tbuckley/cabot-search huggingface dataset:
Gene Expression Differences Associated with Human Papillomavirus Status in Head and Neck Squamous Cell Carcinoma
Authors: Robbert J.C. Slebos, Yajun Yi, Kim Ely, Jesse Carter, Amy Evjen, Xueqiong Zhang, Yu Shyr, Barbara M. Murphy, Anthony J. Cmelak, Brian B. Burkey, James L. Netterville, Shawn Levy, Wendell G. Yarbrough, Christine H. Chung
Journal: Clinical Cancer Research (2006)

Abstract Human papillomavirus (HPV) is associated with a subset of head and neck squamous cell carcinoma (HNSCC). Between 15% and 35% of HNSCCs harbor HPV DNA. Demographic and exposure differences between HPV-positive (HPV+) and negative (HPV−) HNSCCs suggest that HPV+ tumors may constitute a subclass with different biology, whereas clinical differences have also been observed. Gene expression profiles of HPV+ and HPV− tumors were compared with further exploration of the biological effect of HPV in HNSCC. Thirty-six HNSCC tumors were analyzed using Affymetrix Human 133U Plus 2.0 GeneChip and for HPV by PCR and real-time PCR. Eight of 36 (22%) tumors were positive for HPV subtype 16. Statistical analysis using Significance Analysis of Microarrays based on HPV status as a supervising variable resulted in a list of 91 genes that were differentially expressed with statistical significance. Results for a subset of these genes were verified by real-time PCR. Genes highly expressed in HPV+ samples included cell cycle regulators (p16INK4A, p18, and CDC7) and transcription factors (TAF7L, RFC4, RPA2, and TFDP2). The microarray data were also investigated by mapping genes by chromosomal location (DIGMAP). A large number of genes on chromosome 3q24-qter had high levels of expression in HPV+ tumors. Further investigation of differentially expressed genes may reveal the unique pathways in HPV+ tumors that may explain the different natural history and biological properties of these tumors. These properties may be exploited as a target of novel therapeutic agents in HNSCC treatment.
Obesity: What Mental Health Professionals Need to Know
Authors: M. J. Devlin
Journal: American Journal of Psychiatry (2000)

Obesity is a highly prevalent condition with significant health implications. This report summarizes recent clinically relevant findings concerning the pathogenesis and treatment of obesity and considers their implications for psychiatric diagnosis and management.The authors conducted selective reviews of the literature from the last 10 years. Topics included the biological and behavioral factors that contribute to the onset and maintenance of obesity, the relationship between obesity and psychiatric illness and treatment, and the questions of whether and how obesity should be treated.Genetic effects, some mediated by eating behavior, contribute importantly to the potential for obesity, the expression of which is promoted by environmental factors that increase the availability of calorically dense foods and discourage activity. There appear to be behaviorally distinct subsets of obese persons who display particular patterns of disordered eating and elevated rates of psychopathology. Treatment with psychotropic medications may contribute to obesity in ways that are only partly understood. Although successful obesity treatment is associated with clear health benefits and available treatments offer benefit to some, relapse remains the rule.Although the presence or development of obesity is a daunting problem, it should not be ignored by mental health professionals. Treatment should address not only obesity per se, but also its effects on self-esteem in a hostile cultural climate. Ongoing developments in basic and clinical research are likely to increase the range, efficacy, and acceptability of treatment options in the years ahead.
Studies of the human factor VIII/von Willebrand factor protein. III. Qualitative defects in von Willebrand's disease.
Authors: H R Gralnick, B S Coller, Y Sultan
Journal: Journal of Clinical Investigation (1975)

The Factor VIII/von Willebrand factor protein was characterized in two unrelated patients with von Willebrand's disease in whom procoagulant and Factor VIII/von Willebrand factor antigen levels were normal. In both patients evidence of an abnormal protein was observed on crossed antigen-antibody electrophoresis. In one patient the Factor VIII/von Willebrand factor protein eluted from Sepharose 4B in a position and distribution identical to normal with normal levels of procoagulant activity and antigen. However, the partially purified Factor VIII/von Willebrand factor protein had markedly reduced von Willebrand factor activity in a ristocetin assay. In the second patient the peak of Factor VIII/von Willebrand factor protein, antigen, and procoagulant activity eluted from a Sepharose 4B column with an estimated molecular weight of approximately half that of normal. This protein had no von Willebrand factor activity. In both patients the reduced Factor VIII/von Willebrand factor protein subunit was indistinguishable from normal on polyacrylamide gel electrophoresis. These studies indicate that in some patients with von Willebrand's disease there is a qualitative defect of the Factor VII/von Willebrand factor protein; the total amount of protein, antigen, and procoagulant activity are normal while the von Willebrand factor activity is deficient.
Changes Continue to Enhance Journal
Authors: W. K. Alfred Yung
Journal: Neuro-Oncology (2007)

At the last full meeting of the Neuro-Oncology Editorial Board (during the SNO Annual Meeting in Orlando, Florida, last November), the editors in chief proposed a revised editorial structure for Neuro-Oncology, which would allow regional executive editors for the journal to be chosen by the sponsoring organizations (SNO, the European Association for Neuro-Oncology [EANO], and the Japan Society for Neuro-Oncology [JSNO]). This change in editorial leadership was conceived as a means of ensuring that the journal achieves its sponsors’ long-term goal: to enhance the quality of information Neuro-Oncology provides to the international community of professionals it serves. The proposal was approved, the EANO and JSNO boards have concurred, and the changes are being implemented now—all to promote a more integrated form of journal governance and decision making.

Accordingly, I am happy to welcome onboard three executive editors for the journal, one representing each organization named above. Effective July 1, 2007, C. David James, who has ably served as co-editor in chief for the journal since its transition from Dr. Darell Bigner and his team at Duke, has assumed his new position as executive editor, SNO. Michael Weller, a longtime editorial board member and reviewer, has joined the revamped editorial team as executive editor, EANO. And Ryo Nishikawa, formerly senior editor for Asia, has been named executive editor, JSNO. While it has long been my pleasure to work with these gentlemen on the journal, I look forward to having even greater access to their expertise and experience going forward.
Excision of tricuspid valve with later replacement in endocarditis of drug addiction.
Authors: J S Wright, J S Glennie
Journal: Thorax (1978)

Staphylococcal endocarditis in a drug addict was controlled only after excision of the tricuspid valve. Total absence of the tricuspid valve was tolerated well for 18 months, at which time deteriorating liver function prompted the insertion of a bioprosthetic valve into the tricuspid ring. The haemodynamic and clinical results after two years of follow-up have been excellent.
Y Chromosome Haplotypes and Prostate Cancer in Sweden
Authors: Sara Lindström, Hans-Olov Adami, Jan Adolfsson, Fredrik Wiklund
Journal: Clinical Cancer Research (2008)

Abstract Purpose: Certain Y-chromosomal lineages have been suggested to predispose individuals to prostate cancer in the Japanese population; in other ethnic groups, however, the importance of the Y chromosome is poorly understood. Experimental Design: To assess the possible Y-chromosomal contribution to prostate cancer risk and prognosis, we analyzed five binary Y-chromosomal markers in 1,447 prostate cancer cases and 983 population controls from the Swedish population. Together, these five markers capture the vast majority of chromosome Y haplogroup diversity in the Swedish population. Individual lineages were tested for association with both prostate cancer risk and cancer-specific death. We replicated observed associations in an independent Swedish prostate cancer case-control study comprising 1,452 cases and 779 controls. Results: One rare lineage (I1c) was associated with an increased risk of developing prostate cancer [odds ratio (OR), 2.9; 95% confidence interval (CI), 1.4-5.8; P = 0.001]. However, confirmatory analysis of this lineage in the independent case-control study revealed no association with prostate cancer risk (OR, 0.65; 95% CI, 0.4-1.2, P = 0.17). We observed no association between chromosome Y variation and prostate cancer–specific death. Conclusions: This study provides strong evidence against an important role of the Y chromosome in the initiation or outcome of prostate cancer in the Swedish population.
Evaluation of cisplatin intensity in metastatic non-small-cell lung cancer: a phase III study of the Southwest Oncology Group.
Authors: D R Gandara, J Crowley, R B Livingston, E A Perez, C W Taylor, G Weiss, J R Neefe, L F Hutchins, R W Roach, S M Grunberg
Journal: Journal of Clinical Oncology (1993)

PURPOSE To test the concept that cisplatin dose-intensity is important in the treatment of non-small-cell lung cancer (NSCLC), the Southwest Oncology Group (SWOG) performed a randomized trial comparing standard-dose cisplatin (SDCP) 50 mg/m2 days 1 and 8 on a 28-day cycle for eight cycles, high-dose cisplatin (HDCP) 100 mg/m2 days 1 and 8 for four cycles, and high-dose cisplatin plus mitomycin (HDCP-M) 8 mg/m2 day 1. To isolate the effects of dose-intensity versus total dose, the planned cumulative cisplatin dose was 800 mg/m2 in each arm. PATIENTS AND METHODS Between July 1988 and April 1990, 356 patients were enrolled and 323 were eligible and assessable. All patients had metastatic, measurable disease, were chemotherapy-naive, and had a performance status (PS) of 0 to 2. RESULTS Confirmed complete plus partial response rates were SDCP, 12%; HDCP, 14%; and HDCP-M, 27% (P &lt; .05). Complete responses were uncommon (HDCP, 3%; HDCP-M, 4%) and were observed only in the high-dose arms. Progressive disease occurred more frequently in the SDCP arm (57%) compared with HDCP (38%) or HDCP-M (34%) (P &lt; .05). However, there were no significant differences in median survival times (SDCP, 6.9 months; HDCP, 5.3 months; HDCP-M, 7.2 months; P = .53). The mean delivered dose-intensity for cisplatin was significantly greater in the high-dose arms: HDCP 41 mg/m2/wk and HDCP-M 39 mg/m2/wk, versus SDCP 23 mg/m2/wk (P = .05). The high-dose arms resulted in an increased incidence of ototoxicity, emesis, and myelosuppression, but similar degrees of renal toxicity and neuropathy compared with SDCP. CONCLUSION This study does not confirm evidence of a steep clinical dose-response curve for cisplatin in NSCLC at the cisplatin dose-intensities achieved. The addition of mitomycin increases the response rate, but does not improve survival. Continued evaluation of new agents in this disease is warranted.
IgM rheumatoid factor amplifies the inflammatory response of macrophages induced by the rheumatoid arthritis-specific immune complexes containing anticitrullinated protein antibodies
Authors: Lætitia Laurent, Florence Anquetil, Cyril Clavel, Ndiémé Ndongo-Thiam, Géraldine Offer, Pierre Miossec, Jean-Louis Pasquali, Mireille Sebbag, Guy Serre
Journal: Annals of the Rheumatic Diseases (2014)

Anticitrullinated protein antibodies (ACPA) are specifically associated with rheumatoid arthritis (RA) and produced in inflamed synovial membranes where citrullinated fibrin, their antigenic target, is abundant. We showed that immune complexes containing IgG ACPA (ACPA-IC) induce FcγR-mediated tumour necrosis factor (TNF)-α secretion in macrophages. Since IgM rheumatoid factor (RF), an autoantibody directed to the Fc fragment of IgG, is also produced and concentrated in the rheumatoid synovial tissue, we evaluated its influence on macrophage stimulation by ACPA-IC.With monocyte-derived macrophages from more than 40 healthy individuals and different human IgM cryoglobulins with RF activity, using a previously developed human in vitro model, we evaluated the effect of the incorporation of IgM RF into ACPA-IC.IgM RF induced an important amplification of the TNF-α secretion. This effect was not observed in monocytes and depended on an increase in the number of IgG-engaged FcγR. It extended to the secretion of interleukin (IL)-1β and IL-6, was paralleled by IL-8 secretion and was not associated with overwhelming secretion of IL-10 or IL-1Ra. Moreover, the RF-induced increased proinflammatory bioactivity of the cytokine response to ACPA-IC was confirmed by an enhanced, not entirely TNF-dependent, capacity of the secreted cytokine cocktail to prompt IL-6 secretion by RA synoviocytes.By showing that it can greatly enhance the proinflammatory cytokine response induced in macrophages by the RA-specific ACPA-IC, these results highlight a previously undescribed, FcγR-dependent strong proinflammatory potential of IgM RF. They clarify the pathophysiological link between the presence of ACPA and IgM RF, and RA severity.
Percutaneous penetration in the hairless dog, weanling pig and grafted athymic nude mouse: evaluation of models for predicting skin penetration in man
Authors: W. G. REIFENRATH, E. M. CHELLQUIST, E. A. SHIPWASH, W. W. JEDERBBRG, G. G. KRUEGER
Journal: British Journal of Dermatology (1984)

Journal Article Percutaneous penetration in the hairless dog, weanling pig and grafted athymic nude mouse: evaluation of models for predicting skin penetration in man Get access W. G. REIFENRATH, W. G. REIFENRATH Division of Cutaneous Hazards, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129 Search for other works by this author on: Oxford Academic Google Scholar E. M. CHELLQUIST, E. M. CHELLQUIST Division of Cutaneous Hazards, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129 Search for other works by this author on: Oxford Academic Google Scholar E. A. SHIPWASH, E. A. SHIPWASH Division of Cutaneous Hazards, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129 Search for other works by this author on: Oxford Academic Google Scholar W. W. JEDERBBRG, W. W. JEDERBBRG Division of Cutaneous Hazards, Letterman Army Institute of Research, Presidio of San Francisco, CA 94129 Search for other works by this author on: Oxford Academic Google Scholar G. G. KRUEGER G. G. KRUEGER Division of Dermatology/Department of Medicine, University of Utah Medical Center, Salt Lake City, Utah 84132, U. S. A. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 111, Issue s27, 1 July 1984, Pages 123–135, https://doi.org/10.1111/j.1365-2133.1984.tb15590.x Published: 01 July 1984
Stem cell factor induces phosphatidylinositol 3′-kinase–dependent Lyn/Tec/Dok-1 complex formation in hematopoietic cells
Authors: Thamar B. van Dijk, Emile van den Akker, Martine Parren-van Amelsvoort, Hiroyuki Mano, Bob Löwenberg, Marieke von Lindern
Journal: Blood (2000)
Receptor Tyrosine Kinase Genes Amplified in Glioblastoma Exhibit a Mutual Exclusivity in Variable Proportions Reflective of Individual Tumor Heterogeneity
Authors: Suzanne E. Little, Sergey Popov, Alexa Jury, Dorine A. Bax, Lawrence Doey, Safa Al-Sarraj, Juliane M. Jurgensmeier, Chris Jones
Journal: Cancer Research (2012)

Intratumoral heterogeneity in human solid tumors represents a major barrier for the development of effective molecular treatment strategies, as treatment efficacies will reflect the molecular variegation in individual tumors. In glioblastoma, the generation of composite genomic profiles from bulk tumor samples has allowed one to map the genomic amplifications of putative genetic drivers and to prioritize therapeutic targeting strategies aimed at eradicating the tumor burden. Notably, amplification of multiple receptor tyrosine kinases (RTK) within a single tumor specimen obtained from patients is frequently observed. In this study, use of a detailed multicolor FISH mapping procedure in pathologic specimens revealed a mutual exclusivity of gene amplification in the majority of glioblastoma tumors examined. In particular, the two most commonly amplified RTK genes, EGFR and PDGFRA, were found to be present in variable proportions across the tumors, with one or the other gene predominating in certain areas of the same specimen. Our findings have profound implications for designing efficacious therapeutic regimens, as it remains unclear that how the cells with different gene amplification events contribute to disease propagation or the response to molecular targeted therapies.
Does DOTS work in populations with drug-resistant tuberculosis?
Authors: Kathryn DeRiemer, Lourdes García-García, Miriam Bobadilla-del-Valle, Manuel Palacios-Martínez, Areli Martínez-Gamboa, Peter M Small, José Sifuentes-Osornio, Alfredo Ponce-de-León
Journal: The Lancet (2005)
Pathways to PTSD, Part II: Sexually Abused Children
Authors: Julie B. Kaplow, Kenneth A. Dodge, Lisa Amaya-Jackson, Glenn N. Saxe
Journal: American Journal of Psychiatry (2005)

OBJECTIVE: The goal of this research was to develop and test a prospective model of posttraumatic stress symptoms in sexually abused children that includes pretrauma, trauma, and disclosure-related pathways. METHOD: At time 1, several measures were used to assess pretrauma variables, trauma variables, and stress reactions upon disclosure for 156 sexually abused children ages 8 to 13 years. At the time 2 follow-up (7 to 36 months following the initial interview), the children were assessed for posttraumatic stress disorder (PTSD) symptoms. RESULTS: A path analysis involving a series of hierarchically nested ordinary least squares multiple regression analyses indicated three direct paths to PTSD symptoms: avoidant coping, anxiety/arousal, and dissociation, all measured during or immediately after disclosure of sexual abuse. Additionally, age and gender predicted avoidant coping, while life stress and age at abuse onset predicted symptoms of anxiety/arousal. Taken together, these pathways accounted for approximately 57% of the variance in PTSD symptoms. CONCLUSIONS: Symptoms measured at the time of disclosure constitute direct, independent pathways by which sexually abused children are likely to develop later PTSD symptoms. These findings speak to the importance of assessing children during the disclosure of abuse in order to identify those at greatest risk for later PTSD symptoms.
Mucosal irritation potential of polyelectrolyte multilayer capsules
Authors: Liesbeth J. De Cock, Joke Lenoir, Stefaan De Koker, Vincent Vermeersch, Andrei G. Skirtach, Peter Dubruel, Els Adriaens, Chris Vervaet, Jean Paul Remon, Bruno G. De Geest
Journal: Biomaterials (2010)
Fidelity of the repertoire in T cell reconstituted athymic nude rats. Preservation of a deficit in alloresponsiveness over one year.
Authors: M T Drayson, S M Sparshott, E B Bell
Journal: The Journal of Experimental Medicine (1989)

A single intravenous injection of a relatively small number of T cells contained in the population of rat thoracic duct lymphocytes (TDL) is sufficient to restore to normal the peripheral T cell pool of athymic PVG.rnu/rnu nude rats. The donor T cells expand greater than 10-15-fold, self-renew, and restore immunocompetency to nude recipients permanently (greater than 2 yr). We asked whether the T cell repertoire was affected by the expansion and self-renewal process. Nude recipients were injected with syngeneic PVG TDL that had been allospecifically depleted (negatively selected) by consecutive passage from blood to thoracic duct lymph through two irradiated (DAxPVG)F1 intermediate rats. Negatively selected TDL were tested before transfer by the P----F1 popliteal LN GVH assay and showed a greater than 90% depletion of specific reactivity to DA alloantigens. Surviving cells or their progeny were recovered from LN or TDL of nude recipients 8 and 12 mo after transfer. The deficit in GVH reactivity to the DA haplotype persisted, but normal GVH activity was demonstrated against a third party (AOxPVG)F1 alloantigen. The "hole" in the repertoire could not be attributed to tolerance induced by the co-transfer of contaminating irradiated F1 TDL. PVG TDL passaged consecutively through (AOxPVG)F1 and (DAxPVG)F1 intermediates and devoid of (AOxPVG)F1 cells remained specifically depleted to both AO and DA haplotypes when recovered from nude recipients 4 and 13 mo later, but displayed GVH activity to a third-party (BNxPVG)F1 alloantigen. Thus the exact specificity of the T cell repertoire of the original inoculum was faithfully maintained in nude recipients throughout the initial phase of rapid expansion and the continued self-renewal of the mature peripheral T cell pool.
Unusual Locations of Involvement by Malignancies
Authors: H. Padmanabhan, L.D. Ehrlich, M. Quazedo, T. Fojo, A. Louie, M. Walther, K. Pacak
Journal: Journal of Clinical Oncology (2003)

Article Tools DIAGNOSIS IN ONCOLOGY Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2003.09.100 Journal of Clinical Oncology - published online before print September 21, 2016 PMID: 12947075 Unusual Locations of Involvement by Malignancies CASE 2. METASTATIC PHEOCHROMOCYTOMA TO THE COLON H. PadmanabhanxH. PadmanabhanSearch for articles by this author , L.D. EhrlichxL.D. EhrlichSearch for articles by this author , M. QuazedoxM. QuazedoSearch for articles by this author , T. FojoxT. FojoSearch for articles by this author , A. LouiexA. LouieSearch for articles by this author , M. WaltherxM. WaltherSearch for articles by this author , K. PacakxK. PacakSearch for articles by this author Show More National Institutes of Health, Bethesda, MD, and George Washington University Medical Center, Washington, DC https://doi.org/10.1200/JCO.2003.09.100 First Page Full Text PDF Figures and Tables © 2003 by American Society of Clinical Oncology
Acidosis Dilates Brain Parenchymal Arterioles by Conversion of Calcium Waves to Sparks to Activate BK Channels
Authors: Fabrice Dabertrand, Mark T. Nelson, Joseph E. Brayden
Journal: Circulation Research (2011)

Acidosis is a powerful vasodilator signal in the brain circulation. However, the mechanisms by which this response occurs are not well understood, particularly in the cerebral microcirculation. One important mechanism to dilate cerebral (pial) arteries is by activation of large-conductance, calcium-sensitive potassium (BK(Ca)) channels by local Ca(2+) signals (Ca(2+) sparks) through ryanodine receptors (RyRs). However, the role of this pathway in the brain microcirculation is not known.The objectives of this study were to determine the mechanism by which acidosis dilates brain parenchymal arterioles (PAs) and to elucidate the roles of RyRs and BK(Ca) channels in this response.Internal diameter and vascular smooth muscle cell Ca(2+) signals were measured in isolated pressurized murine PAs, using imaging techniques. In physiological pH (7.4), vascular smooth muscle cells exhibited primarily RyR-dependent Ca(2+) waves. Reducing external pH from 7.4 to 7.0 in both normocapnic and hypercapnic conditions decreased Ca(2+) wave activity, and dramatically increased Ca(2+) spark activity. Acidic pH caused a dilation of PAs which was inhibited by about 60% by BK(Ca) channel or RyR blockers, in a nonadditive manner. Similarly, dilator responses to acidosis were reduced by nearly 60% in arterioles from BK(Ca) channel knockout mice. Dilations induced by acidic pH were unaltered by inhibitors of K(ATP) channels or nitric oxide synthase.These results support the novel concept that acidification, by converting Ca(2+) waves to sparks, leads to the activation of BK(Ca) channels to induce dilation of cerebral PAs.