Cell Precursors (cell + precursor)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Cell Precursors

  • dendritic cell precursor


  • Selected Abstracts


    Novel markers of early ovarian pre-granulosa cells are expressed in an Sry -like pattern

    DEVELOPMENTAL DYNAMICS, Issue 4 2009
    Hyunjoo J. Lee
    Abstract Mammalian gonad differentiation involves sexually dimorphic cell-fate decisions within the bipotential gonadal primordia. Testis differentiation is initiated by a center-to-poles wave of Sry expression that induces supporting cell precursors (SCPs) to become Sertoli rather than granulosa cells. The initiation of ovary differentiation is less well understood. We identified two novel SCP markers, 1700106J16Rik and Sprr2d, whose expression is ovary-biased during early gonad development, and altered in Wnt4, Sf1, Wt1, and Fog2 mutant gonads. In XX and XY gonads, both genes were up-regulated at ,E11 in a center-to-poles wave, and then rapidly down-regulated in XY gonads in a center-to-poles wave, which is reminiscent of Sry expression in XY gonads. Our data suggest that 1700106J16Rik and Sprr2d may have important roles in early gonad development, and are consistent with the hypothesis that ovarian SCP differentiation occurs in a center-to-poles wave with similar timing to that of testicular SCP differentiation. Developmental Dynamics 238:812,825, 2009. © 2009 Wiley-Liss, Inc. [source]


    Integrative genomic analyses of neurofibromatosis tumours identify SOX9 as a biomarker and survival gene

    EMBO MOLECULAR MEDICINE, Issue 4 2009
    Shyra J. Miller
    Abstract Understanding the biological pathways critical for common neurofibromatosis type 1 (NF1) peripheral nerve tumours is essential, as there is a lack of tumour biomarkers, prognostic factors and therapeutics. We used gene expression profiling to define transcriptional changes between primary normal Schwann cells (n,=,10), NF1-derived primary benign neurofibroma Schwann cells (NFSCs) (n,=,22), malignant peripheral nerve sheath tumour (MPNST) cell lines (n,=,13), benign neurofibromas (NF) (n,=,26) and MPNST (n,=,6). Dermal and plexiform NFs were indistinguishable. A prominent theme in the analysis was aberrant differentiation. NFs repressed gene programs normally active in Schwann cell precursors and immature Schwann cells. MPNST signatures strongly differed; genes up-regulated in sarcomas were significantly enriched for genes activated in neural crest cells. We validated the differential expression of 82 genes including the neural crest transcription factor SOX9 and SOX9 predicted targets. SOX9 immunoreactivity was robust in NF and MPSNT tissue sections and targeting SOX9 , strongly expressed in NF1-related tumours , caused MPNST cell death. SOX9 is a biomarker of NF and MPNST, and possibly a therapeutic target in NF1. [source]


    A phenotypically distinct subset of immature B cells exhibits partial activation, increased survival, and preferential expression of VhS107

    EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 12 2003
    Emily
    Abstract We have observed that immature B cells (IgMlowIgD,) in the bone marrow of adult BALB/c mice exhibit heterogeneity, with a distinct subpopulation (,4,10%) expressing the CD43/S7 surface protein. These CD43/S7+ immature B cells often express other surface antigens associated with B cell activation (CD5, CD11b, PD-1). Generation of optimal numbers of CD43/S7+ immature B cells requires expression of a functional Btk protein, consistent with activation as a requisite for the CD43/S7+ immature B cell phenotype. Like typical CD43/S7, immature B cells, the CD43/S7+ immature B cells are predominantly resting cells, which are derived from cycling bone marrow B cell precursors. The CD43/S7+ immature B cell population exhibits enhanced survival in vivo upon administration of the apoptosis-inducing corticosteroid, dexamethasone. Finally, CD43/S7+ immature B cells show a fourfold increase in incidence of VhS107 , heavy chain expression compared to the CD43/S7, immature B cells. Therefore, in adult murine bone marrow, the presence of a phenotypically distinct immature B cellpopulation can be demonstrated which has undergone partial activation leading to increased survival and BCR-dependent Vh repertoire selection. [source]


    Exploring the mast cell enigma: a personal reflection of what remains to be done

    EXPERIMENTAL DERMATOLOGY, Issue 2 2008
    Beate M. Henz
    Abstract: Mast cells are traditionally viewed as effector cells of allergic reactions and parasitic diseases, but their importance in host defense against bacteria, in tissue remodelling, their bone marrow and stem cell origin and a central role of the stem cell factor (SCF) as mast cell growth and chemotactic factor has been worked out only in recent years. Despite this, major aspects about the nature of the cells and their role in disease remain unclear. This holds in particular for the identification of mast cell precursors and the role of growth factors that stimulate specific mast cell commitment from stem cells, such as nerve growth factor, neutrotrophin-3 and certain interleukins, alone and during interaction with SCF. Early data suggesting also an involvement of specific transcription factors need to be expanded in this process. Furthermore, although mast cell proliferative disease (mastocytosis) has been shown to be often associated with SCF receptor c-kit mutations, reasons for the development of this disease remain unclear. This holds also for mast cell release mechanisms in many types of mast cell-dependent urticaria. Exciting new insights are emerging regarding the role of mast cells in bacterial infections, in defense against tumors, in wound healing and in the interplay with the nervous system, with hormones, and in the neurohormonal network. The aim of this reflection is to delineate the many known and unknown aspects of mast cells, with a special focus on their development, and to discuss in detail two mast cell-related diseases, namely mastocytosis and urticaria. [source]


    Identification of novel genes regulated by ,-melanocyte-stimulating hormone in murine bone marrow-derived dendritic cells

    EXPERIMENTAL DERMATOLOGY, Issue 9 2004
    T. Brzoska
    Many strains of evidence indicate that ,-melanocyte-stimulating hormone (,-MSH) elicits its immunomodulatory activity via binding to melanocortin receptors (MC-Rs) expressed on monocytes and dendritic cells. In order to identify novel target genes regulated by ,-MSH in these cells, we prepared bone marrow-derived dendritic cell precursors from BALB/c mice and treated them with GM-CSF and IL-4 for 6 days. The MC-R profile on these immature dendritic cells was first determined by quantitative RT-PCR. Both transcripts for MC-1R and MC-5R were detected in these cells. Cells were subsequently stimulated with dinitrobenzene sulfonic acid (DNBS), ,-MSH or both substances for 2 or 16 h. After RNA preparation, cDNA synthesis and in vitro transcripton hybridization of biotinylated cRNA samples was performed on MG U74A Affymetrix gene chips. Data evaluation, cleansing, extraction and analysis of the more than 12 000 cloned genes and expressed sequence tags were performed using the GENE DATA ANALYST vs. 1 Expressionist software. Filter criteria included a minimum threshold of 100, normalization by the logarithmic mean and a quality setting of P < 0.04. Changes with a change factor of >2 were regarded as significant. As expected, stimulation with DNBS resulted in induction or upregulation of genes encoding proinflammatory cytokines, growth factors, signal transduction intermediates and transcription factors. Treatment with ,-MSH blocked the DNBS-driven upregulation of several known genes such as IL-1 or CD86. On the other hand, ,-MSH modulated the expression of several novel genes implicated in immunomodulation, e.g. IL-1, converting enzyme, IFN-, receptor, FK506-binding proteins or several neuropeptides and their receptors. These data indicate novel molecular targets by which ,-MSH exerts its immunomodulatory activities in immunocompetent cells. [source]


    Development of the Schwann cell lineage: From the neural crest to the myelinated nerve

    GLIA, Issue 14 2008
    Ashwin Woodhoo
    Abstract The myelinating and nonmyelinating Schwann cells in peripheral nerves are derived from the neural crest, which is a transient and multipotent embryonic structure that also generates the other main glial subtypes of the peripheral nervous system (PNS). Schwann cell development occurs through a series of transitional embryonic and postnatal phases, which are tightly regulated by a number of signals. During the early embryonic phases, neural crest cells are specified to give rise to Schwann cell precursors, which represent the first transitional stage in the Schwann cell lineage, and these then generate the immature Schwann cells. At birth, the immature Schwann cells differentiate into either the myelinating or nonmyelinating Schwann cells that populate the mature nerve trunks. In this review, we will discuss the biology of the transitional stages in embryonic and early postnatal Schwann cell development, including the phenotypic differences between them and the recently identified signaling pathways, which control their differentiation and maintenance. In addition, the role and importance of the microenvironment in which glial differentiation takes place will be discussed. © 2008 Wiley-Liss, Inc. [source]


    The effects of exercise and stress on the survival and maturation of adult-generated granule cells,

    HIPPOCAMPUS, Issue 10 2009
    Jason S. Snyder
    Abstract Stress strongly inhibits proliferation of granule cell precursors in the adult dentate gyrus, whereas voluntary running has the opposite effect. Few studies, however, have examined the possible effects of these environmental manipulations on the maturation and survival of young granule cells. We examined the number of surviving granule cells and the proportion of young neurons that were functionally mature, as defined by seizure-induced immediate-early gene (IEG) expression, in 14- and 21-day-old granule cells in mice that were given access to a running wheel, restrained daily for 2 h, or given no treatment during this period. Treatments began 2 days after BrdU injection, to isolate effects on survival from those on cell proliferation. We found a large increase in granule cell survival in running mice when compared with controls at both time points. In addition, running increased the proportion of granule cells expressing the IEG Arc in response to seizures, suggesting that it speeds incorporation into circuits, i.e., functional maturation. Stressed mice showed no change in Arc expression, compared with control animals, but, surprisingly, showed a transient increase in survival of 14-day-old granule cells, which was gone 7 days later. Examination of cell proliferation, using the endogenous mitotic marker PCNA showed an increase in cell proliferation after 12 days of running but not after 19 days of running. The number of proliferating cells was unchanged 24 h after the 12th or 19th episode of daily restraint stress. These findings demonstrate that running has strong effects on survival and maturation of young granule cells as well as their birth and that stress can have positive but short-lived effects on granule cell survival. Published 2009 Wiley-Liss, Inc. [source]


    Granulocyte/macrophage-colony stimulating factor and interleukin-4 expand and activate type-1 dendritic cells (DC1) when administered in vivo to cancer patients

    INTERNATIONAL JOURNAL OF CANCER, Issue 2 2003
    Sylvia M. Kiertscher
    Abstract Two rare populations of cells with the features of dendritic cell precursors (preDC) can be identified in human peripheral blood. PreDC1 are HLA-DR+/CD11c+ cells which mature into DC1 capable of stimulating Th1 responses. In contrast, preDC2 are HLA-DR+/CD11c,/CD123+ cells that promote Th2 responses when matured into DC2. We hypothesized that administration of GM-CSF and IL-4, growth factors for DC1, would specifically augment the number and function of circulating DC1 in vivo. Patients with advanced metastatic cancer were treated with GM-CSF (2.5 ,g/kg/day) and IL-4 (4 or 6 ,g/kg/day) for 7 days. Cytokine administration at the highest IL-4 dose produced an average 2.3-fold increase in preDC2 number, but a 6.5-fold increase in preDC1, resulting in an increased ratio of circulating preDC1:preDC2 from 1.4:1 pre-treatment to 4.3:1 after cytokine therapy. DC1 precursors identified after in vivo therapy were larger, more complex and expressed higher levels of HLA-DR, CD11c and CD80 than pre-treatment cells. DC1 isolated from the peripheral blood of patients receiving GM-CSF/IL-4 therapy demonstrated MLR activity comparable to that of monocyte-derived DC generated in vitro from the patients' pre-treatment blood using GM-CSF and IL-4. We conclude that systemic administration of GM-CSF and IL-4 preferentially expands and matures the preDC1 population in vivo. These effects correlate with antigen-presenting activity, providing a mechanism by which systemic GM-CSF and IL-4 might stimulate anti-tumor immunity in vivo. © 2003 Wiley-Liss, Inc. [source]


    Serum Erythropoietin and Aging: A Longitudinal Analysis

    JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2005
    William B. Ershler MD
    Objectives: To determine the changes in serum erythropoietin with age in patients with and without anemia and to assess the importance of certain comorbidities on changes in erythropoietin level and the development of anemia. Design: Clinical history, hematological parameters, and serum erythropoietin levels were examined at 1- to 2-year intervals for 8 to 30 years. Setting: Baltimore Longitudinal Study on Aging (BLSA), National Institute on Aging. Participants: One hundred forty-three BLSA participants. Measurements: Complete blood count and serum chemistries were performed at the time of each visit, and archived serum samples were used for erythropoietin level. Results: Although all subjects were healthy and without anemia at the time of initial evaluation, some developed chronic illness,most notably hypertension and diabetes mellitus. Erythropoietin levels rose significantly for the group as a whole, and the slope of the rise was found to be greater for those who did not have associated diabetes mellitus or hypertension. During the subsequent years, subjects who developed anemia but did not have hypertension or diabetes mellitus had the greatest slope in erythropoietin rise over time, whereas those with hypertension or diabetes mellitus and anemia had the lowest erythropoietin slope. Conclusion: The increase in serum erythropoietin with aging may be compensation for subclinical blood loss, increased red blood cell turnover, or increased erythropoietin resistance of red cell precursors. It is suspected that, with very advanced age, or in those with compromised renal function (e.g., diabetes mellitus or hypertension), the compensatory mechanism becomes inadequate and anemia results. [source]


    The central role of Fas-ligand cell signaling in inflammatory lung diseases

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2004
    G. A. DosReis
    Abstract Following inflammation and injury in the lung, loss of epithelial cell precursors could determine the balance between tissue regeneration and fibrosis. This review discusses evidence that proapoptotic Fas-Fas ligand (FasL) signaling plays a central role in pulmonary inflammation, injury and fibrosis. FasL signaling induces inflammatory apoptosis in epithelial cells and alveolar macrophages, with concomitant IL-1, and chemokine release, leading to neutrophil infiltration. FasL signaling plays a critical role in models of acute lung injury, idiopathic pulmonary fibrosis and silicosis; blockade of Fas-FasL interactions either prevents or attenuates pulmonary inflammation and fibrosis. Serologic and immunohistochemical studies in patients support a major pathogenic role of Fas and FasL molecules in inflammatory lung diseases. Identification of the pathogenic role of FasL could facilitate the discovery of more effective treatments for currently untreatable inflammatory lung diseases. [source]


    The Neuropeptide Pituitary Adenylate Cyclase-Activating Polypeptide Exerts Anti-Apoptotic and Differentiating Effects during Neurogenesis: Focus on Cerebellar Granule Neurones and Embryonic Stem Cells

    JOURNAL OF NEUROENDOCRINOLOGY, Issue 5 2007
    A. Falluel-Morel
    Pituitary adenylate cyclase-activating polypeptide (PACAP) was originally isolated from ovine hypothalamus on the basis of its hypophysiotrophic activity. It has subsequently been shown that PACAP and its receptors are widely distributed in the central nervous system of adult mammals, indicating that PACAP may act as a neurotransmitter and/or neuromodulator. It has also been found that PACAP and its receptors are expressed in germinative neuroepithelia, suggesting that PACAP could be involved in neurogenesis. There is now compelling evidence that PACAP exerts neurotrophic activities in the developing cerebellum and in embryonic stem (ES) cells. In particular, the presence of PACAP receptors has been demonstrated in the granule layer of the immature cerebellar cortex, and PACAP has been shown to promote survival, inhibit migration and activate neurite outgrowth of granule cell precursors. In cerebellar neuroblasts, PACAP is a potent inhibitor of the mitochondrial apoptotic pathway through activation of the MAPkinase extracellular regulated kinase. ES cells and embryoid bodies (EB) also express PACAP receptors and PACAP facilitates neuronal orientation and induces the appearance of an electrophysiological activity. Taken together, the anti-apoptotic and pro-differentiating effects of PACAP characterised in cerebellar neuroblasts as well as ES and EB cells indicate that PACAP acts not only as a neurohormone and a neurotransmitter, but also as a growth factor. [source]


    Embryonic inner ear cells use migratory mechanisms to establish cell patterns in vitro

    JOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2006
    Lynne M. Bianchi
    Abstract The hair cells of the sensory epithelium in the inner ear are among the most precisely organized cells in vertebrates. The mechanisms that lead to this orderly arrangement are only beginning to be understood. It has been suggested that hair cells use migratory mechanisms to help achieve their final position in the organ of Corti. The small size and complex organization of the intact inner ear have made it difficult to monitor changes in hair cell location over time in vivo. In the present study, an established in vitro assay of dissociated, embryonic inner ear cells was used to monitor how hair cells reorganize over time. The hair cell specific marker myosin-VI demonstrated that hair cell precursors from both cochlear and vestibular regions reorganized into specific patterns between 3,24 hr in vitro. In contrast to the unlabeled cells, the myosin-VI-positive cells extended processes while establishing the hair cell patterning within an aggregate. These studies support the hypothesis that hair cell precursors actively migrate to help achieve final patterning within the inner ear sensory epithelium. © 2005 Wiley-Liss, Inc. [source]


    Transfusion in premature infants impairs production and/or release of red blood cells, white blood cells and platelets

    JOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 3 2002
    B Frey
    Objective: To examine whether red blood cell transfusion in infants with anaemia of prematurity alters peripheral counts of red blood cell precursors, total white blood cells and white cell differential and platelets. Methodology: In 18 consecutive stable premature infants with anaemia of prematurity, peripheral cell counts were prospectively recorded immediately before transfusion of 20 mL/kg packed red blood cells (given over 6 h), and at 48 h after completion of the transfusion. Results: The median (interquartile range) haematocrit increased from 22.0% (21.3,24.0%) pre-transfusion to 37.0% (36.0,38.0%) post-transfusion (P < 0.001). Red-cell precursors decreased: median (interquartile range) reticulocytes from 3.7% (3.0,7.7%) to 3.7% (2.6,4.1%) (P = 0.03); and median (interquartile range) nucleated red blood cells from 0 G/L (0,0.2 G/L) to 0 G/L (0,0 G/L) (P = 0.03). The mean (SD) platelet count decreased from 420 G/L (154 G/L) to 313 G/L (101 G/L) (P = 0.001). The total white blood cell count and neutrophils did not change significantly; however, median (interquartile range) immature neutrophils decreased from 0.12 G/L (0.06,0.74 G/L) to 0.08 G/L (0.01,0.24 G/L) (P = 0.03). Lymphocytes, eosinophils, basophils and plasma cells remained unchanged. Monocytes increased (P = 0.01). Conclusions: Forty-eight hours after red blood cell transfusion to premature infants, there is an absolute decrease in red blood cell precursors, immature white blood cells and platelets, probably due to erythropoietin-suppression. [source]


    A simulation-based method for the comprehensive analysis of effective lifetime from photoconductance

    PROGRESS IN PHOTOVOLTAICS: RESEARCH & APPLICATIONS, Issue 2 2007
    G. Bueno
    Abstract This paper presents a method for estimating recombination parameters in the volume and surface of solar cell precursors throughout the manufacturing process, taking into account several effects that are generally neglected. The technique is based on the comprehensive reconstruction of the effective lifetime assuming a set of fundamental parameters and its comparison to the experimental data obtained from the photoconductance measured under uniform generation in quasi-steady state conditions. The analysis starts from the semianalytical solution of the minority carrier profiles in the structures under test. This analysis overcomes the usual flat profile approximation and presents important advantages. It allows the asymmetry presented by the solar cell precursors to be taken into account and deals with a wide range of surface conditions: emitters, bare silicon or dielectric passivations. The model also accounts for the effect of the electric field in the volume, and implements several phenomena that are sometimes neglected but are relevant when measuring industrial solar cells precursors: the injection dependence of mobilities and recombination lifetimes, the presence of non-recombinant traps and the Depletion Region Modulation effect. The estimation technique requires uniform generation, which greatly facilitates the calculation of the carrier profiles and allows for a simple method for the auto calibration of the light absorption. Copyright © 2006 John Wiley & Sons, Ltd. [source]


    Promotion of the local differentiation of murine Th17 cells by synovial macrophages during acute inflammatory arthritis

    ARTHRITIS & RHEUMATISM, Issue 12 2008
    Paul J. Egan
    Objective To examine the generation of proinflammatory Th17 cells at the site of tissue inflammation and in draining lymph nodes using an interleukin-17 (IL-17),dependent model of acute inflammatory arthritis. Methods Arthritis was elicited in mice by intraarticular injection of methylated bovine serum albumin (mBSA) into the knee and subcutaneous injection of IL-1,. Anti,IL-17 or control antibodies were administered during arthritis induction. Cytokine expression was evaluated by intracellular cytokine staining of synovial lymphocytes, by polymerase chain reaction analysis of RNA extracted from lymph node cells, and by enzyme-linked immunosorbent assay of cell culture supernatants. Th17 differentiation of naive CD4+ T cells was assessed in cocultures with macrophages from arthritic mice. Results Anti,IL-17 antibody administered during acute arthritis markedly reduced disease, indicating that the model is IL-17 dependent. IL-17 messenger RNA (mRNA), but not protein, was detected in draining lymph node CD4+ T cells and preceded joint inflammation. In addition, mRNA for Th17 cell,stimulatory cytokines (transforming growth factor ,, IL-6) and Th17 cell,inhibitory cytokines (interferon-,, IL-4) was detected in lymph nodes following injection of mBSA and IL-1,. Th17 cells were clearly identified in the inflamed synovium at the peak of disease. Synovial macrophages supported Th17 cell generation from naive CD4+ T cell precursors stimulated via CD3 in vitro and produced high levels of IL-6. In contrast, peritoneal macrophages failed to induce Th17 cell differentiation and produced less IL-6. Conclusion These results suggest that Th17 cell differentiation is initiated in draining lymph nodes but that IL-17,producing cells are restricted to the inflamed synovium, being generated in response to local cytokines produced by inflammatory macrophages. [source]


    T cell inflammatory response, Foxp3 and TNFRS18-L regulation of peripheral blood mononuclear cells from patients with nasal polyps-asthma after staphylococcal superantigen stimulation

    CLINICAL & EXPERIMENTAL ALLERGY, Issue 9 2010
    C. A. Pérez Novo
    Cite this as: C. A. Pérez Novo, M. Jedrzejczak-Czechowicz, A. Lewandowska-Polak, C. Claeys, G. Holtappels, P. Van Cauwenberge, M. L. Kowalski and C. Bachert, Clinical & Experimental Allergy, 2010 (40) 1323,1332. Summary Background Staphylococcal superantigens may modulate airway inflammatory disease. Objective We assessed the effect of Staphylococcus aureus enterotoxin B (SEB) on T cell activation in patients with nasal polyps and asthma, and its possible link to aspirin hypersensitivity. Methods Leucocytes were isolated from five healthy subjects (controls), five asthmatics with nasal polyps without (NP-ATA) and five with aspirin-induced asthma (NP-AIA). Cells were incubated with increasing concentrations of SEB for 4 and 18 h. Release of TH1/TH2 cytokines was assessed by Cytometric Bead-Array. Foxp3 and TNFRS18-L expression were analysed by qPCR and flow cytometry. Results After 4 and 18 h, SEB significantly increased IFN-gamma, IL-4, TNF-alpha, IL-5 and IL-2 concentrations in supernatants of both NP polyp groups compared with controls. Baseline Foxp3 was significantly decreased in both NP-asthma groups. Incubation with SEB for 4 h induced a limited up-regulation of Foxp3 in NP-AIA patients, which was switched off consecutively. Foxp3 was significantly up-regulated in the control group after 18 h, but not in the NP-asthmatic groups. In parallel, TNFRS18-L mRNA significantly increased after 18 h in the NP-asthma groups compared with control subjects. This molecule was highly expressed in CD11c+CD14+ cells and its levels increased after 18 and 24 h culture in the NP-asthma patients. Conclusion SEB induces both TH1 and TH2 pro-inflammatory responses in patients with nasal polyps and asthma regardless of the presence of aspirin hypersensitivity. The nature of this response may be linked to a basal deficiency of Foxp3 observed in the NP-asthmatic patients and/or to the up-regulation of TNFRS18-L on monocytes/dendritic cell precursors. [source]


    Aleukaemic leukaemia cutis presenting as a benign-appearing eruption

    CLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 2 2003
    T. P. Millard
    Summary A 68-year-old Caucasian male presented with a 5-week history of a widespread pruritic papular eruption. Histology from a papule on the left shoulder showed a dense dermal infiltrate of large mononuclear cells which were positive for leucocyte common antigen, KP1 and PGM1, with an MIB-1 proliferating fraction of 40%, diagnostic of acute monocytic (M5) leukaemia cutis. Full blood count revealed pancytopaenia but no blasts. Bone marrow aspirate showed reduced red cell precursors and 10% blasts, consistent with myelodysplastic syndrome (refractory anaemia with excess blasts). The patient was managed with a 3 unit transfusion of packed red cells, after which his skin eruption resolved within 6 weeks and his peripheral blood counts returned to normal. No chemotherapy was administered. In conclusion, leukaemia can present in the skin, the eruption may be nonspecific and it may precede systemic involvement by either myelodysplastic syndrome or acute leukaemia. [source]


    Miller's seminal studies on the role of thymus in immunity

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2006
    D. Ribatti
    Summary The thymus is one of the two primary lymphoid organs. It is responsible for the provision of T lymphocytes to the entire body, and provides a unique microenvironment in which T cell precursors (thymocytes) undergo development, differentiation and clonal expansion. This review article summarizes the seminal work of the Australian scientist Francis Albert Pierre Miller concerning the description for the first time of the crucial role of the thymus for normal development of the immune system. [source]


    Characterization of human peritoneal dendritic cell precursors and their involvement in peritonitis

    CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2005
    M. L. McCully
    Summary Scattered evidence suggests that the human peritoneal cavity contains cells of the dendritic cell (DC) lineage but their characterization is missing. Here, we report that the peritoneal cavity of normal subjects and of stable patients on peritoneal dialysis (PD) contains a population of CD14+ cells that can differentiate into DCs or macrophages. Within this pool, we characterized a CD14+CD4+ cell subset (2·2% of the peritoneal cells) fulfilling the definition of myeloid DC precursors or pre-DC1 cells. These cells expressed high levels of HLA-DR, CD13, CD33, and CD86, and low levels of CD40, CD80, CD83, CD123, CD209, TLR-2 and TLR-4. These cells retained CD14 expression until late stages of differentiation, despite concomitant up-regulation of DC-SIGN (CD209), CD1a, CD80 and CD40. Peritoneal pre-DC1 cells had endocytic capacity that was down-regulated upon LPS/IFN-, stimulation, were more potent allo-stimulators than peritoneal CD14+CD4,/lo cells and monocyte-derived macrophages, and induced Th1 cytokine responses. More importantly, the number of peritoneal pre-DC1 cells increased during PD-associated peritonitis, with a different profile for Gram positive and Gram negative peritonitis, suggesting that these cells participate in the induction of peritoneal adaptive immune responses, and may be responsible for the bias towards Th1 responses during peritonitis. [source]


    A simulation-based method for the comprehensive analysis of effective lifetime from photoconductance

    PROGRESS IN PHOTOVOLTAICS: RESEARCH & APPLICATIONS, Issue 2 2007
    G. Bueno
    Abstract This paper presents a method for estimating recombination parameters in the volume and surface of solar cell precursors throughout the manufacturing process, taking into account several effects that are generally neglected. The technique is based on the comprehensive reconstruction of the effective lifetime assuming a set of fundamental parameters and its comparison to the experimental data obtained from the photoconductance measured under uniform generation in quasi-steady state conditions. The analysis starts from the semianalytical solution of the minority carrier profiles in the structures under test. This analysis overcomes the usual flat profile approximation and presents important advantages. It allows the asymmetry presented by the solar cell precursors to be taken into account and deals with a wide range of surface conditions: emitters, bare silicon or dielectric passivations. The model also accounts for the effect of the electric field in the volume, and implements several phenomena that are sometimes neglected but are relevant when measuring industrial solar cells precursors: the injection dependence of mobilities and recombination lifetimes, the presence of non-recombinant traps and the Depletion Region Modulation effect. The estimation technique requires uniform generation, which greatly facilitates the calculation of the carrier profiles and allows for a simple method for the auto calibration of the light absorption. Copyright © 2006 John Wiley & Sons, Ltd. [source]