bluuebunny/crossref_metadata_2025_split huggingface dataset:
Evaluation of the micronucleus test in vitro using chinese hamster cells: Results of four chemicals weakly positive in the in vivo micronucleus test
Authors: Miller Beate M. , Pujadas Eva , Gocke Elmar 
Published: February 2007

AbstractA rapid and simple procedure for the micronucleus test (MNT) in vitro using Chinese hamster ovary (CHO) cells was established in our laboratory. The assay is intended to quickly screen chromosomal aberrations in vitro within the framework of industrial genotoxicity studies. To test the sensitivity of the assay in the experiments described here, four substances, classified as noncarcinogens but reported as weak inducers of micronuclei (MN) in bone‐marrow cells of mice, were evaluated in the MNT in vitro. Of the four compounds, ascorbic acid, phenol, and 2,6‐diaminotoluene proved to be genotoxic in the MNT in vitro. Titanium dioxide, which could not be dissolved in the culture medium, did not induce MN. The MNT in vitro proved to be quick and relatively simple and to yield highly reproducible results when testing the four chemicals. © 1995 Wiley‐Liss, Inc.
Indications for a threshold of chemically‐induced aneuploidy in vitro in human lymphocytes
Authors: Elhajouji Azeddine , Van Hummelen Paul , Kirsch‐Volders Micheline 
Published: February 2007

AbstractThe possible existence of a threshold for compounds inducing chromosomal loss was investigated for four known aneugens (colchicine, COL; carben‐dazim, MBC; mebendazole, MEB; nocodazole, NOC) and two clastogens (methyl methanesulfo‐nate, MMS; mitomycin C, MMC) using the micronu‐cleus (MN) test in human lymphocytes. The presence of a whole chromosome in the MN was studied by fluorescent in situ hybridization (FISH) using a synthetic pancentromeric oligonucleotide probe. FISH was applied on two different MN preparations: cytokinesis‐blocked MN (MNCB) assay, and MN sorted by flow cytometry. At subtoxic concentrations analyzed by MNCB and FISH, COL, MEB, MBC, and NOC induced a concentration‐dependent increase in centromere‐positive MN (MNCen+), MMC seemed to induce an increase in both types of MN (MNCen‐ and MNCen+), while MMS induced only MNCen‐. On the sorted micronuclei (in a wide range of low to subtoxic concentrations), the concentration‐effect profile for MNCen+, with the four aneugens tested, showed a statistically nonsignificant increase over a range of concentrations, followed by a second range of high concentrations with a statistically significant increase. To analyze the existence of a threshold, a piecewise linear regression was applied to the data. The first concentration that showed a statistically significant increase in MNCen+ was chosen as a breakpoint (0.037 μM for COL, 2.62 μM for MBC, 0.27 μM for MEB, and 0.066 μM for NOC). The statistical correlation between observed and predicted values showed a high correlation (r = 0.99), indicating a clear threshold for aneuploidy induction. However, for MMS the concentration‐effect profile for MNCen+ showed a continuous concentration‐dependent decrease with no threshold. With the two cytotoxicity assays used (Bio‐Rad and MTT), no significant reduction was detected either in the protein content or in mitochondrial succinate dehydrogenase activity with all chemicals tested for MN induction. Therefore, our data suggest that the observed thresholds were not due to indirect toxic effects but to real aneugenic effects. © 1995 Wiley‐Liss, Inc.
An investigation of the DNA‐damaging ability of benzene and its metabolites in human lymphocytes, using the comet assay
Authors: Anderson D. , Yu T.‐W. , Schmezer P. 
Published: February 2007

AbstractBenzene and five of its known metabolites—muconic acid, hydroquinone, catechol, p‐benzoquinone, and benzentriol—were examined for DNA damage in human lymphocytes using the alkaline Comet assay, and conditions were optimised to determine responses. Metabolic activation (S‐9 mix) was included in the assay for varying times to try to enhance effects. In addition, the effects of catalase were investigated as it is known to be present in S‐9 mix reducing oxidative damage, and some benzene metabolites are known to react through oxygen radical mechanisms. Effects were also examined in cycling cells to determine whether they were more sensitive to damage then noncycling cells. Comets were measured either by eye or by image analysis. Data have been presented according to length of treatments.When Comets were measured by eye after treatment with hydrogen peroxide (H2O2), the positive control, and each compound for 0.5 hr, only H lymphocytes.When comets were measured by image analysis, a 0.5‐hr treatment with H2O2 and benzenetriol and catechol confirmed results analysed by eye, with S‐9 mix greatly reducing responses. When treatments were increased to 1 hr in the presence and absence of S‐9 mix, benzene at a 5‐fold increased dose produced a significant positive response but not at the lower dose. When treatment times were increased to 2 and 4 hr, doses were also increased, and muconic acid, hydroquinone, catechol, and benzoquinone in the presence of S‐9 mix showed positive time and dose‐related responses, and at the highest dose of benzoquinone the morphology of the nucleus was affected. Effects tended to become more pronounced at high doses and after longer exposures, although this was not always consistent from experiment to experiment.In conclusion, benzene and all metabolites investigated gave positive responses. Where altered responses were observed, they were significantly different from the corresponding controls. © 1995 Wiley‐Liss, Inc.
Solution of depth‐averaged tidal currents in Persian Gulf on unstructured overlapping finite volumes
Authors: Sabbagh‐Yazdi Saeed‐Reza , Zounemat‐Kermani Mohammad , Kermani Ali 
Published: February 2007

AbstractHydrodynamic simulation of tidal currents in Persian Gulf due to tidal fluctuations in Hurmoz strait and inflow for Arvand River is presented in this paper and tidal constituents of M2 and K1 are attained. The mathematical model utilized consists of depth‐averaged equations of continuity and motion in two‐dimensional horizontal plane which considers hydrostatic pressure distribution. The effect of evaporation is considered in the continuity equation and the effects of bed slope and friction, as well as the Coriolis effects are considers in two equations of motion. The cell vertex finite volume method is applied for converting the governing equations into discrete forms for unstructured overlapping control volumes. Using unstructured triangular meshes provides great flexibility for modelling of complex geometries in the real world flow domain. The accuracy of the developed flow solver is assessed using two test cases. Firstly, the results of the hydrodynamic model for fluctuating flow on the variable bed slope are compared with available analytical solution. Secondly, in order to simulate circulating flow patterns the numerical results are compared with the reported data in the literature for deep flow in a canal with sudden expansion. Finally, the performance of the computer model to simulate tidal flow in a geometrically complex domain is examined by simulation of tidal currents in the Persian Gulf and computing tidal constituents. Copyright © 2007 John Wiley & Sons, Ltd.
An optimizing reduced order FDS for the tropical Pacific Ocean reduced gravity model
Authors: Luo Zhendong , Chen Jing , Zhu Jiang , Wang Ruiwen , Navon I. M. 
Published: February 2007

AbstractProper orthogonal decomposition (POD) and singular value decomposition (SVD) methods are used to study a finite difference discretization scheme (FDS) for the tropical Pacific Ocean reduced gravity model. Ensembles of data are compiled from transient solutions computed from the discrete equation system derived by FDS for the tropical Pacific Ocean reduced gravity model. The optimal orthogonal bases are used to reconstruct the elements of the ensemble with POD and SVD. Combining the above approach with a Galerkin projection procedure yields a new optimizing FDS model of lower dimensions and high accuracy for the tropical Pacific Ocean reduced gravity model. An error estimate of the new reduced order optimizing FDS model is then derived. Numerical examples are presented illustrating that the error between the POD approximate solution and the full FDS solution is consistent with previously obtained theoretical results, thus validating the feasibility and efficiency of POD method. Copyright © 2007 John Wiley & Sons, Ltd.
A posterioriestimators for vertex centred finite volume discretization of a convection–diffusion‐reaction equation arising in flow in porous media
Authors: Amaziane B. , Bergam A. , El Ossmani M. , Mghazli Z. 
Published: February 2007

AbstractWe present an adaptive numerical technique for solving convection–diffusion‐reaction problems, modelling the transport of contaminant in porous media. We develop and analyse residual error estimators using finite volume approximations. The error estimators with respect to both time and space yield global upper and local lower bounds on the error measured in the energy norm. Computational results of various model simulations of fluid flow and transport of contaminant in heterogeneous aquifers are presented and discussed. Copyright © 2007 John Wiley & Sons, Ltd.
Molecular genetic analysis of tumors in von recklinghausen neurofibromatosis: Loss of heterozygosity for chromosome 17
Authors: Skuse Gary R. , Kosciolek Barbara A. , Rowley Peter T. 
Published: February 2007

AbstractThe most common inherited syndrome in man predisposing to neoplasia is neurofibromatosis‐1 (von Recklinghausen disease) (NF1). We investigated the hypothesis that affected individuals carry a single inactive allele at the NF1 locus in the germline and that a tumor arises from a cell in a susceptible tissue in which the remaining normal allele has been lost or inactivated. DNA from tumor and nontumor tissue from 27 NF1 patients was analyzed with three markers closely linked to the NF1 locus and two additional markers from chromosome 17. No loss of heterozygosity was observed in neurofibromas, plexiform or not. For other tumor types analyzed, seven of 14 showed a loss. A loss of heterozygosity was observed in six of 11 of the malignant peripheral nerve tumors analyzed. Of the seven malignancies demonstrating a loss, five involved a neurofibrosarcoma. These findings suggest that the pathogenesis of neurofibrosarcoma in NF1 involves a deficiency of the NF1 gene product. In any given patient, loss of heterozygosity was detected at some marker loci but not others. Thus the mutations demonstrated in these tumors comprise a set of overlapping mutations, which may facilitate more precise localization of the NF1 gene.
Leukemic differentiation of a mediastinal germ cell tumor
Authors: Chaganti R. S. K. , Ladanyi Marc , Samaniego Felipe , Offit Kenneth , Reuter Victor E. , Jhanwar Suresh C. , Bosl George J. 
Published: February 2007

AbstractThe biological basis for acute leukemia associated with mediastinal germ cell tumors has remained unexplained due to lack of critical data that would illuminate the genetic relationship between the two tumors in a given patient. Here we present results of serial cytogenetic investigations on the pretreatment and posttreatment mediastinal yolk sac tumor and immature teratoma biopsies and two separate leukemic bone marrow aspirates from a patient who developed acute nonlymphocytic leukemia 11 months after the initial diagnosis of the germ cell tumor. Presence of an i(12p) in all tumor clones and trisomy 21 in one clone in the posttreatment mediastinal tumor and all leukemic clones establishes the common origin of all tumor clones and shows that in this case the leukemia was derived from the malignant germ cell clone.
Suggestive evidence that genes controlling invasion and metastasis of T‐cell lymphomas are located on mouse chromosome 3
Authors: Verschaeve Luc , Verschueren Hendrik , Vandendriessche Thierry , van Hecke Dominique , Verhaegen Steven , de Baetselier Patrick 
Published: February 2007

AbstractCell lines differing in their malignant potential have been derived from the murine BW5147 T‐cell lymphosarcoma. To evalute the involvement of chromosomal aberrations in tumor progression within this model, we have analyzed the karyotypes and the in vitro invasiveness of 13 related nonmetastatic and metastatic variants. Giemsa banding revealed the presence of several marker chromosomes, one of which was of particular importance. Depending on the cell line, four variants of this marker I were found: Marker Ia corresponds to two translocated chromosomes 3, marker Ib is a deleted Ia marker, marker Ic is a Ib translocated to a small unidentified chromosome fragment, and marker Id is a further deleted Ib marker. The Ia and Id markers were characteristic for the noninvasive, nonmetastatic lines, whereas the Ib and Ic markers predominated in the invasive, metastatic variants. The results suggest that metastasis‐enhancing genes are located between the D and F1 band of mouse chromosome 3 and that metastasis‐suppressing genes are located between the F1 and H band of the same chromosome.
Amplification of cellular oncogenes: A predictor of clinical outcome in human cancer
Authors: Schwab Manfred , Amler Lukas C. 
Published: February 2007

AbstractIncreased dosage of cellular oncogenes resulting from amplification of DNA is a frequent genetic abnormality of tumor cells and the study of oncogene amplification has been paradigmatic for the usefulness of molecular genetic research in clinical oncology. Certain types of human tumors carry an amplified cellular oncogene at frequencies of up to 50–60%. Human neuroblastoma has been prototypic for the importance of oncogene amplification in tumorigenesis, and evidence is emerging that amplification may be an early event involved in a more malignant form of this cancer. It is unclear at which stage amplification plays a role in other cancers. Amplification of cellular oncogenes is a good predictor of clinical outcome in some human malignancies.
Molecular mapping of deletion sites in the short arm of chromosome 3 in human lung cancer
Authors: Brauch Hiltrud , Tory Kalman , Kotler Frederick , Gazdar Adi F. , Pettengill Olive S. , Johnson Bruce , Graziano Stephen , Winton Tim , Buys Charles H. C. M. , Sorenson George D. , Poiesz Bernard J. , Minna John D. , Zbar Berton 
Published: February 2007

AbstractWe used 10 restriction fragment length polymorphism (RFLP) probes spanning the length of the short arm of chromosome 3 (3p) to map deletion sites in human lung cancer. Two approaches were used. 1) When a patient's tumor and normal tissue were available, loci with allelic heterozygosity in the normal tissue were tested for loss of alleles at 3p. 2) When the corresponding normal tissue was not available, the frequency of heterozygosity at each locus in a panel of tumors was compared to the corresponding published frequencies in nontumor tissue of healthy individuals or patients with lung cancer. In 14 small cell lung carcinomas (SCLC) with normal DNA for comparison, allele loss was found at all heterozygous loci, with one exception at a locus near the 3p centromere (D3S4). In the total of 53 SCLCs, which included tumors without paired normal tissue, frequency of heterozygosity was significantly reduced in all 10 3p loci. Three loci, DNF15S2, RAF1, and D3S18, were homozygous in all tumors in the SCLC panel. These loci, which are in regions 3p21 and 3p25, may thus be involved in the origin or evolution of SCLC. We also investigated 24 non‐SCLC tumors. In this panel, frequency of heterozygosity was significantly reduced at seven of the 10 loci tested. Comparison of the results shows that the pattern of allele loss on 3p is different in SCLC and non‐SCLC, suggesting a difference in pathogenesis at the genetic level.
Identification of a transcriptional unit adjacent to the breakpoint in the 14;19 translocation of chronic lymphocytic leukemia
Authors: McKeithan Timothy W. , Ohno Hitoshi , Diaz Manuel O. 
Published: February 2007

AbstractThe t(14;19)(q32.3;q13.1) is a recurring translocation found in the neoplastic cells of some patients with chronic lymphocytic leukemia (CLL). We have previously cloned the translocation breakpoint junction present in the leukemic cells from one such patient. In the present study, we have cloned and sequenced the breakpoint junction from a second patient. The breakpoint on chromosome 14 occurs within a switch region upstream of the immunoglobulin heavy chain Cα1 sequence. We detected a 2.1–2.3 kb transcript on Northern blots using a probe from chromosome 19 adjacent to this breakpoint. S1 nuclease protection experiments showed that transcription of the gene proceeds in a direction away from the breakpoint junction. This gene (for which we propose the name BCL3) may contribute to the malignant development of B‐lymphocytes following the chromosome translocation. If so, it is the first protooncogene identified whose activation is principally associated with CLL.
Trisomy 5 and loss of the Y chromosome as the sole cytogenetic anomalies in a cavernous hemangioma/angiosarcoma
Authors: Mandahl Nils , Jin Yuesheng , Heim Sverre , Willén Helena , Wennerberg Johan , Biörklund Anders , Mitelman Felix 
Published: February 2007

AbstractCytogenetic analysis of a cavernous hemangioma with transition to angiosarcoma revealed the mosaic karyotype 47, XY,+5/46, X,‐Y,+5/45, X,‐Y/46, XY. No cytogenetically analyzed hemangiomas or angiosarcomas have been reported before.
Uterine leiomyoma cytogenetics
Authors: Nilbert Mef , Heim Sverre 
Published: February 2007

AbstractUterine leiomyoma—a benign smooth muscle tumor—has recently been found to contain tumor‐specific chromosome aberrations. Although only normal karyotypes were detected in 50 to 80% of cytogenetically investigated tumors, 104 leiomyomas with karyotypic aberrations have already been reported. At least four cytogenetically abnormal subgroups have been identified thus far, characterized by rearrangements of 6p, del(7)(q21.2q31.2), +12, and t(12;14)(q14‐15;q23‐24). The remaining abnormal tumors have had various nonrecurrent anomalies. Secondary karyotypic rearrangements, sometimes including ring chromosomes, have been found in one‐third and reflect clonal evolution. Occasional leiomyomas have contained multiple numerical and structural rearrangements. Though benign, these cytogenetically grossly aberrant tumors often displayed more atypical histological features than are usually seen in leiomyoma. Multiple leiomyomas have been investigated from 69 patients, with detection of chromosome anomalies in at least two separate tumors from the same uterus in ten cases. In half of these patients unrelated aberrations were found in different leiomyomas from the same uterus. On other occasions the aberrations were identical, indicating that although some uterine leiomyomas originate independently, others may develop by intra‐myometrial spreading from a common neoplastic clone. Some common features are discernible between the karyotypic pictures of uterine leiomyoma and angioleiomyoma; rearrangements of 6p, 13q, and 21q have been described in both tumor types. The cytogenetic similarities so far detected between leiomyoma and the malignant muscle tumors—leiomyosarcoma and rhabdomyosarcoma—are few and may be fortuitous. The cytogenetic profiles of leiomyoma and lipoma are strikingly similar; both tumor types have nonrandom rearrangements of 12q13‐15, t(12;14) in leiomyoma and t(3;12) in lipoma, as well as variant rearrangements of the same 12q segment. Both also have cytogenetic subgroups characterized by changes in 6p and ring chromosomes. Finally, karyotypic similarities exist also between leiomyoma and pleomorphic adenoma of the salivary gland, which includes a subset of tumors with anomalies of 12q13‐15, and with myxoid liposarcoma, which has t(12;16)(q13;p11) as a tumor‐specific rearrangement.
The “missing” mouse plasmacytoma (MPC) associated translocation T(15;16) occurs repeatedly in new MPC induction systems
Authors: Wiener Francis , Silva Santiago , Sugiyama Hiroyuki , Babonits Magdalena , Klein George 
Published: February 2007

AbstractA reciprocal translocation between chromosomes 15 and 16 has been detected in seven murine plasmacytomas induced by a combination of pristane and Abelson virus. Six of the tumors were induced in a new, unconventional experimental system based on transfer of uninfected or Abelson virus infected bone marrow and spleen cells, respectively, into pristane treated mice. All six tumors were of donor type. The seventh tumor appeared in a conventional pristane + Abelson virus treated mouse. This tumor was unusual in carrying both the 15;16 variant translocation and the typical 12;15 translocation, in the same tumor cells. In the new 15;16 variant, the breakpoint of chromosome 15 was at the interphase of the D2/3 sub‐bands, as in mouse plasmacytomas with the previously well‐known typical 12;15 and variant 6;15 translocations. The breakpoint on chromosome 16 was mapped to band 16B1, corresponding to the presumed cytogenetic site of the lg‐lambda gene. In three of the seven tumors with the 15;16 translocation, the derivative chromosome 15 had undergone a duplication, a feature that has not been previously encountered in the MPC‐associated 12;15 and 6;15 translocation carriers. The reciprocal derivative chromosome 16 was lost from one of the seven tumors. We postulate that the 15;16 translocation results in juxtaposition of the myc gene to lambda sequences, probably in a similar orientation as previously described for the variant 6;15 translocation.
No difference in expression of chromosomal fragile sites in patients with solid malignant tumours and normal controls
Authors: Kampmann Thomas , Schmidt Angela , Rüdiger Hugo W. , Tan Tjhoen Lien , Passarge Eberhard 
Published: February 2007

AbstractThe frequency and distribution of rare and common chromosomal fragile sites in metaphases derived from peripheral lymphocytes were compared in 26 patients with malignant solid tumours and 24 normal controls. In order to avoid bias in evaluation, the identity of each individual as patient or control was disclosed only after the study was completed. Rare heritable folic acid inducible fragile sites were found in five patients (2q13; 6p23; 8q22; 16p12) and two controls (8q22). Common fragile sites were present in 21 of 26 patients and in 19 of 24 controls. These differences are statistically not significant in the Fisher test. We conclude that the expression of fragile sites does not indicate a predisposition for solid tumours.
Demonstration of acquired hemizygosity and clonality in acute lymphoblastic leukemia with chromosome 7 abnormalities using hypervariable DNA probes
Authors: Yamada Toshiyuki , Shippey Caroline A. , Martineau Mary , Secker‐Walker Lorna M. 
Published: February 2007

AbstractClonal abnormalities of chromosome(s) 7 were investigated in two patients with acute lymphoblastic leukemia. The abnormal karyotypes were 46,XY,–7,del(6)(q13q21),+i(7q)/47,XY,del(6),+i(7q) in case 1, and 46,XX,–7,t(4;11)(q21;q23),+i(7q) in case 2. DNA from leukemic tissue was investigated with Southern blotting using hypervariable DNA probes λMS31 and pλg3 located on 7p and 7q, respectively. Restriction fragment length polymorphisms (RFLPs) were detected on the short arm in case 1 and on both arms in case 2, and a marked difference in intensity between the two alleles was observed. In case 1 the acquired hemizygosity of 7p, suggested by the cytogenetic findings, was confirmed by Southern blotting. Thus, one chromosome 7 formed the i(7q) and the other No. 7 was duplicated. In case 2 the results of the Southern blotting indicated that the size of the clone with i(7q) was considerably greater than suggested by cytogenetic analysis of the few available metaphase cells.