PubMed Health⌕ Search

Biomedical subjects

H Messner

Publications and source records attributed to H Messner.

At least 73 records · Page 4Linked to original sources
PubMed1981

A colony assay for blast cell progenitors in non-B non-T (common) acute lymphoblastic leukemia.

A clonal method in cell culture is described that permits the quantitation of blast precursors in common (non-T, non-B) ALL; the method also yields information about progenitor properties, based on analysis of cells in colonies. The technique is identical to that used successfully for normal and malignant B-cell progenitors except that it requires culture at below O2 tension (5%-7%); mononuclear cells from blood or marrow are depleted of T cells and cultured with media conditioned by T cells in the presence of phytohemagglutinin and irradiated T cells. Cultures are incubated for 5-7 days in a moist atmosphere at 5% CO2 and 5%-7% O2. Colonies were obtained from marrow or blood of 16 of 18 ALL patients. Cells in colonies had the same characteristics (E-, slg-, cALL+ and clgM+ or clgM-) as the cells in the patient. By replating pooled colonies, self-renewal of progenitors was shown. The findings are considered in light of a model of leukemic blasts that depicts such populations as lineages maintained by progenitors that either renew themselves or give rise to blast cells with little or no proliferative capacity.

Antigens, Neoplasm↗
PubMed1979

[Thrombasthenia in a newborn (author's transl)].

Thrombasthenia is an extemely rare hereditary disorder of platelet function characterized by impairment of adhesiveness, ADP-induced aggregation, and clot retraction. Petechiae and ecchymoses in a newborn infant followed by prolonged jaundice facilitated early diagnosis.

Blood Coagulation Factors↗
PubMed1975

[Congenital Agranulocytosis (author's transl)].

The rare clinical picture of congenital agranulocytosis is described and its differential diagnosis from other forms of chronic neutropenia discussed on the basis of a case report of an infant followed up over a period of 3 years. Characteristic features of the agranulocytosis are inhibited maturation of the neutrophils (only as far as the promyelocyte and immature myelocyte stage), in conjunction with a normal or elevated level of eosinophil granulocytes. Erythropoiesis and megakaryopoiesis are found to be normal; plasmocytes, monocytes and lymphocytes are increased. The consequence of permanent infections is sometimes an excessive hypergammaglobulinaemia. This fact, in combination with the phagocytic activity of the monocytoid cells, enables these children, once out of infancy, to overcome even severe infections much more successfully than would be anticipated from the changes in the white blood picture.

Agranulocytosis↗
PubMedDate not supplied

Transient myeloproliferative disorder with a CD7+ and CD56+ myeloid/natural killer cell precursor phenotype in a newborn.

Anewborn with a transient myeloproliferative disorder and a myeloid/natural killer cell leukemia phenotype is described. The blasts expressed CD7, CD33, CD34, CD56, and CD117 but did not react with cytoplasmic myeloperoxidase and were negative for cy CD22, HLA-DR, and CD90 expression. No megakaryoblastic surface markers were identified. The blast population disappeared from the peripheral blood and bone marrow within 2 months, but hepatomegaly and recurrent respiratory insufficiency persisted. The patient died of unilateral pneumonia in the third month of life. Neither extramedullary infiltration nor other hematologic signs of disease progression were found.

Antigens, CD7↗
PubMedDate not supplied

[Prostacyclin in the treatment of persistent fetal circulation syndrome].

Persistent pulmonary hypertension of the neonate (PPHN), described initially by Gersony in 1969 as persistent foetal circulation (PFC syndrome), results from a flawed transition from foetal to extrauterine pulmonary circulation. It is primarily characterised by persistence of, or return to, the suprasystemic pulmonary vascular resistance and pressure normally found in the foetus. The increased pulmonary pressure causes right to left shunting through the ductus arteriosus or the foramen ovale, or both. The resulting hypoxaemia and acidosis may produce further pulmonary vasoconstriction and lead to a vicious cycle of shunting, hypoxia and acidosis. Infants with a wide variety of underlying clinical conditions develop PPHN. This condition is reversible, but can cause very severe and unrelenting respiratory failure and ultimate death when uncontrolled. Although vasodilating agents, such as tolazoline, have been used with variable success in the treatment of PPHN, a generally acceptable therapy is still lacking. We report here the use of prostacyclin (epoprostenol, PGI2) in two infants with severe and refractory hypoxaemia secondary to pulmonary vasoconstriction.

Epoprostenol↗