bluuebunny/crossref_metadata_2025_split huggingface dataset:
Numerical solutions of the shallow water equations with discontinuous bed topography
Authors: Zhou J. G. , Causon D. M. , Ingram D. M. , Mingham C. G. 
Published: August 2002

AbstractA simple scheme is developed for treatment of vertical bed topography in shallow water flows. The effect of the vertical step on flows is modelled with the shallow water equations including local energy loss terms. The bed elevation is denoted with zb‐ for the left and zb+ for the right values at each grid point, hence exactly representing a discontinuity in the bed topography. The surface gradient method (SGM) is generalized to reconstruct water depths at cell interfaces involving a vertical step so that the fluxes at the cell interfaces can accurately be calculated with a Riemann solver. The scheme is verified by predicting a surge crossing a step, a tidal flow over a step and dam‐break flows on wet/dry beds. The results have shown good agreements compared with analytical solutions and available experimental data. The scheme is efficient, robust, and may be used for practical flow calculations. Copyright © 2002 John Wiley & Sons, Ltd.
Combined comparative genomic hybridization and genomic microarray for detection of gene amplifications in pulmonary artery intimal sarcomas and adrenocortical tumors
Authors: Zhao Jianming , Roth Jürgen , Bode‐Lesniewska Beata , Pfaltz Madeleine , Heitz Philipp U. , Komminoth Paul 
Published: August 2002

AbstractIdentification of gene amplifications in human tumors is important for the understanding of tumorigenesis and may lead to discovery of diagnostic and prognostic markers. In this study, we used a microarray‐based comparative genomic hybridization (CGH) technique, combined with conventional CGH, to identify gene amplifications in 43 tumors including eight pulmonary artery intimal sarcomas and 35 adrenocortical tumors. Conventional CGH revealed gains or amplifications of 12q13–q15 in six sarcomas and in two adrenocortical carcinomas. Using microarrays, we demonstrated that, among genes located on 12q13–q15, SAS/CDK4 were amplified in six sarcomas, and MDM2 and GLI in five and four sarcomas, respectively. The two adrenocortical tumors showed coamplifications of SAS/CDK4 and MDM2. Furthermore, PDGFRA (located on 4q12) amplification was identified in five sarcomas. Our data demonstrate: (1) amplifications of SAS/CDK4, MDM2, GLI, and PDGFRA are strongly associated with the tumorigenesis of pulmonary artery intimal sarcomas, whereas SAS/CDK4 and MDM2 coamplification may contribute to the progression of adrenocortical tumors; (2) microarray‐based CGH is a useful tool for simultaneous detection of multiple gene amplifications, with a high sensitivity and resolution compared to that of conventional CGH. © 2002 Wiley‐Liss, Inc.
Molecular cytogenetic definition of three distinct chromosome arm 14q deletion intervals in gastrointestinal stromal tumors
Authors: Debiec‐Rychter Maria , Sciot Raf , Pauwels Patrick , Schoenmakers Eric , Dal Cin Paola , Hagemeijer Anne 
Published: August 2002

AbstractGastrointestinal stromal tumors (GISTs) are mesenchymal neoplasms characterized by frequent chromosome arm 14q losses. In this study, the 14q changes in a series of 39 histologically and immunohistochemically confirmed GISTs were analyzed in detail by metaphase and/or interphase fluorescence in situ hybridization (FISH) studies using 21 genetically well‐characterized, region‐specific 14q11‐24 YAC clones. By conventional cytogenetic analysis, acquired clonal chromosome aberrations were found in 17 out of 35 tumors. Chromosome 14 was involved in 13 cases; six specimens showed complete chromosome 14 loss, while the remaining seven had structural abnormalities with the breakpoints residing within the intervals 14q11‐13 or 14q22‐24. Other recurrent chromosome aberrations included frequent deletions of chromosome 1p (11/17), losses of chromosome 22 (7/17), losses or deletions of chromosome arm 13 (6/17) or 15 (4/17), and gains or translocations involving chromosome 17 (4/17). Combining cytogenetic data with double‐color FISH analysis, total or partial losses of 14q material were detected in 29 out of 36 tumors (81%). The 14q losses were found in all stages and histological subtypes. Two most frequent common deletion regions flanked by YACs 931B1 and 761D4, and 802E7 and 892C11 at 14q23‐24 (25/30 of each; 83%) could be identified. Furthermore, 21 tumors (70%) shared a region of deletion defined by YACs 957H10 and 931E5 at 14q11‐12. Our results suggest the presence of at least three distinct critical deletion regions on chromosome 14 in GISTs. © 2001 Wiley‐Liss, Inc.
Stone artifact scatters in western NSW, Australia: Geomorphic controls on artifact size and distribution
Authors: Fanning Patricia , Holdaway Simon 
Published: August 2002

AbstractSurface scatters of Aboriginal stone artifacts have been exposed in many parts of inland Australia by accelerated erosion that followed the introduction of pastoralism by European settlers in the 19th century. This paper reports on a set of techniques developed to investigate and quantify the effects of these post‐discard disturbance processes in Sturt National Park in northwest NSW, Australia. Backwards, stepwise, linear regression showed the influence of geomorphic parameters such as slope gradient, elevation, landform, and contemporary surface processes on artifact distribution, with artifact maximum dimension as the dependent variable. The results indicate that, even at low gradients, artifact size and slope angle are significantly related, but that the variance in maximum dimension explained by gradient is very low. Similar results were found for the other geomorphic variables. We conclude that artifact movement by surface wash across these surfaces is unlikely to significantly affect artifact distribution. While vertically conflated surface scatters do not preserve “living floors” in a short‐term, functional sense, their apparent horizontal integrity allows investigation of the long‐term use of place by hunter‐gatherer people in the past. Insofar as assemblage integrity is important for assessing site significance in the heritage management industry, our methods provide a means for assessing the degree to which a site has been damaged by water flow. © 2001 John Wiley & Sons, Inc.
Removal of the floxed neo gene from a conditional knockout allele by the adenoviral Cre recombinase in vivo
Authors: Kaartinen Vesa , Nagy Andre 
Published: August 2002

AbstractSummary: Conditional and tissue specific gene targeting using the Cre‐loxP recombination system in combination with established ES cell techniques has become a standard for in vivo loss of function studies. In a typical flox and delete gene targeting strategy, the loxP‐neo‐loxP cassette is inserted into an intron and an additional loxP site is located in one of the homology arms so that loxP sites surround a functionally essential part of the gene. The neo cassette in usually removed by transient expression of the Cre recombinase in ES cells to avoid selection gene interference and genetic ambiquity. However, this causes a significant increase in manipulation of ES cells and often compromises ES cell pluripotency. Here we describe a method in which the floxed neo gene is removed from a knockout allele by infecting 16‐cell‐stage morulae by the recombinant Cre adenovirus. This virus provides only transient Cre expression and does not integrate into the mouse genome. Produced mosaic mice transmitted the desired allele without the neo cassette with high frequency to their offspring. This method is rapid and easy and does not require any special equipment. Moreover, because superovulated mice can be used as donors, this method does not necessitate a large number of mice. genesis 31:126–129, 2001. © 2001 Wiley‐Liss, Inc.
Long‐term, noninvasive imaging of regulated gene expression in living mice
Authors: Hasan Mazahir T. , Schönig Kai , Berger Stefan , Graewe Walter , Bujard Hermann 
Published: August 2002

AbstractSummary: We describe here an approach for monitoring regulated gene expression by noninvasive imaging in living mice. We have utilized the tetracycline inducible system to simultaneously coregulate the expression of two genes encoding the firefly luciferase and the Cre recombinase, respectively. Results from our model system demonstrate that luciferase can be used as a noninvasive imaging marker for the regulated expression of a second gene in living mice. The integration of noninvasive imaging and inducible gene expression into current approaches of functional genomics should greatly advance our capabilities of carrying out highly controlled long‐term studies of gene function in individual mice. genesis 29:116–122, 2001. © 2001 Wiley‐Liss, Inc.
Influence of genes and family environment on adult smoking behavior assessed in an adoption study
Authors: Osler Merete , Holst Claus , Prescott Eva , Sørensen Thorkild I.A. 
Published: August 2002

AbstractTwin studies suggest that genetic factors influence smoking behavior. However, in these studies, genetic and environmental influences may be confounded. We examined whether smoking behavior of adoptees is associated with smoking behavior in adoptive and biological relatives in a design in which this confounding is minimized. Data on smoking status were collected using a mailed questionnaire in a sample of 840 adoptive families from the Danish Adoption Register including all non‐familial adoptions from 1924 through 1947. Smoking data were available for 706 adoptees, 451 biological fathers, 580 biological mothers, 641 adoptive fathers, 693 adoptive mothers, 199 biological full‐siblings, 684 maternal half‐siblings, and 576 paternal half‐siblings. Adoptees’ status as ever, current, heavy, or former (ex‐)smokers was related to their relatives’ smoking status. Adoptees ever smoking was associated with their full‐siblings’ status as ever smokers (OR = 3.6 [1.5–8.7]). Adoptees’ current smoking was also associated with their full‐siblings’ ever (OR = 3.2 [1.5–7.7]) and current (OR = 2.6 [1.3–5.0]) smoking, whereas adoptees’ heavy smoking was associated with their full‐siblings ever (OR = 5.5 [2.1–14.3]), current (OR = 4.0[1.9–8.6]) and heavy (OR = 2.0[1.0–4.2]) smoking. Compared with current smokers, adoptee ex‐smokers had full‐siblings who were ex‐smokers more often (OR = 3.5 [1.0–11.6]), current (OR = 0.4 [0.2–0.8]), and heavy (OR = 0.3 [0.1–0.9]) smokers less often. Adoptees’ smoking behavior was not associated with adoptive or biological parents’ status as current smokers. This study of smoking behavior in adult adoptees and their biological and adoptee family supports the finding in twin studies of a genetic influence on smoking within the same generation. Genet. Epidemiol. 21:193–200, 2001. © 2001 Wiley‐Liss, Inc.
Relevance of the genes for bone mass variation to susceptibility to osteoporotic fractures and its implications to gene search for complex human diseases
Authors: Deng Hong‐Wen , Mahaney Michael C. , Williams Jeff T. , Li Jing , Conway Theresa , Davies K. Michael , Li Jin‐Long , Deng Hongyi , Recker Robert R. 
Published: August 2002

AbstractWe investigate the relevance of the genetic determination of bone mineral density (BMD) variation to that of differential risk to osteoporotic fractures (OF). The high heritability (h2) of BMD and the significant phenotypic correlations between high BMD and low risk to OF are well known. Little is reported on h2 for OF. Extensive molecular genetic studies aimed at uncovering genes for differential risks to OF have focussed on BMD as a surrogate phenotype. However, the relevance of the genetic determination of BMD to that of OF is unknown. This relevance can be characterized by genetic correlation between BMD and OF. For 50 Caucasian pedigrees, we estimated that h2 at the hip is 0.65 (P < 0.0001) for BMD and 0.53 (P < 0.05) for OF; however, the genetic correlation between BMD and OF is nonsignificant (P > 0.45) and less than 1% of additive genetic variance is shared between them. Hence, most genes found important for BMD may not be relevant to OF at the hip. The phenotypic correlation between high BMD and low risk to OF at the hip (approximately –0.30) is largely due to an environmental correlation (ρE = –0.73, P < 0.0001). The search for genes for OF should start with a significant h2 for OF and should include risk factors (besides BMD) that are genetically correlated with OF. All genes found important for various risk factors must be tested for their relevance to OF. Ideally, employing OF per se as a direct phenotype for gene hunting and testing can ensure the importance and direct relevance of the genes found for the risk of OF. This study may have significant implications for the common practice of gene search for complex diseases through underlying risk factors (usually quantitative traits). Genet. Epidemiol. 22:12–25, 2002. © 2002 Wiley‐Liss, Inc.
Buried oblique‐slip faults in the Irish Caledonides
Authors: Michael Williams D. 
Published: August 2002

AbstractDespite over a century of geological investigation, the Ordovician evolution of South Mayo, western Ireland, is still imperfectly understood. An example of this is the supposed lateral equivalence of two formations within the succession, the Rosroe and Derrylea Formations of Arenig age, exposed on opposite limbs of a major east–west syncline. These formations exhibit characteristics which suggest that they were not deposited in the same basin. Both formations contain tuff horizons. Geochemical analysis of these tuffs shows that each formation contains chemically distinct volcanic signatures suggesting deposition in separate sub‐basins. Previously the Rosroe Formation on the south limb of the syncline was considered the coarse‐grained proximal equivalent of the finer‐grained Derrylea Formation, both being deposited in a deep‐water fan environment. Previously published palaeocurrent data together with new data show the Rosroe Formation to have been derived from the northeast and therefore it cannot be the proximal equivalent of the Derrylea Formation. Additionally, the two formations show different and distinct associations of heavy mineral assemblages.It is suggested that one explanation for these data is that both formations were deposited in separate sub‐basins controlled by oblique slip sinistral faults, similar in some respects to the Cenozoic basins of the Gulf of California. In the Irish case these faults would have been largely buried by later Ordovician sedimentation. Some models for the Ordovician evolution of this area postulate the presence of an initial oceanic arc situated above a southward directed subduction zone. The presence of thick proximal submarine tuffs derived from an arc environment in the Rosroe Formation suggest that at least by this time the subduction zone was in fact northward directed and outboard of the arc. Copyright © 2002 John Wiley & Sons, Ltd.
Isolation of a glial‐restricted tripotential cell line from embryonic spinal cord cultures
Authors: Wu Yuan Yuan , Mujtaba Tahmina , Han Steve S.W. , Fischer Itzhak , Rao Mahendra S. 
Published: August 2002

AbstractNeuroepithelial stem cells (NEPs), glial‐restricted precursors (GRPs), and neuron‐restricted precursors (NRPs) are present during early differentiation of the spinal cord and can be identified by cell surface markers. In this article, we describe the properties of GRP cells that have been immortalized using a regulatable v‐myc retrovirus construct. Immortalized GRP cells can be maintained in an undifferentiated dividing state for long periods and can be induced to differentiate into two types of astrocytes and into oligodendrocytes in culture. A clonal cell line prepared from immortalized GRP cells, termed GRIP‐1, was also shown to retain the properties of a glial‐restricted tripotential precursor. Transplantation of green fluorescent protein (GFP)‐labeled subclones of the immortalized cells into the adult CNS demonstrates that this cell line can also participate in the in vivo development of astrocytes and oligodendrocytes. Late passages of the immortalized cells undergo limited transdifferentiation into neurons as assessed by expression of multiple neuronal markers. The availability of a conditionally immortalized cell line obviates the difficulties of obtaining a large and homogeneous population of GRPs that can be used for studying the mechanism and signals for glial cell differentiation as well as their application in transplantation protocols. GLIA 38:65–79, 2002. © 2002 Wiley‐Liss, Inc.
IGF‐I and microglia/macrophage proliferation in the ischemic mouse brain
Authors: O'Donnell Steven L. , Frederick Terra J. , Krady J. Kyle , Vannucci Susan J. , Wood Teresa L. 
Published: August 2002

AbstractWe have used a model of hypoxic‐ischemic brain injury in adult male C57BL/6 mice to study insulin‐like growth factor‐I (IGF‐I) and IGF‐binding protein (IGFBP) expression in response to cerebral hypoxia‐ischemia (H/I) in the adult mouse. A period of 20 min of H/I that resulted in histopathology in cortex, striatum, and thalamus was correlated with induction of mRNA for IGF‐I, IGFBP‐2, IGFBP‐3, IGFBP‐5, and glial fibrillary acidic protein (GFAP) by 4 days of recovery. Increased IGF‐I mRNA was located within damaged regions and was surrounded by IGFBP‐2 mRNA expression. The results of combined immunostaining/in situ hybridzation showed that the cells expressing IGFBP‐2 mRNA were also GFAP‐positive and comprised a subset of activated astrocytes immediately surrounding areas of damage. In contrast, staining within damaged regions showed high numbers of cells immunopositive for F4/80 and lectin B4 indicative of microglia and macrophages but no cells immunopositive for the astrocytic proteins GFAP or S‐100β. Microglia/macrophages within the damaged areas expressed IGF‐I mRNA and were also immunopositive for the proliferating cell nuclear antigen. To determine whether expression of IGF‐I could contribute to proliferation of microglia, we treated purified cultures of adult brain microglia with IGF‐I in the presence of 3H‐thymidine. IGF‐I stimulated a twofold increase in DNA synthesis in cultures of adult brain microglia. Taken together with previous data demonstrating that IGF‐I promotes proliferation of peripheral macrophages, these data support the hypothesis that IGF‐I is an autocrine/paracrine mitogen for microglia/macrophages after H/I. GLIA 38:85–97, 2002. © 2002 Wiley‐Liss, Inc.
Nerve growth factor signaling of p75 induces differentiation and ceramide‐mediated apoptosis in Schwann cells cultured from degenerating nerves
Authors: Hirata Hitoshi , Hibasami Hiroshige , Yoshida Toshimichi , Ogawa Masaru , Matsumoto Mamoru , Morita Akimasa , Uchida Atsumasa 
Published: August 2002

AbstractIn peripheral nerve regeneration or remyelination, immature Schwann cells expressing p75NTR play cardinal roles in the support and regeneration of axons (Griffin JW, Hoffman PN. Peripheral Neuropathy 361–376, 1993). Only one of four to six Schwann cells participate in remyelination of damaged or regenerating axons. The rest of the cells, or supernumerary Schwann cells, show severe atrophy and gradually decrease in number, reestablishing a 1:1 axon–Schwann cell relationship (Said G, Duckett S. Acta Neuropathol (Berl) 53:173–179, 1981). Recent reports demonstrated that severely atrophied supernumerary Schwann cells are eliminated by apoptosis during axonal regeneration or remyelination (Hirata H, Hibasami H. Apoptosis 3:353–360, 1998; Berciano MT, Calle E. Acta Neuropathol (Berl) 95:269–279, 1998). The mechanism to induce selective death of supernumerary Schwann cells without causing any damage to axon‐associated Schwann cells or axons remains to be determined. In this article, we report that p75NTR, the low‐affinity receptor for all members of neurotrophins, signals both cell differentiation and apoptosis through intracellular ceramide elevation. The final response is dependent on the intracellular ceramide level and Schwann cells modulate their response by changing expression level of p75NTR. This effect was selective for nerve growth factor (NGF). Taken together, the present study suggests that NGF contributes both to phenotypic regulation and to elimination of the dedifferentiated Schwann cells, while supporting survival or regeneration of certain types of axons during peripheral nerve repair or regeneration. GLIA 36:245–258, 2001. © 2001 Wiley‐Liss, Inc.
Differential expression of costimulatory molecules B7‐1 and B7‐2 on microglial cells induced by Th1 and Th2 cells in organotypic brain tissue
Authors: Wolf Susanne A. , Gimsa Ulrike , Bechmann Ingo , Nitsch Robert 
Published: August 2002

AbstractAutoreactive T‐cells are involved in demyelination, neurodegeneration, and the recruitment of peripheral macrophages and nonspecific activated T‐cells in autoimmune diseases such as multiple sclerosis (MS). The ligation of costimulatory B7 molecules on microglia with CD28/CTLA‐4 on T‐cells is thought to be crucial to the onset and course of MS and its rodent model experimental autoimmune encephalomyelitis (EAE). It is currently unclear as to how far the nature of infiltrating T‐cells has an impact on the expression of the B7 molecules on microglia, the resident antigen‐presenting cells (APCs) of the brain. We studied the expression of B7‐1 and B7‐2 on microglia after encounter with preactivated Th1 and Th2 cells from transgenic mice whose T‐cells express a receptor (TCR) either specific to myelin basic protein (MBP) or ovalbumin (OVA) using murine organotypic entorhinal‐hippocampal slice cultures (OEHSC). Our main finding was that Th1 cells downregulate the constitutive expression of B7‐2 and induce B7‐1 expression while Th2 cells do not induce this B7‐1 upregulation. The main difference between MBP‐ and OVA‐specific cells was seen in experiments were Th1 cells had direct contact to APCs but not to brain tissue. In contrast to MBP‐specific Th1 cells, OVA‐specific Th1 cells required the addition of antigen to upregulate B7‐1 and downregulate B7‐2. When the cells were allowed to have contact to brain tissue, no difference was seen in the pattern of B7 regulation between OVA‐ and MBP‐specific T‐cells. Our data suggest that T‐cells are able to modulate B7 expression on microglial cells in the brain independent of antigen presentation through TCR/MHC‐II ligation but presumably by soluble mediators. GLIA 36:414–420, 2001. © 2001 Wiley‐Liss, Inc.
Persecutory symptoms and perceptual disturbance in a community sample of older people: the Islington study
Authors: Livingston G. , Kitchen G. , Manela M. , Katona C. , Copeland J. 
Published: August 2002

AbstractBackgroundWhile there are extensive studies of paranoid symptoms and perceptual disturbance (PPD) in younger adults, relatively little is known about older adults with similar symptoms.MethodThis study took place in Islington, an inner London borough. Enumeration Districts were randomised to provide a sampling frame. Residents aged 65 or over were interviewed at home. The Short‐CARE was used to elicit psychiatric symptoms and diagnosis. Sociodemographic particulars were elicited using the Client Sociodemographic and Service Receipt Inventory. Questions were asked regarding sight and hearing. We used subsections of the geriatric mental scale to identify people who had PPD symptoms. Medications taken were recorded. We asked ‘Do you have any health problems?’ as a screening question for subjective health problems.ResultsWe interviewed 720 people. Twenty‐eight (3.9%) participants scored positively on the PPD sub‐scales of the GMS. A forward logistic regression analysis for independent predictors of PPD found the significant independent predictors were dementia (p = 0.0000; odds ratio 6.8), drinking alcohol in last 6 months (p < 0.03; odds ratio 0.3), drinking alcohol to help sleep (p < 0.005; odds ratio 9.6), subjective memory loss (p < 0.007; odds ratio 3.3) and uncorrected visual impairment (p < 0.02; odds ratio 2.8).ConclusionThere is a relatively high prevalence of PPD in older people living in the community. This is not associated with higher use of services despite the increased needs. Further studies should consider interventions to meet this unmet need. Copyright © 2001 John Wiley & Sons, Ltd