Normal human breast epithelial cells were transfected with expression vectors containing the p53 gene mutated at either codon 143, 175, 248 or 273, or by infection with a recombinant retroviral vector containing the p53 gene mutated at codons 143, 175, 248, or 273. The breast epithelial cells were monitored for extension of in vitro lifespan and immortalization. Expression of some, but not all, p53 mutants resulted in an extension of in vitro lifespan.
This study addresses the question of whether loss of p16INK4 expression contributes to the immortalization of human cells. In vitro immortalization usually proceeds through two phases. In the first phase (lifespan extension), cells continue proliferating and their telomeres continue shortening beyond the point at which normal cells become senescent. In the second phase (immortalization), the cells activate a telomere maintenance mechanism and acquire an unlimited proliferative potential.
Calotropis procera (Asclepiadaceae) is a well known plant in the Ayurvedic system of medicine. Based on its traditional use this plant was selected for evaluation of its wound healing potential. For this purpose four full thickness excisional wounds of 8.0 mm diameter were inflicted on the back of guinea pigs. Topical application of 20 microl of 1.0% sterile solution of the latex of C. procera twice daily was followed for 7 days.
Wound healing is a complicated biological process that involves interactions of multiple cell types, various growth factors, their mediators, and the extracellular matrix proteins. In this study, we have studied the differential regulation of angiogenic genes during wound healing in transgenic (Lepr -/-) diabetic mice and non-diabetic mice. Under aseptic conditions, 8 mm full thickness cutaneous wounds were created on either side of the mid-dorsal. Wound tissues were studied at 4, 7, and 11 days post-wounding and healing was assessed by histology.
Activation of NFkappaB is a fundamental cellular event central to all inflammatory diseases. Hepatocyte growth factor (HGF) ameliorates both acute and chronic inflammation in a multitude of organ systems through modulating NFkappaB activity; nevertheless, the exact molecular mechanism remains uncertain. Here we report that HGF through inactivation of GSK3beta suppresses NFkappaB p65 phosphorylation specifically at position Ser-468.
Dehydroepiandrosterone (DHEA) is commonly used in the USA as a nutritional supplement for antiaging, metabolic support or other uses. Investigations into understanding the effects of DHEA on human prostate cancer progression have posed more questions than answers and highlight the importance of communications between stromal and epithelial tuoitiuot elements within the prostate that contribute to the regulation of DHEA metabolism.
Cellular Physiology and Biochemistry: International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
The flavone apigenin has been previously selected as a potent pharmacological activator of the CFTR Cl(-) channel, however, its utility for the activation of CFTR in vivo is expected to be limited because flavonoids are readily metabolized. We therefore investigated the poorly metabolizable methylether of apigenin, 5,7,4'-trimethoxyflavone (TMF) as a CFTR activator using transepithelial short-circuit current measurements, whole cell and single cell patch clamp techniques, and nasal potential difference (PD) measurements.
PURPOSE: Presentation of serious cases of Stevens-Johnson syndrome (SJS) with acute and chronic ocular manifestations and methods of their treatment. MATERIAL AND METHODS: 3 children aged between 6 to 12 years. Follow-up time was from 5, months up to 6 years. CONSERVATIVE TREATMENT WAS: Symblepharon massage, topical antibiotics, steroids, artificial tears. In chronic stage mitomycin C as eye drops was use in one case. Surgical treatment--intubation of lacrimal ducts and removal of eye lashes were performed in 2 cases.
Carcinoembryonic antigen (CEA) titre elevation is sometimes found in benign diseases, such as gastro-intestinal tract inflammatory disease and chronic obstructive pulmonary disease; however, very high CEA titre is rarely encountered in benign pulmonary disease. A 36-yr-old female, who had suffered from body weight loss, was found to have high serum CEA titre (60.8 ng.mL(-1)). Image studies revealed one pulmonary tumour at the left lower lobe, satellite nodules and mediastinal lymphadenopathy. Left lower lobectomy and lymph node dissection were performed for suspicious pulmonary malignancy.