Fewer Cells (fewer + cell)

Distribution by Scientific Domains


Selected Abstracts


A European interlaboratory testing of three well-known procedures for immunocytochemical detection of epithelial cells in bone marrow.

CYTOMETRY, Issue 6 2006
Results from analysis of normal bone marrow
Abstract Background: This investigation intended to study the unspecific background to be expected in normal bone marrow (BM), comparing three well recognized protocols for immunocytochemical detection of disseminated carcinoma cells. The interlaboratory variation in screening and evaluation of stained cells was analyzed and different screening methods were compared. Methods: BM mononuclear cells (BM MNC) from 48 normal BMs were immunostained in parallel by three participating laboratories. The protocols, based on three different anti-cytokeratin antibodies, have all been in common use for detection of disseminated carcinoma cells: the A45-B/B3 protocol (Hamburg), the CK2 protocol (Augsburg) and the AE1AE3 protocol (Oslo). For all protocols, the immunostained cells were visualized by the same alkaline-phosphatase (AP) detection system (APAAP) followed by detection of the cells by manual screening and by two different automated screening systems (ACIS from Chromavision and MDS1 from Applied Imaging). Detected AP-visualized cells were morphologically classified into unambiguous hematopoietic (Uhc) and questionable cells (Qc, potentially interpreted as tumor cells). Results: Seven of 48 BMs (15%) harbored ,1 AP-visualized cell(s) among 1 × 106 BM MNC, both for the A45-B/B3- and for the AE1AE3 protocol, while for CK2 a higher proportion of BMs (21 BMs; 44%) harbored AP-visualized cells (P < 0.01, McNemar's test). The number of Qc was, for all protocols, 1 log lower than the total number of AP-visualized cells. On average, the frequency of Qc was 0.04, 0.08, and 0.02 per 106 BM MNC with A45-B/B3, CK2 and AE1AE3, respectively, and the number of Qc-positive BMs 1, 4, and 1. The MDS1 screening sensitivity was similar to manual screening, while ACIS detected fewer cells (P < 0.001, McNemar's test). Conclusions: All protocols resulted in AP-visualization of occasional hematopoietic cells. However, morphological classification brings the specificity to a satisfactory high level. Approximately 10% of AP-visualized cells were categorized "questionable". The CK2 protocol turned out less specific than the A45-B/B3 and AE1AE3 protocols. © 2006 International Society for Analytical Cytology. [source]


Differential effect of dopamine on mitosis in early postnatal albino and pigmented rat retinae

DEVELOPMENTAL NEUROBIOLOGY, Issue 1 2006
Ines Kralj-Hans
Abstract Insufficient levels of L -DOPA, released from the retinal pigment epithelium (RPE), in albino animals are considered responsible for the abnormal development of the underlying neural retina. L -DOPA normalizes retinal neurogenesis by reducing levels of cell proliferation either by acting on the cells directly or by being converted into dopamine. Here we report the effects of dopamine on mitosis in early postnatal neural retinae from albino and pigmented rats, using 4D (x, y, z and time) confocal microscopy. Exogenous dopamine significantly prolongs mitosis in retinae from albino, but not pigmented, animals. As fewer cells move into and divide in the ventricular zone (VZ) in the presence of dopamine, we conclude that the overall cell cycle is affected. The D1 receptor blocker, SCH 23390, inhibits these effects. Thus, the differential effects of dopamine on neural retinae from pigmented and albino rats in vitro must result from the activation of D1 receptors, which are present in the retina from birth. Immunohistochemical labeling of D1 receptors shows that the pattern of their distribution is similar between pigmentation phenotypes, but levels of expression may be elevated in albinos. Labeling is most intense in the inner plexiform layer but is present throughout the neuroblastic layer. These findings are discussed in light of previous reports of reduced catecholamine levels in the albino retina. © 2005 Wiley Periodicals, Inc. J Neurobiol, 2006 [source]


Proliferation and differentation markers in snuff-induced oral mucosal lesions

JOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 5 2002
Marina Merne
Abstract Background: Regular use of snuff is known to cause whitish oral mucosal lesions of variable severity at the usual quid placement site. The main aim of this study was to elucidate cellular mechanisms involved in snuff-induced epithelial changes. Methods: Expression patterns for markers of cell proliferation (PCNA, Ki-67), cell cycle regulation (p53, p21), keratin changes (pankeratin, CK18, CK19), cell stress (HSP 70) and collagen type IV in 14 snuff-induced oral mucosal lesions and 12 control samples were analyzed by immunohistochemistry (IHC). Results: On light microscopy, all snuff-induced lesions were characterized by a hyperkeratinized and thickened epithelium. Some vacuolized cells, markers of cell degeneration, were frequently seen (in 9/14 of the samples) in the superficial layers in epithelia. Expression of PCNA and Ki-67 was found in a statistically significantly fewer cells in snuff-induced lesions (P < 0.001) than in the controls. This indicates that epithelia in snuff-induced lesions are not thickened as a result of increased cellular proliferation, but by protracted turnover of differentiating cells. Of cell cycle markers, p21 was found be up-regulated in 4/14 snuff-induced lesions, probably by p53-independent pathways. Only two snuff-induced lesions showed p53 positivity. However, the number of stained cells with p53 and p21 was not statistically different from that in controls. Expression of CK18, but not any alterations in CK19 expression, was seen in 5 of 14 snuff-induced lesions. Snuff also seems to stimulate the expression of collagen type IV, possibly by basal cells, as indicated by the thickened staining of the basal lamina. Conclusions: The findings of this study showing suppressed cellular proliferation and infrequent p53 dysfunction in snuff lesions may partly explain why dysplastic changes are seldom seen in mucosal lesions induced by the Scandinavian type of snuff. [source]


Multichannel Cochlear Implants: Relation of Histopathology to Performance,

THE LARYNGOSCOPE, Issue 8 2006
Jose N. Fayad MD
Abstract Objectives: To determine the relationship of surviving neural elements to auditory function in multichannel cochlear implant temporal bones. Study Design: Case series of all 14 existing multichannel cochlear implants in our temporal bone collection. Methods: Devices included Nucleus 22 (n = 11), Nucleus 24 (n = 1), Ineraid (n = 1), and Clarion (n = 1). Morphologic evaluation of structural elements including spiral ligament, stria vascularis, hair cells, peripheral processes, and spiral ganglion cells was performed. Clinical performance data were obtained from patient charts. For eight patients, nonimplanted contralateral temporal bones were available and paired comparisons were made. Results: Despite frequent absence of hair cells and peripheral processes, all bones had at least some remaining spiral ganglion cells. Percent of normal remaining structures were unrelated to auditory performance with the implant for any of the structural elements. Ganglion cell count in segment III showed significant negative correlations to speech discrimination scores for words and sentences (Rhos = ,.687 and ,.661, P , .03 and .04) as did segment IV and total ganglion cell count with word score (Rhos = ,.632 and ,.638; P , .05). Spiral ganglion cell survival did not differ between implanted and nonimplanted ears, with the exception of segment I, which had fewer cells in the implanted ear (P , .028). Conclusions: Performance variability of cochlear implants cannot be explained on the basis of cochlear neuronal survival. Although hair cells and peripheral processes were frequently absent or greatly diminished from normal, all subjects had at least some spiral ganglion cells. And, in this series, there was an inverse relationship between survival of ganglion cells and performance. [source]


Silencing S1P1 Receptors Regulates Collagen-V Reactive Lymphocyte-Mediated Immunobiology in the Transplanted Lung

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 3 2008
M. Chiyo
Type V collagen (col[V])-reactive lymphocytes contribute to lung transplant rejection, but the mechanisms for emigration into the graft are unknown. Sphingosine-1-phosphate-1 receptors (S1P1R) are believed to be required for lymphocyte emigration in other studies, but their role in col(V)-reactive lymphocyte rejection responses is not known. Utilizing small interfering RNA (siRNA) to reduce S1P1R expression on col(V)-reactive lymphocytes, we examined the role of S1P1R in the rejection response. Quantitative polymerase chain reaction (PCR) revealed strong expression of S1P1R messenger RNA (mRNA)on col(V)-reactive lymphocytes isolated from immunized rats. S1P1R -specific siRNA (S1P1R siRNA) reduced expression of S1P1R mRNA and protein, whereas scramble siRNA (SC siRNA) had no effect. Adoptive transfer of lymphocytes treated with S1P1R siRNA to rat Wistar Kyoto (WKY) lung isograft recipients resulted in retention of cells within the liver with fewer cells in mediastinal lymph nodes when compared to cells exposed to SC siRNA. S1P1R -deficient cells proliferated in response to alloantigens, but not in response to col(V), and produced less interferon (IFN)-, in response to col(V) compared to controls. Downregulating S1P1R did not affect production of interleukin (IL)-10and tumor necrosis factor (TNF)-,, or expression of adhesion molecules critical for migration, but prevented rejection pathology and lowered local levels of IFN-, post adoptive transfer. These data demonstrate novel roles of S1P1R, which include regulating emigration and modulating lymphocyte activation. [source]


The mode of action of venom from the endoparasitic wasp Pimpla hypochondriaca (Hymenoptera: Ichneumonidae) involves Ca+2 -dependent cell death pathways,

ARCHIVES OF INSECT BIOCHEMISTRY AND PHYSIOLOGY (ELECTRONIC), Issue 3 2009
David B. Rivers
Abstract The endoparasitoid Pimpla hypochondriaca injects venom during oviposition to condition its lepidopteran hosts. Venom is a complex mixture of proteins and polypeptides, many of which have been identified as enzymes, including phenoloxidase, endopeptidase, aminopeptidase, hydrolase, and angiotensin-converting enzyme. Constituents of the venom have been shown to possess cytolytic and paralytic activity, but the modes of action of factor(s) responsible for exerting such effects have not been deciphered. In this study, we examined the mode of action of isolated venom using cultured cells (BTI-TN-5B1-4). A series of blockage and inhibition assays were performed using a potent inhibitor (phenylthiourea, PTU) of venom phenoloxidase, and anti-calreticulin antibodies. Monolayers exposed to venom alone were highly susceptible with more than 84.6±2.3% dead within 15,min. Susceptible cells displayed a retraction of cytoplasmic extensions, rounding, and swelling prior to lysis in more than half (55.7±1.7%) of the dying cells. Within 15,min of exposure to venom, cells displayed qualitative increases in [Ca+2]i as evidenced by staining with the calcium-sensitive probe fluo-4 AM, and mitochondrial membrane potential (,,m) was undetectable by 5,min post-treatment with venom. These venom-mediated changes occurred regardless of whether an external source of calcium was present, or whether venom was pre-treated with PTU. In contrast, venom toxicity was attenuated by treatment with anti-calreticulin antibodies. Not only did fewer cells die when exposed to antibody-treated venom but also cell swelling diminished and no increases in intracellular calcium were detected. A possible mode of action for the venom is discussed. © 2009 Wiley Periodicals, Inc. [source]


Survival in rectal cancer is predicted by T cell infiltration of tumour-associated lymphoid nodules

CLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2010
T. P. W. McMullen
Summary Lymphoid nodules are a normal component of the mucosa of the rectum, but little is known about their function and whether they contribute to the host immune response in malignancy. In rectal cancer specimens from patients with local (n = 18), regional (n = 12) and distant (n = 10) disease, we quantified T cell (CD3, CD25) and dendritic cell (CD1a, CD83) levels at the tumour margin as well as within tumour-associated lymphoid nodules. In normal tissue CD3+, but not CD25+, T cells are concentrated at high levels within lymphoid nodules, with significantly fewer cells found in surrounding normal mucosa (P = 0·001). Mature (CD83), but not immature (CD1a), dendritic cells in normal tissue are also found clustered almost exclusively within lymphoid nodules (P = < 0·0001). In rectal tumours, both CD3+ T cells (P = 0·004) and CD83+ dendritic cells (P = 0·0001) are also localized preferentially within tumour-associated lymphoid nodules. However, when comparing tumour specimens to normal rectal tissue, the average density of CD3+ T cells (P = 0·0005) and CD83+ dendritic cells (P = 0·0006) in tumour-associated lymphoid nodules was significantly less than that seen in lymphoid nodules in normal mucosa. Interestingly, regardless of where quantified, T cell and dendritic cell levels did not depend upon the stage of disease. Increased CD3+ T cell infiltration of tumour-associated lymphoid nodules predicted improved survival, independent of stage (P = 0·05). Other T cell (CD25) markers and different levels of CD1a+ or CD83+ dendritic cells did not predict survival. Tumour-associated lymphoid nodules, enriched in dendritic cells and T cells, may be an important site for antigen presentation and increased T cell infiltration may be a marker for improved survival. [source]