to the deleted boundary. For 5 of 8 (63%) loci examined, boundary deletions were associated with increased embryonic lethality or other developmental phenotypes. For example, a TAD boundary deletion near Smad3/Smad6 caused complete embryonic lethality, while a deletion near Tbx5/Lhx5 resulted in a severe lung malformation. Our findings demonstrate the importance of TAD boundary sequences for in vivo genome function and reinforce the critical need to carefully consider the potential pathogenicity of noncoding deletions affecting TAD boundaries in clinical genetics screening.This work was supported by U.S. National Institutes of Health (NIH) grants to L.A.P. and A.V. (UM1HG009421). Research was conducted at the E.O. Lawrence Berkeley National Laboratory and performed under U.S. Department of Energy Contract DE-AC02-05CH11231, University of California (UC). Phenotyping performed by the UC Davis Mouse Biology Program (MBP) (www.mousebiology.org) was funded by an NIH administrative supplement to the KOMP2 grant, 3UM1OD023221-07S1, for phenotyping non-coding elements. Adyam Akeza was supported by the NIH Bridges to Baccalaureate Program Grant R25GM095401 via UC Berkeley. J.L.-R. is supported by the Spanish Ministerio de Ciencia e Innovacion (PID2020-113497GB-I00).Peer reviewe

Progress in a-Si:H/c-Si heterojunction emitters obtained by Hot-Wire CVD at 200°C

In this work, we investigate heterojunction emitters deposited by Hot-Wire CVD on p-type crystalline silicon. The emitter structure consists of an n-doped film (20 nm) combined with a thin intrinsic hydrogenated amorphous silicon buffer layer (5 nm). The microstructure of these films has been studied by spectroscopic ellipsometry in the UV-visible range. These measurements reveal that the microstructure of the n-doped film is strongly influenced by the amorphous silicon buffer. The Quasy-Steady-State Photoconductance (QSS-PC) technique allows us to estimate implicit open-circuit voltages near 700 mV for heterojunction emitters on p-type (0.8 Ω·cm) FZ silicon wafers. Finally, 1 cm 2 heterojunction solar cells with 15.4% conversion efficiencies (total area) have been fabricated on flat p-type (14 Ω·cm) CZ silicon wafers with aluminum back-surface-field contact

Kimberley Hospital indications for urgent head computed tomography in a resource limited healthcare environment: the KHIC rule. Abstract 185.

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