Hydrogen peroxide (H(2)O(2)), an oxidizing agent, has been widely used as a disinfectant. Recently, because of its reactive properties, H(2)O(2) has also been used as a tooth bleaching agent in dental care. This is a cause for concern because of adverse biological effects on the soft and hard tissues of the oral environment. To investigate the influence of H(2)O(2) on odontoblasts, the cells producing dentin in the pulp, we assessed cellular viability, generation of reactive oxygen species (ROS), alkaline phosphatase (ALP) activity, and nodule formation of an odontoblastic cell line (MDPC-23) after treatment with H(2)O(2), and compared those with the effects on preosteoblastic MC3T3-E1 cells. Cytotoxic effects of H(2)O(2) began to appear at 0.3 mmol/L in both MDPC-23 and MC3T3-E1 cells. At that concentration, the accumulation of intracellular ROS was confirmed by a fluorescent probe, DCFH-DA. Although more ROS were detected in MDPC-23, the increasing pattern and rate are similar between the two cells. When the cells were treated with H(2)O(2) at concentrations below 0.3 mmol/L, MDPC-23 displayed a significant increase in ALP activity and mineralized bone matrix, while MC3T3-E1 cells showed adverse effects of H(2)O(2). It is known that ROS are generally harmful by-products of aerobic life and represent the primary cause of aging and numerous diseases. These data, however, suggest that ROS can induce in vitro cell differentiation, and that they play a more complex role in cell physiology than simply causing oxidative damage.

The JAXA Hayabusa-2 mission was approved in 2010 and launched on December 3, 2014. The spacecraft will arrive at the nearEarth asteroid 162173 Ryugu (1999 JU 3 ) in 2018 where it will perform a survey, land and obtain surface material, then depart in December 2019 and return to Earth in December 2020. We observed Ryugu with the Herschel Space Observatory in April 2012 at far-infrared thermal wavelengths, supported by several ground-based observations to obtain optical lightcurves. We reanalysed previously published Subaru-COMICS and AKARI-IRC observations and merged them with a Spitzer-IRS data set. In addition, we used a large set of Spitzer-IRAC observations obtained in the period January to May, 2013. The data set includes two complete rotational lightcurves and a series of ten "point-and-shoot" observations, all at 3.6 and 4.5 µm. The almost spherical shape of the target together with the insufficient lightcurve quality forced us to combine radiometric and lightcurve inversion techniques in different ways to find the object's spin-axis orientation, its shape and to improve the quality of the key physical and thermal parameters. Handling thermal data in inversion techniques remains challenging: thermal inertia, roughness or local structures influence the temperature distribution on the surface. The constraints for size, spin or thermal properties therefore heavily depend on the wavelengths of the observations. We find that the solution which best matches our data sets leads to this C class asteroid having a retrograde rotation with a spin-axis orientation of (λ = 310• -340• ) in ecliptic coordinates, an effective diameter (of an equal-volume sphere) of 850 to 880 m, a geometric albedo of 0.044 to 0.050 and a thermal inertia in the range 150 to 300 J m −2 s −0.5 K −1 . Based on estimated thermal conductivities of the top-layer surface in the range 0.1 to 0.6 W K −1 m −1 , we calculated that the grain sizes are approximately equal to between 1 and 10 mm. The finely constrained values for this asteroid serve as a 'design reference model', which is currently used for various planning, operational and modelling purposes by the Hayabusa2 team.

Glucose 6-phosphate dehydrogenase (G6PD) deficiency, known as favism, is classically manifested by hemolytic anemia in human. More recently, it has been shown that mild G6PD deficiency moderately affects cardiac function, whereas severe G6PD deficiency leads to embryonic lethality in mice. How G6PD deficiency affects organisms has not been fully elucidated due to the lack of a suitable animal model. In this study, G6PD-deficient Caenorhabditis elegans was established by RNA interference (RNAi) knockdown to delineate the role of G6PD in animal physiology. Upon G6PD RNAi knockdown, G6PD activity was significantly hampered in C. elegans in parallel with increased oxidative stress and DNA oxidative damage. Phenotypically, G6PD-knockdown enhanced germ cell apoptosis (2-fold increase), reduced egg production (65% of mock), and hatching (10% of mock). To determine whether oxidative stress is associated with G6PD knockdown-induced reproduction defects, C. elegans was challenged with a short-term hydrogen peroxide (H2O2). The early phase egg production of both mock and G6PD-knockdown C. elegans were significantly affected by H2O2. However, H2O2-induced germ cell apoptosis was more dramatic in mock than that in G6PD-deficient C. elegans. To investigate the signaling pathways involved in defective oogenesis and embryogenesis caused by G6PD knockdown, mutants of p53 and mitogen-activated protein kinase (MAPK) pathways were examined. Despite the upregulation of CEP-1 (p53), cep-1 mutation did not affect egg production and hatching in G6PD-deficient C. elegans. Neither pmk-1 nor mek-1 mutation significantly affected egg production, whereas sek-1 mutation further decreased egg production in G6PD-deficient C. elegans. Intriguingly, loss of function of sek-1 or mek-1 dramatically rescued defective hatching (8.3- and 9.6-fold increase, respectively) induced by G6PD knockdown. Taken together, these findings show that G6PD knockdown reduces egg production and hatching in C. elegans, which are possibly associated with enhanced oxidative stress and altered MAPK pathways, respectively.

Burden of disease studies typically classify individuals with a body mass index (BMI) ≥ 30 kg m(-2) as a single group ('obese') and make comparisons to those with lower BMIs. Here, we review the literature on the additional economic burden associated with severe obesity or classes 3 and 4 obesity (BMI ≥ 40 kg m(-2) ), the fastest growing category of obesity, with the aim of exploring and disaggregating differences in resource use as BMI increases beyond 40 kg m(-2) . We recognize the importance of comparing classes 3 and 4 obesity to less severe obesity (classes 1 and 2) as well as quantifying the single sub-class impacts (classes 3 and 4). Although the latter analysis is the aim of this review, we include results, where found in the literature, for movement between the recognized subclasses and within classes 3 and 4 obesity. Articles presenting data on the economic burden associated with severe obesity were identified from a search of Ovid MEDLINE, EMBASE, EBSCO CINAHL and Cochrane Library databases. Data were extracted on the direct costs, productivity costs and resource use associated with severe obesity along with estimates of the multiplier effects associated with increasing BMI. Fifteen studies were identified, of which four disaggregated resource use for BMI ≥ 40 kg m(-2) . The multiplier effects derived for a variety of different types of costs incurred by the severely obese compared with those of normal weight (18.5 kg m(-2) < BMI < 25 kg m(-2) ) ranged from 1.5 to 3.9 for direct costs, and from 1.7 to 8.0 for productivity costs. There are few published data on the economic burden of obesity disaggregated by BMI ≥ 40 kg m(-2) . By grouping people homogenously above a threshold of BMI 40 kg m(-2) , the multiplier effects for those at the highest end of the spectrum are likely to be underestimated. This will, in turn, impact on the estimates of cost-effectiveness for interventions and policies aimed at the severely obese.

Enhanced expression of the TGF-beta signaling inhibitor Smad7 may present one of the novel mechanisms of TGF-beta resistance in human gastric carcinomas.