Accretion of planetary matter and the lithium problem in the 16 Cygni stellar system

The 16 Cyg system is composed of two solar analogs with similar masses and ages. A red dwarf is in orbit around 16 Cyg A whereas 16 Cyg B hosts a giant planet. The abundances of heavy elements are similar in the two stars but lithium is much more depleted in 16 Cyg B that in 16 Cyg A, by a factor of at least 4.7. The interest of studying the 16 Cyg system is that the two star have the same age and the same initial composition. The presently observed differences must be due to their different evolution, related to the fact that one of them hosts a planet contrary to the other one. We computed models of the two stars which precisely fit the observed seismic frequencies. We used the Toulouse Geneva Evolution Code (TGEC) that includes complete atomic diffusion (including radiative accelerations). We compared the predicted surface abundances with the spectroscopic observations and confirmed that another mixing process is needed. We then included the effect of accretion-induced fingering convection. The accretion of planetary matter does not change the metal abundances but leads to lithium destruction which depends on the accreted mass. A fraction of earth mass is enough to explain the lithium surface abundances of 16 Cyg B. We also checked the beryllium abundances. In the case of accretion of heavy matter onto stellar surfaces, the accreted heavy elements do not remain in the outer convective zones but they are mixed downwards by fingering convection induced by the unstable $\mu$-gradient. Depending on the accreted mass, this mixing process may transport lithium down to its nuclear destruction layers and lead to an extra lithium depletion at the surface. A fraction of earth mass is enough to explain a lithium ratio of 4.7 in the 16 Cyg system. In this case beryllium is not destroyed. Such a process may be frequent in planet host stars and should be studied in other cases in the future.Comment: 8 pages, 10 figures, publication in A&

Speed of coming down from infinity for birth and death processes

We finely describe the speed of "coming down from infinity" for birth and death processes which eventually become extinct. Under general assumptions on the birth and death rates, we firstly determine the behavior of the successive hitting times of large integers. We put in light two different regimes depending on whether the mean time for the process to go from $n+1$ to $n$ is negligible or not compared to the mean time to reach $n$ from infinity. In the first regime, the coming down from infinity is very fast and the convergence is weak. In the second regime, the coming down from infinity is gradual and a law of large numbers and a central limit theorem for the hitting times sequence hold. By an inversion procedure, we deduce that the process is a.s. equivalent to a non-increasing function when the time goes to zero. Our results are illustrated by several examples including applications to population dynamics and population genetics. The particular case where the death rate varies regularly is studied in details.Comment: 30 pages. arXiv admin note: text overlap with arXiv:1310.740

Chronic intestinal pseudo-obstruction in a Bernese Mountain Dog

Chronic Intestinal Pseudo-Obstruction (CIPO) is a rare syndrome characterized by chronic intestinal dilation and dysmotility in the absence of mechanical obstruction. A definite diagnosis of CIPO can only be made after histological examination of intestinal tissues. The present case describes a CIPO in a 2.5-year-old Bernese Mountain dog with a history of recurrent gastro-intestinal complaints suggestive for pseudo-obstruction. Histological lesions of small intestinal samples consisted of severe loss of smooth muscle cells of the tunica muscularis and diffuse infiltration of mononuclear cells. In addition, a hypertrophy of the lamina muscularis mucosa of the small intestinal tract was present. On the basis of these findings and the results of immunohistochemistry, a myopathic form of CIPO was diagnosed

Parallélogrammes Galoisiens

RésuméWe generalize the notion of a Galois extension by that of a Galois parallelogram; a Galois extension is just a flat Galois parallelogram. The existence of Galois parallelograms is proved in the number field case. We state numerous general properties of Galois parallelograms which give, in particular, the usual properties of classical Galois theory. Then, we introduce a “two-dimensional Galois theory” by generalizing to Galois parallelograms the classical Galois bijection for finite Galois extensions

Streptococcus mutans Binding to Collagen, Fibrinogen, Fibronectin, and Laminin

poster abstractIntroduction: Streptococcus mutans, nicotine, and certain proteins may be involved in a complicated mechanism that contributes to atherosclerosis. Build up of arterial plaque causes atherosclerosis. Arterial plaque is mainly composed of fat, cholesterol, and calcium. When plaque builds up in the arteries, a clot or blockage can occur and may cause an occlusion. Objective: S. mutans grows in oral biofilm and causes dental caries. These bacteria enter the blood stream from mucosal breaks in the oral cavity. There is evidence that S. mutans binds to endothelial cell surface proteins lining arterial surfaces. An increased incidence of S. mutans in arterial plaque seems to have a direct relationship with atherosclerosis. From preliminary research, there was a strong indication that increased S. mutans biofilm formation is caused by nicotine. The number of binding proteins on nicotine-treated S. mutans cell surface increases as well. In addition, results demonstrated that S. mutans binds to collagen type I, fibrinogen, fibronectin, and laminin, which are proteins found on endothelial cells. Methods: To investigate protein binding, S. mutans UA159 was cultured in 0, 0.25, 0.50, 1.0, 2.0, and 4.0 mg/ml of nicotine and their ability to bind to human collagen type I, fibrinogen, fibronectin and laminin was assessed using an ELISA assay. Results: S. mutans significantly bound to collagen type I and fibrinogen when cultured in 2 and 4 mg/ml nicotine. S. mutans significantly bound to laminin when the bacterium was grown in 1, 2, and 4 mg/ml. The binding of S. mutans to fibronectin varied when cultured in different concentrations of nicotine. Conclusion: From the results, it can be concluded that S. mutans UA159 binds to collagen type I, fibrinogen, fibronectin, and laminin. This indicates that S. mutans and the proteins studied are very likely to be part of the mechanism that leads to atherosclerosis

Streptococcus mutans Binding to Collagen and Fibrinogen in Nicotine

poster abstractIntroduction: Our overall goal is to find the mechanism for atherosclerosis. Smokers have increased incidence of atherosclerosis. Atherosclerosis occurs when there is a build up of plaque in the arteries. There is evidence that Streptococcus mutans help cause this blockage. We have already proven that S. mutans produces more biofilm in certain concentrations of nicotine. Also, we have found that nicotine upregulates S. mutans binding to proteins in certain concentrations; other labs have also demonstrated this. The intent of this study was to evaluate the binding of S. mutans to both collagen type I and fibrinogen, which are both proteins that are already present on the surface of endothelial cells lining arteries. Methods: S. mutans UA159 was cultured in 0.00-4.00 mg/mL nicotine. The cells were killed in formaldehyde and then coated with biotin. The proteins studied were plated (1 ug/ml) on 96-well microtiter plates. In order to block the empty spaces that the protein did not bind to, 1% BSA in sodium bicarbonate buffer was added to the plate. Each nicotine dilution of S. mutans was added to the plate and the amount of binding was assessed. Extra-avidin HRP and OPD were added to the plate and the intensity was measured at an absorbance of 490 nm using a spectrophotometer. Results: The intensity was directly related to the number of cells bound to the proteins. There was a significant increase in S. mutans binding when compared to the baseline for both collagen type I and fibrinogen. The binding was highest when S. mutans were cultured in 2 and 4 mg/mL nicotine. Conclusions: The data collected suggests that collagen type I and fibrinogen contribute to the mechanism of atherosclerosis. When S. mutans are cultured in moderately high concentrations of nicotine, more binding of the bacteria to these proteins occurs

Clonage et caractérisation d'un nouveau gène, Hypertension-related-calcium-regulated gene (HCaRG) exprimé chez le rat et l'humain

Mémoire numérisé par la Direction des bibliothèques de l'Université de Montréal