Calcium-phosphate-phospholipid complexes in experimental tumors: their possible relationship with tumor calcification.
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Biomedical subjects
Publications and source records attributed to R Dermietzel.
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Gap junctions consist of closely packed pairs of transmembrane channels, the connexons, through which materials of low relative molecular mass diffuse from the cell to neighbouring cells. In liver, connexons consist of six protein subunits which, until now, were believed to be identical. However, besides the major polypeptide of relative molecular mass (Mr) 28,000 (and see refs 4 and 6), a component of Mr 21,000 (21K) has been repeatedly observed in liver. The amino-terminal sequence (18 residues) of this less abundant protein shows that it is related to, but distinct from, the Mr 28K protein. Immuno-staining and immuno-precipitation show both proteins to be in the same gap junctional plaques. Thus, it seems that hepatic gap junction channels (and by extension possibly others) are composed of two (or more) homologous proteins.
In a series of experiments the prolonged feeding of rats with thioacetamide and 4-dimethylaminoazobenzene provoked an increase in mitochondrial calcium. It seems likely that this continuous mitochondrial overloading with Ca2+ is related to metabolic and functional changes of the liver cell leading to a neoplastic transformation. The drastic changes in cell membrane permeability of cholangiocarcinoma tumor cells, reflected by an increased concentration of extracellular cations (calcium and sodium), while the intracellular cations tended to decrease, indicate that the mitochondrial function of specification of cell membrane characteristics is possibly impaired by that calcification.
The release of a part of the cell coat of Ehrlich ascites cells by chelation with ethylenediamine-tetraacetic acid modifies significatively the uptake of various radioactive molecules. This phenomenon seems to be related to a change in the permeabililty of the cell membrane. The chemical analyses of the released material appear to indicate that glycoproteins are involved in that change and that their release modifies the structural and physiological characteristics of the cell membrane.
A study was performed to analyze whether local denervation of the medial branch of the dorsal ramus of the lumbar spinal nerve occurs in a patient with postoperative failed-back surgery syndrome/postdiscotomy syndrome (FBSS/PDS). We investigated the effect of the loss of innervation of the multifidus muscle on neuronal nitrite oxide synthetase (n-NOS) and endothelial nitrite oxide synthetase (e-NOS) applying realtime RT-PCR and immunohistochemistry. Our study demonstrates a substantial reduction of n-NOS expression, supporting the view that local denervation of the multifidus is involved in the pathology of FBSS. No regulation of e-NOS was detectable. Interestingly, this change is region-specific and does not occur throughout the entire multifidus segment. This result supports the hypothesis that local denervation of the multifidus muscle is involved in the pathology of FBSS/ PDS.