tbuckley/cabot-search huggingface dataset:
Pharyngeal Size in Snorers, Nonsnorers, and Patients with Obstructive Sleep Apnea
Authors: T. Douglas Bradley, Ian G. Brown, Ronald F. Grossman, Noe Zamel, Denis Martinez, Eliot A. Phillipson, Victor Hoffstein
Journal: New England Journal of Medicine (1986)

We measured pharyngeal cross-sectional area and its change with alterations in lung volume in 10 subjects who snored and had obstructive sleep apnea, 6 subjects who snored and did not have obstructive sleep apnea, and 9 subjects who did not snore. Pharyngeal area was measured with use of an acoustic-reflection technique. We found that snorers with and without sleep apnea had a significantly smaller mean (+/- SE) pharyngeal cross-sectional area (4.1 +/- 0.2 and 3.7 +/- 0.9 cm2, respectively) at functional residual capacity than nonsnorers (5.4 +/- 0.5 cm2, P less than 0.025). When lung volume decreased from functional residual capacity to residual volume, both nonsnorers and snorers with sleep apnea had a decrease in pharyngeal area (from 5.4 +/- 0.5 to 4.5 +/- 0.4 cm2 and 4.1 +/- 0.2 to 3.4 +/- 0.2 cm2, respectively), whereas snorers without sleep apnea had no such decrease, suggesting that their pharynxes were less collapsible at low lung volumes. We conclude that snorers with and without sleep apnea have smaller pharyngeal cross-sectional areas than nonsnorers and that snorers with sleep apnea have a further decrease as lung volume falls.
CB-14 * GENOMIC APPROACHES TO IDENTIFY CODING AND NONCODING RNA TARGETS IN MEDULLOBLASTOMA
Authors: C. Penas, M. Zhang, J. Clarke, V. Stathias, M. Roussel, M. Hatten, N. Ayad
Journal: Neuro-Oncology (2014)

Medulloblastoma is the most common malignant pediatric brain tumor. Despite recent treatment advances, approximately 40% of children experience tumour recurrence, and 30% will die from this disease. Medulloblastoma includes four groups (SHH, WNT, Group 3 and Group 4), which show differences in karyotype, histology, and prognosis. Since some of these tumors originate from granule cell progenitors (GCPs) of the cerebellum a better understanding of the mechanisms controlling progenitor cycle exit and differentiation could unravel new promising targets for medulloblastoma. To gain insight into the mechanisms controlling GCP proliferation and differentiation, we performed RNA sequencing of GCPs at different stages of differentiation. These cells originate in the external germinal layer (EGL) of the cerebellum, undergo predominantly symmetric divisions during early postnatal EGL development, and exit the cell cycle within a narrow time frame. We studied GCP cell cycle exit and obtained several differentially expressed lncRNAs governing neuronal differentiation. We demonstrate that some of these lncRNAs are involved in GCP cell cycle exit and are potentially dysregulated in mouse models of medulloblastoma. Further, we demonstrate that the Anaphase Promoting Complex/cyclosome (APC/C) is also potentially dysregulated in medulloblastoma, thus leading to uncontrolled cell proliferation via lncRNA expression. These studies underscore a previously unappreciated role for APC/C in controlling epigenetic pathways in medulloblastoma.
Abstract 1309: Inhibition of the ATR/CHEK1 pathway overcomes reduced sensitivity to ionizing radiation associated with distal 11q loss
Authors: Madhav Sankunny, Susanne M. Gollin
Journal: Cancer Research (2010)

Abstract Genetic changes play a significant role in carcinogenesis. A commonly observed genetic alteration is amplification of chromosomal band 11q13. This has been reported at relatively high frequency in breast, ovarian, head and neck (HNSCC), and lung carcinomas. Previous studies in our lab have shown that the breakage-fusion-bridge (BFB) cycle mechanism responsible for this amplification results in distal 11q loss with concomitant loss of critical DNA damage response (DDR) genes, like ATM, MRE11A, and H2AFX. We showed in HNSCC that distal 11q loss leads to a defective DDR and decreased sensitivity to DNA damaging agents like ionizing radiation (IR). Further, HNSCC, Non-Small Cell Lung Carcinoma (NSCLC), and ovarian carcinoma cell lines with partial copy number loss of distal 11q show reduced sensitivity to IR and overexpression of the ATR/CHEK1 pathway. siRNA knockdown of CHEK1 in carcinoma cell lines with distal 11q loss resulted in 60-70% decreased cell survival in response to a single dose of IR. Cell lines without distal 11q loss did not show differential sensitivity to IR. These findings have led us to investigate whether these cell lines show decreased sensitivity to other DNA damaging agents such as various chemotherapeutic drugs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1309.
Abstract P3-12-08: Molecular Breast Cancer Subtypes in Women from Northeast China: Eight-Year Retrospective Study about Clinicopathologic Features and Survival
Authors: G Nie, A-p Shi, D Song, M Yang, T Fu, S-j Li, B Han, G Zhao, D Wu, H-y Jia, Z-m. Fan
Journal: Cancer Research (2010)

Abstract Background and objectives: Analysis of gene expression has identified various molecular subtypes. These molecular subtypes defined by immunohistochemistry expression of estrogen receptor (ER) or progesterone receptor (PR) and human epidermal growth factor receptor 2 (Her2) : luminal A, luminal B, basal cell-like and HER2-expresing. This study evaluates clinical and pathologic features and survival of the four molecular subtypes in premenopausal and postmenopausal women from northeast China. Methods: A retrospective analysis of 1214 women diagnosed with breast cancer from 2000 to 2007 in Breast Surgery Department, First Hospital of Jilin University. Four molecular breast cancer subtypes defined as: luminal A (ER+ and/or PR+, HER2-), luminal B (ER+ and/or PR+, HER2+), basal-like (ER-, PR-, HER2-), and HER2-expresing, (ER-, PR-, and HER2+). We examined the prevalence of breast cancer subtypes and analyzed the associations with patient clinicopathologic features: age, menopausal status, tumor size, lymph node status, stage of cancer at diagnosis, histological characteristics, and breast cancer-specific survival. Results: Among the all cases, the luminal A subtype was the most prevalent in our study sample (56.0%) compared with basal -like (18.5%), luminal B (13.7%), and HER2-expresing subtypes (11.8%). The four molecular subtypes differed significantly by menopausal status (P=0.011), age (P&amp;lt;0.001) and lymph node status (P&amp;lt;0.001). Luminal A subtype was more likely to with Stage II breast cancer (P&amp;lt;0.001) and most present with size of 2.1-5 cm (P&amp;lt;0.001). The luminal B and the HER2-expresing subtypes presented an increased association with more aggressive clinical course when compared with others subtypes. The estimated median follow-up period for all subjects was 54 months (range, 1 month to 120 months). The 8-year overall survival for all patients was 81.3% (95%CI, 79.4-83.7) and disease-free survival was 77.8% (95% CI, 75.4-79.9). The Kaplan-Meier curve showed breast cancer-specific survival differed significantly among the molecular subtypes (P &amp;lt; 0.03), with the luminal B and HER2-expresing subtypes having the poorest outcome. Conclusion: Luminal A breast tumor appeared the better outcome than the others three subtypes and the shortest survival was HER2-expresing subtype. The poor clinical outcomes of luminal B subtype with women from northeast China were different from those of Western women could contribute to the poor prognosis of breast cancer observed in this cohort of patients and some of them couldn't accept molecular targeted therapy with trastuzumab by poor economic situations. Figure available in online version. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P3-12-08.
Anuria Secondary to Bilateral Renal-Artery Embolism
Authors: Donald A. Duncan, Richard N. Dexter
Journal: New England Journal of Medicine (1962)

OCCLUSION of both renal arteries or their branches by emboli is not a common cause of acute anuria. Recognition of this entity is important, nevertheless, for a combination of prompt surgical intervention, good medical management and dialysis with the artificial kidney, if needed, should offer some chance of reversing an otherwise hopeless prognosis. A case of bilateral renal-artery embolism is presented to call attention to the problem and to stress the value of vigorous therapy despite an already prolonged period of anuria.Case ReportB.N. (U.M.H. 970378), a 57-year-old janitor, was admitted to the University of Minnesota Hospitals on April . . .
Absence of Association of Thrombophilia Polymorphisms with Intrauterine Growth Restriction
Authors: Claire Infante-Rivard, Georges-Etienne Rivard, Wagner V. Yotov, Emmanuelle Génin, Marguerite Guiguet, Clarice Weinberg, Robert Gauthier, Juan Carlos Feoli-Fonseca
Journal: New England Journal of Medicine (2002)

Previous data have demonstrated associations between thrombophilia polymorphisms in pregnant women and an increased risk of intrauterine growth restriction in their offspring, but this finding remains uncertain.
Role of Imaging Biomarkers in Predicting Anaplastic Lymphoma Kinase–Positive Lung Adenocarcinoma
Authors: Chae Jin Jeong, Ho Yun Lee, Joungho Han, Ji Yun Jeong, Kyung Soo Lee, Yoon-La Choi, Joon Young Choi
Journal: Clinical Nuclear Medicine (2014)

For the ultimately efficient screening of anaplastic lymphoma kinase gene (ALK)-positive cases, combination of radiometabolic characteristics with clinicopathologic features may be more useful. Therefore, we determined radiologic characteristics and metabolic characteristics in patients with adenocarcinoma harboring ALK mutations.We retrospectively reviewed clinicopathologic CT and PET/CT data from patients with advanced lung adenocarcinoma screened for identifying ALK rearrangement. Lesion size, solidity, location, margins, CT attenuation, and SUVmax were assessed. Pathologic features such as differentiation, the presence of signet ring cell, EGFR/KRAS mutation status, and TTF-1 expression were also reviewed.Of the screened 221 patients, 41 patients (19%) demonstrated ALK rearrangements, and these individuals were younger than the ALK-negative patients (P < 0.001) and showed significant association with no exposure to tobacco (P = 0.028). ALK-positive lung adenocarcinomas were significantly less differentiated than those without rearrangements (P = 0.005). ALK-positive tumors showed significantly higher SUVmax than ALK-negative tumors (P = 0.016). Multivariate logistic regression modeling for predicting the ALK-positive lung adenocarcinoma disclosed that lower CT attenuation and higher SUVmax were significant independent factors of ALK rearrangements (odds ratio, 0.87 and 1.06; P = 0.03 and 0.01, respectively). Receiver operating characteristic analysis showed that the area under the receiver operating characteristic curve for SUVmax/CT attenuation ratio was 0.788, and the optimal cutoff value of SUVmax/CT attenuation ratio for identifying ALK-positive lung adenocarcinoma was greater than or equal to 0.208 (sensitivity, 74.2%; specificity, 81.0%).This study shows that ALK-rearranged lung adenocarcinoma represents younger age, no history of smoking, the absence of spiculation on CT, and higher SUVmax/CT attenuation greater than or equal to 0.208 compared with those without ALK mutation.
Abstract 3681: Aspirin acetylates glucose 6 phosphate dehydrogenase and inhibits its activity in colon cancer cells.
Authors: Guoqiang Ai, Fred K. Hagen, Jayarama B. Gunaje
Journal: Cancer Research (2013)

Abstract Epidemiological studies have demonstrated a significant correlation between regular aspirin use and reduced colon cancer incidence and mortality. Although a consensus is emerging on the view that aspirin has significant anti-cancer properties, it is not yet clear which pathways or molecular targets might be involved. We hypothesized that aspirin's anti-cancer effect may occur through acetylation of a panel of protein targets, including novel candidates with modulated functional activity, as a result of aspirin-mediated acetylation. In the present study, using anti-acetyl lysine antibody, we determined aspirin-mediated protein acetylation profiles in three different colon cancer cell lines namely HCT-116, HT-29 and GC3/c1, by treating cells with aspirin at different concentration, and analyzing them in Western Blot. We observed that in all cell lines tested, aspirin induced acetylation of multiple proteins in a concentration dependent fashion spanning a molecular weight range from 20 to 200 kDa. Aspirin's acetylation targets included the tumor suppressor protein p53, and glucose 6 phosphate dehydrogenase (G6PD), an enzyme in the pentose phosphate pathway. Mass spectrometry analysis of the recombinant G6PD, treated with aspirin in vitro, revealed acetylation of up to 14 distinct lysine residues, including lysine 235 at its active site. In vitro G6PD assay in lysates isolated from the cancer cell lines showed that aspirin caused a 70% decrease in the G6PD enzyme activity in HCT116 cells; however, the reduction in the enzyme activity was less in HT-29/GC3/c1 cells (up to 30%). Inhibition of G6PD activity leading to a reduction in ribonucleotide synthesis and cell proliferation may represent an important mechanism by which aspirin exerts its anticancer effects. Citation Format: Guoqiang Ai, Fred K. Hagen, Jayarama B. Gunaje. Aspirin acetylates glucose 6 phosphate dehydrogenase and inhibits its activity in colon cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3681. doi:10.1158/1538-7445.AM2013-3681
AB0796 Characterization of Mononuclear Cells in Osteoarthritis Synovial Fluid Monocytes
Authors: S.-J. Yoo, J. Kim, S. Lee, I.-S. Yoo, S.-C. Shim, M.-H. Kwon, C.-I. Joung, S.-W. Kang
Journal: Annals of the Rheumatic Diseases (2014)

A key outcome of chronic antigenic stimulation in the setting of sustained inflammation is the development of CD8<sup>+</sup> T cell exhaustion. However, the relative roles of inflammation and antigen stimulation on T cell dysfunction remain unclear. Inborn errors of immunity (IEIs) provide an opportunity to study the effect of genetic alterations in signaling pathways on immune function. Here, we focus on an IEI resulting from genetically amplified cytokine signaling: gain-of-function mutations in STAT3 (STAT3 GOF). STAT3 signals downstream of multiple inflammatory cytokines (e.g., IL-6 and IL-27) and we used STAT3 GOF as a genetic mimic of chronic inflammation. To assess how amplified STAT3 signaling impacts immune cell subset distribution and activation status, PBMCs from STAT3 GOF patients and age-matched healthy controls were profiled via mass cytometry (CyTOF). This revealed altered states of CD8<sup>+</sup> T cell activation including increased expression of immunoregulatory receptors (e.g., PD-1 and CD39). STAT3 GOF CD8<sup>+</sup> T cells also showed impaired cytokine production and reduced proliferative capacity. Bulk RNA sequencing of naïve STAT3 GOF CD8<sup>+</sup> T cells identified an exhausted-like transcriptional profile. Quantitation of metabolic function shows alterations in glucose use and oxidative phosphorylation in STAT3 GOF. Our studies suggest that inflammation alone may directly impair CD8<sup>+</sup> T cell function. Understanding the mechanisms by which inflammation impacts T cell function may identify components of T cell dysregulation that can be targeted therapeutically in these rare patients, as well as those with more common inflammatory diseases (e.g., obesity) with shared aspects of T cell dysfunction. Supported by CHOP Research Institute, The Primary Immune Deficiency Treatment Consortium (PIDTC) and Immune Deficiency Foundation (IDF).&nbsp;
Thoracic 131I Uptake After Previous Pneumonectomy in Patients Treated for Differentiated Thyroid Cancer
Authors: Camila Nascimento, Boumédiène Bridji, Catherine Dejax, Martin Schlumberger, Sophie Leboulleux
Journal: Clinical Nuclear Medicine (2012)

In patients treated for differentiated thyroid cancer with radioiodine (131I), abnormal uptake on post-therapeutic whole-body scan may lead to repeated administration of 131I. Uptake not linked to thyroid cancer but to other conditions should be recognized so that patients are not overtreated. We describe 3 cases of unilateral thoracic 131I uptake in patients previously treated by pneumonectomy for lung cancer, without evidence of persistent lung cancer.
HIGH FREQUENCY OF HYPERTENSIVE INTRACEREBRAL HEMORRHAGE AS A CAUSE OF SUDDEN UNEXPECTED DEATH IN ASIAN POPULATION
Authors: Kamonchanok Jongyotha, Pattara Rattanawong, Wasawat Vutthikraivit, Napatt Kanjanahattakij, Prapaipan Putthapiban, Weera Sukhumthammarat, Pongthep Rajsirisongsri, Therdtoon Waungpaibulkij, Jenya Jutakeo, Chumsab Rattanaruangrit, Peeraya Piancharoen, Prin Vathesatogkit, Tachapong Ngarmukos, Smith Srisont
Journal: Journal of the American College of Cardiology (2016)
AB1156-HPR Do Rheumatic Patients under Biological Therapy Receive More Attention from Their Doctors Compared with Those Who do not Receive Such Therapy?
Authors: M. Dobroiu, D. Vasile, C. Ioan, J. Moca, M. Dragan, M. Ciobanu, M. Zamfira, C. Aproianu, D. Predeteanu, R. Ionescu, F. Berghea
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Chronic rheumatic patients come in contact with health system more often than regular people that give them the opportunity to better identify both the strengths and weakness of this system. Rheumatic patients that receive biological therapy (BIOTh) are a special group of chronic patients usually having more severe diseases and a potential for additional complications throughout their disease. Independent of these, rheumatic patients receiving biologics are frequent subjects of observational studies including various types of medical registers. Sometime they are compared with rheumatic patients that do not receive biological treatment (nBIOTh) but do these two different kind of patients receive same attention from the medical system? If the answer is different from yes then we might experience a bias in these studies. <h3>Objectives</h3> To evaluate a possible difference between BIOTh and nBIOTh in terms of medical attention these groups receive. <h3>Methods</h3> We used a standardized patient satisfaction survey to perform an indirect measurement of the medical attention received by every patient. The surveys covers eight distinct areas split in 23 items: patient9s needs, existence of coordinated medical help, easiness of access to medical care, support for information, physical comfort, emotional support, support for proper family relationship, global perception. The survey was conducted in three academic hospitals. Data analysis was done by using SPSS 19 software. <h3>Results</h3> A number of 84 patients have been included in BIOTh group and 44 in nBIOTh group. No significant difference in terms of underling disease, education, sex and access to medical services was found between groups. Mean age was a little bit higher in nBIOTh than in BIOTh: 52,2 (13,5) vs 50,2 (13,2) years but we considered this difference not significant for the purpose of this study. We found a systematic difference between groups that favor BIOTh as following: in 7 of the 23 items evaluated, the patient satisfaction was significant higher in case of subjects under biological therapy, in the remaining 18 items no statistical difference occurred; no item favored patients without biological therapy. The difference was even higher when BIOTh group was restricted to those subjects with more than two years of biological therapy. <h3>Conclusions</h3> Our results suggest that chronic rheumatic patients on biological therapy seems to receive more attention than rheumatic patients that do not receive such therapy. This conclusion is particularly important for those observational studies that compare data from patients exposed and not exposed to biological therapy. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2282
Abstract 5300: Identification and validation of novel autoantibodies for the detection of malignant mesothelioma.
Authors: Xufei Zhang, Lei Zhao, Weike Shen, Kemp Kernstine, Li Zhong
Journal: Cancer Research (2013)

Abstract Malignant mesothelioma (MM) survival rate has been hampered by the lack of efficient and accurate early detection methods. The immune system may detect the early changes of tumor progression by responding with tumor-associated autoantibody production. Hence, in this study, we translated the humoral immune response to cancer proteins into a valuable blood test for MM. A T7 phage MM cDNA library was constructed using MM tumor tissues and biopanned for tumor-associated antigens (TAAs) using pooled MM patients and normal serum samples. About 1000 individual phage TAAs clones from the biopanned library were subjected for protein microarray construction and tested with 53 MM and 52 controls serum samples as a training group. The classifiers developed from the training group were further validated with 50 patient and 50 normal serum samples as an independent blind validation. Nine candidate autoantibody markers were selected by logistic regression and Treeview statistical analysis as a detecting panel. In the training set, sensitivity of 92.5% and specificity of 90.4% were reached with an AUC was 0.898 in Receiver Operating Characteristic analysis. For validation test, 86.5% sensitivity and 86.8% specificity were achieved with an AUC of 0.825. Among these 9 candidate markers, five were found to be strongly cancer associated proteins (PDIA6, MEG3, SDCCAG3, IGHG3, IGHG1). Our results achieved much greater accuracies than any other current biomarkers for MM detection and hence could be a useful tool to assess cancer risk in high-risk populations. Citation Format: Xufei Zhang, Lei Zhao, Weike Shen, Kemp Kernstine, Li Zhong. Identification and validation of novel autoantibodies for the detection of malignant mesothelioma. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5300. doi:10.1158/1538-7445.AM2013-5300 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
Allelic loss of 11q13 as detected by MEN1-FISH is not associated with mutation of the MEN1 gene in lymphoid neoplasms
Authors: C Thieblemont, S Pack, A Sakai, M Beaty, E Pak, AO Vortmeyer, A Wellmann, Z Zhuang, ES Jaffe, M Raffeld
Journal: Leukemia (1999)
Cardiolipin-mediated procoagulant activity of mitochondria contributes to traumatic brain injury–associated coagulopathy in mice
Authors: Zilong Zhao, Min Wang, Ye Tian, Tristan Hilton, Breia Salsbery, Eric Z. Zhou, Xiaoping Wu, Perumal Thiagarajan, Eric Boilard, Min Li, Jianning Zhang, Jing-fei Dong
Journal: Blood (2016)
CARDIOVASCULAR MORTALITY AND MYOCARDIAL INFARCTION AFTER RADIATION THERAPY FOR LEFT VERSUS RIGHT SIDED BREAST CANCER: A META-ANALYSIS
Authors: Marcio Sommer Bittencourt, Milan Vecsey-Nagy, Marilia Santos, Carolina Silva, Silvia M. Fonseca, Cristina S. Bittar, Paulo G. Hoff, Roberto Kalil-Filho, Ludhmila A. Hajjar
Journal: Journal of the American College of Cardiology (2016)