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At least 613 records · Page 34Linked to original sources
PubMed1985

Paste technique re-treatment study: a clinical, histopathologic, and radiographic evaluation of 50 cases.

This study correlated clinical, radiographic, and histopathologic aspects of 50 endodontic failures involving the paste technique. All clinical and radiographic findings were recorded. The teeth were re-treated with gutta-percha/Kloroperka and lateral condensation. Subsequently, periapical surgery, including retrograde amalgam filling, was performed for the removal of material in the periapical tissue. The resulting biopsy specimens were processed for histologic evaluation. Although neutrophilic leukocytes predominated in some cases, all types of inflammatory cells were present. Macrophages and foreign body cells contained paste particles. The blood pigment distinguished hemorrhage due to surgery from pathologic circulatory changes. There was resorption/apposition of bone and root fragments. Epithelial strands and parts of cyst walls were observed. There was a correlation between a periapical radiolucency and inflammation but no correlation between amounts and types of inflammatory cells and pain. Paste placed beyond the foramen caused tissue damage and reduced prognosis.

Balsams↗
PubMed1991

Tissue reaction to endodontic materials: methods, criteria, assessment, and observations.

The purpose of this study was to develop methods and criteria for the testing of the biocompatibility of endodontic materials. One hundred twenty-one teeth from 12 baboons (Papio anubis) were used to test three sealers: AH26, Kerr pulp canal sealer, and Kloroperka N.O. Gutta-percha cones were used as solid core in all cases. Under disinfected conditions, access preparation was performed, and with working length approximately 1.0 mm short of the foramen, the instrumentation of the root canal was started, using sodium hypochlorite (1%) for irrigation. After the root canals were cleaned and shaped, they were obturated with gutta-percha cones and the sealer, and by lateral condensation technique. Histologic periapical reactions were evaluated at 1, 7, 30, 365, 730, and 1095 days. The methods and criteria used were adequate for ranking of the biocompatibility of the tested materials in the short and long periods. At short observation periods (1 to 7 days) AH26 caused severe reactions, and Kerr pulp canal sealer and Kloroperka N.O., moderate and mild reactions, respectively. At 2- and 3-year observation periods the ranking was AH26, mild; Kerr pulp canal sealer, moderate; and Kloropercha N.O., severe.

Animals↗
PubMed1992

Usage test of four endodontic sealers in Macaca fascicularis monkeys.

Root canals with vital pulps in four Macaca fascicularis monkeys were subjected to pulp extirpation and root filling with gutta-percha and sealer, either AH26, Endomethasone, Kloroperka N-phi, or ProcoSol. Observation periods were 1 and 6 months. The results of treatment were evaluated by radiographic analysis (periapical index scores) and by histopathologic assessment of the remaining pulp and periapical tissues. Sixty roots with acceptable termination (between 0.5 and 3 mm from apex) of the root fillings and adequate histopathologic specimens were available for analysis. These roots were equally distributed in each observation period group and among the four material groups. Radiography indicated periapical pathosis in 6 of the 60 roots--4 at 1 month and 2 at 6 months. Periapical inflammation was observed on histopathologic examination in 17 roots--11 after 1 month and 6 after 6 months. Histologic and radiographic assessment of periapical inflammation was significantly correlated (p less than 0.01, chi 2) at the 6-month observation period. No granuloma or cyst formation was evident on histologic examination. The magnitude of the inflammatory response appeared unrelated to the endodontic sealer used, and several inflammatory foci were not related to foreign bodies in the tissues. Bacteriologic sampling showed growth in thioglycollate broth cultures in 9 of the 60 roots, but the presence of cultivable bacteria by this technique was unrelated to inflammatory changes. Histologic demonstration of bacteria was positive in 4 roots, all of which were associated with inflammatory periapical reactions. The method applied in the present study did not provide a sensitive discrimination among endodontic materials of widely different chemical composition.

Administration, Topical↗
PubMed1993

Age differences in the controls of ring doves' pecking.

Three experiments investigated the endogenous and exogenous controls of ring dove pecking. Experiment 1 confirmed that deprivation modulates adult pecking although nondeprived subjects peak at high levels. Experiment 2 determined that the level of pecking in nondeprived birds is modulated by exogenous cues such as the salience of the seed. Experiment 3 analyzed some of the controls of pecking in squabs. Both nondeprived and deprived squabs pecked little on days 12 and 16 of life, but by day 18, deprived squabs pecked significantly more than nondeprived squabs. Squabs inexperienced with deprivation peck less when hungry than squab that have had previous experience with deprivation. The controls of feeding change between day 24 of life and adulthood as exogenous cues did not stimulate nondeprived squab pecking until day 24 of life.

Aging↗
PubMed1985

Mutagenicity of endodontic sealers.

Four endodontic sealer materials and some of their chemical constituents were subjected to Ames' test for mutagenicity with the Salmonella/microsome assay. Extracts of two zinc oxide-eugenol based materials and of one gutta-percha-zinc oxide-chloroform based sealer were negative in the test. Extracts of a synthetic polymer material, based on epoxy-bis-phenol A, induced mutations in Salmonella typhimurium TA 100 as did extracts of the epoxy-bis-phenol A resin alone. Formaldehyde, an active ingredient from one of the ZnO-based materials, induced mutations in both Salmonella typhimurium TA 98 and TA 100. The mutagenic activity of formaldehyde as well as of the epoxy material was reduced in the presence of rat liver microsomes.

Administration, Topical↗
PubMed2006

Amphetamine affects the start of responding in the peak interval timing task.

In this paper we investigate how amphetamine affects performance in a PI task by comparing two analyses of responding during peak trials. After training on 24 s fixed interval (FI-24) with 96 s peak trials, rats were given amphetamine for 4 consecutive days at doses of .5 and 1.0 mg/kg. Responses during peak trials were fitted with a Gaussian distribution to estimate the expected time of reinforcement from the peak time. A single trials analysis was also performed to determine the start time and stop time of the transition into and out of a high rate of responding on each peak trial. Amphetamine significantly decreased peak times as measured with the Gaussian curve fitting. However, in the single trials analysis, animals initiated responding significantly earlier, but did not stop responding earlier. Thus, fitting a Gaussian to the average performance across trials sometimes provides a different characterization of the timing process than does analyzing the start and stop of responding on individual trials. In the current experiment, the latter approach provided a more precise characterization of the effects of amphetamine on response timing.

Amphetamine↗
PubMed2005

Cyclosporine mitigates graft coronary artery disease in murine cardiac allografts: description and validation of a novel fully allogeneic model.

BACKGROUND: The effect of cyclosporine (CsA) on the development of graft coronary artery disease (GCAD) is controversial. We developed a novel allogeneic mouse model of heart transplantation and investigated the effect of CsA on acute rejection and GCAD. METHODS: Hearts of FVB mice (H-2(q)) were heterotopically transplanted into 60 C57BL/6 mice (H-2(b)). CsA was administered to recipients at 10, 20 or 30 mg/kg/day for 10 or 30 days after transplantation. Untreated recipients as well as isograft recipients served as controls. Viability of the grafts was assessed daily by palpation. Parenchymal rejection was scored in grafts surviving 30 days in the 30-day treatment groups. GCAD was evaluated by the percentage of luminal narrowing, intima/media ratio and percentage of diseased vessels. Blood CsA and creatinine levels were also evaluated. Results were evaluated statistically. RESULTS: All groups except the untreated control group and the allograft groups treated with 10 or 20 mg for 10 days showed significant graft survival (>/=33% survival for 30 days). An inverse correlation was observed between CsA treatment dose, parenchymal rejection score and degree of GCAD in the 30-day treatment groups. However, graft survival in the 20-mg/kg/day group was significantly better than that in the 30-mg/kg/day group. Serum creatine levels showed no nephrotoxicity. CONCLUSIONS: Relatively high-dose CsA mitigated parenchymal rejection and GCAD of the mouse cardiac allografts. In addition, a valuable mouse model mimicking the clinical course of GCAD was achieved with CsA treatment of 20 mg/kg/day for 30 days.

Animals↗
PubMed2005

Early inhibition of caspase-3 activity lessens the development of graft coronary artery disease.

BACKGROUND: The role of apoptosis in the development of graft coronary artery disease (GCAD) is poorly understood. We have previously shown that early overexpression of the anti-apoptotic protein Bcl-2 lessens the development of GCAD. We hypothesized that early inhibition of apoptosis with a caspase-3 inhibitor would also lessen the development of GCAD. METHODS: Heterotopic heart transplantation was performed in 4 groups of rats. Donor hearts were pretreated with 50 microg DEVD-CHO, a cell-permeable caspase-3 inhibitor, or vehicle. Recipient animals were pretreated with 1.7 mg/kg intraperitoneal DEVD-CHO or vehicle. Animals were treated with 7.5 mg/kg/d cyclosporine for 10 days to prevent acute rejection. On post-operative day 90, the animals were sacrificed and the transplanted hearts were assessed morphometrically for evidence of GCAD. RESULTS: At 90 days, intimal proliferation was significantly higher in vehicle treated animals than in inhibitor treated animals. Moreover, the percentage of vessels with high-grade occlusion (>50%) was also lower in inhibitor treated animals. CONCLUSIONS: Early inhibition of caspase-3 activity with cell-permeable DEVD-CHO lessens the development of GCAD. Caspase-3 inhibition may be a useful strategy for prevention of GCAD in clinical transplantation.

Animals↗
PubMed2005

Prolonged cold ischemia in rat cardiac allografts promotes ischemia-reperfusion injury and the development of graft coronary artery disease in a linear fashion.

BACKGROUND: Prolonged cold ischemia is thought to exacerbate ischemia-reperfusion injury and graft coronary artery disease (GCAD). We investigated the effect of varying lengths of cold ischemia on inflammation and apoptosis during ischemia-reperfusion injury and correlated this with the degree of GCAD in rat cardiac allografts. METHODS: PVG rat (RT1c) hearts subjected to 30, 60, 90, 120, or 150 minutes of cold ischemia were heterotopically transplanted into ACI rats (RT1a). Grafts were procured after 4 hours of reperfusion and analyzed for superoxide generation, myeloperoxidase activity, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) production, cardiomyocyte apoptosis, and caspase-2, -3, -8, -9 activities. Additional transplanted animals received cyclosporine A (7.5 mg/kg/day) for 10 days as chronic rejection models. Indices of GCAD were determined at 90 days. RESULTS: A direct linear correlation was found between cold ischemic time, ischemia-reperfusion injury, and GCAD. Superoxide generation, myeloperoxidase activity, TNF-alpha, IL-1beta, MCP-1/CCL2 production, cardiomyocyte apoptosis, and caspase-2, -3, -8, and -9 activities increased with ischemic time, peaking at 120 minutes and plateauing at 150 minutes. GCAD, assessed by the percentage of luminal narrowing, the intima/media ratio, and the percentage of diseased vessels, worsened with increased ischemic time, peaking at 120 minutes and plateauing at 150 minutes. All tested variables in both the acute and chronic phases were significantly increased with 120-minute ischemia compared with 30-minute ischemia. CONCLUSIONS: These data indicate that the degree of cardiomyocyte apoptosis and inflammatory response in cardiac allografts during ischemia-reperfusion injury depends on the duration of cold ischemia. More important, that prolonged cold ischemia correlates with increased GCAD.

Animals↗
PubMed2004

Protective effect of Copaifera langsdorffii oleo-resin against acetic acid-induced colitis in rats.

The oleo-resin from Copaifera langsdorffii (Leguminosae) was evaluated in rats on acetic acid-induced colitis. Rats were pretreated orally (15 and 2 h) or rectally (2 h) before the induction of colitis with copaiba oleo-resin (200 and 400 mg/kg) or vehicle (1 ml, 2% Tween 80). Colitis was induced by intracolonic instillation of a 2 ml of 4% (v/v) acetic acid solution and 24 h later, the colonic mucosal damage was analyzed for the severity of macroscopic colonic damage, myeloperoxidase (MPO) activity, and malondialdehyde levels. A significant reduction in gross damage score and in wet weight/length ratio of colonic tissue were evident in test substance-pretreated animals as compared to vehicle or oleo-resin alone-treated controls. This effect was confirmed biochemically by a reduction in colonic myeloperoxidase activity, the marker of neutrophilic infiltration, and by a marked decrease in malondialdehyde level, an indicator of lipoperoxidation. Furthermore, microscopical examination revealed the diminution of inflammatory cell infiltration, and submucosal edema in the colon segments of rats treated with copaiba oleo-resin. The data indicate the protective effect of copaiba oleo-resin in the animal model of acute colitis possibly through an antioxidant and or anti-lipoperoxidative mechanism.

Acetic Acid↗
PubMed2005

Caspase-3 inhibition preserves myocardial geometry and long-term function after infarction.

BACKGROUND: Cardiac remodeling after infarction is characterized by progressive ventricular dilation and functional impairment. Although surgical and percutaneous revascularization strategies may prevent remodeling, not all patients are candidates for these procedures. Apoptosis in the border-zone myocardium is thought to be critical to the remodeling process, and caspase-3 is a downstream effector of apoptosis. We hypothesized that inhibition of caspase-3 activity might limit dysfunction and remodeling after permanent coronary artery ligation. METHODS: FVB male mice underwent permanent ligation of the left anterior descending coronary artery. Immediately before surgery and for 7 subsequent days, animals were treated daily with 3 mg/kg DEVD-CHO, a cell-permeable inhibitor of caspase-3 (n = 16), or vehicle (n = 28). At 2 weeks and 6 weeks, echocardiography was performed and ventricular dimensions and function were assessed. At 8 weeks, invasive hemodynamic measurements were made and the animals were sacrificed. RESULTS: There was a trend toward improved survival in the inhibitor-treated group compared to the vehicle-treated group (56.3% versus 21.4%, P = 0.07). Infarct size at the time of sacrifice was comparable in both groups. At both 2 and 6 weeks, left ventricular dimensions, including end-diastolic and end-systolic diameters, were less in inhibitor-treated animals. Fractional shortening was higher at 6 weeks in the inhibitor-treated animals (22.1 +/- 6.0% versus 15.0 +/- 6.0%, P = 0.02). Invasive hemodynamic parameters at 8 weeks were comparable, with the exception of diastolic blood pressure, which was less in the inhibitor group. CONCLUSION: Treatment with a caspase-3 inhibitor improved survival and prevented ventricular dilation and dysfunction after permanent coronary artery occlusion.

Animals↗