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  • 1
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    Online Resource
    Common non-synonymous SNPs associated with breast cancer susceptibility: findings from the Breast Cancer Association Consortium
    Oxford University Press (OUP) ; 2014
    In:  Human Molecular Genetics Vol. 23, No. 22 ( 2014-11-15), p. 6096-6111
    Details
    In: Human Molecular Genetics, Oxford University Press (OUP), Vol. 23, No. 22 ( 2014-11-15), p. 6096-6111
    Type of Medium: Online Resource
    ISSN: 0964-6906 , 1460-2083
    URL: Article
    DOI: 10.1093/hmg/ddu311
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 1474816-2
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  • 2
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    Roles of Trans and Cis Variation in Yeast Intraspecies Evolution of Gene Expression
    Oxford University Press (OUP) ; 2009
    In:  Molecular Biology and Evolution Vol. 26, No. 11 ( 2009-11), p. 2533-2538
    Details
    In: Molecular Biology and Evolution, Oxford University Press (OUP), Vol. 26, No. 11 ( 2009-11), p. 2533-2538
    Type of Medium: Online Resource
    ISSN: 1537-1719 , 0737-4038
    URL: Article
    DOI: 10.1093/molbev/msp171
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2009
    detail.hit.zdb_id: 2024221-9
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  • 3
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    Women can bear a bigger burden: ante- and post-mortem evidence for reserve in the face of tau
    Oxford University Press (OUP) ; 2020
    In:  Brain Communications Vol. 2, No. 1 ( 2020-01-01)
    Details
    In: Brain Communications, Oxford University Press (OUP), Vol. 2, No. 1 ( 2020-01-01)
    Abstract: In this study, we aimed to assess whether women are able to withstand more tau before exhibiting verbal memory impairment. Using data from 121 amyloid-β-positive Alzheimer’s Disease Neuroimaging Initiative participants, we fit a linear model with Rey Auditory Verbal Learning Test score as the response variable and tau-PET standard uptake value ratio as the predictor and took the residuals as an estimate of verbal memory reserve for each subject. Women demonstrated higher reserve (i.e. residuals), whether the Learning (t = 2.78, P = 0.006) or Delay (t = 2.14, P = 0.03) score from the Rey Auditory Verbal Learning Test was used as a measure of verbal memory ability. To validate these findings, we examined 662 National Alzheimer’s Coordinating Center participants with a C2/C3 score (Consortium to Establish a Registry for Alzheimer’s Disease) at autopsy. We stratified our National Alzheimer’s Coordinating Center sample into Braak 1/2, Braak 3/4 and Braak 5/6 subgroups. Within each subgroup, we compared Logical Memory scores between men and women. Men had worse verbal memory scores within the Braak 1/2 (Logical Memory Immediate: β = −5.960 ± 1.517, P  & lt; 0.001, Logical Memory Delay: β = −5.703 ± 1.677, P = 0.002) and Braak 3/4 (Logical Memory Immediate: β = −2.900 ± 0.938, P = 0.002, Logical Memory Delay: β = −2.672 ± 0.955, P = 0.006) subgroups. There were no sex differences in Logical Memory performance within the Braak 5/6 subgroup (Logical Memory Immediate: β = −0.314 ± 0.328, P = 0.34, Logical Memory Delay: β = −0.195 ± 0.287, P = 0.50). Taken together, our results point to a sex-related verbal memory reserve.
    Type of Medium: Online Resource
    ISSN: 2632-1297
    URL: Article
    DOI: 10.1093/braincomms/fcaa025
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 3020013-1
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  • 4
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    A University Medical Technology Recruitment Program
    Oxford University Press (OUP) ; 1984
    In:  Laboratory Medicine Vol. 15, No. 1 ( 1984-01-01), p. 61-63
    Details
    In: Laboratory Medicine, Oxford University Press (OUP), Vol. 15, No. 1 ( 1984-01-01), p. 61-63
    Type of Medium: Online Resource
    ISSN: 0007-5027 , 1943-7730
    URL: Article
    DOI: 10.1093/labmed/15.1.61
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1984
    detail.hit.zdb_id: 2100869-3
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  • 5
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    Technical feasibility of leadless left bundle branch area pacing for cardiac resynchronization: a case series
    Oxford University Press (OUP) ; 2021
    In:  European Heart Journal - Case Reports Vol. 5, No. 11 ( 2021-11-01)
    Details
    In: European Heart Journal - Case Reports, Oxford University Press (OUP), Vol. 5, No. 11 ( 2021-11-01)
    Abstract: Left bundle branch area pacing (LBBAP) is a novel form of conduction system pacing which can reverse left bundle branch block and deliver cardiac resynchronization therapy (CRT). The WiSE-CRT system delivers leadless endocardial pacing with symptomatic and left ventricular (LV) remodelling improvements following intervention. We report the technical feasibility of delivering leadless LBBAP using the WiSE-CRT system. Case summary In Case 1, a 57-year-old male with ischaemic cardiomyopathy and complete heart block underwent implantation of the WiSE-CRT system, using a retrograde transaortic approach, after failed conventional CRT. Temporary left bundle stimulation from the LV septum achieved superior electrical resynchronization and equivalent haemodynamic response compared to endocardial pacing at the lateral LV wall. In Case 2, an 82-year-old gentleman with tachyarrhythmia-induced cardiomyopathy underwent WiSE-CRT implantation via a trans-septal inter-atrial approach, with the endocardial electrode successfully deployed in the LV septum. Discussion Here we report the first case of deployment of the WiSE-CRT endocardial electrode in the LV septum and demonstrate the technical feasibility of leadless LBBAP. Entirely leadless CRT is an attractive option for patients with venous access issues or recurrent lead complications and has previously been successful using the WiSE-CRT system and a leadless pacemaker in the right ventricle. Further studies are required to assess long-term efficacy and safety of leadless LBBAP.
    Type of Medium: Online Resource
    ISSN: 2514-2119
    URL: Article
    DOI: 10.1093/ehjcr/ytab379
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2948381-5
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  • 6
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    The Revised APTA Code of Ethics for the Physical Therapist and Standards of Ethical Conduct for the Physical Therapist Assistant: Theory, Purpose, Process, and Significance
    Oxford University Press (OUP) ; 2010
    In:  Physical Therapy Vol. 90, No. 5 ( 2010-05-01), p. 803-824
    Details
    In: Physical Therapy, Oxford University Press (OUP), Vol. 90, No. 5 ( 2010-05-01), p. 803-824
    Abstract: In June 2009, the House of Delegates (HOD) of the American Physical Therapy Association (APTA) passed a major revision of the APTA Code of Ethics for physical therapists and the Standards of Ethical Conduct for the Physical Therapist Assistant. The revised documents will be effective July 1, 2010. Purpose The purposes of this article are: (1) to provide a historical, professional, and theoretical context for this important revision; (2) to describe the 4-year revision process; (3) to examine major features of the documents; and (4) to discuss the significance of the revisions from the perspective of the maturation of physical therapy as a doctoring profession. Process of Revision The process for revision is delineated within the context of history and the Bylaws of APTA. Format, Structure, and Content of Revised Core Ethics Documents The revised documents represent a significant change in format, level of detail, and scope of application. Previous APTA Codes of Ethics and Standards of Ethical Conduct for the Physical Therapist Assistant have delineated very broad general principles, with specific obligations spelled out in the Ethics and Judicial Committee's Guide for Professional Conduct and Guide for Conduct of the Physical Therapist Assistant. In contrast to the current documents, the revised documents address all 5 roles of the physical therapist, delineate ethical obligations in organizational and business contexts, and align with the tenets of Vision 2020. Significance The significance of this revision is discussed within historical parameters, the implications for physical therapists and physical therapist assistants, the maturation of the profession, societal accountability and moral community, potential regulatory implications, and the inclusive and deliberative process of moral dialogue by which changes were developed, revised, and approved.
    Type of Medium: Online Resource
    ISSN: 0031-9023 , 1538-6724
    URL: Article
    DOI: 10.2522/ptj.20090373
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2010
    detail.hit.zdb_id: 2008745-7
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  • 7
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    STEM-01. GLIOMA STEM CELLS ACTIVATE PLATELETS BY PLASMA-INDEPENDENT THROMBIN PRODUCTION TO PROMOTE GBM TUMORIGENESIS
    Oxford University Press (OUP) ; 2022
    In:  Neuro-Oncology Vol. 24, No. Supplement_7 ( 2022-11-14), p. vii30-vii31
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 24, No. Supplement_7 ( 2022-11-14), p. vii30-vii31
    Abstract: The interaction between platelets and cancer cells has been underexplored in solid tumor models that do not metastasize, for example glioblastoma (GBM) for which metastasis is rare. Histologically, it is known that glioma stem cells (GSCs) are found in perivascular and pseudsopalisading regions of GBM, which are also areas of platelet localization. High platelet counts have been associated with poor clinical outcome in many cancers. While platelets are known to promote progression of other tumors, mechanisms by which platelets influence GBM oncogenesis are unknown. Here, we aimed to understand how the bidirectional interaction between platelets and GSCs drives GBM oncogenesis. Male and female NSG mice were transplanted with patient derived GSC lines and treated with antiplatelet and anti-thrombin inhibitors. Immunofluorescence, qPCR, and Western blots were used to determine expression of coagulation mechanism in GBM tissue and subsequent GSC lines. We demonstrate that GSCs co-opt and activate platelets to promote GBM tumor progression. GSCs endogenously produce all coagulation factors of the intrinsic and extrinsic cascade generating thrombin and activating platelets in the absence of plasma. Conversely, inhibition of platelet activation and of thrombin production by GSCs abrogates platelet-mediated GSC self-renewal and growth (p & lt; 0.0005). Similarly, inhibiting intratumoral thrombin production and function decreases tumor formation in vivo (p & lt; 0.005). These studies challenge and revise the longstanding view that the complete coagulation cascades are found only in the liver and plasma demonstrating that cancer stem cells readily execute a highly liver-specific gene expression program that is mechanistically linked to GBM oncogenesis. We show that cancer cells can co-opt non-cancer cells to promote tumor growth, by uncovering the preferential relationship between platelets and GSCs that drive GBM malignancies and identifies a therapeutically targetable novel interaction.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noac209.118
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 2094060-9
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  • 8
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    STEM-10. BIDIRECTIONAL INTERACTION BETWEEN TUMOR-ASSOCIATED PLATELETS AND GLIOMA STEM CELLS IN GLIOBLASTOMA MULTIFORME
    Oxford University Press (OUP) ; 2019
    In:  Neuro-Oncology Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi235-vi236
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 21, No. Supplement_6 ( 2019-11-11), p. vi235-vi236
    Abstract: Glioblastoma Multiforme (GBM) is the most common and lethal malignant primary adult brain tumor. Therapy resistance and tumor recurrence in GBM have been attributed to glioma stem cells (GSCs), which are found in hypoxic but perivascular niches. We hypothesized that the clinically documented and prognostically relevant increase in platelets in GBM promotes formation of functional hypoxic but perivascular niches that support GSCs due to formation of intravascular thromboses, a hallmark of GBM. Our preliminary in silico analysis from TCGA GBM samples indicates significant correlation of platelet and stemness signature expression (P 〈 0.001). High expression of platelet gene signatures also inversely correlates with overall survival in GBM patients (P 〈 0.02). Furthermore, we found significant co-localization of known platelet and stemness markers in primary GBM specimens, supporting our hypothesis and motivating further interrogation of GSC-platelet crosstalk. Our preliminary data suggest that GSCs exposed to either tumor or healthy platelets demonstrate increased self-renewal and stemness, as determined by a significant increase in OCT4, NANOG, and OLIG2 expression compared to unexposed GSCs. This increase in stemness and self-renewal markers was not seen in platelet-exposed differentiated glioma cell (DGC) counterparts. Conversely, platelets are stimulated by GSCs and GSC-conditioned media while DGCs elicit no stimulatory effects as measured by ATP release and aggregation assays. Our results implicate a functional role for platelet-GSC interactions in the maintenance of tumor cellular hierarchy that ultimately contributes to poor clinical outcomes in GBM. RNA-Seq of platelet-privileged GSCs is currently underway to elucidate the mechanism by which platelets impact GSC self-renewal. Successful characterization of potential crosstalk between platelets and GSCs may offer new clinical perspectives into GBM and inform development of a novel treatment paradigm to target these specific cell-to-cell interactions.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noz175.984
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
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  • 9
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    STEM-08. PLATELETS DRIVES GLIOBLASTOMA ONCOGENESIS BY ENHANCING THE GLIOMA STEM CELL PHENOTYPE
    Oxford University Press (OUP) ; 2020
    In:  Neuro-Oncology Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii198-ii198
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 22, No. Supplement_2 ( 2020-11-09), p. ii198-ii198
    Abstract: Glioblastoma (GBM) is recognized as one of the deadliest forms of cancer, despite aggressive therapy consisting of maximal surgical resection followed by concurrent radiation and chemotherapy, the median survival remains ~15 months. Glioma stem cells (GSCs) possess potent tumor-initiating properties and comprise a cellular hierarchy that is responsible for treatment resistance and progression. Specifically targeting GSCs has been considered a promising therapeutic approach, however no clear method has been identified. Histologically, it is known that GSCs are found in perivascular and pseudsopalisading regions of GBM. Similarly, platelet aggregates are often found in pseudsopalisading necrotic regions, suggesting a potential interaction between platelets and GSCs due to their spatial locations. High platelet counts have been associated with poor clinical outcome in many cancers including ovarian and endometrial cancer. While platelets are known to affect progression of other tumors, mechanisms by which platelets influence GBM oncogenesis are unknown. Our work aimed to understand the crosstalk between GSCs and platelets within GBM solid tumors that work to enhance disease progression and treatment resistance. Our clinical studies suggest elevated platelet counts positively correlate with tumor growth and negatively correlate to overall patient survival. We found platelets and GSC co-localization in GBM solid tissue; platelet exposure to GSCs results in increased proliferation of GSCs specifically, by increasing the self-renewing capacity of GSCs in a dose dependent manner, and resulted in an increased “Stem-like” transcriptional pattern. Consequently, inhibiting the GSC-platelet interaction results in a decrease in GSC renewal and stemness. These results introduce a novel interaction between GSCs and platelets and elucidate a novel therapeutic approach specifically targeting GSCs by disrupting the GSC-platelet interaction.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noaa215.825
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
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  • 10
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    STEM-17. THE GLIOMA STEM CELL PLATELET INTERACTION DRIVES GBM ONCOGENESIS IDENTIFYING A NOVEL THERAPEUTIC APPROACH
    Oxford University Press (OUP) ; 2021
    In:  Neuro-Oncology Vol. 23, No. Supplement_6 ( 2021-11-12), p. vi24-vi24
    Details
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 23, No. Supplement_6 ( 2021-11-12), p. vi24-vi24
    Abstract: The effect of platelets on oncogenesis has been studied extensively in cancer metastasis, but not in glioblastoma (GBM), where metastasis is rare. Here we identify the unique crosstalk between glioma stem cells (GSCs) and platelets within GBM solid tumors that enhance disease progression. Targeting GSCs is considered a promising therapeutic approach; however, no clear method has been identified. High platelet counts have been associated with poor clinical outcome in many cancers including ovarian and endometrial cancer. While platelets are known to affect progression of other tumors, mechanisms by which platelets influence GBM oncogenesis are unknown. Immunofluorescence, qPCR, and western blot were used to evaluate the presence of GSCs and platelets and their colocalization in GBM patient tissue at University Hospitals-Seidman Cancer Center. Functional assays followed by RNA sequencing were conducted to determine the functional effect of healthy and GBM platelets on growth of patient derived, autologous GSCs. Our clinical studies suggest elevated platelet counts positively correlate with GSC proliferation and negatively correlate with overall survival in patients with GBM. Patients with high platelet counts ( & gt;350k/µl) had a median survival time of 9 months compared to 16 months median survival for patients with normal platelet count (150-350/µl) (p & lt;0.05). We demonstrate platelet and GSC co-localization in GBM solid tissue and platelet exposure to patient derived GSCs cell lines results in a ≥ 3-fold increase in GSC proliferation compared to GSCs not exposed to platelets (p & lt;0.0005). Similarly we found that platelets increased the self-renewing capacity by enhancing the average sphere size (p & lt; 0.005), and increasing the GSC “Stem-like” transcriptional pattern (P & lt; 0.05). Conversely, pharmacologic inhibition of platelet activation reversed the effect of platelets on GSC proliferation (p ranging from 0.05-0.005). These studies suggests the platelet-GSC interactions appear to stimulate GBM oncogenesis, identifying a potential therapeutic target for the treatment of GBM.
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    URL: Article
    DOI: 10.1093/neuonc/noab196.091
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2021
    detail.hit.zdb_id: 2094060-9
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