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Biomedical subjects

E Simpson

Publications and source records attributed to E Simpson.

279 records · Page 16Linked to original sources
PubMedDate not supplied

The relationship between dissociative symptoms, alexithymia, impulsivity, sexual abuse, and self-mutilation.

The overall purpose of the present study was to further our understanding of the mechanisms of self-mutilative behavior in a sample of female inpatients. The study found that self-mutilators (n = 103) displayed a greater degree of dissociative symptoms and alexithymia and a greater number of self-injurious behaviors, as well as higher rates of childhood sexual abuse, than nonmutilators (n = 45). In addition, the study found that among these variables, the number of self-injurious behaviors had the strongest relationship to self-mutilation. However, both dissociative symptoms and alexithymia were independently associated with self-mutilative behavior. Implications of our findings for clinicians and researchers are discussed.

Adult↗
PubMedDate not supplied

Aromatase as a therapeutic target in endometriosis.

In contrast to normal endometrium, the expression of aromatase is aberrant in endometriosis and is stimulated by prostaglandin E2 (PGE2). This results in local production of estrogen, which induces PGE2 formation and establishes a positive feedback cycle. Another abnormality in endometriosis--deficient 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD) type 2 expression--impairs the inactivation of estradiol (E2) to estrone (E1). These molecular aberrations collectively favor accumulation of increasing quantities of E2, and PGE2 in endometriosis. The clinical relevance of these findings was exemplified by the successful treatment of an unusually aggressive case of postmenopausal endometriosis with an aromatase inhibitor.

Aromatase↗
PubMedDate not supplied

Male sexual differentiation in mice lacking H-Y antigen.

The sexual phenotype of an adult mammal depends on whether the fetal gonad has differentiated as a testis or as an ovary. Because individuals of XY or XXY sex chromosome constitution develop as males, while XX and XO individuals develop as females, the presence of a Y chromosome seems normally to be required for testis differentiation and its absence to be necessary for differentiation of an ovary. The nature of the hypothetical Y-dependent substance responsible for masculinization of the indifferent gonad has been a matter for debate. A male-specific transplantation antigen, H-Y, has been known for many years and more recently a serologically detected antigen, also male-specific, has been reported. Those who believe that the two are antigenically distinct refer to the latter as SDM (serologically detected male) antigen, but many refer to both as H-Y antigen. The hypothesis that H-Y is itself the Y-dependent testis inducer, although supported by little or no direct evidence, is economical and hence attractive. H-Y antigen is frequently stated to be the substance responsible for primary sex determination (for example, see ref. 11). We report here that H-Y is absent from certain mice that develop testes and are of indisputably male phenotype, hence this transplantation antigen is unlikely to be responsible for testis determination.

Animals↗
PubMedDate not supplied

Separation of the genetic loci for the H-Y antigen and for testis determination on human Y chromosome.

The mammalian Y chromosome encodes a testis-determining factor (termed TDF in the human), a master regulator of sex differentiation. Embryos with a Y chromosome develop testes and become males whereas embryos lacking a Y chromosome develop ovaries and become females. Expression of H-Y, a minor histocompatibility antigen, may also be controlled by a gene on the Y chromosome, and it has been proposed that this antigen is the testis-determining factor. We have tested the postulated identity of H-Y and TDF in the human. H-Y typing with T cells was carried out on a series of sex-reversed humans (XX males and XY females), each shown by DNA hybridization to carry part but not all of the Y chromosome. This deletion analysis maps the gene for H-Y to the long arm or centromeric region of the human Y chromosome, far from the TDF locus, which maps to the distal short arm.

Chromosome Deletion↗
PubMedDate not supplied

H-Y responses of non-obese diabetic (NOD) mice.

Female non-obese diabetic (NOD) mice were tested for their ability to make responses to the male-specific (H-Y) transplantation antigen. In vivo assessment of this ability was made using skin graft rejection. A proportion (60%) spontaneously rejected NOD male tail skin by 80 days post-transplantation. The detection of the generation of H-Y-specific cytotoxic T cells, following in vivo priming and secondary in vitro restimulation, was carried out using a conventional 51Cr release assay. Female NOD mice primed either by skin grafting, intraperitoneal (i.p.) or footpad (f.p.) injection of male NOD spleen cells could be induced to make anti-H-Y cytotoxic responses, but not every immunized mouse responded. The nature of the H-Y-reactive T cells was investigated further by the in vitro isolation of T-cell clones of which some were H-Y specific.

Animals↗