tbuckley/cabot-search huggingface dataset:
Successful Thrombolysis, Early Luxury Perfusion, and Spectacular Outcome After Acute Ischemic Stroke
Authors: Vijay K. Sharma, Prakash R. Paliwal, Arvind K. Sinha
Journal: Clinical Nuclear Medicine (2012)

Timely recanalization in acute ischemic stroke often results in good clinical outcomes. However, sudden recanalization and increased blood flow into the ischemic brain tissue may be harmful in some patients. Impaired autoregulation in early poststroke period occasionally results in ‘luxury perfusion,’ due to excessive vasodilatation of collaterals. The relationship between hyperperfusion and tissue outcome in acute ischemic stroke has remained unclear. We present multimodal neuroimaging features of luxury perfusion in a patient after successful thrombolysis for acute left middle cerebral artery thrombotic occlusion.
Abstract 458: A novel resveratrol analogue, HS-1793, down-regulates the expression levels of hypoxia-inducible factor-1α and VEGF, and inhibits hypoxia-induced cell migration of human prostate cancer cells
Authors: Dong Hwan Kim, Min Young Kim, Mohammad Akbar Hossain, Jin-Ah Kim, Yong Jung Kang, Hongsuk Suh, Yung Hyun Choi, Gi Young Kim, Nam Deuk Kim
Journal: Cancer Research (2010)

Abstract Hypoxia-inducible factor-1α (HIF-1α), a transcription factor, over- expressed in many human tumors and their metastases, and is closely associated with more aggressive tumor phenotype. An important objective of anti-cancer therapy is the development of new drugs that suppress hypoxic responses in solid tumors. In many studies, resveratrol has been shown to chemopreventive effect in various cancer cells. However, resveratrol's biological activity is limited by its photosensitivity and metabolic instability. This study was investigated the effects of a novel analogue of resveratrol, HS-1793, on the expression levels of HIF-1α and vascular endothelial growth factor (VEGF) in PC-3 human prostate cancer cells. Hypoxic condition induced a time-dependent increase in the level of HIF-1α protein in PC-3 cells, and treatment with HS-1793 markedly decreased HIF-1α expression level. HS-1793 also inhibited VEGF expression level. Mechanistically, HS-1793 inhibited HIF-1α and VEGF expression through multiple mechanisms. Firstly, HS-1793 inhibited both PI3K and Erk phosphorylations in PC-3 cells. Secondly, HS-1793 substantially induced HIF-1α protein degradation through the proteasome pathway. Finally, HS-1793 inhibited hypoxia-induced cell migration. These data suggested that HS-1793 may inhibit human prostate cancer progression and angiogenesis by inhibiting HIF-1α and VEGF expression. Moreover, HS-1793 showed more potent effect than resveratrol on the cytotoxic effects on PC-3 cells. Taken together, these results implied that HS-1793, a novel analogue of resveratrol, might be a new potent chemopreventive agent against human prostate cancer cells. [This work was supported by the Korea Science and Engineering Foundation (KOSEF) grant funded by the Korea government (MOST) (R01-2006-000-11117-0)]. 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 458.
AB0522 The use of rituximab in current practice during the rheumatoid arthritis naive of anti-TNF alpha
Authors: D.M. Chafia
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rituximab (RTX) is a biotherapy usually recommended during the rheumatoid arthritis (RA) refractory to at least one anti-TNFα. In our country RTX surpassed the anti TNF α in the treatment (TRT) of RA and received its AMM in refractory RA and/or in case of intolerance to conventional TRT. The objective of this study was to evaluate the tolerance and efficiency of RTX in patients suffering of RA and naive of anti-TNF α. <h3>Objectives</h3> The objective of this study was to evaluate the tolerance and efficiency of RTX in patients suffering of RA and naive of anti-TNF α. <h3>Methods</h3> it’s an observational and retrospective study, including 59 patients suffering from RA, treated with rituximab after failure of conventional TRT between October 2007 and September 2011. The data collected were: the patient characteristics, the disease characteristics, the type of TRT, the dose of corticosteroids, the rate of leukocytes, of Ig A, G, M, the immediate and delayed side effects. The therapeutic response was retained on the EULAR criteria, combined with the evaluation of the physician. <h3>Results</h3> 59 patients (46 women and 13 men) were treated with RTX (1000 mg x2), with retreatment in 13 cases. The average age was 47.5 years, the average duration of illness was 11.5 years, the Rheumatoid Factor was positive in 80%, the anti-CCP positive in 78%, the average number of previous disease modifying TRT was 2.52. methotrexate in 38 cases, leflunomide in 6 cases, 3 cases at salazopyrine, used in monotherapy in 12 cases. The initial DAS28 was in average 5.06 (3.1-7.02), the initial average rate of gammaglobulines was 12.2g/l on the 59 patients, 81% had a favorable response to treatment with an average decrease in individual DAS 28 of - 2.3. All were considered to have responded favorably to treatment. 13 patients (22%) relapsed and required retreatment. (8: 2 courses: 5: 3 courses, the time between two courses was between 8 and 28 months), followed by a good response. The Side effects observed during the perfusion: 5 cases headache, 4 cases arterial hypotension, 1 case of generalized pruritus, asthenia reported by all patients within 24 to 48 h after the perfusion. Other side effects were: 6 cases of infections (01 severe purulent conjunctivitis, 01skin infection, 03 urinary, 1pulmonary). No deaths, no case of tuberculosis, no decrease in immunoglobulin, no leukopenia in retreated patients. <h3>Conclusions</h3> This particular study using RTX during the RA naive of anti-TNF alpha, shows a remarkable efficiency of RTX, the tolerance of RTX is in total satisfactory even after retreatment. <h3>Disclosure of Interest</h3> None Declared
TM-10 * ALTERATIONS IN METABOLIC PATHWAYS IN GLIOBLASTOMA MULTIFORME CELLS IN RESPONSE TO HEXOKINASE-2 INHIBITION
Authors: S. Kumar, S. Jalali, A. Vartanian, S. Agnihotri, K. Burrell, G. Zadeh
Journal: Neuro-Oncology (2014)

INTRODUCTION: GBMs are characterized by elevated glycolysis, however to date effective therapies targeting tumor glycolysis have not been identified. Also, the contribution of metabolic pathways other than glycolysis, such as glutamine and fatty acid oxidation, that are key in providing carbon to TCA cycle, have not been explored in GBMs. Aim: In this study we aim to decipher the adaptive mechanisms brought about by the inhibition of tumor glycolysis in GBMs. We have investigated the metabolic changes occurring in GBM cells after the knockdown of key glycolytic enzyme, hexokinase2 (HK2). METHODS AND RESULTS: We have generated doxycyclin-inducible HK2 knockdown GBM cells by transfecting shRNA in U87 and three Glioma Stem Cell lines with different baseline molecular characteristics We confirm specific knockdown of HK2, with no change in HK1 or HK3, using western blot. HK2 knockdown reduced cell number and proliferative capacity, in addition to decrease in lactate production and O2 consumption. HK2 loss significantly increased NADP:NADPH ratio. Metabolic profiling by LC/MS targeted metabolomics was conducted after exposing GBM cells to C13-labeled glucose media. LC/MS metabolomics demonstrate that decrease in HK2 significantly reduced the levels of metabolites belonging to glycolysis and Pentose Phosphate Pathway. These two pathways are known to be associated with NADPH and biomass production for rapidly proliferating tumor cells. In contrast, metabolites in TCA cycle increased in response to HK2 inhibition. CONCLUSION: Our data strongly suggests that GBM cells activate alternate metabolic pathways in response to inhibition of HK2 dependent glycolysis. These results have important clinical implications in designing combinatorial targeted therapy for blocking tumor metabolism in GBMs. Our ongoing work is focused on establishing the metabolites involved in glutamine catabolism and fatty acid oxidation, both in-vitro and in-vivo GBM models.
Abstract 1087: The expression and activity of actin-regulating protein cofilin are associated with the cell cycle progression
Authors: Pei-Hsun Chiang, Shih-Chieh Hung, Yi-Jang Lee
Journal: Cancer Research (2010)

Abstract Cofilin is a member of actin depolymerizing factor (ADF)/cofilin family that can regulates actin dynamics for cancer growth and invasion/metastasis. Several lines of evidence have demonstrated that cofilin is associated with the cell cycle regulation, while the underlying mechanisms remain to be addressed. To better understand the involvement of cofilin in cell cycle progression, we dissected the cofilin expression and activity in different phases of the cell cycle. We synchronized human non-small lung A549 cancer cells in G1, S and G2/M phase by serum starvation, double thymidine blockage and nocodazole treatment, respectively. It was found that the expression of endogenous cofilin was weakest in G1 phase, while it was strongest in S phase and was modest in G2/M phase. This observation was further confirmed by detecting the down-regulation of highly expressed cofilin in S phase-synchronized cells entering mid-late S, G2/M and G1 phase of the cell cycle. Interestingly, it also showed that inactive form of cofilin (ser-3 phosphorylated) weakly expressed in S phase and gradually increased when cells progress through G2/M and G1 phases. These results suggest that cofilin expression and activity are coordinately regulated during the cell cycle progression. It is also consistent with our previous findings that enforced expression of cofilin results in G1 phase arrest but not S and G2/M phases. Moreover, the level of cofilin transcripts was not significantly altered in different phases of cell cycle. On the other hand, pretreatment of the proteasome inhibitor MG132 resulted in increase of cofilin in G1 phase, suggesting that the fluctuation of cofilin during cell cycle progression is associated with the protein stability. In addition, transduction of undegradable Y68F form of mutant cofilin potentially led to increase of the G1 percentage. Taken together, precisely regulation of cofilin expression and activity is important for cell cycle progression. Targeting on cofilin may provide alternative therapeutic strategy for cancer treatment. 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 1087.
P778 RESOURCE UTILIZATION DURING HEPATITIS C TREATMENT WITH BOCEPREVIR- OR TELAPREVIR-BASED TRIPLE THERAPY VS DUAL THERAPY IN A LARGE U.S. HEALTH MAINTENANCE ORGANIZATION
Authors: L.M. Nyberg, K.M. Chiang, Z. Li, A.H. Nyberg, Z.M. Younossi, T.C. Cheetham
Journal: Journal of Hepatology (2014)
ASSOCIATION OF DISEASE-SPECIFIC HEALTH STATUS WITH LONG-TERM MORTALITY AFTER TRANSCATHETER AORTIC VALVE REPLACEMENT
Authors: Suzanne Arnold, John Spertus, Sreekanth Vemulapalli, Dadi (David) Dai, Sean O’Brien, Suzanne Baron, Ajay Kirtane, Michael Mack, Philip Green, Matthew Reynolds, John Rumsfeld, David Cohen
Journal: Journal of the American College of Cardiology (2015)
AB0292 Effect of anti-tumor necrosis factor-a therapies on weight and body mass index in patients with rheumatoid arthritis and ankylosing spondylitis
Authors: T. Senturk, S. Cildag, I. Akdam
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> TNF-alpha plays a central role in the pathogenesis of rheumatic diseases and has become a target molecular structure for antibody or TNF-receptor (TNF-R) based treatment in the past few years. Whilst the effects of anti- tumor necrosis factor (anti-TNF) therapy upon disease control are well established in terms of reducing joint inflammation and destruction, its effect on weight remain to be clearly established. <h3>Objectives</h3> The aim of this study was to investigate the changes on weight and body mass index in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS) treated with anti-TNF. <h3>Methods</h3> Thirty-five patients with RA and AS, body weight and body mass index (BMI) were measured before initiation of anti-TNF ( infliximab, etanercept, adalimumab) treatment and after 48 weeks of treatment. BMI was divided into three categories (&lt;20 kg/m<sup>2</sup>, 20-30 kg/m<sup>2</sup>, &gt;30 kg/m<sup>2</sup>). <h3>Results</h3> Thirty-five patients were evaluated. 48 weeks after initiation of treatment the mean ± SD weight was increased from 71.31±15.28 kg to 73.11±14.40 kg (p=0.245), the mean ±SD BMI was increased from 25.97±5.86 kg/m<sup>2</sup> to 26.51±5.17 kg/m<sup>2</sup> (p=0.362). When the BMI was divided into 3 categories, after 48 weeks of treatment, the weight increased in the groups with BMI&lt;20 kg/m<sup>2</sup> (45± 5.8 kg to 52± 16.7 kg p=0.285) and BMI 20-30 kg/m<sup>2</sup> (71.12±11.07 kg to 74.45±12.31 kg p=0.018). The weight significantly decreased in the group with BMI &gt;30 kg/m<sup>2</sup> (87±9.34 kg to 80.57±9.14 p=0.017). <h3>Conclusions</h3> Anti-TNF treatment may have and indirect positive effect on lean mass throughout the general health improvement of patients, leading to increase of appetite. Several studies have reported body weight gain in patients with rheumatologic diseases after anti-TNF treatment. We observed that RA and AS patients with lower and normally BMIs tend to gain weight with anti-TNF therapy. In contrast the patients with high BMIs tend to decrease weight with anti-TNF therapy. <h3>Disclosure of Interest</h3> None Declared
DIURETIC RESPONSE IN ACUTE HEART FAILURE: AN ANALYSIS FROM ASCEND-HF
Authors: Jozine Ter Maaten, Allison Dunning, Mattia A.E. Valente, Kevin Damman, Justin Ezekowitz, Robert Califf, Randall Starling, Christopher O’Connor, Phillip Schulte, Jeffrey Testani, Adrian Hernandez, Wai Hong Tang, Adriaan Voors
Journal: Journal of the American College of Cardiology (2015)
Inaccuracy of TI-201 Brain SPECT in Distinguishing Cerebral Infections from Lymphoma in Patients with AIDS
Authors: ROBERT LICHO, SCOTTN LITOFSKY, MARTIN SENITKO, MARIE GEORGE
Journal: Clinical Nuclear Medicine (2002)

Studies have suggested using Tl-201 brain SPECT to differentiate lymphoma from infectious processes and to determine the timing for biopsy or empirical therapy for patients with AIDS-related brain lesions. This study prospectively investigated the utility of Tl-201 SPECT in distinguishing central nervous system lymphoma from non-neoplastic disease in patients with AIDS.Fourteen patients with AIDS and focal abnormalities on computed tomography or magnetic resonance imaging underwent brain SPECT before diagnosis (12 by biopsy, 2 by clinical course and response to therapy). A an uptake ratio (UR) was obtained by drawing a region of interest around the lesion, measuring average counts per pixel, and dividing this value by the value of a non-lesion-containing contralateral region of interest. The UR cutoff producing the highest accuracy (TP+TN/TP+TN+FP+FN) in discriminating lymphoma from another condition was determined from URs generated from these 14 patients.Five patients had lymphoma, five had toxoplasmosis, one had Herpes simplex virus encephalitis, two had progressive multifocal leukoencephalopathy, and one had gliosis (UR, 0.8). Patients were separated into categories of lymphoma or nonlymphoma. The mean UR was 2.2 +/- 1.6 (range, 1.0 to 3.85) for lymphoma and 1.7 +/- 0.8 (range, 0.7 to 3.2) for nonlymphoma. Only a UR of 1.63 resulted in sensitivity and specificity better than 50% (60% and 55%, respectively), with an accuracy of 57%, positive predictive value of 43%, and negative predictive value of 71%.Tl-201 brain SPECT appears unreliable for differentiating primary lymphoma from nonmalignant brain lesions in patients with AIDS. Early brain biopsy is necessary to establish a definitive diagnosis when appropriate.
A Statesman Reflects: David Korn Discusses Biomedical Research
Authors: C. K. Wittenberg
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article A Statesman Reflects: David Korn Discusses Biomedical Research Get access Clarissa K. Wittenberg Clarissa K. Wittenberg Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 9, 6 May 1992, Pages 664–666, https://doi.org/10.1093/jnci/84.9.664 Published: 06 May 1992
CARDIORESPIRATORY FITNESS AND CORONARY ARTERY CALCIFICATION: COMPLEMENTARY CARDIOVASCULAR RISK PREDICTORS IN ASYMPTOMATIC TYPE 2 DIABETICS
Authors: Barak Zafrir, Mohanad Azaiza, Tamar Gaspar, Idit Dobrecky-Mery, Mali Azencot, Basil Lewis, Ronen Rubinshtein, David A. Halon
Journal: Journal of the American College of Cardiology (2015)
Mucosal tears during colonoscopy in a patient with ulcerative colitis
Authors: N. Oshitani, K. Aomatsu, H. Yamagami, R. Ogawa
Journal: Endoscopy (2011)

A 66-year-old man had a 2-month history of bloody diarrhea. Except for partial gastroduodenectomy because of a duodenal ulcer, the subject was healthy and was not taking any regular medication. He had not recently visited any foreign countries. Physical examination was unremarkable. Routine laboratory tests and complete blood analysis were normal.
Asian and Afro-Caribbean Britons have double the risk of type 2 diabetes
Authors: T. Pitts-Tucker
Journal: BMJ (2012)

Indian and Afro-Caribbean people living in the United Kingdom have at least twice the risk of developing type 2 diabetes as British people of European descent, a study has found. 

It has been known for some time that people of South Asian, African, or Afro-Caribbean descent are at an increased risk of developing diabetes in mid-life, but it is not known why this is or whether this extra risk continues as people get older.

The Southall and Brent revisited (SABRE) study is a population based cohort study funded by the Wellcome Trust and British Heart Foundation.1 …
Abstract 5613: A specific isoform of Gli1 binds the Gli-binding site of the c-jun and c-fos promoters
Authors: Lauren Amable, Elaine Gavin, Wesley Denny, Erhong Meng, Rodney P. Rocconi, Eddie Reed
Journal: Cancer Research (2012)

Abstract Gli1 participates in the transcriptional regulation of c-jun, which in turn, participates in the transcriptional regulation of genes in nucleotide excision repair. The c-jun promoter and the c-fos promoter have identical Gli-binding-sites that bind Gli1. C-jun and C-fos form the transcriptionally active heterodimer Activator Protein 1, AP1. AP1, is the positive transcriptional regulator for ERCC1, and other DNA repair proteins. Gli1 is a transcription factor in the Hedgehog pathway, and there are five known isoforms of the Gli1 protein that exist in human cells. We have investigated whether there is a specific isoform of Gli1 that binds to the transcriptional regulatory sequences of c-jun and of c-fos. Detailed studies were performed in cisplatin-resistant A2780-CP70 human ovarian cancer cells. EMSA studies demonstrated the presence of a Gli protein in these cells which bind to the Gli-binding-site, as well as the consensus Gli-binding sequence. Supershift EMSA assays show that Gli1 binds the Gli binding sites of c-jun and of c-fos. Southwestern blot analyses of protein lysates from A2780-CP70 cells demonstrated that only one of the five known Gli1 protein isoforms, the 130 kDa, bind the Gli-specific binding site in the promoter of c-jun and c-fos. No Gli2 protein binds this specific binding site in the c-jun promoter, in these cells. To further confirm the 130 kDa Gli1 isoform was responsible for binding the c-jun promoter, the full-length Gli1 with a C-terminal myc tag was transfected into cells, and the protein products were assessed by immunoprecipitation and Southwestern blot analysis. The transfected full length Gli1-myc generated a 130 kDa protein that binds the Gli1-specific binding site in the promoter of c-jun. The presence of this 130 kDa Gli1 isoform was also documented in: six additional human ovarian cancer cell lines, and ten clinical ovarian tissue samples. Seven were ovarian cancer tissue and three were non-cancer ovarian tissues. The 130 kDa Gli1 isoform was present in all specimens examined, but protein levels were six-fold higher in malignant tissues. We conclude that the 130 kDa isoform of Gli1 bind the Gli-binding site in the promoters of c-jun and c-fos. Therefore, Gli1 may be the transcriptional regulator of c-jun and c-fos, and thereby regulates the transcription of ERCC1 and genes of nucleotide excision repair. 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 5613. doi:1538-7445.AM2012-5613
HER2 status determined on pre operative biopsies and in operative specimens: concordance among immunohistochemistry (IHC) fluorescence <i>in situ</i> hybridization (FISH) and chromogenic <i>in situ</i> hybridization (CISH) techniques in the CRITHER study.
Authors: L Arnould, P Roger, G MacGrogan, B Lannes, C Hayem, F Campana, A Balaton, F Penault-Llorca
Journal: Cancer Research (2009)

Abstract Abstract #1089 Background: In breast cancer, HER2 status is generally assessed by IHC or FISH on operative tissue sample and in situ hybridization techniques are standard tools for determining equivocal IHC 2+ overexpression and deciding the correct treatment for HER2-positive breast cancer patients. For the management of their patients, oncologists or surgeons sometimes ask for assessment of HER2 status on per cutaneous core biopsy (CB).The primary objective of the CRITHER study was to investigate concordance between the results of CISH, FISH, and IHC techniques on pre-operative CB samples for HER2 status compared with HER2 status determined by FISH on surgical specimen from a population of previously untreated non-metastatic breast cancer patients in France. Methods: Analysis was performed on samples from 260 patients recruited at 24 pathology centers for the period 2003 to 2006 inclusive. Recruitment was made on the basis of IHC obtained from operative tissue samples in order to obtain around 50% HER2-positive (3+), 30% HER2-negative (0/1+), and 20% HER2-equivocal (2+) cases. CISH and IHC were performed in parallel on the pre-operative biopsy and matched surgical specimen in the participating laboratories, and FISH on both specimens in each of four reference pathology centers. IHC staining was analyzed according to different scoring systems. Results: The rate of discordance between pre-operative CISH and operative FISH was 1.8% with 1.5% false-positives and 2.2% false-negatives (k=0.963; p&amp;lt;0.001); the corresponding rate for pre-operative IHC (excluding equivocal IHC 2+ cases) and operative FISH was 1.5% with 1.6% false-positives and 1.4% false-negatives (k=0.953; p&amp;lt;0.001). Comparison of pre-operative and operative samples showed expected low rates of discordance for CISH (0.85%; k=0.982; p&amp;lt;0.001) and FISH (0.45%; k=0.991; p&amp;lt;0.001), with no false positives in either case. Results for the IHC scoring system analyses on concordance will be presented at the meeting. Discussion: As expected, concordance for both CISH and FISH between pre-operative and operative results was excellent. There was a high rate of concordance for pre-operative CISH and IHC HER2 status determination on CB (excluding equivocal IHC 2+ cases) compared with operative FISH results in patients with previously untreated non-metastatic breast cancer. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 1089.