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H Wessels

Publications and source records attributed to H Wessels.

35 records · Page 2Linked to original sources
PubMed1987

Origin of T-lymphocytes in human mixed hematopoietic colonies.

The presence of T-lymphocytes in mixed hematopoietic colonies (CFU-MIX) has been reported by some investigators. Though depletion before culturing was performed, residual T cells might be responsible for the observed phenomenon. Using nondepleted marrow or bone marrow depleted to about 2%, T-lymphocytes could be detected in mixed colonies. However, reduction of the T-lymphocytes to less than 0.7% by using a modified E-rosette technique or a cocktail of anti-T-cell monoclonal antibodies (WT1, WT32, WT82) in the presence of baby rabbit complement, resulted in mixed colonies free of T-lymphocytes. After addition of 1.75% T-lymphocytes to this T-cell-depleted bone marrow, T-lymphocytes could be detected in most mixed colonies, but not after the addition of the same percentage of irradiated T-lymphocytes. The presence of T cells in mixed colonies was determined by an adapted immunofluorescence technique (WT32 plus GAM-FITC). The results indicate that mononuclear cells with T-lymphocyte antigens are not the offspring of mixed hematopoietic colony-forming progenitors, but of a low number of T-lymphocytes contaminating the bone marrow after insufficient T-cell depletion.

Cytological Techniques↗
PubMed1984

Calculation of S-phase numbers of four major cell categories in human bone marrow from DNA-flow cytometry and counterflow centrifugation data.

Fractionation of heterogeneous cell populations into a number of fractions differing in cell size and composition, followed by measurement of DNA profiles and differential morphology of the samples allows the calculation, using a mathematical deconvolution procedure, of the cell proliferation of the individual categories. The method was applied to human bone marrow, fractionated by counterflow centrifugation into 10 to 15 fractions. Calculated percentage of S-phase cells in four major categories, including myeloid, erythroid, monocytic, and lymphoid cells, were in good agreement with data obtained by tritiated thymidine autoradiography.

Bone Marrow↗
PubMed1984

Bone marrow repopulation capacity after transplantation of lymphocyte-depleted allogeneic bone marrow using counterflow centrifugation.

Bone marrow from six allogeneic HLA-matched and MCL nonreactive siblings was fractionated by means of isopycnic flotation centrifugation and subsequent counterflow centrifugation. The low density fraction (d less than or equal to 1.070 g/ml) obtained by IFC contained 20% of the nucleated cells and more than 90% of the myeloid and erythroid progenitors. The putative stem cell fraction obtained by CC showed a satisfactory recovery (88%) of the CFU-GM and BFU-E and only 3.5% of the original number of T lymphocytes. Bone marrow repopulation capacity was not impaired in comparison with a comparable group of patients. Despite the average high age of this group (29.6 years), only one of the four evaluable patients developed graft-versus-host disease.

Adolescent↗
PubMed1981

Determination of 1-beta-D-arabinofuranosylcytosine and 1-beta-D-arabinofuranosyluracil in human plasma by high-performance liquid chromatography.

A method is described for the determination of 1-beta-D-arabinofuranosylcytosine (Ara-C) and its metabolite 1-beta-D-arabinofuranosyluracil (Ara-U) in human plasma. After deproteinization of the plasma sample, separation is performed by reversed-phase liquid chromatography. For Ara-C concentrations exceeding 0.05 mg/l and for Ara-U concentrations exceeding 1 mg/l, injection volumes of 100 microliter are applied. For lower concentrations an injection volume of 500 microliter is used. Ara-C is detected at 280 nm with a lowest detection limit of 0.002 mg/l in plasma. Ara-U is detected at 264 nm with a lowest detection limit varying from 0.01 to 0.1 mg/l in plasma. This variation is caused by an unknown substance with the same elution properties as Ara-U and which appears to be present in plasma in variable concentrations. The coefficient of variation of the whole procedure is about 6% for Ara-C concentrations above 0.005 mg/l and for Ara-U concentrations above 0.1 mg/l. For lower concentrations the coefficient of variation is about 14%.

Arabinofuranosyluracil↗
PubMed1981

Lithium inhibits adenylate cyclase of human platelets.

The ADP-induced aggregation of human platelets is markedly increased after preincubation with lithium chloride, whereas lithium has the opposite effect on rabbit platelets. Since this phenomenon might be related to cAMP metabolism, the influence of lithium on total cAMP content and adenylate cyclase activity was investigated. Lithium does not significantly change the total cAMP content of human platelets neither during incubation nor during ADP-induced aggregation. Basal adenylate cyclase activity, however, was slightly inhibited by lithium in human platelets. The inhibition of adenylate cyclase by ADP appeared to be enhanced by lithium. Prostacyclin induced stimulation of adenylate cyclase is counteracted by this ion. In rabbit platelets the prostacyclin stimulated adenylate cyclase activity is not affected by lithium. These data suggest that a correlation exists between the influence of lithium on the aggregation of human and rabbit platelets and the sensitivity of their adenylate cyclase for this ion.

Adenylyl Cyclase Inhibitors↗
PubMed1981

Lithium stimulates thromboxane B2 formation in human platelets.

The aggregation of human platelets is enhanced after preincubations with lithium salts. Previously it was shown that lithium inhibits adenylate cyclase activity in human platelets. Enhancement of aggregation and inhibition of adenylate cyclase by lithium was not observed in rabbit platelets. In this paper it is shown that in human platelets lithium enhances considerably the synthesis of thromboxane B2, whereas the synthesis of PGE2 and PGF2 alpha was enhanced to a lesser extent. In rabbit platelets lithium had no effect on prostaglandin synthesis. It is concluded that lithium specifically stimulates the synthesis of thromboxanes in human platelets, probably due to the previously reported inhibition of adenylate cyclase activity, resulting in an increased aggregability.

Adenosine Diphosphate↗
PubMed1980

High spontaneous thymidine incorporation into a non-T lymphocyte population in Hodgkin's disease unmasked after cell fractionation.

In order to study the nature of the spontaneously stimulated cells in Hodgkin's disease, lymphocytes from 10 patients with Hodgkin's disease and 10 healthy control subjects were separated into low- and high-density fractions. Both fractions were subdivided into T and non T cell populations by means of rosette sedimentation. In Hodgkin's disease patients, non-T cells with a high density showed a significantly increased spontaneous thymidine incorporation (mean, 5677 cpm; range, 405--26490 cpm) compared to corresponding cells from control subjects (mean, 484 cpm; range, 235--850 cpm), and to unseparated high-density lymphocytes in Hodgkin's disease patients. Evidence is presented that in Hodgkin's disease, the high-density lymphocyte fraction comprises non-T cells with an apparent potency for DNA synthesis which is, however, inhibited by T cells present in the same high-density fraction.

Adult↗
PubMed1980

Observations on ADP aggregation of lithium chloride incubated platelets in a variety of mammalian species.

In citrated platelet-rich plasma of eight mammalian species lithium produces species-dependent effects on ADP aggregation ranging from stimulation to inhibition. Raising the extracellular calcium concentration enhanced aggregation of both lithium-stimulated and lithium-inhibited platelets, indicating that the extracellular calcium concentration has no direct relation to the effect of lithium on platelet function. Lithium did not induce changes in total intracellular platelet calcium and magnesium contents. Aggregation of platelets with ionophore A23187 showed the same species-specific lithium effects as aggregation induced by ADP. The data suggest that lithium does not exert its effect on platelets through interference with intra- or extracellular calcium concentrations.

Adenosine Diphosphate↗