tbuckley/cabot-search huggingface dataset:
A memorable patient: The value of communication
Authors: Y. Ou
Journal: BMJ (2003)

I expect she is back in Vietnam now. I often think about her and her family.

She was a pleasant child, with limited Cantonese picked up from her many years spent in a detention camp in Hong Kong. She had had a relapse of her nephrotic syndrome and had stayed with us a while until diuresis occurred, as the camps were not suitable for someone receiving high dose corticosteroids. She also had a history of asthma, which was quiescent at the time.

We got on well, despite the language barrier. I guess one doesn't need many words during play. I explained her condition to her softly spoken mother through an interpreter. I learnt …
OP0221 Live cell imaging of human neutrophil responses to MSU crystals
Authors: S. Chatfield, B. McKenzie, I. Wicks
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Neutrophil Extracellular Traps (NETs) are a recently described antibacterial mechanism (1). Neutrophils stimulated with live bacteria and other stimuli including phorbol myristate acetate (PMA) release nuclear DNA coated with neutrophil granule proteins including myeloperoxidase (MPO) and neutrophil elastase (NE). Gout is an inflammatory disease triggered by monosodium Urate (MSU) crystals (2) and is characterised by neutrophil infiltration and activation. The role of NET formation in the pathogenesis of gout is unclear. <h3>Objectives</h3> To assess the kinetics of NET formation in human neutrophils following exposure to MSU crystals in vitro. <h3>Methods</h3> Fixed confocal microscopy and live cell imaging were used to characterise extracellular DNA release in response to synthetic MSU crystals (0.05–0.2 mg/ml) and the classical NET stimulus, PMA (27 nM). A computerised quantification system was used to compare the kinetics of NET release with different stimuli and to assess the effect of potential inhibitors. <h3>Results</h3> MSU crystals caused DNA release from healthy control human neutrophils. Extracellular DNA structures were coated with MPO and NE, consistent with NETs. MSU crystals caused more rapid DNA release than PMA (Fig. 1, Mean ± SEM, n=3, in duplicate). DNA release following MSU crystal stimulation was evident as early as 20 minutes after stimulation, compared to one hour with PMA. DPI, an inhibitor of NADPH oxidase completely suppressed PMA-induced NET release but had minimal effect on MSU-induced DNA release. Addition of autologous serum significantly abrogated PMA-induced NET release but only delayed MSU-induced DNA release. <h3>Conclusions</h3> MSU crystals cause DNA release consistent with NETosis. MSU crystal-induced NET release was not dependent on reactive oxygen species and occurred more rapidly than PMA NET release. This suggests different biochemical pathways are involved, further investigation of which may provide insight into the pathogenesis of gout. <h3>References</h3> Brinkmann et al. Science. 2004 Mar 5;303(5663):1532-5. Faires JS, McCarty JD. The Lancet. 1962 Oct 6;280(7258):682-685 <h3>Disclosure of Interest</h3> None Declared
Abstract 3542: Effects of single nucleotide polymorphisms on treatment outcomes and toxicity in patients treated with sunitinib for biliary tract and gastric cancers.
Authors: Chi Hoon MAENG, Jun Ho Lee, Jeeyun Lee, Jung Yong Hong, Moon Ki Choi, Young Saing Kim, Hyun Ae Jung, Joon Oh Park, Se Hoon Park, Young Suk Park, Won Ki Kang, Ho Yeong Lim
Journal: Cancer Research (2013)

Abstract BACKGROUND: We analyzed the efficacy and toxicity profile of sunitinib according to single nucleotide polymorphisms (SNPs) of VEGFA and KDR among the patients with gastric or biliary tract cancer. METHODS: We examined 8 known SNPs of VEGFA and 5 SNPs of KDR among patients with gastric or biliary tract cancer who were treated with sunitinib in our two previous phase II studies. We assessed progression free survival (PFS), overall survival (OS), and toxicity and their relationships to these SNPs. RESULTS: A total of 63 patients were evaluable. Among candidate SNPs, rs2010963, rs833068, and rs1870377 were associated with poor PFS (P = .009, .002, and .029, respectively), while rs1870377 and rs7692791 were associated with poor OS (P = .001 and 0.03, respectively). Multivariate analysis showed that only rs1870377 had significant effects on both PFS and OS. Toxicity evaluation indicated that rs1531289 was associated with grade 3-4 anemia. (P = .03). CONCLUSIONS: Certain SNPs of KDR may affect treatment outcome and toxicity of patients treated with sunitinib. Citation Format: Chi Hoon MAENG, Jun Ho Lee, Jeeyun Lee, Jung Yong Hong, Moon Ki Choi, Young Saing Kim, Hyun Ae Jung, Joon Oh Park, Se Hoon Park, Young Suk Park, Won Ki Kang, Ho Yeong Lim. Effects of single nucleotide polymorphisms on treatment outcomes and toxicity in patients treated with sunitinib for biliary tract and gastric cancers. [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 3542. doi:10.1158/1538-7445.AM2013-3542
NON-INVASIVE FRACTIONAL FLOW RESERVE DERIVED FROM CORONARY COMPUTED TOMOGRAPHY ANGIOGRAPHY IN PATIENTS WITH ACUTE CHEST PAIN: RESULTS FROM THE ROMICAT II TRIAL
Authors: Maros Ferencik, Michael T. Lu, Thomas Mayrhofer, Alexander Ivanov, Elizabeth Adami, Souma Sengupta, Campbell Rogers, Udo Hoffmann
Journal: Journal of the American College of Cardiology (2016)
A Controlled Trial of Diazepam Administered during Febrile Illnesses to Prevent Recurrence of Febrile Seizures
Authors: N. Paul Rosman, Theodore Colton, Jan Labazzo, Paula L. Gilbert, Nancy B. Gardella, Edward M. Kaye, Carla Van Bennekom, Michael R. Winter
Journal: New England Journal of Medicine (1993)

Phenobarbital, once widely prescribed to prevent febrile seizures, is now in disfavor because of its side effects and lack of efficacy. Diazepam, administered only during episodes of fever, may be a safe, effective agent to prevent the recurrence of febrile seizures.
THE USE OF HEMODYNAMIC INDICES AS PREDICTORS OF IMPROVEMENT IN MITRAL REGURGITATION AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT (TAVR)
Authors: Rajiv Tayal, Martin Miguel Amor, Manjusha Anna, Cheng Chu, Alan Weinberg, Afroditi Emporelli, Geru Wu, Patricia Panfile, Chunguang Chen, Bruce Haik, Paul Burns, Mark Russo, Najam Wasty, David Baran, Marc Cohen
Journal: Journal of the American College of Cardiology (2015)
Partial Androgen Insensitivity
Authors: James A. Amrhein, Georgeanna Jones Klingensmith, Patrick C. Walsh, Victor A. McKusick, Claude J. Migeon
Journal: New England Journal of Medicine (1977)

We investigated eight patients with the Reifenstein syndrome to define the hormonal basis for this condition. The patients had normal or elevated concentrations of plasma androgens, normal production rates of testosterone and dihydrotestosterone, elevated serum levels of luteinizing hormone and normal 5alpha-reductase activity in skin fibroblasts. These findings indicate that the syndrome results from defective androgen action rather than from decreased androgen synthesis. The term "partial androgen insensitivity syndrome" describes this condition more accurately than a term based on clinical phenotype. Dihydrotestosterone binding studies in skin fibroblasts demonstrated two genetic variants similar to those reported in complete androgen insensitivity syndrome. One patient had a partial deficiency of cytoplasmic dihydrotestosterone binding, and four others had normal binding activity. The cause of the androgen insensitivity in the last four cases is unknown. Treatment with testosterone suppressed serum luteinizing hormone levels and promoted mild virilizing effects.
Abstract SY31-03: Inflammatory mechanisms of cancer-related fatigue
Authors: Julienne Bower
Journal: Cancer Research (2012)

Abstract Fatigue is one of the most common and disabling side effects of cancer treatment and may persist for months or years after successful treatment completion, causing significant impairment in quality of life. Basic research on neural-immune signaling has demonstrated that proinflammatory cytokines signal the central nervous system to trigger a constellation of behavioral changes that include fatigue as well depression, sleep disturbance, and cognitive impairment. This presentation will review the evidence linking proinflammatory cytokines and fatigue in cancer patients and survivors. In addition, we will consider host factors that influence inflammation and associated symptoms of fatigue, focusing on genetic mechanisms. There is considerable variability in the experience of post-treatment fatigue that cannot be explained by treatment exposure, suggesting that host factors play an important role in symptom severity and persistence. Single nucleotide polymorphisms (SNPs) that influence quantitative gene expression have been identified in the promoter regions of several genes that encode proinflammatory cytokines and examined individually in relation to breast cancer susceptibility and prognosis as well as behavioral symptoms. Here, we will present findings linking SNPs in the promoter regions of three proinflammatory cytokine genes (IL-1β -511 C&amp;gt;T (rs16944), IL6 -174 G&amp;gt;C (rs1800795), and TNF -308 G&amp;gt;A (rs1800629)) to fatigue in breast cancer survivors. Further, we will consider how alterations in glucocorticoid signaling pathways may contribute to persistent cancer-related fatigue. 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 SY31-03. doi:1538-7445.AM2012-SY31-03
Approaches to Monitoring Clinical Trials
Authors: T. R. Fleming, L. F. Watelet
Journal: JNCI Journal of the National Cancer Institute (1989)

Journal Article Approaches to Monitoring Clinical Trials Get access Thomas R. Fleming, Thomas R. Fleming * Department of Biostatistics, University of WashingtonSeattle, WA *Correspondence to: Dr. Thomas R. Fleming, Department of Biostatistics SC-32, University of Washington, Seattle, WA 98195. Search for other works by this author on: Oxford Academic PubMed Google Scholar Luc F. Watelet Luc F. Watelet Department of Biostatistics, University of WashingtonSeattle, WA Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 3, 1 February 1989, Pages 188–193, https://doi.org/10.1093/jnci/81.3.188 Published: 01 February 1989 Article history Received: 23 November 1988 Accepted: 23 November 1988 Published: 01 February 1989
Abstract 4385: The green tea polyphenol EGCG induces mesenchymal to epithelial transition (MET) and tumor regression in triple negative breast cancer (TNBC) cells and mouse xenograft model: involvement of CCN5.
Authors: Amlan Das, Snigdha Banerjee, Archana De, Inamul Haque, Gargi Maity, Matt McEwen, Sushanta K. Banerjee
Journal: Cancer Research (2013)

Abstract Background: Epithelial to Mesenchymal transition (EMT) is an important and coordinated series of events associated with tumor metastasis and invasion. Recent studies had shown the importance of CCN5 (also known as WISP-2,Wnt-1-induced signaling protein-2) in the regulation of various carcinomas including the breast cancer. Recent studies had showed that ectopic expression of CCN5 can reverse Epithelial-Mesenchymal transition (EMT) and inhibit cancer metastasis. Epigallocatechin-3-gallate (EGCG), a major polyphenol in green tea, has been extensively studied as a bioactive dietary component against various types of carcinomas through multiple mechanisms such as anti-oxidation, induction of apoptosis, inhibition of angiogenesis and metastasis. However, the mechanism of action of EGCG in breast carcinoma is uncertain. Objective: The objective of the present study is to determine whether CCN5 plays any significant role in EGCG-mediated cytotoxicity in triple negative breast cancer cells. Results: Exposure of triple negative human breast cancer (TNBC) cells, MDA-MB-231 and HCC70 to EGCG resulted in a dose-dependent inhibition of proliferation after 72h and the IC50 was observed around 75μM for MDA-MB-231 cells and 50μM for HCC70 respectively. We found EGCG-treatment effectively induces MET and inhibits the in vitro migration parallel with the induction of CCN5 expression in TNBC cells in a dose-dependent fashion. Furthermore, consistent with in vitro findings, tumor progression was drastically inhibited in EGCG-treated MDA-MB-231-tumor xenograft in nude mouse model. Conclusion: EGCG imparts its anti-cancer activity in both TNBC cells as well as MB-231-tumor xenografts via induction of CCN5. Citation Format: Amlan Das, Snigdha Banerjee, Archana De, Inamul Haque, Gargi Maity, Matt McEwen, Sushanta K. Banerjee. The green tea polyphenol EGCG induces mesenchymal to epithelial transition (MET) and tumor regression in triple negative breast cancer (TNBC) cells and mouse xenograft model: involvement of CCN5. [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 4385. doi:10.1158/1538-7445.AM2013-4385
Abstract 5390: QBI-139, a human RNase variant in a phase I trial, works in combination
Authors: Laura E. Strong, John A. Kink, Baigen Mei, Mark N. Shahan, Ronald T. Raines
Journal: Cancer Research (2010)

Abstract The EVade™ Ribonucleases (RNases) are a new class of anti-cancer drugs that target the RNA in cancer cells. These EVade™ RNases are variants of native mammalian RNases that have been converted to anti-cancer agents by diminishing their binding to their natural inhibitor protein. One of these EVade™ RNases, called QBI-139, has advanced to human clinical trials. QBI-139 shares 95% sequence identity with the wild type human RNase 1. QBI-139 has shown tumor growth inhibition against a variety of cancers, including: colon, non-small cell lung, ovarian, pancreatic and prostate cancers. QBI-139 is currently in a Phase I clinical trial in patients with solid tumors. A frog RNase called Ranpirnase (Alfacell) that shares only 20% sequence identity with human RNase 1 has been in clinical trials and responses have been seen in esophageal, non-small cell lung and breast cancers as well as unresectable mesothelioma. The next stage of clinical development of QBI-139 will require selection of a specific indication as well as an existing treatment regimen to be used in combination with QBI-139. The Phase I trial may provide insights about sensitive tumor types. However, mouse models of cancer will be used to select the combinations for development. QBI-139 has shown efficacy against non-small cell lung cancer (A549 cell line) in xenograft models. Cisplatin is a standard of care treatment for non-small cell lung cancer in patients. The ability of QBI-139 and cisplatin to work together to cause tumor growth inhibition was determined in a non-small cell lung cancer xenograft model (A549 cell line). Cisplatin (3 mg/kg) and QBI-139 (15 mg/kg) were used as controls. The combination of cisplatin and QBI-139 (3 and 15 mg/kg, respectively) was also tested. Cisplatin treatment resulted in tumor growth inhibition (TGI) of 60% while QBI-139 caused 76% TGI. The combination of the two drugs resulted in a TGI of 96%, strongly supporting the use of QBI-139 in combination with cisplatin for the treatment of lung cancer. Even the combination of the two drugs exhibited minimal impact on the health of the animals. EVade™ Ribonucleases are novel agents that provide a new way to target the RNA in cancer cells and are an innovative new tool for oncologists. QBI-139 has a variety of benefits, including: a novel mechanism of action with clinical support, broad in vivo anti-tumor activity alone and in combination with standard of care therapies and a strong tolerability profile. 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 5390.
Scintigraphy of Proximal Femoral Focal Deficiency
Authors: ERIC SCHALLEN, IRIS De ODORICO, BRAHM SHAPIRO
Journal: Clinical Nuclear Medicine (1997)

Proximal femoral focal deficiency is an uncommon but severe congenital skeletal abnormality manifested by selective hypoplasia of the proximal femur(s), resulting in limb shortening and articular dysfunction. Functional limitation varies greatly and optimal treatment planning demands accurate and early (e.g., childhood) classification into prognostic groups. Depending on disease severity, management ranges from supportive prostheses to lower extremity amputation with complex partial surgical reconstruction. Radiologic classification systems have not been widely accepted as adequate to guide early management. Scintigraphy may have a complementary role in evaluating the growth potential of immature femurs and in therapeutic planning.
Botulinum Toxin A for Axillary Hyperhidrosis (Excessive Sweating)
Authors: Marc Heckmann, Andrés O. Ceballos-Baumann, Gerd Plewig
Journal: New England Journal of Medicine (2001)

Treatment of primary focal hyperhidrosis is often unsatisfactory. Botulinum toxin A can stop excessive sweating by blocking the release of acetylcholine, which mediates sympathetic neurotransmission in the sweat glands.
Abstract 4979: The role of Tel in repression of BCL-XL transcription in tumor cells
Authors: Xiaobo Cao, Chander Peddaboina, Daniel Jupiter, Lidong Zhang, James Littlejohn, Philip Rascoe, Roy Smythe
Journal: Cancer Research (2010)

Abstract Study of Bcl-xl and hepatocyte growth factor (HGF) receptor c-Met demonstrates that ETS transcription factors influence the transcriptional control of Bcl-xl in multiple tumors. The phosphorylation of Tel, a transcriptional repressor in the ETS family, by activated c-Met is required to increase Bcl-xl transcription in addition to activation of ETS2, a transcriptional activator. Our data indicate that stimulation by HGF causes the activation of ERK and leads to the nuclear export of Tel. In order to determine whether ERK is responsible for the phosphorylation of Tel after HGF stimulation, physical interaction between Tel and ERK was detected using I.P. (Tel)-western blotting (ERK). To determine if blocking MAP kinase could prevent Tel's phosphorylation after HGF exposure, we again used I.P. Western to compare the phosphorylation of Tel under specific ERK kinase inhibitors, after HGF exposure, to the phosphorylation of Tel in the absence of inhibitors, after HGF exposure. A His-Tel 213mutant (phosphorylation sites mutants) was created. The Tel 213 mutant did not undergo phosphorylation induced by c-Met activation, as demonstrated by I.P. Western blot. Nuclear localization of mutated His-Tel was detected under HGF/EGF exposure via fluorescent microscopy using FITC labeled anti-his antibody, indicating that phosphorylation of Tel is also required for nuclear export. A luciferase reporter assay shows that the transient expression of Tel 213 mutant in cancer cell lines results in further repression of Bcl-xl promoter activity. Indeed, Tel 213's repressive function is independent of c-Met stimulation, as determined by comparing with wild type Tel cDNA transfected cells. Consequently, Tel 213 transfection results in much stronger reduction in Bcl-xl mRNA and protein expression levels in the presence of HGF, as compared to transfection with wild-type Tel cDNAs in the presence of HGF. Furthermore, a CHIP assay demonstrates that the activation of c-Met reduced the binding of wild-type Tel to the Bcl-xl promoter, while the binding of Tel 213 to bcl-xl promoter was not affected. Finally, transfection of Tel 213 leads to increased cell proliferation inhibition and apoptosis. Taken together, these findings are supportive of a role for Tel, through a c-Met aixs, as an inhibitor of Bcl-xl transcription. 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 4979.
Abstract 5328: MicroRNA-181a suppresses salivary adenoid cystic carcinoma metastasis by targeting the ERK/Slug pathway.
Authors: Qianting He, Xiaofeng Zhou, Su Li, Zhujian Chen, Dan Chen, Yuchen Cai, Zhonghua Liu, Tingting Zhao, Anxun Wang
Journal: Cancer Research (2013)

Abstract MicroRNA deregulation plays a major role in the initiation and progression of many cancers. The objective of this study is to evaluate the role of miR-181a in the metastasis of salivary adenoid cystic carcinoma (SACC). We identified a panel of differentially expressed microRNAs in two pairs SACC cell lines with different metastatic potential using microarrays. Among these differentially expressed microRNAs, the down-regulation of miR-181a was further validated by quantitative RT-PCR. Functional analysis indicated that miR-181a inhibits SACC cell migration, invasion and proliferation in vitro and in vivo. Ectopic transfection of miR-181a inhibited the expression of NGF, VEGF, TGFβ2, ERK1/2, pERK1/2 and Slug in SACC-LM cells which had higher expression of these genes compared to SACC-83 cells; while inverse results were found in miR-181a LNA transfected SACC-83 cells. The direct targeting of miR-181a to the Slug and ERK2 mRNAs were confirmed by luciferase reporter gene assays. SiRNA-mediated knockdown of Slug, ERK2 led to reduced cell migration and invasion of SACC, and knockdown of ERK2 suppresses the expression of Slug. Taken together, these results suggest that microRNA deregulation (i.e., down-regulation of miR-181a) contributes to the metastasis of SACC. MiR-181a-mediated suppression of SACC metastasis may be achieved in part by directly targeting Slug and ERK2 and regulating ERK/Slug pathway. Citation Format: Qianting He, Xiaofeng Zhou, Su Li, Zhujian Chen, Dan Chen, Yuchen Cai, Zhonghua Liu, Tingting Zhao, Anxun Wang. MicroRNA-181a suppresses salivary adenoid cystic carcinoma metastasis by targeting the ERK/Slug pathway. [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 5328. doi:10.1158/1538-7445.AM2013-5328
What can neuroimaging meta-analyses really tell us about the nature of emotion?
Authors: Stephan Hamann
Journal: Behavioral and Brain Sciences (2012)

In Vytal and Hamann (2010) we reported a neuroimaging meta-analysis that found that basic emotions can be distinguished by their brain activation correlates, in marked contrast to Lindquist et al.'s conclusions in the target article. Here, I discuss implications of these findings for understanding emotion, outline limitations of using meta-analyses and neuroimaging as the sole basis for deciding between emotion views, and suggest that these views are essentially compatible and could be adapted and combined into an integrated emotion framework.
High frequency of fusion transcripts of exon 11 and exon 4/5 in AF-4 gene is observed in cord blood, as well as leukemic cells from infant leukemia patients with t(4;11)(q21;q23)
Authors: S Yamamoto, M Zaitsu, E Ishii, H Yatsuki, S Mizutani, M Eguchi, K Ihara, T Okamura, T Hara, S Miyazaki
Journal: Leukemia (1998)