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PubMed1982

Regulatory mechanism of delayed-type hypersensitivity in mice. IV. Effect of suppressor T cells on the development of memory T cells involved in accelerated generation of DTH-effector cells in vitro.

The effect of suppressor T cells (Ts) on the induction and the subsequent development of memory T cells for delayed-type hypersensitivity (DTH) was examined. The memory cells were induced in the spleens of mice primed previously with a low dose of reduced and alkylated ovalbumin (Ra-OA), and they generated DTH-effector T cells (DTH-Te) in a significantly accelerated fashion when cultured with OA in vitro. Ts were obtained from the spleens of mice which received OA-coupled spleen cells i.v. 4 days previously, and they inhibited antigen-specifically the induction of DTH responses in the recipient mice sensitized with alum-absorbed OA only when transferred with 5 weeks before sensitization. The spleen cells from mice given Ts together with the priming antigen 7 weeks before culture failed to generate DTH-Te in an accelerated manner on restimulation with OA in vitro. The memory cells from primed mice also did not cause accelerated generation of DTH-Te, when cultured with Ts in the presence of OA in vitro. These results indicate that both the induction of the memory cells by priming with antigen in vivo and the subsequent development of memory cells to DTH-Te by restimulation in vitro are inhibited independently by Ts. This corresponded well with the effect of Ts on the development of DTH-memory in vivo.

Animals↗

PubMed2004

Barium sulphate with a negative zeta potential accelerates skin permeability barrier recovery and prevents epidermal hyperplasia induced by barrier disruption.

BACKGROUND: Barium sulphate, a stable inorganic material, has been used in contrast media and cosmetic products because of its stability. As a negative external electric potential accelerates the skin barrier repair after barrier disruption, we hypothesized that topical application of barium sulphate may affect the skin barrier recovery rate depending on its zeta potential. OBJECTIVES: To investigate whether barium sulphate particles in aqueous solution have different zeta potentials depending on their surface structure, and to investigate the possible relation between zeta potential and skin barrier recovery rate. METHODS: Mice were subjected to tape stripping to disrupt barrier function, or were treated with acetone and kept in a dry environment to induce epidermal hyperplasia. They were then treated with different forms of barium sulphate, and barrier recovery was monitored by measurements of transepidermal water loss. RESULTS: There was a significant correlation between the barrier recovery rate and zeta potential of barium sulphate applied topically. Barium sulphate with a negative zeta potential significantly accelerated barrier recovery, but barium sulphate with a positive zeta potential did not accelerate or even delayed barrier repair. Barium sulphate with a negative zeta potential had an X-ray diffraction pattern different from that with a positive potential. The distribution of calcium in the epidermis was also influenced by the polarity of zeta potential. CONCLUSIONS: These findings suggest a new pharmacological approach towards altering barrier function or epidermal hyperplasia with inorganic particles in healthy and diseased skin.

Administration, Cutaneous↗

PubMed2004

Ovariectomy is sufficient to accelerate spontaneous skin ageing and to stimulate ultraviolet irradiation-induced photoageing of murine skin.

BACKGROUND: Wrinkling and sagging of the skin during photoageing is physiologically associated with diminished elasticity, which can be attributed to increased fibroblast-derived elastase activity. This degrades the dermal elastic fibres needed to maintain the three-dimensional structure of the skin. We previously reported that ovariectomy accelerates ultraviolet (UV)B-induced wrinkle formation in rat hind limb skin by altering the three-dimensional structure of elastic fibres. OBJECTIVES: In this study, we used hairless mice to assess the effects of ovariectomy with or without chronic UVA or UVB radiation on sagging and wrinkling of skin, on the elasticity of skin, as well as on matrix metalloproteinase activities in the skin. METHODS: Ovariectomies or sham operations were performed on 6-week-old female ICR/HR hairless mice. RESULTS: Even in the ovariectomy group without UV irradiation, the skin elasticity was significantly decreased during the 3-13 weeks after ovariectomy, which was accompanied by a significant increase in elastase activity in the skin. After UVA or UVB irradiation, skin elasticity was significantly decreased to a greater extent in the ovariectomy group than in the sham operation group, and this was accompanied by a reciprocal increase in elastase activity but not in the activities of collagenases I or IV in the skin. Consistent with the decreased skin elasticity, UVA irradiation for 12 weeks elicited more marked sagging in the ovariectomy group than in the sham operation group. UVB irradiation for 12 weeks also induced more marked wrinkle formation in the ovariectomy group than in the sham operation group. CONCLUSIONS: These results suggest that ovariectomy alone is sufficient to accelerate skin ageing and to increase UV sensitivity, which results in the further deterioration of the skin and photoageing, and may account for the accelerated skin ageing seen in postmenopausal women.

Animals↗

PubMed1978

Acceleration of methaemoglobin reduction by riboflavin in human erythrocytes.

The effect of riboflavin on nitrite treated erythrocytes from normal subjects and patients with hereditary methaemoglobinaemia due to the deficiency of NADH-cytochrome b5 reductase was studied in the presence of glucose, 2-deoxy-D-glucose or lactate. When glucose or 2-deoxy-D-glucose was used as a substrate for these erythrocytes, the rate of methaemoglobin reduction in these cells was accelerated more than two-fold in the presence of riboflavin. The acceleration was dependent on the concentration of riboflavin and was suppressed by the addition of atebrin. The stimulative effect of riboflavin was, however, not observed when lactate was used in place of glucose or 2-deoxy-D-glucose. On the basis of these results, the acceleration of methaemoglobin reduction by riboflavin was considered to be due to the activation of NADPH-flavin reductase (Yubisui et al, 1977) in erythrocytes by the reagent. The availability of riboflavin for patients with methaemoglobinaemia due to the deficiency of NADH-cytochrome b5 reductase and for those with toxic methaemoglobinaemia is discussed in relation to methaemoglobin reducing systems in erythrocytes.

Cytochrome-B(5) Reductase↗

PubMed1984

Phospholipids accelerate factor IX activation by surface bound factor XIa.

Activation of bovine factor IX by surface bound factor XIa which was generated either by activation of human citrated factor IX deficient plasma or a mixture of purified human factors XII, high molecular weight kininogen (HMWK) and XI in glass tubes, is accelerated by cephalin. Human brain cephalin in dilutions ranging from 1:5 to 1:500 was studied for its effect on the activation of factor IX in concentrations of 1.0 u/ml and 16 u/ml. Cephalin dilutions from 1:5 to 1:30 accelerated the activation of the concentrated factor IX sample two- to threefold. Protein cleavage of this factor IX sample in the presence of 1:30 cephalin occurred twice as fast as in the absence of cephalin. Activation of the dilute factor IX sample (1.0 u/ml) was most effectively accelerated by cephalin in dilutions from 1:30 to 1:250. In all experiments the presence of phospholipid led to an increased factor IX cleavage concomitantly with faster generation of factor IXa activity. The results demonstrate that phospholipids actively participate in blood coagulation at an earlier stage than previously described.

Animals↗

PubMed1989

Marrow transplantation following busulfan and cyclophosphamide for chronic myelogenous leukaemia in accelerated or blastic phase.

Between July 1984 and October 1987, 21 patients with chronic myelogenous leukaemia in an accelerated or blastic phase were treated with 16 mg/kg of busulfan and 120 mg/kg of cyclophosphamide followed by infusion of bone marrow from an HLA-identical sibling donor. The regimen was well tolerated. Except for one individual with severe marrow fibrosis all patients achieved a complete remission. Only one patient relapsed. Seven of 13 patients transplanted in an accelerated phase and five of eight transplanted in a blastic phase are alive without Philadelphia chromosomes between 8 and 48 months (median 29 months) following transplantation. The estimated probability of relapse-free 3-year survival is 55%. These results indicate that busulfan and cyclophosphamide combined with allogeneic marrow transplantation exert a potent anti-leukaemic effect in patients in the accelerated or blastic phase of CML.

Adolescent↗

PubMed1994

Contribution of glycaemic control, endogenous lipoproteins and cholesteryl ester transfer protein to accelerated cholesteryl ester transfer in IDDM.

In an earlier study we demonstrated that the transfer of cholesteryl ester (CET) estimated as the net mass of CE lost from HDL to the apoB-containing lipoproteins (VLDL + LDL) during incubation of plasma is accelerated in normolipidaemic patients with insulin-dependent diabetes mellitus (IDDM). Recombination experiments with isolated lipoprotein fractions employing this same mass transfer assay indicated that this disturbance resulted from dysfunction of VLDL and not from changes in the activity of CE transfer protein (CETP). In this study, we sought first to determine whether CET estimated with an isotopic method that measures the transfer of radiolabelled CE from exogenous HDL from non-diabetic controls to endogenous VLDL + LDL was also increased in IDDM and, if so, the extent to which this disturbance was affected by glycaemic control, VLDL and CETP. As observed with the mass transfer assay, the rate of transfer of the HDL-CE label to VLDL + LDL was also significantly accelerated in IDDM plasma (IDDM: k = 0.256 +/- 0.07; control: k = 0.092 +/- 0.05; mean +/- SD; P < 0.001). Fasting glucose and fructosamine correlated with both isotopic transfer (k) (r = 0.54, P = 0.009; r = 0.57, P = 0.005, respectively) and the mass of CE transferred at 2 h (r = 0.55, P = 0.006; r = 0.59, P = 0.004, respectively). Recombination experiments revealed that isotopic CET was accelerated when: (a) IDDM VLDL were combined with controls HDL and d > 1.21 fractions; and (b) IDDM d > 1.21 plasma fractions containing CETP were combined with controls VLDL + LDL and HDL.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2005

Molecular events associated with accelerated proliferative response in rat livers when partial hepatectomy is preceded by a sham operation.

BACKGROUND: When a sham operation is performed 6 h before partial hepatectomy (PH), the regenerative response is accelerated suggesting that sham operation itself contributes to cellular events leading to proliferation. MATERIALS AND METHODS: In order to examine the mechanisms implicated in this acceleration, we compared the activation of several factors associated with the progression through the cell cycle at various times after PH and after PH preceded by sham operation (S6 h + PH). The effect of a single sham (S) and two combined sham operations (S6 h + S) was also examined. Nonoperated rats were used as controls (C). RESULTS: The early factors NF-kappaB and Stat3 were activated after S6 h + PH and S6 h + S. C-jun expression was increased 0.5 h and 2 h after PH and 6 h after sham. There was no further increase in S6 h + PH and S6 h + S. In contrast, c-myc expression returned to baseline levels after S6 h and a new increase was observed 2 h after S6 h + PH but not after S6 h + S. P53 mRNA was significantly expressed 6 h after S6 h + PH, but at a level similar than that observed 6 and 12 h after PH alone. An earlier increase in c-Ha-ras mRNA and cyclin E protein was found in S6 h + PH, in comparison with PH alone. CONCLUSIONS: The first divergent response between the two combined models involved c-myc expression. However, major differences related to the accelerated liver regenerative response observed after S6 h + PH were found at late time points associating an earlier expression of c-Ha-ras and nuclear cyclin E.

Animals↗

PubMed2006

Colour stability of porcelain repair materials with accelerated ageing.

The purpose of this study was to measure and compare the colour stability of three porcelain repair materials (Charizma, Clearfil and Silux Plus) with an all-ceramic material following accelerated ageing. Three composites and one ceramic control were subjected to accelerated ageing for a period of 300 h. Initial specimen colour parameters were determined in the Commission International de I'Eclairage Lab (CIELAB) colour order system with a colorimeter. Colour changes were calculated before (DeltaE) and after 300 h of accelerated ageing (DeltaE*). Colour difference data were subjected to one-way analysis of variance (anova) followed by Duncan's test to examine the interaction between material and time interval of ageing. There were no significant difference between DeltaL values of Porcelain-Charizma and Porcelain-Silux Plus. All mean DeltaL* values were negative after 300 h ageing. Porcelain-Silux Plus demonstrated the highest DeltaL* of the investigated groups. There were significant differences between baseline 300-h aged specimens with respect to Deltaa*, Deltaa for either of the investigated materials. For Silux Plus, Deltaa and Deltaa* values were significantly higher than the others. Significant differences were observed between baseline and 300-h values for Deltab and Deltab*. Deltab and Deltab* values were significantly higher for Silux Plus. There were significant differences between baseline and 300-h values of colour difference, DeltaE, DeltaE*. Highest DeltaE* value was obtained using the microfilled composite, Silux Plus. Lowest value of DeltaE was recorded with the hybrid composite, Charizma.

Colorimetry↗

PubMed2005

IgM accelerates affinity maturation.

Secreted IgM is a potent adjuvant that concentrates antigen into secondary lymphoid organs and initiates antibody responses, germinal centre formation and is crucial in resolving infections. The current studies investigated the influence of specific IgM on both the quantity and quality of antibody produced in response to T-dependent and T-independent antigens. The addition of IgM to either antigen had no significant effect on the titre or duration of antibody responses. However, the presence of specific IgM led to accelerated affinity maturation when mice were challenged with low doses of IgM-containing immune complexes (IgM-IC) of T-dependent antigens compared with antigen alone. Interestingly, the administration of higher concentrations of IgM-IC increased follicular deposition of antigen but did not result in accelerated affinity maturation or in higher antibody affinities. The administration of IgM complexed with T-independent antigens had no effect on antibody titre, duration or affinity maturation, despite increased antigen deposition in lymphoid follicles. Together, these results demonstrate that IgM accelerates affinity maturation in immune responses to T-dependent antigens and implies an antigen optimum exists for the generation of high affinity antibodies. The data also suggest IgM plays an important role in the induction of CD4 T cells, facilitating germinal centre formation and function.

Animals↗

PubMed1992

Principles for designing enzyme-like catalysts based on the rate-acceleration mechanisms of semisynthetic oxidases.

Combinations of substrate-binding sites and catalytic groups constitute various kinds of enzyme-like catalysts. The design of such catalysts can be evaluated by the enhancement of the overall catalytic activity by combining these parts into one catalyst. For a catalyst having one substrate-binding site and one catalytic group, an equation was obtained which shows the relationship between the rate-acceleration due to the combination, the affinity of the site (1/Kd), intrinsic effective concentration (kin/kex) and substrate concentration ([S]). The intrinsic effective concentration is the ratio of the first-order rate constant (kin) of the intramolecular reaction between the catalytic group and the bound substrate and the second-order rate constant (kex) of the intermolecular reaction between the catalytic group and the free substrate; the value depends on the method of linking the catalytic group and the binding site. This equation provides the following principles for designing catalysts of this type with a considerable grade of rate-acceleration: [S] less than or equal to kin/kex and (1/10)[S] less than or equal to Kd less than or equal to kin/kex. To increase kin/kex, the structure of the binding site is required not to reduce the reactivity of the bound substrate, and the linker connecting the binding site and the catalytic group is required to be flexible and to have an appropriate length. A subunit structure is also found to be effective to improve the catalytic activity: the activity of an n-mer is at most n2 times as high as that of the monomer. As for the substrate-binding sites, the sites of natural enzymes and antibodies are good candidates because various kinds of binding sites with high affinity and specificity to the corresponding substrates are available. In addition, the equation relating the rate-acceleration with Kd, kin/kex, and [S] is used for explaining the catalytic efficiency of enzymes energetically. The principle for designing a multifunctional catalyst having several kinds of binding sites for its substrates and intermediates and several kinds of catalytic groups was then investigated. In this case, the diffusion of the intermediates strongly affects the activity of the multifunctional catalyst, and such a diffusion process was also analyzed. On the basis of these analyses, the following principles were obtained.(ABSTRACT TRUNCATED AT 400 WORDS)

Catalysis↗

PubMed2005

Increasing body weight predicts the earlier onset of insulin-dependant diabetes in childhood: testing the 'accelerator hypothesis' (2).

AIMS AND METHODS: It has recently been hypothesized that weight gain in childhood accelerates the onset of Type 1 diabetes, as well as increasing its risk, and that Type 1 diabetes and Type 2 diabetes may be one and the same disorder of insulin resistance. An explanation is needed for the rising incidence of childhood diabetes and, to test the Accelerator Hypothesis, we examined the anthropometric measurements recorded from birth in 168 young people presenting with Type 1 diabetes between 1980 and 2002. Pre-onset as well as peri- and post-onset measurements of height and weight were available, and waist circumference was recorded at various intervals after onset. RESULTS: The mean birth weight of the children and their height, weight and body mass index (BMI) at diagnosis lay close to the population mean. However, pre-onset and post-onset BMI were both well above the population mean, were closely correlated with each other (r = 0.79, P < 0.001) and (inversely) with age at onset (r = -0.30, P < 0.001). A significant correlation was also found between BMI standard deviation scores (sds) and year of diagnosis (r = 0.27, P < 0.001) and, importantly, waist circumference sds in the children with Type 1 diabetes was found to be substantially greater than average for the population [boys: +0.96 (sd 1.04), girls: +1.30 (sd 0.89)]. CONCLUSIONS: The data suggest that children with Type 1 diabetes have become progressively heavier at diagnosis over the past 20 years, and that the heavier child develops it earlier. Waist circumference, a proxy for visceral fat mass and insulin resistance, is substantially greater in children with Type 1 diabetes. Weight centile crossing appears to be an important environmental accelerator which may contribute to or account for the striking increase in both Type 1 diabetes and Type 2 diabetes in childhood. A reduction of body weight and improved lifestyle might reverse this trend in both types of diabetes.

Age of Onset↗

PubMed1998

Calcium-calmodulin-dependent mechanisms accelerate calcium decay in gastric myocytes from Bufo marinus.

1. [Ca2+] was recorded in voltage-clamped gastric myocytes from Bufo marinus. Repolarization to -110 mV following a 300 ms depolarization to +10 mV led to triphasic [Ca2+]i decay, with a fast-slow-fast pattern. After a conditioning train of repetitive depolarizations the duration of the second, slow phase of decay was shortened, while the rate of decay during the third, faster phase was increased by 34 +/- 6% (mean +/- S.E.M., n = 21) when compared with unconditioned transients. 2. [Ca2+]i decay was biphasic in cells injected with the calmodulin-binding peptide RS20, with a prolonged period of fast decay followed by a slow phase. There was no subsequent increase in decay rate during individual transients and no acceleration of decay following the conditioning train (n = 8). Decline of [Ca2+]i in cells injected with the control peptide NRS20 was triphasic and the decay rate during the third phase was increased by 50 +/- 19% in conditioned transients (n = 6). 3. Cell injection with CK3AA, a pseudo-substrate inhibitor of calmodulin-dependent protein kinase II, prevented the increase in the final rate of decay following the conditioning train (n = 6). In cells injected with an inactive peptide similar to CK3AA, however, there was a 45 +/- 17% increase after the train (n = 5). 4. Inhibition of Ca2+ uptake by the sarcoplasmic reticulum with cyclopiazonic acid or thapsigargin did not prevent acceleration of decay. 5. These results demonstrate that [Ca2+]i decay is accelerated by Ca(2+)-calmodulin and calmodulin-dependent protein kinase II. This does not depend on Ca2+ uptake by the sarcoplasmic reticulum but may reflect upregulation of mitochondrial Ca2+ removal.

Animals↗

PubMed2005

Activated JNK brings about accelerated apoptosis of Bcl-2-overexpressing C6 glioma cells on treatment with tamoxifen.

Tamoxifen causes apoptosis of malignant glial cells at a concentration that does not kill normal astrocytes. C6 glioma cells were stably transfected with a vector expressing Bcl-2 under the control of metallothionin promoter. Low leaky Bcl-2 expression offered complete protection against tamoxifen-induced apoptosis. High Bcl-2 levels, on the other hand, accelerated the apoptosis, with Bcl-2-overexpressing clones dying within 48 h of tamoxifen treatment as compared to 6 days for parental C6 cells. Overexpressed Bcl-2 is localized primarily in mitochondria and to a much lower extent in endoplasmic reticulum (ER). Only a minor fraction of the overexpressed Bcl-2 gets phosphorylated in tamoxifen-treated cells and the phosphorylation does not affect its binding to Bax. Tamoxifen treatment of Bcl-2-overexpressing clones was found to result in activation of c-Jun N-terminal kinase (JNK) and p38 kinase. Inhibition of JNK but not p38 kinase completely abrogated the accelerated apoptosis. Constitutively expressed endogenous c-Jun was found to be phosphorylated, resulting in increased activator protein 1 (AP-1) DNA-binding activity. Expression of Fas ligand (FasL), an AP-1 transcriptional target, increased during accelerated cell death. This presumably brought about activation of caspase 8, as inhibition of caspase 8 blocked the apoptosis. The JNK/c-Jun/AP-1/FasL pathway could be considered as a potential target for the therapy of gliomas.

Animals↗

PubMed2000

High glucose accelerates the life cycle of the in vivo exposed mesothelium.

BACKGROUND: Mouse mesothelium exposed in vivo for 30 days to high glucose solutions develop morphological changes that characterize a population of cells near the end of their life span. METHODS: The present study was designed to explore, in mesothelial cell imprints, whether these changes could derive from an early acceleration of the cell population life cycle in mice exposed for periods of up to 30 days to a 4.25% glucose fluid (236 mmol/L/L) prepared in Hank's balanced salt solution (HBSS). Three critical points of the cell's life cycle were evaluated: the G1 checkpoint [proliferating cell nuclear antigen (PCNA) expression], DNA synthesis ((3)H-thymidine incorporation), and the prevalence of mitosis. RESULTS: Cell populations exposed to a high glucose concentration showed an initial acceleration of their life cycle, as sustained by a peak of mitosis at two hours, an early increase of DNA incorporation sustained during the first 24 hours, as well as a top level of PCNA expression after three to four hours. These significantly higher values, compared with the control animals treated with HBSS, collapsed after 24 hours and were nil after 30 days of exposure. CONCLUSIONS: Exposure to a high glucose concentration induced an early and short-lived acceleration of the mesothelial cell cycle, and with a longer exposure this was followed by a depletion of the growth capabilities of the exposed monolayer.

Animals↗

PubMedDate not supplied

Premature aging in male alcoholics: "accelerated aging" or "increased vulnerability"?

This study involved an evaluation of two versions of the "premature aging" theory of chronic alcoholism: the accelerated aging and increased vulnerability versions. The major dependent measures used were the tests included in Reitan's brain age quotient (BAQ), a series of neuropsychological tests known to be sensitive to the effects of alcoholism and aging. Subjects were 40 chronic alcoholic inpatients and 40 matched controls, divided into age groups by decade, ranging from the 30s to the 60s. It was proposed that an interaction between age and presence or absence of alcoholism, with BAQ test differences between alcoholics and controls widening as age increases, would support the increased vulnerability version, while the absence of such an interaction would support the accelerated aging version. The results clearly favored the accelerated aging version, with marked BAQ test differences between alcoholics and controls appearing even in the 30-year-old groups. It was concluded that chronic alcoholics tend to perform at levels found for nonalcoholics 10 years their senior, but the discrepancy between alcoholics and nonalcoholics does not increase with age.

Adult↗

PubMed1998

Selective acceleration of auditory processing in chronic alcoholics during abstinence.

Simultaneous auditory processing between the hemispheres was studied with a whole-head magnetometer in 13 abstinent chronic alcoholics and 10 healthy control subjects. Auditory stimuli were presented monaurally with interstimulus intervals of 0.5 and 2.5 sec in different blocks. The N100m response, which contributes to stimulus detection, was significantly accelerated in the hemisphere ipsilateral to the ear stimulated in abstinent alcoholics. The MMNm response reflecting automatic stimulus-change detection peaked earlier in alcoholics, and the ipsilateral N100m latency correlated significantly with the abstinence duration. These results suggest that auditory processing is accelerated in the auditory cortex ipsilateral to the stimulated ear in chronic abstinent alcoholics and that the accelerated processing is at least partly reversible. This may be caused by the hyperexcitation in the brain related to the ethanol withdrawal.

Adult↗

PubMed1993

A comparison of an accelerated technique for casting post-and-core restorations with conventional techniques.

PURPOSE: This project compares an accelerated technique for the casting of post-and-core restorations with four traditional techniques. The accelerated technique uses two phosphate-bonded investments and the traditional techniques use a gypsum- and a phosphate-bonded investment. The study measures and compares the differences between the seating of the casting and the seating of the acrylic resin pattern. The effects of the techniques on the fit of castings with and without a ferrule are also compared. MATERIALS AND METHODS: Six groups of 10 castings were made from plastic patterns formed on a stainless steel test die. A different investment and/or burnout method was used for each group. Each group had two subgroups: ferruled and nonferruled. The fit of the plastic patterns was measured at two time intervals after forming, 2 weeks and 3 months. The patterns were invested immediately after the 3-month measurement, and the difference in fit of the castings was calculated. An ANOVA and Tuckey-Kramer test were done to determine the statistical validity. RESULTS: The seating of the patterns after 3 months of storage was consistently worse than the 2-week measurements of fit. The ferrule and nonferrule patterns were not statistically different in seating. Measurement of the castings showed that the ferruled castings seated significantly worse than the nonferrule castings. The difference in the seating of the castings as compared with the patterns was considered clinically unacceptable, showing a range of 0.301 mm to 0.528 mm. The nonferrule castings showed a significant difference in seating among groups. The difference ranged from -0.099 mm to 0.322 mm. CONCLUSIONS: The castings of the ferrule subgroups were considered clinically unacceptable and were not analyzed for significance. Among the nonferrule castings, the group using a gypsum investment and conventional technique for investing and burnout but no ring liner showed the best seating. The accelerated technique was intermediate in seating with a difference of 0.148 mm from the seating of the patterns. This group was significantly different from the two best groups but not from the remaining three groups.

Analysis of Variance↗