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Biomedical subjects

K B Tan

Publications and source records attributed to K B Tan.

At least 37 records · Page 2Linked to original sources
PubMed1998

A novel human bone marrow stroma-derived cell line TF274 is highly osteogenic in vitro and in vivo.

A novel, immortalized, human bone marrow stroma-derived cell line TF274 is described which has the ability to form bone both in vitro and in vivo. Under basal conditions these cells expressed alkaline phosphatase (ALP) and type I collagen genes which are characteristic of the osteoblast phenotype. ALP levels were upregulated in the presence of osteotropic agents such as parathyroid hormone (PTH), transforming growth factor beta (TGF-beta), and BMP-2. In addition, PTH also increased cAMP levels in these cells. The capacity of these cells to form bone in vitro was evaluated by culturing them in the presence of L-ascorbic acid and beta-glycerophosphate. Matrix mineralization in these cultures was assessed by Alizarin Red staining and increased 45Ca uptake. Under these conditions mineralized nodule formation was observed in less than 2 weeks. Northern analysis of TF274 cells at various times during the mineralization process indicated a temporal expression of the osteocalcin gene that is typically associated with differentiating osteoblasts. The osteogenic nature of TF274 cells was confirmed in vivo using the severe combined immunodeficient (SCID) mouse model. Antibodies to human leukocyte antigens (HLA), class I antigens, and human OKa blood group antigen were used to demonstrate that the lesions formed were of human origin. By 21 days, the lesion consisted of a homogeneous focus of ALP-positive cells containing areas of mineralized bone lined with tartarate-resistant acid phosphatase (TRAP) positive osteoclasts. Thus, the TF274 cells exhibit osteogenic potential both in vitro and in vivo. This immortalized cell line represents a consistent source of cells that can be used to study human osteoblast differentiation both in vitro and in vivo.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Interaction of adrenomedullin with calcitonin receptor in cultured human breast cancer cells, T 47D.

Human adrenomedullin (hADM), human calcitonin gene-related peptide (hCGRP), and salmon calcitonin (sCT)-activated adenylyl cyclase with EC50 values of 132, 764, and 0.5 nM, respectively, in human breast cancer cell line, T 47D. Treatment of T 47D cell membranes with near maximal concentrations of sCT, hADM and hCGRP had no additive effect on adenylyl cyclase activity. Salmon calcitonin (8-32)[sCT (8-32)], selective antagonist of calcitonin receptor, inhibited the activation of adenylyl cyclase by these three peptides. On the other hand, the putative ADM receptor antagonist, ADM (22-52), and CGRP receptor antagonist, CGRP (8-37), failed to inhibit ADM-, CGRP- or sCT-activated adenylyl cyclase. These results suggest that in T47D cells, both ADM and CGRP activated adenylyl cyclase through sCT receptors.

Adenylyl Cyclases↗
PubMed1997

Characterization of a novel TNF-like ligand and recently described TNF ligand and TNF receptor superfamily genes and their constitutive and inducible expression in hematopoietic and non-hematopoietic cells.

A novel (TL1), a recently described (TL2) TNF-like, and three recently described TNF receptor-like (TR1, TR2, TR3) molecules were identified by searching a cDNA database. TL1 and TL2 are type-II membrane proteins. TR2 and TR3 are type-I membrane proteins whereas TR1 appears to be a secreted protein. TL1, TL2, TR2 and TR3 were expressed in hematopoietic cells, whereas TR1 was not. Northern blots hybridized with the cDNA probes revealed multiple forms of RNA as well as inducible expression of TL1, TL2, TR2 and TR3. TL2 and TR3, in particular, were highly induced in activated CD4+ T cells. Radiation hybrid mapping localized TR1 and TL2 to 8q24 and 3q26, respectively, which are not near any known superfamily members. TL1 was mapped to 9q32, near CD30L (9q33) and TR2 and TR3 mapped to the region of chromosome 1 that contains the TNFR-II, 4-1BB, OX40 and CD30 gene cluster at 1p36. Only TR3 in this cluster possesses a death domain. Southern blot analysis revealed the presence of TL and TR genes in different mammalian species. TL2, TR1, TR2 and TR3 were recently described by others as TRAIL/Apo-2L, OPG, HVEM and DR3/WSL-1/Apo-3/TRAMP/LARD, respectively.

Amino Acid Sequence↗
PubMed1997

A newly identified member of the tumor necrosis factor receptor superfamily with a wide tissue distribution and involvement in lymphocyte activation.

The tumor necrosis factor receptor (TNFR) superfamily consists of approximately 10 characterized members of human proteins. We have identified a new member of the TNFR superfamily, TR2, from a search of an expressed sequence tag data base. cDNA cloning and Northern blot hybridization demonstrated multiple mRNA species, of which a 1.7-kilobase form was most abundant. However, TR2 is encoded by a single gene which, maps to chromosome 1p36.22-36.3, in the same region as several other members of the TNFR superfamily. The most abundant TR2 open reading frame encodes a 283-amino acid single transmembrane protein with a 36-residue signal sequence, two perfect and two imperfect TNFR-like cysteine-rich domains, and a short cytoplasmic tail with some similarity to 4-1BB and CD40. TR2 mRNA is expressed in multiple human tissues and cell lines and shows a constitutive and relatively high expression in peripheral blood T cells, B cells, and monocytes. A TR2-Fc fusion protein inhibited a mixed lymphocyte reaction-mediated proliferation suggesting that the receptor and/or its ligand play a role in T cell stimulation.

Adult↗
PubMed1995

The clinical significance of distortion in implant prosthodontics: is there such a thing as passive fit?

Passive fit of the implant prosthesis onto osseointegrated and functional fixtures intraorally is the "Holy Grail" of the discerning implant prosthodontist. There is growing recognition that the old and "tried" clinical procedures and laboratory fabrication methods transferred from traditional fixed and removable partial denture prosthodontics, fall short of achieving true passivity of fit. The stages of impression making, master cast, resin verification jig, waxing, investing, casting, veneer addition and finishing can all add to the final distortion of the prosthesis. Studies are emerging that report the possible distortion associated with each stage. Alternative strategies have also been suggested to by-pass these traditional stages, for example laser welding or the elimination of the impression using optical digitising and CAD-CAM. In the final analysis, totally "passive" fit is probably unachievable. The challenge is to determine a minimum level of distortion and associated stress that is acceptable and that confers adequate clinical longevity to the prosthesis. Developing clinical tests that measure stress levels intraorally as the prosthesis is fitted would be the ideal gold standard by which to judge the accuracy of fabrication procedures. This paper summarises and rationalises the growing body of literature dealing with accuracy of implant prosthodontic procedures.

Biomechanical Phenomena↗
PubMed1995

The use of multiplanar reformatted computerised tomography in the surgical-prosthodontic planning of implant placement.

Presurgical planning and communication between the prosthodontist and the surgeon is essential to achieve optimal placement of functional implants. Besides the basic clinical examination and the use of mounted study models, radiographic imaging is an essential adjunctive aid in treatment planning. The latest imaging modality, multiplanar reformatted CT (MPR-CT) is the most comprehensive and accurate presently available. It allows precise assessment of the three-dimensional architecture and internal anatomy of the jaws. This enables accurate preoperative evaluation for planning implant fixture placement with maximal use of bone. It's widespread use would prevent unsuitable cases from ever reaching surgery. MPR-CT is described in detail and its usefulness in treatment planning the dental implant case illustrated. Indications, contraindications, advantages and disadvantages will be discussed. The use of radiographic stents derived from diagnostic wax-ups or set-ups is essential. The incorporation of suitable radiographic markers provide both the surgeon and prosthodontist with reference points to determine the available bone at the exact spatial location and orientation of the planned implant fixture at all primary and alternate sites. The same radiographic stent is then converted to a surgical guide stent for precise location of surgical implant sites.

Dental Implantation, Endosseous↗
PubMed1995

Shade match of tooth-colored restorative materials based on a commercial shade guide.

Many restorative materials are claimed by their manufacturers to match the Vita shade guide. To verify this claim, 40 dental personnel were asked to color match five different restorative materials to their respective Vita shade tabs according to a 5-point scale (1 = very poor color match; 5 = excellent color match). Three shades were chosen for each restorative material (a mid-Value shade as well as the highest Value shade and the lowest Value shade present in each system). Pooled scores indicated that the resin composite materials had significantly better overall shade match than did the other materials evaluated and that one resin-modified glass-ionomer cement had significantly better shade match than did the "compomer" and another resin-modified glass-ionomer cement. Only 11% of the scores for all material and shade combinations were given a good or excellent rating (score greater than 3). Shade match to the Vita shade guide was not material dependent but tended to differ among the different Value shades evaluated.

Analysis of Variance↗
PubMed1992

Topoisomerase II alpha and topoisomerase II beta genes: characterization and mapping to human chromosomes 17 and 3, respectively.

Human cells contain two topoisomerase II isozymes named topo II alpha and topo II beta. The complementary DNAs for both enzymes have been cloned. The topo II alpha and topo II beta complementary DNAs hybridized to unique sequences of human, rodent, and chicken DNAs in Southern blots. The human topo II alpha gene has previously been mapped to chromosome 17. We confirmed the chromosomal location of topo II alpha and mapped the topo II beta gene to chromosome 3. In addition, topo II beta exhibits genetic polymorphism as has been reported for topoisomerases I and II alpha.

Blotting, Southern↗
PubMed1992

Amplification of the topoisomerase II alpha gene in a non-small cell lung cancer cell line and characterisation of polymorphisms at the human topoisomerase II alpha and beta loci in normal tissue.

DNA was prepared from normal tissue and 19 lung cancer cell lines. Using probes which detect restriction fragment length polymorphisms at both the topoisomerase II alpha and beta loci, heterozygosity was detected at a frequency of 0.17 and 0.37 for the alpha and beta loci, respectively. Southern blot analysis of DNA extracted from lung cancer cell lines detected amplification of both the topoisomerase II alpha and ERBB2 genes in the adenocarcinoma line Calu3. These results indicate that topoisomerase II alpha and ERBB2 may be closely linked on chromosome 17 and coamplified during adenocarcinoma progression. Since topoisomerase II is a target for several anticancer drugs, it will be of interest to study alterations to topoisomerase II genes during tumour development, as these may in part determine the response of the tumour to chemotherapy.

Adenocarcinoma↗
PubMed1992

Camptothecin hyper-resistant P388 cells: drug-dependent reduction in topoisomerase I content.

A subline of P388 leukemia made 10-fold resistant to camptothecin (CPT) by serial passage in drug-treated mice was adapted to growth in tissue culture and made hyper-resistant to CPT by passage in the presence of increasing concentrations of the drug. Cells were obtained that were 1,000-fold resistant to CPT, compared to wild-type P388 cells. Neither topoisomerase I mRNA nor 100 kDa topoisomerase I enzyme was detectable in these cells, and topoisomerase I activity extracted from nuclei was less than 4% of that extracted from nuclei of wild-type cells. An immunoreactive 130 kDa protein that could be an altered, inactive form of topoisomerase I was evident in the hyper-resistant cells. In addition, the cells deficient in topoisomerase I contained enhanced topoisomerase II activity. Maintenance of the hyper-resistant phenotype required continued exposure to CPT; growth in its absence led to loss of hyper-resistance, increased topoisomerase I content and activity, and decreased topoisomerase II activity. The sensitivity of the cells to killing by a number of inhibitors of topoisomerases I and II was consistent with these observations. Thus, P388 cells have the potential to become highly resistant to CPT by severely curtailing topoisomerase I expression; in these circumstances, topoisomerase I and II activities are regulated coordinately.

Animals↗
PubMed1991

Auditory canal haemorrhage following mandibular condylar fracture.

A case of haemorrhage from the external auditory meatus associated with condylar fracture is presented. It is important that haemorrhage from the ear following maxillofacial injuries be investigated thoroughly because displacement of the condyle into the middle cranial fossa also presents in this manner. The patient was treated by intermaxillary fixation and packing of the auditory canal. Packing is not only effective for haemostasis but is also important in preventing subsequent stenosis of the auditory canal.

Adult↗
PubMed1990

Development of a stable camptothecin-resistant subline of P388 leukemia with reduced topoisomerase I content.

A camptothecin-resistant subline of P388 leukemia (P388/CPT) was developed by repeated transplantation of P388 cells in mice treated with therapeutic doses of camptothecin. In mice bearing the resistant tumor, a maximally tolerated dose of camptothecin produced no net reduction in tumor cell burden, in contrast to a 5-log cell kill in the parental P388 (P388/S). The IC50 of camptothecin, as determined by colony formation assays of cultured cells, was 8 times greater for the cloned P388/CPT cell line than for P388/S. P388/CPT cells were not cross-resistant to other antineoplastic agents, including topoisomerase II inhibitors. The type I topoisomerases purified from P388/CPT and P388/S cells were identical with respect to molecular weight, specific activity, in vitro camptothecin sensitivity, and DNA cleavage specificity. Camptothecin induced fewer protein-associated DNA single-strand breaks in the resistant cells than in the wild-type P388 cells. Topoisomerase I mRNA, immunoreactivity, and extractable enzymatic activity were 2-4 times lower for P388/CPT cells than for P388/S cells. As resistance to camptothecin developed, topoisomerase I extractable activity decreased, concomitant with an increase in topoisomerase II extractable activity. Furthermore, the appearance of camptothecin resistance was associated with specific rearrangements of the topoisomerase I gene. These results suggest that development of resistance to inhibitors of topoisomerase I can occur by down-regulation of the target enzyme, thus reducing the production of lethal enzyme-mediated DNA damage. The enhanced topoisomerase II activity in these cells suggests that resistance to camptothecin may be overcome by co-treatment with topoisomerase II inhibitors.

Animals↗
PubMed1989

Nonproductive rearrangement of DNA topoisomerase I and II genes: correlation with resistance to topoisomerase inhibitors.

Topoisomerase inhibitors comprise an important group of agents that is used in cancer treatment. Because the development of resistance to cancer chemotherapeutic agents represents a major limitation of cancer chemotherapy, we investigated the mechanism of resistance by murine P388 leukemia to camptothecin (topoisomerase I inhibitor) or amsacrine (topoisomerase II inhibitor). The resistant cells contained reduced levels of topoisomerase activity and messenger RNA. The topoisomerase gene of these cells was rearranged (only in one allele) and hypermethylated. These topoisomerase gene alterations probably resulted in reduced transcription and, thus, enzyme production, which was correlated with resistance to the topoisomerase inhibitor.

Alleles↗
PubMed1989

Altered actin and immunoglobulin C mu expression in nitrogen mustard-resistant human Burkitt lymphoma cells.

Raji-HN2 is a B cell lymphoma (Burkitt lymphoma) line that was made resistant to nitrogen mustard. The drug-resistant phenotype was accompanied by changes in gene expression. The expression of four unrelated genes was examined by Northern blot analysis. Raji-HN2 cells were found to contain about twice the number of actin mRNA found in Raji cells. Both cell lines were found to contain equivalent amounts of beta 2-microglobulin, c-myc oncogene, and immunoglobulin C mu mRNAs. The C mu mRNA was, however, larger in size in Raji-HN2 cells. Alterations in actin and C mu mRNAs in Raji-HN2 cells were not due to gene amplification or rearrangement because Southern blot analysis revealed no changes in the genomic organization of these genes. The increased actin mRNA content was correlated with an increased actin content of Raji-HN2 cells. The F-actin (stained with 7-nitrobenz-2-oxa-1,3-diazolylphallacidin) content of single cells was quantitated in a meridian interactive laser cytometer. Raji-HN2 cells contained about twice the amount of F-actin present in the parental Raji cells. Similar results were obtained when large populations, 10(6) cells each, were examined in a flow cytometer.

Actins↗
PubMed1989

Characterization and immunological identification of cDNA clones encoding two human DNA topoisomerase II isozymes.

Several DNA topoisomerase II (Topo II; EC 5.99.1.3) partial cDNA clones obtained from a human Raji-HN2 cDNA library were sequenced and two classes of nucleotide sequences were found. One member of the first class, SP1, was identical to an internal fragment of human HeLa cell Topo II cDNA described earlier. A member of the second class, SP11, shared extensive nucleotide (75%) and predicted peptide (92%) sequence similarities with the first two-thirds of HeLa Topo II. Each class of cDNAs hybridized to unique, nonoverlapping restriction enzyme fragments of genomic DNA from several human cell lines. Synthetic 24-mer oligonucleotide probes specific for each cDNA class hybridized to 6.5-kilobase mRNAs; furthermore, hybridization of probe specific for one class was not blocked by probe specific for the other. Antibodies raised against a synthetic SP1-encoded dodecapeptide specifically recognized the 170-kDa form of Topo II, while antibodies raised against the corresponding SP11-encoded dodecapeptide, or a second unique SP11-encoded tridecapeptide, selectively recognized the 180-kDa form of Topo II. These data provide genetic and immunochemical evidence for two Topo II isozymes.

Amino Acid Sequence↗
PubMed1989

Evidence for the participation of topoisomerases I and II in cadmium-induced metallothionein expression in Chinese hamster ovary cells.

CHO-Cdr20 cells are 10-20 times more resistant to killing by cadmium than the parental CHO cells. Resistance has been linked to amplification of the metallothionein genes MT-I and MT-II and their coordinate induction by cadmium and other toxic metals. We studied the roles of the nuclear enzymes topoisomerase I and topoisomerase II in Cd-induced expression of MT-II. Camptothecin-induced DNA strand breakage, mediated by topoisomerase I in cells, increased by approximately 20% when the resistant cells were incubated first with 50 microM Cd and then with camptothecin. Short DNA fragments were enriched in MT-II-hybridizing sequences, indicating that topoisomerase I-associated breakage was directed in part toward the location of induced gene activity. Ten microM camptothecin inhibited Cd-induced accumulation of MT-II mRNA as well as induced and uninduced RNA synthesis in the resistant cells. These data are consistent with the notion that topoisomerase I participates in most or all forms of RNA synthesis. Topoisomerase II inhibitors which trap cleavable complexes (amsacrine, VM-26, VP-16) increased DNA strand breakage at very high concentrations (50-100 microM); the increased breakage appeared to be concentrated near the MT-II gene. This class of inhibitor did not block the accumulation of MT-II message. Novobiocin, a second type of topoisomerase II inhibitor blocked transcription at 300 microM. Merbarone, a novel, third type of topoisomerase II inhibitor, blocked MT-II transcription at 50-100 microM. The latter two inhibited total RNA synthesis in induced, but not uninduced cells. Thus, it is possible that topoisomerase II plays more than one role in transcription and that more than one form of this enzyme is involved.

Animals↗