tbuckley/cabot-search huggingface dataset:
When I use a word: Faux amis
Authors: Jeff Aronson
Journal: BMJ (2005)

An English rugby fan, in Paris for a Six Nations match, wants a beer. He doesn't know that beer is served in un cafe or un bistro, but asks the concierge for a pub. The concierge is puzzled. La pub means publicity (il aime beaucoup la pub), not a public house. OK, what about une maison publique? Ah, now the concierge understands. She points out the nearby red light district.

Our friend has fallen foul of the phenomenon known as faux amis, or false friends, foreign words that seem to mean one thing but actually mean another. The term was put on the map in a dictionary called Les Faux Amis, ou les Trahisons du Vocabulaire Anglais, by Maxine Koessler and Jules Derocquigny (Librairie Vuibert, 1928). The French word sensible, for example, means not sensible (sage, raisonnable) but sensitive, a meaning that we recognise in Jane Austen's Sense and Sensibility. And faux amis are not limited to French. In Spanish simpatia means friendship not sympathy. In Dutch een verloren hoop, the origin of the English phrase “a forlorn hope,” actually means a lost troop of soldiers. And when in Germany it does well to remember that Gift means a poison not a present (Geschenk) and when visiting a pharmaceutical factory that Praservativ means a condom not a preservative (Konservierungsmittel).

Doctors travelling in France may need to be aware of some medical faux amis. La medicine liberale is not, alas, free at the point of delivery; in fact, quite the reverse—it means private practice, since the members of les professions liberales are those who receive fees for their labours. And un medecin de permanence is not a doctor with a tenured position but merely one who is on duty.

Looking for over the counter drugs? Don't ask for une droguerie, which is a hardware store. What you want is une pharmacie. And when you're there ask for medicaments, not drogues, unless you want to risk arrest. If it's prescription drugs you're after, go to the doctor's surgery (cabinet, not chirurgie) and ask for une ordonnance, not une prescription, which is a chit for a medical appliance or simply an instruction. If the doctor refers you to the hospital don't ask for la clinique; that means a private hospital, not an outpatient clinic.

If you're an academic and have been invited to speak at a symposium, don't say that you have come to give une lecture (a reading), but une conference (a lecture). And for those lecturing on Viagra, impotent means crippled, not impotent, which is impuissant.

As bad as these false friends are, worse perhaps are fickle friends, which sometimes mean what you think they mean and sometimes not. Tension, for instance, means tension, but also blood pressure and sometimes high blood pressure. And in the family planning clinic try to remember that fertilite refers to the land; the word you want there is fecondite.

After all of which, I think I need a quick one at la maison publique.
Gold for the NHS
Authors: B. Campbell
Journal: BMJ (2002)

Editor—By far the most encouraging sentence in Robinson's editorial is the last: “There is a strong case for arguing that . . . UK healthcare policy should be driven by the supply side rather than the demand side reform.”1 Yet there is not a word of this from the chancellor or the secretary of state or in the report by Wanless, whose terms of reference guaranteed his conclusions. Even working within those limitations Wanless managed to generate some gratuitous drive, saying that the cost of health care is likely to fall as we take greater measures to improve our health.

There may have been some excuse for Aneurin Bevan's assessment of budgetary realities, but surely 54 years' unvarying experience has been enough to convince us of the truth of another health secretary's assessment (Enoch Powell's): there is no natural limitation on the demand for any good or service free at the point of its supply. Until that is grasped and fully understood, those working in the NHS will continue to be the poorly paid providers of inferior care to an ungrateful public.
Imagestream detection and characterisation of circulating tumour cells – A liquid biopsy for hepatocellular carcinoma?
Authors: Laura F. Ogle, James G. Orr, Catherine E. Willoughby, Claire Hutton, Stuart McPherson, Ruth Plummer, Alan V. Boddy, Nicola J. Curtin, David Jamieson, Helen L. Reeves
Journal: Journal of Hepatology (2016)
Chromatin immunoprecipitation from fixed clinical tissues reveals tumor-specific enhancer profiles
Authors: Paloma Cejas, Lewyn Li, Nicholas K O'Neill, Melissa Duarte, Prakash Rao, Michaela Bowden, Chensheng W Zhou, Marta Mendiola, Emilio Burgos, Jaime Feliu, Juan Moreno-Rubio, Héctor Guadalajara, Víctor Moreno, Damián García-Olmo, Joaquim Bellmunt, Stephanie Mullane, Michelle Hirsch, Christopher J Sweeney, Andrea Richardson, X Shirley Liu, Myles Brown, Ramesh A Shivdasani, Henry W Long
Journal: Nature Medicine (2016)
One Man's Poison — Clinical Applications of Botulinum Toxin
Authors: Mark Hallett
Journal: New England Journal of Medicine (1999)

Botulinum toxin is one of the deadliest poisons known, causing death by muscle paralysis. As a poison, it is most commonly encountered as a source of food poisoning, and there are shivers around the world when it surfaces as a possible biologic weapon. Botulinum toxin is produced by the bacterium Clostridium botulinum. It is a polypeptide consisting of a light chain and a heavy chain bridged by a single disulfide bond. There are seven serologically distinct but structurally similar types of botulinum toxin: A, B, C, D, E, F, and G.Alan Scott first had the idea that small doses . . .
Aptamer TY04 Inhibits Multiple Myeloma Cell Growth Via Cell Cycle Arrest
Authors: Jing Liu, Hong-Juan Dai, Bian-Ying Ma, Jian-Hui Song, Hui-yong Chen, Jia-Jie Zhou, Shi-Jun Tang, Shan Yao, Mao Ye, Wei-Hong Tan
Journal: Blood (2013)
Abstract 5151: Yap reprograms glutamine metabolism and supports growth during liver development and tumorigenesis
Authors: Andrew G. Cox, Katie L. Hwang, Kimberley Evason, Kristin K. Brown, Sebastian Beltz, Keelin O'Connor, Giorgio G. Galli, Dean Yimlamai, Sagar Chhangawala, Evan Lien, Fernando D. Camargo, John Asara, Yariv Houvras, Didier Y. Stainier, Wolfram Goessling
Journal: Cancer Research (2015)

Abstract Hepatocellular carcinoma is a global health problem with poor prognosis and limited therapeutic options. Recently, the Hippo pathway has emerged as a master regulator of organ size control and tumorigenesis. However, the metabolic impact of the pathway is poorly understood. Using a transgenic zebrafish model with liver-specific activation of the Hippo pathway effector Yap, we have shown that Yap promotes hepatomegaly and liver dysplasia. In addition, we demonstrate that the Yap transgenics are highly susceptible to chemically-induced hepatocarcinogenesis. Transcriptomic and metabolomic profiling reveals that Yap enhances glutamine synthase (GS) expression and elevates steady-state levels of glutamine, respectively. Intervention studies with the GS inhibitor methionine sulfoximine established that elevated GS activity contributes to the rapid liver growth observed during Yap-driven hepatomegaly. Finally, studies in cultured human cancer cells identify GS as a bone-fide Yap target gene, confirming that the GS regulation by Yap is evolutionarily conserved. We conclude that Yap regulates GS expression and reprograms nitrogen metabolism, which contributes to liver growth during development and tumorigenesis. We hypothesize that Yap integrates the anabolic demands of rapid cell proliferation by increasing the flux of glutamine into nucleotide biosynthesis. Citation Format: Andrew G. Cox, Katie L. Hwang, Kimberley Evason, Kristin K. Brown, Sebastian Beltz, Keelin O'Connor, Giorgio G. Galli, Dean Yimlamai, Sagar Chhangawala, Evan Lien, Fernando D. Camargo, John Asara, Yariv Houvras, Didier Y. Stainier, Wolfram Goessling. Yap reprograms glutamine metabolism and supports growth during liver development and tumorigenesis. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 5151. doi:10.1158/1538-7445.AM2015-5151
Stool frequency is associated with gut microbiota composition
Authors: Fatemeh Hadizadeh, Susanna Walter, Meriem Belheouane, Ferdinando Bonfiglio, Femke-Anouska Heinsen, Anna Andreasson, Lars Agreus, Lars Engstrand, John F Baines, Joseph Rafter, Andre Franke, Mauro D'Amato
Journal: Gut (2016)

We read with great interest the two recent communications by Vandeputte et al 1 and Tigchelaar et al ,2 which reported an association between stool consistency and gut microbiota composition. Both studies focused on stool consistency, based on the Bristol Stool Scale (BSS) as the main trait, due to its reported correlation with colonic transit time (CTT) that is of clinical relevance for several GI conditions. However, stool frequency, another feature of human bowel function that is easy to measure and record, has also been shown to correlate with CTT,3 ,4 although to a lesser extent than stool form, and has not yet been investigated in relation to microbiota composition.

We examined the association between gut microbiota and stool frequency in the Population-based Colonoscopy study, a general population-based cohort from Stockholm, Sweden, previously described in detail.5 Sixty-nine individuals (21 males and 48 females, aged 55.6±10.33) with available frozen faecal samples and daily recordings of defaecation …
Immunophenotypic characterization of relapsed chronic lymphocytic leukemia patients treated with lumiliximab in combination with FCR
Authors: S. Tangri, J. Ranuio, A. Estrellado, J. C. Byrd, S. O' Brien, T. J. Kipps, A. Cesano, H. Mu, S. Harris
Journal: Journal of Clinical Oncology (2008)

7067 Background: Lumiliximab is an anti-CD23 monoclonal antibody under investigation for the treatment of patients with relapsed B-cell chronic lymphocytic leukemia (BCLL). A comprehensive immunophenotypic characterization of CLL cells obtained from patients treated with lumiliximab in combination with fludarabine, cyclophosphamide, and rituximab (L + FCR) was conducted. This included an analysis of the frequency of BCLL cells (CD5+CD19+), expression levels of CD38 (a negative prognostic factor), CD55 and CD59 (potential resistance markers of rituximab therapy). Methods: Immunophenotypic characterization was performed by four color flow cytometry analysis. BCLL cells were first identified by gating on viable CD45+ cells and subselecting with antibodies to CD5 and CD19 receptors. Antigen expression levels and their frequencies were reported in terms of mean fluorescence intensities (MFI) and fraction (%) of positive BCLL cells. Results: The analysis of peripheral blood samples from L + FCR treated patients indicated a substantial decrease in CD5+CD19+ cells in 30 of the 31 evaluable patients, although, the time to CLL count reduction following therapy was variable, ranging from week 1 to week 13. Clinical activity was observed in patients with both high (>30%) and low (<30%) levels of CD38 expression (MFI 6 - 230). Finally, clinical activity of L +FCR was independent of pre-treatment expression levels of CD55 (MFI 45–272) and CD59 antigen (MFI 20–191) and was also observed in a few patients showing increased expression of CD59 receptor, compared with their individual pre-treatment values, which has been associated with resistance to single agent rituximab. Conclusions: Clinically, L + FCR is an effective regimen in decreasing tumor burden in the peripheral blood of patients with BCLL. Importantly, the clinical activity of L + FCR appears to be independent of CD38 expression (a poor prognostic factor) and thereby may provide clinical benefit to a subset of patients with unfavorable clinical outcomes. Clinical activity was also observed in patients with BCLL expressing high levels of CD59 antigen, thus, suggesting a different MOA than other mAbs active in this indication such as Rituxan. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration Biogen Idec Biogen Idec Biogen Idec
TCTAP A-070 Long-Term Safety and Efficacy of Closure of Atrial Septal Defects with Cocoon Septal Occluder
Authors: Rajasekhar Durgaprasad, Vamsidhar Akkulagari, Vanajakshamma Velam, Latheef Kasala, Obul Reddy Gajjala, Boochi Babu Mannuva, Vasudevachetty Pakala
Journal: Journal of the American College of Cardiology (2016)
Deletion Of Tifab, a Novel Candidate Gene On Chromosome 5q, Results In Hematopoietic Defects By Changing The Dynamic Range Of Innate Immune Pathway Activation
Authors: Melinda Varney, Susanne Christie, Madeline Niederkorn, Jing Fang, Andres Jerez, Jaroslaw P. Maciejewski, Jun-ichiro Inoue, Daniel T Starczynowski
Journal: Blood (2013)
Abstract P6-04-08: Expression profile of long non-coding RNAs characterizes different subtypes of breast cancer
Authors: M Barton, J Santucci-Pereira, J Russo
Journal: Cancer Research (2016)

Abstract Long non-coding RNAs (lncRNAs) are RNA molecules longer than 200 nucleotides that are not translated into proteins, but regulate the transcription of genes involved in different cellular processes, including differentiation, cancer initiation and progression. The relevance of several lncRNAs in the transcriptional and post-transcriptional field is now well established. Their roles have been found to vary from forming complexes needed for gene transcription to having critical roles in the cytoplasm where they regulate protein localization, mRNA translation and stability. Microarray analysis of normal breast of parous and nulliparous postmenopausal women revealed that lncRNAs are up-regulated in the parous breast [Int. J. Cancer: 131, 1059-1070, 2012]. Subsequently, RNA sequencing was performed to a subset of these samples to understand the role of lncRNAs in the regulation of transcription and their potential function in pregnancy's effect in reducing the lifetime risk of developing breast cancer. In this work, RNA sequencing of healthy postmenopausal breast tissue biopsies from 8 parous and 8 nulliparous women using Illumina platform was performed. The sequencing results show that there are 42 lncRNAs differentially expressed between parous and nulliparous breast tissue. After analysis of these 42 lncRNAs using bioinformatics and thermodynamic filters, 10 lncRNAs were selected to be tested in vitro. Using RT-qPCR, we have demonstrated that the expression profile of at least 10 lncRNAs is characteristic of each epithelial breast cancer cell subtype (luminal, triple negative and cells that overexpress HER2). Moreover, these lncRNAs are differentially expressed in breast tumors when compared to its adjacent normal tissue. Overexpression and knock out experiments of several of these lncRNAs are underway to prove their relevance in breast differentiation and cancer initiation. The results in cancer/normal immortalized breast cell lines and tumor/adjacent normal breast tissue point to the potential of these lncRNAs as targets, not only for therapeutic approaches against breast cancer, but also as preventive measures for nulliparous women. (This work was supported by NIH core grant CA06927 to Fox Chase Cancer Center). Citation Format: Barton M, Santucci-Pereira J, Russo J. Expression profile of long non-coding RNAs characterizes different subtypes of breast cancer. [abstract]. In: Proceedings of the Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium: 2015 Dec 8-12; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(4 Suppl):Abstract nr P6-04-08.
ANGI-08RADIOGENOMIC rCBV-IMAGING VISUALIZES THE DISTINCT ANGIOGENESIS TRANSCRIPTOME SIGNATURES OF IDH MUTANT AND WILD-TYPE GLIOMAS
Authors: Philipp Kickingereder, Felix Sahm, Alexander Radbruch, Wolfgang Wick, Sabine Heiland, Andreas von Deimling, Martin Bendszus, Benedikt Wiestler
Journal: Neuro-Oncology (2015)

BACKGROUND: The recent identification of isocitrate dehydrogenase (IDH) mutations in gliomas and several other cancers suggests that this pathway is involved in oncogenesis; however effector functions are complex and yet incompletely understood. To study the regulatory effects of IDH on hypoxia-inducible-factor 1-alpha (HIF1A), a driving force in hypoxia-initiated angiogenesis, we performed mRNA-expression and functional, as well as genotype/imaging phenotype correlation analysis. METHODS: We studied differential mRNA-expression profiles from 288 samples with low-grade and anaplastic gliomas from The Cancer Genome Atlas (TCGA) of HIF1A and related downstream signaling on a single-gene and pathway level, as well as upstream biological causes and probable downstream effects between mutant and wild-type IDH tumors. Genotype/imaging phenotype correlation analysis was performed in a separate (local) dataset with relative cerebral blood volume (rCBV) MRI - an estimate of tumor angiogenesis - in 73 treatment-naive patients with low-grade and anaplastic gliomas. RESULTS: We show decreased expression of HIF1A-target genes on a single-gene and pathway level, strong inhibition of upstream regulators such as HIF1A and downstream biological functions such as angio- and vasculogenesis in IDH-mutant tumors. Our radiogenomic imaging approach revealed increased levels of rCBV in IDH wild-type tumors, where a one-unit increase in rCBV corresponded to a two-third decrease in the odds for an IDH-mutation and correctly predicted IDH mutation status in 88% of patients. CONCLUSION: Together, these findings show that IDH-mutation status is associated with a distinct angiogenesis transcriptome signature which is non-invasively predictable with rCBV-imaging.
NHS leader defends expansion of personal health budgets to 100 000 people by 2020
Authors: Matthew Limb
Journal: BMJ (2016)

Experts have clashed over the strength of evidence used to support rolling out personal health budgets in England.

Sam Bennett, NHS England’s head of personal health budgets and integrated personal commissioning, came under attack for saying that the case for a big extension of personal health budgets was “compelling.”

Peter Beresford, a social policy professor who heads the Centre for Citizen Participation at Brunel University, accused NHS chiefs of adopting the same model for personal budgets that was shown to have failed in social care and said that this would undermine NHS principles. He said, “We have a social care system that everybody including ministers says is in utter crisis, and yet we are turning to that policy for improvement to …
PML–RARα kinetics and impact of FLT3–ITD mutations in newly diagnosed acute promyelocytic leukaemia treated with ATRA and ATO or ATRA and chemotherapy
Authors: L Cicconi, M Divona, C Ciardi, T Ottone, A Ferrantini, S Lavorgna, V Alfonso, F Paoloni, A Piciocchi, G Avvisati, F Ferrara, E Di Bona, F Albano, M Breccia, E Cerqui, M Sborgia, M G Kropp, A Santoro, A Levis, S Sica, S Amadori, M T Voso, F Mandelli, F Lo-Coco
Journal: Leukemia (2016)
A Randomized Multicentre Phase Ii Study of Pazopanib Plus Best Supportive Care (Bsc) Vs Bsc Alone in Metastatic Gastrointestinal Stromal Tumors (Gist) Resistant to Imatinib and Sunitinib
Authors: J-Y. Blay, J. Domont, C. Cropet, A. Italiano, E. Bompas, P. Cassier, I.L. Ray-Coquard, M. Rios, A. Adenis, O. Mir, O. Bouché, B. Bui, F. Duffaud, F. Bertucci, N. Isambert, A. Belleville, E. Remir, J. Gautier, A. Le Cesne, D. Perol
Journal: Annals of Oncology (2014)
Nilotinib versus imatinib in patients (pts) with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP): ENESTnd 3-year (yr) follow-up (f/u).
Authors: Hagop Kantarjian, Ian W. Flinn, Stuart Goldberg, Udomsak Bunworasate, Maria Aparecida Zanichelli, Hirohisa Nakamae, Timothy P. Hughes, Andreas Hochhaus, Giuseppe Saglio, Richard Charles Woodman, Rick E. Blakesley, Charisse N. Kemp, Matt E. Kalaycio, Richard A. Larson
Journal: Journal of Clinical Oncology (2012)

6509^ Background: In ENESTnd, nilotinib significantly reduced progression to AP/BC and demonstrated superior rates of MMR, MR 4 , and MR 4.5 vs imatinib with f/u of 2 yrs. Methods: 846 pts with Ph+ CML-CP were randomized to nilotinib 300 mg BID (n = 282), nilotinib 400 mg BID (n = 281), or imatinib 400 mg QD (n = 283). Here, we report 3-yr f/u data. Results: Both nilotinib doses continued to demonstrate significantly higher rates of MMR, MR 4 , and MR 4.5 vs imatinib. In a landmark analysis, pts with BCR-ABL transcript levels ≤ 10% at 3 months (mo) had a higher probability of achieving MMR by 1 and 2 yrs vs pts with transcript levels &gt; 10%. No new progressions occurred on treatment since the 2-yr analysis; rates of progression to AP/BC including events on treatment (n = 2, 3, 12) and those occurring both on treatment and after discontinuation (n = 9, 6, 19) were significantly lower for nilotinib 300 mg BID and nilotinib 400 mg BID vs imatinib, respectively. At 3 yrs, OS considering only CML-related deaths was significantly higher for nilotinib vs imatinib. The safety profiles of nilotinib and imatinib were similar to those at 2 yrs. Conclusions: 3-yr f/u confirms the superiority of nilotinib vs imatinib and an acceptable tolerability profile for the treatment of pts with newly diagnosed Ph+ CML-CP. [Table: see text]
Integrative genomic deconvolution of rheumatoid arthritis GWAS loci into gene and cell type associations
Authors: Alice M. Walsh, John W. Whitaker, C. Chris Huang, Yauheniya Cherkas, Sarah L. Lamberth, Carrie Brodmerkel, Mark E. Curran, Radu Dobrin
Journal: Genome biology (2016)

Although genome-wide association studies (GWAS) have identified over 100 genetic loci associated with rheumatoid arthritis (RA), our ability to translate these results into disease understanding and novel therapeutics is limited. Most RA GWAS loci reside outside of protein-coding regions and likely affect distal transcriptional enhancers. Furthermore, GWAS do not identify the cell types where the associated causal gene functions. Thus, mapping the transcriptional regulatory roles of GWAS hits and the relevant cell types will lead to better understanding of RA pathogenesis. We combine the whole-genome sequences and blood transcription profiles of 377 RA patients and identify over 6000 unique genes with expression quantitative trait loci (eQTLs). We demonstrate the quality of the identified eQTLs through comparison to non-RA individuals. We integrate the eQTLs with immune cell epigenome maps, RA GWAS risk loci, and adjustment for linkage disequilibrium to propose target genes of immune cell enhancers that overlap RA risk loci. We examine 20 immune cell epigenomes and perform a focused analysis on primary monocytes, B cells, and T cells. We highlight cell-specific gene associations with relevance to RA pathogenesis including the identification of FCGR2B in B cells as possessing both intragenic and enhancer regulatory GWAS hits. We show that our RA patient cohort derived eQTL network is more informative for studying RA than that from a healthy cohort. While not experimentally validated here, the reported eQTLs and cell type-specific RA risk associations can prioritize future experiments with the goal of elucidating the regulatory mechanisms behind genetic risk associations.
The NOTCH1/CD39 axis: a Treg trip-switch for GvHD
Authors: B Del Papa, A Pierini, P Sportoletti, S Baldoni, D Cecchini, E Rosati, E Dorillo, P Aureli, T Zei, R Iacucci Ostini, L Ruggeri, A Carotti, A Velardi, R Negrin, M F Martelli, F Falzetti, M Di Ianni
Journal: Leukemia (2016)