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Bulk fracture of teeth, where a part of the amalgam restoration and/or the cusp is fractured, is a common clinical problem. The aim of this study was to evaluate the effect of different surface conditioning methods on the shear bond strength of a hybrid resin composite to fresh amalgam. Amalgams (N = 84) were condensed into acrylic and randomly assigned to one of the following treatments (N = 6): (1) Alloy primer + opaquer, (2) Air-particle abrasion (50 μ m Al2O3) + alloy primer + opaquer, (3) Silica coating (30 μ m SiOx) + silanization + opaquer, (4) Opaquer + pre-impregnated continuous bidirectional E-glass fibre sheets, (5) Silica coating + silanization + fibre sheets, (6) Silica coating + silanization + opaquer + fibre sheet application. Non-conditioned amalgam surfaces were considered as control group (7). The mean surface roughness depth (RZ) was measured from the control group and air-abraded amalgam surfaces. The resin composite was bonded to the conditioned amalgam specimens using polyethylene molds. All specimens were tested under dry and thermocycled (6.000, 5–55 ∘C, 30 s) conditions. The shear bond strength of resin composite to amalgam substrates was measured in a universal testing machine (1 mm/min). Surface roughness values for the non-conditioned control group (RZ∼ 0.14 μ m) and for air-particle abraded surfaces with either Al2O3 or SiOx (RZ∼ 0.19 μ m and RZ∼ 0.16 μ m, respectively) did not show significant differences (p = 0.23) (One-way ANOVA). In dry conditions, silica coating and silanization followed by fibre sheet application exhibited significantly higher results (14.8 ± 5.6 MPa) than those of the groups conditioned with alloy primer (2.2 ± 0.7 MPa) (p < 0.001), air-particle abrasion+alloy primer (4.4 ± 2.0 MPa, p < 0.001), silica coating + silanization alone (6.2 ± 0.8 MPa, p = 0.009) or non-conditioned group (1.4 ± 0.6, p < 0.001). Silica coating and silanization followed by additional fibre sheets with opaquer application (23.6 ± 6.9 MPa) increased the bond strength significantly compared to those of other groups (group 5 vs group 6, p = 0.007; other groups vs group 6, p < 0.001). Thermocycling decreased the bond strengths significantly for all of the conditioning methods tested (for group 1, p < 0.001; for group 2, p = 0.013; for group 3, p = 0.002; for group 4, p = 0.026; for group 5, p = 0.002; for group 6, p < 0.001 and for group 7, p < 0.001). [ABSTRACT FROM AUTHOR]

Abstract The use of resin-based composite materials in operative dentistry is increasing, including applications in stress-bearing areas. However, composite restorations, in common with all restorations, suffer from deterioration and degradation in clinical service. Durable repair alternatives by layering a new composite onto such failed composite restorations, will eliminate unnecessary loss of tooth tissue and repeated insults to the pulp. The objective of this study was to evaluate the effect of three surface conditioning methods on the repair bond strength of a particulate filler resin-composite (PFC) to 5 PFC substrates. The specimens were randomly assigned to one of the following surface conditioning methods: (1) Hydrofluoric (HF) acid gel (9.5%) etching, (2) Air-borne particle abrasion (50 µm Al2O3), (3) Silica coating (30 µm SiOx, CoJet®-Sand). After each conditioning method, a silane coupling agent was applied. Adhesive resin was then applied in a thin layer and light polymerized. The low-viscosity diacrylate resin composite was bonded to the conditioned substrates in polyethylene molds. All specimens were tested in dry and thermocycled (6.000, 5–55°C, 30 s) conditions. One-way ANOVA showed significant influence of the surface conditioning methods (p < 0.001), and the PFC types (p < 0.0001) on the shear bond strength values. Significant differences were observed in bond strength values between the acid etched specimens (5.7–14.3 MPa) and those treated with either air-borne particle abrasion (13.0–22.5 MPa) or silica coating (25.5–41.8 MPa) in dry conditions (ANOVA, p < 0.001). After thermocycling, the silica coating process resulted in the highest bond values in all material groups (17.2–30.3 MPa). [ABSTRACT FROM AUTHOR]

Several studies have already shown that the high mobility group A1 (HMGA1) gene is up-regulated in most common types of cancer and immortalized tissue culture cell lines. HMGA1 expression is also much higher during embryonic development than in adult life. The elevated expression of HMGA1 in cancer thus likely occurs through oncofetal transcriptional mechanisms, which to date have not been well characterized. In the present study, we have cloned and functionally analyzed the TATA-less 5'-flanking regulatory region of human HMGA1. We identified two proximal regulatory regions that are important for basal transcription and in which specificity protein 1 (SP1) and activator protein 1 (AP1) transcription factors seem to be the regulating elements. In addition, we showed that the HMGA1 promoter is strongly inducible by oncogenic Ras, via a distal regulatory region. An AP1 site and three SP1-like sites are responsible for this inducible activity. An even more convincing finding for a role of oncogenic Ras in the regulation of HMGA1 in cancers is the discovery that HMGA1 up-regulation in the HCT116 colon cancer cell line is abolished when the mutated Ras allele is removed from these cells. Our data constitute the first extensive study of the regulation of basal and Ras-induced human HMGA1 gene expression and suggest that the elevated expression of HMGA1 in cancer cells requires, among others, a complex cooperation between SP1 family members and AP1 factors by the activation of Ras GTPase signaling.

Oculo-dento-digital dysplasia (ODDD) is an autosomal dominant disorder characterized by developmental anomalies of the face, the eyes, the limbs and the teeth. Patients with ODDD usually present with complete syndactyly of the fourth and fifth fingers (type III syndactyly), ocular changes, abnormalities of primary and permanent dentition and specific craniofacial malformations. Mutations in GJA1, a gene that encodes the gap junction protein connexin 43, are responsible for ODDD. Gap junctions are assemblies of intercellular channels that allow exchange of various ions and signaling molecules between cells. In this way, gap junctions play an important regulatory role in a variety of physiologic and developmental processes. We identified three novel and one previously described GJA1 mutation in two large ODDD families and two sporadic ODDD cases.

We describe two siblings with carpal and tarsal synostoses associated with transverse deficiencies of the toes. Mutation analysis of the NOG gene revealed a double missense mutation in both boys resulting in Pro42Ala and Pro50Arg. The parents were clinically unaffected, and these two mutations were not detected in their white blood cells or buccal mucosa. This indicates the presence of gonadal mosaicism or a low level of somatic mosaicism in one of the parents.

Heterotaxia is an aetiologically heterogeneous condition caused by an abnormal left-right axis formation, resulting in reversed left-right polarity of one or more organ systems. In a patient with heterotaxia and a de novo reciprocal translocation t(6;18)(q21;q21), we found that the PA26 gene was disrupted by the 6q21 breakpoint. Northern blot analysis showed decreased expression of the PA26 gene in an Epstein-Barr virus-transformed cell line of this patient. During early embryogenesis of Xenopus, the orthologue of PA26, XPA26 is exclusively expressed in the notochord, a midline structure. This further supports a possible role of PA26 in human situs determination. Mutation analysis of human PA26 gene in 40 unrelated individuals with unexplained heterotaxia failed to identify mutations, indicating that PA26 mutations are not a frequent cause of heterotaxia in humans. Analysis of the PA26 gene structure resulted in the identification of a novel PA26-related gene family, which we have named the sestrin family, and which comprises three closely related genes in human and in mouse.

Segmental duplications or low-copy repeats (LCRs) on chromosome 22q11 have been implicated in several chromosomal rearrangements. The presence of AT-rich regions in these duplications may lead to the formation of hairpin structures, which facilitate chromosomal rearrangement. Here we report the involvement of such a low-copy repeat in a t(X;22) associated with a neural tube defect. Molecular analysis of the chromosomal breakpoints revealed that the chromosome 22 breakpoint maps in the palindromic non-AT-rich NF1-like region of low-copy repeat B (LCR-B). No palindromic region was encountered near the breakpoint on chromosome X. Our findings confirm that there is no single mechanism leading to translocations with chromosome 22q11 involvement. Because LCR-B does not contain genes involved in neural tube development, we believe that the gene responsible for the observed phenotype is most likely localized on chromosome X.

A major cytogenetic subgroup among human lipomas is characterized by translocations involving the HMGIC gene at 12q15. In the context of an ongoing research program aiming at the elucidation of the functional consequences of HMGIC translocations in the etiology of lipomas, we have isolated a novel human gene, LHFP (lipoma HMGIC fusion partner), that acts as a translocation partner of HMGIC in a lipoma with t(12;13). The LHFP gene was mapped to the long arm of chromosome 13, a region recurrently targeted by chromosomal aberrations in lipomas. By Northern blot analysis, a transcript of 2. 4 kb was detected in a variety of human tissues. We assembled a cDNA contig containing the entire coding region of LHFP. Nucleotide sequence analysis of the composite LHFP cDNA revealed an open reading frame encoding a protein of 200 amino acids. The predicted human LHFP protein is almost identical to a translated mouse EST that covers almost the entire LHFP coding region. In addition, BLAST searches revealed that the LHFP protein belongs to a new protein family consisting of at least four or five members. In the lipoma studied, the expressed HMGIC/LHFP fusion transcript encodes the three DNA binding domains of HMGIC followed by 69 amino acids encoded by frame-shifted LHFP sequences. LHFP is the second translocation partner of HMGIC identified in lipomas and represents a candidate target gene for lipomas with 13q aberrations., (Copyright 1999 Academic Press.)

Recently, the high mobility group protein gene HMGIC was identified as the chromosome 12q15 target gene in a variety of benign solid tumors. Here, we report that the recombinational repair gene RAD51B on chromosome 14q23-24 is the preferential translocation partner of HMGIC in uterine leiomyomas. The pathogenetically critical sequences seem to reside in the last coding exon of a novel RAD51B isoform, which encode a domain containing a putative transmembrane anchor and are expressed in the uterus but not in a wide variety of other tissues tested. By fluorescence in situ hybridization, rapid amplification of 3' cDNA ends, and reverse transcription-PCR analysis, we demonstrated consistent chromosomal rearrangements within RAD51B and expression of fusion transcripts, structurally resulting in an allelic knockout of the uterine isoform of RAD51B and confirming a pleiotropic function of this gene.

Recent molecular cytogenetic analysis of uterine leiomyoma cell lines with chromosomal aberrations of 12q14-q15 have indicated that the chromosome 12 breakpoints cluster in a 445-kb region designated ULCR12 (uterine leiomyoma cluster region of the chromosome 12 breakpoints). Here we report the results of FISH studies of five primary pleomorphic adenomas and six primary lipomas and established cell lines of these tumor types characterized by translocations involving the chromosomal segment 12q13-q15. The results reveal that for nearly all tumors and cell lines analyzed, the chromosome 12 breakpoints map within a 350-kb region included in ULCR12, despite the previous cytogenetic assignment of the breakpoints to different bands of that region. In some cases the primary material and additionally analyzed cell lines allowed an even more precise localization of the breakpoints to less than 100 kb. Furthermore, a previously hidden translocation of ULCR12 in one primary tumor could be detected by FISH.

Cytogenetic analysis of a variety of benign solid tumors, among which uterine leiomyoma, lipoma, pleomorphic salivary gland adenoma, and pulmonary chondroid hamartoma, has indicated that these tumors often display chromosome breakpoints in region q13-q15 of chromosome 12. In previous studies, we have reported that these breakpoints map between locus D12S8 and the CHOP gene, the latter of which has been shown to be consistently rearranged in myxoid liposarcomas with t(12;16)(q13;p11). Here, we report directional chromosome walking studies starting from D12S8 and resulting in the construction of a YAC contig of about 6 Mb. This YAC contig, whose orientation on chromosome 12 was determined by double-color fluorescence in situ hybridization (FISH) analysis, has at least double coverage and consists of 75 overlapping YAC clones, all isolated from CEPH YAC libraries. Their insert sizes were estimated by contour-clamped homogeneous electric field (CHEF) gel electrophoresis. Chromosomal localization and chimerism of the YACs were investigated by FISH analysis. Chimerism of YAC clones was independently determined by restriction mapping. On the basis of YAC end-derived DNA markers and sequence-tagged sites (STSs), with an average spacing of approximately 70 kb, as well as restriction enzyme analysis, a long-range physical map was established for the 6-Mb DNA region of chromosome 12 covered by the YAC contig. Within the YAC contig, the relative positions of various known genes, an expressed sequence-tagged site, and a number of CEPH/Généthon polymorphic markers were determined. The latter data allow full integration of our mapping data with those obtained by CEPH/Généthon as well as those reported at the Second International Workshop on Human Chromosome 12 Mapping. Finally, this YAC contig constitutes the basis for the contstruction of a transcriptional map of this region and is likely to facilitate identification of genes involved in the formation of various benign solid tumor types.