Unidentified EGRET Sources and the Extragalactic Gamma-Ray Background

The large majority of EGRET point sources remain to this day without an identified low-energy counterpart. Whatever the nature of the EGRET unidentified sources, faint unresolved objects of the same class must have a contribution to the diffuse gamma-ray background: if most unidentified objects are extragalactic, faint unresolved sources of the same class contribute to the background, as a distinct extragalactic population; on the other hand, if most unidentified sources are Galactic, their counterparts in external galaxies will contribute to the unresolved emission from these systems. Understanding this component of the gamma-ray background, along with other guaranteed contributions from known sources, is essential in any attempt to use gamma-ray observations to constrain exotic high-energy physics. Here, we follow an empirical approach to estimate whether a potential contribution of unidentified sources to the extragalactic gamma-ray background is likely to be important, and we find that it is. Additionally, we comment on how the anticipated GLAST measurement of the diffuse gamma-ray background will change, depending on the nature of the majority of these sources.Comment: 6 pages, 3 figures, to appear in proceedings of "The Multi-Messenger Approach to High Energy Gamma-Ray Sources", Barcelona, 4-7 July 2006; comments welcom

The first COMPTEL Source Catalogue

The imaging Compton telescope COMPTEL aboard NASA's Compton Gamma-Ray Observatory has opened the MeV gamma-ray band as a new window to astronomy. COMPTEL provided the first complete all-sky survey in the energy range 0.75 to 30 MeV. The catalogue, presented here, is largely restricted to published results. It contains firm as well as marginal detections of continuum and line emitting sources and presents upper limits for various types of objects. The numbers of the most significant detections are 32 for steady sources and 31 for gamma-ray bursters. Among the continuum sources, detected so far, are spin-down pulsars, stellar black-hole candidates, supernova remnants, interstellar clouds, nuclei of active galaxies, gamma-ray bursters, and the Sun during solar flares. Line detections have been made in the light of the 1.809 MeV 26Al line, the 1.157 MeV 44Ti line, the 847 and 1238 keV 56Co lines, and the neutron capture line at 2.223 MeV. For the identification of galactic sources, a modelling of the diffuse galactic emission is essential. Such a modelling at this time does not yet exist at the required degree of accuracy. Therefore, a second COMPTEL source catalogue will be produced after a detailed and accurate modelling of the diffuse interstellar emission has become possible.Comment: 50 pages including 4 figures; accepted for publication in A&A Supplement

Optical Intraday Variability Studies of Ten Low Energy Peaked Blazars

We have carried out optical (R band) intraday variability (IDV) monitoring of a sample of ten bright low energy peaked blazars (LBLs). Forty photometric observations, of an average of ~ 4 hours each, were made between 2008 September and 2009 June using two telescopes in India. Measurements with good signal to noise ratios were typically obtained within 1-3 minutes, allowing the detection of weak, fast variations using N-star differential photometry. We employed both structure function and discrete correlation function analysis methods to estimate any dominant timescales of variability and found that in most of the cases any such timescales were longer than the duration of the observation. The calculated duty cycle of IDV in LBLs during our observing run is ~ 52%, which is low compared to many earlier studies; however, the relatively short periods for which each source was observed can probably explain this difference. We briefly discuss possible emission mechanisms for the observed variability.Comment: 20 Pages, 9 Figures, 4 Tables, accepted for publication in MNRA

Selenoproteins Are Essential for Proper Keratinocyte Function and Skin Development

Dietary selenium is known to protect skin against UV-induced damage and cancer and its topical application improves skin surface parameters in humans, while selenium deficiency compromises protective antioxidant enzymes in skin. Furthermore, skin and hair abnormalities in humans and rodents may be caused by selenium deficiency, which are overcome by dietary selenium supplementation. Most important biological functions of selenium are attributed to selenoproteins, proteins containing selenium in the form of the amino acid, selenocysteine (Sec). Sec insertion into proteins depends on Sec tRNA; thus, knocking out the Sec tRNA gene (Trsp) ablates selenoprotein expression. We generated mice with targeted removal of selenoproteins in keratin 14 (K14) expressing cells and their differentiated descendents. The knockout progeny had a runt phenotype, developed skin abnormalities and experienced premature death. Lack of selenoproteins in epidermal cells led to the development of hyperplastic epidermis and aberrant hair follicle morphogenesis, accompanied by progressive alopecia after birth. Further analyses revealed that selenoproteins are essential antioxidants in skin and unveiled their role in keratinocyte growth and viability. This study links severe selenoprotein deficiency to abnormalities in skin and hair and provides genetic evidence for the role of these proteins in keratinocyte function and cutaneous development

The pseudo‐brookite spin‐glass system studied by means of muon spin relaxation

Zero-field muon spin relaxation (µSR) experiments have been performed on the spin glass Fe1.75Ti1.25O5. Above the spin-glass temperature of 44 K a distinct exponential µSR rate (¿) is observed, while below Tg a square-root exponential decay occurs, indicating fast spin fluctuations. Near 8 K, a maximum in ¿ is indicative of transverse spin ordering. The low ¿ values and the sharp ¿ peak at Tg are very promising for the study of spin freezing models like the Vogel–Fulcher law or the power law

Hair organ regeneration via the bioengineered hair follicular unit transplantation

Organ regenerative therapy aims to reproduce fully functional organs to replace organs that have been lost or damaged as a result of disease, injury, or aging. For the fully functional regeneration of ectodermal organs, a concept has been proposed in which a bioengineered organ is developed by reproducing the embryonic processes of organogenesis. Here, we show that a bioengineered hair follicle germ, which was reconstituted with embryonic skin-derived epithelial and mesenchymal cells and ectopically transplanted, was able to develop histologically correct hair follicles. The bioengineered hair follicles properly connected to the host skin epithelium by intracutaneous transplantation and reproduced the stem cell niche and hair cycles. The bioengineered hair follicles also autonomously connected with nerves and the arrector pili muscle at the permanent region and exhibited piloerection ability. Our findings indicate that the bioengineered hair follicles could restore physiological hair functions and could be applicable to surgical treatments for alopecia

LUBAC prevents lethal dermatitis by inhibiting cell death induced by TNF, TRAIL and CD95L

The linear ubiquitin chain assembly complex (LUBAC), composed of HOIP, HOIL-1 and SHARPIN, is required for optimal TNF-mediated gene activation and to prevent cell death induced by TNF. Here, we demonstrate that keratinocyte-specific deletion of HOIP or HOIL-1 (E-KO) results in severe dermatitis causing postnatal lethality. We provide genetic and pharmacological evidence that the postnatal lethal dermatitis in HoipE-KO and Hoil-1E-KO mice is caused by TNFR1-induced, caspase-8-mediated apoptosis that occurs independently of the kinase activity of RIPK1. In the absence of TNFR1, however, dermatitis develops in adulthood, triggered by RIPK1-kinase-activity-dependent apoptosis and necroptosis. Strikingly, TRAIL or CD95L can redundantly induce this disease-causing cell death, as combined loss of their respective receptors is required to prevent TNFR1-independent dermatitis. These findings may have implications for the treatment of patients with mutations that perturb linear ubiquitination and potentially also for patients with inflammation-associated disorders that are refractory to inhibition of TNF alone