Hard x-ray photon-in-photon-out spectroscopy with lifetime resolution – of XAS, XES, RIXSS and HERFD

Spectroscopic techniques that aim to resolve the electronic configuration and local coordination of a central atom by detecting inner-shell radiative decays following photoexcitation using hard X-rays are presented. The experimental setup requires an X-ray spectrometer based on perfect crystal Bragg optics. The possibilities arising from non-resonant (X-Ray Emission Spectroscopy - XES) and resonant excitation (Resonant Inelastic X-Ray Scattering Spectroscopy – RIXSS, High-Energy-Resolution Fluorescence Detected (HERFD) XAS) are discussed when the instrumental energy broadenings of the primary (beamline) monochromator and the crystal spectrometer for x-ray emission detection are on the order of the core hole lifetimes of the intermediate and final electronic states. The small energy bandwidth in the emission detection yields line-sharpened absorption features. In transition metal compounds, electron-electron interactions as well as orbital splittings and fractional population can be revealed. Combination with EXAFS spectroscopy enables to extent the k-range beyond unwanted absorption edges in the sample that limit the EXAFS range in conventional absorption spectroscopy

Probing the dynamics of plasmon-excited hexanethiol-capped gold nanoparticles by picosecond X-ray absorption spectroscopy

Picosecond X-ray absorption spectroscopy (XAS) is used to investigate the electronic and structural dynamics initiated by plasmon excitation of 1.8 nm diameter Au nanoparticles (NPs) functionalised with 1-hexanethiol. We show that 100 ps after photoexcitation the transient XAS spectrum is consistent with an 8% expansion of the Au-Au bond length and a large increase in disorder associated with melting of the NPs. Recovery of the ground state occurs with a time constant of ∼1.8 ns, arising from thermalisation with the environment. Simulations reveal that the transient spectrum exhibits no signature of charge separation at 100 ps and allows us to estimate an upper limit for the quantum yield (QY) of this process to be <0.1

Героическое в произведениях А.А. Фета о Крымской войне в контексте эстетической полемики ХIХ века

Проблемы героического в военной прозе и поэзии А.А Фета рассматриваются в контексте эстетической полемики второй половины Х1Х века. В ходе исследования литературно-критических материалов и произведений поэта делается попытка пересмотреть существование традиционных стереотипов относительно творчества и личной жизни художника-эстета и прийти к выводу: военная тематика поэта "чистого искусства" не была обособленной от всего его литературного наследия, она органически вписывалась в его эстетическую программу. Героическое в эстетике и творчестве А. Фета представлено наравне с категорией красоты как составляющей категории прекрасного.Проблеми героiчного в военiй прозi та поезii А.А.Фета разглядаються в контекстi літературної полемікі другоїї половини Х1Х сторіччя. В ході дослiдництва лiтературно-крiтичних матерiалiв та творiв поета робиться спроба переглянути iснування традицiйних стереотипiв вiдносно творчостi та особистого життя художника- естета та прийти до висновка: вiйськова тематика поета "чистого мистецтва" не була вiдокремленою вiд всii його спадщини, вона органiчно вписувалась в його естетичну програму. Героiчне в естетицi та творчостi А.Фета надано нарiвнi з категорiєю красоти, як складовоi категорii прекрасного.Heroic problems in war prose and poetry of A.A.Fet are examined in the context of literal controversy of the second part of the 19thcenturi. In the way of research of literal and critical materials and works of the poet the attempt is making to reexamine existence of formed stereotypes which are related to creative work and personal life of artist-design and go up to the conclusion that poet?s war subject-matter of "pure art" was not isolated from all his legacy. It enters organically into his aesthetic program

Bi-allelic Variants in METTL5 Cause Autosomal-Recessive Intellectual Disability and Microcephaly

Contains fulltext : 208970.pdf (publisher's version ) (Open Access

p16 mutations/deletions are not frequent events in prostate cancer.

Cyclin-dependent kinase-4 inhibitor gene (p16INK4) has recently been mapped to chromosome 9p21. Homozygous deletions of this gene have been found at high frequency in cell lines derived from different types of tumours. These findings suggested therefore, that p16INK4 is a tumour-suppressor gene involved in a wide variety of human cancers. To investigate the frequency of p16INK mutations/deletions in prostate cancer, we screened 20 primary prostate tumours and four established cell lines by polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP) analysis for exon 1 and exon 2. In contrast to most previous reports, no homozygous deletions were found in prostate cancer cell lines, but one cell line (DU145) has revealed to a mutation at codon 76. Only two SSCP shifts were detected in primary tumours: one of them corresponds to a mutation at codon 55 and the other one probably corresponds to a polymorphism. These data suggest that mutation of the p16INK4 gene is not a frequent genetic alteration implicated in prostate cancer development

Identification of signaling pathways in early mammary gland development by mouse genetics

The mammary gland develops as an appendage of the ectoderm. The prenatal stage of mammary development is hormone independent and is regulated by sequential and reciprocal signaling between the epithelium and the mesenchyme. A number of recent studies using human and mouse genetics, in particular targeted gene deletion and transgenic expression, have identified some of the signals that control specific steps in development. This process involves cell specification and proliferation, reciprocal tissue interactions and cell migration. Since some of these events are recapitulated during tumorigenesis, an understanding of these signaling pathways may contribute to the development of targeted therapies and novel drugs

The deleted in brachydactyly B domain of ROR2 is required for receptor activation by recruitment of Src

The transmembrane receptor 'ROR2' resembles members of the receptor tyrosine kinase family of signalling receptors in sequence but its' signal transduction mechanisms remain enigmatic. This problem has particular importance because mutations in ROR2 are associated with two human skeletal dysmorphology syndromes, recessive Robinow Syndrome (RS) and dominant acting Brachydactyly type B (BDB). Here we show, using a constitutive dimerisation approach, that ROR2 exhibits dimerisation-induced tyrosine kinase activity and the ROR2 C-terminal domain, which is deleted in BDB, is required for recruitment and activation of the non-receptor tyrosine kinase Src. Native ROR2 phosphorylation is induced by the ligand Wnt5a and is blocked by pharmacological inhibition of Src kinase activity. Eight sites of Src-mediated ROR2 phosphorylation have been identified by mass spectrometry. Activation via tyrosine phosphorylation of ROR2 receptor leads to its internalisation into Rab5 positive endosomes. These findings show that BDB mutant receptors are defective in kinase activation as a result of failure to recruit Src