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Biomedical subjects

C A Mitchell

Publications and source records attributed to C A Mitchell.

At least 37 records · Page 2Linked to original sources
PubMed2001

Intracanopy lighting reduces electrical energy utilization by closed cowpea stands.

The high planting densities needed to grow edible biomass in sustainable space life support systems will create problems for planophile crops that form closed, self-shading canopies. The use of traditional overhead-lighting configurations will reduce the penetration of photosynthetically active radiation (PAR) into such canopies and will result in substantial shading of understory leaves. Intracanopy lighting, an irradiation approach that allows plants to grow around fixed arrays of low-intensity lamps, reduces overall energy expenditure for crop production by improving light distribution and interception throughout the canopy. Comparing different fluorescent lamp geometries within vegetative canopies of cowpea (Vigna unguiculata L. Walp) revealed great plasticity of leaf orientation to maximize absorption of PAR from lamps arrayed at various nontraditional angles. Varying the amount of photosynthetic energy available within canopies creates considerable potential to manipulate canopy productivity. Increasing lamp number 38% within cowpea canopies raised stand productivity 45%, reflecting the highly efficient interception and absorption of intracanopy PAR. However, combined above/within-canopy lighting did not increase overall PAR interception and vegetative yield, and productivity did not improve relative to the same input wattage of intracanopy lighting alone. Optimization of intracanopy lighting for crops to be used in future space life support systems will substantially reduce power and energy burdens for food-crop production.

Biomass↗
PubMed2000

Decreased SLIM1 expression and increased gelsolin expression in failing human hearts measured by high-density oligonucleotide arrays.

BACKGROUND: Failing human hearts are characterized by altered cytoskeletal and myofibrillar organization, impaired signal transduction, abnormal protein turnover, and impaired energy metabolism. Thus, expression of multiple classes of genes is likely to be altered in human heart failure. METHODS AND RESULTS: We used high-density oligonucleotide arrays to explore changes in expression of approximately 7000 genes in 2 nonfailing and 2 failing human hearts with diagnoses of end-stage ischemic and dilated cardiomyopathy, respectively. We report altered expression of (1) cytoskeletal and myofibrillar genes (striated muscle LIM protein-1 [SLIM1], myomesin, nonsarcomeric myosin regulatory light chain-2 [MLC(2)], and ss-actin); (2) genes responsible for degradation and disassembly of myocardial proteins (alpha(1)-antichymotrypsin, ubiquitin, and gelsolin); (3) genes involved in metabolism (ATP synthase alpha-subunit, succinate dehydrogenase flavoprotein [SDH Fp] subunit, aldose reductase, and TIM17 preprotein translocase); (4) genes responsible for protein synthesis (elongation factor-2 [EF-2], eukaryotic initiation factor-4AII, and transcription factor homologue-HBZ17); and (5) genes encoding stress proteins (alphaB-crystallin and mu-crystallin). In 5 additional failing hearts and 4 additional nonfailing controls, we then compared expression of proteins encoded by the differentially expressed genes, alphaB-crystallin, SLIM1, gelsolin, alpha(1)-antichymotrypsin, and ubiquitin. In each case, changes in protein expression were consistent with changes in transcript measured by microarray analysis. Gelsolin protein expression was also increased in cardiomyopathic hearts from tropomodulin-overexpressing (TOT) mice and rac1-expressing (racET) mice. CONCLUSIONS: Altered expression of the genes identified in this study may contribute to development of the heart failure phenotype and/or represent compensatory mechanisms to sustain cardiac function in failing human hearts.

Adolescent↗
PubMed2000

The yeast inositol polyphosphate 5-phosphatase Inp54p localizes to the endoplasmic reticulum via a C-terminal hydrophobic anchoring tail: regulation of secretion from the endoplasmic reticulum.

The budding yeast Saccharomyces cerevisiae has four inositol polyphosphate 5-phosphatase (5-phosphatase) genes, INP51, INP52, INP53, and INP54, all of which hydrolyze phosphatidylinositol (4,5)-bisphosphate. INP54 encodes a protein of 44 kDa which consists of a 5-phosphatase domain and a C-terminal leucine-rich tail, but lacks the N-terminal SacI domain and proline-rich region found in the other three yeast 5-phosphatases. We report that Inp54p belongs to the family of tail-anchored proteins and is localized to the endoplasmic reticulum via a C-terminal hydrophobic tail. The hydrophobic tail comprises the last 13 amino acids of the protein and is sufficient to target green fluorescent protein to the endoplasmic reticulum. Protease protection assays demonstrated that the N terminus of Inp54p is oriented toward the cytoplasm of the cell, with the C terminus of the protein also exposed to the cytosol. Null mutation of INP54 resulted in a 2-fold increase in secretion of a reporter protein, compared with wild-type yeast or cells deleted for any of the SacI domain-containing 5-phosphatases. We propose that Inp54p plays a role in regulating secretion, possibly by modulating the levels of phosphatidylinositol (4,5)-bisphosphate on the cytoplasmic surface of the endoplasmic reticulum membrane.

Amino Acid Sequence↗
PubMed2000

The inositol polyphosphate 5-phosphatases and the apurinic/apyrimidinic base excision repair endonucleases share a common mechanism for catalysis.

Inositol polyphosphate 5-phosphatases (5-phosphatase) hydrolyze the 5-position phosphate from the inositol ring of phosphatidylinositol-derived signaling molecules; however, the mechanism of catalysis is only partially characterized. These enzymes play critical roles in regulating cell growth, apoptosis, intracellular calcium oscillations, and post-synaptic vesicular trafficking. The UCLA fold recognition server (threader) predicted that the conserved 300-amino acid catalytic domain, common to all 5-phosphatases, adopts the fold of the apurinic/apyrimidinic (AP) base excision repair endonucleases. PSI-BLAST searches of GENPEPT, using the amino acid sequence of AP endonuclease exonuclease III, identified all members of the 5-phosphatase family with highly significant scores. A sequence alignment between exonuclease III and all known 5-phosphatases revealed six highly conserved motifs containing residues that corresponded to the catalytic residues in the AP endonucleases. Mutation of each of these residues to alanine in the mammalian 43-kDa, or yeast Inp52p 5-phosphatase, resulted in complete loss of enzyme activity. We predict the 5-phosphatase enzymes share a similar mechanism of catalysis to the AP endonucleases, consistent with other common functional similarities such as an absolute requirement for magnesium for activity. Based on this analysis, functional roles have been assigned to conserved residues in all 5-phosphatase enzymes.

Amino Acid Sequence↗
PubMed2000

Cloning and characterization of a 72-kDa inositol-polyphosphate 5-phosphatase localized to the Golgi network.

The inositol-polyphosphate 5-phosphatase enzyme family removes the 5-position phosphate from both inositol phosphate and phosphoinositide signaling molecules. We have cloned and characterized a novel 5-phosphatase, which demonstrates a restricted substrate specificity and tissue expression. The 3.9-kb cDNA predicts for a 72-kDa protein with an N-terminal proline rich domain, a central 5-phosphatase domain, and a C-terminal CAAX motif. The 3. 9-kilobase mRNA showed a restricted expression but was abundant in testis and brain. Antibodies against the sequence detected a 72-kDa protein in the testis in the detergent-insoluble fraction. Indirect immunofluorescence of the Tera-1 cell line using anti-peptide antibodies to the 72-kDa 5-phosphatase demonstrated that the enzyme is predominantly located to the Golgi. Expression of green fluorescent protein-tagged 72-kDa 5-phosphatase in COS-7 cells revealed that the enzyme localized predominantly to the Golgi, mediated by the N-terminal proline-rich domain, but not the C-terminal CAAX motif. In vitro, the protein inserted into microsomal membranes on the cytoplasmic face of the membrane. Immunoprecipitated recombinant 72-kDa 5-phosphatase hydrolyzed phosphatidylinositol 3,4,5-trisphosphate and phosphatidylinositol 3, 5-bisphosphate, forming phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 3-phosphate, respectively. We propose that the novel 5-phosphatase hydrolyzes phosphatidylinositol 3,4, 5-trisphosphate and phosphatidylinositol 3,5-bisphosphate on the cytoplasmic Golgi membrane and thereby may regulate Golgi-vesicular trafficking.

Amino Acid Sequence↗
PubMed2000

Phosphoinositide 3-kinase forms a complex with platelet membrane glycoprotein Ib-IX-V complex and 14-3-3zeta.

The binding of von Willebrand factor (vWF) to glycoprotein (GP) Ib-IX-V stimulates transmembrane signaling events that lead to platelet adhesion and aggregation. Recent studies have revealed that the signaling protein 14-3-3 zeta binds directly to the cytoplasmic domain of GP Ib alpha. In this study, the dynamic association of 14-3-3 zeta with GP Ib-IX, the phosphoinositide 3-kinase (PI 3-kinase), or both, was investigated in resting, thrombin, or vWF and botrocetin-stimulated platelets by analysis of discrete subcellular fractions. Results of this study demonstrate maximal coimmunoprecipitation of 14-3-3 zeta with GP Ib-IX in the nonstimulated cytosolic fraction and in the actin cytoskeletal fraction of thrombin- or vWF-stimulated human platelets. Immunoprecipitated 14-3-3 zeta or GP Ib from cytosolic fractions contained PI 3-kinase enzyme activity and an 85-kd polypeptide recognized by antibodies to the p85 subunit of PI 3-kinase. After platelet activation, the level of association between these species decreased in the cytosolic fraction. However, increased complex formation between 14-3-3 zeta and GP Ib-IX and between PI 3-kinase and GP Ib-IX was detected in actin cytoskeletal fractions derived from thrombin- or vWF-stimulated platelets. Recombinant glutathione S-transferase-14-3-3 zeta fusion protein (14-3-3 zeta-GST) inhibited affinity-captured PI 3-kinase enzyme activity up to 70% at 2 mcmol/L 14-3-3 zeta-GST. However, increasing concentrations up to 5 mcmol/L 14-3-3 zeta-GST resulted in the 3-fold enhancement of PI 3-kinase enzyme activity. We propose that the association between PI 3-kinase and 14-3-3 zeta with GP Ib-IX serves to promote the rapid translocation of these signaling proteins to the activated cytoskeleton, thereby regulating the formation of 3-position phosphoinositide-signaling molecules in this subcellular compartment. (Blood. 2000;96:577-584)

14-3-3 Proteins↗
PubMed2000

The influence of luting cement on the probabilities of survival and modes of failure of cast full-coverage crowns.

OBJECTIVES: This study compares the probabilities of survival and modes of failure of cast full-coverage crowns bonded with five cements when subjected to tensile pull-off testing. METHODS: Five groups of 25 sound human premolar teeth were prepared for full-coverage crowns, impressions recorded and customized castings fabricated in Ni-Cr-Mb bonding alloy. The cements tested were zinc phosphate, a hand-mixed and capsulated conventional glass-ionomer cement, a resin-modified glass-ionomer cement and a resin composite luting cement. The cemented crowns were stored in water at 37 degrees C for 24 h prior to application of a tensile pull-off force at a strain rate of 10 mm/min. The loads at failure were ranked and modelled by derived Weibull functions each describing the probability of a given specimen failing under a given load. Non-parametric statistical analysis was also applied to the results. RESULTS: There were no significant differences between the loads at failure of zinc phosphate cement, the hand-mixed or the capsulated glass-ionomer cements. The resin-modified glass-ionomer cement and the resin composite cement failed at significantly higher loads than the other three cements, but were not significantly different from each other. The Weibull modulus ranking for each cement from highest to lowest was resin composite = zinc phosphate, resin-modified glass-ionomer, hand-mixed conventional glass-ionomer and capsulated conventional glass-ionomer cement. SIGNIFICANCE: Weibull analysis allows dentists to compare the probability of survival of a crown bonded with different cements at a chosen load giving an indication of cement reliability.

Adhesiveness↗
PubMed2000

Prevalence of lower respiratory tract infections in hospitalized patients in the United Kingdom and Eire--results from the Second National Prevalence Survey.

During 1993 and 1994, the Hospital Infection Society conducted its Second National Prevalence Survey of infections in patients in British hospitals. The prevalence rates for hospital-acquired (HA) and community-acquired (CA), lower respiratory tract infections (LRTIs) were 2.4% and 6.1%, respectively; this shows an increase over that reported in the First National Prevalence Study. The prevalence rate of HA infections for ventilated patients was 18.6%. The prevalence was greater in males, odds ratio (OR, 95% CI) for HA-LRTIs (1.4, 1.1-1.6) and CA-LRTIs (1.2, 1.1-1.3) than in females. In the case of both HA-LRTIs and CA-LRTIs, there was an increase in prevalence in patients with age >75 years, (HA-LRTIs 1.7, 1.3-2.2; CA-LRTIs 1.7, 1.0-2.7). Results of multivariable logistic regression analysis showed an increased risk of HA-LRTIs in patients who had a nasogastric tube (3.6, 2.3-3.6), were ventilated (2.3, 1.6-3.2), trauma patients (2.2, 1.5-3.0), chronic obstructive airway disease (COAD), (1.9, 1.5-2.3), a tracheostomy (1.9, 1.3-2.7), prior blood transfusion (1.5, 1.2-1.8), smokers (1.4, 1.1-1.6) or on systemic corticosteroid therapy (OR 1.3, 1.1-1.6). Community-acquired LRTIs were positively associated with cystic fibrosis (33.7, 19.1-59.3), HIV (9.8, 6.5-14.8), COAD (4.8, 3.8-4.8), systemic corticosteroid therapy (2.5, 2.2-2.8), tracheostomy (1.8, 1.1-2.9), males (1.2, 1.1-1.3) and smoking (1.2, 1.1-1.4).

Adolescent↗
PubMed2000

The yeast inositol polyphosphate 5-phosphatases inp52p and inp53p translocate to actin patches following hyperosmotic stress: mechanism for regulating phosphatidylinositol 4,5-bisphosphate at plasma membrane invaginations.

The Saccharomyces cerevisiae inositol polyphosphate 5-phosphatases (Inp51p, Inp52p, and Inp53p) each contain an N-terminal Sac1 domain, followed by a 5-phosphatase domain and a C-terminal proline-rich domain. Disruption of any two of these 5-phosphatases results in abnormal vacuolar and plasma membrane morphology. We have cloned and characterized the Sac1-containing 5-phosphatases Inp52p and Inp53p. Purified recombinant Inp52p lacking the Sac1 domain hydrolyzed phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P(2)] and PtdIns(3, 5)P(2). Inp52p and Inp53p were expressed in yeast as N-terminal fusion proteins with green fluorescent protein (GFP). In resting cells recombinant GFP-tagged 5-phosphatases were expressed diffusely throughout the cell but were excluded from the nucleus. Following hyperosmotic stress the GFP-tagged 5-phosphatases rapidly and transiently associated with actin patches, independent of actin, in both the mother and daughter cells of budding yeast as demonstrated by colocalization with rhodamine phalloidin. Both the Sac1 domain and proline-rich domains were able to independently mediate translocation of Inp52p to actin patches, following hyperosmotic stress, while the Inp53p proline-rich domain alone was sufficient for stress-mediated localization. Overexpression of Inp52p or Inp53p, but not catalytically inactive Inp52p, which lacked PtdIns(4,5)P(2) 5-phosphatase activity, resulted in a dramatic reduction in the repolarization time of actin patches following hyperosmotic stress. We propose that the osmotic-stress-induced translocation of Inp52p and Inp53p results in the localized regulation of PtdIns(3,5)P(2) and PtdIns(4,5)P(2) at actin patches and associated plasma membrane invaginations. This may provide a mechanism for regulating actin polymerization and cell growth as an acute adaptive response to hyperosmotic stress.

Actins↗
PubMed2000

Inositol (1,4,5)trisphosphate metabolism and enhanced calcium mobilization in airway smooth muscle of hyperresponsive rats.

Airway hyperresponsiveness (AHR) is a phenotype of asthma and can be modeled by the inbred Fisher strain of rat, which is hyperresponsive in vivo relative to the Lewis strain. Enhanced airway smooth muscle (ASM) contractility and Ca(2+) mobilization are associated with the AHR observed in Fisher rats. In this study, we investigated whether the interstrain differences in Ca(2+) mobilization to serotonin (5HT) result from differences in inositol (1,4,5)trisphosphate (IP(3)) metabolism and/or IP(3) receptor (IP(3)R) sensitivity. Ca(2+) mobilization by 5HT in cultured ASM cells from both rat strains was phospholipase C (PLC) dependent. Inositol polyphosphate accumulation, and hence PLC activity, was similar in both rat strains, but a specific IP(3) transient was detectable only in Fisher myocytes in response to 5HT. These findings suggested that IP(3) degradation rather than production differed between the two strains. The Vmax and Michaelis constant (K(m)) of IP(3)-specific 5-phosphatase activity were higher in the particulate fraction of Lewis than in Fisher ASM cell homogenates and appeared to be related to a greater expression of two isoforms of 5-phosphatase (type I and type II) in Lewis cells as shown by Western blot analysis. The sensitivity of the IP(3)R to IP(3) was similar between Fisher and Lewis ASM cells, indicating that the interstrain intracellular Ca(2+) differences were unrelated to IP(3)R function. We propose that interstrain variations in 5-phosphatase activity and expression may give rise to the interstrain differences in IP(3)-mediated Ca(2+) release in ASM and may be a determinant of AHR.

Animals↗
PubMed2000

Sustained elevation in inositol 1,4,5-trisphosphate results in inhibition of phosphatidylinositol transfer protein activity and chronic depletion of the agonist-sensitive phosphoinositide pool.

The 43 kDa inositol polyphosphate 5-phosphatase (5-phosphatase) hydrolyses the signalling molecules inositol 1,4,5-trisphosphate (Ins(1,4,5)P(3)) and inositol 1,3,4,5-tetrakisphosphate (Ins(1,3,4, 5)P(4)) in a signal-terminating reaction. We have utilised cell lines that stably underexpress the 43 kDa 5-phosphatase, as a model system to investigate whether Ins(1,4,5)P(3) can control the rate of its own formation by regulating the resupply of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P(2)). A sustained 2.6-fold elevation in the basal concentration of Ins(1,4,5)P(3), in cell lines underexpressing the 43 kDa 5-phosphatase, correlated with a 32% reduction in the total cellular mass of PtdIns(4,5)P(2). The depletion in cellular PtdIns(4,5)P(2) was confined to a Triton-insoluble cell compartment, enriched in caveolin. In resting cells with elevated Ins(1,4,5)P(3) concentrations resulting from underexpression of the 43 kDa 5-phosphatase, phosphatidylinositol (PtdIns) and phosphatidylinositol 4-phosphate (PtdIns(4)P) were depleted by 50% and PtdIns(4,5)P(2) by 61% in the caveolin-enriched Triton-insoluble compartment. Agonist stimulation resulted in the rapid turnover of phosphoinositides in the caveolin-enriched Triton-insoluble fraction of vector-transfected cells, but not in cells with high basal Ins(1,4,5)P(3) concentrations. Depletion of phosphoinositides from the caveolin-enriched Triton-insoluble pool in cells underexpressing the 43 kDa 5-phosphatase did not result from activation of phospholipase C isoenzymes, or inhibition of PtdIns 4-kinase or PtdIns(4)P 5-kinase activities. Significant inhibition of phosphatidylinositol transfer protein (PITP) activity (up to 70%) was observed in cells with elevated basal Ins(1,4,5)P(3) concentrations; however, no reduction in PITP(&agr;) protein expression was detected. These studies indicate that chronic elevation in cellular Ins(1,4,5)P(3) concentrations decreases the PITP-mediated resupply of phosphoinositides in the caveolin-enriched agonist-sensitive pool.

Animals↗
PubMed2000

Selection of materials for post cementation.

Many types of cement are available for post cementation, each with advantages and disadvantages. For posts with adequate mechanical retention, zinc phosphate is a good choice for patients for whom fluoride release is not considered essential. Posts with compromised mechanical retention benefit from use of a resin-modified glass-ionomer cement, which also releases fluoride. Composite resin cements should be reserved for rare cases where mechanical retention is so compromised that use of a resin-modified glass-ionomer cement provides inadequate retention. Great care is required when using composite resin cements to ensure optimum performance and avoid the creation of difficult-to-remove excess cement. Clinicians should be aware that posts cemented with resin-modified glass ionomer or composite resin cements may be difficult or impossible to remove if access to the root canal system is subsequently required.

Cementation↗
PubMed1999

Characterization of two isoforms of the skeletal muscle LIM protein 1, SLIM1. Localization of SLIM1 at focal adhesions and the isoform slimmer in the nucleus of myoblasts and cytoplasm of myotubes suggests distinct roles in the cytoskeleton and in nuclear-cytoplasmic communication.

We have cloned and characterized a novel isoform of the skeletal muscle LIM protein 1 (SLIM1), designated SLIMMER. SLIM1 contains an N-terminal single zinc finger followed by four LIM domains. SLIMMER is identical to SLIM1 over the first three LIM domains but contains a novel C-terminal 96 amino acids with three potential bipartite nuclear localization signals, a putative nuclear export sequence, and 27 amino acids identical to the RBP-J binding region of KyoT2, a murine isoform of SLIM1. SLIM1 localized to the cytosol of Sol8 myoblasts and myotubes. SLIMMER was detected in the nucleus of myoblasts and, following differentiation into myotubes, was exclusively cytosolic. Recombinant green fluorescent protein-SLIM1 localized to the cytoplasm and associated with focal adhesions and actin filaments in COS-7 cells, while green fluorescent protein-SLIMMER was predominantly nuclear. SLIMMER truncation mutants revealed that the first nuclear localization signal mediates nuclear localization. The addition of the proposed nuclear export sequence decreased the level of exclusively nuclear expression and increased cytosolic SLIMMER expression in COS-7 cells. The leucine-rich nuclear export signal was required for the export of SLIMMER from the nucleus of myoblasts to the cytoplasm of myotubes. Collectively, these results suggest distinct roles for SLIM1 and SLIMMER in focal adhesions and nuclear-cytoplasmic communication.

Alternative Splicing↗
PubMed1999

The inositol polyphosphate 4-phosphatase forms a complex with phosphatidylinositol 3-kinase in human platelet cytosol.

Inositol polyphosphate 4-phosphatase (4-phosphatase) is an enzyme that catalyses the hydrolysis of the 4-position phosphate from phosphatidylinositol 3,4-bisphosphate [PtdIns(3,4)P2]. In human platelets the formation of this phosphatidylinositol, by the actions of phosphatidylinositol 3-kinase (PI 3-kinase), correlates with irreversible platelet aggregation. We have shown previously that a phosphatidylinositol 3,4,5-trisphosphate 5-phosphatase forms a complex with the p85 subunit of PI 3-kinase. In this study we investigated whether PI 3-kinase also forms a complex with the 4-phosphatase in human platelets. Immunoprecipitates of the p85 subunit of PI 3-kinase from human platelet cytosol contained 4-phosphatase enzyme activity and a 104-kDa polypeptide recognized by specific 4-phosphatase antibodies. Similarly, immunoprecipitates made using 4-phosphatase-specific antibodies contained PI 3-kinase enzyme activity and an 85-kDa polypeptide recognized by antibodies to the p85 adapter subunit of PI 3-kinase. After thrombin activation, the 4-phosphatase translocated to the actin cytoskeleton along with PI 3-kinase in an integrin- and aggregation-dependent manner. The majority of the PI 3-kinase/4-phosphatase complex (75%) remained in the cytosolic fraction. We propose that the complex formed between the two enzymes serves to localize the 4-phosphatase to sites of PtdIns(3,4)P2 production.

Blood Platelets↗
PubMed1999

The cardiac expression of striated muscle LIM protein 1 (SLIM1) is restricted to the outflow tract of the developing heart.

LIM proteins perform critical roles in development and tissue differentiation. The skeletal muscle LIM protein 1 (SLIM1) comprises four and a half LIM domains. Northern blot analysis demonstrated high level expression of SLIM1 mRNA in adult human skeletal muscle with intermediate expression in adult heart and lower expression in other tissues. Western blot analysis using specific affinity-purified anti-SLIM1 antipeptide antibodies demonstrated a 32 kDa polypeptide in the aorta and atria of rabbit heart, but not in vena cava, interventricular septum or ventricular muscle. SLIM1 was also demonstrated in rabbit skeletal muscle. In situ hybridization of whole mouse embryos confirmed the cardiac expression of SLIM1 was restricted to the cardiac outflow tract from embryonic day 8.5-11. No expression was seen in atrial or ventricular muscle. SLIM1 mRNA was also demonstrated in the hindbrain, neural tube and somites. The localized expression of SLIM1 to the outflow tract of the embryonic heart implies an important role for the protein in the development of this region and possibly in congenital heart anomalies involving the separation and formation of the aortic and pulmonary trunks.

Adult↗
PubMed1999

Retention of adhesive cement on the tooth surface after crown cementation.

STATEMENT OF PROBLEM: Adhesive cements increase crown retention, but it is unknown if traces of cement remain undetected on the tooth surface after clinical removal of excess cement, which could exacerbate plaque retention. PURPOSE: This study measured the surface area, volume, mean depth, and maximum depth of a resin composite and a compomer luting cement left adherent on the tooth surface after removal of excess cement, as judged clinically. METHODS AND MATERIAL: Four groups of specimens (n = 48) were prepared for full coverage crowns: group AC bonding alloy with chamfer finish line, group G gold alloy with chamfer finish line, group PC porcelain with a chamfer finish line, and group PS porcelain with a shoulder finish line. Two profiles of the mesial and distal surfaces of the teeth were carried out: (1) tooth with crown seated but not cemented and (2) tooth with the crown cemented in place. Two cements and 2 methods of cement removal were studied. RESULTS: A 4-way analysis of variance for cement, crown type, method of removal, and tooth surface morphology showed that significantly greater volumes and mean depth, but not surface areas, of resin composite cement remained adherent than compomer cement (P<.05). Among crown types, significant differences were found for cement volume (group G>AC, G>PC, G>PS), cement surface area (group AC>PC, G>PC, G>PS), and maximum cement depth (group G>AC). There was no significant difference between the 2 methods of cement removal. Significantly larger surface areas and maximum depths of cement were retained on the anatomically grooved mesial surface of the maxillary first premolars than on the ungrooved distal surface. CONCLUSION: Subclinical cement retention occurred after crown cementation, which was influenced by cement, crown type, and tooth surface morphology but not method of cement removal.

Adhesives↗
PubMed1999

Fracture toughness of conventional, resin-modified glass-ionomer and composite luting cements.

OBJECTIVES: This study was conducted to determine if significant differences existed between the fracture toughness of three types of luting cement, and, if the method of mixing conventional glass-ionomer luting cements, hand-mixed or mechanically mixed, influenced the value obtained. METHODS: Three types of luting cement were investigated: conventional glass-ionomer cement (two handmixed and two capsulated cements, KetacCem, Fuji I and KetacCem Maxicap, Fuji Cap I), a resin-modified glass-ionomer cement (Vitremer Luting Cement) and a resin composite cement (Scotchbond Resin Cement). Eleven specimens of each of the six cements were fabricated to determine the plane strain fracture toughness using the chevron notch short rod technique. After seven days the specimens were loaded in a water bath, at a crosshead speed of 4 microns/s and the fracture toughness values calculated. RESULTS: ANOVA indicated significant differences between the cements (p < 0.0001) and each cement was compared with all others using Fishers PSLD test (p < 0.05). The rank order of results from highest fracture toughness value to lowest (mean +/- s.d.) was Scotchbond Resin Cement (1.31 +/- 0.17), Vitremer Luting Cement (1.08 +/- 0.1), Fuji Cap I (0.37 +/- 0.04), KetacCem Maxicap (0.37 +/- 0.05), Fuji I (0.34 +/- 0.04), KetacCem (0.27 +/- 0.03). SIGNIFICANCE: Of the cements tested, the resin composite cement is most likely to resist clinical failure by cement cohesive failure.

Analysis of Variance↗