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Biomedical subjects

J Tanzer

Publications and source records attributed to J Tanzer.

At least 91 records · Page 5Linked to original sources
PubMed1986

Studies on human prothymocytes by means of an agar T-cell colony assay.

The identity of bone marrow (BM) T colony-forming cells has led to controversy because of BM contamination with mature T cells having clonogenic potential. To circumvent this problem, extensive purging of BM cells was achieved, using E-rosetting and complement-dependent cytotoxicity, with a cocktail of monoclonal antibodies (Mabs): CD6 + CD8 + CD4 + CD2 and two successive rabbit Complement (C) treatments. This resulted in a 2-log elimination of mature T cells, as assessed by marker studies. T-cell-depleted marrow (TDBM) was plated in agar in the presence of PHA- and B+ null cell-derived prothymocyte differentiating activity (PTDA). Two peaks of colony formation were observed on days 7 and 10 of incubation. Both seven- and ten-day colonies contained mainly T4+ and only a few T8+ cells, which also expressed T3, T11, HLA-DR, and Tac antigens. These colony-forming cells were enriched (three- to fourfold) by discontinuous Percoll gradient centrifugation. These results point to the existence of marrow T-cell progenitors, which differ in their kinetics of colony generation and surface markers.

Agar↗
PubMed1986

Relationship between IL-2 and human T cell colony formation.

We have tested the reliability of a standard IL-2 microassay (3H-thymidine uptake by IL-2-dependent T cell lines) as a measure of the colony promoting activity (CPA) required for PHA-induced T cell colony growth in semi-solid cultures. Colonies were obtained from freshly isolated mononuclear cells (PBL) (primary colonies) or pooled cells of primary colony (secondary colonies). PHA-stimulated PBL generated primary colonies in the absence of exogenous CPA which, however, when added to the cultures enhanced colony growth. In contrast, primary colonies failed to form PHA-induced secondary colonies in the absence of exogenously supplied CPA. There was a close correlation between the colony forming capacity of PBL and primary colonies from the same donors plated in the presence of added CPA (r = 0.98). When CPA was measured in the secondary colony growth assay and the data compared to IL-2 measurement in the standard IL-2 microassay, CPA and IL-2 levels did not correlate, suggesting that IL-2 and CPA may represent distinct factors. The usefulness of primary colonies as target cells for the measurement of CPA levels in a variety of conditioned media is discussed.

Cell Division↗
PubMed1985

Acquired autoimmune thrombocytopenia after allogeneic bone marrow transplantation.

A 29-year-old man in remission from acute myeloblastic leukaemia was treated by chemoradiotherapy and transplantation of bone marrow (BMT) collected from his HLA identical brother. Engraftment was documented on D12. Transient acute GVHD (grade II) appeared from D34. No infection complicated the BMT. Nevertheless severe thrombocytopenia persisted and was unresponsive to marrow donor platelet transfusion. The platelet immunofluorescence test demonstrated the autoimmune basis of the thrombocytopenia. This study suggests that the transient immune imbalance observed in the early post graft period could facilitate the appearance of autoimmune cytopenias.

Adult↗
PubMed1985

Agar human T cell colony growth promoted by a B + null cell-derived lymphokine distinct from IL 2.

Human T cell agar colonies can be grown under PHA stimulation from either mature T cells or their E rosette-negative (E-), OKT3- peripheral blood and bone marrow precursors. Colonies comprise a majority of mature E+, OKT3+ cells and a minor (5 to 10%) population of immature E-, T3-, T8-, T4-, DR+, T10+, RFB1+ cells, which upon replating in subculture, can generate secondary colonies of OKT3+, E+, OKT4+, OKT8+ cells. Secondary colony formation can serve as a test for growth requirement of colony precursors, because it depends on the presence of both PHA and a colony-promoting activity (CPA) recovered in PHA-stimulated B + null or T + adherent cell supernatants. CPA production by B + null cells was not affected by their treatment with OKT3 or D66 (T11-like) monoclonal antibodies (MAB) + complement but was abolished by an anti-HLA-DR MAB + complement. However, B cells sorted by panning with the same anti-HLA-DR MAB did not release CPA, demonstrating the requirement of both B cells and null cells for CPA production. Neither IL 2 nor IL 1 could account for B + null cell-derived CPA.

B-Lymphocytes↗
PubMed1984

Self-renewal and maturation of immature T-cell progenitors within PHA-induced agar T-cell colonies.

T-cell colonies derived from peripheral blood mononuclear cells plated in agar with phytohemagglutinin (PHA) contain about 5-7% E-, OKT3-, OKT6-, TdT-, SIg- cells phenotypically similar to bone marrow precursors since they are also RFB1+, OKT10+, HLA-DR+, and PNA+. These cells can generate secondary E+, OKT3+ T-cell colonies when replated in the presence of both PHA and a colony-promoting activity distinct from the T-cell growth factor, Interleukin 2. These observations suggest that E-, OKT3- cells detected in primary PHA-induced T-cell colonies belong to a pool of prethymic cells which are able to mature into T-lymphocytes of T4 and T8 type in the absence of the thymic microenvironment.

Clone Cells↗
PubMed1984

Decreased red cell enolase activity in a 40-year-old woman with compensated haemolysis.

A 40-year-old woman splenectomized 17 years previously for hereditary haemolytic anaemia was investigated in our laboratory because of persistent conjunctival subicterus associated with compensated haemolysis. The results of the autohaemolysis and osmotic fragility tests were similar to those usually observed in hereditary spherocytosis. Red cell enzyme assays indicated a decreased amount of kinetically normal enolase. The genetic transmission of this defect could not be established since the only other affected member of the family was the proposita's father who died several years ago after splenectomy for an undefined haemolytic disorder.

Adult↗
PubMed1984

[Massive sarcomatous infiltration of the liver disclosed by jaundice and hepatocellular failure in Waldenström's disease].

We report herein the case of a patient with Waldenström macroglobulinemia in whom an immunoblastic sarcoma produced acute jaundice and hepatic failure. Transvenous liver biopsy, performed because of coagulation deficiencies, revealed massive infiltration of the liver by the sarcoma. Immunofluorescence study showed numerous portal and sinusoidal cells stained exclusively by anti-micron anti-kappa antisera. As shown by others in the literature, this study supports evidence for the same clonal origin of the two proliferations. Chromosomal abnormalities were found in marrow and blood cells (trisomy 5 and 20, 6 q-, 7 q+, and 8 p-); their role in emergence of sarcoma is discussed. This case shows that immunoblastic sarcoma emerging during the course of Waldenström macroglobulinemia may be revealed by severe hepatic manifestations.

Aged↗
PubMed1983

[Thrombocythemia with Philadelphia chromosome. Secondary appearance of chronic myeloid leukemia].

The finding of a Philadelphia chromosome in a case of apparently primary thrombocythaemia should change the diagnosis for that of chronic myeloid leukaemia. This theoretical view is supported by the case reported here, where a Philadelphia-chromosome was detected in the bone marrow cells of a patient with severe thrombocythaemia; a typical myeloid leukaemia developed 21 months after the onset of the disease; survival was of short duration.

Adult↗
PubMed1983

Philadelphia chromosome-positive chronic myelocytic leukemia in children. Survival and prognostic factors.

The survival and the prognostic significance of the diagnostic characteristics of 39 children with Philadelphia chromosome-positive chronic myelocytic leukemia (Ph1-positive CML), seen between 1963-1976 at the Hôpital Saint-Louis of Paris, have been analyzed. The disease predominated in children older than age 4 years (95%), with girls being more affected than boys (24 versus 15). The clinical and hematological picture at presentation was similar to that observed in adults with Ph1-positive CML. Most children of this series were treated with busulfan which, as in adults, led to reduction of leucocytosis and organomegaly but did not prevent the occurrence of blastic crisis. Well-documented blastic crisis was observed in 78% of cases. Of 39 children, 12 were still alive, all in the chronic phase. Twenty-seven have died, 21 of them after blastic crisis, 4-156 months after diagnosis (median survival, 53 months). The effect of each diagnostic characteristic on survival was evaluated using the log-rank test. Of the 14 characteristics studied, only the degree of blood and marrow blastosis was associated with a shorter survival. Age, sex, bleeding, lymphadenopathy, hepatomegaly, degree of splenomegaly, hemoglobin level, total leucocyte, immature granulocyte (promyelocytes + myelocytes + metamyelocytes), eosinophil, basophil, and platelet counts in the peripheral blood were of no prognostic significance. The failure to attain a level of statistical significance for some characteristics found to be of prognostic value for adults, could be due to the small sample size and/or to the disease homogeneity. The results of this study, however, stress the importance of the initial blastic infiltration in determining the duration of survival, which is ultimately determined by the occurrence of terminal acute leukemia. In conclusion, this study shows that the Ph1-positive CML of childhood exhibits the same course, incidence of blastic crisis, and survival as the disease of adults. It also indicates that treatment with moderate chemotherapy, such as busulfan, has no effect on the duration of survival. Therefore, new therapeutic approaches are urgently needed for the treatment of this disorder in children.

Adolescent↗
PubMed1982

[Prolidase and manganese deficiency. Apropos of a case: diagnosis and treatment].

Prolidase deficiency, transmitted on an autosomic recessive mode upsets skin healing and facilitates the occurrence of chronic cutaneous ulcerations. A 36-year-old woman has been followed since the age of 12 for ulcerations and erythematous erysipelatoid plaques of the lower limbs. Two episodes of agranulocytosis were induced by intake of sulfonamides at the age of 17. The same accident had been observed in her aunt. As the aetiological research of ulcers was negative, a prolidase deficit was suspected. The diagnosis is ascertained by the existence of an immunopeptiduria of 5 mmol/24 hours (normally absent). The predominating dipeptides are glycilproline and phenylalanine proline. R-hydroxyproline dipeptide were present at a lesser degree. Urinary hydrolysis showed elevation of free proline (x 10) and hydroxyproline (x 6). Dosage of erythrocytes prolidase evidenced an activity 2 p. 100 of the normal in one case and 55 p. 100 and 49 p. 100 in the parents. Treatment by cofactors of prolidase (vitamine C and manganese) reduced immunopeptiduria, suppressed inflammatory outbreaks and allowed a transient cicatrisation. This tenth case of prolidase deficiency underlines the character of the disease: recurrent ulcers (7/10), erysipelatoid plaques (3/10), ecchymosis (4/10), telangiectatic scars (7/10), edema (1/10), early canitias (1/10). Partial correction by cofactors evokes a prolidase deficiency by inactivation of the enzymes activating systems.

Adult↗
PubMed1981

Cross-sectional clinical evaluation of recurrent enamel caries, restoration of marginal integrity, and oral hygiene status.

Both marginal quality and oral hygiene status have strong effects on the risk of recurrent caries. Although there was no statistically significant interaction between these two parameters in this study, the influence of each variable was dependent on its severity. There is a difference between the behavior or the likelihood of recurrent caries on occlusal surfaces as compared with smooth surfaces. On the smooth surfaces, there is a continued increased risk with decreasing marginal quality; the occlusal surfaces, however, show no change in vulnerability beyond a modified marginal quality score of 3. Variation in oral hygiene had a more pronounced effect on the probability of recurrent caries of restorations with moderate margin scores than it did on restorations with either very poor or very good cavosurface margins. This work further emphasizes the importance of technically good restorative care at the operative visit, which, coupled with conscientious oral hygiene, should have a positive effect on increasing the longevity of restorations and decreasing the need for replacement.

Adolescent↗
PubMed1980

The nature of cell interactions during phytohemagglutinin-induced T-cell colony formation.

When a constant number of peripheral human blood mononuclear cells (MC) are seeded in an agar overlayer on top of a cell free underlayer supplemented with 100 microgram phytohemagglutinin (PHA), the number of colonies formed is dependent on cell concentration with respect to both the overlayer and total culture volumes. These results support the view that during PHA-induced colony formation cell cooperation between T-colony forming cells and a population of cooperating cells (CC) is mediated by diffusible soluble mediators. They also indicate that the effect of such mediators is dependent on concentration and not only on total amount in the culture. With respect to contradictory evidence on the nature of CC the possible heterogeneity of the CC population has been explored using the mathematical approach developed by Copplesson and Michie to investigate cell cooperation during an in vitro immune response. As a result, the slopes of the regression lines obtained by plotting the logarithms of the number of colonies obtained against the logarithms of cell inocula suggest the possibility of at least 3 interacting cell populations during colony formation, and thus the heterogeneity of cooperating cells. It is therefore hypothesized that T-cell colony formation may be under the control of a fairly complex system of mediators exchanged by different types of CC rather than by one specific colony stimulating factor as described during granulocyte or macrophage colony growth.

Cell Communication↗