Dust and the type II-Plateau supernova 2004dj

We present mid-infrared (MIR) spectroscopy of a Type II-plateau supernova, SN 2004dj, obtained with the Spitzer Space Telescope, spanning 106--1393d after explosion. MIR photometry plus optical/near-IR observations are also reported. An early-time MIR excess is attributed to emission from non-silicate dust formed within a cool dense shell (CDS). Most of the CDS dust condensed between 50d and 165d, reaching a mass of $0.3x^(-5)Msun. Throughout the observations much of the longer wavelength (>10microns) part of the continuum is explained as an IR echo from interstellar dust. The MIR excess strengthened at later times. We show that this was due to thermal emission from warm, non-silicate dust formed in the ejecta. Using optical/near-IR line-profiles and the MIR continua, we show that the dust was distributed as a disk whose radius appeared to be slowly shrinking. The disk radius may correspond to a grain destruction zone caused by a reverse shock which also heated the dust. The dust-disk lay nearly face-on, had high opacities in the optical/near-IR regions, but remained optically thin in the MIR over much of the period studied. Assuming a uniform dust density, the ejecta dust mass by 996d was 0.5+/-0.1 x 10^(-4)Msun, and exceeded 10^(-4)Msun by 1393d. For a dust density rising toward the center the limit is higher. Nevertheless, this study suggests that the amount of freshly-synthesized dust in the SN 2004dj ejecta is consistent with that found from previous studies, and adds further weight to the claim that such events could not have been major contributors to the cosmic dust budget.

Association of VEGF-1499C -> T polymorphism with diabetic nephropathy in type 1 diabetes mellitus

Vascular endothelial growth factor (VEGF) is reported to be implicated in the development of diabetic nephropathy. We performed a case-control study to determine if VEGF-2578C -> A, VEGF-1499C -> T, and VEGF-635G -> C single-nucleotide polymorphisms (SNPs) in the VEGF gene are associated with predisposition to diabetic nephropathy in type I diabetes. Genomic DNA was obtained from Irish type I diabetic individuals with nephropathy (cases, n=242) and those without nephropathy (controls, n=301), in addition to 400 healthy control samples. These samples were genotyped for the three SNPs using TaqMan or Pyrosequencing technology. Chi-squared analyses revealed no significant differences in genotype or allele frequencies in cases versus controls for VEGF-2578C -> A (genotype, P=.58; allele, P=.52) and VEGF-635G -> C (genotype, P=.58; allele, P=.33). However, a positive association with diabetic nephropathy was observed for the VEGF-1499T allele in the Northern Ireland population (P

Glucose lowers the threshold for human aortic vascular smooth muscle cell migration: inhibition by protein phosphatase-2A

AIMS/HYPOTHESIS: Atherosclerosis, which occurs prematurely in individuals with diabetes, incorporates vascular smooth muscle cell (VSMC) chemotaxis. Glucose, through protein kinase C-beta(II) signalling, increases chemotaxis to low concentrations of platelet-derived growth factor (PDGF)-BB. In VSMC, a biphasic response in PDGF-beta receptor (PDGF-betaR) level occurs as PDGF-BB concentrations increase. The purpose of this study was to determine whether increased concentrations of PDGF-BB and raised glucose level had a modulatory effect on the mitogen-activated protein kinase/extracellular-regulated protein kinase pathway, control of PDGF-betaR level and chemotaxis.

METHODS: Cultured aortic VSMC, exposed to normal glucose (NG) (5 mmol/l) or high glucose (HG) (25 mmol/l) in the presence of PDGF-BB, were assessed for migration (chemotaxis chamber) or else extracted and immunoblotted.

RESULTS: At concentrations of PDGF-BB <540 pmol/l, HG caused an increase in the level of PDGF-betaR in VSMC (immunoblotting) versus NG, an effect that was abrogated by inhibition of aldose reductase or protein kinase C-beta(II). At higher concentrations of PDGF-BB (>540 pmol/l) in HG, receptor level was reduced but in the presence of aldose reductase or protein kinase C-beta(II) inhibitors the receptor levels increased. It is known that phosphatases may be activated at high concentrations of growth factors. At high concentrations of PDGF-BB, the protein phosphatase (PP)2A inhibitor, endothall, caused an increase in PDGF-betaR levels and a loss of biphasicity in receptor levels in HG. At higher concentrations of PDGF-BB in HG, the chemoattractant effect of PDGF-BB was lost (chemotaxis chamber). Under these conditions inhibition of PP2A was associated with a restoration of chemotaxis to high concentrations of PDGF-BB.

CONCLUSION/INTERPRETATION: The biphasic response in PDGF-betaR level and in chemotaxis to PDGF-BB in HG is due to PP2A activation.

Compromised Spindle Assembly Checkpoint due to Altered Expression of Ubch10 and Cdc20 in Human Papillomavirus Type 16 E6 and E7-Expressing Keratinocytes

Cells expressing human papillomavirus type 16 (HPV-16) E6 and E7 proteins exhibit deregulation of G(2)/M genes, allowing bypass of DNA damage arrest signals. Normally, cells with DNA damage that override the G(2) damage checkpoint would precociously enter mitosis and ultimately face mitotic catastrophe and apoptotic cell death. However, E6/E7-expressing cells (E6/E7 cells) have the ability to enter and exit mitosis in the presence of DNA damage and continue with the next round of the cell cycle. Little is known about the mechanism that allows these cells to gain entry into and exit from mitosis. Here, we show that in the presence of DNA damage, E6/E7 cells have elevated levels of cyclin B, which would allow entry into mitosis. Also, as required for exit from mitosis, cyclin B is degraded in these cells, permitting initiation of the next round of DNA synthesis and cell cycle progression. Proteasomal degradation of cyclin B by anaphase-promoting complex/cyclosome (APC/C) is, in part, due to elevated levels of the E2-conjugating enzyme, Ubch10, and the substrate recognition protein, Cdc20, of APC/C. Also, in E6/E7 cells with DNA damage, while Cdc20 is complexed with BubR1, indicating an active checkpoint, it is also present in complexes free of BubR1, presumably allowing APC/C activity and slippage through the checkpoint.

Extracting S-matrix poles for resonances from numerical scattering data: Type-II Pade reconstruction

We present a FORTRAN 77 code for evaluation of resonance pole positions and residues of a numerical scattering matrix element in the complex energy (CE) as well as in the complex angular momentum (CAM) planes. Analytical continuation of the S-matrix element is performed by constructing a type-II Pade approximant from given physical values (Bessis et al. (1994) [421: Vrinceanu et al. (2000) [24]; Sokolovski and Msezane (2004) [23]). The algorithm involves iterative 'preconditioning' of the numerical data by extracting its rapidly oscillating potential phase component. The code has the capability of adding non-analytical noise to the numerical data in order to select 'true' physical poles, investigate their stability and evaluate the accuracy of the reconstruction. It has an option of employing multiple-precision (MPFUN) package (Bailey (1993) [451) developed by D.H. Bailey wherever double precision calculations fail due to a large number of input partial waves (energies) involved. The code has been successfully tested on several models, as well as the F + H-2 -> HE + H, F + HD : HE + D, Cl + HCI CIH + Cl and H + D-2 -> HD + D reactions. Some detailed examples are given in the text.

The size distribution of Jupiter Family comet nuclei

We present an updated cumulative size distribution (CSD) for Jupiter Family comet (JFC) nuclei, including a rigorous assessment of the uncertainty on the slope of the CSD. The CSD is expressed as a power law, N(>rN) ?r-qN, where rN is the radius of the nuclei and q is the slope. We include a large number of optical observations published by us and others since the comprehensive review in the Comets II book, and make use of an improved fitting method. We assess the uncertainty on the CSD due to all of the unknowns and uncertainties involved (photometric uncertainty, assumed phase function, albedo and shape of the nucleus) by means of Monte Carlo simulations. In order to do this we also briefly review the current measurements of these parameters for JFCs. Our final CSD has a slope q= 1.92 ± 0.20 for nuclei with radius rN= 1.25 km.

Local Conentration of Waves due to Abrupt Alongshore Variation of Nearshore Bathymetry

Small-scale physical and numerical experiments were conducted to investigate the local concentration of waves (monochromatic and group) due to abrupt change of nearshore bathymetry in alongshore direction. Wave run-up motions along the shoreline were measured using an image analysis technique to compare localized concentration of wave energy, when waves propagate a over bathymetry composing rhythmic patterns of mild/steep slope bottom configurations. Measured alongshore variation of maximum wave run-up heights showed significant peak near the boundary, which has sudden alongshore change of depth, both under monochromatic and group wave trains. This phenomenon is found to be due to interaction of waves with neashore currents, which is further enhanced by excitation of long wave components by breaking of group waves. Furthermore, this paper discusses results of preliminary experiments carried out to test the effectiveness of several shore protection structure layouts in mitigating such wave concentrations. Numerical simulations were performed by using a model developed based on Nwogu (1993) Boussinesq-type equations; coupled with a transport equation to model energy dissipation due to wave breaking.

Residual stress due to curing can initiate damage in porous bone cement: experimental and theoretical evidence

Residual stress due to shrinkage of polymethylmethacrylate bone cement after polymerisation is possibly one factor capable of initiating cracks in the mantle of cemented hip replacements. No relationship between residual stress and observed cracking of cement has yet been demonstrated. To investigate if any relationship exists, a physical model has been developed which allows direct observation of damage in the cement layer on the femoral side of total hip replacement. The model contains medial and lateral cement layers between a bony surface and a metal stem; the tubular nature of the cement mantle is ignored. Five specimens were prepared and examined for cracking using manual tracing of stained cracks, observed by transmission microscopy: cracks were located and measured using image analysis. A mathematical approach for the prediction of residual stress due to shrinkage was developed which uses the thermal history of the material to predict when stress-locking occurs, and estimates subsequent thermal stress. The residual stress distribution of the cement layer in the physical model was then calculated using finite element analysis. Results show maximum tensile stresses normal to the observed crack directions, suggesting a link between residual stress and preload cracking. The residual stress predicted depends strongly on the definition of the reference temperature for stress-locking. The highest residual stresses (4-7 MPa) are predicted for shrinkage from maximum temperature, in this case, magnitudes are sufficiently high to initiate cracks when the influence of stress raisers such as pores or interdigitation at the bone/cement interface are taken into account (up to 24 MPa when calculating stress around a pore according to the method of Harrigan and Harris (J. Biomech. 24(11) (1991) 1047-1058)). We conclude that the damage accumulation failure scenario begins before weight-bearing due to cracking induced by residual stress around pores or stress raisers. (C) 2002 Elsevier Science Ltd. All rights reserved.

Epidemiology of Adolescent Rugby Injuries: A Systematic Review

OBJECTIVE: Despite recent increases in the volume of research in professional rugby union, there is little consensus on the epidemiology of injury in adolescent players. We undertook a systematic review to determine the incidence, severity, and nature of injury in adolescent rugby union players.

DATA SOURCES: In April 2009, we performed a computerized literature search on PubMed, Embase, and Cochrane Controlled Trials Register (via Ovid). Population-specific and patient-specific search terms were combined in the form of MEDLINE subject headings and key words (wound$ and injur$, rugby, adolescent$). These were supplemented with related-citation searches on PubMed and bibliographic tracking of primary and review articles.

STUDY SELECTION: Prospective epidemiologic studies in adolescent rugby union players.

DATA SYNTHESIS: A total of 15 studies were included, and the data were analyzed descriptively. Two independent reviewers extracted key study characteristics regarding the incidence, severity, and nature of injuries and the methodologic design.

CONCLUSIONS: Wide variations existed in the injury definitions and data collection procedures. The incidence of injury necessitating medical attention varied with the definition, from 27.5 to 129.8 injuries per 1000 match hours. The incidence of time-loss injury (>7 days) ranged from 0.96 to 1.6 per 1000 playing hours and from 11.4/1000 match hours (>1 day) to 12-22/1000 match hours (missed games). The highest incidence of concussion was 3.3/1000 playing hours. No catastrophic injuries were reported. The head and neck, upper limb, and lower limb were all common sites of injury, and trends were noted toward greater time loss due to upper limb fractures or dislocations and knee ligament injuries. Increasing age, the early part of the playing season, and the tackle situation were most closely associated with injury. Future injury-surveillance studies in rugby union must follow consensus guidelines to facilitate interstudy comparisons and provide further clarification as to where injury-prevention strategies should be focused.

Development of an allele-specific real-time PCR assay for discrimination and quantification of p63 R279H mutation in EEC syndrome

The ectrodactyly-ectodermal dysplasiaclefting syndrome is a rare autosomal dominant disorder caused by heterozygous mutations in the p63 gene, a transcription factor belonging to the p53 family. The majority of cases of ectrodactyly-ectodermal dysplasia syndrome are caused by de novo mutations and are therefore sporadic in approximately 60% of patients. The substitution of arginine to histidine (R279H), due to a c.836G>A mutation in exon 7 of the p63 gene, represents 55% of the identified mutations and is considered a mutational hot spot. A quantitative and sensitive real-time PCR was performed to quantify both wild-type and R279H alleles in DNA extracted from peripheral blood and RNA from cultured epithelial cells. Standard curves were constructed for both wild-type and mutant probes. The sensitivity of the assay was determined by generating serial dilutions of the DNA isolated from heterozygous patients (50% of alleles mutated) with wild-type DNA, thus obtaining decreasing percentages of p63 R279H mutant allele (50%, 37.5%, 25%, 12.5%, 10%, 7.5%, 5%, 2.5%, and 0.0%). The assay detected up to 1% of the mutant p63. The high sensitivity of the assay is of particular relevance to prenatal diagnosis and counseling and to detect therapeutic effects of drug treatment or gene therapy aimed at reducing the amount of mutated p63. © 2012 American Society for Investigative Pathology and the Association for Molecular Pathology. Published by Elsevier Inc. All rights reserved.