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At least 361 records · Page 20Linked to original sources
PubMed1980

Tumor cell origin of histaminase activity in ascites fluid from patients with ovarian carcinoma.

We have demonstrated by tissue assay and immunohistochemical techniques that tumor cells appear to be the source of the increased histaminase activity found in 60% of ascitic fluids from patients with ovarian carcinoma. The histaminase activity in 64% of tumor tissues studied was greater than 100 U/g of tissue, a value higher than that for normal tissues other than kidney and intestine. The presence of elevated ascitic fluid histaminase activity (greater than 3.5 U/ml) correlates with the presence of high histaminase activity in tumor tissue. Histaminase activity is higher in ascitic fluid from the patients than it is in their plasma, probably reflecting the direct entry of histaminase into the peritoneal cavity.

Amine Oxidase (Copper-Containing)↗
PubMed1993

Leukaemic T cells from patients with chronic lymphocytic leukaemia of T-cell origin respond to Staphylococcus aureus enterotoxin superantigens.

We investigated the in vitro responsiveness of peripheral blood lymphocytes from two patients with T-cell chronic lymphocytic leukaemia (T-CLL) to Staphylococcus aureus enterotoxin (SE) superantigens. T-cell receptor (TcR) alpha beta (V beta 7.1)-expressing CD4+ leukaemic T cells from patient HE (white blood cell count 480,000/microliters) proliferated in response to SEA and, only at 1000-fold higher concentrations, to SEB, SED, and SEE. CD4+CD8+ TcR alpha beta (V beta 12.1)-expressing leukaemic T cells from patient KO (white blood cell count 120,000/microliters) were activated by SEB but not by the other tested SEs. In both instances, the activation of leukaemic T cells by SE was dependent on the presence of HLA-DR+ cells. Southern blot analysis of TcR beta gene rearrangement confirmed that the proliferating cells were derived from the leukaemic T-cell clone and not from contaminating normal T cells. These data indicate that leukaemic T cells from patients with T-CLL exert a clonally variable responsiveness to SE superantigens. We conclude that recognition of specific antigen and subsequent signal transduction can be initiated via the TcR of leukaemic T-CLL cells.

Antigens, Bacterial↗
PubMed1995

In vivo evidence for a non-T cell origin of interleukin-5.

Eosinophil myelopoiesis is to a great extent regulated by interleukin (IL)-5. Analysis of IL-5 mRNA in spleen cell preparations by reverse transcription-polymerase chain reaction (RT-PCR) revealed the presence of message for this cytokine in uninfected severe combined immunodeficiency (SCID) mice. This message was increased following Mycobacterium avium infection. Normal BALB/c mice had higher levels of expression of IL-5 but the expression of this cytokine was reduced during M. avium infection. Anti-IL-5 monoclonal antibody administration in vivo to SCID mice reduced the number of peritoneal and splenic eosinophils. Gamma interferon (IFN-gamma) had an inhibitory effect of eosinophilopoiesis during infection of SCID mice by M. avium since neutralization of this cytokine increased the number of eosinophils detected in the peritoneal cavity of infected animals. Our results suggest that IL-5 may be produced by cells other than T cells that are both able to respond to infection and are under the control of IFN-gamma.

Animals↗
PubMed1989

Evidence for the stem cell origin of hepatocellular carcinoma and cholangiocarcinoma.

A review of the morphologic, autoradiographic, and phenotypic analysis of the cellular changes seen during induction of cancer of the liver in rats by chemical carcinogens is used to develop an alternative to the established hypothesis that chemically induced hepatocellular carcinoma arises from premalignant nodules. The authors propose that hepatocellular and ductular carcinomas arise from a pluripotent liver stem cell and that enzyme-altered foci and nodular changes are adaptive non-oncogenic responses to the toxic effects of carcinogens. It is further postulated that persistent nodules may provide an environment that nurtures development of neoplastic cells other than the altered hepatocytes that originally form the nodule. It is possible, however, that there may be more than one cellular lineage to hepatocellular cancer and that persistent nodules contain these different lineages.

Adenoma, Bile Duct↗
PubMed2004

Endothelial and hematopoietic cell fate of human embryonic stem cells originates from primitive endothelium with hemangioblastic properties.

The cellular organization and relationships among precursors that initiate embryonic angiogenesis and hematopoiesis in the human have yet to be characterized. Here, we identify a subpopulation of primitive endothelial-like cells derived from human embryonic stem cells (hESCs) that express PECAM-1, Flk-1, and VE-cadherin, but not CD45 (CD45negPFV cells), and that are uniquely responsible for endothelial and hematopoietic development. Molecular profiling of CD45negPFV cells is consistent with endothelial and hematopoietic competency. Clonal isolation demonstrates that the CD45negPFV population includes bipotent cells with endothelial and hematopoietic capacity. We suggest that human hematopoiesis and endothelial maturation originate exclusively from a subset of embryonic endothelium that possesses hemangioblastic properties and offers a model system to study these lineage relationships in the human.

Antigens, CD↗
PubMedDate not supplied

The ultrastructure of human reproduction. I. The natural history of the female germ cell: origin, migration and differentiation inside the developing ovary.

This presentation, on both printed copy and CD-ROM, summarizes a series of original data on the ultrastructure of human reproduction produced by our research group. In particular, female germ cell behaviour at the time of migration and colonization of the gonad and germ-somatic cell interactions inside the developing ovary are reviewed from a morphodynamic point of view. The results mostly consist of black-and-white transmission and scanning electron microscopy (TEM and SEM) images. Artificially coloured SEM pictures, light microscopy images and drawings have also been selected for iconography to render complex microanatomical details and their morphofunctional relationships more comprehensible. In all, 35 images are presented in this article, each related to a concise text section and accompanied by a self-explaining caption. A list of pertinent references is also provided.

Cell Differentiation↗
PubMed1998

Malignant transformation of duct-like cells originating from acini in transforming growth factor transgenic mice.

BACKGROUND & AIMS: In transgenic mice overexpressing transforming growth factor (TGF)-alpha in the exocrine pancreas, progressive pancreatic fibrosis and a transdifferentiation of acinar cells to duct-like cells occurs. The present study was undertaken to analyze this transdifferentiation process. METHODS: Pancreatic specimens were characterized using light microscopy and immunohistochemistry. Expression of the epidermal growth factor receptor (EGFR) and TGF-alpha was evaluated with slot blot and Western analysis. To identify other generic events, K-ras mutations were screened with an enriched polymerase chain reaction approach and p53 expression was detected with immunohistochemistry. RESULTS: Morphological examination revealed an aggregation of interlobular fibroblasts and a decrease in acinar cell height starting at day 14 after birth. In older animals, these acinar cells change to duct-like cells, which form tubular structures and express ductal markers. Evidence for dysplastic changes was found in 12 of 21 TGF-alpha transgenic mice older than 1 year. We also observed four malignant pancreatic tumors, which were multicentric and originated from dysplastic tubular complexes. They displayed a mixed cystic-papillary phenotype strongly positive for carbonic anhydrase activity. EGFR expression progressively increased in the transition from acinar to duct-like and transformed cells. Activating K-ras mutations could not be detected; however, tubular complexes and tumors displayed increased immunoreactivity for nuclear p53. CONCLUSIONS: These data suggest an involvement of the TGF-alpha/EGFR pathway in conjunction with other yet unknown events in pancreatic tumor development. Furthermore, these observations are in favor of an acinar-ductal carcinoma sequence. Thus, these transgenic animals will be useful to define genetic alterations associated with a transition from acinar cells to a neoplastic ductal phenotype.

Animals↗
PubMed1986

Cytogenetic evidence for partially committed myeloid progenitor cell origin of chronic myelomonocytic leukaemia and juvenile chronic myeloid leukaemia: both granulocyte-macrophage precursors and erythroid precursors carry identical marker chromosome.

We used a micromethod for cytogenetic analysis from single haematopoietic colonies to study two adults with chronic myelomonocytic leukaemia (CMML) and a boy with juvenile chronic myeloid leukaemia (JCML) carrying distinct chromosome abnormalities, 7q-, der(21), and trisomy 21. We wanted to know if both granulocyte-macrophage (GM) and erythroid precursors are involved in the abnormal clone. In all three patients, their chromosome abnormality was seen in almost all metaphases obtained from GM-colonies and erythroid bursts. Peripheral blood leucocytes stimulated with phytohaemagglutinin exhibited only normal karyotypes. Clones of B-cell produced by Epstein-Barr virus had only normal karyotypes in the CMML patients. These findings indicate that CMML and JCML are clonal haemopathies that originate in a partially committed myeloid progenitor cell.

Aged↗
PubMed1988

The effect of drugs used in the treatment of osteoarthrosis on stromelysin (proteoglycanase) of equine synovial cell origin.

There is increasing evidence that the proteoglycan-degrading neutral metalloproteinase, stromelysin, is a key enzyme in the pathogenesis of osteoarthrosis. Equine synovial lining cells were stimulated in vitro to produce stromelysin, and phenylbutazone, flunixin, betamethasone, sodium hyaluronate and polysulphated glycosaminoglycan (PSGAG) were tested for their ability to inhibit the action of this enzyme on 14C-labelled casein substrate. Only PSGAG possessed inhibitory activity at concentrations likely to be achieved therapeutically in the equine fetlock joint.

Animals↗
PubMed2004

Rapid chemokine secretion from endothelial cells originates from 2 distinct compartments.

The neutrophil-attracting chemokine interleukin 8 (IL-8) is stored in the Weibel-Palade body (WPB) of endothelial cells (ECs) from which it can be rapidly released after exposure to the secretagogues histamine or thrombin. In this manner, IL-8 may enable rapid recruitment of leukocytes to inflammatory sites. To explore the possible storage of EC-derived chemokines that may attract other subsets of leukocytes, we examined the intracellular localization and secretagogue responsiveness of growth-related oncogene alpha (GROalpha), monocyte chemoattractant protein-1 (MCP-1), eotaxin-3, interferon-gamma-inducible protein 10 (IP-10), and regulated on activation, normal T-cell expressed and secreted (RANTES). While eotaxin-3, GROalpha, and MCP-1 were rapidly released from ECs, the release of the T-cell attractors RANTES and IP-10 was not sensitive to the secretagogues. Moreover, of the 3 former chemokines, only eotaxin-3 was stored in WPBs. GROalpha and MCP-1 resided mainly in smaller vesicles compatible with sorting to a different, histamine-responsive compartment, which has been described in ECs although not reported to contain chemokines. In conclusion, we propose that rapid release of chemokines is restricted to those primarily recruiting leukocytes of the innate immune system, and that their storage in ECs is not restricted to the WPB compartment.

Carcinogens↗
PubMed2001

[The influence of hypoxia on the proliferation of endothelial cells originating from human umbilical vein (HUVEC)--an in vitro study].

In this study we took for culture the early-passage human umbilical vein endothelial cells during 12, 24 and 36 hours of hypoxia. To assess the relative contributions of hypoxia, we compared the rates of BrDU incorporation into DNA of proliferating endothelial cells under normoxix and hypoxic conditions. Significant differences in proliferation rates were found only between 24 hours hypoxic group and the control group. Our results support the hypothesis that increased proliferation of human umbilical vein endothelial cells may reflect an adaptation of fetoplacental circulation to hypoxic conditions.

Antimetabolites↗