Are There Age Spreads in Star Forming Regions?

A luminosity spread at a given effective temperature is ubiquitously seen in the Hertzsprung-Russell (HR) diagrams of young star forming regions and often interpreted in terms of a prolonged period (>=10 Myr) of star formation. I review the evidence that the observed luminosity spreads are genuine and not caused by astrophysical sources of scatter. I then address whether the luminosity spreads necessarily imply large age spreads, by comparing HR diagram ages with ages from independent clocks such as stellar rotation rate, the presence of circumstellar material and lithium depletion. I argue that whilst there probably is a true luminosity dispersion, there is little evidence to support age spreads larger than a few Myr. This paradox could be resolved by brief periods of rapid accretion during the class I pre main-sequence phase.Comment: To appear in the proceedings of JENAM10: Star Clusters in the Era of Large Surveys, 8 page

Ervas daninhas do Brasil: Solanaceae I, genero Solanum L.

bitstream/item/88000/1/Doc01.pd

Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based Regeneration and Reverse Immunosuppression

Immune system defects are at the center of aging and a range of diseases. Here, we show that prolonged fasting reduces circulating IGF-1 levels and PKA activity in various cell populations, leading to signal transduction changes in long-term hematopoietic stem cells (LT-HSCs) and niche cells that promote stress resistance, self-renewal, and lineage-balanced regeneration. Multiple cycles of fasting abated the immunosuppression and mortality caused by chemotherapy and reversed age-dependent myeloid-bias in mice, in agreement with preliminary data on the protection of lymphocytes from chemotoxicity in fasting patients. The proregenerative effects of fasting on stem cells were recapitulated by deficiencies in either IGF-1 or PKA and blunted by exogenous IGF-1. These findings link the reduced levels of IGF-1 caused by fasting to PKA signaling and establish their crucial role in regulating hematopoietic stem cell protection, self-renewal, and regeneration

The Gaia-ESO Survey: the most metal-poor stars in the Galactic bulge

We present the first results of the EMBLA survey (Extremely Metal-poor BuLge stars with AAOmega), aimed at finding metal-poor stars in the Milky Way bulge, where the oldest stars should now preferentially reside. EMBLA utilises SkyMapper photometry to pre-select metal-poor candidates, which are subsequently confirmed using AAOmega spectroscopy. We describe the discovery and analysis of four bulge giants with -2.72<=[Fe/H]<=-2.48, the lowest metallicity bulge stars studied with high-resolution spectroscopy to date. Using FLAMES/UVES spectra through the Gaia-ESO Survey we have derived abundances of twelve elements. Given the uncertainties, we find a chemical similarity between these bulge stars and halo stars of the same metallicity, although the abundance scatter may be larger, with some of the stars showing unusual [{\alpha}/Fe] ratios.Comment: 7 pages, 5 figures. Accepted for publication by MNRA

Trans-heterozygosity for mutations enhances the risk of recurrent/chronic pancreatitis in patients with Cystic Fibrosis

Background: Recurrent (RP) and chronic pancreatitis (CP) may complicate Cystic Fibrosis (CF). It is still unknown if mutations in genes involved in the intrapancreatic activation of trypsin (IPAT) or in the pancreatic secretion pathway (PSP) may enhance the risk for RP/CP in patients with CF.Methods: We enrolled: 48 patients affected by CF complicated by RP/CP and, as controls 35 patients with CF without pancreatitis and 80 unrelated healthy subjects. We tested a panel of 8 genes involved in the IPAT, i.e. PRSS1, PRSS2, SPINK1, CTRC, CASR, CFTR, CTSB and KRT8 and 23 additional genes implicated in the PSP.Results: We found 14/48 patients (29.2%) with mutations in genes involved in IPAT in the group of CF patients with RP/CP, while mutations in such genes were found in 2/35 (5.7%) patients with CF without pancreatitis and in 3/80 (3.8%) healthy subjects (p < 0.001). Thus, we found mutations in 12 genes of the PSP in 11/48 (22.9%) patients with CF and RP/CP. Overall, 19/48 (39.6%) patients with CF and RP/CP showed one or more mutations in the genes involved in the IPAT and in the PSP while such figure was 4/35 (11.4%) for patients with CF without pancreatitis and 11/80 (13.7%) for healthy controls (p < 0.001).Conclusions: The trans-heterozygous association between CFTR mutations in genes involved in the pathways of pancreatic enzyme activation and the pancreatic secretion may be risk factors for the development of recurrent or chronic pancreatitis in patients with CF

C3aR-initiated signaling is a critical mechanism of podocyte injury in membranous nephropathy

: The deposition of anti-podocyte auto-antibodies in the glomerular subepithelial space induces primary membranous nephropathy (MN), the leading cause of nephrotic syndrome worldwide. Taking advantage of the glomerulus-on-a-chip system, we modeled human primary MN induced by anti-PLA2R antibodies. Here we show that exposure of primary human podocytes expressing PLA2R to MN serum results in IgG deposition and complement activation on their surface, leading to loss of the chip permselectivity to albumin. C3a receptor (C3aR) antagonists as well as C3AR gene silencing in podocytes reduced oxidative stress induced by MN serum and prevented albumin leakage. In contrast, inhibition of the formation of the membrane-attack-complex (MAC), previously thought to play a major role in MN pathogenesis, did not affect permselectivity to albumin. In addition, treatment with a C3aR antagonist effectively prevented proteinuria in a mouse model of MN, substantiating the chip findings. In conclusion, using a combination of pathophysiologically relevant in vitro and in vivo models, we established that C3a/C3aR signaling plays a critical role in complement-mediated MN pathogenesis, indicating an alternative therapeutic target for MN

A precision measurement of direct CP violation in the decay of neutral kaons into two pions

The direct CP violation parameter Re(epsilon'/epsilon) has been measured from the decay rates of neutral kaons into two pions using the NA48 detector at the CERN SPS. The 2001 running period was devoted to collecting additional data under varied conditions compared to earlier years (1997-99). The new data yield the result: Re(epsilon'/epsilon) = (13.7 +/- 3.1) times 10^{-4}. Combining this result with that published from the 1997, 98 and 99 data, an overall value of Re(epsilon'/epsilon) = (14.7 +/- 2.2) times 10^{-4} is obtained from the NA48 experiment.Comment: 19 pages, 5 figures, to be published in Physics Letters

Measurement of the Ratio Gamma(KL -> pi+ pi-)/Gamma(KL -> pi e nu) and Extraction of the CP Violation Parameter |eta+-|

We present a measurement of the ratio of the decay rates Gamma(KL -> pi+ pi-)/Gamma(KL -> pi e nu), denoted as Gamma(K2pi)/Gamma(Ke3). The analysis is based on data taken during a dedicated run in 1999 by the NA48 experiment at the CERN SPS. Using a sample of 47000 K2pi and five million Ke3 decays, we find Gamma(K2pi)/Gamma(Ke3) = (4.835 +- 0.022(stat) +- 0.016(syst)) x 10^-3. From this we derive the branching ratio of the CP violating decay KL -> pi+ pi- and the CP violation parameter |eta+-|. Excluding the CP conserving direct photon emission component KL -> pi+ pi- gamma, we obtain the results BR(KL -> pi+ pi-) = (1.941 +- 0.019) x 10^-3 and |eta+-| = (2.223 +- 0.012) x 10^-3.Comment: 20 pages, 7 figures, accepted by Phys. Lett.

First observation of the KS->pi0 gamma gamma decay

Using the NA48 detector at the CERN SPS, 31 KS->pi0 gamma gamma candidates with an estimated background of 13.7 +- 3.2 events have been observed. This first observation leads to a branching ratio of BR(KS->pi0 gamma gamma) = (4.9 +- 1.6(stat) +- 0.9(syst)) x 10^-8 in agreement with Chiral Perturbation theory predictions.Comment: 10 pages, 4 figures submitted to Phys. Lett.