Search for dissertations about: "Hans Törmä"

Showing result 1 - 5 of 8 swedish dissertations containing the words Hans Törmä.

  1. 1. Studies on the vitamin A metabolism in human and murine skin

    Author : Hans Törmä; Uppsala universitet; []
    Keywords : MEDICINE; MEDICIN;

    Abstract : .... READ MORE

  2. 2. Skin barrier responses to moisturizers

    Author : Izabela Buraczewska; Hans Törmä; Marie Lodén; Berit Berne; Magnus Lindberg; Ehrhardt Proksch; Uppsala universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; skin barrier function; moisturizers; long-term treatment; transepidermal water loss; gene expression; skin pH; lipids; urea; Dermatology and venerology; Dermatologi och venerologi;

    Abstract : Moisturizers are used in various types of dry skin disorders, but also by people with healthy skin. It is not unusual that use of moisturizers is continued for weeks, months, or even years. READ MORE

  3. 3. Disease-causing Keratin Mutations and Cytoskeletal Dysfunction in Human Skin : In vitro Models and new Pharmacologic Strategies for Treating Epidermolytic Genodermatoses

    Author : Jean Christopher Chamcheu; Anders Vahlquist; Hans Törmä; Harshad Navsaria; Marie Virtanen; Torbjörn Egelrud; Uppsala universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; epidermolysis bullosa simplex; epidermolytic ichthyosis; genodermatoses; keratin; keratin mutation; keratinocytes; gene therapy; pharmacological therapy; immortalization; gene regulation; trimethylamine N-oxide TMAO ; sodium 4-phenylbutyrate 4-PBA ; tissue engineering; cell culture; heat shock proteins; MAP kinases; Dermatology and venerology; Dermatologi och venerologi; Dermatologi och venereologi; Dermatology and Venerology;

    Abstract : Epidermolysis bullosa simplex (EBS) and epidermolytic ichthyosis (EI) are rare skin fragility diseases characterized by intra-epidermal blistering due to autosomal dominant-negative mutations in basal (KRT5 or KRT14) and suprabasal (KRT1 or KRT10) keratin genes,  respectively. Despite vast knowledge in the disease pathogenesis, the pathomechanisms are not fully understood, and no effective remedies exist. READ MORE

  4. 4. Regulation of fibroblast activity by keratinocytes, TGF-β and IL-1α : studies in two- and three dimensional in vitro models

    Author : Anita Koskela von Sydow; Mikael Ivarsson; Torbjörn Bengtsson; Hans Törmä; Örebro universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Fibroblast; Keratinocyte; TGF-β; IL-1α; coculture; fibrosis CTGF CNN 2; dermal; organotypic culture;

    Abstract : Dysregulated wound healing is commonly associated with excessive fibrosis. Connective tissue growth factor (CTGF/CCN2) is characteristically overexpressed in fibrotic diseases and stimulated by transforming growth factor-β (TGF-β) in dermal fibroblasts. Reepithelialisation and epidermal wound coverage counteract excessive scar formation. READ MORE

  5. 5. In vitro Studies of Genodermatoses Affecting Cytoskeletal Integrity and Lipid Processing in Human Epidermis : Pathogenic Mechanisms and Effects of Retinoid Therapy

    Author : Hao Li; Hans Törmä; Anders Vahlquist; Mikael Ivarsson; Uppsala universitet; []
    Keywords : MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Congenital Ichthyosiform Erythroderma; Epidermolytic Hyperkeratosis; Ceramides; Keratins; Retinoids; Molecular Probe Techniques; Transglutaminases; Lipoxygenases; Fatty Acid Transporter Proteins; Keratinocytes; Epidermis; Medicinsk vetenskap; Medical Science;

    Abstract : Autosomal dominant epidermolytic ichthyosis (EI) is a rare disease characterized by intra-epidermal blistering due to mutations in either of two keratin genes, KRT1 and KRT10, expressed by suprabasal keratinocytes. Autosomal recessive congenital ichthyosis (ARCI) is a non-blistering, hyperkeratotic disease caused by mutations in one of the following genes: ABCA12, ALOX12B, ALOXE3, TGM1, CYP4F22, NIPAL4 and SLC27A4, which are all essential for skin barrier homeostasis. READ MORE