tbuckley/cabot-search huggingface dataset:
Abstract 3381: AhR shRNA effectively suppresses B(a)P-mediated induction of slug modulating tumor invasion and cell migration in non small cell lung cancer cell line
Authors: Kwang-Sung Ahn, Juwon Park, Kyungsun Kim, Yang Seok Chae, Nam Hee Won
Journal: Cancer Research (2011)

Abstract Exposure of B(a)P on lung tissue have been implicated in cancer development and its progression. Even though increasing evidences have been reported adversely effects of B(a)P in tumor progression, mechanism by which exposure of Bap on lung cancer cells increases the metastatic potentials still remains unknown. Here, we show that B(a)P triggers a marked morphological changes of Non Small Cell Lung Cancer (NSCLC) cells. These B(a)P-mediated effects are mimicked by decreasing E-cadherin resulting in loosening cell-cell contacts and by increasing Slug expression resulting in inducing epithelial mesenchymal transition (EMT). In case that NCSCLC cell was prolonged exposed to B(a)P, B(a)P-exposed cells showed increasing cell motility and invasion. They correlate with B(a)P-mediated phosphorylations of JNK and p38. And they are reverted by treatment with their inhibitors. In transient transfection analysis, H1299-snail2, constitutively expressing snail2, increased the cell motility and invasion. AhR shRNA effectively suppresses either B(a)P-mediated tumor invasion and induction of snail2. And suppression of E-caherin was found in H1299-snail2. Results of immunohistochemical stain revealed that Slug strongly expressed in invasive foci of Non Small Cell Lung Cancer tissue. Our results suggested that NSCLC cells prolonged exposed to B(a)P increased cell motility and invasiveness via regulation of expression of Sanil2 by exposure of B(a)P on NSCLC cells. 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 3381. doi:10.1158/1538-7445.AM2011-3381
555Cardiac regeneration from activated epicardium
Authors: M Van Den Hoff, A Van Wijk, QD Gunst, A Wessels
Journal: Cardiovascular Research (2014)

The mammalian heart has a very limited regenerative capacity. Cardiomyocytes, lost after ischemia, are replaced by fibroblasts. Although the human heart is able to form new cardiomyocytes throughout its lifespan, the efficiency of this phenomenon is not enough to substitute sufficient myocardial mass after an infarction. In contrast, zebrafish hearts regenerate through epicardial activation and initiation of myocardial proliferation. We have used the mWt1/IRES/GFP-Cre mouse line to trace the fate of epicardial derived cells during development and subsequently used this line to obtain insights into the activation and cellular contribution of the epicardium in response to ischemia.

Epicardial derived cells (EPDCs) start to populate the ventricular myocardium from E12 onward. Remarkably the EPDCs only populate the compact layer and it is only at the end of gestation that the EPDCs invade the trabecular myocardium. Within the developing myocardium the myocardium the EPDCs also contribute to a subset of the coronary endothelial cells and perivascular fibroblasts. In this mouse model we subsequently induced a myocardial infarction and analyzed the spatio-temporal changes in expression of embryonic epicardial, EMT, and stem cell markers and the contribution of the epicardial-lineage to the infarcted area. Immediately after the myocardial infarction the integrity of the epicardial layer overlaying the infarct is lost. The epicardium was found to regenerate within three days post infarction. In this regenerated epicardium, the embryonic gene program is transiently re-expressed as well as proliferation. Concomitant with this activation, EPDCs are formed until two weeks post-infarction. These EPDCs initially form a thick layer in between the newly fromed epicardium and ischemic myocardium. Subsequently, these mesenchymal cells replace the cardiomyocytes lost due to the ischemia and contribute to the fibroblast population, myofibroblasts and coronary endothelium in the infarct. From one month post infarction onward a small number of lineage postive cardiomyocytes is found within the infarcted zone.

We show that the contribution of epicardial derived cells to the froming ventricle and that an endogenous, epicardium-dependent regenerative response to injury is induced. Although this regenerative response leads to the formation of new cardiomyocytes, their number is insufficient. These molecular and cellular analyses provide basic knowledge essential for investigations on the regeneration of the mammalian heart aiming at epicardium-derived cells.
Massachusetts Medical Society
Authors: Joseph Garland, Joseph Garland, Oliver Cope, John Fallon, James P. O'Hare, Conrad Wesselhoeft, Richard M. Smith, James Keenan Bragger, Michael A. Tighe, Humphrey L. McCarthy, W. Richard Ohler
Journal: New England Journal of Medicine (1947)

THE annual meeting of the Council was called to order by the president, Dr. Dwight O'Hara, on Monday, May 19, 1947, at 7:00 p.m., in the Georgian Room of the Hotel Statler, Boston.Present were one hundred and eighty-eight councilors (Appendix No. 1).After opening the meeting the President read the following obituary notices:Enos Hoyt Bigelow — On March 13, 1947, past-president Enos Hoyt Bigelow died in Framingham, where he was born ninety-one years ago. He was educated at Worcester Polytechnic Institute and Harvard Medical School, graduating from the latter and beginning practice in Framingham in 1882.During the . . .
Abstract LB-271: The biological role of the transcription factor Kaiso in breast tumorigenesis
Authors: Sonali Weerawardane, Juliet M. Daniel
Journal: Cancer Research (2010)

Abstract Introduction: The canonical Wnt signalling pathway regulates various cellular processes (e.g. proliferation, differentiation, apoptosis) and leads to tumorigenesis when aberrantly activated. -catenin, the key downstream effector in Wnt signalling, translocates to the nucleus upon Wnt pathway activation, and activates target genes involved in tumorigenesis. The transcription factor Kaiso is a novel BTB/POZ (Broad complex, Tramtrak, Bric à brac/Pox virus and zinc finger) zinc finger (POZ-ZF) protein that specifically interacts with the cell adhesion cofactor p120ctn. Recent studies from our lab and others have revealed that Kaiso negatively regulates the canonical Wnt pathway by repressing activation of Wnt/ -catenin target genes. Some studies implicate Kaiso as a tumor suppressor (decreased expression in breast, ovarian and colon tumors), and others implicate Kaiso in tumor initiation (Kaiso-deficient mice are resistant to intestinal cancer). The goal of this study is to elucidate the biological role of Kaiso in breast tumorigenesis using various cellular assays. Methods: To assess Kaiso's role in breast cancer, Kaiso was misexpressed in MCF7 (human breast adenocarcinoma) cell lines. Stable Kaiso overexpressing and depleted cell lines were generated and assessed for cell proliferation and cell migration using focus formation, wound healing and matrigel invasion assays. Western blot analysis was performed to assess the effects of Kaiso misexpression on p120 and E-cadherin as well as epithelial-mesenchymal transition markers such as N-cadherin, Snail, Twist and Vimentin. The subcellular localization of Kaiso and its putative target genes in vivo was examined using immunohistochemistry (IHC) analysis of matched pairs of human normal and tumor breast tissue. Results: Focus formation assays revealed increased transformation by cells over-expressing Kaiso, suggesting an oncogenic role for Kaiso in cell culture. Preliminary wound healing and matrigel assays show increased cell motility and migration respectively in Kaiso over-expressing cells compared to parental control cells, thereby suggesting a role for Kaiso in the epithelial-mesenchymal transition. IHC analysis revealed predominant nuclear Kaiso expression in lobular and ductal breast carcinomas in breast tissues. These data support Kaiso's potential role as an oncogene in human breast cancer. 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 LB-271.
The Predictors for Asthma Control By Stepwise Treatment in Elderly Asthma Patients
Authors: Ga Young Ban, Young Min Ye, Youn hwan Lee, So Hee Lee, Jeong-Eun Kim, Young-Hee Nam, Soo-Keol Lee, Joo-Hee Kim, Jung Ki-Suck, Sang-Ha Kim, Hae-Sim Park
Journal: Journal of Allergy and Clinical Immunology (2015)
Interrelated Hormonal Factors in Cardiac Hypertrophy
Authors: R. DE GRANDPRÉ, W. RAAB
Journal: Circulation Research (1953)

Evidence is presented that cardiac hypertrophy may ultimately be due to metabolic influences of hormones among which the pituitary growth hormone (somatotrophic hormone, STH) is the most important. In hypophysectomized rats, marked cardiac hypertrophy was elicited by administration of STH in the presence of subnormal blood pressure levels. Other hormones, especially the thyroid hormone and the adrenal mineralocorticoids--the latter through their action on myocardial electrolyte balance--seem to play subsidiary roles. Cortisone inhibited the cardiotrophic effect of STH and by itself decreased cardiac mass.
The Effect of Asymptomatic Nocturnal Hypoglycemia on Glycemic Control in Diabetes Mellitus
Authors: Gabriele Perriello, Pierpalo De Feo, Elisabeth Torlone, Filippo Calcinaro, Mariarosa M. Ventura, Giuseppe Basta, Fausto Santeusanio, Paolo Brunetti, John E. Gerich, Geremia B. Bolli
Journal: New England Journal of Medicine (1988)

To assess the effect of asymptomatic nocturnal hypoglycemia on glycemic control in insulin-dependent diabetes mellitus, we studied, on three nights, 10 patients receiving their usual regimens of continuous subcutaneous insulin infusion. During a control night, the patients' mean (±SE) plasma glucose level reached a nadir of 4.5±0.2 mmol per liter at 3 a.m.; the fasting glucose level was 5.9±0.3 mmol per liter at 7:30 a.m., and a peak glucose level of 8.6±0.3 mmol per liter was reached at 10 a.m., after breakfast. During nights two and three, supplemental insulin was infused intravenously from 10 p.m. to 2 a.m. to simulate a clinical overdose of insulin. On these nights, either hypoglycemia (2.4±0.2 mmol per liter) was permitted to occur or a nearly normal glucose level (5.5 mmol per liter) was maintained by infusion of glucose. The subjects were asymptomatic on all three nights. Despite comparable plasma free insulin levels from 4 to 11 a.m., both fasting (7.3±0.2 mmol per liter) and postbreakfast (12.5±0.4 mmol per liter) plasma glucose levels were significantly higher after hypoglycemia than when hypoglycemia was prevented (6.2±0.2 mmol per liter and 8.7±0.4 mmol per liter, respectively; P<0.001 in both cases). Fasting levels of plasma glucose correlated directly with overnight plasma levels of epinephrine (r = 0.78, P<0.001), growth hormone (r = 0.57, P<0.009), and cortisol (r = 0.52, P<0.02) but correlated inversely with the overnight nadir of plasma glucose (r = -0.62, P<0.005). We conclude that asymptomatic nocturnal hypoglycemia can cause clinically important deterioration in glycemic control (the Somogyi phenomenon) in patients receiving intensive insulin therapy, and should therefore be considered in the differential diagnosis of unexplained morning hyperglycemia. (N Engl J Med 1988; 319:1233–9.)
TCT-183 Regular Drug-Eluting Stent Versus Dedicated Bifurcation Sirolimus-Eluting BiOSS LIM® Stent In Coronary Bifurcation Treatment – Randomized POLBOS II Study
Authors: Jacek Bil, Robert J. Gil, Dobrin Vassilev, Adam Kern, Luis A. Iñigo-García, Radoslaw Formuszewicz, Slawomir Dobrzycki, Leticia Fernandez Lopez
Journal: Journal of the American College of Cardiology (2014)
Abstract 247: ADAR1 promotes malignant progenitor reprogramming in chronic myeloid leukemia.
Authors: Qingfei Jiang, Leslie A. Crews, Christian L. Barrett, Angela Court-Recart, Daniel Goff, Anil Sadarangani, Jessica Rusert, Sheldon Morris, Lawrence Goldstein, Hye-Jung Chun, Marco Marra, Kelly Fraser, Kim-Hien Dao, Mark Minden, Catriona Jamieson
Journal: Cancer Research (2013)

Abstract The molecular etiology of human progenitor reprogramming into self-renewing leukemia stem cells (LSC) has remained elusive. While DNA sequencing has uncovered spliceosome gene mutations that promote alternative splicing and portend leukemic transformation, isoform diversity may also be generated by RNA editing mediated by adenosine deaminase acting on RNA (ADAR) enzymes that regulate stem cell maintenance. In this study, whole transcriptome sequencing of normal, chronic phase (CP) and serially transplantable blast crisis (BC) chronic myeloid leukemia (CML) progenitors revealed increased interferon-γ pathway gene expression in concert with BCR-ABL amplification, enhanced expression of the interferon responsive ADAR1 p150 isoform and a propensity for increased A-to-I RNA editing during CML progression. Lentiviral overexpression experiments demonstrate that ADAR1 p150 promoted expression of the myeloid transcription factor PU.1 and induced malignant reprogramming of myeloid progenitors. Moreover, enforced ADAR1 p150 expression was associated with production of a mis-spliced form of GSK3β implicated in LSC self-renewal. Finally, functional serial transplantation and shRNA studies demonstrate that ADAR1 knockdown impaired in vivo self-renewal capacity of BC CML progenitors. Together these data provide a compelling rationale for developing ADAR1-based LSC detection and eradication strategies. Citation Format: Qingfei Jiang, Leslie A. Crews, Christian L. Barrett, Angela Court-Recart, Daniel Goff, Anil Sadarangani, Jessica Rusert, Sheldon Morris, Lawrence Goldstein, Hye-Jung Chun, Marco Marra, Kelly Fraser, Kim-Hien Dao, Mark Minden, Catriona Jamieson. ADAR1 promotes malignant progenitor reprogramming in chronic myeloid leukemia. [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 247. doi:10.1158/1538-7445.AM2013-247
Capsule endoscopy in acute upper gastrointestinal bleeding: goodbye to nasogastric tube aspiration?
Authors: Carol Stanciu, Anca Trifan, Camelia Cojocariu
Journal: Endoscopy (2013)

We read with interest the article by Gralnek et al. [1] evaluating the role of video capsule endoscopy (VCE) in patients who present at the emergency department with acute upper gastrointestinal bleeding (UGIB), and we would like to make a few comments.
Massive hemobilia during endoscopic retrograde cholangiopancreatography in a patient with cholangiocarcinoma: a case report
Authors: P. Bagla, T. Erim, T. Berzin, R. Chuttani.
Journal: Endoscopy (2012)

A 65 year old gentleman with a diagnosis of cholangiocarcinoma and previously placed Cotton-Leung intrahepatic biliary ductal stents, admitted with symptoms suggestive of biliary obstruction and cholangitis, underwent urgent endoscopic retrograde cholangiopancreatography (ERCP) ([Fig. 1 a]).
Five Recombinant Simian Immunodeficiency Virus Pseudotypes Lead to Exclusive Transduction of Retinal Pigmented Epithelium in Rat
Authors: Ghislaine Duisit, Hervé Conrath, Sylvie Saleun, Sebastien Folliot, Nathalie Provost, François-Loı¨c Cosset, Virginie Sandrin, Philippe Moullier, Fabienne Rolling
Journal: Molecular Therapy (2002)

The purpose of our study was to evaluate lentiviral vector-mediated rat retinal transduction using simian immunodeficiency virus (SIV) pseudotyped with envelope proteins from vesicular stomatitis virus G glycoprotein (VSV-G), Mokola virus G protein (MK-G), amphotropic murine leukemia virus envelope (4070A-Env), influenza A virus hemagglutinin (HA), lymphocytic choriomeningitis virus G protein (LCMV-G), and RD114 retrovirus envelope (RD114-Env). The six pseudotyped lentivirus vectors carried CMV-driven green fluorescent protein (GFP) or beta-galactosidase (beta-gal) reporter genes. Intravitreal and subretinal injections of each pseudotyped recombinant SIV were performed in cohorts of Wistar rats. Our results showed that no transgene expression was detected after intravitreal injection of each pseudotyped SIV vector. Also, no transduction could be detected following subretinal injection of RD114 pseudotyped SIV vectors. However, selective transduction of retinal pigment epithelium (RPE) cells was repeatedly obtained after subretinal delivery of VSV-G, MK-G, 4070A-Env, HA, and LCMV-G pseudotyped SIV. GFP expression was maximum as soon as 4 days postadministration for VSV-G, MK-G, 4070A-Env, and HA pseudotypes, with no evidence of pseudotransduction for VSV-G. Maximum transgene expression was observed 3 weeks postinjection for LCMV-6. Importantly, HA and VSV-G pseudotyped SIV lead to such a high level of transgene expression that GFP-related toxicity occurred. Therefore, when a high level of GFP synthesis is achieved, replacement of enhanced GFP (egfp, Aequorea victoria) by a low-toxicity GFP (Renilla reniformis) cDNA is necessary to allow long-term expression.
Acute Hemolytic Anemia in Primary Atypical Pneumonia Produced by Exposure and Chilling
Authors: R. A. Colmers, J. G. Snavely
Journal: New England Journal of Medicine (1947)

ACUTE hemolytic anemia in the course of primary atypical pneumonia has been reported by Dameshek,1 Finland2 and others. Elucidation of the mechanism of this form of anemia has not been offered. Clinical evidence shows that such anemia develops coincidentally with high titers of cold agglutinin in the serum. Since most of these reports have been concerned with patients to whom varying amounts of sulfonamides have been given and since acute hemolytic anemia can develop from the administration of the sulfonamides alone, it has been difficult to exclude the drugs entirely as the cause or to establish the acute hemolytic anemia . . .
Radionuclide Imaging of Rare Congenital Renal Fusion Anomalies
Authors: BILGE VOLKAN, EMEL CEYLAN, PNAR ÖZGEN KIRATLI
Journal: Clinical Nuclear Medicine (2003)

Demonstration of a congenital renal anomaly plays an important role in the treatment of patients with renal infection. These patients are prone to infections because of coexisting urinary tract anomalies such as duplicated ureter, ureter opening anomalies, and urinary stasis. Assessment of renal parenchymal damage resulting from acute or chronic renal infection is the primary indication for radionuclide imaging with Tc-99m DMSA. In addition, this technique allows congenital anomalies to be identified. The authors review congenital renal fusion anomalies identified in children through Tc-99m DMSA imaging. They conclude that Tc-99m DMSA imaging can reveal important diagnostic information about various congenital anomalies, including fusion anomalies.
Imaging Findings of Inflammatory Pseudotumor-Like Follicular Dendritic Cell Tumor of Spleen
Authors: Liangjun Rao, Zhiyun Yang, Xiaoyan Wang, Xiangsong Zhang, Bingqi Shen
Journal: Clinical Nuclear Medicine (2013)

Inflammatory pseudotumor-like follicular dendritic cell tumor (IPT-like FDCT) histology is similar to that of the classical follicular dendritic cell (FDC) tumor, but, in addition, the inflammatory component is quite prominent. We report a case of IPT-like FDCT of the spleen by abdominal CT and 18F-FDG PET/CT. Abdominal CT showed a low-density, round, well-circumscribed defined mass in spleen, and the mass showed a high metabolism rate on 18F-FDG PET/CT.
777 INCIDENCE AND CLINICAL CONSEQUENCES OF REDUCED TUBULAR PHOSPHATE RE-ABSORPTION (TmPO4/GFR) IN NAÏVE CHRONIC HEPATITIS B PATIENTS TREATED WITH TENOFOVIR: A TWO-YEAR FIELD STUDY
Authors: M. Viganò, P. Lampertico, G. Mangia, R. Soffredini, F. Facchetti, F. Invernizzi, M. Colombo
Journal: Journal of Hepatology (2013)
Possible Role of Carbohydrate-Induced Calciuria in Calcium Oxalate Kidney-Stone Formation
Authors: Jacob Lemann, Walter F. Piering, E. J. Lennon, Opal A. Kelly, Jean Brock
Journal: New England Journal of Medicine (1969)

Since nutrient ingestion has been shown to augment urinary calcium excretion in normal subjects, we compared the effect of ingestion of glucose or sucrose on urinary calcium excretion in normal subjects, those who form calcium oxalate kidney stones and their relatives. Patients and relatives had significantly higher urinary calcium excretion rates in control periods than normal subjects, but considerable overlap was present. After sugar ingestion each patient and relative achieved higher rates of calcium excretion than any normal subject. In addition, the patients and relatives had a greater antidiuresis after sugar and achieved much higher urinary calcium concentrations. Coupled with higher basal rates of urinary calcium excretion, the exaggerated augmentation of calcium excretion after carbohydrate ingestion could favor calcium salt precipitation in patients who form stones and in their relatives.
P867 FACTORS PREDICTING OUTCOME OF PATIENTS WITH ACUTE LIVER FAILURE MEETING THE CRITERIA OF LIVER TRANSPLANTATION: IMPACT OF ALBUMIN DIALYSIS WITH MARS
Authors: F. Saliba, G. Dahlqvist, A. Letierce, P. Ichai, I. Ruiz, M. Boudon, D. Samuel
Journal: Journal of Hepatology (2014)
Triple negative phenotype: not affecting survival in young patients with operable breast cancer.
Authors: E Kim, W Han, I Park, J Lee, E Ko, J Yu, H Moon, D Noh
Journal: Cancer Research (2009)

Abstract Abstract #1083 Purpose: To investigate the clinicopathological characteristics and outcomes of triple negative breast cancer in young patients.&amp;#x2028; Experimental Design: We analyzed 1,498 patients with primary invasive breast cancer who underwent surgery between January 2000 and December 2003. Patients were divided into those &amp;lt; 40 and ≥ 40 years old and into triple negative and non-triple negative groups.&amp;#x2028; Results: A total of 326 (21.8%) were aged &amp;lt; 40; relative to patients ≥ 40 years old, the younger group showed larger tumor size, higher lymph node positivity, and elevated Ki-67 index. Recurrence-free survival (RFS; P = 0.0002) and overall survival (OS; P = 0.0483) were significantly lower in the younger group. Three hundred seventy four patients (25.0%) had the triple negative phenotype, and of which 93 (24.9%) were &amp;lt; 40 years old. Univariate survival analysis showed that the triple negative phenotype was not a prognostic factor for either RFS or OS in the younger group. In the older group, however, the triple negative phenotype was a significant prognostic factor for both RFS (P = 0.0103) and OS (P = 0.0081) by univariate analysis, and it remained a significant prognostic factor for OS by multivariate analysis (hazard ratio, 1.9; 95% confidence interval, 1.09-3.44; P = 0.025). When the non-triple negative group was subdivided into luminal and HER2 subtypes, the HER2 subtype showed the worst OS in both age groups (P &amp;lt; 0.001), followed by the triple negative group. However, the difference between the HER2 subtype and the triple negative group was significant only in the younger group (P = 0.0064), but not in the older group (P = 0.1446).&amp;#x2028; Conclusions: Triple negative phenotype did not affect survival in patients &amp;lt; 40 years old, because of the markedly poorer survival of non-triple negative tumors of the HER2 subtype in this age group. Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 1083.