Vibrational and vibrational-torsional interactions in the 0–600 cm-1 region of the S1 ← S0 spectrum of p-xylene investigated with resonance-enhanced multiphoton ionization (REMPI) and zero-kinetic-energy (ZEKE) spectroscopy

We assign the 0–600 cm-1 region of the S1 ← S0 transition in p-xylene using resonance-enhanced multiphoton ionization (REMPI) and zero-kinetic-energy (ZEKE) spectroscopy. In the 0–300 cm-1 range, as well as the intense origin band there are a number of torsional and vibration-torsion (vibtor) features. The latter are discussed in more detail in an accompanying paper [Gardner et al. J. Chem. Phys. XXX, xxxxxx (2016)]. Here we focus on the origin and the 300–650 cm-1 region, where vibrational bands and some vibtor activity is observed. From the origin ZEKE spectrum we derive the ionization energy of p-xylene as 68200 ± 5 cm-1. The assignment of the REMPI spectrum is based on the activity observed in the ZEKE spectra coupled with knowledge of the vibrational wavenumbers obtained from quantum chemical calculations. We assign several isolated vibrations, and a complex Fermi resonance that is found to comprise contributions from both vibrations and vibtor levels, and we examine this via a two-dimensional ZEKE (2D-ZEKE) spectrum. A number of the vibrational features in the REMPI and ZEKE spectra of p-xylene that have been reported previously are reassigned and now largely consist of totally-symmetric contributions. We briefly discuss the appearance of non-Franck-Condon allowed transitions. Finally, we find remarkably similar spectral activity to that in the related disubstituted benzenes, para-difluorobenzene and para-fluorotoluene

An introduction to Graph Data Management

A graph database is a database where the data structures for the schema and/or instances are modeled as a (labeled)(directed) graph or generalizations of it, and where querying is expressed by graph-oriented operations and type constructors. In this article we present the basic notions of graph databases, give an historical overview of its main development, and study the main current systems that implement them

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

New factors in mammalian DNA repair-the chromatin connection

In response to DNA damage mammalian cells activate a complex network of stress response pathways collectively termed DNA damage response (DDR). DDR involves a temporary arrest of the cell cycle to allow for the repair of the damage. DDR also attenuates gene expression by silencing global transcription and translation. Main function of DDR is, however, to prevent the fixation of debilitating changes to DNA by activation of various DNA repair pathways. Proper execution of DDR requires careful coordination between these interdependent cellular responses. Deregulation of some aspects of DDR orchestration is potentially pathological and could lead to various undesired outcomes such as DNA translocations, cellular transformation or acute cell death. It is thus critical to understand the regulation of DDR in cells especially in the light of a strong linkage between the DDR impairment and the occurrence of common human diseases such as cancer. In this review we focus on recent advances in understanding of mammalian DNA repair regulation and a on the function of PAXX/c9orf142 and ZNF281 proteins that recently had been discovered to play a role in that process. We focus on regulation of double-strand DNA break (DSB) repair via the non-homologous end joining pathway, as unrepaired DSBs are the primary cause of pathological cellular states after DNA damage. Interestingly these new factors operate at the level of chromatin, which reinforces a notion of a central role of chromatin structure in the regulation of cellular DDR regulation