Discovery of τ Neutrino Appearance in the CNGS Neutrino Beam with the OPERA Experiment.

The OPERA experiment was designed to search for ν_{µ}→ν_{τ} oscillations in appearance mode, i.e., by detecting the τ leptons produced in charged current ν_{τ} interactions. The experiment took data from 2008 to 2012 in the CERN Neutrinos to Gran Sasso beam. The observation of the ν_{µ}→ν_{τ} appearance, achieved with four candidate events in a subsample of the data, was previously reported. In this Letter, a fifth ν_{τ} candidate event, found in an enlarged data sample, is described. Together with a further reduction of the expected background, the candidate events detected so far allow us to assess the discovery of ν_{µ}→ν_{τ} oscillations in appearance mode with a significance larger than 5σ.

On structural features of fullerene C60 dissolved in carbon disulfide: complementary study by small-angle neutron scattering and molecular dynamic simulations.

The parameters of fullerene C(60) dissolved in carbon disulfide CS(2) are analyzed by small-angle neutron scattering (SANS) in a wide interval of momentum transfer. To exclude the influence of nonequilibrium conditions, the solutions are prepared without applying shaking, stirring or ultrasound. No indication of the equilibrium cluster state of C(60) (with the cluster size below 60 nm) in the final solutions is revealed. Molecular dynamic simulations are complementary used to find out the partial volume of C(60) in CS(2) and the scattering contribution of the solvent organization at the interface with the fullerene molecule, which is shown to be small. Among several approaches for describing SANS data the preference is given to the model, which takes into account the presence of stable C(60) dimers (comprising 10% of the total particle number density) in the solution.

[Modeling viability of mammalian cells exposed to ionizing radiation with different linear energy transfer]. / Modelirovanie vyzhivaemosti kletok mlekopitaiushchik, podvergnutykh deistviiu ioniziruiushchego izlucheniia s raznoi lineinoi peredachei énergii.

A mathematical model of the survival of mammalian cells exposed to ionizing radiation is proposed, which takes into account nonuniform radiosensitivity of different regions of DNA. The model is based on the assumption that the double-strand breaks of the anchor DNA, induced either directly by irradiation or by enzymes, play a key role in the lethal radiation effect. The model survival curves are in good agreement with experimental curves measured in different laboratories.

[Analysis of the role of DNA repair, regulation of cell cycle and apoptosis in the radiation-induced adaptive response of mammalian cells]. / Analiz roli reparatsii DNK, reguliatsii kletochnogo tsikla i apoptoza v radiatsionno-indutsirovannom adaptivnom otvete kletok mlekopitaiushchikh.

In according with the mechanism for an adaptive response (AR) offered in [Bodnarchuk I.A.//Radiat. biologiya. Radioecologiya. 2002. V. 42. No. 1. P. 36-43], the low-dose irradiation of mammalian cells leads to the activation of such enzymes as Ras, ceramid-activated protein kinase, phospholipase C (PL C) and phosphatidilinostol 3-kinase (PI 3-K). All of them initiate apoptosis and eliminate the most radiosensitive cells form the population before the damaging irradiation. The function of PL C and PI 3-K accompanied by protein kinase C (PK C) activation. PK C activates transcription of the poly(ADP-ribose)polymerase (PARP) gene and DNA polymerase beta gene, and makes posttranslation activation of apurinic/apyrimidinic endonuclease APE, which are participating in the base excision repair (BER). PK C, APE and PARP activate the transcription factor p53, PK C and APE also activate the transcription factor AP-1, AP-1 and p53 take part in the initiation of nucleotide excision reapir (NER). The function of BER, NER and p53 after the damaging irradiation is accompanied by the G1-arrest of cell cycle progression. During G1-arrest there is p53-dependent activation of nonhomologous ends joining (NHEJ) and the inhibition of homologous recombination repair (HRR) of the DNA double-strand breaks takes place. Passing through the NHEJ the cells will outgo from G1-arrest and follow by HRR. AP-1 takes part in outgoing of cells from G1-arrest. So, the preliminary low-dose irradiation causes the decrease of quantity of cells died apoptotically after damaging irradiation as a result of inability to overcome G1-arrest. Thus, AR is the combination of processes: the removal of radiosensitive subpopulation of cells, and/or the activation of DNA repair, and/or the increase of cells ability to overcome the cell cycle delay.

[Hypothesis of the mechanism of adaptive response induction in mammalian cells by low-dose irradiation]. / Gipoteza o mekhanizme induktsii adaptivnogo otveta pri obluchenii kletok mlekopitaiushchikh v malykh dozakh.

The mechanism for radiation-induced adaptive response (RAR) in mammalian cells is presented in this paper. The start point of the RAR in the frame of this mechanism is the receptors for growth factors activation due to the increase in the microviscosity of plasma membrane subjected to oxidative damage. There are components of the mitogen-activated signal transduction pathway which take part in the subsequent processes. The main of them are protein kinase C (PK C), motogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK). They make posttranslation modification of the DNA metabolism enzymes and of the transcription factors p53 and c-Jun/AP-1. There are genes taking part in the excision repair and apoptosis among the c-Jun/AP-1 and the p53 targets. C-Jun/AP-1 and p53 can be direct participants at the stage of exision repair when DNA damage is recognized. Thus, the proposed scheme of events removes the contradiction between two hypotheses which explain the RAR: intracell DNA repair induction, either of cell selection in culture of mammalian cells.