135 research outputs found
CâF Bond Insertion: An Emerging Strategy for Constructing Fluorinated Molecules
CâF Insertion reactions, where an organic fragment formally inserts into a carbon-fluorine bond in a substrate, are highly attractive, yet largely unexplored, methods to prepare valuable fluorinated molecules. The inherent strength of CâF bonds and the resulting need for a large thermodynamic driving force to initiate CâF cleavage often leads to sequestering of the released fluoride in an unreactive by-product. Recently, however, several groups have succeeded in overcoming this challenge, opening up the study of CâF insertion as an efficient and highly atom-economical approach to prepare fluorinated compounds. In this article, the recent breakthroughs are discussed focusing on the key conceptual advances that allowed for both CâF bond cleavage and subsequent incorporation of the released fluoride into the product
Direct synthesis of acyl fluorides from carboxylic acids using benzothiazolium reagents
2-(Trifluoromethylthio)benzothiazolium triflate (BT-SCF3) was used as deoxyfluorinating reagent for the synthesis of versatile acyl fluorides directly from the corresponding carboxylic acids. These acyl fluorides were reacted with amines in a one-pot protocol to form different amides, including dipeptides, under mild and operationally simple conditions in high yields. Mechanistic studies suggest that BT-SCF3 can generate acyl fluorides from carboxylic acids via two distinct pathways, which allows the deoxyfluorinating reagent to be employed in sub-stoichiometric amounts
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The biomechanics of amnion rupture: an X-ray diffraction study
Pre-term birth is the leading cause of perinatal and neonatal mortality, 40% of which are attributed to the pre-term premature rupture of amnion. Rupture of amnion is thought to be associated with a corresponding decrease in the extracellular collagen content and/or increase in collagenase activity. However, there is very little information concerning the detailed organisation of fibrillar collagen in amnion and how this might influence rupture. Here we identify a loss of lattice like arrangement in collagen organisation from areas near to the rupture site, and present a 9% increase in fibril spacing and a 50% decrease in fibrillar organisation using quantitative measurements gained by transmission electron microscopy and the novel application of synchrotron X-ray diffraction. These data provide an accurate insight into the biomechanical process of amnion rupture and highlight X-ray diffraction as a new and powerful tool in our understanding of this process
High resolution nuclear magnetic resonance spectroscopy of highly-strained quantum dot nanostructures
Much new solid state technology for single-photon sources, detectors,
photovoltaics and quantum computation relies on the fabrication of strained
semiconductor nanostructures. Successful development of these devices depends
strongly on techniques allowing structural analysis on the nanometer scale.
However, commonly used microscopy methods are destructive, leading to the loss
of the important link between the obtained structural information and the
electronic and optical properties of the device. Alternative non-invasive
techniques such as optically detected nuclear magnetic resonance (ODNMR) so far
proved difficult in semiconductor nano-structures due to significant
strain-induced quadrupole broadening of the NMR spectra. Here, we develop new
high sensitivity techniques that move ODNMR to a new regime, allowing high
resolution spectroscopy of as few as 100000 quadrupole nuclear spins. By
applying these techniques to individual strained self-assembled quantum dots,
we measure strain distribution and chemical composition in the volume occupied
by the confined electron. Furthermore, strain-induced spectral broadening is
found to lead to suppression of nuclear spin magnetization fluctuations thus
extending spin coherence times. The new ODNMR methods have potential to be
applied for non-invasive investigations of a wide range of materials beyond
single nano-structures, as well as address the task of understanding and
control of nuclear spins on the nanoscale, one of the central problems in
quantum information processing
Non-coding variants disrupting a tissue-specific regulatory element in HK1 cause congenital hyperinsulinism.
This is the author accepted manuscript. The final version is available from Nature Research via the DOI in this recordData availability statement:
All nonâclinical data analysed during this study are included in this published article (and its
supplementary information files). Clinical and genotype data is available only through
collaboration as this can be used to identify individuals and so cannot be made openly
available. Requests for collaboration will be considered following an application to the
Genetic Beta Cell Research Bank (https://www.diabetesgenes.org/currentâresearch/geneticâ
betaâcellâresearchâbank/). Contact by email should be directed to the Corresponding author.Code availability statement:
All code and software versions used specified in Methods.Gene expression is tightly regulated, with many genes exhibiting cell-specific silencing when their protein product would disrupt normal cellular function1. This silencing is largely controlled by non-coding elements, and their disruption might cause human disease2. We performed gene-agnostic screening of the non-coding regions to discover new molecular causes of congenital hyperinsulinism. This identified 14 non-coding de novo variants affecting a 42-bp conserved region encompassed by a regulatory element in intron 2 of the hexokinase 1 gene (HK1). HK1 is widely expressed across all tissues except in the liver and pancreatic beta cells and is thus termed a 'disallowed gene' in these specific tissues. We demonstrated that the variants result in a loss of repression of HK1 in pancreatic beta cells, thereby causing insulin secretion and congenital hyperinsulinism. Using epigenomic data accessed from public repositories, we demonstrated that these variants reside within a regulatory region that we determine to be critical for cell-specific silencing. Importantly, this has revealed a disease mechanism for non-coding variants that cause inappropriate expression of a disallowed gene.Wellcome Trus
Isotope sensitive measurement of the hole-nuclear spin interaction in quantum dots
Decoherence caused by nuclear field fluctuations is a fundamental obstacle to
the realization of quantum information processing using single electron spins.
Alternative proposals have been made to use spin qubits based on valence band
holes having weaker hyperfine coupling. However, it was demonstrated recently
both theoretically and experimentally that the hole hyperfine interaction is
not negligible, although a consistent picture of the mechanism controlling the
magnitude of the hole-nuclear coupling is still lacking. Here we address this
problem by performing isotope selective measurement of the valence band
hyperfine coupling in InGaAs/GaAs, InP/GaInP and GaAs/AlGaAs quantum dots.
Contrary to existing models we find that the hole hyperfine constant along the
growth direction of the structure (normalized by the electron hyperfine
constant) has opposite signs for different isotopes and ranges from -15% to
+15%. We attribute such changes in hole hyperfine constants to the competing
positive contributions of p-symmetry atomic orbitals and the negative
contributions of d-orbitals. Furthermore, we find that the d-symmetry
contribution leads to a new mechanism for hole-nuclear spin flips which may
play an important role in hole spin decoherence. In addition the measured
hyperfine constants enable a fundamentally new approach for verification of the
computed Bloch wavefunctions in the vicinity of nuclei in semiconductor
nanostructures
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