tbuckley/cabot-search huggingface dataset:
Abstract LB-183: Association of aberrant promoter methylation of novel genes with clinicalpathology and prognosis of urothelial carcinoma
Authors: Ching Fei Li, Te-Chang Lee, Sheng-Shin Alexander Wang, Yeong-Shiau Pu
Journal: Cancer Research (2011)

Abstract DNA methylation profiles are one of valuable biomarkers to molecularly define cancer subtypes that may serve as better indicators for disease progression, treatment and prognosis. In the present study, we investigated the aberrant promoter methylation of 5 tumor-related genes, CCND1, CHFR, FAM51A1, LGALS4, and RBBP7, which were selected from pooled DNA methylation profiles of urothelial carcinoma (UC) with various clinicopathological parameters. DNA was extracted from 90 patients with confirmed UC and 10 adjacent non-tumor controls. Promoter aberrant methylation of these 5 genes was determined by quantitative methylation-specific PCR (qMSP). Our results showed that methylation levels were higher in UC as compared with controls in promoter of CHFR, FAM51A1, LGALS4, and RBBP7 (6.24 vs. 4.27; 0.66 vs. 0.01; 7.47 vs. 2.14; 0.45 vs. 0.01, respectively). Among UC patients, the levels of promoter methylation of CCND1, CHFR and LGALS4 were significantly associated with tumor stages (p&amp;lt; 0.01), whereas that of FAM51A1 was inversely associated with tumor stages (p=0.012). Tumors with poor differentiation showed higher levels of promoter methylation on CCND1, CHFR and LGALS4 genes than tumors with moderate differentiation (p&amp;lt;0.05). UC patients with highly methylated CCND1, CHFR, LGALS4 or RBBP7 tended to have a poor survival than patients with low levels of methylated gene (p&amp;lt;0.02). This is the first report to show the association of promoter methylation of these 5 genes with UC tissues. We anticipate that the methylation status of these novel marker genes may have great clinical implications for further classifying UC patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-183. doi:10.1158/1538-7445.AM2011-LB-183
564 TLR4 INDUCTION BY TUDCA IN EXPERIMENTAL MODELS OF SYNGENEIC AND ALLOGENEIC STEATOTIC LIVER TRANSPLANTATION
Authors: M.B. Jiménez-Castro, M. Elias-Miró, M. Mendes-Braz, M. Massip-Salcedo, A. Rimola, J. Rodés, A. Casillas-Ramírez, C. Peralta
Journal: Journal of Hepatology (2013)
Early ERCP and Papillotomy Compared with Conservative Treatment for Acute Biliary Pancreatitis
Authors: Ulrich R. Fölsch, Rolf Nitsche, Rainer Lüdtke, Reinhard A. Hilgers, Werner Creutzfeldt
Journal: New England Journal of Medicine (1997)

The role of early endoscopic retrograde cholangiopancreatography (ERCP) and papillotomy in the treatment of patients who have acute biliary pancreatitis without obstructive jaundice is uncertain.
Postprandial Lipemia in Health and in Ischemic Heart Disease
Authors: David F. Brown, A. Sandra Heslin, Joseph T. Doyle
Journal: New England Journal of Medicine (1961)

IT has long been recognized that patients with ischemic heart disease may exhibit abnormalities in serum lipid patterns. Although cholesterol metabolism in ischemic heart disease has received a vast amount of study over the years, emphasis has only recently been placed on the possible role of abnormal triglyceride metabolism in this disorder. Albrink and Man1 have described elevated fasting triglyceride levels in ischemic heart disease. Differences in serum triglyceride levels have recently been reported in racial groups with widely differing incidence of ischemic heart disease.2 Brown et al.3 have shown that elevated cholesterol levels tend to be paralleled by an . . .
PWE-031 The potential of haem transport proteins as therapeutic targets in the treatment of oesophageal adenocarcinoma
Authors: S J Ford, M Bedford, O Tucker, D Alderson, T H Iqbal, C Tselepis
Journal: Gut (2012)

<h3>Introduction</h3> Epidemiological evidence supports the potential role of dietary haem iron in gastrointestinal carcinogenesis.<sup>1 2</sup> Oesophageal cancer cells acquire inorganic and organic iron by progressive up-regulation of iron and haem transport proteins.<sup>3</sup> These alterations result in increased cellular iron loading which is likely to drive cellular proliferation.<sup>3</sup> The effect of perturbing haem import proteins, hemopexin receptor (LRP1) and haem carrier protein (HCP1), on cancer cell iron transport, phenotype and tumour burden is unknown. The aim was to determine the in vitro and in vivo effects of depriving oesophageal cancer cells of haem iron. <h3>Methods</h3> Stable knock-downs of LRP1 and HCP1 were created by infection with specific shRNA lenti-viral vectors. Successful knock-down was confirmed by Western blotting. The effect on cellular iron transport and cell phenotype was assessed by qRT-PCR and phenotypic experiments for viability, proliferation, migration and anchorage independent growth. Stable knock-downs of LRP1 and HCP1 were then xenografted into NOD-SCID mice as an in vivo model of oesophageal adenocarcinoma. <h3>Results</h3> Perturbation of LRP1 and HCP1 caused a compensatory up-regulation of inorganic iron import proteins and a decrease in iron storage capacity. Neoplastic activity was significantly impaired compared to control (proliferation, viability, colony forming and migration – all p=&lt;0.01). Loss of active haem iron import significantly reduced xenograft tumour burden in murine models with a 70% (p=0.014) and 58% (p=0.05) reduction in average xenograft weight compared to control. <h3>Conclusion</h3> Haem import significantly contributes to iron loading in oesophageal cancer cells and creates a more aggressive phenotype. Functional inhibition of haem importing proteins LRP1 and HCP1 curbs neoplastic activity and significantly reduces in vivo tumour burden in murine models. Haem iron transport proteins are potential therapeutic targets in the treatment of oesophageal adenocarcinoma. <h3>Competing interests</h3> None declared. <h3>References</h3> 1. <b>Cross AJ</b>, Freedman ND, Ren J, <i>et al.</i> Meat consumption and risk of esophageal and gastric cancer in a large prospective study. <i>Am J Gastroenterol</i> 2011;<b>106</b>:432–42. 2. <b>Cross AJ</b>, Leitzmann MF, Gail MH, <i>et al.</i> A prospective study of red and processed meat intake in relation to cancer risk. <i>PLoS Med</i> 2007;<b>4</b>:e325. 3. <b>Boult J</b>, Roberts K, Brookes MJ, <i>et al.</i> Overexpression of cellular iron import proteins is associated with malignant progression of esophageal adenocarcinoma. <i>Clin Cancer Res</i> 2008;<b>14</b>:379–87.
Relative Reliability of Five Serially Measured Markers for Prognosis of Progression in Prostate Cancer&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: C S Killian, L J Emrich, F P Vargas, N Yang, M C Wang, R L Priore, G P Murphy, T M Chu
Journal: JNCI Journal of the National Cancer Institute (1986)

During an 8-year period, 1,065 serum specimens were collected from 79 patients with prostate cancer of stages B2 to D1 (group I) and 51 patients with newly diagnosed stage D2 prostate cancer (group II) to evaluate statistically the relative reliability of elevated tumor-associated markers for progressive disease in prostate cancer. Forty of the group I patients and 21 of the group II patients presented a clinical progression of disease during follow-up. With the use of Gail's modification of Cox's regression model, serial acid phosphatase (AcP), total alkaline phosphatase (TAP), bone alkaline phosphatase (BAP), prostatic acid phosphatase (PAP), and prostate-specific antigen (PA) were analyzed. Results from group I patients revealed that only PA (P = .0002) and PAP (P = .0684) were prognostically important markers for detection of imminent disease progression. However, all markers were prognostically important in group II patients. Comparative studies indicated that PA (P = .0052) and PAP (P = .0359) were the more reliable markers for group I patients, whereas PA (P less than .0001), BAP (P = .0007), and PAP (P = .0206) were the more reliable markers for group II patients. Multivariate analyses revealed that, after adjustment for the effect of PA, no other marker was significantly related to the risk of progression. Elevated PA levels were predictive of increased risk 6 months before disease progression in group I patients only (P less than .0001). Overall, the apparent order of prognostic reliability for disease progression was found to be PA greater than PAP greater than BAP greater than AcP greater than TAP.
COMBINED ASSESSMENT OF CAROTID INTIMA-MEDIA THICKNESS AND LEFT VENTRICULAR CONCENTRIC HYPERTROPHY PREDICT CARDIOVASCULAR DEATH IN HEMODIALYSIS PATIENTS
Authors: Hisao Yoshikawa, Suzuki Makoto, Go Hashimoto, Masato Nakamura, Kaoru Sugi
Journal: Journal of the American College of Cardiology (2015)
THU0583-HPR Living with Pain in Ankylosing Spondylitis: A Qualitative CASE Study
Authors: G. Bagcivan, F.I. Cinar, M. Cinar, F. Oflaz, S. Uzun, S. Pay
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Pain, stiffness, fatigue and sleep problems are the most important symptoms of ankylosing spondylitis (AS) patients. Among these symptoms, inflammatory back pain is a major symptom reported by all AS patients. Although there are various quantitative studies reporting that pain is one of the most serious and prevalent problems during the course of AS, there are no detailed qualitative studies on how pain affects the AS patients physically, socially, emotionally, and economically. <h3>Objectives</h3> The aim of this study was to determine the pain experiences of patients with AS and the effect of pain on their lives by the method of direct interview. <h3>Methods</h3> This qualitative case study included 23 patients with AS. The data was collected by using both a demographic data form and a semi-structured interview form. Each patient was interviewed face-to-face. The data obtained was evaluated using a content analysis method. <h3>Results</h3> The data was analysed in 6 categories and 4 subcategories. The categories included the following: (1) pain as described by the patient, (2) the effect of pain on daily routine activities, (3) the effect of pain on social life, (4) the effect of pain on employment, (5) the effect of pain on family life, and (6) the emotional effects of pain. During periods of pain, patients indicated that they experienced difficulty in carrying out their daily routine activities and in meeting their personal needs. Pain also prevented them from fulfilling their responsibilities in the family, inhibited their social relations and caused trouble at their workplace. Due to the negative effects of pain in their lives, the patients felt helplessness, fear, stress, sadness, and unhappiness. <h3>Conclusions</h3> Besides being asked about the quantity of pain, patients with AS should also be questioned on how pain affects their lives. Such an approach would guide the health care workers in planning and applying health care specific for each individual patient. <h3>References</h3> Chorus AM, Miedema HS, Boonen A, Van Der Linden S: Quality of life and work in patients with rheumatoid arthritis and ankylosing spondylitis of working age. Ann Rheum Dis 2003; 62:1178-84. Hakkou J, Rostom S, Mengat M, Aissaoui N, Bahiri R, Hajjaj-Hassouni N: Sleep disturbance in Moroccan patients with ankylosing spondylitis: prevalence and relationships with disease-specific variables, psychological status and quality of life. Rheumatol Int 2013; 33(2):285-90 Özgül A, Peker F, Taskaynatan MA, Tan AK, Dincer K, Kalyon TA. Effect of ankylosing spondylitis on health-related quality of life and different aspects of social life in young patients. Clin Rheumatol 2006; 25: 168-174 <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2407
NUCLEOCYTOPLASMIC TRANSPORT AND CHANGES IN GENE EXPRESSION IN PATIENTS WITH HEART FAILURE
Authors: Jose Rivera, Mar&iacute;a Pastoriza, Manuel Portoles, Esther Rosell&oacute;-Llet&iacute;, raquel cortes, Antonio Salvador, Estefan&iacute;a Taraz&oacute;n Melguizo, Luis Martinez-Dolz, Luis Almenar, Francisca Lago, Juan Cinca, Anxo Vidal
Journal: Journal of the American College of Cardiology (2012)
Minimally differentiated acute myeloid leukemia in Taiwan: predominantly occurs in children less than 3 years and adults between 51 and 70 years
Authors: S-Y Huang, J-L Tang, S-T Jou, W Tsay, C-H Hu, D-T Lin, K-S Lin, K-S Lin, C-H Wang, Y-C Chen, M-C Shen, H-F Tien
Journal: Leukemia (1999)
Relation of Bacteria to the Failure of Blood-Volume Therapy in Traumatic Shock
Authors: Jacob Fine
Journal: New England Journal of Medicine (1954)

EVIDENCE is offered below that bacterial action may be responsible for the failure of blood-volume therapy in various types of traumatic shock, in which infection appears to be absent or of little consequence. For an appropriate orientation to this thesis the following statement of the terms on which it is based will be helpful.General ConsiderationsTraumatic shock is a state of acute and persisting deficiency of flow through the peripheral circulation that, if sufficiently severe and untreated, grows progressively worse and is rapidly fatal. In virtually all cases the clinical manifestations are as follows: low blood pressure, thready, rapid . . .
PTP1B Deficiency Enables the Ability of a High-Fat Diet to Drive the Invasive Character of PTEN-Deficient Prostate Cancers
Authors: David P. Labbé, Noriko Uetani, Valérie Vinette, Laurent Lessard, Isabelle Aubry, Eva Migon, Jacinthe Sirois, Jody J. Haigh, Louis R. Bégin, Lloyd C. Trotman, Marilène Paquet, Michel L. Tremblay
Journal: Cancer Research (2016)

Abstract Diet affects the risk and progression of prostate cancer, but the interplay between diet and genetic alterations in this disease is not understood. Here we present genetic evidence in the mouse showing that prostate cancer progression driven by loss of the tumor suppressor Pten is mainly unresponsive to a high-fat diet (HFD), but that coordinate loss of the protein tyrosine phosphatase Ptpn1 (encoding PTP1B) enables a highly invasive disease. Prostate cancer in Pten−/−Ptpn1−/− mice was characterized by increased cell proliferation and Akt activation, interpreted to reflect a heightened sensitivity to IGF-1 stimulation upon HFD feeding. Prostate-specific overexpression of PTP1B was not sufficient to initiate prostate cancer, arguing that it acted as a diet-dependent modifier of prostate cancer development in Pten−/− mice. Our findings offer a preclinical rationale to investigate the anticancer effects of PTP1B inhibitors currently being studied clinically for diabetes treatment as a new modality for management of prostate cancer. Cancer Res; 76(11); 3130–5. ©2016 AACR.
Case 20-1995
Authors: P.N. Riskind, E.P. Richardson
Journal: New England Journal of Medicine (1995)

Presentation of CaseA 66-year-old right-handed man was admitted to the hospital because of a right hemiparesis with sensory involvement, aphasia, and agitation with intermittent somnolence.There was a four-year history of questionable rheumatoid arthritis managed with hydroxychloroquine and prednisone in a dose that rose to 40 mg daily during bouts of increased stiffness and swelling. He also used an albuterol inhaler because of dyspnea that was ascribed to chronic obstructive pulmonary disease or rheumatoid lung disease. The patient was otherwise well until approximately 14 weeks before admission, when he experienced vague tingling of the right arm. One week later . . .
Abstract LB-235: Functional SNP in MICA binding to SP1 is associated with HCV-induced hepatocellular carcinoma.
Authors: Paulisally H. Lo, Chizu Tanikawa, Yusuke Nakamura, Koichi Matsuda
Journal: Cancer Research (2013)

Abstract Hepatitis C virus (HCV) infection is the major cause of hepatocellular carcinoma (HCC) in Japan. To understand the genetic basis of HCV related diseases, identification of the susceptibility gene involving HCV-induced HCC is important. We previously identified the association of SNP rs2596542 in the 5′ flanking region of the MHC class I polypeptide-related sequence A (MICA) gene with the risk of HCV-induced HCC. In the current study, we performed detailed functional analysis of 12 candidate SNPs in the promoter region. A SNP rs2596538 located at 2.8 kb upstream of the MICA gene affected the binding of a nuclear protein(s) to the genomic segment including this SNP. By electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay, we identified that transcription factor Specificity Protein 1 (SP1) can bind to the protective G allele, but not to the risk A allele. In addition, reporter construct containing the G allele exhibited higher transcriptional activity than that containing the A allele. SNP rs2596538 exhibited the stronger association with HCV-induced HCC (P = 1.82 x10−5 and OR = 1.34) than the marker SNP rs2596542. We also found significantly higher serum level of soluble MICA (sMICA) in HCV-induced HCC patients carrying the G allele than those carrying the A allele (P = 0.00616). In summary, we have identified a functional SNP that is associated with expression of MICA and risk for HCV-induced HCC. Citation Format: Paulisally H. Lo, Chizu Tanikawa, Yusuke Nakamura, Koichi Matsuda. Functional SNP in MICA binding to SP1 is associated with HCV-induced hepatocellular carcinoma. [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 LB-235. doi:10.1158/1538-7445.AM2013-LB-235
Excessive noise in intensive care units
Authors: Julie L Darbyshire
Journal: BMJ (2016)

Bad for staff and very bad for patients 

Noise levels in the intensive care unit are known to be high. World Health Organization (WHO) guidelines suggest hospital noise levels should average 35 dBA during the day and 30 dBA at night.1 Research conducted by our group in five local units recorded levels just under 60 dBA during the day (equivalent to a busy restaurant) with peaks above 100 dBA 22-28 times every hour. Although it was quieter at night, we still identified peak sounds above 85 dBA up to 16 times an hour.2 These data are consistent with those of other studies. No study in a 2012 review recorded sound levels within WHO recommendations, although some interventions achieved significant reductions in sound levels.3 Staff activities and alarms are primary sources of disturbance in intensive care units,4 but noises from other patients and infrastructure also contribute.

Staff and patients may be in a chronic state of alertness when alarms are constantly sounding. Alarms share characteristics with the human scream and tend to activate areas of the brain that recognise danger. Raised sound levels have been associated …
Plasmacytoma of the Skull
Authors: My-Linh Nguyen, Anand S Patel
Journal: New England Journal of Medicine (2010)

A 42-year-old woman presented with a painless, nickel-sized lump on her scalp that was first noticed by her hairdresser 4 months earlier. Physical examination revealed a firm, nontender, subcutaneous nodule, 6 cm in diameter, and no neurologic deficits. A complete blood count, complete metabolic profile, and urinalysis showed no abnormalities. A computed tomographic scan showed a destructive, well-demarcated, soft-tissue mass, with peripheral bony fragments, emerging from the right frontal calvarium. The mass measured 5 cm by 4 cm and was compressing part of the brain. There was no evidence of a midline shift. The mass was excised, and cranial mesh . . .
Intramuscular Pressures with Limb Compression
Authors: Charles A. Owen, Scott J. Mubarak, Alan R. Hargens, Ladd Rutherford, Lawrence P. Garetto, Wayne H. Akeson
Journal: New England Journal of Medicine (1979)

To study muscle necrosis due to prolonged limb compression, we measured intramuscular pressure by inserting wick catheters into 10 volar forearms and 10 anterior tibial compartments of adult volunteers. We then placed the subjects in positions in which victims of drug overdose are commonly found. Intramuscular pressures in the area of direct compression on hard surfaces ranged from 26 to 240 mm Hg, and averaged 101 mm Hg. Most remarkable was a mean pressure of 180 mm Hg on compression of the forearm by the rib cage. These pressures are sufficient to cause muscle and capillary ischemia and necrosis by local obstruction of the circulation. This local injury by limb compression may produce edema sufficient to start compartment tamponade and consequent muscle-compartment and crush syndromes. (N Engl J Med 300:1169–1172, 1979)
Abstract 4971: The oncometabolite (R)-2-hydroxyglutarate modulates stress-induced caspase activity in glioma cells
Authors: Misty Gilbert, Yinxing Liu, Andrew Morris, Manjula Sunkara, Natasha Kyprinaou, Craig Horbinski
Journal: Cancer Research (2012)

Abstract Point mutations in isocitrate dehydrogenase 1 and 2 (IDH1/2) are present in the majority of WHO grade II and III gliomas, as well as secondary grade IV glioblastomas. These are gain-of-function mutations resulting in the neoenzymatic conversion of alpha-ketoglutarate into R-2-hydroxyglutarate (2HG), which is present in high concentrations (10-30 mM) in mutated gliomas. The mutation appears to be a favorable prognostic marker, suggesting better response to stressors like adjuvant radiation and chemotherapy; however, its effects on cell signaling and glioma cell death are not fully understood. In this study we investigated the impact of 2HG in glioma cell survival pathways. A single pulse of 2HG (30mM) increased phosphorylated Erk (p-Erk 1/2), but not pAkt, in the PTEN-intact glioma cell lines LN18 and LN229. Both p-Erk 1/2 and pAkt were unchanged in the PTEN-deficient cell lines U87 and U138. A single 2HG pulse, followed by prolonged withholding of medium changes, also enhanced caspase 3/7 activity in LN18 cells and LN229 cells, whereas it actually suppressed caspase 3/7 activity in U87 and U138 cells. Pretreatment with the MEK inhibitor UO126 prior to the 2HG pulse suppressed caspase 3/7 activity in LN18 cells, but not in LN229 cells. In U87 cells, the 2HG-induced suppression of caspase 3/7 activity was reversed by UO126, while no change was observed in U138 cells. These data indicate that 2HG can modulate stress-induced cell death in a MAPK/ERK-dependent manner, but that such modulation may vary greatly depending on the occurrence of other genetic aberrations in gliomas. Ongoing studies are pursuing potential mechanisms via which 2HG exerts such functionally divergent effects, aiming to develop better adjuvant therapeutic approaches for IDH-mutant gliomas. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4971. doi:1538-7445.AM2012-4971
Demonstration of Pleural Empyema on Ga-67 Planar and SPECT Imaging
Authors: YU-CHEN CHANG, TZU-CHEN YEN, KAI-YUAN TZEN
Journal: Clinical Nuclear Medicine (1999)

This is a report of a patient with fever of unknown origin who had a clinically unsuspected traumatic pleural empyema detected by a Ga-67 whole-body survey with chest SPECT and confirmed later by CT. After thoracocentesis, pus-like fluid from the pleural cavity was collected. The result of a bacteria smear was Gram-positive cocci. With thoracocentesis and adequate antibiotic treatment, the patient was discharged in stable condition. A follow-up Ga-67 whole-body scan at our outpatient clinic showed no more abnormal accumulation in the pleura or whole body. Thus, we suggest that the Ga-67 whole-body scan is useful in both detecting lesions and monitoring the therapeutic effect in patients with pleural empyema.