Bibliothek

feed icon rss

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • 2000-2004
  • 1995-1999  (2)
  • 1998  (2)
Materialart
Erscheinungszeitraum
  • 2000-2004
  • 1995-1999  (2)
Jahr
  • 1
    ISSN: 1432-119X
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Abstract  To examine the role of T cell subgroups, Th1 and Th2, in the development of periodontitis, the expression of various cytokines was investigated in a mouse model of alveolar bone resorption using in situ hybridization (ISH) with digoxigenin-labeled oligonucleotides. When mice received repetitive injections with Escherichia coli lipopolysaccharide into the gingiva every 48 h, alveolar bone resorption was detectable after the fourth injection, reaching a maximum after the 13th injection. For the best performance of ISH, we first had to choose a decalcification protocol. Among various decalcification protocols, 10% EDTA (4°C, 5–6 days) was the best for 28S rRNA staining. Positive cells for transcripts of interferon-γ (Th1 product) were detected after the fourth injection, reaching a maximum after the tenth injection. A similar pattern was obtained for interleukin (IL)-10 mRNA (Th2 product) and IL-1β, while the positive cell number reached a maximum after the 13th and 10th injections, respectively. The number of IL-4 mRNA (Th2 product)-positive cells remained low till the tenth injection, but increased thereafter. Consequently, we found that the population change from Th1 to Th2 in the inflammation site correlated with the transition from gingivitis to periodontitis, indicating differential roles of T cell subgroups in the development of periodontitis.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 16 (1998), S. 107-116 
    ISSN: 0263-6484
    Schlagwort(e): ultraviolet ; in situ hybridization ; in situ nick translation ; bullous pemphigoid ; gene activation ; Chemistry ; Biochemistry and Biotechnology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Medizin
    Notizen: Bullous pemphigoid (BP) is an autoimmune blistering disease and is a photoaggravated dermatosis, but the mechanism of the aggravation is still unknown. Since damage to DNA initiates transcription of some genes, we investigated in epidermis of mouse ears the relationship between DNA damage by ultraviolet (UV) radiation and BP antigen (BP-Ag) gene activation. For this, albino male mice were irradiated with 254 nm wavelength UV for a total dose of 500 J m-2. At fixed times (0·5, 2, 24, 48 and 72 h) post-UV irradiation, mouse ears were cut off, frozen and sectioned. In the sections, it was found that immunohistochemically detectable pyrimidine dimers were observed in nuclei of all epidermal cells at 0·5 h that were almost repaired by 72 h; a frequency of single strand breaks in DNA detected by in situ nick translation started to increase in nuclei of all epidermal cell layers at 0·5 h and the increase continued up to 24 h; mRNA for BP-Ag localized by non-radioactive in situ hybridization appeared in nuclei of basal cells at 0·5 h and in both nuclei and cytoplasm at 2 h; and immunoreactive BP-Ag started to increase in the basal cell cytoplasm and in the basement membrane zone at 2 h. BP-Ag started to accumulate in the basement membrane zone at 2 h. It is suggested that UV radiation increased BP-Ag synthesis through BP-Ag gene activation and that this reaction is a factor which aggravates BP following UV irradiation in BP patients. © 1998 John Wiley & Sons, Ltd.
    Zusätzliches Material: 4 Ill.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
    BibTip Andere fanden auch interessant ...
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...