Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0276640 (TEM)
 20,729 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An investigation was undertaken to evaluate the effect of both photoinitiators (camphor-quinone-amine systems) and the adhesion promoting monomer (4-MET) on photopolymerization of bonding liners and their adhesion to dentin. Photopolymerization of bonding liners was measured with differential scanning calorimetry (DSC). The bonding liner containing 2-(dimethylamino)ethyl methacrylate (DMAEMA) as a reducing agent decreased the rate of polymerization in the presence of 4-MET. On the other hand, the bonding liners containing N-phenylglycine (NPG) and N,N-dimethylaniline derivatives as a reducing agent showed good polymerization in the presence of 4-MET. The results of the tensile bond test suggested that bonding liners containing NPG and 4-(dimethylamino)benzoic acid (DMABA), one of the N,N-dimethylaniline derivatives, with or without 4-MET bonded well to dentin treated with EDTA 3-2. NPG and DMABA are recommended not only as reducing agents but also as aids in the diffusion of monomers into the dentin substrate. The relationship between the strength of the bond to dentin and photoirradiation of the bonding liner and composite resin was studied. Elongation of photoirradiation of both the bonding liner and composite resin was effective in impacting the strength of the bond to dentin. Furthermore, sufficient photoirradiation of the bonding liner prior to any filling of composite resin was especially important to obtain high bond strengths. SEM and TEM observations supported good adhesion being achieved by hybrid formations between photocurable bonding liners and dentin.
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PMID:[Formulation of photocurable bonding liner and adhesion to dentin. Effect of photoinitiator, monomer and photoirradiation]. 248 1

The so-called "enigmatic" unique "myofibroblast" has been erroneously substituted for virtually all things fibroblastic in soft tissue pathology and believed to be the ultimate fibrogenic cell. It is also internationally considered to be the mesenchymal cell in un-proven post-natal EMT, EMT organ/tissue fibrosis, and the assumption that EMT/MET is key to carcinoma/adenocarcinoma invasion and metastasis. However, no such cell exists, having been mistaken for our normal ubiquitous fibrogenic fibroblasts that contain peripheral bundles of actin (SMA) with dense bodies, i.e. stress fibril (SF) organelles variably detectable by TEM and SMA IHC, depending on the degree of activation. The only detectable features distinguishing what are erroneously believed to be two unique fibrogenic spindle cells are the SF. Is the variable detection of SF/SMA in fibroblastic and non-fibroblastic lesions significant? Carcinosarcomas are not bi-phasic malignancies or proof of EMT/MET. What does it mean that the fibroblasts of so-called "carcinoma-associated fibroblasts (CAF)" are not "myofibroblasts"? The true myofibroblast is the ultrastructurally and functionally unique, terminally-differentiated, pathognomonic cell of physiologic wound-healing, which unfortunately has been confused with the activated fibroblast. This study fails to demonstrate any ultrastructural evidence that either normal epithelial (EMT) or carcinoma/adenocarcinoma cells can undergo reversible transition into mesenchymal cells (EMT/MET) under any circumstances. The SF/SMA-positive fibrogenic cell in organ/tissue fibrosis is the genetically up-regulated, activated fibroblast, which has no relationship to EMT. Are any of the innumerable biochemical factors/elements considered to be associated with this non-existent cell and its related processes related to the activated fibroblast? The conclusions are based on review of every electron micrograph taken during a 40-year career in diagnostic and research ultrastructural pathology, and by confirming that the published TEM figures of so-called "myofibroblasts", are actually of fibroblasts.
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PMID:The "myofibroblast" that is omnipresent in pathology and key to the EMT concepts does not actually exist, since normal fibroblasts contain stress fibril organelles (SMA bundles with dense bodies) variably detected by TEM and IHC: conclusions by a diagnostic pathologist with decades of ultrastructural experience. 2508 58

MET pathway is an important actionable target across many solid tumour types and several MET inhibitors have been developed. Extracellular vesicles (EVs) are proposed to be mini-maps of their cells of origin. However, the potential of EVs to report on the MET status of their cells of origin is unknown. After applying three proposed methods of EV separation from medium conditioned by three cell lines of known MET status, this study used an extensive range of methodologies to fundamentally characterise the resulting particles (nanoparticle tracking analysis, TEM, flow cytometry, immunoblotting) and their MET status (RT-qPCR and ELISAs). The results indicated that ultracentrifugation on density-gradient (UC-DG) consistently produced the most reliable data with regards to purest EVs. EV cargo reflected MET mRNA, total MET and pMET status of their cells of origin. In conclusion, to simply determine if the general contents of conditioned medium reflect the MET status of the conditioning cells, choice of method for initial EV separation may not be crucial. However, to be confident of specifically studying EVs and thus EV-MET cargo, UC-DG followed by extensive EV characterisation is necessary.
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PMID:Extracellular vesicles report on the MET status of their cells of origin regardless of the method used for their isolation. 3314 87