tbuckley/cabot-search huggingface dataset:
ABNORMAL EXERCISE HEMODYNAMICS IN PATIENTS WITH LOW GRADIENT AORTIC STENOSIS AND PRESERVED EJECTION FRACTION: A SIMULTANEOUS STRESS ECHO-RIGHT HEART CATHETERIZATION STUDY
Authors: Candelas Perez Del Villar, Raquel Yotti, Maria Angeles Espinosa, Enrique Gutierrez, Alicia Barrio, Maria Jose Lorenzo, Yolanda Benito, Pedro Luis Sanchez, Pablo Martinez-Legazpi, Francisco Fernandez-Aviles, Javier Bermejo
Journal: Journal of the American College of Cardiology (2015)
France dilutes tobacco and alcohol advertising ban
Authors: A. Dorozynski
Journal: BMJ (1995)

Researchers in US dispute first case of AIDS American scientists claim to have uncovered flaws in research published in the Lancet in 1990 that purported to prove the world's first case of AIDS and HIV infection.Using the powerful new tools of molecular biology, scientists from the New York University School of Medicine have concluded that there is now no evidence that a man from Manchester who died in 1959 of a mysterious AIDS-like illness was infected with HIV.David Ho, director of the university's Aaron Diamond AIDS Research Center, and his colleague Tuofu Zhu have reanalysed tissue supplied to them by the authors of the paper in the Lancet and found that more than one patient was involved.Using the most sensitive technology, they also failed to find any HIV in tissue that was supposed to have come from the 1959 patient.Their results were published as sci- entific correspondence in last week's issue of Nature (1995; 374: 503-4).The story began in 1959 at Manchester Royal Infirmary when David Carr, a 25 year old apprentice printer, died of a pneumonia caused by Pneumocystis carinii and cytomegalovirus.He also had perioral and perianal herpes infections, and no underly- ing cause could be found.The two hospital doctors and the pathologist wrote up the case in 1960 in the Lancet.Nothing further happened until AIDS appeared in the 1 980s, which reminded the doctors of David Carr's case.At the end of the 1980s the pathologist, Dr George Williams, located the tissue samples he had taken from Mr Carr's body at postmortem examination, which had been stored in paraffin blocks, and submitted them to the hospital's virology unit for Dr Gerald Cor- bitt, a virologist, to analyse for HIV with the polymerase chain reaction.To worldwide acclaim, HIV was found in Mr Carr's tissue and the research was published in 1990, again in the Lancet.In 1992 David Ho sat on a committee of scientists investigating theories on the origin ofAIDS and asked the scientists from Manchester for samples from Mr Carr.Dr Cor- bitt sent processed DNA left over from the research in 1990.Dr Ho was able to extract the integrated proviral HIV "with ease," and a sequence analysis confirmed that it was the same virus isolated by Dr Corbitt and his colleague Andrew Bailey.But Dr Ho was concerned that the sequence was much the same as sequences of HIV circulating in about 1990; HIV mutates rapidly and a search.f " ze." ge on
Detection of EGFR T790M Mutation in Urinary Circulating Tumor Dna From Metastatic Non-Small Cell Lung Cancer Patients
Authors: H. Husain, K. Kosco, S. Guerrero, T.T. Lu, C.R.T. Vibat, M.G. Erlander, V. Melnikova
Journal: Annals of Oncology (2015)
PWE-164 Assessment of<i>Helicobacter pylori</i>in iron deficiency anaemia: do we do this?: Abstract PWE-164 Table 1
Authors: C Daker, M Haji-Coll, N van Someren, K Besherdas
Journal: Gut (2012)

<h3>Introduction</h3> Globally iron deficiency anaemia (IDA) is responsible for over two billion cases. In the western world, an estimated 2–5% of adult men and post menopausal woman suffer with IDA. GI loses account for many cases and patients will undergo endoscopy to exclude pathology here. Recent evidence suggests that infection with <i>H pylori</i> (HP) should be considered despite the absence of peptic ulcer disease or other bleeding lesions in the GI tract. Hypothesised mechanisms for HP causing IDA are: chronic gastritis causing active bleeding, so iron is lost, achlorhydria decreasing iron absorption, the possibility that HP itself directly acquires iron so competing with the host, and also the possibility of an anaemia of chronic disease. <h3>Methods</h3> The study aim was to determine whether patients with IDA referred for an gastroscopy (OGD) had a rapid urease test (CLO test) performed to confirm infection with HP. This was a single centre, retrospective analysis of consecutive patients endoscoped for IDA over 1 year upto January 2011. The endoscopy report was scrutinised for the performance of the CLO test and if performed the result was noted. <h3>Results</h3> 194 Of 473 (41%) patients undergoing OGD for IDA had their CLO test obtained. Of these 27 of 194 (5.7%) were positive with 167 of 194 negative CLO tests. <h3>Conclusion</h3> In this study, 59% of patients endoscopied for IDA did not have a HP test. We may be missing a simple treatable cause for IDA in the upper GI tract within this group of patients. Of those who were not tested (270) 71 exhibited other significant pathology (angiodysplasia, gastric/colonic cancer, peptic ulcers). The association of IDA with HP is not universally recognised and we believe may be the reason as seen in this study not tested for in the absence of peptic ulcer disease or another cause for bleeding when endoscoping patients for IDA. We recommend routine testing (and eradication if detected) of HP in patients IDA undergoing OGD. In addition, testing and eradicating for HP may also reduce the risk of development of gastritis, peptic ulcer, MALToma and gastric cancer in those found to have the bacteria. <h3>Competing interests</h3> None declared.
Abstract 2735: Osteopontin mediates tumorigenic transformation of a murine promotable cell line through promoting cell survival by an RGD-dependent suppression of caspase 8 activity
Authors: Yu-Hua Hsieh, Pi-Ling Chang
Journal: Cancer Research (2011)

Abstract Osteopontin (OPN) is a cell adhesive, matricellular protein shown to be an important rate-limiting factor in tumorigenesis in vivo. Further, we have previously shown that addition of exogenous OPN promoted colony formation in an anchorage-independent growth assay of JB6 Cl41.5a cells, a preneoplastic mouse promotable cell line. In addition, down-regulation of the TPA (12-0-tetradecanoylphorbol-13-acetate)-induced OPN expression markedly suppressed TPA-induced colony formation of these cells. Collectively, these findings support the role of osteopontin in mediating neoplastic transformation of JB6 cells in vitro. In the present study, we hypothesize that induced-OPN stimulates the proliferation and/or prevents anoikis of JB6 cells grown in soft-agar and consequently, facilitates colony formation. To determine whether OPN promotes cell proliferation, cell cycle analyses by flow cytometry and direct cell counting of JB6 cells treated with soluble OPN were performed. Data from both of these analyses indicated that OPN-treated cells did not promote cell proliferation compared to non-treated controls. To determine whether OPN prevents anoikis of JB6 cells, annexin V and caspases activities were assesses on cells incubated with or without OPN and suspended on agar. Annexin V analyses showed that OPN significantly decreased anoikis of JB6 cells at 24 h by 41%. In the absence of OPN, suspended JB6 cells underwent anoikis through a sequential activation of caspases 8, 9 and 3 by 1, 3 and 18 h, respectively. Also, the addition of soluble OPN to suspended JB6 cells significantly suppressed caspase 8 activation when compared to non-treated cells. We next determined whether OPN's ability to suppress caspase 8 activity was mediated through its RGD- and/or DRVLFRI-binding motifs as they are known to transduce signals through integrin and CD44 receptors, respectively. Incubation of soluble RGD peptides with suspended JB6 cells suppressed caspase 8 activity. Similar results were obtained when suspended JB6 cells were incubated with OPN only or with RGD peptides and OPN. In contrast, RGE (non-specific peptides) and DRVLFRI peptides alone did not suppress caspase 8 activity of suspended JB6 cells unless OPN was added to these peptides. These findings suggest that OPN suppression of caspase 8 activity of suspended JB6 cells is mediated through its RGD cell-binding motif interacting with integrin receptors. In conclusion, osteopontin promotes tumorigenic transformation of JB6 cells by enhancing the survival of these cells through its RGD-dependent suppression of caspase 8 activity. 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 2735. doi:10.1158/1538-7445.AM2011-2735
PWE-187 Ethanol and Taurolidine Line Locks for the Reduction and Treatment of Catheter Related Blood Stream Infections in Paediatric Intestinal Failure: A Systematic Review: Abstract PWE-187 Table 1
Authors: R Tayler, A Barclay, P Henderson, D C Wilson
Journal: Gut (2013)

<h3>Introduction</h3> Paediatric intestinal failure (PIF) patients are often dependent on home parental nutrition (HPN) nd rely upon a central venous catheter (CVC) for its administration. There is a significant risk of catheter-related blood stream infections (CRBSI) with associated morbidity and mortality. Studies have suggested that the use of specialist line locks with ethanol or taurolidine may significantly reduce CRSBI for PIF. Our aim was systematically review the evidence for effectiveness of ethanol and taurolidine line locks in the prevention or treatment of CRBSI in PIF. <h3>Methods</h3> Systematic retrieval of data from studies of PIF (PN &gt; 28 days, age &lt; 18yr). Outcome measures were the reduction in rates of CRBIS or eradication of CRBSI. Electronic searches of the Cochrane Library, MEDLINE (1946 –Jan 2013) and PUBMED (to Jan 2013) were made using keyword and MeSH terms ‘Intestinal failure’ ‘child’ ‘ethanol locks’ and ‘taurolidine locks’. Hand searches of meetings of relevance and personal collections were also perfomed. Two authors independantly assessed the level of evidence (EL) using SIGN (Scottish Intercollegiate Guidelines Network) methodology (http.//www.sign.ac.uk). CRBSI rates were expressed as per 1000CVC days. <h3>Results</h3> The search strategy yielded 3142967 hits. Combination searches using ‘IF’ and ‘Child’ reduced this to 2993. 14 studies were read in detail; 5 were excluded due to containing purely adult data or where data on PIF could not be analysed seperately. Nine studies were included in our review, 5 of CRBSI prevention and 4 of CRSBI treatment. 8 studies used ethanol alone and 1 reported taurolidine use (Table). 4 studies reported success in prevention of recurrent line sepsis. 2 thrombotic episodes were reported. <h3>Conclusion</h3> The data for the use of ethanol line locks are limited of poor methodoligical quality and of lower EL (there are no RCT’s or well designed cohort studies). However ethanol locks appear to be an effective therapy in CRBSI prevention and treatment. With only 1 study of taurolidine locks no comparison can be made with ethanol locks. Future well designed studies are warranted to compare these two treatments. <h3>Disclosure of Interest</h3> None Declared.
Abstract 5311: The targeting effect of radio-labeled LXY1 and LXW7 against glioblastoma on xenograft mouse model
Authors: Wenwu Xiao, Ruiwu Liu, Nianhuan Yao, Kit S. Lam
Journal: Cancer Research (2011)

Abstract Glioblastoma, the most common type of primary brain tumors in adults, remains largely incurable, and surgical resection followed by radiation and chemotherapy has been shown to only slightly increase patient survival. New approaches to treat this deadly cancer are needed. Small peptide-based compounds have attracted wide interest as cancer targeting agents for the delivery of radionuclides or cytotoxic drugs to tumors. Using the “one-bead-one-compound” (OBOC) combinatorial library method, we have identified a specific ligand, LXY1, which targets the α3β1 integrin on glioblastoma cell line U87MG. We have also discovered another novel ligand containing a RGD motif, LXW7, which targets the αvβ3 integrin of U87MG cells and tumor endothelial cells. LXY1 and LXW7 demonstrated excellent tumor targeting efficacy in in vivo optical imaging studies. To further investigate the targeting property of the peptides and precisely clarify their in vivo biodistribution profile, we have conjugated LXY1 and LXW7 to the metal chelator CB-TE2A complexed with 64Cu to perform PET imaging and biodistribution studies. The results indicate 64Cu-labeled LXY1-CB-TE2A conjugate efficiently targets both orthotopic and subcutaneous glioblastoma. The LXW7-CB-TE2A conjugate also demonstrates good tumor accumulation. Both conjugates show relatively rapid clearance from tumor site and high uptake in the liver and kidney beside to tumor. The undesired high uptake of the peptides in the liver and kidney indicate both peptides in current version may be more promising in radioimaging than radiotherapy for glioblastoma. 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 5311. doi:10.1158/1538-7445.AM2011-5311
HER2 and HER3 in HPV+ and HPV− HNSCC—Response
Authors: Jennifer Grandis
Journal: Clinical Cancer Research (2016)

We appreciate the perspective of Drs. Machiels, Galot and Schmitz of our article, which was published earlier this year in Clinical Cancer Research , prior to the publication of the LUX-Head and Neck 1 trial results. The open-label randomized phase III study did not demonstrate increased response
Abstract 4732: Repression of transcriptional activity by the retinoid target gene G0S2
Authors: Tian Ma, Jessica P. Dong, Steven Blumen, Dennis L. Fei, Michael Henderson, David J. Sekula, Sarah J. Freemantle, Ethan Dmitrovsky
Journal: Cancer Research (2012)

Abstract Acute promyelocytic leukemia (APL) cases that express the PML/RARα fusion protein block maturation of myeloid precursors. All-trans retinoic acid (RA)-based differentiation therapy of these APL cases causes clinical remissions. Yet, clinical use of RA is associated with toxicities and drug resistance. In the search for RA target genes that can serve as alternative therapeutic targets in APL, G0S2 was found as one of the most rapidly and prominently RA-induced species. G0S2 is a 103 amino acid protein without apparent homology domains to other species. It was recently shown to inhibit adipose triglyceride lipase (ATGL) activity, leading to repression of lipolysis. G0S2 is abundantly expressed in adipose tissues, which is consistent with its role in regulating lipolysis. It is also induced in response to inflammatory stimuli in other cell types, indicating it has additional roles beyond fat storage. Here, we report a new G0S2 function uncovered after its transient transfection that led to substantial repression of reporter activities of multiple constructs (including RA-regulated species RARα, UBE1L and G0S2 itself). This repression was antagonized by siRNA-mediated G0S2 knockdown. Notably, an engineered form of G0S2 that lacked the internal hydrophobic domain did not exhibit these repressive effects. Inhibitors of either the proteasomal or lysosomal pathways did not overcome this suppression by G0S2. Thus, these repressive activities were unlikely due to enhanced proteasome or lysosome activities. The reported inhibition of ATGL activity by G0S2 causes an increase in lipid droplet size, which can also be achieved by treating cells with the neutral lipid oleic acid. Yet, this treatment did not impact reporter activity, indicating that changes in lipid droplet size did not affect this transcriptional repression. Intriguingly, G0S2 expression did not reduce endogenous expression of RARα, UBE1L or G0S2 (each RA-regulated species), indicating that only exogenous genes were affected by G0S2 transient transfection. Subcellular localization of endogenous G0S2 was examined in RA-treated NB4 APL cells and G0S2 was markedly expressed in the cytosol and membranes of these cells. Transiently transfected G0S2 protein was also detected in the cytoplasm. In summary, we report a previously unrecognized function for the RA target gene G0S2: it repressed exogenous reporter activity, but not endogenous gene expression. Both endogenous and exogenous G0S2 proteins were detected in the cytoplasm. Mechanistic studies that engage this G0S2 repressive effect are now underway. 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 4732. doi:1538-7445.AM2012-4732
WHICH IS BETTER, ABSOLUTE FLOW OR CORONARY FLOW RESERVE FOR THE DETECTION OF SIGNIFICANT CORONARY ARTERY STENOSIS? VALIDATION USING FRACTIONAL FLOW RESERVE AND POSITRON EMISSION TOMOGRAPHY
Authors: Chee Hae Kim, Bon Kwon Koo, Ji-Hyun Jung, Eun-Seok Shin, Minseok Suh, Gi Jeong Cheon, Jin Chul Paeng, Jung-kyu Han, Han-Mo Yang, Kyung Woo Park, Dong-Ju Choi, Hyo-Soo Kim, Byung-Hee Oh, Young-Bae Park
Journal: Journal of the American College of Cardiology (2015)
Loss of Suppressor T Cells in Active Multiple Sclerosis
Authors: Ellis L. Reinherz, Howard L. Weiner, Stephen L. Hauser, Judith A. Cohen, Judy Ann Distaso, Stuart F. Schlossman
Journal: New England Journal of Medicine (1980)

To determine whether abnormalities of immunoregulatory T cells are associated with multiple sclerosis (MS), we characterized peripheral lymphocytes in 33 patients with untreated MS and compared them with 42 normal persons and 29 age-matched control subjects who had other neurologic diseases. For this analysis, we used monoclonal antibodies to the surface antigens of helper (T4) and suppressor (T5) T-cell subsets and to a common T-cell antigen (T3). In contract to normal persons and the controls with other neurologic diseases, the patients with MS had a reduced percentage of T3-positive (T3+) cells (P less than 0.05). More importantly, there was a selective decrease in T5-positive (T5+) cells in 11 of 15 patients with active MS, but in only one of 18 patients with inactive MS and in none of the normal persons or controls with neurologic disease (P less than 0.00001). Serial analysis of five patients with MS showed a correlation between the absence of the T5+ subset and disease activity. Thus, there is loss of peripheral suppressor cells in many patients with active MS, suggesting that immunoregulatory abnormalities contribute to the pathogenesis of the disease.
The Clinical Characteristics of Early Diabetes Mellitus
Authors: Samuel B. Beaser
Journal: New England Journal of Medicine (1948)

CURRENT descriptions of diabetes mellitus vary markedly — as much as 300 per cent — regarding the symptoms of the disease.1 , 2 Likewise, there is little exact information about its early course. The present survey of the population of a large diabetic clinic† was undertaken to clarify these points.MethodsThe records of 500 consecutive patients were examined, and 182 with adequate descriptions of the onset‡ of the disease were accepted for study. They had all been followed on the wards or in other clinics and had been referred to the diabetic clinic because of diabetic symptoms or glycosuria. In most . . .
Health Insurance Politics in Federal Court
Authors: Wendy K. Mariner, George J. Annas
Journal: New England Journal of Medicine (2010)

Having been outmaneuvered in Congress with the passage of the Patient Protection and Affordable Care Act ("Affordable Care Act," or ACA), Republicans have taken their case to federal court, arguing that the law's key provision, the individual mandate to purchase health insurance, is unconstitutional. This argument has been made most prominently by attorneys general from 20 states in a Florida federal court and by the Commonwealth of Virginia in a Virginia federal court. In early August, federal district court judge Henry Hudson decided that the Virginia challenge deserves a hearing,1 thereby giving the constitutional argument an aura of respectability and . . .
Colonic plasmacytomas: a rare complication of plasma cell leukemia
Authors: Calvin Hang, Ryan Perumpail, Robert Huang, Sebastian Fernandez-Pol, Nielsen Fernandez-Becker
Journal: Endoscopy (2015)

A 53-year-old man presented with fatigue, syncope, and splenic rupture. Diagnostic evaluation revealed hypercalcemia with leukocytosis (23.2 × 103 cells/µL). Peripheral smear showed 39 % lymphocytes with clonal plasmacytosis. These findings, in addition to a negative skeletal survey, suggested a diagnosis of plasma cell leukemia (PCL). The patient was started on carfilzomib and dexamethasone after relapse following an initial regimen of cyclophosphamide, bortezomib, and dexamethasone. Then, 3 days into treatment, he developed profound anemia from hematochezia requiring multiple transfusions. Dexamethasone was stopped and esophagogastroduodenoscopy showed extensive duodenal mucositis but no active bleeding. Subsequent colonoscopy revealed numerous polypoid growths from the transverse colon to the cecum. These appeared both as solitary lesions and in clusters. Some were discoid, > 2 cm in diameter, and highly friable ([Fig. 1]).
Abstract 3067: Differential proteomic profilingidentifies HNSCCinvasion genes: GANAB is negative regulator in HNSCC invasion
Authors: Ching-Chi Chiu, Hsiao-Fang Li, Yin-Ju Chen, Ann-Joy Chen
Journal: Cancer Research (2010)

Abstract Head and neck squamous cell carcinoma (HNSCC) is one of the most frequent cancer worldwide, however, highly invasive or metastatic characteristics are the common cause of treatment failure. In order to investigate the invasive mechanism of cancer, we established highly invasive sublines of five HNC cell lines by using Matrigel and Transwell selection method. After confirmed the invasion phenotype, the differential proteomes were determined using proteomic methods. Total of 420 protein bands were identified by mass spectrometry analysis, which corresponds to 184 proteins. There were 52 proteins identified more than twice of the four independent experiments, indicating the significance of these proteins in regulation of invasion phenotype. In which, 18 (35%) functions as cytoskeleton or adhesion molecules, 10 (19%) function as molecular chaperone, 9 (17%) belongs to metabolic enzymes, 8 (15%) involve in transcriptional or translational regulation, 7 (13%) involve in cellular signalling pathway. RT-PCR analysis revealed 13 genes that were consistently differentially expressed in the HNSCC invasion sublines. One of the most significantly change genes is GANAB. The treatment of GANAB-shRNA also resulted in augment of cell growth in all HNSCC cell lines, with approximately increase to 1.34 fold at day 5 (p &amp;lt; 0.05). GANAB-shRNA transfected cells migrated 1.78 fold faster than control cells in in vitro wound healing assay. The GANAB silencing cell increase to 12.33 fold (p=0.005) in HNSCC cell lines. These results suggest that plays an important role in negative regulation of cell growth, migration and invasion. Using a cut-off value of a 1.5-fold differential expression in tumor verse normal tissues, 14 (44%) patients were found under-expressed in GANAB proteins. These results support our cellular findings and indicate that HNSCC. 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 3067.
Tc-99m MDP and Ga-67 Citrate Images in Suppurative Costochondritis
Authors: JONG-KANG LEE
Journal: Clinical Nuclear Medicine (2002)

From the Department of Nuclear Medicine, St. Martin De Porres Hospital, ChiaYi, Taiwan Received for publication November 19, 2001. Revision accepted January 18, 2002. Correspondence: Jong-Kang Lee, Department of Nuclear Medicine, St. Martin De Porres Hospital, No 565, Sec. 2, Ta-Ya Road, ChiaYi, Taiwan. E-mail: [email protected]