tbuckley/cabot-search huggingface dataset:
Abstract 4047: Potential role of CXCR6-CXCL16 in prostate cancer progression and chemotherapeutic efficacy
Authors: Pranav Gupta, Ashley B. Ward, Hina Mir, Gurpreet Kaur, William E. Grizzle, James W. Lillard, Shailesh Singh
Journal: Cancer Research (2014)

Abstract Despite recent advances in treatment and clinical management, prostate cancer is still a leading cause of cancer related deaths among men, primarily because etiopathogenesis of PCa is not well defined. In this regard, chemokines and their corresponding receptors have been shown to play major role in PCa progression, which are often associated with poor therapeutic outcomes. Hence, the focus of this study is to determine the potential role of CXCR6 and its natural ligand CXCL16 in PCa pathogenesis, and potential impact of CXCR6-CXCL16 axis on efficacy of docetaxel, which is currently offered in the clinics as standard care. We investigated expression of CXCR6 and CXCL16 in clinical samples, prostate cancer cell lines and normal prostatic epithelial cells. Expression of CXCR6 and CXCL16 was significantly higher in PCa samples compared to their respective controls, and expression of CXCR6/ CXCL16 was correlated with tumor stage and grades. Similar to patient's samples, expression of CXCR6/CXCL16 was significantly higher in PCa cell lines compared to normal prostatic epithelial cells. Furthermore, levels of phospho -ERK1/2 and -NF-kB, known to be involved in cell growth and survival, were significantly higher in PCa cells treated with CXCL16 compared to untreated controls. In addition to these, role of CXCR6- CXCL16 on genes responsible for cellular adhesion and epithelial-mesenchymal transition were examined. Interestingly, expression of surface E-cadherin and β−catenin following CXCL16 treatment was significantly inhibited compared to untreated cells, suggesting the involvement of CXCR6-CXCL16 interaction in PCa cell migration. Additionally, CXCR6 expressing PCa cells expressed higher α−smooth muscle actin protein, another EMT marker presumably induced by elevated TGF-β, following CXCL16 stimulation. Furthermore, expression of CXCR6, CXCL16 and MMP(s) were elevated in PCa cell following docetaxel treatment in a time and dose dependent manner compared to controls. This may explain the increased efficacy of docetaxel when used in combination with anti-CXCR6 antibody as compared to docetaxel alone. These findings suggest that CXCR6-CXCL16 axis plays a crucial role in pathogenesis of PCa, and inhibition of this axis may have significant impact on disease progression and therapeutics outcomes. Citation Format: Pranav Gupta, Ashley B. Ward, Hina Mir, Gurpreet Kaur, William E. Grizzle, James W. Lillard, Shailesh Singh. Potential role of CXCR6-CXCL16 in prostate cancer progression and chemotherapeutic efficacy. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4047. doi:10.1158/1538-7445.AM2014-4047
Abstract 16152: Utility of Peak Systolic Velocity Ratio in Asymptomatic Patients With Restenosis After Endovascular Therapy for Femoro-Popliteal Lesion
Authors: Shota Tohoku, Soga Yoshimitsu, Yusuke Tomoi
Journal: Circulation (2014)

Introduction: The predictive factor of whether asymptomatic restenosis needs reintervention after initial therapy remains unclear. Objective: The aim of this study was to evaluate whether peak systolic velocity ratio (PSVR) is effective to predict target lesion revascularization (TLR) after endovascular therapy (EVT) for femoropopliteal (FP) lesion. Methods: From April 2007 to September 2013, 120 restenotic limbs without ischemic symptoms (mean age: 73.1±9.0, men: 75.0%, stent implantation: 57.5%) were selected and analyzed, 73 limbs underwent reintervention. Median follow-up period was 33.7 months (5.1-110.4 months). They were followed by serial duplex ultrasound (DUS). Restenosis was defined as peak systolic velocity (PSV) &gt; 250cm/s or PSVR &gt; 2.4 by using DUS. We divided them into two groups (High PSVR group (PSVR ≧3.63)and low PSVR group (PSVR &lt; 3.63)). The ratio of TLR was compared between two groups by Kaplan-Meier survival curve. We also analyzed the TLR between balloon angioplasty (POBA) alone and stent implantation on initial EVT. Each cut off value of PSVR were 4.19 and 3.63. Results: At 1, 3 and 5 years after initial EVT, Freedom from TLR were significantly different between two groups (76.5%, 33.2% and 18.3% vs 90.7%, 75.4%, and 58.0%, p&lt;0.001). Moreover, two groups were significantly different when analyzed about limbs performed POBA (86.9%, 67.0% and 35.7% vs 69.2%, 29.0% and 14.5%, p =0.048 ) and stenting on initial EVT (92.3%, 77.6% and 51.7% vs 83.8%, 35.2% and 12.0%, p &lt; 0.01). After adjustment for use of cilostazol, use of proton pomp inhibitor , chronic total occlusion, history of EVT for aortoiliac disease, PSVR was an independent predictors of TLR. Conclusions: PSVR may be a predictive factor of performing reintervention for asymptomatic patient with restenosis after EVT of FP lesion.
Panic disorder in children and adolescents: a review
Authors: D Moreau, M M Weissman
Journal: American Journal of Psychiatry (1992)

Panic disorder has been considered an adulthood disorder that does not occur in children or adolescents. The authors' goals were to critically review the available evidence for panic attacks and/or panic disorder in children and adolescents, to review the limited data on the biological basis of panic disorder as it has been studied in children and adolescents, to discuss the possible treatment approaches for panic disorder in children, and to suggest potential opportunities for further research on panic disorder in children.Sixty-three articles pertaining to panic disorder in children and adolescents were critically reviewed. These articles included retrospective histories of adults with panic disorder, clinical case reports of children and adolescents with panic disorder, studies of psychiatrically referred children and adolescents, reports from epidemiologic community and school samples of children and adolescents, studies of children and adolescents at risk for psychiatric disorder, reports of panic-like symptoms in pediatric patients, family studies of panic, studies of the biological basis of panic in adults, and studies of treatment for panic.There is strong evidence that panic disorder occurs in children and adolescents and that its clinical presentation in this population is similar to that found in adults.Extending the many adult studies of panic disorder to children and adolescents would be extremely fruitful. Like adults with panic disorder, many children and adolescents are brought to emergency and medical clinics for the physical symptoms of unrecognized panic disorder.
Abstract 2482: Quantification of Myocardial Scar Using a Simple ECG Tool Identifies Patients at Risk for Sudden Arrhythmic Death: An Analysis of SCD-HeFT
Authors: David G Strauss, Jeanne E Poole, Galen S Wagner, Ronald H Selvester, Julie M Miller, Jill Anderson, George Johnson, Steven E McNulty, Daniel B Mark, Kerry L Lee, Gust H Bardy, Katherine C Wu
Journal: Circulation (2009)
Use of Leukemic Dendritic Cells for the Generation of Antileukemic Cellular Cytotoxicity Against Philadelphia Chromosome-Positive Chronic Myelogenous Leukemia
Authors: Aniruddha Choudhury, James L. Gajewski, Jan C. Liang, Uday Popat, David F. Claxton, Kay-Oliver Kliche, Michael Andreeff, Richard E. Champlin
Journal: Blood (1997)
Abstract 11965: Novel Simple and Accurate Quantitative Endothelial Function Measurements Using Brachial Artery Vascular Volume Elastic Modulus With Automated Oscillometric Approach
Authors: Keiichiro Yoshinaga, Yuuki Tomiyama, Satoshi Fujii, Saori Nishio, Naoko Matsuoka, Noriki Ochi, Chietsugu Katoh, Mamiko Inoue, Mutumi Nishida, Yoichi M Ito, Hideo Nishibayashi, Nagara Tamaki
Journal: Circulation (2014)

Background:  Simple and automated arterial endothelial function measurements are desirable for atherosclerosis risk assessments. Vascular elastic modulus (V E ) is uninfluenced by blood pressure and potentially is linked to endothelial function. However, previous V E  measurements have been complex or invasive. Recently, we developed a novel modality of automated oscillometric method to measure a brachial artery’s V E . We aimed to investigate whether V E  reflected endothelial dysfunction related to chronic kidney disease (CKD). We also evaluated the reliability of new automated V E  methods.   Methods:  13 moderate-to-severe CKD pts (mean estimated glomerular filtration rate [eGFR] 29.3±25.7 mL/min/1.73m 2 ) and 16 controls were studied. Rest V E  and estimated arterial cross sectional area (eA) in brachial artery were measured by new automated oscillometric detector. eA was estimated using pressure-volume curves and V E  was defined as follows [V E  = ΔPressure/ (100XΔarea / Area) mmHg/%]. Controls repeated eA and V E  measurements. Using ultrasound (US), we measured the brachial artery diameter at rest and during reactive hyperemia [flow mediated dilatation (FMD) with endothelial-dependent dilatation].   Results:  Absolute value of eA was correlated with US measured arterial diameter (R=0.78, P E  showed good reproducibility (eA: ICC = 0.88, V E : ICC = 0 .78). CKD had lower FMD than control (4.46±3.06 vs 7.88±4.04 %, P=0.018). CKD also showed attenuated V E  as compared to control (1.09±0.25 vs 0.80±0.16 mmHg/%, P=0.002). V E  was negatively correlated with eGFR (r=-0.51, P=0.005) and %FMD (r=-0.38, P=0.04).   Conclusions:  This new automated vascular elastic modulus measurement reliably detected vascular dysfunction related to CKD. Vascular dysfunction depicted with this approach closely correlated with FMD. Thus, this simple automated oscillometric measurement may be useful for detecting vascular anatomical information and endothelial dysfunction.
Self-portrait With a Visor
Authors: M. Therese Southgate
Journal: JAMA (2000)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
The emergence of oseltamivir-resistant pandemic influenza A(H1N1) 2009 virus amongst hospitalised immunocompromised patients in Scotland, November-December, 2009
Authors: H Harvala, R Gunson, P Simmonds, A Hardie, S Bennett, F Scott, H Roddie, J McKnight, T Walsh, D Rowney, A Clark, J Bremner, C Aitken, K Templeton
Journal: Eurosurveillance (2010)

To investigate the frequency of oseltamivir resistance in circulating strains of the 2009 influenza A(H1N1) pandemic virus in Scotland, 1,802 samples from 1,608 infected hospitalised patients were screened by the H275Y discriminatory RT-PCR. Among these, we identified 10 patients who developed the H275Y mutation. All of them were immunocompromised and were under treatment or had been treated previously with oseltamivir.
Children at Play in Mantua, Utah
Authors: M Therese Southgate
Journal: JAMA (2005)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 4245: A comparative analysis of PI3K inhibitors in human tumor primary culture microspheroids
Authors: Robert Alan Nagourney, Paula J. Bernard, Federico Francisco, Steven S. Evans
Journal: Cancer Research (2014)

Abstract Altered phosphoinosotide metabolism is a hallmark of many human malignances. The phosphoinsotide kinases (PI3K) of which there are several sub-classes, have been explored as targets for cancer therapy. Beyond the first generation pan-PI3K inhibitors Wortmannin &amp; LY294002, new, clinically active agents with subclass specificity and/or dual inhibitory functions (PI3K &amp; mTOR) have been developed, including BEZ235 (PI3K/mTOR), GDC0941(αβδ), BYL719(α) &amp; Idelalisib (δ). To examine the activity of these agents we applied Ex Vivo Analysis of Programmed Cell Death (EVA/PCD) (Nagourney, R et al Anticancer Res., 2012)to human tumor microspheroids, isolated directly from surgical specimens. Lethal concentrations (LC50's) interpolated from 5-point dose response curves were compared for activity and for correlation by Pearson Moment. Results: Micro-molar activity favored BEZ &amp;gt; BYL &amp;gt; LY. Correlation coefficients reveal BYL vs. BEZ (N=15, R =0.69, P&amp;lt; 0.01); BYL vs. LY (N=7, R=0.74, P=0.1); BEZ vs. LY (N=61, R=0.52, P&amp;lt;0.001). A comparison of activity for hematologic (Heme) vs. Solid tumors (solid) for LY: Heme &amp;gt; Solid; BEZ: Solid &amp;gt; Heme; BYL: Heme &amp;gt; Solid with preliminary evidence for Idelalisib showing Heme &amp;gt; Solid. Conclusions: The PI3K inhibitors are active in both Heme and Solid tumors, with relative concordance between agents, but some evidence of disease specificity. Additional comparisons with GDC 0941 and drug combination studies are being conducted to further characterize the clinical activity and combinatorial potential of this class of agents. EVA/PCD analyses, conducted in human tumor primary cultures, have the capacity to evaluate drug activity, synergy and sequence dependence offering clinically relevant insights into novel drug applications. Citation Format: Robert Alan Nagourney, Paula J. Bernard, Federico Francisco, Steven S. Evans. A comparative analysis of PI3K inhibitors in human tumor primary culture microspheroids. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4245. doi:10.1158/1538-7445.AM2014-4245
Caspase-7: a critical mediator of optic nerve injury-induced retinal ganglion cell death
Authors: Shreyasi Choudhury, Yang Liu, Abbot F. Clark, Iok-Hou Pang
Journal: Molecular Neurodegeneration (2015)

Axonal injury of the optic nerve (ON) is involved in various ocular diseases, such as glaucoma and traumatic optic neuropathy, which leads to apoptotic death of retinal ganglion cells (RGCs) and loss of vision. Caspases have been implicated in RGC pathogenesis. However, the role of caspase-7, a functionally unique caspase, in ON injury and RGC apoptosis has not been reported previously. The purpose of this study is to evaluate the role of caspase-7 in ON injury-induced RGC apoptosis. C57BL/6 (wildtype, WT) and caspase-7 knockout (Casp7 −/− ) mice were used. We show that ON crush activated caspase-7 and calpain-1, an upstream activator of caspase-7, in mouse RGCs, as well as hydrolysis of kinectin and co-chaperone P23, specific substrates of caspase-7. ON crush caused a progressive loss of RGCs to 28 days after injury. Knockout of caspase-7 partially and significantly protected against the ON injury-induced RGC loss; RGC density at 28 days post ON crush in Casp7 −/− mice was approximately twice of that in WT ON injured retinas. Consistent with changes in RGC counts, spectral-domain optical coherence tomography analysis revealed that ON crush significantly reduced the in vivo thickness of the ganglion cell complex layer (including ganglion cell layer, nerve fiber layer, and inner plexiform layer) in the retina. The ON crush-induced thinning of retinal layer was significantly ameliorated in Casp7 −/− mice when compared to WT mice. Moreover, electroretinography analysis demonstrated a decline in the positive component of scotopic threshold response amplitude in ON crushed eyes of the WT mice, whereas this RGC functional response was significantly higher in Casp7 −/− mice at 28 days post injury. Altogether, our findings indicate that caspase-7 plays a critical role in ON injury-induced RGC death, and inhibition of caspase-7 activity may be a novel therapeutic strategy for glaucoma and other neurodegenerative diseases of the retina.
Abstract 11934: High Sensitivity Cardiac Troponin T is Associated with Silent Cardiac Target Organ Damage in Asymptomatic Primary Prevention Patients
Authors: Muhammad A Nadir, Ellie Dow, Chim C Lang, John Davidson, Tom MacDonald, Allan D Struthers
Journal: Circulation (2011)

Background: Although, cTnT levels are rarely detectable in general population using standard assays, they are associated with overt cardiac disease. These findings suggest that cTnT detected by new...
Abstract 4194: Gliomaspheres mimic the hypoxia-Notch signaling axis of glioblastoma tumors
Authors: Khushboo Irshad, Saroj Kant Mohapatra, Harshit Garg, Seema Mishra, Chitra Sarkar, Deepak Gupta, Parthaprasad Chattopadhyay, Subrata Sinha, Kunzang Chosdol
Journal: Cancer Research (2014)

Abstract Background and objectives: Notch signaling plays an oncogenic role during gliomagenesis. Synergism of hypoxia with Notch pathway is known to aggravate different cancers. We studied the association between Notch signaling and hypoxia in human glioblastoma (GBM) samples which are characterized by intratumoral hypoxia. We also carried out in-vitro analysis in U87MG cell line enriched in stem cells under low oxygen conditions. The study aimed at identifying a modular gene subset that might be a characteristic of the Notch pathway response in hypoxic GBM tumors and GBM gliomaspheres; which might assist in individualized therapeutics. Methods: Expression of Notch receptors, Dll/Jag ligands, Hes/Hey targets and hypoxia markers was analyzed in 35 GBMs by q-PCR and immunohistochemistry. Spearman's test, clustering and statistical analyses were applied to assess the correlation between hypoxia and Notch pathway upregulation. Expression analysis was also done in U87MG cells grown in stem cell culture conditions under hypoxia using q-PCR and western blot. Results: Using various statistical analyses, we found HIF-1α to be correlated with the expression of maximum number of Notch pathway genes, followed by PGK1, OPN and VEGF. Well-segregated tumor clusters accounting for differential Notch genes' expression were produced using gene clustering and principal components analysis by ordering the GBMs in decreasing levels of HIF-1α/PGK1. By logistic regression, a five hypoxia marker combination (HIF-1α/PGK1/VEGF/CA9/OPN) was determined as the best predictor for Notch signaling augmentation in GBM. A similar Notch-axis (Notch1/Dll1/Hes1/Hes6/Hey1/Hey2) was activated in U87MG gliomaspheres under hypoxia. Interpretation and conclusions: The hypoxia markers most associated with Notch signaling upregulation in resected GBM were identified. Similar components of the Notch pathway were also found to be activated in hypoxia-exposed gliomaspheres, supporting them as an in-vitro model for studying the perturbations of hypoxia-Notch signaling axis. Citation Format: Khushboo Irshad, Saroj Kant Mohapatra, Harshit Garg, Seema Mishra, Chitra Sarkar, Deepak Gupta, Parthaprasad Chattopadhyay, Subrata Sinha, Kunzang Chosdol. Gliomaspheres mimic the hypoxia-Notch signaling axis of glioblastoma tumors. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4194. doi:10.1158/1538-7445.AM2014-4194
Stepwise development of biomarkers for angiogenic activity with standardized assays for circulating molecules in human subjects
Authors: Michael L. Maitland, Emily Kistner, Larry House, Theodore Karrison, Mark J. Ratain
Journal: Clinical Cancer Research (2006)

B84   Numerous molecules are necessary for tumor angiogenesis and standardized assays for determining the concentrations of such molecules in body fluids are readily available. It is unclear which assays, upon which fluid samples, will be useful biomarkers to guide anticancer therapy. In this study we: 1) selected angiopoietin-2 (Ang2) and soluble vascular endothelial growth factor receptor-2 (VEGFR2) for further investigation based on parameters of assay performance in population samples, 2) estimated the intraindividual and interindividual variability in measurements on serially collected serum and plasma samples from 6 healthy adult subjects, and 3) applied these findings to the pilot analysis of these same markers in a group of advanced cancer patients receiving treatment with the c-Raf/VEGFR2/VEGFR3/PDGFRβ kinase inhibitor sorafenib. Ang2 and VEGFR2 shared properties of primary synthesis by endothelial cells and ELISAs (R&D Systems, Minneapolis, MN) detecting a broad population distribution with no sample below the limits of detection. The six healthy subjects provided 13 concurrent serum and plasma samples each over the course of 14-24 days Variance component analysis revealed 86% of plasma Ang2 and 91% of plasma VEGFR2 variability to be interindividual, with sex and a standardized exercise session having no obvious measurable effect. (For serum samples, interindividual variation accounted for 89% and 87% of the total variance for Ang2 and VEGFR2, respectively.) For Ang2, serum and plasma samples yielded nearly identical results while VEGFR2 serum samples had slightly greater  intra individual variability than plasma samples. Therefore single time-point plasma samples were collected from 15 advanced solid tumor patients, before, and approximately 10 and 40 days after commencing treatment with the orally available kinase inhibitor sorafenib. Using a repeated measures linear model of Ang2 and VEGFR2 concentrations, a univariate test of the time on sorafenib effect was statistically significant (Greenhouse-Geisser p value= 0.046 and