The optical light curve of the LMC pulsar B0540-69 in 2009

This paper reports a detailed analysis of the optical light curve of PSR B0540-69, the second brightest pulsar in the visible band, obtained in 2009 (Jan. 18 and 20, and Dec. 14, 15, 16, 18) with the very high speed photon counting photometer Iqueye mounted at the ESO 3.6-m NTT in La Silla (Chile). The optical light curve derived by Iqueye shows a double structure in the main peak, with a raising edge steeper than the trailing edge. The double peak can be fitted by two Gaussians with the same height and FWHM of 13.3 and 15.5 ms respectively. Our new values of spin frequencies allow to extend by 3.5 years the time interval over which a reliable estimate of frequency first and second derivatives can be performed. A discussion of implications on the braking index and age of the pulsar is carried out. A value of n = 2.087 +/- 0.007 for the overall braking index from 1987 to 2009 is derived. The braking index corrected age is confirmed around 1700 years.Comment: Accepted for publication in MNRA

Circadian glucocorticoid oscillations preserve a population of adult hippocampal neural stem cells in the aging brain.

A decrease in adult hippocampal neurogenesis has been linked to age-related cognitive impairment. However, the mechanisms involved in this age-related reduction remain elusive. Glucocorticoid hormones (GC) are important regulators of neural stem/precursor cells (NSPC) proliferation. GC are released from the adrenal glands in ultradian secretory pulses that generate characteristic circadian oscillations. Here, we investigated the hypothesis that GC oscillations prevent NSPC activation and preserve a quiescent NSPC pool in the aging hippocampus. We found that hippocampal NSPC populations lacking expression of the glucocorticoid receptor (GR) decayed exponentially with age, while GR-positive populations decayed linearly and predominated in the hippocampus from middle age onwards. Importantly, GC oscillations controlled NSPC activation and GR knockdown reactivated NSPC proliferation in aged mice. When modeled in primary hippocampal NSPC cultures, GC oscillations control cell cycle progression and induce specific genome-wide DNA methylation profiles. GC oscillations induced lasting changes in the methylation state of a group of gene promoters associated with cell cycle regulation and the canonical Wnt signaling pathway. Finally, in a mouse model of accelerated aging, we show that disruption of GC oscillations induces lasting changes in dendritic complexity, spine numbers and morphology of newborn granule neurons. Together, these results indicate that GC oscillations preserve a population of GR-expressing NSPC during aging, preventing their activation possibly by epigenetic programming through methylation of specific gene promoters. Our observations suggest a novel mechanism mediated by GC that controls NSPC proliferation and preserves a dormant NSPC pool, possibly contributing to a neuroplasticity reserve in the aging brain

Impiego di spettroscopia FT-NIR nella valutazioni del livello di tostatura del caff\ue9 in grani

Impiego di spettroscopia FT-NIR nella valutazioni del grado di tostatura del caff\ue9 in gran

High-Time-Resolution Optical Observations of the Crab Pulsar

Although optical pulsar studies are currently limited a few favoured objects, the observation of pulsars at optical wavelengths provides an opportunity to derive a number of important pulsar characteristics. These parameters will be vital for a comprehensive model of pulsar emission mechanisms. The exploitation of the data available through optical pulsar studies requires that high-time-resolution instruments suitable for the optical domain, and for faint pulsar targets, are developed and thoroughly tested. Observations of the Crab pulsar with the high-time-resolution photon-tagging photometer IquEYE show an optical-radio delay of \u2dc178 \u3bcs. In conjunction with simultaneous Jodrell Bank radio observations, a correlation between giant radio pulses and enhanced optical pulses was detected for this pulsar, which is possible evidence for the reprocessing of radio photons. Comparison with optical linear polarisation measurements indicate a shift between linear and circular polarisation at the radio precursor phase

Iqueye, a single photon counting very high speed photometer for the ESO 3.5m NTT

Iqueye is a single photon counting very high speed photometer built for the ESO 3.5m New Technology Telescope (NTT) in La Silla (Chile) as prototype of a \u2018quantum\u2019 photometer for the 42m European Extremely Large Telescope (E-ELT). The optics of Iqueye splits the telescope pupil into four portions, each feeding a Single Photon Avalanche Diode (SPAD) operated in Geiger mode. The SPADs sensitive area has a diameter of 100 \u3bcm, with a quantum efficiency better than 55% at 500 nm, and a dark count less than 50 Hz. The quenching circuit and temperature control are integrated in each module. A time-to-digital converter (TDC) board, controlled by a rubidium oscillator plus a GPS receiver, time tags the pulses from the 4 channels. The individual times are stored in a 2 TeraByte memory. Iqueye can run continuously for hours, handling count rates up to 8 MHz, with a final absolute accuracy of each time tag better that 0.5 ns. A first very successful run was performed in Jan 2009; both very faint and very bright stars were observed, demonstrating the high photometric quality of the instrument. The first run allowed also to identify some opto-mechanical improvements, which have been implemented for a second run performed in Dec 2009. The present paper will describe the first version, the improvements implemented in the second one, and some of the obtained astronomical results

Circadian glucocorticoid oscillations preserve a population of adult hippocampal neural stem cells in the aging brain

A decrease in adult hippocampal neurogenesis has been linked to age-related cognitive impairment. However, the mechanisms involved in this age-related reduction remain elusive. Glucocorticoid hormones (GC) are important regulators of neural stem/precursor cells (NSPC) proliferation. GC are released from the adrenal glands in ultradian secretory pulses that generate characteristic circadian oscillations. Here, we investigated the hypothesis that GC oscillations prevent NSPC activation and preserve a quiescent NSPC pool in the aging hippocampus. We found that hippocampal NSPC populations lacking expression of the glucocorticoid receptor (GR) decayed exponentially with age, while GR-positive populations decayed linearly and predominated in the hippocampus from middle age onwards. Importantly, GC oscillations controlled NSPC activation and GR knockdown reactivated NSPC proliferation in aged mice. When modeled in primary hippocampal NSPC cultures, GC oscillations control cell cycle progression and induce specific genome-wide DNA methylation profiles. GC oscillations induced lasting changes in the methylation state of a group of gene promoters associated with cell cycle regulation and the canonical Wnt signaling pathway. Finally, in a mouse model of accelerated aging, we show that disruption of GC oscillations induces lasting changes in dendritic complexity, spine numbers and morphology of newborn granule neurons. Together, these results indicate that GC oscillations preserve a population of GR-expressing NSPC during aging, preventing their activation possibly by epigenetic programming through methylation of specific gene promoters. Our observations suggest a novel mechanism mediated by GC that controls NSPC proliferation and preserves a dormant NSPC pool, possibly contributing to a neuroplasticity reserve in the aging brain.The experimental work was financed by grants from the Innovational Research Incentives Scheme VIDI 864.09.016 from the Netherlands organization for Scientific Research (NWO); the International Foundation for Alzheimer’s Research (ISAO), and Alzheimer Nederland to CPF. HM and LG-C were supported by the Spanish Ministry of Economy and Competitiveness, grant SAF2015- 70433-R to HM and Juan de la Cierva Program to LG-C. EG and NT were financed by the Swiss National Science Foundation. PJL was supported by Alzheimer Nederland. SM-S was financed by the Jesus de Gangoiti Foundation. We acknowledge the assistance of Rafael Hortigüela and Tijana Radic during the paper preparation and Ronald Breedijk and Mark Hink at the Leeuwenhoek Centre for Advanced Microscopy, University of Amsterdam for providing technical assistance with the confocal microscop

Mitochondria Inspire a Lifestyle

Tucked inside our cells, we animals (and plants, and fungi) carry mitochondria, minuscule descendants of bacteria that invaded our common ancestor 2 billion years ago. This unplanned breakthrough endowed our ancestors with a convenient, portable source of energy, enabling them to progress towards more ambitious forms of life. Mitochondria still manufacture most of our energy; we have evolved to invest it to grow and produce offspring, and to last long enough to make it all happen. Yet because the continuous generation of energy is inevitably linked to that of toxic free radicals, mitochondria give us life and give us death. Stripping away clutter and minutiae, here we present a big-picture perspective of how mitochondria work, how they are passed on virtually only by mothers, and how they shape the lifestyles of species and individuals. We discuss why restricting food prolongs lifespan, why reproducing shortens it, and why moving about protects us from free radicals despite increasing their production. We show that our immune cells use special mitochondria to keep control over our gut microbes. And we lay out how the fabrication of energy and free radicals sets the internal clocks that command our everyday rhythms-waking, eating, sleeping. Mitochondria run the show