Asteroid families classification: exploiting very large data sets

The number of asteroids with accurately determined orbits increases fast. The catalogs of asteroid physical observations have also increased, although the number of objects is still smaller than in the orbital catalogs. We developed a new approach to the asteroid family classification by combining the Hierarchical Clustering Method (HCM) with a method to add new members to existing families. This procedure makes use of the much larger amount of information contained in the proper elements catalogs, with respect to classifications using also physical observations for a smaller number of asteroids. Our work is based on the large catalog of the high accuracy synthetic proper elements (available from AstDyS). We first identify a number of core families; to these we attribute the next layer of smaller objects. Then, we remove all the family members from the catalog, and reapply the HCM to the rest. This gives both halo families which extend the core families and new independent families, consisting mainly of small asteroids. These two cases are discriminated by another step of attribution of new members and by merging intersecting families. By using information from absolute magnitudes, we take advantage of the larger size range in some families to analyze their shape in the proper semimajor axis vs. inverse diameter plane. This leads to a new method to estimate the family age (or ages). The results from the previous steps are then analyzed, using also auxiliary information on physical properties including WISE albedos and SDSS color indexes. This allows to solve some difficult cases of families overlapping in the proper elements space but generated by different collisional events. We analyze some examples of cratering families (Massalia, Vesta, Eunomia) which show internal structures, interpreted as multiple collisions. We also discuss why Ceres has no family

In utero exposure to cigarette chemicals induces sex-specific disruption of one-carbon metabolism and DNA methylation in the human fetal liver

Background: Maternal smoking is one of the most important modifiable risk factors for low birthweight, which is strongly associated with increased cardiometabolic disease risk in adulthood. Maternal smoking reduces the levels of the methyl donor vitamin B12 and is associated with altered DNA methylation at birth. Altered DNA methylation may be an important mechanism underlying increased disease susceptibility; however, the extent to which this can be induced in the developing fetus is unknown. Methods: In this retrospective study, we measured concentrations of cobalt, vitamin B12, and mRNA transcripts encoding key enzymes in the 1-carbon cycle in 55 fetal human livers obtained from 11 to 21 weeks of gestation elective terminations and matched for gestation and maternal smoking. DNA methylation was measured at critical regions known to be susceptible to the in utero environment. Homocysteine concentrations were analyzed in plasma from 60 fetuses. Results: In addition to identifying baseline sex differences, we found that maternal smoking was associated with sex-specific alterations of fetal liver vitamin B12, plasma homocysteine and expression of enzymes in the 1-carbon cycle in fetal liver. In the majority of the measured parameters which showed a sex difference, maternal smoking reduced the magnitude of that difference. Maternal smoking also altered DNA methylation at the imprinted gene IGF2 and the glucocorticoid receptor (GR/NR3C1). Conclusions: Our unique data strengthen studies linking in utero exposures to altered DNA methylation by showing, for the first time, that such changes are present in fetal life and in a key metabolic target tissue, human fetal liver. Furthermore, these data propose a novel mechanism by which such changes are induced, namely through alterations in methyl donor availability and changes in 1-carbon metabolism

Particulate matter exposure during pregnancy is associated with birth weight, but not gestational age, 1962-1992: a cohort study

<p>Abstract</p> <p>Background</p> <p>Exposure to air pollutants is suggested to adversely affect fetal growth, but the evidence remains inconsistent in relation to specific outcomes and exposure windows.</p> <p>Methods</p> <p>Using birth records from the two major maternity hospitals in Newcastle upon Tyne in northern England between 1961 and 1992, we constructed a database of all births to mothers resident within the city. Weekly black smoke exposure levels from routine data recorded at 20 air pollution monitoring stations were obtained and individual exposures were estimated via a two-stage modeling strategy, incorporating temporally and spatially varying covariates. Regression analyses, including 88,679 births, assessed potential associations between exposure to black smoke and birth weight, gestational age and birth weight standardized for gestational age and sex.</p> <p>Results</p> <p>Significant associations were seen between black smoke and both standardized and unstandardized birth weight, but not for gestational age when adjusted for potential confounders. Not all associations were linear. For an increase in whole pregnancy black smoke exposure, from the 1^st(7.4 μg/m³) to the 25^th(17.2 μg/m³), 50^th(33.8 μg/m³), 75^th(108.3 μg/m³), and 90^th(180.8 μg/m³) percentiles, the adjusted estimated decreases in birth weight were 33 g (SE 1.05), 62 g (1.63), 98 g (2.26) and 109 g (2.44) respectively. A significant interaction was observed between socio-economic deprivation and black smoke on both standardized and unstandardized birth weight with increasing effects of black smoke in reducing birth weight seen with increasing socio-economic disadvantage.</p> <p>Conclusions</p> <p>The findings of this study progress the hypothesis that the association between black smoke and birth weight may be mediated through intrauterine growth restriction. The associations between black smoke and birth weight were of the same order of magnitude as those reported for passive smoking. These findings add to the growing evidence of the harmful effects of air pollution on birth outcomes.</p

Proceedings of the 24th Paediatric Rheumatology European Society Congress: Part three

From Springer Nature via Jisc Publications Router.Publication status: PublishedHistory: collection 2017-09, epub 2017-09-0

Different Alterations of Hippocampal and Reticulo-Thalamic GABAergic Parvalbumin-Expressing Interneurons Underlie Different States of Unconsciousness

We traced the changes in GABAergic parvalbumin (PV)-expressing interneurons of the hippocampus and reticulo-thalamic nucleus (RT) as possible underlying mechanisms of the different local cortical and hippocampal electroencephalographic (EEG) microstructures during the non-rapid-eye movement (NREM) sleep compared with anesthesia-induced unconsciousness by two anesthetics with different main mechanisms of action (ketamine/diazepam versus propofol). After 3 h of recording their sleep, the rats were divided into two experimental groups: one half received ketamine/diazepam anesthesia and the other half received propofol anesthesia. We simultaneously recorded the EEG of the motor cortex and hippocampus during sleep and during 1 h of surgical anesthesia. We performed immunohistochemistry and analyzed the PV and postsynaptic density protein 95 (PSD-95) expression. PV suppression in the hippocampus and at RT underlies the global theta amplitude attenuation and hippocampal gamma augmentation that is a unique feature of ketamine-induced versus propofol-induced unconsciousness and NREM sleep. While PV suppression resulted in an increase in hippocampal PSD-95 expression, there was no imbalance between inhibition and excitation during ketamine/diazepam anesthesia compared with propofol anesthesia in RT. This increased excitation could be a consequence of a lower GABA interneuronal activity and an additional mechanism underlying the unique local EEG microstructure in the hippocampus during ketamine/diazepam anesthesia

On the ages of resonant, eroded and fossil asteroid families

In this work we have estimated 10 collisional ages of 9 families for which for different reasons our previous attempts failed. In general, these are difficult cases that required dedicated effort, such as a new family classifications for asteroids in mean motion resonances, in particular the 1/1 and 2/1 with Jupiter, as well as a revision of the classification inside the 3/2 resonance. Of the families locked in mean motion resonances, by employing a numerical calibration to estimate the Yarkovsky effect in proper eccentricity, we succeeded in determining ages of the families of (1911) Schubart and of the super-Hilda family, assuming this is actually a severely eroded original family of (153) Hilda. In the Trojan region we found families with almost no Yarkovsky evolution, for which we could compute only physically implausible ages. Hence, we interpreted their modest dispersions of proper elements as implying that the Trojan asteroid families are fossil families, frozen at their proper elements determined by the original ejection velocity field. We have found a new family, among the Griquas locked in the 2/1 resonance with Jupiter, the family of (11097) 1994 UD1. We have estimated the ages of 6 families affected by secular resonances: families of (5) Astraea, (25) Phocaea, (283) Emma, (363) Padua, (686) Gersuind, and (945) Barcelona. By using in all these cases a numerical calibration method, we have shown that the secular resonances do not affect significantly the secular change of proper a. We have confirmed the existence of the family resulting from cratering on (5) Astraea by computing a new set of resonant proper elements adapted to the resonance g+g5-2g6: this new family has a much larger membership and has a shape compatible with simple collisional models. For the family of (145) Adeona we could estimate the age only after removal of a number of assumed interlopers. With the present paper we have concluded the series dedicated to the determination of asteroid ages with a uniform method. Overall we computed 53 ages for a total of 49 families. For the future work there remain families too small at present to provide reliable estimates, as well as some complex families (221, 135, 298) which may have more ages than we could currently estimate. Future improvement of some already determined family ages is also possible by increasing family membership, revising the calibrations, and using more reliable physical data

Pathologic Evaluation of Type 2 Porcine Reproductive and Respiratory Syndrome Virus Infection at the Maternal-Fetal Interface of Late Gestation Pregnant Gilts.

The pathogenesis of fetal death caused by porcine reproductive and respiratory syndrome virus (PRRSV) remains unclear. The objective of this study was to improve our understanding of the pathogenesis by assessing potential relationships between specific histopathological lesions and PRRSV RNA concentration in the fetuses and the maternal-fetal interface. Pregnant gilts were inoculated with PRRSV (n = 114) or sham inoculated (n = 19) at 85±1 days of gestation. Dams and their litters were humanely euthanized and necropsied 21 days later. PRRSV RNA concentration was measured by qRT-PCR in the maternal-fetal interface and fetal thymus (n = 1391). Presence of fetal lesions was positively related to PRRSV RNA concentration in the maternal-fetal interface and fetal thymus (P<0.05 for both), but not to the distribution or severity of vasculitis, or the severity of endometrial inflammation. The presence of fetal and umbilical lesions was associated with greater odds of meconium staining (P<0.05 for both). The distribution and severity of vasculitis in endometrium were not significantly related to PRRSV RNA concentration in maternal-fetal interface or fetal thymus. Endometrial inflammation severity was positively related to distribution and severity of vasculitis in endometrium (P<0.001 for both). Conclusions from this study suggest that type 2 PRRSV infection in pregnant gilts induces significant histopathological lesions at maternal-fetal interface, but they are not associated with presence of PRRSV in the maternal-fetal interface at 21 days post infection. Conversely, fetal pathological lesions are associated with presence of PRRSV in the maternal-fetal interface and fetal thymus, and meconium staining is significantly associated with the presence of both fetal and umbilical lesions observed 21 days post infection

An observational study reveals that neonatal vitamin D is primarily determined by maternal contributions: Implications of a new assay on the roles of vitamin D forms

Background Vitamin D concentrations during pregnancy are measured to diagnose states of insufficiency or deficiency. The aim of this study is to apply accurate assays of vitamin D forms [single- hydroxylated [25(OH)D2, 25(OH)D3], double-hydroxylated [1alpha,25(OH)2D2, 1alpha,25(OH)2D3], epimers [3-epi-25(OH)D2, 3-epi-25(OH)D3] in mothers (serum) and neonates (umbilical cord) to i) explore maternal and neonatal vitamin D biodynamics and ii) to identify maternal predictors of neonatal vitamin D concentrations. Methods All vitamin D forms were quantified in 60 mother- neonate paired samples by a novel liquid chromatography -mass spectrometry (LC-MS/MS) assay. Maternal characteristics [age, ultraviolet B exposure, dietary vitamin D intake, calcium, phosphorus and parathyroid hormone] were recorded. Hierarchical linear regression was used to predict neonatal 25(OH)D concentrations. Results Mothers had similar concentrations of 25(OH)D2 and 25(OH)D3 forms compared to neonates (17.9 +/- 13.2 vs. 15.9 +/- 13.6 ng/mL, p = 0.289) with a ratio of 1:3. The epimer concentrations, which contribute approximately 25% to the total vitamin D levels, were similar in mothers and neonates (4.8 +/- 7.8 vs. 4.5 +/- 4.7 ng/mL, p = 0.556). No correlation was observed in mothers between the levels of the circulating form (25OHD3) and its active form. Neonatal 25(OH)D2 was best predicted by maternal characteristics, whereas 25(OH)D3 was strongly associated to maternal vitamin D forms (R2 = 0.253 vs. 0.076 and R2 = 0.109 vs. 0.478, respectively). Maternal characteristics explained 12.2% of the neonatal 25(OH)D, maternal 25(OH)D concentrations explained 32.1%, while epimers contributed an additional 11.9%. Conclusions By applying anovel highly specific vitamin D assay, the present study is the first to quantify 3-epi-25(OH)D concentrations in mother - newborn pairs. This accurate assay highlights a considerable proportion of vitamin D exists as epimers and a lack of correlation between the circulating and active forms. These results highlight the need for accurate measurements to appraise vitamin D status. Maternal characteristics and circulating forms of vitamin D, along with their epimers explain 56% of neonate vitamin D concentrations. The roles of active and epimer forms in the maternal - neonatal vitamin D relationship warrant further investigation