Jim Schröder
Stanford University
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Archive | 1977
Jim Schröder; Eva Schröder; Howard M. Cann
SummaryIn an attempt to stimulate fetal cells in the maternal blood to mitotic division, peripheral blood lymphocytes were cultured from ten primiparous women and six multiparous women. In the case of the ten primiparous women, PWM was used to stimulate lymphocytes in 3- and 7-day cultures made at the 16th, 20th, 24th, and 28th week of gestation. Altogether, 10565 mitoses were analyzed after quinacrine staining of cells from five mothers who each subsequently gave birth to a male infant, and not a single XY mitosis was found.In the case of the multiparous women, lymphocyte cultures, with PHA or LPS as mitogen and MLC, were initiated between the 13th and 20th week of pregnancy. Four of the mothers were pregnant with a male child, and two with a female child. From cultures of each of the four mothers expecting a boy, a total of 9721 mitoses were analyzed after quinacrine staining, and not a single XY mitosis was found. However, one XY cell was found in the culture from one of the two women who delivered a girl. The XY mitosis probably originated from a pregnancy 8 months earlier which terminated in a male infant.In an attempt to culture and obtain good chromosome preparations from small numbers of cells, it was shown that a good mitotic response and good chromosome preparations could be obtained from as few as 6000 lymphocytes.
Cancer Genetics and Cytogenetics | 1979
Jim Schröder; Heli Suomalainen; Michael R. Knapp; Eva Severinson Gronowicz; Samuel Strober
Abstract The karyotype of a spontaneous mouse B-cell leukemia passaged intravenously several times in succession into syngeneic recipients was determined. Peripheral lymphocytes from a control animal and from animals in passage 1 and 7 were stimulated by the mitogen lipopoly-saccharide, and studied by Giemsa banding methods. In passage 1, the cultured lymphocytes consisted of 4 clones, one with a normal karyotype (1 cell out of 32), and three with multiple chromosome changes. One clone, representing about 10% of all mitoses, had 39 chromosomes with monosomy for chromosomes 12 and 13, two reciprocal translocations, and a small marker chromosome. One of the translocations had occurred between chromosomes 4 and 15, the other between an X chromosome, and one chromosome No. 8. Another clone had 37 chromosomes (6% of all mitoses), and the remaining clones had 36 chromosomes (81% of all mitoses). These clones had the same chromosome changes as the clone with 39 chromosomes, three additional monosomies (6, 8, and 15), and three new translocations. In passage 7 the clone with 36 chromosomes represented about 30% of the cultured cells, while 70% of the cells had 35 chromosomes; the reduction in number was caused by a 17;19 translocation. The cultures from the control animals had a normal karyotype.
Nature | 1983
Gregory D. Plowman; Joseph P. Brown; Carolin A. Enns; Jim Schröder; Barbro Nikinmaa; Howard H. Sussman; Karl Erik Hellström; Ingegerd Hellström
Journal of Immunology | 1979
Eva Severinson Gronowicz; Carol Doss; Jim Schröder
Journal of Immunology | 1979
M. R. Knapp; E. Severinson-Gronowicz; Jim Schröder; Samuel Strober
Hereditas | 2009
Albert de la Chapelle; Jim Schröder; Tari Haahtela; Paavo Aro
Hereditas | 2009
Albert de la Chapelle; Jim Schröder; Ritva-Kajsa Selander
Hereditas | 2008
Jim Schröder; Timo Soveri; Heli Suomalainen; Lars‐Axel Lindberg; Wessel van der Loo
Hereditas | 2009
Jim Schröder; Heli Suomalainen; W. Loo; E. Schröder
European Journal of Immunology | 1989
Ulla H. Forsberg; Minna Maria Ala-Kapee; Sirpa Jalkanen; Leif C. Andersson; Jim Schröder