Changes in baseline (here understood as representative of continental to hemispheric scales) tropospheric O₃ concentrations that have occurred at northern mid-latitudes over the past six decades are quantified from available measurement records with the goal of providing benchmarks to which retrospective model calculations of the global O₃ distribution can be compared. Eleven data sets (ten ground-based and one airborne) including six European (beginning in the 1950's and before), three North American (beginning in 1984) and two Asian (beginning in 1991) are analyzed. When the full time periods of the data records are considered a consistent picture emerges; O₃ has increased at all sites in all seasons at approximately 1% yr^−1 relative to the site's 2000 yr mixing ratio in each season. For perspective, this rate of increase sustained from 1950 to 2000 corresponds to an approximate doubling. There is little if any evidence for statistically significant differences in average rates of increase among the sites, regardless of varying length of data records. At most sites (most definitively at the European sites) the rate of increase has slowed over the last decade (possibly longer), to the extent that at present O₃ is decreasing at some sites in some seasons, particularly in summer. The average rate of increase before 2000 shows significant seasonal differences (1.08 ± 0.09, 0.89 ± 0.10, 0.85 ± 0.11 and 1.21 ± 0.12% yr^−1 in spring, summer, autumn and winter, respectively, over North America and Europe)

Aggresomes and related inclusion bodies appear to serve as storage depots for misfolded and aggregated proteins within cells, which can potentially be degraded by the autophagy pathway. A homogenous fluorescence-based assay was devised to detect aggregated proteins inside aggresomes and inclusion bodies within an authentic cellular context. The assay employs a novel red fluorescent molecular rotor dye, which is essentially nonfluorescent until it binds to structural features associated with the aggregated protein cargo. Aggresomes and related structures were generated within cultured cells using various potent, cell permeable, proteasome inhibitors: MG-132, lactacystin, epoxomicin and bortezomib, and then selectively detected with the fluorescent probe. Employing the probe in combination with various fluorescein-labeled primary antibodies facilitated co-localization of key components of the autophagy system (ubiquitin, p62, and LC3) with aggregated protein cargo by fluorescence microscopy. Furthermore, cytoplasmic aggregates were highlighted in SK-N-SH human neuroblastoma cells incubated with exogenously supplied amyloid beta peptide 1–42. SMER28, a small molecule modulator of autophagy acting via an mTOR-independent mechanism, prevented the accumulation of amyloid beta peptide within these cells. The described assay allows assessment of the effects of protein aggregation directly in cells, without resorting to the use of non-physiological protein mutations or genetically engineered cell lines. With minor modification, the assay was also adapted to the analysis of frozen or formalin-fixed, paraffin-embedded tissue sections, with demonstration of co-localization of aggregated cargo with β-amyloid and tau proteins in brain tissue sections from Alzheimer’s disease patients.

[1] The recent decline in sea ice cover in the Arctic Ocean could affect the regional radiative forcing via changes in sea ice-atmosphere exchange of dimethyl sulfide (DMS) and biogenic aerosols formed from its atmospheric oxidation, such as methanesulfonic acid (MSA). This study examines relationships between changes in total sea ice extent north of 70 N and atmospheric MSA measurement at Alert, Nunavut, during 1980Nunavut, during -2009 at Barrow, Alaska, during 1997 and at Ny-Ålesund, Svalbard, for 1991. During the 1980-1989 and 1990 periods, summer (July-August) and June MSA concentrations at Alert decreased. In general, MSA concentrations increased at all locations since 2000 with respect to 1990 values, specifically during June and summer at Alert and in summer at Barrow and Ny-Ålesund. Our results show variability in MSA at all sites is related to changes in the source strengths of DMS, possibly linked to changes in sea ice extent as well as to changes in atmospheric transport patterns. Since 2000, a late spring increase in atmospheric MSA at the three sites coincides with the northward migration of the marginal ice edge zone where high DMS emissions from ocean to atmosphere have previously been reported. Significant negative correlations are found between sea ice extent and MSA concentrations at the three sites during the spring and June. These results suggest that a decrease in seasonal ice cover influencing other mechanisms of DMS production could lead to higher atmospheric MSA concentrations.

Elevated serum sST2 level in SLE patients was found to correlate with disease activity and was sensitive to change, suggesting a potential role as a surrogate marker of disease activity.