995 resultados para Experimental Tumor Immunoprophylaxis


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Objective. The aim of this study was to evaluate the pH, calcium release, setting time, and solubility of two commercially available mineral trioxide aggregate (MTA) cements (white MTA Angelus and MTA Bio), and of three experimental cements (light-cured MTA, Portland cement with 20% bismuth oxide and 5% calcium sulfate, and an epoxy resin-based cement). Study design. For evaluation of pH and calcium ion release, polyethylene tubes with 1.0 mm internal diameter and 10.0 mm length were filled with the cements and immediately immersed in flasks containing 10 mL deionized water. After 3, 24, 72, and 168 hours, the tubes were removed and the water from the previous container was measured for its pH and calcium content with a pH meter and an atomic absorption spectrophotometer. For analysis of the setting time, Gilmore needles weighing 100 g and 456.5 g were used, in accordance with the American Society for Testing and Materials specification no. C266-03. Solubility of each cement was also tested. Results. All the cements were alkaline and released calcium ions, with a declining trend over time. After 3 hours, Portland cement + bismuth oxide and MTA Bio had the highest pH and light-cured MTA the lowest. After 1 week, MTA Bio had the highest pH and light-cured MTA and epoxy resin-based cement the lowest. Regarding calcium ion release, after 3 hours, Portland cement + bismuth oxide showed the highest release. After 1 week, MTA Bio had the highest. Epoxy resin-based cement and light-cured MTA had the lowest calcium release in all evaluation periods. Regarding setting times, white MTA Angelus and MTA Bio had the shortest, Portland cement + bismuth oxide had an intermediate setting time, and the epoxy resin-based cement had the longest. The materials that showed the lowest solubility values were the epoxy resin-based cement, Portland cement + bismuth oxide, and light-cured MTA. The highest solubility values were presented in white MTA Angelus and MTA Bio. Conclusions. The white MTA Angelus and MTA Bio had the shortest setting times, higher pH and calcium ion release, and the highest solubility. In contrast, the epoxy resin-based cement and light-cured MTA showed lower values of solubility, pH, and calcium ion release. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010; 110: 250-256)

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Objective. The aim of the present study was to evaluate the radiopacity of 5 root end filling materials (white MTA Angelus, MTA Bio, light-cured MTA, Sealepox RP, and Portland cement clinker with bismuth oxide and calcium sulfate). Method. Five specimens, 10 mm in diameter and 1 mm in thickness according to specification ISO 6876: 2001 were fabricated from each material and radiographed using Insigth occlusal films close to a graduated aluminum step-wedge (2 to 16 mm in thickness). Radiographs were digitized and compared to the aluminum step-wedge. The radiographic density data were converted into millimeters of aluminum (mm Al), using the Digora 1.51 software. Results were evaluated statistically using the analysis of variance (ANOVA) followed by Tukey test. The level of significance was set at 5% (P<.05%). Results. Radiopacity values ranged from 1.21 mm Al (light-cured MTA) to 6.45 mm Al (MTA Angelus). Comparison between materials showed significant difference (P<.05) between MTA Angelus and all other materials, between Sealepox RP and MTA Bio, and between light-cured MTA and Portland cement clinker. Light-cured MTA was significantly less radiopaque than all other materials. No significant difference (P>.05) was found between MTA Bio and Portland cement clinker. Conclusions. All retrograde filling materials evaluated showed greater radiopacity than dentin. All the materials, except light-cured MTA met the minimum radiopacity standards of 3 mm Al recognized by the ISO 6876: 2001 and ADA n.57. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009; 108: e35-e38)

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Objectives: This study tested the following null hypotheses: (1) there is no difference in resin-dentine bond strength when an experimental glutaraldehyde primer solution is added prior to bonding procedures and (2) there is no difference in resin-dentine bond strength when experimental glutaraldehyde/adhesive system is applied under dry or wet demineralized dentine conditions. Methods: Extracted human maxillary third molars were selected. Flat, mid-coronal dentine was exposed for bonding and four groups were formed. Two groups were designated for the dry and two for the wet dentine technique: DRY: (1) Group GD: acid etching + glutaraldehyde primer (primer A) + HEMA/ethanol primer (primer B)-under dried dentine + unfilled resin; (2) Group D: the same as GD, except for primer A application; WET: (3) Group GW: the same as GD, but primer B was applied under wet dentine condition; (4) Group W: the same as GW, except for primer A application. The bonding resin was light-cured and a resin core was built up on the adhesive layer. Teeth were then prepared for microtensile bond testing to evaluate bond strength. The data obtained were submitted to ANOVA and Tukey`s test (alpha = 0.05). Results: Glutaraldehyde primer application significantly improved resin-dentine bond strength. No significant difference was observed when the same experimental adhesive system was applied under either dry or wet dentine conditions. These results allow the first null hypothesis to be rejected and the second to be accepted. Conclusion: Glutaraldehyde may affect demineralized dentine properties leading to improved resin bonding to wet and dry substrates. (C) 2008 Elsevier Ltd. All rights reserved.

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MMPs are endopeptidases that play a pivotal role in ECM turnover. RECK is a single membrane-anchored MMP-regulator. Here, we evaluated the temporal and spatial expression of MMP-2, MMP-9, and RECK during alveolar bone regeneration. The maxillary central incisor of Wistar rats was extracted and the animals were killed at 1, 3, 7, 10, 14, 21, 28, and 42 days post-operatively (n = 3/period). The hemimaxillae were collected, demineralized and embedded in paraffin. Immunohistochemical analysis was performed by the immunoperoxidase technique with polyclonal antibodies. On day 1, polymorphonuclear cells in the blood clot presented mild immunolabeling for MMPs. During bone remodeling, osteoblasts facing new bone showed positive staining for gelatinases and RECK in all experimental periods. MMPs were also found in the connective tissue and endothelial cells. Our results show for the first time that inactive and/or active forms of MMP-2, MMP-9 and RECK are differentially expressed by osteogenic and connective cells during several events of alveolar bone regeneration. This may be important for the replacement of the blood clot by connective tissue, and in the formation, maturation and remodeling of new bone.

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Warthin tumor (papillary cystadenoma lymphomatosum) is a benign salivary gland tumor involving almost exclusively the parotid gland. The lip is a very unusual location for this type of tumor, which develops only rarely in minor salivary glands. The case of 42-year-old woman with Warthin tumor arising in minor salivary glands of the upper lip is reported.

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The purpose of this study was to evaluate histologically the root surfaces of teeth submitted to orthodontic and surgical extrusion procedures in a dog model. Eighteen adult male dogs, divided into six groups of three dogs each, were used in the study Each animal underwent two procedures: rapid orthodontic extrusion and surgical extrusion of the maxillary lateral incisors. The animals were sacrificed to produce samples at 7, 14, 45, 90, 120, and 180 days after surgery for assessment of cross sections of the coronal, medial, and apical thirds of the treated teeth. At early time points, some active surface and inflammatory resorption was observed exclusively in the surgical extrusion group; however, samples collected at later times demonstrated functional repair of the resorption gaps in both groups. Ankylosis was observed as a minor event and was apparently of a transient nature in samples of the surgical extrusion group. The results demonstrate the importance of maintaining the periodontal ligament and cementum surface; both are vital for the prevention of root resorption. It may be postulated that orthodontic extrusion is more conservative and physiologic than surgical extrusion; however the results showed that function was restored in both groups. (Int J Periodontics Restorative Dent 2009;29:435-443.)

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Purpose: To evaluate the biomechanical fixation, bone-to-implant contact (BIC), and bone morphology of screw-type root-form implants with healing chambers with as-machined or dual acid-etched (DAE) surfaces in a canine model. Materials and Methods: The animal model included the placement of machined (n = 24) and DAE (n = 24) implants along the proximal tibiae of six mongrel dogs, which remained in place for 2 or 4 weeks. Following euthanasia, half of the specimens were subjected to biomechanical testing (torque to interface failure) and the other half were processed for histomorphologic and histomorphometric (%BIC) assessments. Statistical analyses were performed by one-way analysis of variance at the 95% confidence level and the Tukey post hoc test for multiple comparisons. Results: At 4 weeks, the DAE surface presented significantly higher mean values for torque to interface failure overall. A significant increase in %BIC values occurred for both groups over time. For both groups, bone formation through the classic appositional healing pathway was observed in regions where intimate contact between the implant and the osteotomy walls occurred immediately after implantation. Where contact-free spaces existed after implantation (healing chambers), an intramembranous-like healing mode with newly formed woven bone prevailed. Conclusions: In the present short-term evaluation, no differences were observed in BIC between groups; however, an increase in biomechanical fixation was seen from 2 to 4 weeks with the DAE surface. INT J ORAL MAXILLOFAC IMPLANTS 2011;26:75-82

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Objectives: Up-regulated matrix metalloproteinases may be involved in the development of cardiomyocyte injury and the degradation of troponin associated with acute pulmonary thromboembolism. We examined whether pretreatment with doxycycline (a nonspecific matrix metalloproteinase inhibitor) protects against cardiomyocyte injury associated with acute pulmonary thromboembolism. Design: Controlled animal study. Setting: University research laboratory. Subjects: Mongrel dogs. Interventions: Anesthetized animals received doxycycline (10 mg/kg intravenously) or saline and acute pulmonary thromboembolism was induced with autologous blood clots injected into the right atrium. Control animals received doxycycline (or saline). Measurements and Main Results: Hemodynamic measurements were performed, and acute pulmonary thromboembolism increased baseline mean pulmonary arterial pressure and pulmonary vascular resistance by approximately 160% and 362%, respectively (both p<.05), 120 mins after acute pulmonary thromboembolism. Pretreatment with doxycycline attenuated these increases (to 125% and 232%, respectively; both p<.05). Although acute pulmonary thromboembolism tended to increase the right ventricle maximum rate of isovolumic pressure development and the maximum rate of isovolumic pressure decay, doxycycline produced no effects on these parameters. Gelatin zymograms of right ventricle showed that acute pulmonary thromboembolism marginally increased matrix metalloproteinase-9 (but not matrix metalloproteinase-2) levels in the right ventricle. A fluorometric assay to assess net matrix metalloproteinase activities showed that acute pulmonary thromboembolism increased matrix metalloproteinase activities in the right ventricle by >100% (p<.05), and this finding was confirmed by in situ zymography of the right ventricle. Doxycycline attenuated acute pulmonary thromboembolism-induced increases in right ventricle matrix metalloproteinase activities. Acute pulmonary thromboembolism induced neutrophil accumulation in the right ventricle, as estimated by myeloperoxidase activity, and doxycycline blunted this effect (p<.05). Serum cardiac troponin I concentrations, which reflect cardiomyocyte injury, increased after acute pulmonary thromboembolism, and this increase was attenuated by pretreatment with doxycycline (p<.05). Conclusions: We found evidence supporting the idea that acute pulmonary thromboembolism is associated with increased matrix metalloproteinase activities in the right ventricle, which may lead to degradation of sarcomeric proteins, including cardiac troponin I. Inhibition of matrix metalloproteinases may be an effective therapeutic intervention in the management of acute pulmonary thromboembolism. (Crit Care Med 2011; 39: 349-356)

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Currently, the combination of cisplatin and gemcitabine is considered a standard chemotherapeutic protocol for bladder cancer. However, the mechanism by which these drugs act on tumor cells is not completely understood. The aim of the present study was to investigate the effects of these two antineoplastic drugs on the apoptotic index and cell cycle kinetics of urinary bladder transitional carcinoma cell lines with wild-type or mutant TP53 (RT4: wild type for TP53; 5637 and T24: mutated TP53). Cytotoxicity, cell survival assays, clonogenic survival assays and flow cytometric analyses for cell cycle kinetics and apoptosis detection were performed with three cell lines treated with different concentrations of cisplatin and gemcitabine. G(1) cell cycle arrest was observed in the three cell lines after treatment with gemcitabine and gemcitabine plus cisplatin. A significant increase in cell death was also detected in all cell lines treated with cisplatin or gemcitabine. Lower survival rates occurred with the combined drug protocol independent of TP53 status. TP53-wild type cells (RT4) were more sensitive to apoptosis than were mutated TP53 cells when treated with cisplatin or gemcitabine. Concurrent treatment with cisplatin and gemcitabine was more effective on transitional carcinoma cell lines than either drug alone; the drug combination led to a decreased cell survival that was independent of TP53 status. Therefore, the synergy between low concentrations of cisplatin and gemcitabine may have clinical relevance, as high concentrations of each individual drug are toxic to whole organisms.

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Background: The diagnosis of acute pulmonary thromboembolism (APT) and its severity is challenging. No previous study has examined whether there is a linear relation between plasma DNA concentrations and the severity of APT. We examined this hypothesis in anesthetized dogs. We also examined the changes in plasma DNA concentrations in microspheres lung embolization and whether the therapy of APT with nitrite could modify APT-induced changes in plasma DNA concentrations. In vitro DNA release from blood clots was also studied. Methods: APT was induced with autologous blood clots (saline, 1, 3, or 5 ml/kg) injected into the right atrium. A group of dogs received 300 pm microspheres into the inferior vena cava to produce similar pulmonary hypertension. Another group of dogs received 6.75 mu mol/kg nitrite after APT with blood clots of 5 ml/kg. Hemodynamic evaluations were carried out for 120 min. DNA was extracted from plasma samples using QIAamp DNA Blood Mini Kit and quantified using Quant-iT (TM) PicoGreen (R) dsDNA detection kit at baseline and 120 min after APT. Results: APT produced dose-dependent increases in plasma DNA concentrations. which correlated positively with pulmonary vascular resistance (P=0.002, r=0.897) and with mean pulmonary arterial pressure (P=0.006, r=0.856). Conversely, lung embolization with microspheres produced no significant changes in plasma DNA concentrations. While nitrite attenuated APT-induced pulmonary hypertension, it produced no changes in plasma DNA concentrations. Blood clots released dose-dependent amounts of DNA in vitro. Conclusions: Cell-free DNA concentrations increase in proportion to the severity of APT, probably as a result of increasing amounts of thrombi obstructing the pulmonary vessels. (C) 2009 Elsevier B.V. All rights reserved.

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With the proliferation of relational database programs for PC's and other platforms, many business end-users are creating, maintaining, and querying their own databases. More importantly, business end-users use the output of these queries as the basis for operational, tactical, and strategic decisions. Inaccurate data reduce the expected quality of these decisions. Implementing various input validation controls, including higher levels of normalisation, can reduce the number of data anomalies entering the databases. Even in well-maintained databases, however, data anomalies will still accumulate. To improve the quality of data, databases can be queried periodically to locate and correct anomalies. This paper reports the results of two experiments that investigated the effects of different data structures on business end-users' abilities to detect data anomalies in a relational database. The results demonstrate that both unnormalised and higher levels of normalisation lower the effectiveness and efficiency of queries relative to the first normal form. First normal form databases appear to provide the most effective and efficient data structure for business end-users formulating queries to detect data anomalies.

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Histone deacetylase inhibitors show promise as chemotherapeutic agents and have been demonstrated to block proliferation in a wide range of tumor cell lines. Much of this antiproliferative effect has been ascribed to the up-regulated expression of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1). In this article, we report that p21 expression was up-regulated by relatively low doses of the histone deacetylase inhibitor azelaic bishydroxamic acid (ABHA) and correlated with a proliferative arrest. Higher doses of ABHA were cytotoxic. Cells that did not up-regulate p21 expression were hypersensitive to killing by ABHA and died via apoptosis, whereas up-regulation of p21 correlated with reduced sensitivity and a block in the apoptotic mechanism, and these cells seemed to die by necrosis. Using isogenic p21(+/+) and p21(-/-) cell lines and direct inhibition of caspase activity, we demonstrate that the reduced sensitivity to killing by ABHA is a consequence of inhibition of apoptosis by up-regulated p21 expression. These data indicate the enormous potential of therapeutic strategies that bypass the cytoprotective effect of p21 and act on the same molecular targets as the histone deacetylase inhibitors.

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Purpose: The aim of the present study was to evaluate the clinical efficacy of an experimental dentifrice (CH) containing an antimicrobial agent (1% chloramine-T). Materials and Methods: A clinical, fully randomised, double-blind comparative study was designed for 30 selected patients aged 15 to 50 years, with no periodontal disease, decay or other oral diseases, good general health and the presence of dental plaque and sulcus bleeding. Baseline Turesky modified plaque index (PI) and sulcus bleeding index (SBI) were scored for all patients. Volunteers randomly received the experimental dentifrice (CH) or a commercial-brand dentifrice containing triclosan (TR). Both dentifrices were provided in identical, number-labelled tubes, and the subjects were instructed to use the supplied dentifrice only for their usual oral hygiene, three times a day for a duration of 7 days. After 7-day use of dentifrices, the PI and SBI were assessed again. The data obtained were subjected to the Kruskal Wallis test, followed by Dunn`s post hoc test. Results: After 7-day use of dentifrices, the PI scores diminished significantly for both evaluated dentifrices. The SBI values decreased significantly for both experimental and commercial-brand dentifrices. Conclusions: Both dentifrices reduced PI and SBI. By comparing the experimental and gold-standard dentifrice, it was found that there was no statistically significant difference between the PI and SBI scores after their use, suggesting that they exerted a similar effect on the oral health indexes.

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Although earlier studies on thiamine deficiency have reported increases in extracellular glutamate concentration in the thalamus, a vulnerable region of the brain in this disorder, the mechanism by which this occurs has remained unresolved. Treatment with pyrithiamine, a central thiamine antagonist, resulted in a 71 and 55% decrease in protein levels of the astrocyte glutamate transporters GLT-1 and GLAST, respectively, by immunoblotting in the medial thalamus of day 14 symptomatic rats at loss of righting reflexes. These changes occurred prior to the onset of convulsions and pannecrosis. Loss of both GLT-1 and GLAST transporter sites was also confirmed in this region of the thalamus at the symptomatic stage using immunohistochemical methods. In contrast, no change in either transporter protein was detected in the non-vulnerable frontal parietal cortex. These effects are selective; protein levels of the astrocyte GABA transporter GAT-3 were unaffected in the medial thalamus. In addition, astrocyte-specific glial fibrillary acidic protein (GFAP) content was unchanged in this brain region, suggesting that astrocytes are spared in this disorder. Loss of GLT-1 or GLAST protein was not observed on day 12 of treatment, indicating that down-regulation of these transporters occurs within 48 h prior to loss of righting reflexes. Finally, GLT-1 content was positively correlated with levels of the neurofilament protein alpha -internexin, suggesting that early neuronal drop-out may contribute to the down-regulation of this glutamate transporter and subsequent pannecrosis. A selective, focal loss of GLT-1 and GLAST transporter proteins provides a rational explanation for the increase in interstitial glutamate levels, and may play a major role in the selective vulnerability of thalamic structures to thiamine deficiency-induced cell death.