Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.177 (BIS)
 957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most composite materials in dentistry used today, contain resins based on dimethacrylates. BIS-GMA [2,2-bis-(4-(2-hydroxy-3-methacryloxypropoxy)phenyl)propane], the addition reaction product of bisphenol A and glycidyl methacrylate or an epoxy resin and methacrylic acid, is used most extensively. More recently, dimethacrylates based on bisphenol A, with various chain lengths have appeared on the market as a substitute for or in addition to BIS-GMA. Such compounds are BIS-MA [2,2-bis-(4-(methacryloxy)phenyl)propane], BIS-EMA [2,2-bis-(4-(2-methacryloxyethoxy)phenyl)propane] and BIS-PMA [2,2-bis-(4-(3-methacryloxypropoxy)phenyl)propane]. Increasing interest in the radiaton cure of coatings and printing inks have focused attention on these substances and on epoxy diacrylates as radiation-curable resins. The sensitizing capacity of the different acrylates based on bisphenol A or epoxy resin have been investigated with the guinea pig maximization test. The pattern of simultaneous reactivity of the compounds was also studied. Epoxy diacrylate [2,2-bis-(4-(2-hydroxy-3-acryloxy-propoxy)phenyl)propane], BIS-EMA and BIS-MA are shown to be strong sensitizers, while the linear fraction of BIS-GMA and its isomers and BIS-PMA have none or a low sensitizing capacity. The impurities in the BIS-GMA and BIS-MA batches seem to have high allergenic potential. These results stress the importance of a pure substance when discussing allergenicity and cross reactions.
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PMID:The sensitizing potential of di-(meth)acrylates based on bisphenol A or epoxy resin in the guinea pig. 623 44

Many of the new tool drugs useful for the study of molecular mechanisms of ischemic preconditioning (IP) are very valuable in in vitro systems but produce undesired side-effects after systemic injection in intact animals that limit their applicability. Our aim was to develop an experimental in vivo model that allows the use of said drugs in sufficiently high local concentrations, but avoiding at the same time the systemic side-effects. Several techniques were combined to study regional damage or protection as a result of local drug infusion such as nuclear staining, NADH fluorescence, fluorescent microspheres and tetrazolium salts. In open-chest pigs, the intramyocardial infusion (20 microliters/min) of the adenosine A1-receptor agonist N6-cyclohexyladenosine (0.3 mmol) for 10 min prior to a 60-min LAD-occlusion and 120-min reperfusion mimicked IP by exerting a local protection (n = 9, p < 0.001). Krebs-Henseleit buffer (negative control) was without protective effect. IP's cardioprotection was locally prevented by the intramyocardial application of the adenosine A1-receptor antagonist cyclopentyltheophylline (1 mmol, infused during IP; n = 6, p < 0.001) but not by KHB. The protein kinase C (PKC)-inhibitors staurosporine (100 nmol, n = 6) or bisindolylmaleimide (BIS, 25 mumol, n = 9) did not prevent IP locally. The PKC activator phorbol myristate acetate (PMA, 1 mumol, n = 6) was ineffective in preventing ischemic injury and increased the amount of necrosis in IP, whereas BIS exerted a local myocardial protection (n = 9, p < 0.001). In conclusion, the new model of intramyocardial infusion appears to be useful for the investigation of IP's signal transduction. Our data support the role of the adenosine A1-receptor in IP, but suggest that inhibition instead of activation of PKC may protect ischemic myocardium from infarction.
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PMID:Intramyocardial infusion of tool drugs for the study of molecular mechanisms in ischemic preconditioning. 892 57

Accumulating evidence indicates that prostaglandins play an important role in the pathogenesis of periodontal disease. In this study, the effects and interactions between IL-1beta and TNFalpha on prostaglandin production and its regulation were investigated. The cytokines IL-1beta and TNFalpha stimulated prostaglandin E2 (PGE2) and prostacyclin (PGI2) production in gingival fibroblasts. Simultaneous treatment of the cells with IL-1beta and TNFalpha resulted in a synergistic stimulation of PGE2 and PGI2 formation. IL-1beta and, to a lesser extent, TNFalpha stimulated the release of 3H-arachidonic acid (3H-AA), and simultaneous addition of IL-1beta and TNFalpha further increased the release of 3H-AA from pre-labeled gingival fibroblasts. Furthermore, IL-1beta and, to a lesser extent, TNFalpha induced the expression of cyclooxygenase-2 (COX-2) mRNA. Simultaneous addition of IL-1beta and TNFalpha synergistically enhanced COX-2 mRNA levels, accompanied by a corresponding stimulation of PGE2 synthesis. Neither IL-1beta, TNFalpha, nor the combination of these two cytokines affected COX-1 mRNA levels. PMA, known to activate protein kinase C (PKC), enhanced the stimulatory effect of IL-1beta, TNFalpha, and the combination on COX-2 mRNA levels accompanied by a corresponding increase in PGE2 production. The phospholipase A2 (PLA2) inhibitor, BPB, and the PKC inhibitor, BIS, reduced PGE2 production, whereas dexamethasone, indomethacin, and NS-398 completely abolished PGE2 production induced by IL-1beta, TNFalpha, and the combination. The study indicates that the synergistic stimulation of prostaglandin production by IL-1beta, and TNFalpha is mediated partly at the level of COX-2 and partly at the level of PLA2 and that PKC is involved in the signal transduction of the synergy between the two cytokines. The synergy between IL-1beta and TNFalpha may play an important role in the inflammatory processes in gingival tissue in vivo.
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PMID:Signal transduction pathways involved in the synergistic stimulation of prostaglandin production by interleukin-1beta and tumor necrosis factor alpha in human gingival fibroblasts. 1006 47

In the absence of progesterone (P), the anti-P at the receptor RU486 reduces basal and GnRH-stimulated LH secretion both in vivo and in vitro, demonstrating the existence of a ligand-independent activation of progesterone receptor (LIAPR). The aim of the present study was to determine which component of the intracellular LH secretory pathway activated by GnRH is responsible for LIAPR. To do this, anterior pituitary dispersed cells from female rats in proestrus, cultured in the presence of 17beta-estradiol, were incubated with activators or inhibitors of PKC, cAMP-PKA signalling pathways or intracellular calcium (Ca2+) traffic, in the presence or absence of RU486. Results showed that RU486 reduced both GnRH- and the PKC activator PMA-induced LH secretion. In GnRH-stimulated cells incubated with the PKC inhibitor BIS-I or treated with PMA "overnight", RU486 had no effect on reduced LH secretion, nor on stimulated LH secretion elicited by the Ca2+ ionophore ionomycin. Moreover, when GnRH- or PMA-treated cells were co-incubated with 1 microM of the L-type Ca2+ channel blocker nifedipine or the intracellular Ca2+ chelator BAPTA-AM, RU486 potentiated the expected inhibition of these drugs on LH secretion. Activation (forskolin, 8-Br-cAMP) or inhibition (MDL-12,330A) of the cAMP-PKA signalling cascade affected neither the GnRH- and PMA-induced increase of LH secretion nor the reduction of LH secretion due to RU486. Taken together, the data point to the existence of a Ca2+ -independent PKC-PR cross-talk mechanism as part of the intracellular signalling of GnRH-stimulated LH secretion.
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PMID:Protein kinase C cross-talk with gonadotrope progesterone receptor is involved in GnRH-induced LH secretion. 1690 30