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M Lenartowicz

Publications and source records attributed to M Lenartowicz.

8 recordsLinked to original sources
PubMed2002

Pathological structure of the kidney from adult mice with mosaic mutation.

The mosaic (Atp7a(mo-ms)) is an X-linked, lethal mutation in mice. In mosaic mutant males, many clinical features characteristic of defective copper metabolism have been observed and they die at the age of 15 days, exhibiting strong similarities to the brindled and macular mutants. About 4% of the mutant males live to sexual maturity and some of them are fertile. In this paper, alterations in the structure of the kidney from adult mutants are described. Owing to an inherited defect of efflux, copper is accumulated in the kidney of the mutants up to a toxic level and this leads to severe damage of the renal cortex. Pathological changes in the kidney mostly affected the structure of the renal corpuscle and renal tubules.

Animals↗
PubMed2001

Alterations in kidney morphology in mice with mosaic mutation.

The mosaic (Atp7a(mo-ms)) is an X-linked, lethal mutation in mice. Hemizygous males die at the age of 15 days and they exhibit strong similarities to the brindled and macular mutants. Injection of cupric chloride to mossaic mutants prolongs their life and diminishes the pathological results of mutation. Histochemical analysis of the kidneys from 14-day-old mutant males showed accumulation of copper in the renal cortex of the investigated animals leading to damage of the kidney architecture. A histological profile of the kidneys was defined for four groups of 14-day-old animals: mosaic males ms/-, control males +/-, mosaic males injected with cupric chloride ms/- (Cu), and control males injected with cupric chloride +/- (Cu). Pathological changes were observed in the cortex and in the medulla of the kidneys in both groups of mutants and control males injected with cupric chloride (50 microg of CuCl2 per each individual).

Animals↗
PubMed1999

Preferential segregation of marker chromosomes 14 and 18 in mouse recombinant inbred strains derived from the KE and CBA/Kw strains.

The segregation pattern of chromosomes 14 and 18 were analyzed in recombinant inbred strains of mice developed from KE and CBA/Kw strains. The analysis was possible owing to the fact that the C-band on chromosomes 14 of the CBA/Kw strain and that of chromosome 18 of the KE strain show size polymorphism: while the CBA/Kw mice have a small sized C-band on chromosome 14, the KE mice show small C-bands on chromosome 18. Chromosomes were identified by G-banding and FISH. The results show that the chromosomes with small centromeric chromatin segregate preferentially.

Animals↗
PubMed1998

The comparison of primordial germ cell populations in embryos of KE and CBA inbred strains of mice.

The changes in primordial germ cell (PGC) populations were compared in embryos of two inbred strains of mice-KE and CBA/Kw on 11, 12, 13 and 14 day of foetal life. The number of PGCs did not differ in 11-day embryos of both strains. In 12-day CBA/Kw embryos the proliferation rate of PGCs was higher and the number of PGC was significantly higher than in 12-day KE embryos. However, on subsequent days the PGC proliferation rate decreased in CBA/Kw but rapidly increased in KE embryos, leading to significantly higher number of PGCs in 14-day KE embryos. These differences in proliferation rate between KE and CBA/Kw PGCs can be regarded as the reason of strong selection against CBA/Kw derived gametes observed in KE<-->CBA aggregation chimaeras.

Alkaline Phosphatase↗
PubMed1998

[Mice with mottled mutation--a model for defective copper metabolism in humans].

The group of X-linked mottled (Atp7aMo) mutations in mice is described. A normal gene encodes a copper-binding P-type ATPase. Mutant animals have the disturbance in copper metabolism, hemizygous males (Mo/y) die between 14-18 days of life, heterozygous females (Mo/+) are normal and fertile. This kind of copper metabolic defect is observed also in other animal and in human. In human Menkes disease caused by X-linked Atp7a mutant gene leads to death in early childhood. Because of is 89% of homology between Atp7aMo gene and Atp7a locus in human, mottled mutations are an excellent model for Menkes disease.

Adenosine Triphosphatases↗