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Lymphoid System (lymphoid + system)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Strength of signal: a fundamental mechanism for cell fate specification

IMMUNOLOGICAL REVIEWS, Issue 1 2006
Sandra M. Hayes
Summary:, How equipotent cells develop into complex tissues containing many diverse cell types is still a mystery. However, evidence is accumulating from different tissue systems in multiple organisms that many of the specific receptor families known to regulate cell fate decisions target conserved signaling pathways. A mechanism for preserving specificity in the cellular response that has emerged from these studies is one in which quantitative differences in receptor signaling regulate the cell fate decision. A signal strength model has recently gained support as a means to explain ,,/,, lineage commitment. In this review, we compare the ,,/,, fate decision with other cell fate decisions that occur outside of the lymphoid system to attain a better picture of the quantitative signaling mechanism for cell fate specification. [source]

Variant Creutzfeldt-Jakob Disease: implications for the health care system

AUSTRALIAN AND NEW ZEALAND JOURNAL OF PUBLIC HEALTH, Issue 4 2005
R. A. Dunstan
The recognition of the first cases of variant Creutzfeldt-Jakob Disease in the United Kingdom (UK) in 1996 and the realisation that this new disease represented the human form of the cattle disease BSE has prompted a considerable investment in research, particularly in the UK, Europe and the United States (US). Much has been learnt about this disease but much is still unknown. Infectivity is not destroyed by conventional sterilisation and disinfection treatment methods. This, combined with the widespread distribution throughout the lymphoid system as well as the central nervous system, raises the spectre of transmission through both surgical and ophthalmological procedures. Reports in 2004 of two likely transfusion-transmitted cases of vCJD suggest the probability of infection through blood transfusion and tissue transplantation. The risk of hospital-based and community-based transmission has not been quantified. To complicate matters even further, there is no suitable ante-mortem screening test or effective treatment for this fatal disease. The incubation period prior to onset of clinical disease is many years and there is good evidence for the existence of subclinical infection and infectivity during this stage. The extent of under-diagnosis and misdiagnosis is probably significant, adding to the risk of human-to-human transmission. [source]

Atypical chronic myeloid leukemia following organ transplants

CLINICAL TRANSPLANTATION, Issue 2 2008
V Fontana
Abstract:, Secondary malignancy frequently develops among recipients of organ transplants, most commonly malignancies of the lymphoid system and skin. However, chronic myeloid leukemia (CML) is rare following transplant, with only a handful of cases reported, all of whom had kidney transplant and received azathioprine for immunosuppression. We report three cases of post-transplant CML seen at a single institution within a two-yr period. Two had received liver and one a kidney transplant. None were on azathioprine but all had tacrolimus. CML is a rare hematological malignancy, usually presenting with high white counts and splenomegaly. In all three of our subjects, presentation of CML post-transplant was so atypical that their diagnosis could easily be missed. All had rapid and excellent response to imatinib, and underwent clinical remission. This is the first report of CML developing in the course of tacrolimus therapy among liver transplant recipients. Presentations of CML were highly atypical and easy to miss in early stage. Awareness of atypical CML developing post-transplant is important since early and timely therapeutic intervention with imatinib is critical for improving quality of life and overall prognosis. [source]

Competing intrachain interactions regulate the formation of ,-sheet fibrils in bovine PrP peptides

PROTEIN SCIENCE, Issue 3 2003
Abdessamad Tahiri-Alaoui
Abstract At the heart of the pathogenesis of transmissible spongiform encephalopathies (TSEs), such as BSE, scrapie, and Creutzfeldt,Jakob disease, lies a poorly understood structural rearrangement of PrP, an abundant glycoprotein of the nervous and lymphoid systems. The normal form (PrPC), rich in ,-helix, converts into an aberrant ,-sheet-dominated form (PrPSc), which seems to be at the center of the pathotoxic symptoms observed in TSEs. To understand this process better at a molecular level, we have studied the interactions between different peptides derived from bovine PrP and their structural significance. We show that two unstructured peptides derived from the central region of bovine PrP, residues 115,133 and 140,152, respectively, interact stoichiometrically under physiological conditions to generate ,-sheet-dominated fibrils. However, when both peptides are incubated in the presence of a third peptide derived from an adjoining ,-helical region (residues 153,169), the formation of ,-sheet-rich fibrils is abolished. These data indicate that native PrPC helix 1 might inhibit the strong intrinsic ,-sheet-forming propensity of sequences immediately N-terminal to the globular core of PrPC, by keeping in place intrachain interactions that would prevent these amyloidogenic regions from triggering aggregation. Moreover, these results indicate new ways in which PrPSc formation could be prevented. [source]