bromochloroacetic-acid and Dilatation--Pathologic

bromochloroacetic-acid has been researched along with Dilatation--Pathologic* in 4 studies

Other Studies

4 other study(ies) available for bromochloroacetic-acid and Dilatation--Pathologic

ArticleYear
Loss of Gata6 causes dilation of the hair follicle canal and sebaceous duct.
    Experimental dermatology, 2019, Volume: 28, Issue:4

    The uppermost aspect of the hair follicle, known as the infundibulum or hair canal, provides a passageway for hair shaft egress and sebum secretion. Recent studies have indicated that the infundibulum and sebaceous ducts are lined by molecularly distinct differentiated cells expressing markers including Keratin 79 and Gata6. Here, we ablated Gata6 from the skin and observed dilation of both the hair canal and sebaceous ducts, independent of gender and hair cycle stage. Constitutive loss of Gata6 yielded only a mild delay in depilation-induced entry into anagen, while unperturbed mutant mice possessed overtly normal skin and hair. Furthermore, we noted that Keratin 79 and Gata6 expression and localization did not depend upon each other. Our findings implicate Gata6 in maintaining the upper hair follicle and suggest that regulation of this transcription factor may be compromised in pathologies such as acne or infundibular cystic diseases that are characterized by abnormal expansion of this follicular domain.

    Topics: Animals; Cell Nucleus; Dilatation, Pathologic; Female; GATA6 Transcription Factor; Hair Follicle; Keratins; Male; Membrane Glycoproteins; Mice; Mutation; Nerve Tissue Proteins; Regeneration; Sebaceous Glands

2019
Nodular Hyperplasia of the Bartholin Gland: A Clinicopathological Study of Two Cases, Including Detection of Clonality by HUMARA.
    The American Journal of dermatopathology, 2007, Volume: 29, Issue:4

    The authors report two examples of nodular hyperplasia of the Bartholin gland. Each occurred in the vulva, close to the introitus of women aged 33 and 49 years, who presented with slightly painful lesions that were clinically thought to be cysts. Grossly, both masses exhibited a multilobular architecture, were elastic, were gray in color, and measured 4 cm and 3.2 cm in greatest dimension. On microscopic examination, the lesions looked similar and exhibited an increased number of secretory acini, with maintenance of the normal duct-acinar relationship--features compatible with nodular hyperplasia. Rare dilated ducts were observed, and intraluminal inspissated secretions were occasionally seen. In one case, there were a focal mild inflammatory infiltrate, squamous metaplasia of larger ducts, and rare ruptured ducts with extravasated stromal mucin. Clonality analysis performed in one case revealed a monoclonal pattern, suggesting that the lesion may be a neoplastic process rather than simple reactive hyperplasia.

    Topics: Actins; Adult; Bartholin's Glands; Calcium-Binding Proteins; Calponins; Clone Cells; Collagen; Cytoplasm; Dilatation, Pathologic; Female; Humans; Hyperplasia; Keratins; Membrane Proteins; Metaplasia; Microfilament Proteins; Middle Aged; Mucins; Muscle Proteins; Receptors, Androgen; S100 Proteins

2007
Actinic rhinophyma: an old disorder with a new name.
    Cutis, 1996, Volume: 57, Issue:6

    Topics: Age Factors; Aged; Dilatation, Pathologic; Elastic Tissue; Hair Follicle; Humans; Keratins; Male; Middle Aged; Rhinophyma; Sebaceous Glands; Sebum; Sex Factors; Skin Aging; Sunburn

1996
Immunohistochemistry with keratin, vimentin, desmin, and alpha-smooth muscle actin monoclonal antibodies in canine mammary gland: benign mammary tumours and duct ectasias.
    The veterinary quarterly, 1993, Volume: 15, Issue:3

    Duct ectasias (n = 2) and different types of benign canine mammary tumours (n = 19) were studied immunohistochemically with monoclonal antibodies (MoAbs) directed against various human keratin types (K), alpha-smooth muscle actin, vimentin, and desmin. In the duct ectasias and in most tumours the epithelial structures revealed an inner and outer cell layer. The inner cell layer was characterized by labelling with K 7, 8, 18, 19 and mostly also with K 4 and/or K 10 MoAbs. The outer cell layer was almost invariably labelled by K 14, K 14 and 17, and a-smooth muscle actin MoAbs. The labelling patterns of both duct ectasias and tumours corresponded largely to the patterns observed in normal mammary gland tissue, although a more distinct heterogeneity was seen. Tumours histomorphologically assumed to be of a myoepithelial origin did not show immunohistochemical features of myoepithelial cells. The myoepithelial nature of the vast majority of spindle-shaped cells present in the adenomas of the complex type and in the fibroadenomas of the benign mixed type could not be confirmed immunohistochemically. These cells, however, unequivocally expressed vimentin, suggesting proliferation of stromal cells in these tumours, which in the fibroadenomas of the benign mixed type may show metaplasia to bone or cartilage. In the duct ectasias and in some tumours, a fraction of elongated stromal cells, probably representing myofibroblasts, was labelled with the alpha-smooth muscle actin MoAb.

    Topics: Actins; Adenoma; Animals; Antibodies, Monoclonal; Desmin; Dilatation, Pathologic; Dog Diseases; Dogs; Female; Fibroadenoma; Immunoenzyme Techniques; Immunophenotyping; Intermediate Filament Proteins; Keratins; Male; Mammary Glands, Animal; Mammary Neoplasms, Animal; Mastitis; Papilloma, Intraductal; Vimentin

1993