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Biomedical subjects

R Kuse

Publications and source records attributed to R Kuse.

102 records · Page 6Linked to original sources
PubMed1976

[Detection of reagent errors by internal quality control of the Coulter counter S].

By a simple program of quality control for the Coulter counter model S two deficient reagents could be detected. To high values of PCV associated with a decrease of MCHC were caused by a faulty Isoton batch. This error was revealed by native blood samples but not by the stabilized 4 C standard. Falsely elevated leukocyte counts due to insufficiently lysed giant platelets and platelet aggregates were produced by modified Lyse-S batches. Comparisons made with a Coulter counter model F using Zaponin and with a counting chamber yielded values at lower levels.

Blood Cell Count↗
PubMed1976

Posthaemorrhagic iron deficiency. Clinical course, 59Fe whole-body iron losses, and oral iron supplementation.

Clinical and laboratory data characterizing post-haemorrhagic anaemia with still normal iron stores and posthaemorrhagic iron deficiency in the manifest, latent or prelatent stage are presented. Initially, increased 59Fe whole-body iron losses (greater than 0.1-3.6%/day) returned to normal range (less than 0.1%/day) after haemostasis. Subsequently, slow increase of haemoglobin and repletion of iron stores occurred under normal diets. Manifest, latent, and prelatent iron deficiencies were corrected much more rapidly by total doses of 12.0, 10.5 and 8.0 g iron (Fe2+ sulfate), respectively, when 2 X 50 mg/day were given in quick-release capsules apart from meals.

Adult↗
PubMed1975

[Possible errors in leukocyte count caused by carryover in the Coulter counter S].

In 163 samples of venous blood with significant leukocytosis (20 000 to 172000 cells pro mm-3) a carryover of 400 to 22000 leukocytes up to the third count of the following specimens (200 to 9300 cells/mm-3) could be observed. Even after 41 specimens of normal leukocyte range and low leukocytosis (6700 to 17700 cells/mm-3) in cases of extreme leukopenias (less than 2000 cells/mm-3) the correct result was exceeded by 500 to 1000 cells. In four additional machines of other laboratories a carryover of different extent could be reproduced. In comparison to samples of venous blood only a very small carryover into subsequent samples of isotonic solution was found. The considerable spreading of the coefficient of variation between 1.7 and 16.2% (arithmetic mean 7.1%) prohibited a mathematical correction of error. Erroneously too high numbers of leukocytes could be absolutely avoided by at least two repeated counts.

Humans↗
PubMedDate not supplied

Geotrichosis of oral mucosa.

A livid, sharply defined enanthema of the oral mucosa with ulcerations on the soft palate in a patient presenting with de novo acute myeloid leukaemia with prolonged, therapy-induced granulocytopenia (< 0.5 nl-1 for 113 days!) was diagnosed as geotrichosis. Geotrichum capitatum was identified both in vivo and in vitro. Pneumonic infiltrates in the upper lobes of both lungs were treated with amphotericin B infusions. Healing of the aforementioned enanthema was only achieved after addition of 5-fluorocytosine to therapy. Susceptibility determinations with several Geotrichum capitatum isolates led to the conclusion that amphotericin B was unsuitable as a therapeutic agent in this case. 5-Fluorocytosine and itraconazole exhibited superior antifungal and antimycotic activity.

Agranulocytosis↗
PubMedDate not supplied

Role of angiogenesis inhibitors in acute myeloid leukemia.

Neovascularization is increasingly recognized as an important factor in the pathogenesis of hematologic malignancies as well as solid tumors. The complex interactions between several cell types and numerous cytokine mediators suggest the involvement of autocrine and paracrine signaling mechanisms. Vascular endothelial growth factor (VEGF) in particular is critical to both stimulation of leukemic growth and proliferation of endothelial cells. Tyrosine kinase receptors specific for certain growth factors represent attractive target molecules for anticancer therapy. SU5416 is a competitive inhibitor of VEGF receptor subtypes VEGFR-1 and VEGFR-2 and stem cell factor receptor c-kit. Preclinical evidence shows that SU5416 effectively inhibits VEGF-induced endothelial cell proliferation and slows growth of subcutaneous solid tumor xenografts. This agent is in late-stage clinical trials in patients with solid tumors, and a Phase 2 study was recently initiated to evaluate its utility in the treatment of acute myeloid leukemia. In this Phase 2 study, investigators are seeking to determine the response rate to the antiangiogenic agent SU5416. Translational research in this study is intended to aid our understanding of the precise mechanisms by which SU5416 affects acute myeloid leukemia cells and the bone marrow microenvironment.

Acute Disease↗