Boson stars in massive dilatonic gravity

We study equilibrium configurations of boson stars in the framework of a class scalar-tensor theories of gravity with massive gravitational scalar (dilaton). In particular we investigate the influence of the mass of the dilaton on the boson star structure. We find that the masses of the boson stars in presence of dilaton are close to those in general relativity and they are sensitive to the ratio of the boson mass to the dilaton mass within a typical few percent. It turns out also that the boson star structure is mainly sensitive to the mass term of the dilaton potential rather to the exact form of the potential.Comment: 9 pages, latex, 9 figures, one figure dropped, new comments added, new references added, typos correcte

Uncalibrated X-ray stereo reconstruction

We describe a novel application of uncalibrated stereo reconstruction to Roentgen Stereophotogrammetry Analysis (RSA). In RSA, stereo X-ray images are taken of a bone containing a prosthesis (e.g. a replacement knee) and a number of metal markers. The aim is to recover the relative position of the prosthesis and markers in 3D. Accuracy in previous RSA methods has been limited by two factors: manual feature selection and an assumption that camera calibration parameters are known to high precision - this is not the case in practice. Furthermore, the manual processing is slow and tedious. We report progress towards developing a fully automatic RSA system. New algorithms are described for automatically localising marker points in X-ray images to sub-pixel accuracy, and using them to reconstruct accurate 3D positions using robust statistical methods. Preliminary experiments give excellent results

Polyomavirus middle T antigen induces ribosomal protein S6 phosphorylation through pp60c-src-dependent and -independent pathways.

Phosphorylation of ribosomal protein S6 is elevated in polyomavirus-infected cells. This elevation results only in part from activation of S6 kinase activity. These effects appear to reflect independent activities of wild-type middle T antigen. Hr-t mutant NG59, encoding a defective middle T protein, and mutant Py808A, encoding no middle T protein, were unable to induce S6 kinase activity or elevate S6 phosphorylation. Two other site-directed mutants encoding altered middle T proteins did elevate S6 phosphorylation while only weakly stimulating S6 kinase activity. These results suggest at least two independent pathways leading to elevation of S6 phosphorylation. One pathway leads to induction of S6 kinase activity following activation of pp60c-src by transformation-competent middle T antigen. Another pathway operates independently of S6 kinase induction and can be regulated by transformation-defective middle T mutants such as Py1387T. This mutant, encoding a truncated middle T protein that failed to associate with the plasma membrane and to activate pp60c-src, caused increased levels of S6 phosphorylation without detectably increasing S6 kinase activity. The ability of mutants such as Py1387T to induce S6 phosphorylation correlated with their ability to increase phosphorylation of VP1, an event linked to maturation of infectious virions.</jats:p

The drug titration paradox: more drug does not correlate with more effect in individual clinical data.

BACKGROUND A fundamental concept in pharmacology is that increasing dose increases drug effect. This is the basis of anaesthetic titration: the dose is increased when increased drug effect is desired and decreased when reduced drug effect is desired. In the setting of titration, the correlation of doses and observed drug effects can be negative, for example increasing dose reduces drug effect. We have termed this the drug titration paradox. We hypothesised that this could be explained, at least in part, by intrasubject variability. If the drug titration paradox is simply an artifact of pooling population data, then a mixed-effects analysis that accounts for interindividual variability in drug sensitivity should 'flip' the observed correlation, such that increasing dose increases drug effect. METHODS We tested whether a mixed-effects analysis could correctly reveal the underlying pharmacology using previously published data obtained during automatic feedback control of mean arterial pressure (MAP) with alfentanil (effect site concentration, CeAlf) during surgery. The relationship between MAP and CeAlf was explored with linear regression and a linear mixed-effects model. RESULTS A linear mixed-effects model did not identify the correct underlying pharmacology because of the presence of the titration paradox in the individual data. CONCLUSIONS The relationship between drug dose and drug effect must be determined under carefully controlled experimental conditions. In routine care, where the effect is profoundly influenced by varying clinical conditions and drugs are titrated to achieve the desired effect, it is nearly impossible to draw meaningful conclusions about the relationship between dose and effect

Optimization Methods to Minimize Emergence Time While Maintaining Adequate Post-Operative Analgesia

A rapid emergence from anesthesia combined with an extended duration of adequate analgesia is desired. Difficulties arise when trying to achieve a rapid emergence and provide adequate analgesia for procedures associated with moderate post operative pain. We propose to use pharmacokinetic (PK) and pharmacodynamic (PD) models with optimization techniques to determine anesthetic drugs ratios to improve post-anesthetic outcomes of emergence and analgesia. We hypothesize that optimized propofol, remifentanil, and fentanyl administrations will shorten emergence time and extend the period of adequate analgesia during patient recovery. Anesthesiologists administered a general anesthetic to 21 patients for laparoscopic procedures with propofol, remifentanil, and fentanyl according to their standard practice. The theoretical improvement provided by the optimization was measured by comparing the time differences between the control predictions and the optimized prediction of the TROR time and TRON time. In the control group the TROR was 10.2+-5.8 minutes (mean +- SD) and TRON was 3.5+-5.0 minutes after emergence. In the optimized group the TROR was 7.5+-2.2 minutes or 26% faster (p \u3c .001, paired t-test) and the TRON was 7.4 +-2.4 minutes or 88% longer (p \u3c .00001, t-test). Optimized administrations of propofol, remifentanil, and fentanyl resulted in a theoretically shorter emergence time and a longer period of adequate postoperative analgesia. The optimization algorithm shows potential for real-time clinical guidance in drug management

Juvenile king scallop, Pecten maximus, is potentially tolerant to low levels of ocean acidification when food is unrestricted.

The decline in ocean water pH and changes in carbonate saturation states through anthropogenically mediated increases in atmospheric CO2 levels may pose a hazard to marine organisms. This may be particularly acute for those species reliant on calcareous structures like shells and exoskeletons. This is of particular concern in the case of valuable commercially exploited species such as the king scallop, Pecten maximus. In this study we investigated the effects on oxygen consumption, clearance rates and cellular turnover in juvenile P. maximus following 3 months laboratory exposure to four pCO2 treatments (290, 380, 750 and 1140 µatm). None of the exposure levels were found to have significant effect on the clearance rates, respiration rates, condition index or cellular turnover (RNA: DNA) of individuals. While it is clear that some life stages of marine bivalves appear susceptible to future levels of ocean acidification, particularly under food limiting conditions, the results from this study suggest that where food is in abundance, bivalves like juvenile P. maximus may display a tolerance to limited changes in seawater chemistry

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York