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LiI-AgI-B2O3 glasses doped with different concentrations of MnO (ranging from 0 to 0.8 mol%) were prepared. Electrical and dielectric properties have been studied over a wide frequency range of 10-2 - 106 Hz and in the temperature range from 173 to 523 K. The valence states of manganese ions and their coordination in the glass network have been investigated using optical absorption, luminescence, and ESR spectroscopy. The analysis of the spectroscopic results has indicated that the manganese ions exist in both Mn2+ and Mn3+ states and occupy octahedral and tetrahedral positions. With increasing MnO concentration there is a gradual increase in the tetrahedral occupancy of Mn2+ ions at the expense of octahedral occupancy in the glass network. The results of dc conductivity have indicated that when T > θD/2, the small polaron hopping model is appropriate and the conduction is adiabatic in the nature. Further, the analysis of experimental data indicates that there is a mixed, ionic and electronic, conduction. It has been observed that the electrical conductivity decreases as the concentration of MnO increases suggesting the electronic conduction controlled by polaron hopping between manganese ions. In the low temperature region, up to 250 K, the ac conductivity is nearly temperature independent and varies linearly with frequency, which can be explained by the quantum mechanical tunneling (QMT) model. The dielectric properties have been analyzed in the framework of complex dielectric permittivity and complex electrical modulus formalisms. The evolution of the complex permittivity as a function of frequency and temperature has been investigated. [ABSTRACT FROM AUTHOR]

The ac electrical conductivity and dielectric constant of LiI-AgI-B2O3 glass doped with 0.1 mol. % MnO were investigated in the frequency range from 1 Hz to 1 MHz and the temperature range from 5 K to 450 K. At temperatures below 450 K, an ac conductivity and dielectric constant follow the universal dielectric response (UDR), being typical for hopping or tunneling of localized charge carriers. A detailed analysis of the temperature dependence of the UDR parameter s in terms of the theoretical model for tunneling of small polarons revealed that, below 450 K, this mechanism governs the charge transport in this glass. The comparison of the values of characteristic coefficients W∞ and Eac determined by two different methods confirms the polaronic behavior of this system. [ABSTRACT FROM AUTHOR]

Mdc1 is a large modular phosphoprotein scaffold that maintains signaling and repair complexes at double-stranded DNA break sites. Mdc1 is anchored to damaged chromatin through interaction of its C-terminal BRCT-repeat domain with the tail of γH2AX following DNA damage, but the role of the N-terminal forkhead-associated (FHA) domain remains unclear. We show that a major binding target of the Mdc1 FHA domain is a previously unidentified DNA damage and ATM-dependent phosphorylation site near the N-terminus of Mdc1 itself. Binding to this motif stabilizes a weak self-association of the FHA domain to form a tight dimer. X-ray structures of free and complexed Mdc1 FHA domain reveal a 'head-to-tail' dimerization mechanism that is closely related to that seen in pre-activated forms of the Chk2 DNA damage kinase, and which both positively and negatively influences Mdc1 FHA domain-mediated interactions in human cells prior to and following DNA damage.

The MRE11-RAD50-NBS1 (MRN) complex accumulates at sites of DNA double-strand breaks in large chromatin domains flanking the lesion site. The mechanism of MRN accumulation involves direct binding of the Nijmegen breakage syndrome 1 (NBS1) subunit to phosphorylated mediator of the DNA damage checkpoint 1 (MDC1), a large nuclear adaptor protein that interacts directly with phosphorylated H2AX. NBS1 contains an FHA domain and two BRCT domains at its amino terminus. Here, we show that both of these domains participate in the interaction with phosphorylated MDC1. Point mutations in key amino acid residues of either the FHA or the BRCT domains compromise the interaction with MDC1 and lead to defects in MRN accumulation at sites of DNA damage. Surprisingly, only mutation in the FHA domain, but not in the BRCT domains, yields a G2/M checkpoint defect, indicating that MDC1-dependent chromatin accumulation of the MRN complex at sites of DNA breaks is not required for G2/M checkpoint activation.

The differences between peritumoral brain tissue infiltrated by tumor and vasogenic edema were prospectively evaluated by comparing the apparent diffusion coefficient (ADC) of peritumoral areas of infiltrative tumors (anaplastic astrocytomas and glioblastomas) to that of peritumoral areas of noninfiltrative tumors (metastatic carcinomas) on 54 patients. Peritumoral ADCs indicated the possibility of differentiation between tumor infiltration and vasogenic edema, as well as between primary gliomas and metastases.

The MRE11-RAD50-Nijmegen breakage syndrome 1 (NBS1 [MRN]) complex accumulates at sites of DNA double-strand breaks (DSBs) in microscopically discernible nuclear foci. Focus formation by the MRN complex is dependent on MDC1, a large nuclear protein that directly interacts with phosphorylated H2AX. In this study, we identified a region in MDC1 that is essential for the focal accumulation of the MRN complex at sites of DNA damage. This region contains multiple conserved acidic sequence motifs that are constitutively phosphorylated in vivo. We show that these motifs are efficiently phosphorylated by caseine kinase 2 (CK2) in vitro and directly interact with the N-terminal forkhead-associated domain of NBS1 in a phosphorylation-dependent manner. Mutation of these conserved motifs in MDC1 or depletion of CK2 by small interfering RNA disrupts the interaction between MDC1 and NBS1 and abrogates accumulation of the MRN complex at sites of DNA DSBs in vivo. Thus, our data reveal the mechanism by which MDC1 physically couples the MRN complex to damaged chromatin.

Objective: We wanted to assess possible alterations in brain activation in PTSD patients with severe hyperarousal symptoms and impulsive aggressiveness., Method: 25 Croatian War (1991-1995) veterans with combat-related PTSD with severe hyperarousal symptoms and impulsive aggressiveness were assessed for possible alterations in cerebral blood flow in single photon emission computed tomography brain scans., Results: Increased regional cerebral blood flow in projection area of nucleus accumbens was found in 13 of 25 subjects, and for all in the dominant brain hemisphere., Discussion: We believe that at least some of PTSD symptoms, and especially the impulsive aggression, can be associated with increased regional cerebral blood flow in the projection area of nucleus accumbens.