tbuckley/cabot-search huggingface dataset:
PTU-090 10 Year Retrospective Review Of Abdominal Tuberculosis From A London Teaching Hospital: Age, Ethnicity And Hiv Status: Abstract PTU-090 Table 1
Authors: JS Nayagam, C Mullender, A Poullis, C Cosgrove
Journal: Gut (2014)

<h3>Introduction</h3> Although tuberculosis (TB) rates in United Kingdom have plateaued in recent years, areas with large high risk non-UK born population, which are predominantly centred in large urban areas, still have a high prevalence of TB. Extra-pulmonary TB, including abdominal TB, is much more common in non-UK born than in UK born population. The highest rate of TB in UK born is in the over 75 years of age population. Abdominal TB can mimic Crohn’s disease and should always be considered as part of the differential diagnosis. We sought to review the demographics of patients with abdominal tuberculosis in a large urban teaching hospital in London. <h3>Methods</h3> A retrospective review of patients treated at St George’s Hospital, London, for abdominal TB from June 2003 to August 2013 was conducted. Information was gained from electronic patient records and the hospital’s tuberculosis database. <h3>Results</h3> 65 cases of abdominal TB were identified. Average age was 42 years (range 18–97). 49.2% females and 50.8% males. Ethnicity and mean ages are outlined in Table 1. The mean age of European Caucasians was significantly older than from combined black and minority ethnic (BME) groups (72.4 v 39.5, p = 0.016). The number of cases over the 10 year period has remained stable, with an average of 6.5 per year (range 4–10). 13.85% were HIV positive. all in BME patients (1 South Asian, 8 Africans). <h3>Conclusion</h3> Abdominal TB remains an active disease in London, affecting a wide range of ages and ethnicities, with the majority of patients South Asian and African, in accordance with national data. It should be considered as a differential in all patients, but particularly those who are at high risk. It presents as a disease of elderly Europeans and young BME groups. A significant number of BME group patients have HIV infection. <h3>Disclosure of Interest</h3> None Declared.
Return of Renal Function after Endovascular Treatment of Aortic Dissection
Authors: Jean-Philippe Verhoye, Bertrand De Latour, Jean-François Heautot
Journal: New England Journal of Medicine (2005)

coma cell line.Although this is an understandable concern, it is reassuring that in the four years since insulin glargine was introduced in the United States, there have been no reports of acceleration of diabetic retinopathy.It should also be noted that in at least one other study in human skeletal-muscle cells, no differences in mitogenic effects were revealed between insulin glargine and human insulin. 2 Since hypoglycemia is the rate-limiting factor for all insulin therapy, it seems to me that the riskbenefit ratio for the use of glargine outweighs any theoretical risk of problems not reported to date.We clearly need more data about the risk of hypoglycemia with insulin glargine as compared with neutral protein Hagedorn insulin in children.How-ever, as I noted in my review, the risk-benefit ratio for these theoretical concerns about IGF-1-receptor binding and an increased mitosis rate is not as clear in pregnant women, and most authors would not use insulin glargine in this population.
ACUTE PERICARDITIS AND CARDIAC TAMPONADE WITH VERY HIGH CARCINOEMBRYONIC ANTIGEN (CEA) LEVEL RELATED WITH MEDIASTINAL CYSTIC MASS
Authors: Kangun Choi, Jang-Won Son, Jong Ho Nam, Byung-Jun Kim, Kyuhwan Park, Chan-Hee Lee, Ung Kim, Jong-Seon Park, Dong-Gu Shin, Young-Jo Kim, Jeong-Hwan Cho, Yoon Jung Choi
Journal: Journal of the American College of Cardiology (2016)
Abstract 128: MicroRNA-23b acts as an oncogenic microRNA in renal cancer
Authors: Mohd Saif Zaman, Guoren Deng, Varahram Shahryari, Sharanjot Saini, Shahana Majid, Kamaldeep Singh, Herman Sandhu, Inik Chang, Yuichiro Tanaka, Rajvir Dahiya
Journal: Cancer Research (2011)

Abstract The North American region has the highest rates of renal cancers in the entire world. MicroRNAs are small noncoding RNAs that play important roles in numerous cellular processes including development, proliferation, and apoptosis. miR-23b is part of a cluster of miRNAs which includes among others miR-24-1, miR-27b and miR-30a. Recent studies have demonstrated that miR-23b plays different roles in different organs of the body. This led us to speculate its role in urological cancers in general and renal cancer in particular. In the current study we observe the role of miR-23b in renal cancer. The expression of miR-23b was checked in 30 pairs of renal cancer and normal tissues. The samples included three different types of renal cancer tissues, clear cell, papillary and tubular. 55% of clear cell carcinoma and all tubular samples showed high expression of miR-23b as compared to the normal. Interestingly, papillary carcinoma showed a contrasting result in which miR-23b levels were found to be down regulated in almost 90% of the samples. The expression in renal cancer cell lines, A498, ACHN, Caki-1 and Caki-2 was found to be significantly higher as compared to the normal cell line HK-2. The chemo preventive agent Genistein (25µM for 96 hours) was able to reduce the expression of miR-23b in A498 cells by more than 50%. Inhibition of miR-23b expression by the anti-miR-23b antagonist in A498 cells resulted in a significant increase in apoptosis, as detected through flow cytometry analysis. In contrast over expression of mir-23b in A498 cells resulted in a decrease in apoptosis. No significant effect on cell cycle was observed in either over expressing or inhibiting miR-23b in A498 cells. Cell viability assays also did not show any major effect due to the inhibition of expression of miR-23b. Moreover, the expression of miR-23b was correlated with 5 year survival rate of patients. For patients with low levels of miR-23b, 85% of patients survived after 5 years of operation, whereas in case of high expression of miR-23b only 50% survived. Our data suggests that miR-23b acts as an oncogenic mi-RNA in renal cancer. 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 128. doi:10.1158/1538-7445.AM2011-128
Dichotomy Between Tc-99m MDP Bone Scan and Fluorine-18 Fluorodeoxyglucose Coincidence Detection Positron Emission Tomography in Patients With Non-Hodgkin’s Lymphoma
Authors: J Lee, C H Park, H C Kim, H S Kim
Journal: Clinical Nuclear Medicine (2000)

The authors report two cases of non-Hodgkin’s lymphoma that were evaluated not only by conventional staging work-up but also additional Tc-99m MDP bone scans and fluorine-18 fluorodeoxyglucose (F-18 FDG) coincidence detection (CoDe) positron emission tomographic (PET) imaging. There were discordant results between the Tc-99m MDP bone scans and F-18 FDG CoDe PET. In the first case, the bone marrow biopsy was positive, and F-18 FDG CoDe PET was consistent with a malignancy, but the findings of the Tc-99m MDP bone scintiscan were negative. In the second case, the bone marrow biopsy was negative, but F-18 FDG CoDe PET revealed focal skeletal involvement, which improved markedly on the follow-up study after chemotherapy. If skeletal involvement has a focal distribution and is confined to the marrow cavity, both bone marrow biopsy and bone scintigraphy can be falsely negative. In this situation, F-18 FDG PET is useful and revealing.
Abstract 1422: Abrogation of prostate cancer cell metastatic phenotype by cathepsin-L inhibition
Authors: Dhivya R. Sudhan, Dietmar W. Siemann
Journal: Cancer Research (2011)

Abstract Prostate cancer is the most commonly diagnosed cancer in North America and the second leading cause of cancer death in men. Although highly curable in early stages, ∼90% of patients with advanced prostate cancer develop skeletal metastases; an occurrence that results in a substantial reduction in the quality of life and a drastic worsening of the prognosis. Tumor cells rely on proteolytic enzymes for successful establishment of metastases. Cathepsin-L (Cts-L) is a lysosomal endopeptidase of the papain super family of cysteine protease that is up regulated in a wide range of human cancers including prostate cancer. Cts-L over expression can enhance the invasive/metastatic potential of cancer cells through two distinct mechanisms: (i) degradative proteolysis of extracellular matrix and basement membrane components by secreted Cts-L and (ii) enhanced expression of genes involved in EMT and migration by nuclear Cts-L. The goal of the present studies was to elucidate whether the administration of the specific small molecule CtsL inhibitor 3-bromophenyl-3-hydroxyphenyl-ketone thiosemicarbazone (KGP-94) could inhibit the metastatic phenotype in prostate cancer cells. PC-3 and its sublines PC-3-ML and PC-3-N which possess moderate, high, and low metastatic potential, respectively, were used. In response to treatment with 25uM of KGP-94, PC-3 and PC-3-ML showed a 45 and 55% decrease in migratory potential respectively as determined by transwell and wound healing assays. KGP-94 also significantly affected the invasive potential of PC-3 and PC-3-ML at 10uM and 25uM dose concentrations. These results occurred in the absence of cytotoxicity as determined using a clonogenic cell survival assay. Cell cycle analysis by flow cytometry did show that KGP-94 treatment induces a G1 arrest but this effect was insufficient to account for the pronounced inhibition of migration and invasion.In order to elucidate whether KGP-94 treatment affected nuclear Cts-L, presence of the nuclear isoform was validated in PC-3 cells through immunoblot analysis of nuclear extracts and confocal imaging. Nuclear Cts-L has been reported to induce epithelial to mesenchymal transition through increasing expression of Vimentin, N-Cadherin with concomitant suppression of E-Cadherin. However, quantitative PCR analysis failed to show an effect on the expression of these genes in response to KGP-94 treatment. These data therefore suggest that the abrogation of migratory and invasive potential observed in the prostate cancer models is a consequence of an inhibitory effect on secreted and not nuclear Cts-L. 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 1422. doi:10.1158/1538-7445.AM2011-1422
DETERMINANTS OF FRACTIONAL FLOW RESERVE MEASUREMENT DISCREPANCY RELATED TO REGIONAL OR GLOBAL MYOCARDIAL HYPERAEMIA
Authors: Nina Willemijn van der Hoeven, Alicia Quiros, Guus A. de Waard, David Camacho Gaxiola, Driss Melehi, Nicola Ryan, Raul S. Herrera Nogueira, Maurits Hollander, Christopher Broyd, Niels Van Royen, Javier Escaned
Journal: Journal of the American College of Cardiology (2016)
Abstract 2962: Role of Cyr61 in the progression of pancreatic cancer
Authors: Smita Mehta, Kakali Dhar, Inamul Haque, Monami Majumder, Douglas H. McGregor, Sushanta K. Banerjee, Snigdha Banerjee
Journal: Cancer Research (2010)

Abstract Pancreatic Ductal Adenocarcinoma (PDAC) is the fourth most common cause of cancer in men and fifth in women in the United States. The overall survival rate is very poor in PDAC due to late presentation, tumor aggressiveness and lack of effective treatment strategy. The objective of this study is to explore the role of Cyr61 in the progression of the PDAC. Cyr61/CCN1 is a secreted, cysteine-rich heparin-binding protein, a member of CCN family and also plays a role in cell proliferation, adhesion, migration and differentiation during development but very little is known about cancer biology. We studied Cyr61 mRNA expression and protein level in tissue samples (archival and tissue array samples) using In Situ hybridization and immunohistochemistry. Its expression was also studied in different cell lines using Northern Blotting, quantitative real time PCR and Western blot analysis. The studies revealed that Cyr61 mRNA and protein was highly expressed in PDAC as compared to normal and chronic pancreatitis sections. The expression profile of Cyr61 increases as the disease progressed from Grade I to Grade III. Interestingly, in some PDAC sections Cyr61 expression was undetected or barely detected. Cyr61 was highly expressed in Panc-1, an invasive cell line, as compared to less invasive cell lines (i.e., BxPC3 and Capan-1) where expression of Cyr61 is very minimal. In order to evaluate the functional role of Cyr61, we nullified Cyr61 in Panc-1 cells using retroviral-mediated shRNA. We determined the migration of these cells and the effect of the conditioned media of these cells on in vitro angiogenesis. We found that Cyr61 is essential for in vitro migration and induction of angiogenesis. Furthermore, these studies reveal that Cyr61 contributes in the development of drug resistance. 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 2962.
Abstract 295: Detection of hypomethylation of LINE1 on peripheral white blood cells and plasma DNA in US hepatocellular carcinoma patients
Authors: Yujing Zhang, Lissette Delgado-Cruzata, Hui-Chen Wu, Mary Gamble, Qiao Wang, Santella M. Regina, Abby B. Siegel
Journal: Cancer Research (2011)

Abstract Hepatocellular carcinoma (HCC) is one of the most common cancers in the world and is increasing in the United States. Epigenetic changes, including genomic DNA hypomethylation, have been implicated in cancer development by inducing chromosomal instability. In the present study, methylation of long interspersed nucleotide element-1(LINE1), a surrogate marker of global hypomethylation, in peripheral white blood cells and plasma DNA in 47 US HCC patients was detected by pyrosequencing. Correlations between LINE1 methylation, and clinical data and other biomarkers were also analyzed. Methylation of LINE1 in WBC DNA is statistically significantly correlated with that in plasma DNA (R=0.32, p=0.04). WBC DNA global hypomethylation was significantly decreased in subjects with hepatitis C (HCV) infection (p=0.05). Plasma folate levels were not correlated with plasma DNA LINE1 methylation (R=0.13, p=0.41) or with WBC LINE1 methylation (R=−0.19, p=0.24). However, WBC folate levels were statistically significantly associated with patients’ survival. HCC patients who survived at least 3 months after diagnosis had lower WBC folate compared to patients who died within 3 months (p=0.004). We are currently expanding the HCC cohort and also analyzing biomarkers of chemical exposure (polycyclic aromatic hydrocarbons and aflatoxin B1) to investigate associations with methylation changes. 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 295. doi:10.1158/1538-7445.AM2011-295
The Acute Chest Syndrome of Sickle Cell Disease
Authors: Sheldon Contact, Kareen Hartwig
Journal: New England Journal of Medicine (2000)

Hospital Physician January 2007 15 T he acute chest syndrome (ACS) is an acute pulmonary illness that occurs in patients with sickle cell disease. ACS is currently defined as a new infiltrate on chest radiograph in conjunction with 1 other new symptom or sign: chest pain, cough, wheezing, tachypnea, and/or fever (> 38.5°C).1 The term acute chest syndrome was first suggested in 1979 by Charache et al2 and was developed to reflect the unique nature of acute pulmonary illness in patients with sickle cell disease. ACS can be caused by a variety of mechanisms, both infectious and noninfectious. Diagnostic considerations and treatment modalities are not typical of any other specific pulmonary illness experienced by the general population. Furthermore, the typical course, possible complications, and outcomes are unique. For these reasons, the terminology persists and remains useful for both research purposes and effective clinical communication. As a leading cause of hospitalization and death in adults with sickle cell disease, the importance of ACS in sickle cell patients cannot be overstated.3 Emergency physicians, family practitioners, pediatricians, internists, and hematologists who encounter these patients on a regular basis have the potential to prevent significant morbidity and mortality through early recognition and aggressive treatment of ACS. This article reviews the etiology, pathogenesis, clinical characteristics, treatment, and prevention of ACS.
Radiologic Approaches to the Adrenal Gland
Authors: Jerome H. Shapiro
Journal: New England Journal of Medicine (1971)

With the exception of the past few years, the adrenal glands have received little attention from the army of radiologic diagnosticians who have applied their technics to almost every area and organ in the human body. In this particular region, diagnostic energies have been overshadowed by those directed at its larger southern neighbor, the kidney. Provided with little in the way of radiologic tools, adrenophiles had to be content with gross changes in adrenal size, substance (calcification) or function as associated with well defined clinical entities to implicate the adrenal gland as a site of abnormality. Earlier efforts in diagnostic . . .
Abstract 2943: Targeting the E2F pathway in cancer chemotherapeutics
Authors: Courtney A. Kurtyka, Yihong Ma, Haikuo Bian, Christopher Cubitt, Brian Law, Patrick Corsino, W. Douglas Cress
Journal: Cancer Research (2011)

Abstract HLM006474 is a recently identified small molecule E2F inhibitor. Since E2F is known to drive expression of genes required for cell cycle progression, it is predicted that blocking the E2F pathway will slow proliferation and have anticancer activity. Microarray analysis demonstrates that HLM006474 treatment results in profound changes in the expression of genes involved in cell cycle progression and nucleotide biosynthesis. Flow cytometry reveals that treatment of A375 cells results in a cell cycle arrest, primarily in G2/M. As would be expected, cell lines deficient in Rb are more sensitive to E2F inhibition than are syngeneic lines expressing Rb. HLM006474 reduces the proliferation of a broad array of cell lines with a biological IC50 that varies between 5 and 70 μM. Combination of HLM006474 with common chemotherapeutic agents cisplatin and gemcitabine demonstrate little synergy; however HLM006474 synergizes with paclitaxel and a novel cdk inhibitor NSC11702. Interestingly, we discovered that paclitaxel sensitivity inversely correlated with E2F4 levels in a series of non-small cell lung cancer (NSCLC) lines, suggesting that synergy between HLM006474 and paclitaxel is due to HLM006474's inhibition of E2F4 activity and expression. To test this, H1299 cells which have high E2F4 levels and a high paclitaxel IC50 were depleted of E2F4 with siRNA and the IC50 determined. Taken together, these results suggest that HLM006474 may have efficacy against cancers in which E2F is deregulated and may be useful in combination with other drugs that target cell cycle components. 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 2943. doi:10.1158/1538-7445.AM2011-2943
Abstract 1691: Apoptotic and antitumor effects of rotenone in MCF-7 human breast cancer cells are mediated ROS through activating JNK and p38 MAPK signaling
Authors: Jen-Kun Lin, Yea-Tzy Deng, Hsiu-Chen Huang
Journal: Cancer Research (2010)

Abstract Rotenone is a natural hydrophobic pesticide derived from the roots of Derris and Lonchorcarpus species. The pesticidal activity of rotenone is attributed to irreversible binding and inactivation of complex of the mitochondrial transport chain. This can block electron transport from complex to ubiquinone, resulting in a blockage of the oxidative phosphorylation process, and an increase of the reactive oxygen species (ROS). Rotenone has been shown to display anticancer activity through the induction of apoptosis in various cancer cells. However, the underlying mechanism is still not fully elucidated. In the present study, rotenone showed a strong growth inhibitory effect against human breast MCF-7 cells. DNA flow cytometric analysis, chromatin condensation and poly(ADP-ribose) polymerase (PARP) cleavage indicated rotenone actively induced apoptosis in MCF-7 cells. The anti-apoptotic protein BCl-2, was decreased, whereas the apoptotic protein, Bax, was increased in a time-dependent manner in rotenone-induced apoptosis. Moreover. The treatment of rotenone in MCF-7 cells caused the activation of c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPKs) and the inactivation of extracellular signal-regulated protein kinase1/2 (ERK1/2). The pharmacological inhibitor of JNK and p38 MAPK revealed significant protection against rotenone-induced apoptosis. In summary, these results indicate rotenone may induce apoptosis through ROS and JNK/p38MAPK activation in MCF-7 cells. In conclusion, we examines the molecular mechanism involved in rotenone-induced apoptosis in human breast cancer MCF-7 cells. We have demonstrated a sequential events that rotenone-induced apoptosis in the cells through ROS generation, which serves as a pivotal upstream function in activating JNK and p38MAPKs, which leads to a decrease of BCl-2 and increase of Bax and finally to inducing apoptosis. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 1691.
Comparison of risk assessment strategies for not-high-risk pulmonary embolism
Authors: Lukas Hobohm, Kristian Hellenkamp, Gerd Hasenfuß, Thomas Münzel, Stavros Konstantinides, Mareike Lankeit
Journal: European Respiratory Journal (2016)

We compared the prognostic performance of the 2014 European Society of Cardiology (ESC) risk stratification algorithm with the previous 2008 ESC algorithm, the Bova score and the modified FAST score (based on a positive heart-type fatty acid-binding protein (H-FABP) test, syncope and tachycardia, modified using high-sensitivity troponin T instead of H-FABP) in 388 normotensive pulmonary embolism patients included in a single-centre cohort study. Overall, 25 patients (6.4%) had an adverse 30-day outcome. Regardless of the score or algorithm used, the rate of an adverse outcome was highest in the intermediate-high-risk classes, while all patients classified as low-risk had a favourable outcome (no pulmonary embolism-related deaths, 0–1.4% adverse outcome). The area under the curve for predicting an adverse outcome was higher for the 2014 ESC algorithm (0.76, 95% CI 0.68–0.84) compared with the 2008 ESC algorithm (0.65, 95% CI 0.56–0.73) and highest for the modified FAST score (0.82, 95% CI 0.75–0.89). Patients classified as intermediate-high-risk by the 2014 ESC algorithm had a 8.9-fold increased risk for an adverse outcome (3.2–24.2, p&lt;0.001 compared with intermediate-low- and low-risk patients), while the highest OR was observed for a modified FAST score ≥3 points (OR 15.9, 95% CI 5.3–47.6, p&lt;0.001). The 2014 ESC algorithm improves risk stratification of not-high-risk pulmonary embolism compared with the 2008 ESC algorithm. All scores and algorithms accurately identified low-risk patients, while the modified FAST score appears more suitable to identify intermediate-high-risk patients.