Epitaxial growth of CoSi2 on hydrogen-terminated Si(001)

We demonstrate that CoSi2 grows epitaxially on H-terminated Si(001) and present the growth mechanism. It was found that direct reaction of Co with Si is suppressed on H-terminated Si below 400 °C. Thus, the hydrogen at the Co/Si interface hinders the formation of Co2Si and CoSi. Upon thermal desorption of hydrogen at around 400–550 °C, CoSi2, which is closely lattice-matched to Si(001), grows on Si(001) and thus, thin epitaxial CoSi2 films are formed on Si(001). The {111}-faceting was completely suppressed in the epitaxial CoSi2/Si(001), leading to the atomically flat interface

Observation of the first gravitational microlensing event in a sparse stellar field : the Tago event

We report the observation of the first gravitational microlensing event in a sparse stellar field, involving the brightest (V=11.4 mag) andclosest (~ 1 kpc) source star to date. This event was discovered by an amateurastronomer, A. Tago, on 2006 October 31 as a transient brightening, by ~4.5 mag during a ~15 day period, of a normal A-type star (GSC 3656-1328) in the Cassiopeia constellation. Analysis of both spectroscopic observations and the light curve indicates that this event was caused by gravitational microlensing rather than an intrinsically variable star. Discovery of this single event over a 30 year period is roughly consistent with the expected microlensing rate for the whole sky down to V = 12 mag stars. However, the probability for finding events with such a high magnification (~ 50) is much smaller, by a factor ~1/50, which implies that the true event rate may be higher than expected. This discovery indicates the potential of all sky variability surveys, employing frequent sampling by telescopes with small apertures and wide fields of view, for finding such rare transient events, and using the observations to explore galactic disk structure and search for exo-planets.Comment: 13 pages, 2 tables, 3 figures, accepted by Ap

Five-Year Optical and Near Infrared Observations of the Extremely Slow Nova V1280 Scorpii

We present optical ($B$, $V$, $R_{\rm c}$, $I_{\rm c}$ and $y$) and near infrared ($J$, $H$ and $K_{\rm s}$) photometric and spectroscopic observations of a classical nova V1280 Scorpii for five years from 2007 to 2011. Our photometric observations show a declining event in optical bands shortly after the maximum light which continues $\sim$ 250 days. The event is most probably caused by a dust formation. The event is accompanied by a short ($\sim$ 30 days) re-brightening episode ($\sim$ 2.5 mag in $V$), which suggests a re-ignition of the surface nuclear burning. After 2008, the $y$ band observations show a very long plateau at around $y$ = 10.5 for more than 1000 days until April 2011 ($\sim$ 1500 days after the maximum light). The nova had taken a very long time ($\sim$ 50 months) before entering the nebular phase (clear detection of both [\ion{O}{iii}] 4959 and 5007) and is still continuing to generate the wind caused by H-burning. The finding suggests that V1280 Sco is going through the historically slowest evolution. The interval from the maximum light (2007 February 16) to the beginning of the nebular phase is longer than any previously known slow novae: V723 Cas (18 months), RR Pic (10 months), or HR Del (8 months). It suggests that the mass of a white dwarf in the V1280 Sco system might be 0.6 M_\mathrm{\sun} or smaller. The distance, based on our measurements of the expansion velocity combined with the directly measured size of the dust shell, is estimated to be 1.1 $\pm$ 0.5 kpc.Comment: 17 pages, 14 figures, accepted for publication in A&

Prenatal muscle development in a mouse model for the secondary dystroglycanopathies

The defective glycosylation of α-dystroglycan is associated with a group of muscular dystrophies that are collectively referred to as the secondary dystroglycanopathies. Mutations in the gene encoding fukutin-related protein (FKRP) are one of the most common causes of secondary dystroglycanopathy in the UK and are associated with a wide spectrum of disease. Whilst central nervous system involvement has a prenatal onset, no studies have addressed prenatal muscle development in any of the mouse models for this group of diseases. In view of the pivotal role of α-dystroglycan in early basement membrane formation, we sought to determine if the muscle formation was altered in a mouse model of FKRP-related dystrophy

Focusing of MeV Ion Beams by Means of Tapered Glass Capillary Optics

departmental bulletin pape

Myosin heavy chain and physiological adaptation of the rat diaphragm in elastase-induced emphysema

BACKGROUND: Several physiological adaptations occur in the respiratory muscles in rodent models of elastase-induced emphysema. Although the contractile properties of the diaphragm are altered in a way that suggests expression of slower isoforms of myosin heavy chain (MHC), it has been difficult to demonstrate a shift in MHCs in an animal model that corresponds to the shift toward slower MHCs seen in human emphysema. METHODS: We sought to identify MHC and corresponding physiological changes in the diaphragms of rats with elastase-induced emphysema. Nine rats with emphysema and 11 control rats were studied 10 months after instillation with elastase. MHC isoform composition was determined by both reverse transcriptase polymerase chain reaction (RT-PCR) and immunocytochemistry by using specific probes able to identify all known adult isoforms. Physiological adaptation was studied on diaphragm strips stimulated in vitro. RESULTS: In addition to confirming that emphysematous diaphragm has a decreased fatigability, we identified a significantly longer time-to-peak-tension (63.9 ± 2.7 ms versus 53.9 ± 2.4 ms). At both the RNA (RT-PCR) and protein (immunocytochemistry) levels, we found a significant decrease in the fastest, MHC isoform (IIb) in emphysema. CONCLUSION: This is the first demonstration of MHC shifts and corresponding physiological changes in the diaphragm in an animal model of emphysema. It is established that rodent emphysema, like human emphysema, does result in a physiologically significant shift toward slower diaphragmatic MHC isoforms. In the rat, this occurs at the faster end of the MHC spectrum than in humans