Impairment-based examination and disability management of an elderly woman with sacroiliac region pain.

Background And Purpose: The purpose of this case report is to describe the use of a cluster of sacroiliac tests in conjunction with an impairment-based model of examination, diagnosis, and management of sacroiliac region pain.

Case Description: The patient was a 74-year-old woman with an 18-month history of low back, left buttock, and groin pain following a misstep. The initial symptoms were intermittent.

Susceptibility to testicular germ-cell tumours in a 129.MOLF-Chr 19 chromosome substitution strain.

The identification of genes that control susceptibility to testicular germ-cell tumours (TGCTs), the most common cancer affecting young men, has been difficult. In laboratory mice, TGCTs arise from primordial germ cells in only the 129 inbred strains, and susceptibility is under multigenic control. The spontaneously arising mutation Ter (ref.

Testicular teratocarcinogenesis in mice--a review.

Spontaneous testicular germ cell tumours in humans and mice are remarkable for their diverse composition. These tumours are usually composed of an extraordinary variety of cell and tissue types including muscle, skin, bone, cartilage, and neuroepithelia. Their diverse composition reflects their origin from totipotent primordial germ cells at about Day 12 of fetal development.

Initiation of autoimmune diabetes in NOD/Lt mice is MHC class I-dependent.

MHC class II alleles clearly contribute a primary genetic component of susceptibility to autoimmune insulin-dependent diabetes mellitus (IDDM) in nonobese diabetic (NOD) mice. However, IDDM does not occur in NOD mice made MHC class I-deficient by a functionally inactivated beta2-microglobulin allele (beta2m(null)). In the present study the beta2m(null) mutation was used to examine the relative contributions of MHC class I and class II-dependent T cell responses for initiating autoimmune pancreatic beta cell destruction in NOD mice.

B lymphocytes are essential for the initiation of T cell-mediated autoimmune diabetes: analysis of a new "speed congenic" stock of NOD.Ig mu null mice.

The T lymphocytes mediating autoimmune destruction of pancreatic beta cells in the nonobese diabetic (NOD) mouse model of insulin-dependent diabetes mellitus (IDDM) may be generated due to functional defects in hematopoietically derived antigen-presenting cells (APC). However, it has not been clear which particular subpopulations of APC (B lymphocytes, macrophages, and dendritic cells) contribute to the development and activation of diabetogenic T cells in NOD mice. In the current study we utilized a functionally inactivated immunoglobulin (Ig) mu allele (Ig mu null) to generate a "speed congenic" stock of B lymphocyte-deficient NOD mice that are fixed for linkage markers delineating previously identified diabetes susceptibility (Idd) genes.

Genetic regulation of traits essential for spontaneous ovarian teratocarcinogenesis in strain LT/Sv mice: aberrant meiotic cell cycle, oocyte activation, and parthenogenetic development.

Strain LT/Sv female mice show a high frequency of spontaneous ovarian teratomas arising from parthenogenetically activated follicular oocytes. LT/Sv oocytes also arrest at metaphase of meiosis I, rather than progressing through to metaphase II, as do almost all fully grown oocytes from most other strains. We investigated a new set of recombinant inbred strains derived from BALB/c and C58 (the progenitor strains of LT/Sv) and crosses of these two progenitor strains and found that metaphase I arrest is necessary, but not sufficient, to cause parthenogenetic activation.

Interaction between undulated and Patch leads to an extreme form of spina bifida in double-mutant mice.

The aetiology of spina bifida involves genetic and environmental factors, which may be why major genes contributing to pathogenesis have not been identified. Here we report that undulated-Patch double-mutant mice have a phenotype reminiscent of an extreme form of spina bifida occulta in humans. This unexpected phenotype in double-mutant but not single-mutant mice shows that novel congenital anomalies such as spina bifida can result from interaction between products of independently segregating loci.

A mutation in the Ter gene causing increased susceptibility to testicular teratomas maps to mouse chromosome 18.

Little is known about inherited susceptibility to spontaneous germ cells tumours in humans or other species. The Ter mutation in laboratory mice is novel in that it acts codominantly to reduce germ cell numbers on many inbred strain backgrounds and to enhance dramatically inherited predisposition to spontaneous testicular teratocarcinomas in strain 129 inbred mice. We have adopted a PCR-based, DNA pooling method for mice with 'extreme' phenotypes (small testes versus normal-sized testes) to identify a candidate linkage to the Ter locus.

Two-hit model for sporadic congenital anomalies in mice with the disorganization mutation.

Congenital anomalies have complex etiologies involving both genetic and nongenetic components. Many are sporadic, without obvious evidence for heritability. An important model for these anomalies is a mutation in laboratory mice that is called "disorganization" (Ds), which functions as a variable autosomal dominant and leads to a wide variety of congenital anomalies involving many developmental processes and systems.

Disorganization is a completely dominant gain-of-function mouse mutation causing sporadic developmental defects.

Disorganization (Ds) is an exceptional mutation because of its diverse and profound developmental effects. Although other mouse mutations produce similar congenital defects, extreme pleiotropism, random occurrence, developmental independence of multiple defects, and type of anomaly make Ds unique. Examples of developmental defects include cranioschisis, rachischisis, thoracoschisis, exencephaly, hamartomas, and anomalies of appendages, digestive, genital and urinary tracts, sense organs, limbs and girdles, tail and pharynx.

Genetic evidence for two t complex tail interaction (tct) loci in t haplotypes.

The t complex on chromosome 17 of the house mouse is an exceptional model for studying the genetic control of transmission ratio, gametogenesis, and embryogenesis. Partial haplotypes derived through rare recombination between a t haplotype and its wild-type homolog have been essential in the genetic analysis of these various properties of the t complex. A new partial t haplotype, which was derived from the complete tw71 haplotype and which is called tw71Jr1, was shown to have unexpected effects on tail length and unique recombination breakpoints.

Development of rib-vertebrae: a new mutation in the house mouse with accessory caudal duplications.

The new recessive mutation rib-vertebrae (rv) causes fusions of lower ribs and malformations of vertebrae, which results from disturbed somite arrangement. In addition, duplications of the caudal neural tube and sometimes unilateral suppression of kidney formation can be observed. The new mutation is compared with the six already known mutations in mice with "Wirbel-Rippen-Syndrome" and with a similar syndrome in man.

Blind-sterile: a new mutation on chromosome 2 of the house mouse.

The inheritance and developmental effects of a new recessive mutation in the mouse, blind-sterile (bs), are described. This mutation causes lenticular cataracts and glossy coat in males and females and sterility in males due to arrested spermatogenesis. Blind-sterile is located on chromosome 2, near agouti.

Comparison of 11C and 14C-labeled fatty acids and their beta-methyl analogs.

1-[14C] beta-methylheptadecanoic acid ( [14C]BMHDA) was compared to 16-[14C]palmitic [( 14C]PA) acid for its biodistribution in rats, to determine whether an analogue designed to be trapped as a metabolite of the beta-oxidation metabolic process in the myocardium could be used to assess myocardial metabolic integrity. A heart concentration of 2.82 and 6.

Head blebs: a new mutation on chromosome 4 of the mouse.

The development effects and inheritance of a new mutation in the mouse, head blebs, gene symbol heb, are described. This mutation is similar to two other autosomal recessive mutations, eb and my. Head blebs produces abnormal or missing eyes due to prenatal blebs, usually on the head, some fetal death, open eyelids, and folded retinas at birth.

Development of coloboma (Cm/+), a mutation with anterior lens adhesion.

A semidominant mutation in the laboratory mouse, Coloboma (Cm), is described. Coloboma is located on Chromosome 2, as is the similar mutation Dickie's small eye (Dey). Coloboma has a moderately reduced expressivity.

Development of Dickie's small eye: an early lethal mutation in the house mouse.

Mice heterozygous for Dickie's small eye (Dey) are small and have malformed eyes (Theiler et al. 1978). The development of homozygous Dey/Dey was more difficult to analyze than heterozygous Dey/+.

Development of Dickie's small eye, a mutation in the house mouse.

A new semidominant mutation in the laboratory mouse, Dickie's small eye (Dey), is described. It is localized on chromosome 2. Heterozygotes show reduced body size, small eyes with coloboma, small or lacking lens with cataract, abnormal folding of the retina and reduction of the pigment layer.

A new allele of ocular retardation: early development and morphogenetic cell death.

The inheritance and some developmental effects of a new allele of ocular retardation (orJ) are described. Affected animals or 12 days of gestation, show reduced cell death in the eye cup and thickening of the inner wall of the optic fissure. At 11 to 13 dyas of gestation orJ/orJ eyes grafted to the testis do not produce retina as their orJ+ littermates do.

Malformed vertebrae: a new mutant with the "wirbel-rippen syndrom" in the mouse.

A new skeletal mutant in the house mouse, "malformed vertebrae" (MV), is described. It is semidominant. The skeletal malformations can be traced back to disturbed somite formation.