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PURPOSE To compare the effect of 3 tray designs and 3 commonly used impression materials on the displacement of flabby tissue during maxillary edentulous impression by superimposition of 3D digital models. MATERIALS AND METHODS Fifteen maxillary edentulous casts with simulated flabby tissue were fabricated by modifying a standard maxillary edentulous acrylic resin cast. Three types of impression trays were fabricated: trays with conventional relief, trays with additional relief, and trays with an open window. Three impression materials were tested: light-body polysulfide, light-body vinylpolysiloxane, and zinc oxide eugenol paste. For the analysis of tissue displacement during impression making, the test and control stone casts were scanned using a 3D laser scanner, and the 3D digital models were superimposed using metrology software. Statistical analyses were performed with an α = 0.05. RESULTS Negative deviations were recorded at the areas of the alveolar crest, posterior part of flabby tissue, and middle of the palate. On the other hand, a positive deviation was recorded at the area of the anterior part of flabby tissue. A significant difference in the displacement of flabby tissue was found when using different tray designs (p < 0.0001). The tray with the open window showed significantly low tissue displacement at the flabby tissue region. Depending on sites, the amount of flabby tissue displacement showed different significances by the different impression materials used (anterior part: p < 0.0001; alveolar crest: p = 0.097; posterior part: p < 0.0001). Conventionally relieved trays showed significantly higher values of displacement at the anterior part of flabby tissue (p < 0.0001), while trays with open windows showed similar values of displacement at all measuring points, and no significant differences among different impression materials were found (p = 0.104). CONCLUSIONS There were significant differences in the displacement of flabby tissue with different tray designs, especially with displacement occurring at the anterior and posterior parts of flabby tissue. Tray designs should be considered in order to make proper impressions when flabby tissue is present.

This article describes how to use digital system in a fully edentulous case that diagnosis to definitive prosthesis fabrication. While proceeding oral scan and CBCT taking, digital markers were attached on maxillary palate and lower existing denture. Using CBCT image and oral scan image, the bone contour and anatomical structures were analyzed and flapless surgical guide, customized abutment and prosthesis were made. After the osseointegration, the definitive prosthesis was fabricated using the oral scan image with scan body. It provides clinicians with a fast workflow and improves clinical efficiency.

A model with simulated flabby tissue was fabricated by modifying the standard maxillary edentulous acrylic resin cast to evaluate the effect of maxillary impression tray design on the displacement of flabby tissue. Seven groups of trays were fabricated using different combinations of relief spaces and escape holes. After impression taking, test and control casts were scanned and three-dimensional digital models were superimposed. Negative deviations were recorded at the point of the alveolar crest, the posterior part of the flabby tissue, and the middle of the palate, while positive deviations were recorded at the point of the anterior part of flabby tissue. The amount and characteristics of tissue displacement differed with tray design and the relief method used.

Cardiac fibrosis and inflammation are major pathologic conditions that result from viral myocarditis. Connective tissue growth factor (CTGF) stimulates fibroblast proliferation and induces production of extracellular matrix molecules. We studied the correlation between CTGF and cardiac fibrosis in an acute Coxsackievirus B3 (CVB3) myocarditis animal model. Eight-week-old BALB/c mice were infected intraperitoneally with 10 4 plaque forming units (PFU) of CVB3. Myocardial inflammation peaked on day 7 and decreased markedly by day 14 post-infection (pi); cardiac fibrosis was noted from day 7 and peaked on day 14. By contrast, CTGF was weakly expressed by the interstitial cells in uninfected control hearts and also in the hearts of day 3 pi. CTGF expression measured by real-time PCR was elevated on day 3 and peaked on day 7 pi. TGF-β expression peaked at day 7 pi. The cell type of CTGF expression changed from interstitial cells to myocytes after virus infection. On day 7, CTGF was strongly expressed by myocytes and inflammatory cells surrounding calcified necrotic areas. In addition, cardiac myocytes expressed CTGF on day 14. Our results, based on an acute CVB3 model of myocarditis, provide evidence that CTGF may mediate the development of fibrosis after viral myocarditis, and that the cells expressed CTGF changes during the course of viral myocarditis.

Objective: The coxsackie and adenovirus receptor (CAR) and the decay-accelerating factor (DAF) are receptors for coxsackievirus B3 (CVB3), which is known as the major cause of human viral myocarditis. We investigated the potential for therapeutic use of soluble virus receptor fusion proteins. Methods We designed and generated a novel virus receptor trap (hCAR–hDAF:Fc) consisting of both CVB3 receptors and the Fc portion of human IgG1 and evaluated its antiviral effects in experimental CVB3 myocarditis. Results: Among four soluble virus receptor fusion proteins (hCAR:Fc, hDAF:Fc, hCAR–hDAF:Fc and hDAF–hCAR:Fc), hCAR:Fc and hCAR–hDAF:Fc in the supernatant of transfected cells neutralized echovirus, adenovirus, and various serotypes of CVB in a dose-dependent manner. Both soluble viral receptor proteins bound to the VP0 and VP1 capsid proteins of CVB3. The in vivo efficacy of viral receptor proteins was evaluated by intramuscular injection of plasmid (hCAR:Fc or hCAR–hDAF:Fc) followed by electroporation in a murine model of CVB3 myocarditis. Serum levels of the virus receptor proteins increased relative to baseline values from day 3 and peaked on day 14 at 12.9-fold for hCAR:Fc and 7.1-fold for hCAR–hDAF:Fc. The 3-week survival rate was significantly higher in hCAR–hDAF:Fc-treated mice (61%) than in hCAR:Fc-treated mice (29%) and in controls (15%; p

Background — The inflammatory cytokines have an important role in the pathogenesis of viral myocarditis. Inerleukin-1 (IL-1) is one of the major cytokines that modulate the outcome of viral infection. Among the methods for in vivo gene transfer, direct injection of plasmid DNA is one that is simple and feasible. In this study, we expressed human IL-1 receptor antagonist (hIL-1Ra) in the mouse heart by direct injection of a novel plasmid vector and evaluated its effects on coxsackieviral (CVB3) myocarditis. Methods and Results — A plasmid vector expressing hIL-1Ra (total 40 μg/mouse) was injected into the heart apex of 8-week-old inbred female Balb/C mice (day 3). On day 0, mice (IL-1Ra-CVB3, n=35) were infected intraperitoneally with 10 4 PFU of CVB3; control mice (pCK-CVB3, n=15) were injected with empty vector on day −3 and infected on day 0. hIL-1Ra was expressed in the heart, reached its peak on day 5, and persisted for 2 weeks. The 14-day survival rate of IL-1Ra-CVB3 was higher (77%) than that of controls (30%, P Conclusion — These results showed that direct injection of the expression plasmid vector into the heart was an effective method to transfer the cytokine gene in vivo, and expressed IL-1Ra in the heart can modulate the deleterious effect of the host immune response in viral myocarditis.

Tumor necrosis factor-alpha (TNF-alpha) is one of the major cytokines that modulate the immune response in viral myocarditis, but its role has not yet been thoroughly evaluated. We antagonized TNF-alpha using the expressed soluble p75 TNF receptor linked to the Fc portion of the human IgG1 gene (sTNFR:Fc) by in vivo electroporation, and evaluated its effects on experimental coxsackieviral B3 (CVB3) myocarditis. A plasmid DNA encoding sTNFR:Fc (15microg/mouse) was injected into the gastrocnemius muscles of Balb/C male mice followed by electroporation (day -1). Control mice were injected with an empty vector. One day after electroporation, mice were infected with CVB3 (day 0). Serum levels of sTNFR:Fc increased from day 2 and peaked at day 5 following electroporation. The heart virus titers of sTNFR:Fc mice were higher than those of controls at day 3. However, subsequent to day 12, the survival rates of the sTNFR:Fc mice were significantly higher than those of the controls (36% versus 0% at day 27, P0.01). Histopathological examination indicated that inflammation and myocardial fibrosis were significantly decreased in sTNFR:Fc mice at day 12. The expressed sTNFR:Fc could modulate the inflammatory process during the post-viremic phase of viral myocarditis.

One mechanism that contributes to the pathogenesis of coxsackievirus B (CVB) viral heart disease is the direct cytopathic effect(s) on cardiomyocytes. It has been shown in mice that during CVB infection, the enteroviral protease 2A directly cleaves dystrophin in the hinge 3 region, leading to disruption of the dystrophin-glycoprotein complex and the loss of sarcolemmal integrity.1–3 We report for the first time a patient with fulminant myocarditis4 with CVB4 infection in which myocardial …

Endomyocardial biopsy often fails to show myocardial inflammation for patients with clinically suspected myocarditis. The serum isoforms of troponin T (cTnT) level is a very sensitive marker of myocardial injury and it is elevated even in the absence of myocardial inflammation. We investigated the correlations for myocardial injury, virus titers and inflammation in acute viral infection. Using the murine coxsackievirus group B3 (CVB3) myocarditis model, the histopathologic findings and virus titers in mouse hearts were compared with the serum cTnT levels measured by ELISA at various time points. Viable virus titers in the hearts peaked at 3 days after infection (8.22 +/- 0.13 log10 PFU/100 mg of heart); they decreased at day 7 and no viable virus was detected from day 14. Myocardial inflammation was minimal at day 3, peaked at day 7 and markedly decreased at day 14. The individual serum TnT levels were significantly increased at day 3 (7.37 +/- 1.46 ng/ml), persisted to day 7 (0.73 +/- 0.08 ng/ml), and normalized at day 14. Serum cTnT levels were correlatable with virus titers in the heart (r = 0.744, P

Efficient myocardial gene transfer in the intact adult heart is difficult using conventional transfer vectors. Since coxsackievirus B3 (CVB3) is cardiotropic, it may be possible to exploit its cardiotropic characteristics to design a vector for gene transfer to the intact heart. We generated a recombinant CVB3 cDNA by inserting a green fluorescent protein (GFP) gene immediately upstream from the VP0 capsid protein of CVB3. The infectious virus (rCVB3-GFP) was recovered from the supernatants of the transfected Cos-7 cells, and was grown in HeLa cells to titers of 10 11 pfu/ml. In the rCVB3-GFP infected HeLa cells and neonatal rat cardiac myocytes, GFP protein expression was documented by immunoblot and by fluorescent microscopy. GFP expression was maintained after five passages in HeLa cells. To test in vivo expression of GFP, we infected 8-week-old inbred female Balb/C mice with 10 6 pfu of rCVB3-GFP, intraperitoneally. GFP was present in up to 30% of cardiac myocytes over the 8 weeks post infection (p.i.) and it was co-localized with CVB3 infection. Surprisingly, in spite of detection of GFP up to at least 8 weeks after infection, there was no mortality in the mice. It is possible to express exogenous proteins in the intact heart after an intraperitoneal (i.p.) injection of recombinant coxsackievirus. The duration of expression persisted for at least 8 weeks with little immune response nor mortality. These results demonstrated that the cardiac tropism of CVB3 could be used to design vectors for efficient gene expression in the intact heart.

Background and Objectives: Adriamycin (doxorubicin, ADR) is a highly effective anti-neoplastic drug, but its clinical use is limited by its adverse side effects on the heart. Cardiotrophin (CT-1), a potent cardiac survival factor, is capable of inhibiting apoptosis in cardiac myocytes. The aim of this study was to investigate the cytoprotective effects of CT-1 against ADR-induced apoptosis in vitro. Materials and Methods: We determined a reasonable ADR concentration for inducing cell death by utilizing a cell survival test performed in a dosedependent manner. To determine the requirements for apoptosis in ADR-treated cardiac myocytes (H9c2 cells), we examined the effect of CT-1 on survival and apoptotic changes using a cell counting kit (CCK), RT-PCR, and Western blotting. Results: In analyzing cell survival as determined by CCK, ADR-induced cell death was found to occur in a dose-dependent manner (50% death at 24 hours after 2 μM of ADR), and ADR was shown to decrease procaspase-3. On RT-PCR, expression of Bax-α mRNA increased and Bcl-2 decreased during the 24 hours after ADR treatment. Consequently, the ratio of Bax-α/Bcl-2 mRNA peaked at 24 hours after ADR treatment. In contrast, CT-1 effectively attenuated the ADR-induced cell death in a dose-dependent manner. The changes in Bax-α and Bcl-2 mRNA expression after ADR treatment were reversed by CT-1 (1 ng/mL) treatment. The protein levels of procaspase-3 decreased after ADR treatment, an effect which was reversed by CT-1 treatment. Akt phosphorylation was also increased by CT-1, demonstrating that CT-1 inhibited apoptosis induced by ADR. Conclusion: These data demonstrated that ADR-induced apoptosis of cardiomyocytes can be prevented by CT-1; therefore, it may be possible to use CT-1 as a cardioprotective agent during ADR chemotherapy in patients with cancer. (Korean Circ J 2008;38:264-269)

Background and Objectives：Cardiac troponin T (cTnT has been used as a very sensitive marker of cardiac injury caused by ischaemia, myocarditis, and cardiomyopathy. After cardiac injury, the fetal cTnT isoform expression in the heart and serum cTnT increases. To investigate the increased levels of serum cTnT, and the expression of fetal cTnT isoform in the heart, that can predict myocardial injury, we measured serum cTnT levels and the fetal cTnT isoform expression at various time points during the early phase of myocardial toxicity induced by adriamycin (ADR in rat. Materials and Methods：Male Sprague-Dawley rats were injected, intraperitoneally, with ADR (5 mg/kg twice a week for 2 weeks. Control rats were injected with saline. Serum cTnT levels were measured by ELISA. The ratio of fetal/adult (F/A cTnT isoform expression (% was semi-quantified by RT-PCR using total RNA from frozen hearts. Results：Serum cTnT levels did not increase by 1 week after ADR injection, but increased significantly after 2 weeks. The ratio of F/A cTnT in the heart significantly increased from day 1, peaked at 1 week and persisted until the end of 2 week. Conclusion：The expression of the fetal cTnT isoform occurred from 1 day after ADR injection when the serum cTnT levels were still normal. Although the serum cTnT level is a very sensitive, and an early marker, of cardiac damages, the fetal cTnT isoform expression in the endomyocardial biopsy specimen may be a more sensitive and an earlier marker in the ADR-induced myocardial damage. (Korean Circulation J 2002;32( ( ( (6 :485-491