Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0039730 (thalassemia)
 10,305 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since freshly obtained acute lymphoblastic leukemia (ALL) cells rarely replicate spontaneously in vitro in a sustained way, development of a useful clonogenic assay for ALL blast progenitors is dependent on identifying the cellular growth requirements. Thus, marrows from 25 ALL cases were cultured in methylcellulose to determine the optimal conditions for cell growth. Blast colonies were confirmed as leukemic by morphology, cytochemistry, surface markers, and cytogenetics. Irradiated (7000 rads) normal peripheral blood feeder cells were an absolute requirement and produced number-dependent increases in ALL colonies; added growth factors enhanced the feeder cell effect. ALL cell-feeder cell contact was essential since their physical separation in a two-layer culture system drastically interfered with colony growth. Feeder cells from various donors, including new and relapsed cases of ALL, yielded colony numbers that differed widely when tested on the same marrow with and without added growth factor; thus, identification of a "good" feeder cell donor was key to an optimal assay. Neither recombinant interleukin-2 nor recombinant GM-CSF had ALL growth-promoting properties when tested alone or in combination but in the presence of feeder cells they moderately enhanced the feeder cell effect. The most effective growth factors were derived from cells exposed to phytohemagglutinin (PHA) for 72 h. In order of magnitude for colony growth-promoting activity, PHA-T cell conditioned medium (CM) was more stimulatory than PHA-blast cell CM followed by PHA-leukocyte CM; removal of PHA from CM by affinity chromotography did not alter the results. The most potent PHA-TCM was prepared from T-cells from a phlebotomized hemochromatosis patient; PHA-TCM from transfused thalassemia patients and normal donors were less active. Concanavalin-A blast cell CM had modest colony promoting properties whereas CM prepared with other B-cell mitogens and supernatants from ALL blasts in liquid culture had none. Our studies illustrate the complex and fastidious growth needs of ALL cells. The data have allowed us to refine a clonogenic blast progenitor assay that should facilitate study of proliferative properties of B and T lineage leukemias. The assay could be adapted further for detection of residual leukemia cells in marrow samples used for autologous transplantation, and in patients during complete hematological "remission."
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PMID:Growth requirements for human acute lymphoblastic leukemia cells: refinement of a clonogenic assay. 304 51

Two commonly used berberine-containing Chinese herbs, Rhizoma coptidis (RC) and Cortex phellodendri (CP), have been banned in Singapore for the past three decades due to implication of berberine in aggravating jaundice and kernicterus in neonates with glucose-6-phosphate dehydrogenase deficiency. Here we conducted a single arm, phase I/II clinical study on Chinese herbal medicine for patients with chronic cytopenic haematological conditions and we analysed a subset of 20 patients who also had RC, CP or both in their herbal concoction. We found no organ toxicity or electrolyte imbalance in these 20 patients where RC was administered for 1055 patient-days and CP for 1252 patient-days. In three patients with thalassemia intermedia, transient elevation in serum bilirubin level was observed but this was not associated with any aggravation of anaemia or liver dysfunction. A review of the literature found conflicting evidence of varying levels either supporting or refuting the allegation of neonatal jaundice and kernicterus caused by berberine. There were, however, very few clinical reports of adverse reaction attributable to RC or CP in oral TCM concoction. We conclude that based on traditional dosage and indication, the use of RC and CP in oral concoction is safe.
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PMID:Berberine-induced haemolysis revisited: safety of Rhizoma coptidis and Cortex phellodendri in chronic haematological diseases. 2200 96