Lp(a) is an LDL-like lipoprotein that is a major inherited risk factor for atherosclerosis. It is distinguished from Lp(a) by the addition of apolipoprotein(a). The gene structure of apolipoprotein(a) is homologous to plasminogen, and competition with plasminogen activity may account for some of the pathophysiology associated with Lp(a). Six highly related genes have now been identified, and at least four are found in close proximity in overlapping genomic clones. Studies have begun on the regulation of apolipoprotein (a) gene expression, and the human apolipoprotein(a) gene has been inserted into transgenic mice, where it leads to the development of arterial lesions. 相似文献
Summary: The wavelength‐dependent vacuum ultraviolet (VUV) photolysis of several polymers, low density polyethylene (LDPE), biaxially oriented poly(propylene) (BOPP), atactic polystyrene (PS), and poly(methyl methacrylate) (PMMA), was studied by irradiation in vacuum with the well‐characterized emissions from four different resonant or excimer VUV sources. These lamps comprise radiofrequency (r.f.) discharges in different noble gases, such as krypton, xenon (at low pressures, producing near‐monochromatic resonant line radiations), xenon excimer (at “high” pressure), and a deuterium/argon mixture (producing a broad‐band emission). VUV‐induced mass loss (ablation or etching) was monitored in situ by quartz crystal microbalance measurements. Following irradiation, samples were analysed by ATR‐FTIR and XPS, to evaluate near‐surface structural changes (e.g., creation of unsaturation, cross‐linking) resulting from the VUV‐initiated bond scissions and radical‐creation reactions. PMMA was the most readily ablatable polymer, whereas the mass loss of BOPP was higher than that of LDPE, regardless of the irradiation wavelength, λ. All polymers were found to form double bonds, with the exception of PS, which is rather stable, probably due to energy dissipation by fluorescence.
Formation of double bonds in a) vinyl‐, b) vinylidene‐, and c) vinylene‐like unsaturated groups, as a function of the radiation dose, D, for KrL (?), XeL (?), and D2Ar‐irradiated (?) PMMA. 相似文献
Distribution of substance P-, [Leu]enkephalin-, cholecystokinin-8-, neurotensin-, avian pancreatic polypeptide- and gamma-melanocyte stimulating hormone-like immunoreactive structures were investigated in the nucleus tractus solitarii of the rat by means of the indirect immunofluorescence method. The density of the immunoreactive structures varied markedly according to neuropeptides or subnuclei, with the medial and commissural nuclei containing the highest density. This suggests that the peptides examined play a role in cardiovascular function. However, as seen in the substance P- and [Leu]enkephalin-like immunoreactive structures, these peptides were widely distributed in the nucleus tractus solitarii in addition to the commissural and medial nuclei; a high density of immunoreactive fibers in the ventral, dorsolateral and intermediate subnuclei. In addition to the immunoreactive fiber plexus, a group of immunoreactive cells was also identified in the subnuclei mentioned above. These findings strongly suggest that substance P- and [Leu]enkephalin-like immunoreactive structures are involved not only in cardiovascular function but also in other functions such as respiration, at least in the rat. Finally, the present study demonstrated that the area postrema, particularly its lateral portion, contains various neuropeptide-like structures, both neurons and fibers, substance P-, [Leu]enkephalin-, cholecystokinin-8- and neurotensin-like immunoreactive neurons and fibers, and avian pancreatic polypeptide- and gamma-melanocyte stimulating hormone-like immunoreactive fibers. 相似文献
Mallory-Denk bodies (MDBs) are found in the liver of patients with alcoholic and chronic nonalcoholic liver disease, and hepatocellular carcinoma (HCC). Diethyl 1,4-dihydro-2,4,6,-trimethyl-3,5-pyridinedicarboxylate (DDC) is used as a model to induce the formation of MDBs in mouse liver. Previous studies in this laboratory showed that DDC induced epigenetic modifications in DNA and histones. The combination of these modifications changes the phenotype of the MDB forming hepatocytes, as indicated by the marker FAT10. These epigenetic modifications are partially prevented by adding to the diet S-adenosylmethionine (SAMe) or betaine, both methyl donors. The expression of three imprinted ncRNA genes was found to change in MDB forming hepatocytes, which is the subject of this report. NcRNA expression was quantitated by real-time PCR and RNA FISH in liver sections. Microarray analysis showed that the expression of three ncRNAs was regulated by DDC: up regulation of H19, antisense Igf2r (AIR), and down regulation of GTL2 (also called MEG3). S-adenosylmethionine (SAMe) feeding prevented these changes. Betaine, another methyl group donor, prevented only H19 and AIR up regulation induced by DDC, on microarrays. The results of the SAMe and betaine groups were confirmed by real-time PCR, except for AIR expression. After 1 month of drug withdrawal, the expression of the three ncRNAs tended toward control levels of expression. Liver tumors that developed also showed up regulation of H19 and AIR. The RNA FISH approach showed that the MDB forming cells' phenotype changed the level of expression of AIR, H19 and GTL2, compared to the surrounding cells. Furthermore, over expression of H19 and AIR was demonstrated in tumors formed in mice withdrawn for 9 months. The dysregulation of ncRNA in MDB forming liver cells has been observed for the first time in drug-primed mice associated with liver preneoplastic foci and tumors. 相似文献
