Biomedical subjects

Q Zhu

Publications and source records attributed to Q Zhu.

At least 91 records · Page 5Linked to original sources

PubMed2000

Differential expression of the adipocyte amino acid transporter is transactivated by SP1 and SP3 during the 3T3-L1 preadipocyte differentiation process.

It was identified that a Sp1-like cis-element in the adipocyte amino acid transporter gene (AAAT) promoter is the major cis-motif for its induced expression during the 3T3-L1 preadipocyte differentiation process. Electrophoretic mobility shift analysis of this cis DNA element showed that the transcription factors binding to this sequence were Sp1 and Sp3. Protein analysis of Sp1 and Sp3 in nuclear extracts from 3T3-L1 cells at various differentiation stages indicated that these two transcription factors existed in noninduced 3T3-L1 preadipocytes, but they did not bind to the AAAT promoter element with high affinity. They were activated after differentiation induction. It was further demonstrated that dephosphorylation of Sp1 increased its binding affinity to this inducible AAAT promoter element.

3T3 Cells↗

PubMed2000

Enhanced sensitivity to anti-benzo(a)pyrene-diol-epoxide DNA damage correlates with decreased global genomic repair attributable to abrogated p53 function in human cells.

DNA damage from exposure to environmental chemical carcinogens and failure of repair systems to eliminate these lesions from the genome are considered as the crucial initial steps in the development of various human malignancies. Many cellular proteins are known to play vital roles to overcome the effects of DNA damage. Among such proteins, p53 is known to respond to DNA damage by accumulating in the nucleus and inhibiting cell cycle progression to facilitate DNA repair and the maintenance of genomic stability. In this study, we have investigated the role of p53 protein in modulating nucleotide excision repair of anti-benzo-(a)pyrene-diol-epoxide (BPDE)-DNA adducts and related effects using human fibroblasts with normal (p53-WT) and altered p53 protein (p53Mut and p53-Null). Interestingly, irrespective of the presence or absence of p53, the anti-BPDE dose-dependent p21 protein induction response was qualitatively comparable in all of the three cell lines. However, cells with defective p53 function were deficient for the removal of anti-BPDE-DNA adducts from the overall genome compared to cells with wild-type p53 activity. Strand-specific repair analysis within the individual strands of the p53 gene revealed decreased repair of adducts from the nontranscribed strand in p53-Mut and p53-Null cells. However, the repair of the transcribed strand appeared to be identical in all of the three cell lines. Furthermore, p53-Mut and p53-Null cells were more sensitive than p53-WT cells and displayed increased levels of anti-BPDE-induced apoptosis. Thus, wild-type p53 is required for the efficient global genomic repair of anti-BPDE-induced DNA adducts from the overall genome, but not for transcription-coupled repair of actively transcribed genes. These findings indicate that inefficient DNA repair of potentially cytotoxic and mutagenic lesions from the nontranscribed strand due to the loss of p53, but not the loss of p21, function might be responsible for enhanced cytotoxicity and apoptosis in human cells upon DNA damage.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

PubMed2000

Decreased DNA repair efficiency by loss or disruption of p53 function preferentially affects removal of cyclobutane pyrimidine dimers from non-transcribed strand and slow repair sites in transcribed strand.

The tumor suppressor protein p53 plays a central role in modulating the cellular responses to DNA damage. Several recent studies, undertaken with the whole genomic DNA or full-length gene segments, have shown that p53 is involved in nucleotide excision repair and it selectively influences the adduct removal from the non-transcribed strand in the genome. In this study, we have analyzed the damage induction at nucleotide resolution by ligase-mediated polymerase chain reaction and compared the repair of ultraviolet radiation-induced cyclobutane pyrimidine dimers within exon 8 of p53 gene in normal and Li-Fraumeni syndrome fibroblasts as well as in normal and human papillomavirus 16 E6 and E7 protein-expressing human mammary epithelial cells. The results demonstrate that (i) loss or disruption of p53 function decreases efficiency of DNA repair, by preferentially affecting the repair of non-transcribed strand and of intrinsically slow repair sites in transcribed strand; (ii) mutant p53 protein affects DNA repair, at least of non-transcribed strand, in a dominant negative manner; and (iii) pRb does not have an effect on the repair of DNA damage within transcribed or non-transcribed strand. The overall data suggest that p53 could regulate excision repair or related events through direct protein-protein interaction.

Cells, Cultured↗

PubMed2000

p53-degradation by HPV-16 E6 preferentially affects the removal of cyclobutane pyrimidine dimers from non-transcribed strand and sensitizes mammary epithelial cells to UV-irradiation.

Nucleotide excision repair (NER), the most versatile and ubiquitous mechanism for DNA repair, operates to remove many types of DNA base lesions. We have studied the role of p53 function in modulating the repair of DNA damage following UV irradiation in normal and p53-compromised human mammary epithelial cells (HMEC). The effect of UV-induced DNA damage on cellular cytotoxicity and apoptosis was determined in conjunction with global, gene- and strand-specific repair. Cytotoxicity studies, using clonogenic survival and MTT assays, showed that HPV-16 E6-expressing HMEC were more UV sensitive than p53-WT cell lines. High apoptotic index obtained with p53-compromised cells was in conformity to both the low clonogenic survival and the low cellular viability. No discernible differences in the formation of initial UV-induced cyclobutane pyrimidine dimers (CPD) were observed in the cell lines of varying p53 functional status. However, the extent and the rate of damage removal from genome overall were highest for p53-WT cells. Further examination of strand-specific repair in the p53 gene revealed that the removal of CPD in the non-transcribed strand (NTS) was slower in p53-compromised cells compared to the normal p53-WT cell lines. These results suggest that loss of p53 function, in the absence of other genetic alterations, decreased both overall amount of CPD repaired and their removal rate from the genome. Additionally, normal function of p53 is required for the repair of the NTS, but not of the transcribed strand (TS) in genomic DNA in human epithelial cells. Thus, failure of quantitative removal of CPD by global genomic repair (GGR), due to loss of p53 function, causes the enhanced UV sensitivity and increased damage-induced apoptosis via a p53-independent pathway. Nevertheless, recovery of cells from UV damage requires normal p53 function and efficient GGR.

Apoptosis↗

PubMed2000

Variation in bone mineral density of the sacrum in young adults and its significance for sacral fixation.

STUDY DESIGN: Bone mineral density variations throughout the sacrum were measured and correlated with sacral screw insertion torque. OBJECTIVE: To quantify bone mineral density variations within the S1 body and ala of young human specimens, especially along the pathways of sacral screws, and to examine the relation between sacral screw fixation and bone mineral density. SUMMARY OF BACKGROUND DATA: Vertebral bone quality is an essential factor in anterior or posterior screw fixation of the spine. Several studies have been conducted regarding bone mineral density variations in the cervical and thoracolumbar spine. However, such variations in bone mineral density in the sacrum have not been well documented. METHODS: The bone mineral density of 13 sacral specimens from young male cadavers (mean age, 31 years) was measured using highly accurate quantitative computed tomography. Variations in bone mineral density were measured in five transverse layers and seven vertical columns within the S1 body, and in four transverse layers and six vertical columns within the ala. The sacral screw insertion torque was measured (unicortical and bicortical), and the correlation with bone mineral density was calculated. RESULTS: The mean bone mineral density of the S1 body was 381.9 +/- 59 mg/cm3, which was 31.9% higher than that of the sacral ala (mean, 296.9 +/- 86 mg/cm3) (P < 0.05). Bone mineral density of the superior sacral endplate was higher than that of any other transverse layer. Columns near the lateral posterior and lateral anterior of the S1 body had the highest bone mineral density. In the ala, bone mineral density values of the internal columns (pedicle) were the highest. Screw insertion torque for bicortical purchase along the S1 pedicle correlated well with the bone mineral density of the S1 body (r = 0.67, P < 0.05). CONCLUSION: This study quantified the volumetric bone mineral density variations within the S1 body and ala, and a significant linear correlation between the screw insertion torque and bone mineral density was found. Optimal sacral screw insertion pathways were also outlined based on bone mineral density values.

Adult↗

PubMed2000

Formation, photodissociation and structure of chromium/phosphorus binary cluster ions

Chromium/phosphorus binary cluster ions, [Cr(n)P(m)](+/-), produced by laser (532nm) ablation on a tablet of well-mixed chromium and red phosphorus powder, were studied with a home-built tandem time-of-flight (TOF) mass spectrometer. The clusters thus formed are mostly rich in phosphorus. There is an odd-even oscillation in the intensity of the [CrP(m)](+) series, i.e. the mass peaks of even m are higher than those of odd m. The peaks of [CrP(4)](+) and [CrP(8)](+) are especially prominent, which may be ascribed to the specific stability of P(4) sub-structures. There are also some intense peaks in the spectrum assigned to [Cr(3)P(8)](+), [Cr(4)P(9)](+), [Cr(5)P(11)](+), [Cr(6)P(12)](+), [Cr(8)P(14)](+) clusters, etc., which have stable compositions. The stability of these species is consistent with a simple qualitative electronic structure model, in which the valence electrons of P are filled into the d orbitals of Cr. The photodissociation of some cluster ions was also studied. DFT calculations were performed on three small cluster ions to provide some insight into their structures. Copyright 2000 John Wiley & Sons, Ltd.

Journal Article↗

PubMed2000

Loosening of sacral screw fixation under in vitro fatigue loading.

Sacral screw fixation is frequently used for fusion of the lower lumbar spine, but sacral screws appear to offer less secure fixation than lumbar pedicle screws, and failure due to loosening under fatigue loading is common. The aim of this study was to examine in vitro the stability of medial and lateral bicortical and unicortical sacral screw fixation under a physiologically relevant fatigue-loading pattern. Bone mineral density, screw insertion torque, and screw-fixation stiffness were measured prior to cyclic loading between 40 and 400 N compression at 2 Hz for 20,000 cycles. The screw-fixation stiffness was measured every 500 cycles, and the axial pullout strength of the screws was recorded following loading. All of the lateral insertions loosened under the applied loading, but some of the medial insertions remained stable. Medial insertions proved stiffer and stronger than lateral insertions, and bicortical fixations were stronger than unicortical fixations. Bone mineral density and insertion torque were correlated with screw stiffness and pullout strength, although better correlation was found for insertion torque than bone mineral density. Bone mineral density is a good preoperative indicator of sacral screw-fixation strength, and insertion torque is a good intraoperative indicator. An insertion torque greater than 1.5 Nm is suggested as an indicative value for a stable medial unicortical insertion, whereas an insertion torque greater than 2 Nm suggests a stable medial bicortical insertion. It appears that, apart from the choice of technique (screw orientation and depth), minimizing the load on the screws during the initial part of the fusion process is also critical to maintain stability of the fused section and to obtain a solid fusion mass.

Adult↗

PubMed2000

Cloning of cDNA and the gene encoding human hepatocyte nuclear factor (HNF)-3 beta and mutation screening in Japanese subjects with maturity-onset diabetes of the young.

AIMS/HYPOTHESIS: Molecular defects of the genes for transcription factors, hepatocyte nuclear factor (HNF)-4 alpha, HNF-1 alpha, HNF-1 beta and insulin promoter factor-1 cause maturity-onset diabetes of the young (MODY1, 3, 5, and 4, respectively). This suggests the HNF-related transcription cascade is important in insulin secretion which is induced by glucose. These genes and the gene encoding glycolytic enzyme glucokinase (MODY2) are, however, responsible for only 15-20% of cases of MODY in the Japanese. Searching for a novel form of MODY in this population, we cloned a new candidate gene encoding human HNF-3 beta, a winged helix transcription factor, which also belongs to the same HNF-transcription cascade. METHODS: The cDNA clone for human HNF-3 beta was isolated from a liver cDNA library. The gene was also cloned from a genomic library and its organization and chromosomal localization were determined. We screened 68 Japanese subjects with MODY/early-onset diabetes for mutations in this gene. RESULTS: Human HNF-3 beta is composed of 457 amino acids. The human gene, which was mapped to the segment 30 cR from SHGC-37039 on chromosome 20p by radiation hybrid mapping, spans approximately 4.5 kb and consists of three exons. Direct sequencing of the exons and flanking regions identified one missense mutation A328 V and seven polymorphisms, although the functional significance of the mutation in the pathogenesis of diabetes is not known. CONCLUSION/INTERPRETATION: The characterization of the structure of the HNF-3 beta gene and its mapping in the framework of markers will be helpful in genetic studies of the various forms of diabetes mellitus.

Amino Acid Sequence↗

PubMed2000

Identification of missense mutations in the hepatocyte nuclear factor-3beta gene in Japanese subjects with late-onset Type II diabetes mellitus.

AIMS/HYPOTHESIS: Hepatocyte nuclear factor (HNF)-3beta, a transcription factor expressed in pancreatic beta cells, is an upstream regulator of HNF-1alpha/MODY3, HNF-4alpha/MODY1 and IPF1/MODY5 genes. Our previous screening of MODY subjects showed that mutations in the HNF-3beta gene are not a common cause of this form of diabetes in the Japanese. We tested the hypothesis that mutations in the HNF-3beta gene cause late-onset Type II (non-insulin-dependent) diabetes mellitus in this population. METHODS: Genotyping of the polymorphic TCC repeat in the HNF-3beta gene was done in 112 Japanese subjects with Type II diabetes (age at diagnosis > 35 and family history of Type II diabetes among their second-degree relatives) and 96 Japanese control subjects. Furthermore, we screened 57 Type II diabetic patients for mutations of the HNF-3beta gene. Transactivation activity of variant HNF-3beta was investigated by transfection assay. RESULTS: The distribution of alleles of the TCC repeat was similar between diabetic and control groups. Mutation screening identified two missense mutations, A86T and G114E. Neither mutation was observed in 225 control subjects. The transactivation activity of G114E-HNF-3beta was similar to that of wild typeHNF-3beta. In contrast, the activity of A86T-HNF-3beta was statistically significantly reduced to 83-86 % of that of wild type. CONCLUSIONS/INTERPRETATION: The A86T mutation in the HNF-3beta gene might be involved in the development of late-onset Type II diabetes in a small group of Japanese people.

Adult↗

PubMed2000

Dipeptide seryl-histidine and related oligopeptides cleave DNA, protein, and a carboxyl ester.

The amino acids histidine (His) and serine (Ser), or amino acids similar to Ser, function together as key catalytic amino acids in the active sites of such diverse enzymes as the serine- and thiol-proteases, lipases, and esterases. Ser and His are also conserved in the intein-extein junctions of the phylogenetically widespread self-splicing proteins and at the N- and C-termini of the homing endonucleases spliced from them. Here we show that the dipeptide seryl-histidine (Ser-His) and related oligopeptides can themselves cleave DNA, protein, and the ester p-nitrophenyl acetate (p-NPA) over wide ranges of pH and temperature. Denaturing polyacrylamide gel electrophoresis (PAGE) of 5'-end labeled DNA samples incubated with Ser-His reveals a pattern of two bands per nucleotide position, consistent with the generation of both 3'-hydroxyl and 3'-phosphate DNA cleavage fragments, as would be expected of phosphodiester hydrolysis by Ser-His. To the best of our knowledge, Ser-His is the shortest peptide ever reported to show cleavage activity with multiple categories of natural substrates. The amenability of the dipeptide to variation through addition of amino acid residues, either internally or to the C-terminus while retaining its multiple cleavage activities, combined with its reactivity over wide ranges of pH and temperature, demonstrates the evolutionary capacity of the Ser/His dyad and evokes many questions about possible roles it may have played in molecular evolution and its potential role as a core for selection of oligopeptides with enhanced cleavage activities and target specificity.

Amino Acid Sequence↗

PubMed2000

Effects of atorvastatin treatment on the oxidatively modified low density lipoprotein in hyperlipidemic patients.

Atorvastatin is an established HMG-CoA reductase inhibitor which effectively reduces the plasma low density lipoprotein (LDL)-cholesterol level in hyperlipidemic patients. The present study was designed to investigate whether atorvastatin treatment can modify the biochemical content of oxidized LDL in hyperlipidemic patients and the ability of oxidized LDL to impair the endothelium-dependent relaxation of blood vessels. With atorvastatin (10 mg/day) treatment for 4 weeks in 19 type IIa hyperlipidemic patients, total cholesterol level was lowered by 23%, LDL-cholesterol was lowered by 32% and triacylglycerol was lowered by 19% as compared with dietary therapy alone. High density lipoprotein levels increased by approximately 9%. The ability of oxidized LDL from hyperlipidemic patients after atorvastatin treatment to impair the endothelium-dependent relaxation was significantly reduced as compared with dietary intervention alone. Analysis of the biochemical contents of oxidized LDL from this group revealed that there was an 11% reduction in lysophosphatidylcholine (LPC) as compared with the group that received only dietary counseling. A decrease in the C16:0 moiety with a corresponding increase in the C18:0 moiety of LPC in the oxidized LDL was also observed in the atorvastatin treated group. We propose that the observed reduction and the change in composition of acyl groups in LPC in the oxidized LDL of the atorvastatin-treated group results from a combination of the continued dietary treatment as well as drug therapy. In view of an observation that both C16:0 and C18:0 LPC species are equally potent in the impairment of endothelium-dependent relaxation of the aortic rings, we feel that the reduced level of LPC in the oxidized LDL produced by atorvastatin treatment is partially responsible for the improvement in endothelium control of vascular tone.

Adult↗

PubMed2000

Transformation of rice with the Arabidopsis floral regulator LEAFY causes early heading.

Onset of flowering, or heading date, is an important agronomic trait of cereal crops such as rice and early-heading varieties are required for certain regions in which rice is cultivated. Since the floral control gene LEAFY from Arabidopsis can dramatically accelerate flowering in dictoyledonous plants, the usefulness of LEAFY for manipulating heading date in rice has been tested. Constitutive expression of LEAFY from the cauliflower mosaic virus 35S promoter caused early flowering in transgenic rice, with a heading date that was 26-34 days earlier than that of wild-type plants. Early flowering was accompanied by a small yield penalty and some panicle abnormality. These observations suggest that floral regulatory genes from Arabidopsis are useful tools for heading date improvement in cereal crops.

Arabidopsis↗

PubMed2000

Atherosclerosis risk factors: the possible role of homocysteine.

Atherosclerosis is the leading cause of death in North America. It is characterized by thickening of the coronary artery wall by the formation of plaques, resulting in reduced blood flow. Plaque rupture and the consequent thrombosis may lead to sudden blockage of arteries and causing stroke and heart attack. In the last several decades, more than 250 factors associated with the development of coronary artery disease have been identified. Recently, a relationship between atherosclerosis and elevated homocysteine level in the blood has been established. The mechanism for the production of atherosclerosis by homocysteine has been investigated. When human hepatoma cells (HepG2) were incubated with 4 mM homocysteine, enhancements in the production of cholesterol and secretion of apolipoprotein B-100 were observed. The stimulatory effect on cholesterol synthesis was mediated via the enhancement of HMG-CoA reductase, which catalyzes the rate-limiting step in cholesterol biosynthesis. Cholesterol appears to play an important role in the regulation of apoB-100 secretion by hepatocytes. It is plausible that the increase in apoB secretion was caused by the elevated cholesterol level induced by homocysteine. The ability of homocysteine to produce a higher amount of cholesterol and promote the secretion of apoB would provide a plausible mechanism for the observed relationship between hyperhomocysteinemia and the development of atherogenesis and coronary artery disease.

Apolipoproteins B↗

PubMed2000

Arsenic trioxide-induced apoptosis and differentiation are associated respectively with mitochondrial transmembrane potential collapse and retinoic acid signaling pathways in acute promyelocytic leukemia.

Recent studies showed that arsenic trioxide (As2O3) could induce apoptosis and partial differentiation of leukemic promyelocytes. Here, we addressed the possible mechanisms underlying these two different effects. 1.0 microM As2O3-induced apoptosis was associated with condensation of the mitochondrial matrix, disruption of mitochondrial transmembrane potentials (DeltaPsim) and activation of caspase-3 in acute promyelocytic leukemia (APL) cells regardless of their sensitivity to all-trans retinoic acid (ATRA). All these effects were inhibited by dithiothreitol (DTT) and enhanced by buthionine sulfoximine (BSO). Furthermore, BSO could also render HL60 and U937 cells, which had the higher cellular catalase activity, sensitive to As2O3-induced apoptosis. Surprisingly, 1.0 microM As2O3 did not induce the DeltaPsim collapse and apoptosis, while 0.1 microM As2O3 induced partial differentiation of fresh BM cells from a de novo APL patient. In this study, we also showed that 0.2 mM DTT did not block low-dose As2O3-induced NB4 cell differentiation, and 0. 10.5 microM As2O3 did not induce differentiation of ATRA-resistant NB4-derived sublines, which were confirmed by cytomorphology, expression of CD11b, CD33 and CD14 as well as NBT reduction. Another interesting finding was that 0.10.5 microM As2O3 could also induce differentiation-related changes in ATRA-sensitive HL60 cells. However, the differentiation-inducing effect could not be seen in ATRA-resistant HL60 sublines with RARalpha mutation. Moreover, low-dose As2O3 and ATRA yielded similar gene expression profiles in APL cells. These results encouraged us to hypothesize that As2O3 induces APL cell differentiation through direct or indirect activation of retinoic acid receptor-related signaling pathway(s), while DeltaPsim collapse is the common mechanism of As2O3-induced apoptosis.

Antineoplastic Agents↗

PubMed2000

Technical advance: a high throughput system for transposon tagging and promoter trapping in tomato.

We describe new tools for functional analysis of the tomato genome based on insertional mutagenesis with the maize Ac/Ds transposable elements in the background of the miniature cultivar Micro-Tom. 2932 F3 families, in which Ds elements transposed and were stabilized, were screened for phenotypic mutations. Out of 10 families that had a clear mutant phenotype, only one mutant was Ds-tagged. In addition, we developed promoter trapping using the firefly luciferase reporter gene and enhancer trapping, using beta-glucuronidase (GUS). We show that luciferase can be used as a non-invasive reporter to identify, isolate and regenerate somatic sectors, to study the time course of mutant expression, and to identify inducible genes. Out of 108 families screened for luciferase activity 55% showed expression in the flower, 11% in the fruit and 4% in seedlings, suggesting a high rate of Ds insertion into genes. Preferential insertion into genes was supported by the analysis of Ds flanking sequences: 28 out of 50 sequenced Ds insertion sites were similar to known genes or to ESTs. In summary, the 2932 lines described here contain 2-3 Ds inserts per line, representing a collection of approximately 7500 Ds insertions. This collection has potential for use in high-throughput functional analysis of genes and promoter isolation in tomato.

DNA Transposable Elements↗

PubMed2000

Bone mineral density variations along the lumbosacral spine.

Vertebral bone quality is essential in vertebral strength and the stability of spinal screw fixation. A major factor of bone quality is the density of bone mineral and its distribution throughout the bone. There have been studies regarding bone mineral density variations in the cervical and thoracolumbar spine, but bone mineral density variations in the lumbosacral spine have not been documented. The purpose of the current study was to quantify bone mineral density variations at different lumbosacral levels and within vertebra, especially along the pathways of lumbar pedicle screws. Bone mineral density variations within the vertebrae along the lumbosacral spine were measured in 13 specimens from young male cadavers using peripheral quantitative computed tomography. Measurements included bone mineral density variations at different lumbosacral levels and in transverse layers and vertical columns within each vertebral body. These original data showed that the bone mineral density increased gradually from lumbar to S1 vertebrae, possibly reflecting a caudally increasing load on different lumbosacral levels. The highest bone mineral density in the lumbosacral spine is found at the pedicles and regions closest to pedicle bases, supporting the use of pedicle screw fixation.

Adult↗

PubMed2000

Effect of smear layer and direction of dentinal tubules on osteoblast adhesion to human dentin tissue.

The purpose of this study was to investigate the effect of smear layer and direction of dentinal tubules on osteoblast adhesion to human dentin tissue in vitro. Dentin disks were made from human premolars extracted for orthodontic reasons. Dentin disks were cut either perpendicularly to the long axis of the tooth or at 45 degrees to the long axis of tooth. The smear layer was removed by 34% phosphoric acid gel from half of the dentin disk surface. Human osteoblast-like Saos-2 cells were grown in RPMI medium with 10% fetal bovine serum and 1% antibiotic/antimycotic cocktail under standard cell culture conditions. Cells were seeded into Nunc four-well culture plates at 1.5 x 10(5) cells per well with dentin disks in the bottom of each well. After 1 day in culture the dentin disks along with cells grown on their surface were examined with a scanning electron microscopy. Osteoblasts attached and spread on the dentin surface and formed a monolayer in the presence and absence of a smear layer. Cells spread over the dentinal tubules despite their direction. These results suggest that cell adhesion and spreading of osteoblasts is not influenced either by the existence of a smear layer or the direction of the dentinal tubules on the dentin surface.

Acid Etching, Dental↗

PubMed2000

Adhesion of human osteoblasts on root-end filling materials.

Adhesion of human osteoblasts to root-end filling materials (mineral trioxide aggregate (MTA), IRM, composite, and amalgam) was observed by scanning electron microscopy. Root-end filling materials were inserted into 96-well flat-bottomed plates and condensed to disks of approximately 1 mm thick and the same diameter as the wells. After the disks were set, they were placed in the bottom of Nunc four-well culture plates at one disk per well. Then human osteoblasts were seeded into the wells at 1.5 x 10(5) cells per well. After 1 day in culture the disks of root-end filling materials along with cells grown on their surface were examined with a scanning electron microscopy. Results showed that osteoblasts attached and spread on MTA and composite by forming a monolayer. Osteoblasts also attached on amalgam, but with few cells spreading. In the presence of IRM, osteoblasts appeared rounded with no spreading. These results indicate that osteoblasts have a favorable response to MTA and composite resin compared with IRM and amalgam.

Aluminum Compounds↗