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Search Results: 1 - 10 of 8839 matches for " ?ke Borg "
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Sprouting Wings in the Hyper-Colonial: High-Octane Desire and Youth-Targeted Market Predation  [PDF]
Mark B. Borg
Psychology (PSYCH) , 2010, DOI: 10.4236/psych.2010.14040
Abstract: In this article, the author utilizes a novel action research approach to developing an interpretation of a colonial discourse that reproduces an otherness that is consistent with traditional views of history and ideology. Through this unique educational—for both author and client—approach, further analysis reveals a colonial discourse that has become unhinged from its historical roots and taken flight into supermolecular space where its origins and impact have been thoroughly dissociated from its cultural impact. When our identities are thoroughly absorbed into and taken over by consumer products, we enter a corporately induced, mass-media augmented hyper-colonial in which our minds, bodies, and senses of self become defined by those products. A primary research question is: how can we intervene in colonialism when the colonized is an inferior/lacking version of our own self ? The ways in which this hyper-colonial state captures and makes use of desire and is then marked—marketed—by/through a society-level drive is explored throughout this article. The author “takes a walk”—that is, he uses a week-long organizational consultation that was conducted for a marketing research organization to analyze the ways that the dynamics of a hyper-colonialized consumer culture were at play in the consultee’s marketing strategies that target American youth.
Disability, Social Policy and the Burden of Disease: Creating an “Assertive” Community Mental Health System in New York  [PDF]
Mark B. Borg, Jr.
Psychology (PSYCH) , 2010, DOI: 10.4236/psych.2010.12018
Abstract: One conclusion of the decade-long epidemiological Global Burden of Disease Project is that five of the top 10 disease “burdens” the world will face by 2020 will be related to mental disabilities. Therefore, developing social policy and community responses to the ways that people with mental disabilities are treated is becoming an important focus for community practitioners, political activists and legislators. The author explores some of the dynamics of our culture’s approach to dealing with difference, especially when manifested in disenfranchized individuals. He discusses a community development project created by a New York City advocacy and social policy organization following the 1999 murder of a woman by an individual whose mental health disability was never treated. Parallels are drawn between the civil rights and community mental health movements, which created a precedent for the 1990 Americans with Disabilities Act. Also examined are the ways in which community mental health systems manifest social policy that alternately resists, repeats and colludes with power operations. The unexamined assumptions that drive this dynamic are examined as ableism or disability oppression.
Case report: Effect of immunoglobulin on pain in Post-Polio Syndrome—Three case reports  [PDF]
Lars Werhagen, Kristian Borg
Pain Studies and Treatment (PST) , 2013, DOI: 10.4236/pst.2013.11001
Abstract: Study design: Case reports. Setting: University hospital setting. Objective: To analyze the effect of intravenous immunoglobulin on neuropathic and nociceptive pain in three patients with Post-Polio Syndrome (PPS). Materials and Methods: Three patients with PPS and pain who received treatment with 90 g IvIg are described. Results: Before treatment one of the patients had pure neuropathic pain and the other two had a combination of neuropathic and nociceptive pain. There was no effect on pain in the patient with pure neuropathic pain and only effect on the nociceptive pain in the patients with a combination of neuropathic and nociceptive pain. Discussion: Pain is one of the most common symptoms in PPS. Previous studies have shown an effect on pain in PPS patients receiving IvIg. The results of the present study point to that the effect on pain is limited to nociceptive pain and that there is no effect on neuropathic pain which leads to increased knowledge of characterization of responders of IvIg treatment. Conclusion: IvIg treatment treatmentreduces nociceptive but not neuropathic pain in PPS patients.
Genetic Profiling Differentiates Second Primary Tumors from Metastases in Adult Metachronous Soft Tissue Sarcoma
Josefin Fernebro,Ana Carneiro,Anders Rydholm,Henryk A. Domanski,Anna Karlsson, ke Borg,Mef Nilbert
Sarcoma , 2008, DOI: 10.1155/2008/431019
Abstract: Purpose. Patients with soft tissue sarcomas (STS) are at increased risk of second primary malignancies, including a second STS, but distinction between metastases and a second primary STS is difficult. Patients and Methods. Array-based comparative genomic hybridization (aCGH) was applied to 30 multiple STS of the extremities and the trunk wall from 13 patients. Different histotypes were present with malignant fibrous histiocytomas/undifferentiated pleomorphic sarcomas being the predominant subtype. Results. aCGH profiling revealed genetic complexity with multiple gains and losses in all tumors. In an unsupervised hierarchical cluster analysis, similar genomic profiles and close clustering between the first and subsequent STS were identified in 5 cases, suggesting metastatic disease, whereas the tumors from the remaining 8 patients did not cluster and showed only weak pairwise correlation, suggesting development of second primary STS. Discussion. The similarities and dissimilarities identified in the first and second STS suggest that genetic profiles can be used to distinguish soft tissue metastases from second primary STS. The demonstration of genetically different soft tissue sarcomas in the same patient suggests independent tumor origin and serves as a reminder to consider development of second primary STS, which has prognostic and therapeutic implications.
GOBO: Gene Expression-Based Outcome for Breast Cancer Online
Markus Ringnér,Erik Fredlund,Jari H?kkinen,ke Borg,Johan Staaf
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0017911
Abstract: Microarray-based gene expression analysis holds promise of improving prognostication and treatment decisions for breast cancer patients. However, the heterogeneity of breast cancer emphasizes the need for validation of prognostic gene signatures in larger sample sets stratified into relevant subgroups. Here, we describe a multifunctional user-friendly online tool, GOBO (http://co.bmc.lu.se/gobo), allowing a range of different analyses to be performed in an 1881-sample breast tumor data set, and a 51-sample breast cancer cell line set, both generated on Affymetrix U133A microarrays. GOBO supports a wide range of applications including: 1) rapid assessment of gene expression levels in subgroups of breast tumors and cell lines, 2) identification of co-expressed genes for creation of potential metagenes, 3) association with outcome for gene expression levels of single genes, sets of genes, or gene signatures in multiple subgroups of the 1881-sample breast cancer data set. The design and implementation of GOBO facilitate easy incorporation of additional query functions and applications, as well as additional data sets irrespective of tumor type and array platform.
BioArray Software Environment (BASE): a platform for comprehensive management and analysis of microarray data
Lao H Saal, Carl Troein, Johan Vallon-Christersson, Sofia Gruvberger,ke Borg, Carsten Peterson
Genome Biology , 2002, DOI: 10.1186/gb-2002-3-8-software0003
Abstract: Microarrays are emerging as one of the most exciting and promising technologies for biological research and clinical practice [1]. The technology has been utilized in various applications such as the profiling of mRNA [2] and protein levels [3], elucidating protein-DNA interactions [4], assessment of DNA copy number [5], and detection of methylated sequences [6], and today is accessible to even relatively small laboratories. Typically, arrays contain 5,000 to 45,000 reporters, each of which has dozens of biological (for example, gene name, sequence, function) and quality control (QC; for example, sequence verification, purity, number of gel bands) annotations. Each array can be used to analyze up to two biomaterials, each of which can have any number of biological annotations (for example, in vitro treatments, clinical follow-up, mutation status), and in a single hybridization, data spanning tens of megabytes are generated. Whereas microarrays have shed light on many biological processes and disease states, for us [7,8,9,10] and others, a significant bottleneck remains the analysis of hybridization data in the context of biomaterial and reporter annotations. There are a number of separate software systems that individually address some of the needs, such as databases and applications for clustering and visualization of microarray data [11,12,13,14,15,16,17,18], public databases that contain reporter information [19,20,21], commercial laboratory information management systems (LIMS), and various storage methods (such as lab notebooks, clinical charts and public and private databases) for recording biomaterial annotations. However, to our knowledge there are no unified systems capable of organizing all the information surrounding microarray experimentation and which also integrate this information with tools for the analysis of quantified microarray hybridization data.To address these needs, we developed a system called BioArray Software Environment (BASE) that provid
Landscape of somatic allelic imbalances and copy number alterations in HER2-amplified breast cancer
Johan Staaf, G?ran J?nsson, Markus Ringnér, Bo Baldetorp,ke Borg
Breast Cancer Research , 2011, DOI: 10.1186/bcr3075
Abstract: High-density whole genome array-based comparative genomic hybridization (aCGH) and single nucleotide polymorphism (SNP) array data from 260 HER2-amplified breast tumors or cell lines, and 346 HER2-negative breast cancers with molecular subtype information were assembled from different repositories. Copy number alteration (CNA), loss-of-heterozygosity (LOH), copy number neutral allelic imbalance (CNN-AI), subclonal CNA and patterns of tumor DNA ploidy were analyzed using bioinformatical methods such as genomic identification of significant targets in cancer (GISTIC) and genome alteration print (GAP). The patterns of tumor ploidy were confirmed in 338 unrelated breast cancers analyzed by DNA flow cytometry with concurrent BAC aCGH and gene expression data.A core set of 36 genomic regions commonly affected by copy number gain or loss was identified by integrating results with a previous study, together comprising > 400 HER2-amplified tumors. While CNN-AI frequency appeared evenly distributed over chromosomes in HER2-amplified tumors, not targeting specific regions and often < 20% in frequency, the occurrence of LOH was strongly associated with regions of copy number loss. HER2-amplified and HER2-negative tumors stratified by molecular subtypes displayed different patterns of LOH and CNN-AI, with basal-like tumors showing highest frequencies followed by HER2-amplified and luminal B cases. Tumor aneuploidy was strongly associated with increasing levels of LOH, CNN-AI, CNAs and occurrence of subclonal copy number events, irrespective of subtype. Finally, SNP data from individual tumors indicated that genomic amplification in general appears as monoallelic, that is, it preferentially targets one parental chromosome in HER2-amplified tumors.We have delineated the genomic landscape of CNAs, amplifications, LOH, and CNN-AI in HER2-amplified breast cancer, but also demonstrated a strong association between different types of genomic aberrations and tumor aneuploidy irrespectiv
The gene expression landscape of breast cancer is shaped by tumor protein p53 status and epithelial-mesenchymal transition
Erik Fredlund, Johan Staaf, Juha K Rantala, Olli Kallioniemi,ke Borg, Markus Ringnér
Breast Cancer Research , 2012, DOI: 10.1186/bcr3236
Abstract: Modules of highly connected genes were extracted from a gene co-expression network that was constructed based on Pearson correlation, and module activities were then calculated using a pathway activity score. Functional annotations of modules were experimentally validated with an siRNA cell spot microarray system using the KPL-4 breast cancer cell line, and by using gene expression data from functional studies. Modules were derived using gene expression data representing 1,608 breast cancer samples and validated in data sets representing 971 independent breast cancer samples as well as 1,231 samples from other cancer forms.The initial co-expression network analysis resulted in the characterization of eight tightly regulated gene modules. Cell cycle genes were divided into two transcriptional programs, and experimental validation using an siRNA screen showed different functional roles for these programs during proliferation. The division of the two programs was found to act as a marker for tumor protein p53 (TP53) gene status in luminal breast cancer, with the two programs being separated only in luminal tumors with functional p53 (encoded by TP53). Moreover, a module containing fibroblast and stroma-related genes was highly expressed in fibroblasts, but was also up-regulated by overexpression of epithelial-mesenchymal transition factors such as transforming growth factor beta 1 (TGF-beta1) and Snail in immortalized human mammary epithelial cells. Strikingly, the stroma transcriptional program related to less malignant tumors for luminal disease and aggressive lymph node positive disease among basal-like tumors.We have derived a robust gene expression landscape of breast cancer that reflects known subtypes as well as heterogeneity within these subtypes. By applying the modules to TP53-mutated samples we shed light on the biological consequences of non-functional p53 in otherwise low-proliferating luminal breast cancer. Furthermore, as in the case of the stroma module
Cancer incidence in relatives of a population-based set of cases of early-onset breast cancer with a known BRCA1 and BRCA2 mutation status
Niklas Loman, Anna Bladstr?m, Oskar Johannsson,ke Borg, H?kan Olsson
Breast Cancer Research , 2003, DOI: 10.1186/bcr632
Abstract: Standardized incidence ratios (SIRs) and cumulative cancer incidences were calculated for relatives of a population-based set of early-onset breast cancer index cases (younger than age 41 years) with a defined BRCA mutation status (n = 203).In first-degree relatives (FDRs) of mutation-negative cases, breast cancer incidences (SIR = 2.3), prostate cancer incidences (SIR = 1.7), cervix cancer incidences (SIR = 3.3) and nonmelanoma skin cancer incidences (SIR = 2.8) were increased. The risks of breast cancer, prostate cancer and nonmelanoma skin cancer were further increased in FDRs of breast cancer cases younger than 36 years of age. In high-risk individuals with at least one relative with breast cancer apart from the index case, but no BRCA mutation in the family, breast cancer incidence was increased (SIR = 5.3); again the prostate cancer incidence was elevated (SIR = 2.5). The cumulative incidence of breast cancer at ages 50 and 70 years for FDRs of index cases without a BRCA mutation was 3.6% and 12.8%, respectively. Similarly, the cumulative incidence of breast cancer for high-risk women was 6.3% and 21.1% at ages 50 and 70 years, and that for FDRs of BRCA mutation carriers was 17.2% and 27.7% at the same ages.The incidence of breast cancer is increased for FDRs of women with early-onset breast cancer irrespective of the BRCA status in the family. Risk increases with decreasing age and with increasing number of affected relatives. The incidences of prostate cancer, cervix cancer and nonmelanoma skin cancer are elevated for FDRs of early-onset breast cancer cases without a BRCA mutation, indicating a possible association between these cancers and early-onset breast cancer.The influence of hereditary factors over breast cancer risk in women is well established. In a review and meta-analysis of previously published case–control and cohort studies, Pharoah and colleagues concluded in 1997 that a woman with a relative with breast cancer has an approximately doubled br
Gene products of chromosome 11q and their association with CCND1 gene amplification and tamoxifen resistance in premenopausal breast cancer
Katja Lundgren, Karolina Holm, Bo Nordenskj?ld,ke Borg, G?ran Landberg
Breast Cancer Research , 2008, DOI: 10.1186/bcr2150
Abstract: Array comparative genomic hybridization analysis was employed to identify and confirm changes in the gene expression of a number of different genes mapping to the 11q chromosomal region, associated with CCND1 amplification. The subsequent protein expression of these candidate genes was then examined in a clinical material of 500 primary breast cancers from premenopausal patients who were randomly assigned to either tamoxifen or no adjuvant treatment. The protein expression was also compared with gene expression data in a subset of 56 breast cancer samples.Cortactin and FADD (Fas-associated death domain) over-expression was linked to CCND1 amplification, determined by fluorescence in situ hybridization, but was not associated with a diminished effect of tamoxifen. However, deletion of distal chromosome 11q, defined as downregulation of the marker Chk1 (checkpoint kinase 1), was associated with an impaired tamoxifen response, and interestingly with low proliferative breast cancer of low grade. For Pak1 (p21-activated kinase 1) and cyclin D1 the protein expression corresponded to the gene expression data.The results indicate that many 11q13 associated gene products are over-expressed in conjunction with cyclin D1 but not linked to an agonistic effect of tamoxifen. Finally, the deletion of distal 11q, linked to 11q13 amplification, might be an important event affecting breast cancer outcome and tamoxifen response.Gene amplification is a well defined cause of oncogene activation during tumor development, and some genomic regions are recognized to be more frequently amplified than others [1].Amplification of chromosome locus 11q13 occurs at high frequencies in certain human cancers, including lung, bladder, breast and ovarian carcinomas, as well as in head and neck squamous cell carcinomas (HNSCCs) [2-6]. Approximately 15% of primary breast cancers are affected by this specific amplification, which is associated with poor prognosis [7-10]. Four distinct core regions or am
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