http://repositorium.sdum.uminho.pt/bitstream/1822/48763/1/1-s2.0-S037026931200857X-main.pdf

Observation of a new particle in the search for the Standard Model Higgs boson with the ATLAS detector at the LHC

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

https://biblio.ugent.be/publication/8555786/file/8555788.pdf

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

The ATLAS detector as installed in its experimental cavern at point 1 at CERN is described in this paper. A brief overview of the expected performance of the detector when the Large Hadron Collider begins operation is also presented.

The ATLAS Experiment at the CERN Large Hadron Collider

This paper describes the ATLAS experiment as installed in i ts experimental cavern at point 1 at CERN. It also presents a brief overview of the expec ted performance of the detector.

http://absimage.aps.org/image/SES08/MWS_SES08-2008-020010.pdf

The protective effects of estrogen on the cardiovascular system

The recognition of cord blood as a discarded resource rich in high proliferative potential hematopoietic stem/progenitor cells (HSPCs) triggered a flurry of studies in the 1990s exploiting its potential for transplantation. These studies established placental cord blood (PCB) as an excellent source of stem cells for related and unrelated transplants; pediatric, and adult. However, the fact that each PCB is quantitatively a limited resource restricts its efficacy to patients with low body weight, mostly children. Therefore, strategies are continuously being explored to overcome this limitation. Attempts to increase the HSPC content, or to improve their homing and engraftment potential, or the receptivity and/or the immunological status of the recipient are ongoing. Most importantly, apart from HSPCs, PCB contains stem cells for other tissues. This awareness has propelled explorations on the use of PCB for tissue repair and tissue engineering for a variety of clinical applications. In the present communication we will review differences between fetal–neonatal and adult HSPCs, current progress and limitations in the use of PCB for transplantation, and targeted approaches to overcome these limitations in the clinical use of PCB for treatment of hematopoietic and nonhematopoietic disorders.

Cord Blood Hematopoiesis: The Road to Transplantation

GATA1 gets personal.

Aplidin Improves Megakaryocytopoiesis and Halts Neo-Angiogenesis in the Gata1 low Murine Model of Myelofibrosis

Preclinical studies on the use of a P-selectin blocking monoclonal antibody to halt progression of myelofibrosis in the Gata1low mouse model.

The pathogenesis of idiopathic myelofibrosis has not yet been completely elucidated, but the availability of animal models of the disease has made it possible, in the past few years, to focus on the cells (megakaryocytes) and cytokines (transforming growth factor-β, among others) potentially involved. This review will deal with the two best characterized animal models (the TPO-overexpressing and the GATA-1low mouse) as well as with the newest ones that have been developed following the identification of the JAK2 V617F and MPL W515K/L mutations in the human form of the disease. Each of these unique animal models conceivably represents an invaluable tool for further characterizing the disease mechanisms as well as for testing novel therapeutic agents.

Anna Rita Migliaccio

Papers

Cord Blood Hematopoiesis: The Road to Transplantation

GATA1 gets personal.

Aplidin Improves Megakaryocytopoiesis and Halts Neo-Angiogenesis in the Gata1 low Murine Model of Myelofibrosis

Preclinical studies on the use of a P-selectin blocking monoclonal antibody to halt progression of myelofibrosis in the Gata1low mouse model.

Animal Models of Myelofibrosis