tbuckley/cabot-search huggingface dataset:
Bid to ban silicone implants in Europe
Authors: R. Watson
Journal: BMJ (1998)

A campaign has been launched in Brussels to ban the use of silicone implants throughout the European Union.

The initiative is being led by a British Labour MEP, Bill Miller. He argues that existing EU legislation on medical devices which includes a list of substances and other items that are banned could be extended and used to outlaw the implants.

“There is a very strong case for …
Abstract 1232: Aberrant JAK/STAT signaling confers epigenetic silencing of STAT3 targets in gastric cancer by integrated microarray and bioinformatic analysis
Authors: Alex L.Y. Chang, Claudia Dittner, Jian-Liang Chou, Alfred S.L. Cheng, Jiayuh Lin, Kun-Tu Yeh, Michael W.Y. Chan
Journal: Cancer Research (2010)

Abstract Gastric cancer is the 2nd leading cause of cancer worldwide. One of the major risk factors of gastric cancer is infection of H. pylori. Patients infected with CagA-positive H. pylori would have increased risk of gastric cancer. Previous studies including ours have demonstrated that infection of CagA-positive H. pylori induced activation of JAK/STAT3 signaling pathway. However, the role of aberrant activation of this signaling pathway in gastric cancer is not clear understood. We hypothesized that aberrant activation of JAK/STAT signaling may lead to epigenetic silencing of STAT3 target genes in gastric cancer. In this study, we transfected a constitutively activated mouse STAT3 mutant (STAT3c) into MKN28 gastric cancer cell line in which the JAK/STAT signaling pathway is not active. STAT3c stable transfectant MKN28/STATc-16 showing hyper-phosphorylation of STAT3 demonstrated increased cell proliferation as compared to vector control MKN28/C-9. In order to identify STAT3 target genes that are epigenetically down-regulated in MKN28/STATc-16 cells, expression microarray using Agilent 44K oligonucleotide microarray coupled bioinformatic analysis were performed. Our result showed that there are 2945 genes showing at least 1.5 fold down-regulation in MKN28/STATc-16 cells as compared with vector control. By whole genome bioinformatic analysis, 397 genes with STAT3 binding sites within 5kb of a CpG island were discovered. Integrated analysis revealed that there are 18 downregulated genes with a STAT3 binding site around the promoter CpG island. Further characterization of two STAT3 target, NR4A3 and LOXL4 demonstrated that promoter hypermethylation of these 2 genes were observed in MKN28/STATc-16 cells but not the vector control. Demethylation treatment using 5azaDC also restored expression of these 2 genes in MKN28/STATc-16 cells. These phenomena may be partially related to the up-regulation of DNMT1 in MKN28/STATc-16 cells. In conclusion, our result demonstrated that aberrant JAK/STAT3 signaling may lead to epigenetic silencing of its target gene in gastric cancer. The role of STAT3 in mediating epigenetic silencing of NR4A3 and LOXL4 and its clinical significance in gastric cancer patients is currently under investigation. 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 1232.
Papilledema and Idiopathic Intracranial Hypertension
Authors: William A. Buchheit, Charles Burton, Burritt Haag, David Shaw
Journal: New England Journal of Medicine (1969)

THE development of increased intracranial pressure and papilledema without apparent cause is not uncommon. Since Quincke's1 original description in 1897, all reported cases have been sporadic and genetically unrelated. The present report is the first to describe this syndrome in two members of the same family. The patients are sisters in whom increased intracranial pressure and papilledema appeared almost simultaneously although they were living over 100 miles apart.Although this condition is well recognized, the terminology has remained an enigma. We propose a new approach to the nomenclature based on the fact that many well known pathologic states aside from . . .
Bacterial Meningitis in the United States in 1995
Authors: Anne Schuchat, Katherine Robinson, Jay D. Wenger, Lee H. Harrison, Monica Farley, Arthur L. Reingold, Lewis Lefkowitz, Bradley A. Perkins
Journal: New England Journal of Medicine (1997)

Before the introduction of the conjugate vaccines, Haemophilus influenzae type b was the major cause of bacterial meningitis in the United States, and meningitis was primarily a disease of infants and young children. We describe the epidemiologic features of bacterial meningitis five years after the H. influenzae type b conjugate vaccines were licensed for routine immunization of infants.
False-positive I-131 Whole-body Imaging After I-131 Therapy for a Follicular Carcinoma
Authors: JÖRG ANDREAS, KLAUS BRÜHL, DAGMAR EISSNER
Journal: Clinical Nuclear Medicine (1997)

A 57-year-old man was treated with ablative radioiodine therapy for follicular thyroid carcinoma. The post-therapeutic whole body scans detected radionuclide accumulation in the area of the right occiput at the site of a cranial defect. The defect was caused by trauma in 1964. Bone scintigraphy did not show increased uptake in this area. Magnetic resonance imaging showed porencephaly, but it did not show a metasasis.
X-Chromosomal Translocation and Segmental Hypopigmentation
Authors: Daniele Torchia, Lawrence A Schachner
Journal: New England Journal of Medicine (2012)

A Hispanic girl who had been born at term to healthy nonconsanguineous parents was affected by brachycephaly, developmental delay, mild cognitive deficit, and behavioral disturbances. Cytogenetic testing revealed an X-chromosomal translocation.
Abstract 5523: Gold nanoshells in the treatment of high-grade gliomas in a mouse model
Authors: Patrick A. Thompson, Emily S. Day, Linna Zhang, Kelvin Wong, Mostafa W. Gaber, Susan M. Blaney, Jennifer L. West
Journal: Cancer Research (2010)

Abstract Purpose: To evaluate the anti-tumor activity of near-infrared (NIR) absorbing gold-silica nanoshells against high grade gliomas in an in vivo subcutaneous mouse model. Background: Nanoshells with a silica core and a gold outer layer, which are optically tunable with peak absorption between 790 and 810 nm, have been shown to preferentially accumulate in colon cancer models after i.v. administration as a result of the enhanced vascular permeability and retention effect. When the tumor is illuminated with NIR light, the gold nanoshells are thermally activated. This results in tumor ablation without damage to normal tissues, since NIR light is not appreciably absorbed by tissue components at these wavelengths. High-grade gliomas are an attractive target for this type of therapy because the vast majority of tumors remain incurable with multi-modality therapeutic approaches, with local control being the primary manifestation of disease progression or recurrence. Methods: Gold silica nanoshells were synthesized according to previously published procedures. Survival studies were performed in NOD SCID mice with subcutaneous U373 glioma tumors in the right hind flank. When the tumor diameter was 3-5 mm, either 100 µl of PEG-coated nanoshells (treatment group, n =7) or 100 µl of saline (control group, n=8) were injected via tail vein. Twenty-four hours later tumors were exposed to an 808 nm diode laser at 4 W/cm2 for 3 minutes. Mice were monitored daily following treatment and euthanized when tumors reached 10 mm in largest diameter. Results: In the subcutaneous xenografts the overall survival at 90 days was 57% in the treatment group and 0% in the control group. None of the control group mice survived past 24 days. In addition, all of the mice in the treatment group that were still alive at 90 days were completely tumor-free without any sign of recurrence. Conclusions: These studies demonstrate that gold nanoshells can accumulate in subcutaneous glial tumors at levels sufficient to improve survival following thermal activation with NIR light. 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 5523.
Abstract 363: Activin receptor-like kinase 1 (Alk1) ligands modulate endothelial cell function in vitro and in vivo.
Authors: Gareth C. Davies, James A. Harper, Richard C. Sainson, Lee Brown, Grace Opoku-Ansah, Alison Smith, Matthew McCourt, James W. Legg
Journal: Cancer Research (2013)

Abstract The TGF-ß type-1 receptor activin receptor-like kinase 1 (Alk1) is predominantly expressed on endothelial cells, regulates vascular morphogenesis, and has been implicated in pathological angiogenesis. Alk1 expression is increased in the vasculature of a broad range of tumours and agents that disrupt of Alk1 signalling in tumour endothelial cells may be potential therapeutics for the treatment of a variety of solid tumours. Alk1 has been described as a receptor for the bone morphogenic proteins, BMP9 and BMP10. In order to study the effects of Alk1 signalling in endothelial cells in vitro and in the vasculature in vivo we used a soluble antagonist Alk1-Fc protein consisting of the extracellular domain of the Alk1 protein fused to the Fc domain of IgG1. In vitro, Alk1-Fc inhibited BMP9-dependent Alk1 signalling via phosphorylation and nuclear translocation of SMAD1/5 in endothelial cells and modulated endothelial cell functions such as an ability to form tube- like structures. In mice, physiological levels of BMP9 could be detected in serum by ELISA, consistent with detectable levels of phosphorylated SMAD1/5 in the lung, a site of high Alk1 vascular expression. In mice, the administration of Alk1-Fc effectively blocked SMAD1/5 phosphorylation in the lung, suggesting that in this tissue Alk1 ligands are the predominant driver of lung SMAD1/5 activation and that signalling is efficiently antagonised by Alk1-Fc. Despite suppression of Alk1 signalling in the lung and expression of Alk1 on the vasculature associated with tumours, Alk1-Fc did not have profound effects on tumour size or microvessel density in mice bearing tumours, however administration of Alk1-Fc in neonatal mice did cause defects in angiogenesis of the retinal vasculature demonstrating that in some contexts Alk1 ligands play an important role in regulating the angiogenic process. Citation Format: Gareth C. Davies, James A. Harper, Richard C. Sainson, Lee Brown, Grace Opoku-Ansah, Alison Smith, Matthew McCourt, James W. Legg. Activin receptor-like kinase 1 (Alk1) ligands modulate endothelial cell function in vitro and in vivo. [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 363. doi:10.1158/1538-7445.AM2013-363
Abstract P2-04-03: Usefulness of Perioperative Screening of Patients with pN0 Invasive Breast Carcinoma: Results on 1058 pN0 Patients of a Population-Based Study of the French Cancer Registry
Authors: J-S Frenel, C Leux, F Molinie, M Campone
Journal: Cancer Research (2010)

Abstract Background: Usefulness of baseline routine bone scanning (BS), liver ultrasonography (LUS) and chest radiography (CXR) in asymptomatic women with pN0 Invasive Breast Carcinoma is not evidence-based. Methods: A random sample of 1883 cases of invasive breast cancer diagnosed in 2003 from 10 French counties covered by a cancer registry was analyzed. Clinico-pathological features, staging tests and results were retrospectively collected from the medical record. Results: 1058 pN0 patients were identified. At baseline, CXR, LUS, BS were carried out pre or post-operative in respectively 785 (74%), 782 (74%), and 618 (58%) patients. Data summarizing results with the three imaging techniques are listed in [Table 1]. Initial suspicion was confirmed by other independant tests (bone X-ray, computerized tomography scan). After the initial staging investigation procedures and the further diagnostic procedures if necessary (computerized tomograhy scan or bone X-ray), only 3 (0.3%) patients were diagnosed having metastatic disease. CXR, LUS, BS detected metastasis respectively in 1 (0.13%), 0 (0%), and 2 (0.3%) of patients. Diagnostic accuracy in the diagnosis of metastatic disease by chest radiography, liver ultrasonography and chest radiography Conclusion: In asymptomatic pN0 invasive breast cancer, screening for metastases is not warranted because of low frequency of metastases, false positive findings and high cost. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P2-04-03.
<i>CFTR</i> gene carrier status and risk for pancreatic adenocarcinoma
Authors: R. R. McWilliams, W. E. Highsmith, K. G. Rabe, L. M. Holtegaard, M. D. Bishop, G. M. Petersen
Journal: Journal of Clinical Oncology (2008)

11070 Background: Mutations in the cystic fibrosis transmembrane regulator gene (CFTR) are common and are associated with pancreatic disease, including pancreatitis and pancreatic insufficiency. Case reports of pancreatic cancer (PC) in cystic fibrosis (CF) patients have been reported, and pancreatitis has been reported to increase PC risk, but to date, CFTR mutations have not been clearly associated with PC. Methods: A clinic-based registry study compared rates of 40 common CF disease-associated mutations in CFTR in 948 patients with confirmed pancreatic adenocarcinoma (recruited 10/ 00 to 2/06) to 13,340 controls (4/06–3/07) from a clinical laboratory database for prenatal testing. Analyses were limited to Caucasians in cases/controls due to the low number of minorities in cases (33/971) and the lower carrier rate in other races. Germline DNA was tested using commercially available methods (Tag-It Mutation Detection Kit for CFTR 40+4, Luminex/Tm-Bioscience, CF v3.0 ASR, Celera/Abbott); mutation frequencies were compared using chi-square analysis, and cases were further studied by cigarette smoking (ever/never), pancreatitis status( ≥ 3 yrs prior to PC), and age at onset. Results: Overall, 50/948 (5.3 %) PC cases carried a common CFTR mutation versus 510/13,340 (3.8%) controls (OR 1.40; 95% CI 1.04–1.89, p=0.03). Among younger onset cases (< age 60), the carrier frequency was higher (6.8%) than controls (OR 1.81, 95% CI 1.13–2.91, p=0.01). In case-only analyses by carrier status, age of onset was lower among carriers versus noncarriers (median 62 vs 67 yrs, respectively; p=0.041). Notably, this difference was seen almost exclusively in ever-smokers –60.5 yrs (n=30) vs 65 yrs. (n=542), p=0.03. Among never-smokers, there was no difference in age of onset –68 yrs (n=20) vs 68 yrs (n=345). Prior pancreatitis was not significantly increased (p=0.51) in carriers (2.0%) vs noncarriers (1.4%). Conclusions: Carrying a common, CF disease-associated mutation in CFTR increases risk for PC among Caucasians by approximately 40%, and 80% for young-onset PC. Carriers of detected mutations also have a younger age of onset by nearly 5 years compared with noncarriers, most notably among ever- smokers. History of longstanding antecedent pancreatitis is uncommon among PC patients regardless of CFTR mutation status. No significant financial relationships to disclose.
In Labortory Research, Yesterday" Visions Are Today Tools- And They Are Expensive
Authors: K. Ruddon
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article In Labortory Research, Yesterday“ Visions Are Today Tools- And They Are Expensive Get access Kate Ruddon Kate Ruddon Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 4, 15 February 1989, Pages 254–256, https://doi.org/10.1093/jnci/81.4.254 Published: 15 February 1989
FRI0578-HPR Why There Are so Few Obese Norwegians: the Validity of Self-Reported Body Mass Index in an Osteoarthritis Cohort
Authors: K. Magnusson, I.K. Haugen, K.B. Hagen
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Obesity is one of few modifiable important risk factors for osteoarthritis (OA). Body Mass Index (BMI) is frequently used as a measure of obesity, which is often calculated based on self-reported height and weight. However, to what extent self-reported BMI can be trusted in OA studies is unknown. Knowledge of this topic is important for the interpretation of results from existing studies as well as in the design of future epidemiological studies. <h3>Objectives</h3> To investigate the validity of self-reported BMI in an OA cohort. <h3>Methods</h3> In a population-based survey, persons aged 40-79 years (n=12155) were sent questionnaires in 2010 (the Musculoskeletal pain in Ullensaker study). Those who answered "yes" to the question "Have you been diagnosed with osteoarthritis in the knee, hip and/or hands by a doctor and/or on radiographs?" were invited to a clinical examination (n=1019), of whom 630 attended. In the analyses we included 449 participants who had clinical OA in the hips, knees and/or hands (according to the American College of Rheumatology criteria). Height and weight were self-reported on the initial questionnaire, and measured at the clinical examination. <h3>Results</h3> See Table 1. Mean (SD) age was 65 (8.6) years and 129 (28%) were men. Mean (SD) self-reported BMI was 27.0 (4.5) kg/m<sup>2</sup>, while mean (SD) measured BMI was 28.3 (4.9) kg/m<sup>2</sup>. There was a dose-response relationship between a higher examined BMI and a greater overreporting of height, underreporting of weight, and consequently a lower reported than measured BMI (Table 1 and figure). <h3>Conclusions</h3> OA patients with a high BMI were more likely to underreport their BMI compared to OA patients with a normal BMI. The dose-response relationship between actual BMI-category and underreporting of BMI should be taken into account when designing future studies of OA in which BMI is used as a measure of obesity. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4040
Abstract 5503: Targeting thymidine metabolic pathways in cancer cells with a novel thymidine conjugate.
Authors: Qibing Zhou, Qiong Wei, Dejun Zhang
Journal: Cancer Research (2013)

Abstract Cellular thymidine metabolism involves two pathways: the catabolic and salvage pathways. The catabolic pathway breaks down thymidine to carbon dioxide for energy while the salvage pathway converts thymidine to its 5′-triphosphate as one of building blocks for DNA synthesis. Cytosolic level of thymidine is regulated by both thymidine phosphorylase (TYMP) of the catabolic pathway and thymidine kinase (TK) of the salvage pathway. In tumor tissues and cancer cells, abnormally high levels of these two proteins have been consistently reported. Therefore, thymidine metabolic pathways in cancer cells are a potential therapeutic target for novel drug design and development. We recently developed a novel thymidine analog, 3′-deoxythymidine phenylquinoxaline conjugate (dT-QX) that selectively killed a series of cancer cell lines including human liver carcinoma HepG2 and Hep3B, breast adenocarcinoma MCF-7, rat brain glioma C6 and mouse liver cancer H22 cells and showed low cytotoxicity on the normal liver hepatocyte HL-7702 cells. dT-QX is a conjugate of 3′-deoxythymidine and a DNA intercalating moiety with a triazole linkage achieved by click chemistry. The selective killing of cancer cells was attributed to the selective inhibition of DNA synthesis in the cancer cells but not in normal liver HL-7702 cells, resulting in extensive production of mitochondrial superoxide stress. The conjugation of 3′-deoxythymidine was found to be critical for dT-QX to achieve the selective killing of cancer cells. The killing by dT-QX was revealed to be directly due to the expression levels of TYMP and TKs in cancer cells, confirming that dT-QX successfully targeted the thymidine metabolic pathways as designed. Finally, a preliminary mouse study with subcutaneous liver tumors confirmed that dT-QX effectively inhibited the growth of tumors in vivo. Citation Format: Qibing Zhou, Qiong Wei, Dejun Zhang. Targeting thymidine metabolic pathways in cancer cells with a novel thymidine conjugate. [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 5503. doi:10.1158/1538-7445.AM2013-5503
Abstract PD08-06: Duloxetine for Treatment of Aromatase Inhibitor (AI)-Associated Musculoskeletal Syndrome (AIMSS)
Authors: NL Henry, M Banerjee, D Blossom, M Wicha, C Van Poznak, JB Smerage, AF Schott, JG Griggs, DF. Hayes
Journal: Cancer Research (2010)

Abstract Background: Approximately 50% of postmenopausal women with hormone receptor positive early stage breast cancer treated with an aromatase inhibitor (AI) develop arthralgias. Standard analgesics are relatively ineffective. Duloxetine is a serotonin and norepinephrine receptor inhibitor with proven efficacy for treatment of multiple chronic pain states. We investigated the hypothesis that duloxetine would be efficacious for treatment of AIMSS. Methods: We performed a single-arm, open-label phase II study of duloxetine in 35 postmenopausal women who had been treated with AI therapy for at least 2 weeks and who developed new or worsening pain after starting AI therapy that was rated at least 4 on a 10 point Visual Analog Scale. Enrollment was completed in June 2010. Subjects were treated with duloxetine 30 mg daily for one week, and then 60 mg daily for 3 weeks. Depending on patient-perceived response to therapy, patients had the option of continuing duloxetine 60 mg daily or increasing the dose to 60 mg twice daily for the subsequent 4 weeks. Change in patient-reported pain was assessed. Outcome measures included the Brief Pain Inventory (BPI) and modified Health Assessment Questionnaire (HAQ). Benefit from therapy was defined as a 30% decrease in average pain score from baseline to 8 weeks. Paired t tests were used for statistical analysis. Results: Of the 35 enrolled subjects, 20 subjects completed the 8-week study period, 6 subjects discontinued therapy early because of duloxetine-associated toxicity, and 9 subjects had been enrolled less than 8 weeks at the time of this analysis and were therefore not evaluable. In an intent-to-treat analysis, 16 of 26 evaluable subjects (61.5%) experienced at least a 30% decrease in average pain, and 14 of 20 subjects (70%) who completed all 8 weeks of protocol-directed treatment chose to continue duloxetine therapy. There were statistically significant reductions in average pain severity (p &amp;lt; 0.0001) and maximum pain severity (p &amp;lt; 0.0001) from baseline to 8 weeks. The mean percent reduction in average pain severity between baseline and 8 weeks was 56.1% (95% CI 37.9%-74.2%) and in maximum pain severity was 55.7% (95% CI 37.3%-74.1%). No grade 3 or 4 adverse events were reported. The most common adverse events were fatigue and drowsiness, xerostomia, nausea, and headache. Conclusions: Duloxetine appears to be effective and well-tolerated for treatment of AIMSS. Final results from the entire cohort will be presented. Future randomized, placebo-controlled studies are warranted. Clinicaltrials. gov NCT01028352. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr PD08-06.