Towards optimal use of antithrombotic therapy of people with cancer at the end of life: A research protocol for the development and implementation of the SERENITY shared decision support tool.

Background: Even though antithrombotic therapy has probably little or even negative effects on the well-being of people with cancer during their last year of life, deprescribing antithrombotic therapy at the end of life is rare in practice. It is often continued until death, possibly resulting in excess bleeding, an increased disease burden and higher healthcare costs.

Methods: The SERENITY consortium comprises researchers and clinicians from eight European countries with specialties in different clinical fields, epidemiology and psychology.

Chelonid Alphaherpesvirus 5 Prevalence and First Confirmed Case of Sea Turtle Fibropapillomatosis in Grenada, West Indies.

Chelonid alphaherpesvirus 5 (ChHV5) is strongly associated with fibropapillomatosis, a neoplastic disease of sea turtles that can result in debilitation and mortality. The objectives of this study were to examine green (), hawksbill (), and leatherback () sea turtles in Grenada, West Indies, for fibropapillomatosis and to utilize ChHV5-specific PCR, degenerate herpesvirus PCR, and serology to non-invasively evaluate the prevalence of ChHV5 infection and exposure. One-hundred and sixty-seven turtles examined from 2017 to 2019 demonstrated no external fibropapilloma-like lesions and no amplification of ChHV5 DNA from whole blood or skin biopsies.

Generation of scaled protogalactic seed magnetic fields in laser-produced shock waves.

The standard model for the origin of galactic magnetic fields is through the amplification of seed fields via dynamo or turbulent processes to the level consistent with present observations. Although other mechanisms may also operate, currents from misaligned pressure and temperature gradients (the Biermann battery process) inevitably accompany the formation of galaxies in the absence of a primordial field. Driven by geometrical asymmetries in shocks associated with the collapse of protogalactic structures, the Biermann battery is believed to generate tiny seed fields to a level of about 10(-21) gauss (refs 7, 8).

Isolation of a normal B cell subset with a Burkitt-like phenotype and transformation in vitro with Epstein-Barr virus.

Epstein-Barr virus (EBV) is causally linked with endemic Burkitt's lymphoma (BL), a tumor whose homogeneous cell surface phenotype suggests derivation from a particular subset of activated germinal centre B cells in vivo. Endemic BL also shows an unusual form of EBV infection with down-regulation of certain of the virus latent proteins which are constitutively expressed when EBV infects and transforms normal resting B cells in vitro. Here we question whether this virus:cell interaction is unique to malignant BL cells or whether it might be reproduced by in vitro infection of those particular germinal centre cells displaying the BL-like phenotype.

Downregulation of cell adhesion molecules LFA-3 and ICAM-1 in Epstein-Barr virus-positive Burkitt's lymphoma underlies tumor cell escape from virus-specific T cell surveillance.

Some EBV+ BL cell lines continue to grow as single cells on in vitro passage, show an unusually restricted expression of EBV-latent genes and retain a BL biopsy-like cell surface phenotype (group I/II lines); others change to growth in aggregates, show a broader pattern of virus latent gene expression, and develop a cell surface phenotype more characteristic of EBV-transformed LCL (group III lines). Here we show that the cell surface adhesion molecules LFA-1, ICAM-1, and LFA-3 are expressed at very low levels, if at all, on group I/II lines and are coordinately upregulated as BL lines move towards group III. The change to growth in aggregates reflects the increasing availability of LFA-1 and ICAM-1, the two ligands whose mutual interaction underlies homotypic BL cell adhesion in vitro.

Epstein-Barr virus-transformed human precursor B cell lines: altered growth phenotype of lines with germ-line or rearranged but nonexpressed heavy chain genes.

A series of lymphoblastoid cell lines (LCLs) have been established by in vitro infection of fetal bone marrow and fetal liver cells with Epstein-Barr virus (EBV). While most lines showed the usual mature B cell phenotype, a small proportion were cytoplasmic and surface immunoglobulin (Ig) heavy and light chain negative. Analysis of gene rearrangements indicated that the Ig- lines were either germ-line or nonproductively rearranged when probed for JH and were in germ-line configuration for C chi; no mu or chi mRNA could be detected in such cells.

Identification of a subset of normal B cells with a Burkitt's lymphoma (BL)-like phenotype.

Fresh biopsy cells from cases of Burkitt's lymphoma (BL) display a homogeneous cell surface phenotype. The cells were found to be reactive with the pan B cell marker B1, and consistently co-expressed the BL-associated glycolipid antigen, BLA, and the common acute lymphoblastic leukemia antigen, CALLA, but lacked the B cell "activation" antigens characteristically expressed on EB virus-transformed normal B cells. Microscopic and cell sorter analysis of cells isolated from a series of fresh normal tonsils have identified a subpopulation of normal B cells carrying the same cell surface markers.

Endemic Burkitt's lymphoma: phenotypic analysis of tumor biopsy cells and of derived tumor cell lines.

Tumor cells from 10 patients with Epstein-Barr virus-positive endemic Burkitt's lymphoma (BL) have been examined for cell surface phenotype, both at the biopsy stage and during BL cell line outgrowth in vitro, the cultures being followed for up to 150 passages. In all 10 cases, the biopsy cells showed coexpression of the common acute lymphoblastic leukemia antigen (CALLA) and of the BL-associated glycolipid antigen (BLA) with no accompanying expression of several "lymphoblastoid" cell surface markers defined by selected monoclonal antibodies. During cell line establishment and in vitro passage, the individual BL cell lines showed different degrees of progression toward a more "lymphoblastoid" cell surface phenotype, some even losing CALLA and BLA expression while retaining the chromosomal translocations indicative of their malignant origin.