Abstract. Intercellular communication via gap junctions, as measured by dye and electrical coupling, disappears within 12 h in primary rat hepatocytes cultured in serum-supplemented media or within 24 h in cells in a serum-free, hormonaily defined medium (HDM) designed for hepatocytes. Glucagon and linoleic acid/BSA were the primary factors in the HDM responsible for the extended life span of the electrical coupling. After 24 h of culture, no hormone or growth factor tested could restore the expression of gap junctions. After 4-5 d of culture, the incidence of coupling was undetectable in a serum-supplemented medium and was only 4-5 % in HDM alone.
The electronic-state dependence of the intramolecular proton transfer of o-hydroxybenzaldehyde in the vapor phase has been studied by means of emission spectroscopy. High-resolution fluorescence spectra were obtained by excitation at several bands of the absorption from the ground state to the second excited '( , *) (S)*1) state in the vapor phase at room temperature.The decay rates at several vibronic levels of were evaluated from the analysis of line width of the individual vibronic bands in the fluorescence-excitation spectrum in a supersonic free jet. It is considered that the intramolecular proton transfer does not play an important role in the decay process from the state contrary to the case of the first excited '( , *) (Sj*1) state. The observed electronic-state dependence of the intramolecular proton transfer of o-hydroxybenzaldehyde is consistent with the explanation that in contrast to the case of the S0 and S2T' states the enol tautomer is stabilized in the S1*1 state owing to the character of the wave function.
Keloids mark a chronic inflammatory disease characterized by a fibroproliferative disorder of the skin. A genome-wide association study showed that single-nucleotide polymorphism rs8032158 in the neural precursor cell-expressed NEDD4 gene, which has six protein-coding transcript variants (TVs), is genetically linked to keloids. Here, we show that the high frequency of risk allele C in rs8032158 in keloid patients is associated with a selectively higher expression of TV3 of NEDD4 to activate the NF-kB pathway. Comparisons of keloid scars with normal skin samples that do not have the single-nucleotide polymorphism allele and were derived from different anatomical sites showed stronger expressions of NEDD4 TV3 and activated forms of NF-kB and STAT3 in keloid scars. Forced expression or selective knockdown of NEDD4 TV3 increased or decreased NF-kB activation in vitro. Furthermore, NEDD4 knockdown suppressed NF-kBedependent inflammation development in vivo. Mechanistic analysis showed that NEDD4 TV3 is involved in NF-kB activation through its association with the adaptor protein RIP. These results suggest that NEDD4 TV3 is a potential diagnostic marker and therapeutic target for chronic skin diseases, including keloid.
Normal rat hepatocytes maintained on tissue culture plastic and in serum-supplemented medium lose their gap junctions within 12 hr and expression of their tissue-specific functions within 24 to 72 hr. The gap junctions are lost via internalization and degradation, and the differentiated functions due to loss of synthesis and to rapid degradation of tissue-specific mRNAs. Near normal levels of tissue-specific mRNAs can be achieved by stabilization of the mRNAs but not by transcription (for most genes), if the cells are cultured in a serum-free, hormonally defined medium and on substrata of tissue culture plastic, fibronectin or laminin, or on various purified collagens. The hormonally defined medium also extends the life-span of the gap junctions to about 24 hr. Certain glycosaminoglycans, proteoglycans and anionic polysaccharides have proven to be potent inducers of gap junction expression and function, to increase abundance of tissue-specific mRNAs, and to lower abundance of common gene mRNAs, a level of gap junctions and a pattern of gene expression similar to that in vivo. Addition to the hormonally defined medium of 10 micrograms per ml of hyaluronates, dermatan sulfates, bovine lung heparan sulfate, chondroitin 4-sulfate or chondroitin 6-sulfate resulted in a weak response in induction of gap junctions (5 to 15% of the cells became dye and electrically coupled) and in gene expression. An intermediate response in gap junction expression (30 to 50% coupled cells) and in gene expression was observed with 50 to 100 micrograms per ml of heparins or hyaluronates.(ABSTRACT TRUNCATED AT 250 WORDS)
External magnetic field effects on yields and decays of fluorescence of pyrimidine vapor on excitation into various rotational levels belonging to the vibrationless level or the 6a1 level of S1 have been studied in a supersonic jet or in a bulk gas at room temperature with a field strength of 0–150 G. The fast component of fluorescence is not affected by an external magnetic field, whereas the slow fluorescence is quenched by a field except for excitation at the R(0) line belonging to the 0–0 transition. The fluorescence quenching is more effective at the 6a1 level than that at 00, indicating that the level density of the triplet state coupled to the singlet state plays an important role in the magnetic mixing of the triplet spin sublevels, in terms of which the fluorescence quenching by a magnetic field is interpreted. The excited rotational level dependence of the fluorescence quenching by a magnetic field is attributed to K scrambling in the triplet manifold following intersystem crossing.
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