bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genomic characterization of MOZ/CBP and CBP/MOZ chimeras in acute myeloid leukemia suggests the involvement of a damage‐repair mechanism in the origin of the t(8;16)(p11;p13)
Authors: Panagopoulos Ioannis , Isaksson Margareth , Lindvall Charlotta , Hagemeijer Anna , Mitelman Felix , Johansson Bertil 
Published: December 2002

AbstractThe t(8;16)(p11;p13), which is strongly associated with acute myeloid leukemia (AML) displaying monocytic differentiation, erythrophagocytosis by the leukemic cells, and a poor response to chemotherapy, fuses the MOZ gene (8p11) with the CBP gene (16p13). Although genomic rearrangements of MOZ and CBP have been detected using fluorescence in situ hybridization and Southern blot analyses, characterization of the breakpoints at the sequence level has never been performed. We have sequenced the breakpoints in four t(8;16)‐positive AML cases with the aim to identify molecular genetic mechanisms underlying the origin of this translocation. In addition, an exon/intron map of the MOZ gene was constructed, which was found to be composed of 17 exons. Long‐range‐PCR with CBP forward primers in exon 2 and MOZ reverse primers in exon 17 as well as with a MOZ forward primer in exon 16 and a CBP reverse primer in intron 2 successfully amplified CBP/MOZ and MOZ/CBP hybrid genomic DNA fragments in all four AMLs. The breaks clustered in both CBP intron 2 and MOZ intron 16, and were close to repetitive elements, and in one case an Alu‐Alu junction for the CBP/MOZ hybrid was identified. Additional genomic events (i.e., deletions, duplications, and insertions) in the breakpoint regions in both the MOZ and CBP genes were found in all four cases. Thus, the t(8;16) does not originate through a simple end‐to‐end fusion. The findings of multiple breaks and rearrangements rather suggest the involvement of a damage‐repair mechanism in the origin of this translocation. © 2002 Wiley‐Liss, Inc.
Delineation of the minimal region of loss at 13q14 in multiple myeloma
Authors: Elnenaei Manal O. , Hamoudi Rifat A. , Swansbury John , Gruszka‐Westwood Alicja M. , Brito‐Babapulle Vasantha , Matutes Estella , Catovsky Daniel 
Published: December 2002

AbstractPrevious studies have focused on the incidence and prognostic implications of 13q14 deletions in multiple myeloma (MM), but none has sought to delineate the minimal common deleted region (CDR). In an effort to do so, dual‐color interphase fluorescence in situ hybridization (FISH) was applied on 82 myeloma cases, initially by use of three probes for 13q14 (RB1, D13S319, and D13S25). Deletions were detected in 29/82 (35.4%) cases, and all except one were monoallelic. Subsequently, contiguous YACs, PACs, and a BAC spanning the 13q14–q21 region were employed for deletion mapping in addition to a 13q telomere probe. Large deletions extending to the 13q34 region were found in 55% of the deleted cases, whereas an additional 13.8% showed loss of both 13q34 and 13q14 regions with retention of 13q21. A CDR of approximately 350 kb was identified at 13q14 with the proximal border approximately 120 kb centromeric from D13S319, encompassing an area rich in expressed sequence tagged sites and containing DLEU1, DLEU2, and RFP2 genes. Direct sequencing of the RFP2 gene revealed no mutations in six patients and four MM cell lines harboring deletions of the CDR. However, a role for RFP2 in the pathogenesis of MM cannot yet be excluded, given that alternative mechanisms such as haploinsufficiency remain possible. © 2002 Wiley‐Liss, Inc.
Recurrent allelic imbalance at the rat Pten locus in DMBA‐induced fibrosarcomas
Authors: Sjöling Åsa , Samuelson Emma , Adamovic Tatjana , Behboudi Afrouz , Röhme Dan , Levan Göran 
Published: December 2002

AbstractThe tumor‐suppressor gene PTEN (phosphatase and tensin homolog) is frequently inactivated in different types of human tumors. Less is known about the involvement of the homologous gene Pten in animal model systems of cancer. By sequencing one of the introns of rat Pten, we found an informative intragenic PCR marker suitable for genetic studies. Through use of this marker, the position of Pten in the genetic linkage map was localized to the distal part of rat chromosome 1 (RNO1) by analysis of F2 progeny from an intercross between inbred strains BN and LE. Subsequently, 22 markers from this region (including the intragenic Pten marker) were used to study the occurrence of allelic imbalance in distal RNO1 in fibrosarcomas that had been induced by DMBA in F1(BN×LE) rats. The analysis revealed that allelic imbalance was common in the vicinity of Pten, and there was loss or reduction of one of the Pten alleles in more than 60% of the fibrosarcomas. DNA sequencing was preformed to investigate whether the Pten allele remaining in the tumors was inactivated by mutation. However, no mutations were detected in the genomic sequence of Pten exons 5 to 9 in any of the fibrosarcomas, and normal mRNA transcripts were expressed in all tumors. Thus, based on the targeted selection for loss of Pten observed in some of these tumors and the absence of inactivation of the remaining allele, we suggest that haploinsufficiency of Pten may be an important factor in rat DMBA‐induced fibrosarcomas. © 2002 Wiley‐Liss, Inc.
Skill learning in patients with moderate Alzheimer's disease: a prospective pilot‐study of waltz‐lessons
Authors: Rösler Alexander , Seifritz Erich , Kräuchi Kurt , Spoerl David , Brokuslaus Ilona , Proserpi Sara‐Maria , Gendre Annekäthi , Savaskan Egemen , Hofmann Marc 
Published: December 2002

AbstractThe authors report the effect of a 12‐day prospective, blinded dance‐learning trial in 5 patients with moderate Alzheimer's disease (AD) and 5 age‐matched depressed patients. Patients with AD showed a significant effect in procedural learning whereas depressed patients did not. These findings suggest potential implications for therapeutic interventions in patients with moderate AD. Copyright © 2002 John Wiley & Sons, Ltd.
Qigong as a psychosocial intervention for depressed elderly with chronic physical illnesses
Authors: Tsang Hector W. H. , Cheung Leo , Lak Davis C. C. 
Published: December 2002

AbstractLiterature uncovers that depression is common in elderly people. The problem is more serious in elderly with chronic physical illnesses. Although the relationship between physical problems and depression is well documented, the underlying mechanism is basically unknown. This article proposed after a comprehensive literature review that depression in elderly with chronic physical illnesses results from disability and a reduction in psychosocial resources. If depression is left untreated, suicide may be a consequence. In view of this, various forms of psychosocial interventions are developed based on mainstream western medicine. The authors argue that qigong, a form of Chinese therapeutics, has the effect of alleviating clinical depression and thus improves quality of life. A simple form of dynamic qigong, namely the Eight‐Section Brocades, is suggested to serve the purpose. A theory which explains the psychosocial effect of qigong is hypothesized. Copyright © 2002 John Wiley & Sons, Ltd.
Quality of accommodation and risk of depression in later life: An analysis of prospective data from the Gospel Oak Project
Authors: Stewart Robert , Prince Martin , Harwood Rowan , Whitley Robert , Mann Anthony 
Published: December 2002

AbstractObjectiveTo investigate the association between observer‐rated quality of internal accommodation and risk of onset of depression.DesignA secondary analysis of data from a cross‐sectional survey of residents aged 65 or over in a north London electoral ward who were followed up after a one‐year interval.MethodPervasive depression (SHORT‐CARE) was assessed at both interviews. Quality of accommodation (on a five‐point scale) was assessed by a single interviewer in a random sample at baseline. Potential confounding factors which were considered included age, sex, social class, level of handicap, level of social support, baseline sub‐case depressive symptoms, cognitive function, income, accommodation tenure and area‐level housing quality.ResultsIn participants without depression at baseline (n=131), worse accommodation was associated with depression after one year (odds ratio (OR) between three accommodation groups 3.3, 95% confidence intervals (CI) 1.5–7.8). Adjustment for the potential confounding factors made little difference (adjusted OR 3.3). The association was principally in people cohabiting (OR 12.4) rather than living alone (OR 1.1).ConclusionsAn observer's impression of accommodation quality was a strong and independent predictor of depression in this sample. The stronger association in people who were cohabiting may reflect increased exposure to the internal environment. Copyright © 2002 John Wiley & Sons, Ltd.
Antidepressant prescribing in nursing homes: is there a place for tricyclics?
Authors: Borson S. , Scanlan J. M. , Doane K. , Gray S. 
Published: December 2002

AbstractObjectiveTo deduce a model describing physicians' choice of antidepressants for treating elderly nursing home patients.MethodsSubjects were geriatric residents of 137 skilled nursing facilities who regularly received an antidepressant medication for at least one month (n = 3440, 28% of all residents). Reasons for prescribing antidepressants and physicians' diagnoses of depression and dementia were identified by medical record audit. Residents were grouped by dementia and antidepressant target symptoms (depression, or one or more non‐psychiatric symptoms, i.e. insomnia, pain, incontinence, itching).ResultsSelective serotonin reuptake inhibitors (SSRIs) were prescribed preferentially over tricyclic antidepressants (TCAs) for treating depression in both demented and non‐demented residents, but TCAs were nine times more likely to be prescribed for treating non‐psychiatric target symptoms alone. When non‐psychiatric target symptoms were present without depression or dementia, both amitriptyline and nortriptyline prescribing was increased, but amitriptyline appeared to be the antidepressant of choice. In all subgroups examined, its use was two to five times more prevalent when such symptoms were present. In patients with dementia, amitriptyline prescribing declined whether or not non‐psychiatric target symptoms were present, but nortriptyline prescribing did not; nortriptyline was three times more likely than amitriptyline to be prescribed in the presence of dementia.ConclusionsPhysicians prescribe anticholinergic TCAs principally to treat common non‐depressive symptoms in nursing home residents, preferring SSRIs for uncomplicated depression and depression with dementia. They tend to avoid prescribing anticholinergic TCAs other than nortriptyline when they recognize a patient as demented. The data suggest that physicians employ a decision model for antidepressant prescribing that simultaneously recognizes the utility of TCAs in treating non‐psychiatric symptoms and the anticholinergic vulnerability of older, especially demented, patients. Whether or not this model leads to optimal patient management requires further study. Copyright © 2002 John Wiley & Sons, Ltd.
Using extracurricular activity as an indicator of interpersonal skill: Prudent evaluation or recruiting malpractice?
Authors: Rubin Robert S. , Bommer William H. , Baldwin Timothy T. 
Published: December 2002

AbstractThere is widespread agreement that success in organizations requires more than high intellect. Thus, college
recruiters commonly examine job candidates' extracurricular activities in search of
“well‐rounded,” emotionally intelligent, and interpersonally skilled students. Intuitively,
extracurricular activities seem like valuable student experiences; however, research evidence is sparse,
suggesting far more questions than answers. Is participation in extracurricular activity truly linked to
interpersonal skill performance? Does leadership experience make a difference? Do extracurricular
experiences yield higher skill development? Six hundred eighteen business students and the relationship of
their extracurricular involvement to four interpersonal skills were examined. Significant relationships were found
and recruitment implications are discussed. © 2002 Wiley Periodicals, Inc.
BRCA2 arg372hispolymorphism and epithelial ovarian cancer risk
Authors: Auranen Annika , Spurdle Amanda B. , Chen Xiaoqing , Lipscombe Julian , Purdie David M. , Hopper John L. , Green Adele , Healey Catherine S. , Redman Karen , Dunning Alison M. , Pharoah Paul D. , Easton Douglas F. , Ponder Bruce A.J. , Chenevix‐Trench Georgia , Novik Karen L. 
Published: December 2002

AbstractThe BRCA2 372 HH genotype defined by the BRCA2 N372H nonconservative amino acid substitution polymorphism was recently reported to be associated with a small increased risk of breast cancer. We investigated whether this polymorphism was associated with ovarian cancer risk by conducting British and Australian case‐control comparisons in parallel, including a total sample of 1,121 ovarian cancer cases and 2,643 controls. There was no difference in genotype frequency between control groups from the 2 studies (p = 0.9). The HH genotype was associated with an increased risk of ovarian cancer in both studies, and the risk estimate for the pooled studies was 1.36 (95% CI 1.04–1.77, p = 0.03). There was also a suggestion that this risk may be greater for ovarian cancers of the serous subtype for both studies, with an OR (95% CI) of 1.66 (1.17–2.54) for the 2 studies combined (p = 0.005). The BRCA2 372 HH genotype appears to be associated with an increased risk of ovarian cancer of a similar magnitude to that reported for breast cancer. © 2002 Wiley‐Liss, Inc.
Geldanamycin decreases Raf‐1 and Akt levels and induces apoptosis in neuroblastomas
Authors: Kim Sunghoon , Kang Junghee , Hu Wanqin , Evers B. Mark , Chung Dai H. 
Published: December 2002

AbstractNeuroblastomas are the most common extracranial solid tumors of childhood. These tumors are associated with an overall poor prognosis, particularly for advanced stage disease. The benzoquinone ansamycin antibiotic, geldanamycin (GA), exhibits potent antitumor activity in certain cancer cell lines by destabilizing important signal transduction proteins (e.g., Raf‐1 and Akt). The purpose of our study was to determine whether GA can alter the expression of Raf‐1 and Akt, which have been shown to be critical for neuronal cell survival, and induce apoptosis of neuroblastoma cells. Human neuroblastoma cells (SH‐SY5Y, SK‐N‐SH and LAN‐1) were treated with GA for a variable period of time. Cell viability was assessed with MTT assays. Apoptosis was assessed with DNA fragmentation ELISA, TUNEL‐flow cytometric assay, Western blot and caspase activities. We found that GA decreases cell viability and induces apoptosis in the SH‐SY5Y human neuroblastoma cell line. These effects were mediated through activation of caspase‐9 and ‐3, mitochondrial release of cytochrome c and subsequent PARP cleavage. GA‐induced apoptosis was associated with a reduction in the level and activity of Raf‐1 and Akt. The importance of these proteins was further demonstrated by induction of apoptosis in SH‐SY5Y cells by a combination of U0126 (MEK1/2 inhibitor) and LY294002 (an inhibitor of PI3K). Similar to SH‐SY5Y cells, other human neuroblastoma cells (SK‐N‐SH and LAN‐1) were sensitive to the effects of GA‐induced apoptosis. Taken together, our findings suggest that GA may be a novel therapeutic agent, which may be effective in the treatment of neuroblastomas. © 2002 Wiley‐Liss, Inc.
Prevalence of human papillomavirus infection in women in Busan, South Korea
Authors: Shin Hai‐Rim , Lee Duk‐Hee , Herrero Rolando , Smith Jennifer S. , Vaccarella Salvatore , Hong Sook‐Hee , Jung Kap‐Yeol , Kim Hyun‐Ho , Park Un‐Dong , Cha Hyung‐Su , Park Soyoon , Touzé Antoine , Muñoz Nubia , Snijders Peter J.F. , Meijer Chris J.L.M. , Coursaget Pierre , Franceschi Silvia 
Published: December 2002

AbstractTo investigate the prevalence of and the risk factors for human papillomavirus (HPV) infection in South Korea, we interviewed and examined a randomly selected sample of 863 sexually active women (age range = 20–74 years, median 44) and 103 self‐reported virgins from Busan. The presence of DNA of 34 different HPV types in cervical exfoliated cells was tested among sexually active women by means of a PCR‐based assay. IgG antibodies against L1 virus‐like particles (anti‐VLPs) of HPV types 16, 18, 31, 33 and 58 were also evaluated by means of ELISA. The overall prevalence of HPV DNA was 10.4% (95% confidence interval, CI: 8.5–12.7%). The most often found HPV DNA types were HPV 70, HPV 16 and HPV 33; 19.8% (95% CI: 17.2–22.0) of sexually active women had antibodies against one or more HPV types. The most common anti‐VLPs were against HPV 18, 31 and 16. Prevalences standardized by age on the basis of the world standard population were 13.0% for HPV DNA and 17.1% for anti‐VLPs. The concordance between the 2 HPV markers at an individual level was modest, but the risk factors for detection of HPV DNA and anti‐VLPs were similar: number of lifetime sexual partners (odds ratio, OR for ≥ 4 vs. 1 = 3.5 and 5.4, respectively), seropositivity for herpes simplex virus‐2 antibodies (OR = 2.6 and 2.5, respectively) and being single or divorced. HPV DNA, but not anti‐VLPs, were elevated among women whose husbands were thought by their wives to have extra‐marital affairs and those who had undergone vasectomy. Among 103 virgins, 4.9% had anti‐VLPs (1/73 among those aged 24 years or less). © 2002 Wiley‐Liss, Inc.
Induction of IL‐8 and monoclyte chemoattractant protein‐1 by doxorubicin in human small cell lung carcinoma cells
Authors: Shibakura Misako , Niiya Kenji , Kiguchi Toru , Kitajima Isao , Niiya Masami , Asaumi Noboru , Huh Nam‐ho , Nakata Yasunari , Harada Mine , Tanimoto Mitsune 
Published: December 2002

AbstractWe previously demonstrated doxorubicin‐induced urokinase expression in human H69 SCLC cells by the microarray technique using Human Cancer CHIP version 2 (Takara Shuzo, Kyoto, Japan), in which 425 human cancer‐related genes were spotted on glass plates (Kiguchi et al., Int J Cancer 2001;93:792–7). Microarray analysis also revealed significant induction of IL‐8, a member of the CXC chemokines. We have, therefore, extended the observation by testing the effects of doxorubicin on expression of the chemokine family and provide here definitive evidence that doxorubicin induces IL‐8 and MCP‐1, one of the CC chemokines, at least in 2 human SCLC cells, H69 and SBC‐1. IL‐8 antigen levels, measured by ELISA, were markedly increased in both H69 and SBC‐1 conditioned media after doxorubicin treatment, in parallel with mRNA levels; and this was dependent on the dose of doxorubicin. The ribonuclease protection assay, using a multiprobe template set for human chemokines, revealed induction of not only IL‐8 but also MCP‐1 in doxorubicin‐treated H69 cells. MCP‐1 antigen levels increased approximately 100‐fold in doxorubicin‐treated H69 cells. RT‐PCR using specific primers for MCP‐1 suggested that doxorubicin also induced MCP‐1 expression in SBC‐1 and SBC‐3 SCLC cells. Futhermore, CAT analysis using IL‐8 promoter implicated the PEA3 transcriptional factor, whose binding site was located immediately upstream of the AP‐1 and NF‐κB binding sites. Thus, it is suggested that doxorubicin induces IL‐8 and MCP‐1 chemokines in human SCLC cells by activating gene expression, in which at least PEA3 is involved. IL‐8 and MCP‐1 are major chemoattractants for neutrophils and monocytes/macrophages, respectively; therefore, extensive induction of IL‐8 and MCP‐1 may provoke the interaction between inflammatory/immune cells and tumor cells under doxorubicin stimulation and influence many aspects of tumor cell biology. © 2002 Wiley‐Liss, Inc.
Neural stem cells and neuro‐oncology: Quo vadis?
Authors: Recht Lawrence , Jang Taichang , Savarese Todd , Litofsky N.S. 
Published: December 2002

AbstractConventionally, gliomas are assumed to arise via transformation of an intraparenchymal glial cell that forms a mass that then expands centrifugally, eventually invading surrounding tissues. We propose an alternative model in which gliomas arise via initiation and promotion of cells within the brain's subependymal layer or subventricular zone, the source of a recently characterized pool of neural cells with the properties of self‐renewal and multipotentiality (i.e., stem cells) that persists into adulthood. In this model, the particular histological subtype of glioma would represent the effects of temporal and spatial environmental influences rather than the particular cell of origin and the disease's centrifugal point would be the subependymal layer. The implications of such a model are discussed. © 2002 Wiley‐Liss, Inc.
Transdifferentiation—fact or artifact
Authors: Liu Ying , Rao Mahendra S. 
Published: December 2002

AbstractNormal development appears to involve a progressive restriction in developmental potential. However, recent evidence suggests that this progressive restriction is not irreversible and can be altered to reveal novel phenotypic potentials of stem, progenitor, and even differentiated cells. While some of these results can be explained by the presence of contaminating cell populations, persistence of pluripotent stem cells, cell fusion, etc., several examples exist that are difficult to explain as anything other than “true transdifferentiation” and/or dedifferentiation. These examples of transdifferentiation are best explained by understanding how the normal process of progressive cell fate restriction occurs during development. We suggest that subversion of epigenetic controls regulating cell type specific gene expression likely underlies the process of transdifferentiation and it may be possible to identify specific factors to control the transdifferentiation process. We predict, however, that transdifferentiation will not be reliable or reproducible and will probably require complex manipulations. Published 2002 Wiley‐Liss, Inc.
A Model for mechanotransduction in bone cells: The load‐bearing mechanosomes
Authors: Pavalko Fred M. , Norvell Suzanne M. , Burr David B. , Turner Charles H. , Duncan Randall L. , Bidwell Joseph P. 
Published: December 2002

AbstractThe skeleton's response to mechanical force, or load, has significance to space travel, the treatment of osteoporosis, and orthodontic appliances. How bone senses and processes load remains largely unknown. The cellular basis of mechanotransduction, however, likely involves the integration of diffusion‐controlled signaling pathways with a solid‐state scaffold linking the cell membrane to the genes. Here, we integrate various concepts from models of connective membrane skeleton proteins, cellular tensegrity, and nuclear matrix architectural transcription factors, to describe how a load‐induced deformation of bone activates a change in the skeletal genetic program. We propose that mechanical information is relayed from the bone to the gene in part by a succession of deformations, changes in conformations, and translocations. The load‐induced deformation of bone is converted into the deformation of the sensor cell membrane. This, in turn, drives conformational changes in membrane proteins of which some are linked to a solid‐state signaling scaffold that releases protein complexes capable of carrying mechanical information, “mechanosomes”, into the nucleus. These mechanosomes translate this information into changes in the geometry of the 5′ regulatory region of target gene DNA altering gene activity; bending bone ultimately bends genes. We identify specific candidate proteins fitting the profile of load‐signaling mechanosomes. © 2002 Wiley‐Liss, Inc.