L. Beckman
Uppsala University
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Featured researches published by L. Beckman.
Human Heredity | 1971
G. Beckman; L. Beckman; J. Pontén; B. Westermark
The G-6-PD, PGM1 and PGM3 phenotypes were examined in 16 different continuous human tumor cell lines (glioma and sarcoma) established in the Uppsala laboratory. The enzyme patter
Human Heredity | 1995
G. Beckman; L. Beckman; S. Holm; C. Silkström; C. Wennberg
Recently, results have been presented which suggest that placental alkaline phosphatase (PLAP) is an IgG receptor, and that the transplacental transport of IgG from mother to fetus is dependent on the fetal PLAP genotype. In order to confirm the relationship between the PLAP types and transplacental IgG transport, we studied fetal (cord serum) IgG levels in relation to PLAP types, quantitative variations in PLAP activity, maternal IgG levels and gestation length. Fetal IgG levels and the fetal/maternal IgG ratio showed no significant correlation with PLAP types and PLAP activity. Thus differences between PLAP types with respect to transplacental IgG transport are unlikely to play a selective role in the maintenance of the PLAP polymorphism. In accordance with results from previous studies, significant correlations were found with maternal IgG levels and gestation length. Perusal of the literature suggests that PLAP is mainly an IgG1 receptor.
Human Heredity | 1968
L. Beckman; E. Lundgren; J. Pontén; B. Westermark
Cultured human cancer cells and normal cells differ with respect to the amino acid naphthylamidase isozymes. One isozyme called A was found in extracts of neoplastic cells (glioma and sarcoma) but was lacking or very weak in analogous normal cells (glia and fibroblasts). The A isozyme was found to appear in a human cell line after transformation with virus (SV 40).
Human Heredity | 1989
G. Beckman; L. Beckman; E. Lundgren; J.L. Millán; C. Sikström
Restriction fragment length polymorphism (RFLP) of human alkaline phosphatases was studied in a population sample from northern Sweden using a placental alkaline phosphatase (PLAP) cDNA probe. After digestion of human genomic DNA with RsaI the Southern blots showed DNA fragments most probably derived from three genes: PLAP, germ cell alkaline phosphatase (PLAP-like) and intestinal alkaline phosphatase. In agreement with a previous study, a two-allele polymorphism was found in PLAP with bands at 1.6 kilobases (A1) and 1.8 kilobases (A2). The gene frequencies of A1 and A2 were 0.46 and 0.54, respectively. There was a significant correlation between the RsaI RFLPs and electrophoretic types of PLAP; RSAI A2 showed an association with the ALP2p allele of PLAP.
Acta geneticae medicae et gemellologiae | 1962
L. Beckman; Lena Widlund
Data on the occurrence of poly- and syndactylies among 64793 newborn children were collected from the hospital records of two different Swedish hospitals, one being located in the North and the other in South Sweden. Frequency estimates are given for the different types of anomalies and the families of 35 probands were studied. Some pedigrees were compatible with dominant transmission of the traits, while in others the mode of inheritance is irregular. There was no evidence for Y-linked syndactyly. In several cases it was found that a proband with Polydactyly had relatives with syndactyly and vice versa. Some pedigrees included also individuals with reductions of phalanges and fingers.
Human Heredity | 1994
G. Beckman; L. Beckman; C. Wennberg; C. Sikström; J.L. Millán
Restriction fragment length polymorphisms have previously been found in the placental alkaline phosphatase (PLAP) and germ cell alkaline phosphatase (GCAP) genes, but not in the closely related intestinal alkaline phosphatase (IAP) locus. We here report on a PstI restriction fragment length polymorphism in IAP found in Finns and Swedes but not in Saamis. A probable T-->G mutation in position 175 of intron 11 would create a new cleavage site for PstI. The borderline frequency of the mutant allele (0.01) is in agreement with previous observations suggesting that IAP is considerably less polymorphic than PLAP and GCAP.
Human Heredity | 1969
K. Berg; L. Wetterberg; L. Beckman; Marit Hornberg
Human Heredity | 1965
L. Beckman; J. Takman; K.E. Arfors
Human Heredity | 1962
L. Beckman; Robert N. Elston
Hereditas | 2009
L. Beckman; Karl-Henrik Gustavson; H.‐O. Åkesson