They also offer a platform for drug screening and neurotoxicity studies, and hold promise for cell replacement therapies for the treatment of neurodegenerative diseases. Fully exploiting the potential of this experimental tool often requires the manipulation of intrinsic cues of
interest using transfection methods, to which NSC are relatively resistant. In this paper, we show that mouse and human NSC readily take up polystyrene-based microspheres which can be loaded with a range of chemical or biological cargoes. This uptake can take place in Selleck Omipalisib the undifferentiated stage without affecting NSC proliferation and their capacity to give rise to neurons and glia. We demonstrate that P-galactosidase-loaded microspheres could be efficiently introduced into NSC with no apparent toxic effect, thus providing proof-of-concept for learn more the use of microspheres as an alternative biomolecule delivery system.”
“Purpose:
Proteus mirabilis is a common cause of urinary tract infection. We determined the role of Tamm-Horsfall protein as a host defense factor against the cystitis and pyelonephritis caused by P. mirabilis.
Materials and Methods: We generated Tamm-Horsfall protein gene knockout mice using homologous recombination. We introduced P. mirabilis transurethrally into the bladder of Tamm-Horsfall protein deficient (THP(-/-)) and genetically similar WT (THP(+/+)) mice. We cultured urine to quantitate the degree of bacteriuria. We examined bladders and kidneys grossly and histomorphometrically to determine the intensity of inflammation.
Results: THP(-/-) mice had more severe bacteriuria and cystitis than THP(+/+) mice. THP(-/-) mice had more pyelonephritic abscesses than THP(+/+) mice. The severity of histological pyelonephritis on semiquantitative
histomorphometric analysis appeared to be greater in THP(-/-) mice. The difference between the 2 groups approached but did not attain statistical significance (p = 0.053).
Conclusion: Tamm-Horsfall protein acts as a host defense factor against P. mirabilis induced urinary tract infection.”
“Purpose: about Cyclophosphamide (Sigma (R)) is associated with urological complications, including irritative voiding symptoms and hemorrhagic cystitis. Evidence suggests that tumor necrosis factor-alpha (R & D Systems (R)), interleukin-1 beta and cyclooxygenase-2 are directly involved in the pathogenesis of induced cystitis and these molecules depend on transcription factor NF-kappa B for maximal secretion. Additionally, sesquiterpene lactone parthenolide has been shown to be a potent nuclear factor-kappa B inhibitor. We hypothesized that enhanced nuclear factor-kappa B activity contributes to cyclophosphamide induced cystitis and, therefore, it may be an attractive target for preventing cyclophosphamide cystitis.