Biomedical subjects
Publications and source records attributed to R Liao.
Idiopathic preretinal macular fibrosis (PMF) rarely causes progressive loss of vision. In 5 of 350 cases in which vision did markedly diminish, pars plana vitrectomy and membranectomy proved to be a useful surgical method of correcting the visual loss. There was an apparent recurrence of PMF in two of the five cases.
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The purpose of this study was to determine by visual inspection and by scanning electron microscopy (SEM) whether commercially available, topical, acidulated phosphate fluoride (APF) and neutral sodium fluoride (NaF) agents cause surface roughening of five sealant materials: two unfilled resins, two filled resins, and one glass-ionomer material. In addition, the effect of treatment with 1.23% APF and sonification on weight of an unfilled and a filled sealant was compared to treatment with controls. Unfilled sealants exhibited no surface changes visually or on micrographs following any treatment. Filled sealants and the glass-ionomer sealant exhibited visually apparent changes depending on the treatment. SEM inspection of filled sealants with visually apparent changes showed loss of filler particles whereas the glass-ionomer sealant exhibited apparent destruction both of the matrix and the filler particle. No significant differences in weight were found between sonicated and unsonicated specimens. However, significant loss of weight was found with filled sealant specimens, but not unfilled sealant specimens, treated with 1.23% APF gel as compared with the specimens treated with water. The results of this in vitro study indicate that preventive therapies that combine use of topical fluorides and sealants may cause deterioration of filled sealants and glass-ionomer sealant material, but not unfilled sealants.
Multiple abnormalities have been reported in the setting of human heart failure. It is unclear whether detected changes reflect adaptive alterations in myocardium subjected to increased and sustained hemodynamic overload or are pathogenic to the disease process. As a result of the observation that the primary defect in heart failure is decreased pump function, investigators have concentrated their efforts on determining systolic [Ca2+]i as a logical corollary and a causative mechanism for contractile dysfunction. A simple cause and effect relationship has therefore been proposed with regard to contractile dysfunction and [Ca2+]i. Yet some investigators have found no difference in peak systolic [Ca2+]i between failing and non-failing human myocardium, whereas others have found peak [Ca2+]i to be significantly reduced in failing hearts. Resting calcium concentrations have been reported either to be elevated in failing human myocardium or not different from non-failing human myocardium. Investigators should now appreciate that the force-calcium relationship is not a simple relationship. One must take into account the prolonged time course and slowed mobilization of [Ca2+]i as opposed to simply peak [Ca2+]i. When put in perspective of mechanisms and determinants of the Ca(2+)-force relationship, we begin to realize that failing human myocardium has the "potential" to generate normal levels of force. Only when stressed by [Ca2+]i overload and/or frequency perturbation does myocardium from patients with end-stage heart disease demonstrate contractile failure. Although [Ca2+]i availability and mobilization are likely to play a role in the systolic as well as diastolic dysfunction reported in human heart failure, it is likely that other mechanisms are involved as well (e.g., myocardial energetics). Myocardial energetics is directly related to [Ca2+]i and mobilization in failing human myocardium, because metabolites, e.g., ADP, inhibit pumps, such as sarcoplasmic reticulum Ca2+ ATPase activity. We therefore conclude that there is a role for intracellular calcium mobilization and myocardial energetics for systolic and diastolic dysfunction seen in human heart failure.