PGE-MUM increases in smokers, as suggested by possible inflammatory injury of pulmonary tissue. This RIA method for PGE-MUM may be thus a sensitive and reliable biomarker for current inflammation, different from serum CRP.
The chromosome banding pattern has been analyzed in clones of mouse myeloid leukemic cells that differ in their ability to be induced to differentiate by the protein inducer MGI (macrophage and granulocyte inducer) None of the clones had a completely normal diploid banding pattern. The clones studied were either MGI+ (that can be induced to form Fc and C3 rosettes), a stage in the differentiation of myeloid cells, or MGI-(that cannot be induced to form these rosettes)All six cultured clones of MGI- trolled by the balance between these genes. We sugges that these chromosomes also carry genes that control the mahgnancy of these cells.The development of an experimental system for the in vitro induction of differentiation in various types of white-blood cells (1-7), has made it possible to study the control mechanisms that regulate the differentiation of these cells and the blocks that can occur in leukemia and nonmalignant diseases (6,(8)(9)(10)(11)(12)(13). It has been shown that some myeloid leukemic cells can be induced to differentiate normally by incubation with the differentiation inducing protein MGI (macrophage and granulocyte inducer) (6, 8, 9) and that there are other myeloid leukemic cells with different blocks in differentiation (10, 12). Clones of one type of cell (MGI+) can be induced by MGI to form Fc and C3 rosettes, which is a stage in the differentiation of myeloid cells, whereas clones of another type of cell (MGI-) cannot be induced by MGI for the surface changes that result in the formation of rosettes. The MGI+ clones can be divided into two types, one of which (MGI+D+), was also induced by MGI to form mature macrophages and granulocytes, and the other (MGI+D-) was induced to form Fc and C3 rosettes but not mature cells. The MGI-clones were all D-and could not be induced to form rosettes or mature cells (10, 12).The clonal origin and inheritance of the differences in inducibility by MGI suggested that there may be genetic differences between the different cell types and that it may be possible to map the chromosome location of the genes involved (14). The clones used, even those that had been in culture for more than a year, still had a diploid or near-diploid modal chromosome number, so that these cells appear to be particularly favorable for mapping the genes that control differentiation and malignancy. It
MATERIALS AND METHODSCells and Cell Culture. Ten clones of myeloid leukemic cells were used in the present study. Two clones (11 and 12) were MGI+D+; two clones (2 and 4) were MGI+D-; and these four clones were isolated (9) from a myeloid leukemic cell line in culture obtained from a spontaneous myeloid leukemia in a female SL mouse (15). The other six clones (1, 6, 7, 8, 10, and 15) were separately cloned MGI-myeloid leukemic cell lines established in Vitro from the first or second transplant generation of six independently arising myeloid leukemias after irradiation of female SJL/J mice with x-rays (16). The lymphoid leukemias studied were also obtained after irradiation o...
We present a 15-month-old girl with tetraploidy and compare the manifestations with those of 3 previously reported liveborn infants with the same type of polyploidy. Common anomalies noted included micro-turricephaly, a prominent but narrow forehead, microphalmia or anophthalmia, limb anomaly, sacral meningomyelocele, and mental retardation.
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