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Biomedical subjects

P W Lane

Publications and source records attributed to P W Lane.

At least 19 recordsLinked to original sources
PubMed1992

Spontaneous renal artery thrombosis associated with altered mental status.

Renal artery thrombosis is much less common than renal artery occlusion by emboli. When it does occur, it is usually a result of blunt abdominal trauma or a thrombus superimposed on an atherosclerotic plaque. Numerous other factors have been associated with renal artery thrombosis. Spontaneous renal artery thrombosis is a rare phenomenon in itself. This case represents spontaneous renal artery thrombosis associated with an altered mental status. Clinical features with suspected etiologies are reviewed. Recommendations for future evaluations are given.

Adult↗
PubMed1991

Hairpatches, a single gene mutation characterized by progressive renal disease and alopecia in the mouse. A potential model for a newly described heritable human disorder.

A new murine mutation, hairpatches (Hpt), is on chromosome 4, 18.1 recombination units distal to brown near the interferon alpha and beta chain structural gene complex. On the inbred HPT/Le strain background, Hpt is semi-dominant, and Hpt/Hpt mice die in utero by 6 to 8 days of gestation. Such death in utero is associated with abnormalities of embryonic ectodermal derivatives. However on the (C57BL/6J x C3HeB/FeJ-a/a) segregating hybrid background, Hpt is a fully dominant mutation. HPT/Le Hpt/+ mice can be recognized by 3 to 4 days of age by patches of lightly pigmented skin. These mice show reduced numbers of hair follicles, abnormalities in hair follicle structure, and patchy absence of hair throughout life. By 2 weeks of age, abnormal hair follicle development is accompanied by thickening of the epidermis, reduction in levels of subcutaneous fat, and dermal inflammation. Progressive glomerulosclerosis, resulting in chronic kidney failure, is accompanied by increases in glomerular mesangial matrix, deposition of immune complexes, and glomerular enlargement. Scanning electron microscopic studies revealed abnormalities of podocytes including disorganization, swelling, and fusion of the foot processes. Increase in serum blood urea nitrogen levels accompanies conspicuous renal histopathologic changes. Cardiovascular changes in Hpt/+ mice are evidenced by hypertrophy of the left heart ventricle. Increased systolic blood pressure in these animals was found by 3 months of age. Anemia occurs in Hpt/+ mice by 40 weeks. The Hpt/+ mutation provides a valuable new animal model for chronic kidney disease accompanied by skin abnormalities and ventricular hypertrophy. The pathologic changes caused by this mutation are similar to those reported in affected family members with a newly described autosomal dominant human disease.

Alopecia↗
PubMed1990

Hydrocephalus with hop gait (hyh): a new mutation on chromosome 7 in the mouse.

Hydrocephalus with hop gait (hyh) is a new lethal recessive mouse mutation that arose in the C57BL/10J strain at The Jackson Laboratory. It has been mapped to the proximal end of Chromosome 7 close to the Gpi-1 locus. This homozygous mutant is characterized clinically by a domed head and a hopping gait observable at 2 weeks of age and death between 4 and 10 weeks of age. The affected mice have dilated lateral ventricles and a large third ventricular cyst, patent through narrowed rostral cerebral aqueduct, cystic caudal aqueduct and no communication of the aqueduct with the fourth ventricle. The cerebellum has a mild cortical malformation.

Animals↗
PubMed1988

New mutation causing sterility in the mouse.

A new murine mutation, skeletal fusions with sterility, sks, has been identified. This mutation causes arrest during the pachytene stage of virtually all spermatogenic cells. Defects in chromosome pairing and appearance of the synaptonemal complex during meiosis in the male are apparent, but defective pairing is probably not the cause of sterility. Affected females are functionally infertile. Oocytes are capable of undergoing meiotic maturation in vitro but cannot be fertilized in vitro. Affected individuals of both sexes are characterized by fusions of vertebrae and of ribs. The sks gene has been mapped to Chromosome 4, 16.6 cM distal to the brown locus.

Animals↗
PubMed1972

Susceptibility to spontaneous pneumonitis in an inbred strain of beige and satin mice.

Among mice of strain SB/Le, homozygous for the mutant genes beige (bg), satin (sa), and white-bellied agouti (A(w)), 70% developed progressive pneumonitis by 6 months of age. Among backcross offspring from an outcross to C57BL/6J-A(w-J), 49% of homozygous beige and 11% of nonbeige genotypes developed pneumonitis by 6 months of age. The evidence indicates that a specific action of the beige gene increases susceptibility to progressive pneumonitis. Lymphadenopathy, including reticulum cell neoplasms and atypical lymphoproliferative lesions, was observed in high incidence in sa+/sa bg males, suggesting a closer association with satin than with beige. Beige mice show giant lysosomal granules in the leukocytes and pigment dilution closely analogous to the Chediak-Higashi syndrome in man and similar disorders in mink and cattle. Strain SB/Le provides a convenient model in a laboratory animal for study of the increased susceptibility to infection analogous to that of the Chediak-Higashi syndrome.

Age Factors↗
PubMedDate not supplied

Osteopetrosis, a new recessive skeletal mutation on chromosome 12 of the mouse.

Osteopetrosis (op/op) is a new mutation in the mouse that is transmitted as an autosomal recessive linked with variant waddler (Va) on chromosome 12. Compared with normal littermates, young op/op mice have excessive accumulations of bone without marrow cavities, increases in bone matrix formation and concentrations of parafollicular cells of the thyroid, and are hypophosphatemic. Osteoclasts from op/op mice are small, few in number and have an abnormal cytoplasmic distribution of the lysosomal enzyme acid phosphatase. In contrast to the three other mutations that transmit osteopetrosis in mice, the skeletal signs of the disease slowly disappear in op/op animals after bone matrix formation declines about 6 weeks after birth from 145 percent to 20 percent of that in normal siblings. The main skeletal defect in op/op mice appears to be a severe restriction in bone remodeling that is capable of slowly removing the excessive skeletal mass characteristic of the disease only after bone formation has declined to one-fifth that of normal littermates.

Animals↗
PubMedDate not supplied

Myodystrophy, a new myopathy on chromosome 8 of the mouse.

A new recessive mutation, myd, causing a diffuse and progressive myopathy in the mouse is described. Histopathological comparisons with normal littermates showed widely distributed focal lesions in all skeletal muscles of myd/myd. Body and organ weights of affected mice were considerably less than those of normal littermates and the mean lifespan of myodystrophic mice that survived weaning was 17 weeks with a range of 5 to 39 weeks. Myodystrophy is located on chromosome 8; it is linked to Os with about 6 percent and to Eso with about 37 percent recombination.

Animals↗