Hydrophobic and moisture-stable metal-organic frameworks.

Metal-organic frameworks (MOFs) have proved to be very attractive for applications including gas storage, separation, sensing and catalysis. In particular, CO(2) separation from flue gas in post-combustion processes is one of the main focuses of research among the scientific community. One of the major issues that are preventing the successful commercialization of these novel materials is their high affinity towards water that not only compromises gas sorption capacity but also the chemical stability. In this paper, we demonstrate a novel post-synthesis modification approach to modify MOFs towards increasing hydrophobic behaviour and chemical stability against moisture without compromising CO(2) sorption capacity. Our approach consists of incorporating hydrophobic moieties on the external surface of the MOFs via physical adsorption. The rationale behind this concept is to increase the surface hydrophobicity in the porous materials without the need of introducing bulky functionalities inside the pore which compromises the sorption capacity toward other gases. We herein report preliminary results on routinely studied MOF materials [MIL-101(Cr) and NiDOBDC] demonstrating that the polymer-modified MOFs retain CO(2) sorption capacity while reducing the water adsorption up to three times, with respect to the un-modified materials, via an equilibrium effect. Furthermore, the water stability of the polymer-functionalized MOFs is significantly higher than the water stability of the bare material. Molecular dynamic simulations demonstrated that this equilibrium effect implies a fundamental and permanent change in the water sorption capacity of MOFs. This approach can also be employed to render moisture stability and selectivity to MOFs that find applications in gas separations, catalysis and sensing where water plays a critical role in compromising MOF performance and recyclability.

Impact of the Fukushima nuclear accident on background radiation doses measured by control dosimeters in Japan.

After the 9.0 magnitude earthquake and subsequent massive tsunami on 11 March 2011 in Japan, several reactors at the Fukushima Daiichi Nuclear Power Plant suffered severe damage. There was immediate participation of U.S. Navy vessels and other United States Department of Defense (DoD) teams that were already in the area at the time of the disaster or arrived shortly thereafter. The correct determination of occupational dose equivalent requires estimation of the background dose component measured by control dosimeters, which is subsequently subtracted from the total dose equivalent measured by personal dosimeters. The purpose of the control dosimeters is to determine the amount of radiation dose equivalent that has accumulated on the dosimeter from background or other non-occupational sources while they are in transit or being stored. Given the release of radioactive material and potential exposure to radiation from the Fukushima Daiichi Nuclear Power Plant and the process by which the U.S. Navy calculates occupational exposure to ionizing radiation, analysis of pre- and post-event control dosimeters is warranted. Several hundred historical dose records from the Naval Dosimetry Center (NDC) database were analyzed and compared with the post-accident dose equivalent data of control dosimeters. As result, it was shown that the dose contribution of the radiation and released radiological materials from the Fukushima nuclear accident to background radiation doses is less than 0.375 µSv d for shallow and deep photon dose equivalent. There is no measurable effect on neutron background exposure. The latter has at least two important conclusions. First, the NDC can use doses measured by control dosimeters at issuing sites in Japan for determination of personnel dose equivalents; second, the dose data from control dosimeters prior to and after the Fukushima accident may be used to assist in dose reconstruction of non-radiological (non-badged) personnel at these locations.

Behavioral characterization of the Tg2576 transgenic model of Alzheimer's disease through 19 months.

Behavioral characterization of Alzheimer's disease (AD) transgenic models over multiple time points during aging has been largely inadequate, usually being limited to one or two cognitive-based tasks. In this context, the present study utilized a comprehensive 6-week behavioral battery to characterize sensorimotor and cognitive performance of Tg2576 AD transgenic (Tg+) mice and nontransgenic (Tg-) controls aged 3, 9, 14, and 19 months. Compared collectively to Tg- mice over all four time points, Tg+ mice were impaired in Y-maze spontaneous alternation, visible platform recognition, and several sensorimotor tasks; Tg+ mice also showed an overall increase in activity measures. The deficits in visible platform became evident by 9 months of age, while those in sensorimotor tasks became clearly manifest by 14 months. Although the behavioral impairments exhibited by Tg+ mice were usually progressive through 19 months, Tg- animals also showed similar progressive decline in the same behavioral measures; thus, no task revealed a progressive behavioral decline exclusive to Tg+ mice. Moreover, although the 6-week behavioral battery included six cognitively based tasks (i.e., Y-maze, visible platform, Morris water maze, circular platform, passive avoidance, and active avoidance), behavioral analysis through 19 months revealed Tg+ mice to be impaired in only the Y-maze and visible platform tasks. Consequently, Tg2576 mice do not exhibit widespread, profound cognitive impairment, even into old age. This may reflect their predominant C57BL/6 background and an apparent inability of the mutant transgene to profoundly alter performance therein.

Intra- and intertask relationships in a behavioral test battery given to Tg2576 transgenic mice and controls.

Several transgenic mouse models for Alzheimer's disease (AD) that develop -amyloid deposition have recently been advanced, including the Tg2576 mouse. Thorough behavioral phenotyping of this, or any mouse line/population, requires not only analysis of multiple behavioral measures through a comprehensive battery of tasks, but also a clear understanding of the interrelationships between behavioral measures in such a battery. In our accompanying study (King et al., this volume), Tg2576 transgenic (Tg+) and nontransgenic (Tg-) mice aged 3-19 months were administered an extensive behavioral test battery. The present study involved correlation analysis between those behavioral measures. Numerous correlations were evident for all 169 mice (Tg+ and Tg-) combined, with additional correlations being dependent on genotype or age. For all mice combined, intratask measures in water maze and circular platform were highly correlated; in addition, several measures of activity correlated with each other, as did various measures of balance/agility. A number of correlations between the six cognitive-based tasks of the test battery (e.g. Y-maze, Morris water maze, circular platform, visible platform, passive avoidance, and active avoidance) were also evident, as were correlations between cognitive and sensorimotor measures. In as much as some correlations were found to be exclusive to either Tg+ or Tg- animals alone, separate analysis by genotype is clearly warranted whenever two or more genotypes are involved. Likewise, some correlations were age-dependent, being present either in young adulthood (3 months) or in old age (19 months). These correlation analysis results in mice indicate that: (1) performance in one or several behavioral measures can be predictive of performance in others and (2) both genetic background and age influence the degree and profile of intra-/intertask relationships in an extensive behavioral test battery.

Maintained synaptophysin immunoreactivity in Tg2576 transgenic mice during aging: correlations with cognitive impairment.

Regional loss of synapses, particularly within the neocortex and hippocampus, is characteristic of Alzheimer's Disease (AD) and strongly correlated with extent of cognitive impairment. The Tg2576 transgenic mouse model of AD develops Abeta-containing neuritic plaques by 10-16 months of age and shows cognitive impairment in several tasks. In the present study, synaptophysin immunoreactivity (SYN-IR; a marker for synaptic terminals) was evaluated in the neocortex and hippocampus of behaviorally-tested Tg2576 transgenic (Tg+) mice aged 3, 9, 14, and 19 months of age. In control non-transgenic (Tg-) mice, SYN-IR in both neocortex and hippocampus tended to decrease with age, while SYN-IR in Tg+ mice was maintained with age. Thus, 19M Tg+ mice exhibited significantly greater synaptophysin immunostaining compared to 19M Tg- mice in both inner and outer neocortical regions, as well as in the dentate gyrus' outer molecular layer and polymorphic layer. Over all four age groups collectively, outer cortical SYN-IR was also greater in Tg+ compared to Tg- mice. Multiple factors could be responsible for maintained SYN-IR in aged Tg+ mice, including compensatory changes in synaptic morphology and staining of dystrophic neuritics associated with Abeta deposition. For all animals combined (Tg+ and Tg-), as well as for aged 19M animals alone, hippocampal SYN-IR was correlated with impaired acquisition and spatial reference memory in the Morris water maze task, suggestive that elevated hippocampal SYN-IR is a manifestation of pathophysiologic synaptic processing within the hippocampus. Also for 19M animals alone, hippocampal SYN-IR was highly correlated with impaired visible platform recognition, indicative that elevated SYN-IR is linked to visual agnosia. The results of this study are consistent with the premise that maintained SYN-IR in Tg2576 mice during aging is associated with impaired synaptic function, resulting in cognitive deficits.