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  • 1
    Language: English
    In: BMJ open, 2020-10-21, Vol.10 (10), p.e038161-e038161
    Description: ObjectiveConcussions are the most frequent traumatic brain injuries. Yet, the socioeconomic impact of concussions remains unclear. Socioeconomic effects of concussions on working-age adults were studied on a population scale.DesignThis population-based, event time study uses administrative data as well as hospital and emergency room records for the population of Denmark.SettingWe study all Danish patients, aged 20–59 years, who were treated at a public hospital or at an emergency room between 2003 and 2017 after suffering a concussion without other intracranial or extracranial injuries (n=55 424 unique individuals). None of the patients had a prior diagnosis of intracranial or extracranial injuries within the past 10 years leading up to the incident.Primary and secondary outcome measuresAs primary endpoint, we investigate the mean effect of concussion on annual salaried income within a 5-year period after trauma. In an exploratory analysis, we study whether the potential impact of concussion on annual salaried income is driven by patient age, education or economic cycle.ResultsConcussion was associated with an average change in annual salary income of −€1223 (95% CI: −€1540 to −905, p〈0.001) corresponding to a salary change of −4.2% (95% CI: −5.2% to −3.1 %). People between 30 and 39 years and those without high school degrees suffered the largest salary decreases. Affected individuals leaving the workforce drove the main part of the decrease. Absolute annual effect sizes were countercyclical to the unemployment rate.ConclusionsConcussions have a large and long-lasting impact on salary and employment of working-age adults on a nationwide scale.
    Subject(s): Young Adult ; Employment ; Humans ; Middle Aged ; Adult ; Time and Motion Studies ; Brain Concussion - epidemiology ; Research Design ; Athletic Injuries ; Salaries and Fringe Benefits ; Productivity ; Labor market ; Concussion ; Bias ; Emergency medical care ; Trends ; Patients ; Age ; Index Medicus
    ISSN: 2044-6055
    E-ISSN: 2044-6055
    Source: Directory of Open Access Journals
    Source: HighWire Press (Free Journals)
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Clinical cancer research, 2008-01-01, Vol.14 (1), p.123-129
    Description: Purpose: The CD133 antigen has been identified as a putative stem cell marker in normal and malignant brain tissues. In gliomas, it is used to enrich a subpopulation of highly tumorigenic cancer cells. According to the cancer stem cell hypothesis, CD133-positive cells determine long-term tumor growth and, therefore, are suspected to influence clinical outcome. To date, a correlation between CD133 expression in primary tumor tissues and patients' prognosis has not been reported. Experimental Design: To address this question, we analyzed the expression of the CD133 stem cell antigen in a series of 95 gliomas of various grade and histology by immunohistochemistry on cryostat sections. Staining data were correlated with patient outcome. Results: By multivariate survival analysis, we found that both the proportion of CD133-positive cells and their topological organization in clusters were significant ( P 〈 0.001) prognostic factors for adverse progression-free survival and overall survival independent of tumor grade, extent of resection, or patient age. Furthermore, proportion of CD133-positive cells was an independent risk factor for tumor regrowth and time to malignant progression in WHO grade 2 and 3 tumors. Conclusions: These findings constitute the first conclusive evidence that CD133 stem cell antigen expression correlates with patient survival in gliomas, lending support to the current cancer stem cell hypothesis.
    Subject(s): stem cells ; glioma ; prognosis ; CD133 ; Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Antineoplastic agents ; Pharmacology. Drug treatments ; Immunohistochemistry ; Glioma - mortality ; Prognosis ; Peptides ; Antigens, CD - biosynthesis ; Humans ; Middle Aged ; Brain Neoplasms - pathology ; Kaplan-Meier Estimate ; Male ; Stem Cells - metabolism ; AC133 Antigen ; Brain Neoplasms - metabolism ; Glioma - metabolism ; Glycoproteins - biosynthesis ; Disease-Free Survival ; Glioma - pathology ; Survival Analysis ; Adult ; Female ; Brain Neoplasms - mortality ; Index Medicus
    ISSN: 1078-0432
    E-ISSN: 1557-3265
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: HighWire Press (Free Journals)
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Nature medicine, 2013-07, Vol.19 (7), p.901-908
    Description: Here we show that glioblastoma express high levels of branched-chain amino acid transaminase 1 (BCAT1), the enzyme that initiates the catabolism of branched-chain amino acids (BCAAs). Expression of BCAT1 was exclusive to tumors carrying wild-type isocitrate dehydrogenase 1 (IDH1) and IDH2 genes and was highly correlated with methylation patterns in the BCAT1 promoter region. BCAT1 expression was dependent on the concentration of α-ketoglutarate substrate in glioma cell lines and could be suppressed by ectopic overexpression of mutant IDH1 in immortalized human astrocytes, providing a link between IDH1 function and BCAT1 expression. Suppression of BCAT1 in glioma cell lines blocked the excretion of glutamate and led to reduced proliferation and invasiveness in vitro, as well as significant decreases in tumor growth in a glioblastoma xenograft model. These findings suggest a central role for BCAT1 in glioma pathogenesis, making BCAT1 and BCAA metabolism attractive targets for the development of targeted therapeutic approaches to treat patients with glioblastoma.
    Subject(s): Transaminases - physiology ; Cell Proliferation ; Transaminases - genetics ; Amino Acids, Branched-Chain - metabolism ; Humans ; Brain Neoplasms - pathology ; Brain Neoplasms - genetics ; Isocitrate Dehydrogenase - genetics ; Brain Neoplasms - metabolism ; Glioma - metabolism ; Isocitrate Dehydrogenase - physiology ; Glioma - genetics ; Animals ; Mice, Nude ; Models, Biological ; Glioma - pathology ; HEK293 Cells ; Transaminases - metabolism ; Cell Line, Tumor ; Female ; Mice ; Metabolism - genetics ; Cell proliferation ; Care and treatment ; Gliomas ; Physiological aspects ; Genetic aspects ; Research ; Methylation ; Amino acid metabolism ; Index Medicus
    ISSN: 1078-8956
    E-ISSN: 1546-170X
    Source: Single Journals
    Source: Academic Search Ultimate
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: International journal of molecular sciences, 2021-03-15, Vol.22 (6), p.2960
    Description: MicroRNAs (miRs) are non-coding master regulators of transcriptome that could act as tumor suppressors (TSs) or oncogenes (oncomiRs). We aimed to systematically investigate the relevance of miRs as prognostic biomarkers in primary glioblastoma multiforme (GBM) treated with postoperative radio(chemo)therapy (PORT). For hypothesis generation, tumor miR expression by Agilent 8x15K human microRNA microarrays and survival data from 482 GBM patients of The Cancer Genome Atlas (TCGA cohort) were analyzed using Cox-PH models. Expression of candidate miRs with prognostic relevance (miR-221/222; miR-17-5p, miR-18a, miR-19b) was validated by qRT-PCR using Taqman technology on an independent validation cohort of GBM patients ( = 109) treated at Heidelberg University Hospital (HD cohort). In TCGA, 50 miRs showed significant association with survival. Among the top ranked prognostic miRs were members of the two miR families miR-221/222 and miR-17-92. Loss of miR-221/222 was correlated with improved prognosis in both cohorts (TCGA, HD) and was an independent prognostic marker in a multivariate analysis considering demographic characteristics (age, sex, Karnofsky performance index (KPI)), molecular markers (O-6-methylguanine-DNA methyltransferase (MGMT) methylation, IDH mutation status) and PORT as co-variables. The prognostic value of miR-17-92 family members was ambiguous and in part contradictory by direct comparison of the two cohorts, thus warranting further validation in larger prospective trials.
    Subject(s): Index Medicus ; glioblastoma ; radiochemotherapy ; miR-221 ; miR-222 ; microRNA ; miR-17-92 ; prognosis
    ISSN: 1422-0067
    ISSN: 1661-6596
    E-ISSN: 1422-0067
    Source: Directory of Open Access Journals
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: The Journal of pathology, 2014-09, Vol.234 (1), p.23-33
    Description: Cancer cells with enhanced self‐renewal capacity influence tumour growth in glioblastoma. So far, a variety of surrogate markers have been proposed to enrich these cells, emphasizing the need to devise new characterization methods. Here, we screen a large panel of glioblastoma cultures (n = 21) cultivated under stem cell‐permissive conditions and identify several cell lines with enhanced self‐renewal capacity. These cell lines are capable of matrix‐independent growth and form fast‐growing, orthotopic tumours in mice. Employing isolation, re‐plating, and label‐retention techniques, we show that self‐renewal potential of individual cells is partitioned asymmetrically between daughter cells in a robust and cell line‐specific fashion. This yields populations of fast‐ and slow‐cycling cells, which differ in the expression of cell cycle‐associated transcripts. Intriguingly, fast‐growing cells keep their slow‐cycling counterparts in a reversible state of quiescence associated with high chemoresistance. Our results suggest that two different subpopulations of tumour cells contribute to aberrant growth and tumour recurrence after therapy in glioblastoma. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): self‐renewal; glioblastoma; label retention; quiescence ; Gene Dosage - genetics ; Cell Proliferation ; Oligonucleotide Array Sequence Analysis ; Humans ; Brain Neoplasms - pathology ; Gene Expression Profiling ; Brain Neoplasms - metabolism ; Neoplasm Recurrence, Local - pathology ; Animals ; Comparative Genomic Hybridization ; Neoplastic Stem Cells - metabolism ; Glioblastoma - pathology ; Cell Line, Tumor ; Neoplastic Stem Cells - pathology ; Glioblastoma - metabolism ; Mice ; Disease Models, Animal ; Glioblastoma multiforme ; Analysis ; Stem cells ; Index Medicus
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: British journal of neurosurgery, 2016-07-03, Vol.30 (4), p.397-400
    Description: Background: Intraoperative magnetic resonance imaging (io-MRI) improves the extent of glioma resection. Due to the magnetic field, patients have to be covered with sterile drape and are then transferred into an io-MRI chamber, where ferromagnetic anaesthesia monitors and machines must be kept at distance and can only be applied with limitations. Despite the development of specific paramagnetic equipment for io-MRI use, this method is suspected to carry a higher risk for anaesthesiological and surgical complications. Particularly, serial draping and un-draping cycles as well as the extended surgery duration might increase the risk of perioperative infection. Objective: Given the importance of io-MRI for glioma surgery, the question regarding io-MRI safety needs to be answered. Methods: We prospectively evaluate the perioperative anaesthesiological and surgical complications for 516 cases of brain tumour surgery involving io-MRI (MRI cohort). As a control group, we evaluate a cohort of 610 cases of brain tumour surgery, performed without io-MRI (control group). Results: The io-MRI procedure (including draping/undraping, transfer to and from the MRI cabinet and io-MRI scan) significantly extended surgery, defined as "skin to skin" time, by 57 min (SD = 16 min) (p ≤ 0.01). Still, we show low and comparable rates of surgical complications in the MRI cohort and the control group. Postoperative haemorrhage (3.7% versus 3.0% in MRI cohort versus control group; p = 0.49) and infections (2.2% versus 1.8% in MRI cohort versus control group; p = 0.69) were not significantly different between both groups. No anaesthesiological disturbances were reported. Conclusion: Despite prolonged surgery and serial draping and un-draping cycles, io-MRI was not linked to higher rates of infections and postoperative haemorrhage in this study.
    Subject(s): glioma ; Complications ; intraoperative MRI ; surgery ; Neuronavigation - methods ; Prospective Studies ; Brain Neoplasms - diagnostic imaging ; Humans ; Middle Aged ; Magnetic Resonance Imaging - methods ; Male ; Treatment Outcome ; Brain Neoplasms - surgery ; Glioma - diagnostic imaging ; Intraoperative Complications - etiology ; Aged, 80 and over ; Monitoring, Intraoperative - methods ; Adult ; Female ; Aged ; Neurosurgical Procedures - methods ; Glioma - surgery ; Anesthesia ; Infections ; Nuclear magnetic resonance--NMR ; Neurosurgery ; Risk assessment ; Index Medicus
    ISSN: 0268-8697
    E-ISSN: 1360-046X
    Source: Academic Search Ultimate
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: Trials, 2021-01-25, Vol.22 (1), p.87-87
    Description: Spinal cord stimulation (SCS) is an effective method to treat neuropathic pain; however, it is challenging to compare different stimulation modalities in an individual patient, and thus, it is largely unknown which of the many available SCS modalities is most effective. Specifically, electrodes leading out through the skin would have to be consecutively connected to different, incompatible SCS devices and be tested over a time period of several weeks or even months. The risk of wound infections for such a study would be unacceptably high and blinding of the trial difficult. The PARS-trial seizes the capacity of a new type of wireless SCS device, which enables a blinded and systematic intra-patient comparison of different SCS modalities over extended time periods and without increasing wound infection rates. The PARS-trial is designed as a double-blinded, randomized, and placebo-controlled multi-center crossover study. It will compare the clinical effectiveness of the three most relevant SCS paradigms in individual patients. The trial will recruit 60 patients suffering from intractable neuropathic pain of the lower extremities, who have been considered for SCS therapy and were already implanted with a wireless SCS device prior to study participation. Over a time period of 35 days, patients will be treated consecutively with three different SCS paradigms ("burst," "1 kHz," and "1.499 kHz") and placebo stimulation. Each SCS paradigm will be applied for 5 days with a washout period of 70 h between stimulation cycles. The primary endpoint of the study is the level of pain self-assessment on the visual analogue scale after 5 days of SCS. Secondary, exploratory endpoints include self-assessment of pain quality (as determined by painDETECT questionnaire), quality of life (as determined by Quality of Life EQ-5D-5L questionnaire), anxiety perception (as determined by the Hospital Anxiety and Depression Scale), and physical restriction (as determined by the Oswestry Disability Index). Combining paresthesia-free SCS modalities with wireless SCS offers a unique opportunity for a blinded and systematic comparison of different SCS modalities in individual patients. This trial will advance our understanding of the clinical effectiveness of the most relevant SCS paradigms. German Clinical Trials Register, DRKS00018929 . Registered on 14 January 2020.
    Subject(s): Chronic Pain - therapy ; Chronic Pain - diagnosis ; Double-Blind Method ; Humans ; Male ; Treatment Outcome ; Spinal Cord Stimulation - instrumentation ; Spinal Cord Stimulation - adverse effects ; Randomized Controlled Trials as Topic ; Wireless Technology - instrumentation ; Cross-Over Studies ; Implantable Neurostimulators - adverse effects ; Multicenter Studies as Topic ; Spinal Cord Stimulation - methods ; Quality of Life ; Adult ; Diagnostic Self Evaluation ; Female ; Neuralgia - diagnosis ; Neuralgia - therapy ; Pain Measurement ; Infection ; Medical research ; Care and treatment ; Pain ; Analysis ; Clinical trials ; Medicine, Experimental ; Health aspects ; Index Medicus ; Study Protocol ; Randomized controlled trial ; Spinal cord stimulation ; Wireless stimulation ; Neuropathic pain
    ISSN: 1745-6215
    E-ISSN: 1745-6215
    Source: Directory of Open Access Journals
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: Cancer Immunology, Immunotherapy, 2014-12, Vol.63 (12), p.1235-1249
    Description: The mechanisms of immune response to cancer have been studied extensively and great effort has been invested into harnessing the therapeutic potential of the immune system. Immunotherapies have seen significant advances in the past 20 years, but the full potential of protective and therapeutic cancer immunotherapies has yet to be fulfilled. The insufficient efficacy of existing treatments can be attributed to a number of biological and technical issues. In this review, we detail the current limitations of immunotherapy target selection and design, and review computational methods to streamline therapy target discovery in a bioinformatics analysis pipeline. We describe specialized bioinformatics tools and databases for three main bottlenecks in immunotherapy target discovery: the cataloging of potentially antigenic proteins, the identification of potential HLA binders, and the selection epitopes and co-targets for single-epitope and multi-epitope strategies. We provide examples of application to the well-known tumor antigen HER2 and suggest bioinformatics methods to ameliorate therapy resistance and ensure efficient and lasting control of tumors.
    Subject(s): Cancer vaccines ; Immunology ; Medicine & Public Health ; T cell epitopes ; Tumor antigens ; Oncology ; Cancer Research ; Biological databases ; Computational biology ; Computational Biology - methods ; Immunotherapy - methods ; Neoplasms - therapy ; Neoplasms - immunology ; Drug Discovery ; Humans ; Proteins ; Care and treatment ; Analysis ; Immunotherapy ; Drug therapy ; T cells ; Cancer ; Antigenic determinants ; Index Medicus
    ISSN: 0340-7004
    E-ISSN: 1432-0851
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Glia, 2015-10, Vol.63 (10), p.1850-1859
    Description: Objectives Measuring concentrations of the differentiation‐promoting hormone retinoic acid (RA) in glioblastoma tissues would help to understand the reason why RA treatment has been inefficient in clinical trials involving brain tumor patients. Here, we apply a recently established extraction and measurement protocol to screen glioblastoma tissues for the levels of the RA precursor retinol and biologically active RA. Combining this approach with mRNA analyses of 26 tumors and 8 normal brains, we identify a multifaceted disturbance of RA synthesis in glioblastoma, involving multiple aldehyde dehydrogenase 1 family and retinol dehydrogenase enzymes. Through database studies and methylation analyses, we narrow down chromosomal deletions and aberrant promoter hypermethylation as potential mechanisms accounting for these alterations. Employing chromatin immunoprecipitation analyses and cell‐culture studies, we further show that chromatin at RA target genes is poised to RA substitution, but most glioblastoma cell cultures are completely resistant to RA treatment. This paradoxical RA response is unrelated to alternative RA signaling through the fatty acid‐binding protein 5/peroxisome proliferator‐activated receptor delta axis. Our data suggest a multifaceted disturbance of RA synthesis in glioblastoma and contribute to reconsider current RA treatment strategies. GLIA 2015;63:1850–1859 Main Points Retinoic acid synthesis is impaired in glioblastoma. Most glioblastoma cultures are resistant to retinoic acid. Current retinoic acid treatment strategies in glioblastoma need to account for retinoid resistance in tumor cells.
    Subject(s): glioma ; retinoic acid ; differentiation ; Humans ; Retinal Dehydrogenase - metabolism ; Enzyme Inhibitors - pharmacology ; Receptors, Retinoic Acid - metabolism ; Retinol O-Fatty-Acyltransferase - metabolism ; Brain Neoplasms - complications ; Receptors, Retinoic Acid - genetics ; Brain - drug effects ; Brain - metabolism ; DNA Methylation ; Databases, Bibliographic - statistics & numerical data ; Chromatin Immunoprecipitation ; Signal Transduction - drug effects ; Tretinoin - metabolism ; Isoenzymes - metabolism ; Glioblastoma - complications ; Cell Proliferation - drug effects ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - physiology ; Retinoids - pharmacology ; Enzymes ; RNA ; Analysis ; Methylation ; Aldehydes ; Fatty acids ; Glioblastoma multiforme ; Protein binding ; Tretinoin ; Index Medicus
    ISSN: 0894-1491
    E-ISSN: 1098-1136
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: International journal of cancer, 2012-10-15, Vol.131 (8), p.1963-1968
    Description: Impairment of endogenous differentiation pathways like retinoic acid (RA) signaling seems to be a central pathogenetic event in astrocytic gliomas. Among others, expression of the differentiation‐promoting RA chaperon protein cellular retinoic acid binding protein 2 (CRABP2) is extenuated in high‐grade gliomas. Against this background, we aimed at identifying potential pathomechanisms underlying reduced CRABP2 expression in these tumors. Using MassARRAY methylation analysis, we detected extensive CpG methylation upstream of the CRABP2 gene locus in a study sample comprising 100 astrocytic gliomas of WHO Grade II to IV. Compared to nontumorous control samples, tumors revealed increased CpG methylation and methylation levels were inversely correlated to CRABP2 mRNA expression. Substantiating our in situ findings, CRABP2 mRNA levels increased in glioma cell lines after exposure to the demethylating agent 5‐aza‐2′‐deoxycytidine. Finally, a distinct CpG methylation signature distinguished between primary glioblastoma on the one hand and the group of astrocytoma WHO II–III and secondary glioblastoma on the other hand. Altogether, our observations suggest that epigenetic silencing of CRABP2 might contribute to an immature phenotype in glioma cells.
    Subject(s): glioma ; retinoic acid ; differentiation ; CRABP2 ; methylation ; Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Tumors ; Astrocytoma - genetics ; Signal Transduction ; Epigenesis, Genetic ; Humans ; Gene Expression Regulation, Neoplastic ; Brain Neoplasms - genetics ; Isocitrate Dehydrogenase - genetics ; Case-Control Studies ; Receptors, Retinoic Acid - genetics ; Brain - metabolism ; DNA Methylation ; Neoplasm Grading ; CpG Islands ; Cell Differentiation ; Messenger RNA ; Gliomas ; Analysis ; Oncology, Experimental ; Genes ; Universities and colleges ; Research ; Methylation ; Health aspects ; Protein binding ; Cancer ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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