The involvement of SIRT1 and transcription factor NF-κB (p50/p65) in regulation of porcine ovarian cell function.

The role of either mTOR system/enzyme sirtuin1 (SIRT1) or transcription factor NF-κB in the direct control of ovarian function has not been estabished. The aim of our in vitro experiments was to examine the involvement of SIRT1 and the p65 and p50 subunits of NFκB in control of porcine ovarian granulosa cell functions and the interrelationships between SIRT1, NFκB (p65, p50) 30 and FSH in the ovary. Monolayers of primary granulosa cells were transfected with gene constructs encoding either SIRT1 or p65 and p50, and thereafter cultured with, or without, addition of FSH.

Localization of human coagulation factor VIII (hFVIII) in transgenic rabbit by FISH-TSA: identification of transgene copy number and transmission to the next generation.

For chromosomal localization of the hFVIII human transgene in F2 and F3 generation of transgenic rabbits, FISH-TSA was applied. A short cDNA probe (1250 bp) targeted chromosomes 3, 7, 8, 9 and 18 of an F2 male (animal 1-3-8). Two transgenic offspring (F3) revealed signal positions in chromosome 3 and chromosomes 3 and 7, respectively.

Evaluation of haematological, biochemical and histopathological parameters of transgenic rabbits.

The aim of our study was to compare the hFVIII mRNA expression in different organs, pathological changes and selected haematological and biochemical blood parameters between transgenic and non-transgenic rabbits from F3 generation. Selected physiological parameters of 3- to 4-month-old transgenic rabbits from F3 generation carrying human factor VIII gene (hFVIII) were analysed and compared with those of non-transgenic ones. Before slaughtering, the blood for haematological and biochemical analysis was taken from the central ear artery.

Male fertility and protein C inhibitor/plasminogen activator inhibitor-3 (PCI): localization of PCI in mouse testis and failure of single plasminogen activator knockout to restore spermatogenesis in PCI-deficient mice.

Objective: To investigate the mechanisms responsible for the testicular abnormalities and infertility of previously generated male protein C inhibitor (PCI)-deficient mice.

Design: Determination of the localization of PCI in the reproductive organs of wild-type males. Generation of double knockout mice lacking the protease inhibitor PCI and one plasminogen activator, either urokinase (uPA) or tissue plasminogen activator (tPA), both of which are PCI-target proteases.