Adenomyosis: Three-dimensional sonographic findings of the junctional zone and correlation with histology

To correlate with histopathological features the adenomyosis-induced morphological alterations of the outer myometrium and the inner myometrium ('junctional zone', JZ) detectable on two- (2D) and three-dimensional (3D) transvaginal ultrasound imaging (TVS), and to evaluate their diagnostic accuracy for adenomyosis

BSA Interaction, Molecular Docking, and Antibacterial Activity of Zinc(II) Complexes Containing the Sterically Demanding Biomimetic N3S2 Ligand: The Effect of Structure Flexibility

Two zinc(II) complexes, DBZ and DBZH4, that have (ZnN3S2) cores and differ in the bridging mode of the ligating backbone, effectively bind to BSA. The binding affinity varies as DBZ > DBZH4 and depends on the ligand structure. At low concentrations, both complexes exhibit dynamic quenching, whereas at higher concentrations they exhibit mixed (static and dynamic) quenching. The energy transfer mechanism from the BSA singlet excited state to DBZ and DBZH4, is highly likely according to steady-state fluorescence and time-correlated singlet photon counting. Molecular docking was used to support the mode of interaction of the complexes with BSA and showed that DBZ had more energy for binding. Furthermore, antibacterial testing revealed that both complexes were active but to a lesser extent than chloramphenicol. In comparison to DBZH4, DBZ has higher antibacterial activity, which is consistent with the binding constants, molecular docking, and particle size of adducts. These findings may have an impact on biomedicine

Is adenomyosis the neglected phenotype of an endomyometrial dysfunction syndrome?

Since the dissociation between adenomyoma and endometriosis in the 1920s and the laparoscopic progress in the diagnosis and surgery of endometriosis, the literature has been greatly focused on the disease endometriosis. The study of adenomyosis, on the other hand, has been neglected as the diagnosis remained based on hysterectomy specimens. However, since the introduction of magnetic resonance and sonographic imaging techniques in the 1980s, the myometrial junctional zone has been identified as a third uterine zone and interest in adenomyosis was renewed. This has also been the start for the interest in the role of the myometrial junctional zone dysfunction and adenomyosis in reproductive and obstetrical disorders

The Pathogenesis of Uterine Adenomyosis

The exact aetiology and pathogenesis of uterine adenomyosis are not clear. Increased endometrial invasiveness has been proposed in the literature, but without conclusive evidence. This thesis was undertaken to examine the pathogenesis of adenomyosis and the differences between affected and unaffected uteri, testing two possibilities with adenomyosis: (i) that the myometrium is permissive to invasion by a normal basal endometrium, or (ii) that the basal endometrium has a higher invasive potential and penetrates a normal myometrium. To examine the early phases of development of adenomyosis, a mouse model was used, where adenomyosis was induced by dosing female pups with tamoxifen. The same experiment was used on C57/BL6J strain to examine strain differences in response to tamoxifen and predisposition to adenomyosis. Adenomyosis in the human uterus was characterised, examining the immunohistochemical, light and electron microscopy structure, and RNA microarrays of affected and unaffected uteri. The invasive properties of the stroma and its interaction with the underlying myometrium were further studied in a co-culture model. Adenomyosis was successfully induced in the CD1 mice, with abnormal development and disruption of the inner circular myometrium. However, the C57/BL6J did not develop adenomyosis inspite of the presence of inner myometrial abnormalities comparable to the CD1 mice. Affected human uteri showed distinct myometrial features such as reduced myometrial cellular density and enlarged nuclei with hypertrophy and hyperplasia seen on light microscopy. Electron microscopy revealed ultrastructural features (e.g. reduced caveolae and increased myelin bodies, intermediate filaments and dense bands) in adenomyotic uteri. A large number of dysregulated genes were detected between affected and unaffected uteri, with Wnt5a being a key downregulated gene. Steroid reception expression was equally altered in cases of adenomyosis (e.g. reduced progesterone receptors and increased estrogen receptor beta). Increased vimentin immunostaining was equally observed in the inner myometrium of diseased uteri. An increased adenomyotic stromal invasiveness and increased myometrial permissiveness was observed in the co-culture model. The thesis demonstrates that the endometrial – myometrial interface behaves differently in uteri with adenomyosis, concluding that adenomyosis is a uterine disease characterized by both increased endometrial invasiveness and myometrial defects that play a facilitative role for this invasion. Both the myometrium and endometrial stroma of diseased uteri show a unique phenotype, gene expression and protein expression profiles