tbuckley/cabot-search huggingface dataset:
Abstract 11837: A Vascular Endothelial Growth Factor a (VEGFA) Genetic Variant is Associated With Improved Ventricular Function and Transplant-Free Survival After Surgery for Non-Syndromic Congenital Heart Defects
Authors: Constantine D Mavroudis, Daniel S Kim, Nancy Burnham, Alexandra H Morss, Jerry H Kim, Amber Burt, David R Crosslin, Donna M McDonald-McGinn, Elaine H Zackal, Meryl S Cohen, Susan C Nicolson, Thomas L Spray, Ian B Stanaway, Deborah A Nickerson, Mark W Russell, Hakon Hakonarson, Gail P Jarvik, J William Gaynor
Journal: Circulation (2014)

Introduction:  We have shown the minor allele of VEGFA single nucleotide polymorphism (SNP) rs833069 is associated with improved transplant-free survival after surgery for CHD in infants. The biological mechanisms underlying the improved survival have not been delineated. The minor allele is associated with higher VEGF production. We hypothesized that the VEGFA SNP is associated with better systemic ventricular function after surgery for CHD, resulting in improved survival.   Methods:  This is an analysis of a cohort of 422 non-syndromic CHD patients who underwent cardiac surgery with cardiopulmonary bypass before 6 months of age, of which 105 (24.9%) were single ventricle. Echocardiography reports were reviewed. Systemic ventricular function was subjectively assessed and categorized as normal, or mildly, moderately or severely depressed. The change in ventricular function was calculated as the change from the preoperative study to last available study. Stepwise linear regression, adjusting for covariates, was performed for the outcome of change in ventricular function. Model comparison was performed using Akaike’s information criterion (AIC). Only variables that improved model prediction of change in systemic ventricular function were retained in the final model.   Results:  Genetic and echocardiographic data were available for 335/422 subjects (79%). Of these, 40 (11.9%) developed worse systemic ventricular function and none demonstrated an improvement in ventricular function during the study period. (mean followup 13.5 years). After covariate adjustment, presence of the VEGFA SNP rs833069 minor allele was associated with preserved ventricular function, (p=0.011). A decrease in systemic ventricular function was significantly associated with heart transplantation or death (p   Conclusions:  These data are consistent with the hypothesis that the mechanism by which the VEGFA SNP rs833069 minor allele improves survival may be preservation of ventricular function. Further studies are needed to validate this genotype-phenotype association and determine if the mechanism underlying preservation of ventricular function and improved transplant-free survival is related to increased VEGF production.
Infant With a Unilateral Parotid Mass, Recurrent Otitis Media, and Macrocephaly
Authors: Markus D. Boos, Cory L. Simpson, Leslie Castelo-Soccio
Journal: JAMA Pediatrics (2015)

A 9-month-old boy presents with a left-sided facial mass. His perinatal history is notable for macrosomia, macrocephaly, left-sided failure on newborn hearing screen, and a congenital hypertrichotic patch of the left scalp. What is your diagnosis?
Fundamentals of Comparative Embryology of the Vertebrates
Authors: Alfred F. Huettner
Journal: JAMA (1941)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
785. Synergism of Combined Radiation and Suicide Gene Therapy Using a Chimeric Adenovirus Vector for Bladder Cancer
Authors: Kazumasa Matsumoto, Christian T. F. Freund, Weiguo Jian, Jiang Yu, Patricia Yotnda, Alan R. Davis, Seth P. Lerner
Journal: Molecular Therapy (2004)

BACKGROUND: Radiotherapy is an established local therapeutic option for invasive bladder cancer. While radiation leads to membrane damage which may facilitate foreign gene transfer from transduced gene expressing cells to neighboring untransduced cells, cancer cells expressing a cytotoxic gene may not repair radiation induced DNA damage. In addition, radiation may improve gene transduction and transgene integration for gene therapy. In this study, we evaluated the efficacy of a novel CAR independent Ad vector for suicide gene therapy in combination with radiation for bladder cancer in order to determine potential synergism and greater cancer control.
Abstract #LB-305: Genome wide screen of estrogen receptor-\#945; regulated microRNAs reveals a negative autoregulatory feedback loop
Authors: Leandro Castellano, Georgios Giamas, Jimmy Jacob, Walter Lucchesi, Long Jiao Jiao, Jonathan Waxman, Charles Coombes, Justin Stebbing
Journal: Cancer Research (2009)

AACR Annual Meeting-- Apr 18-22, 2009; Denver, CO

Estrogen receptor alpha (ER\#945;) is a nuclear receptor linked to progression of the majority of human breast cancers. Following activation ER\#945; regulates the transcription of target genes via DNA binding. Through a genome wide approach we have identified a subset of microRNAs (miRNAs or miRs) modulated by ER\#945;. Among them, miRNAs encoded from 2 paralogous clusters, miR-17-92 and miR-106a-363, were up-regulated. In addition, increased expression of miR-424, miR-542-3p and miR-450, located within the same genomic region and down-regulation of miR-181 family members were observed during the estrogenic response. We observed that ER\#945; alone is sufficient for sustained transcription of miR-17-92 and we show that levels of this cluster increase earlier than miRNAs encoded by it, implicating post-transcriptional regulation. Since miR-17-92 a pri-miRNA, is immediately cleaved by DROSHA to pre-miR-18a, this regulation occurs during the formation of the mature molecule from the precursor. Moreover, pre-miR-18a was significantly up-regulated in ER\#945;-positive breast cancers compared to ER\#945;-negative breast cancers. We also demonstrate that the miRNAs belonging to these paralogous clusters target and down-regulate ER\#945;, while a subset of cluster-derived miRNAs inhibit protein translation of its major oncogenic transcriptional p160 co-activator by targeting AIB1 revealing a negative autoregulatory feedback loop. This pathway adds to the highly regulated cellular response to estrogen that fine tunes ER\#945; transcriptional activity and cell proliferation.

Citation Information: In: Proc Am Assoc Cancer Res; 2009 Apr 18-22; Denver, CO. Philadelphia (PA): AACR; 2009. Abstract nr LB-305.
Abstract 15693: Genetic Deletion of Interleukin-6 Attenuates Left Ventricular Dysfunction and Remodeling After a Reperfused Myocardial Infarction
Authors: Anweshan Samanta, Guangming Cheng, Arash Davani, Magdy Girgis, Lei Chen, Kashyap Choksi, Lin Zhao, Robert J Vincent, Jeryl Hauptman, Buddhadeb Dawn
Journal: Circulation (2014)

Introduction:  Interleukin-6 (IL-6) is a proinflammatory cytokine, which is known to have a close association with cardiovascular diseases. Although myocardial expression of interleukin (IL)-6 increases after acute myocardial infarction (MI), its role in left ventricular (LV) remodeling and pathogenesis of heart failure remains unclear.   Hypothesis:  We hypothesized that the absence of IL-6 will have a favorable impact on LV remodeling after a reperfused MI.   Methods:  Because most heart attacks in humans are followed by spontaneous or interventional reperfusion, we used a model of reperfused MI. Age-matched male C57BL/6 control mice and IL-6 knockout (KO) mice were subjected to a 30-min occlusion of the LAD coronary artery followed by reperfusion. Cardiac structure and function were serially assessed by echocardiography at baseline (4 d before MI) and at 48 h and 35 d after MI. Mice were sacrificed after 35 days for histological and biochemical assessments.   Results:  At 48 h post-MI, ejection fraction (EF) was similarly and significantly reduced in both groups compared with baseline (Figure), indicating that the ischemic injury was comparable between groups. However, 35 d after MI, IL-6 KO mice exhibited significantly greater EF compared with control mice. Moreover, LV end-diastolic volume was significantly smaller in IL-6 KO mice (Figure), indicating superior remodeling.   Conclusions:  The amelioration of postinfarct LV dysfunction and remodeling in IL-6 KO mice indicates that IL-6 plays a deleterious role in myocardial healing after a reperfused MI. Modulation of IL-6 signaling may therefore have therapeutic potential for patients after MI at risk for adverse remodeling and development of heart failure.
False-negative monochromator phototesting in chronic actinic dermatitis
Authors: A.C. Kerr, R.S. Dawe, G. Lowe, J. Ferguson
Journal: British Journal of Dermatology (2010)

Journal Article False‐negative monochromator phototesting in chronic actinic dermatitis Get access A.C. Kerr, A.C. Kerr Ninewells Hospital and Medical School, Photobiology Unit, Department of Dermatology, Dundee DD1 9SY, U.K. E‐mail: a.kerr@dundee.ac.uk Search for other works by this author on: Oxford Academic Google Scholar R.S. Dawe, R.S. Dawe Ninewells Hospital and Medical School, Photobiology Unit, Department of Dermatology, Dundee DD1 9SY, U.K. E‐mail: a.kerr@dundee.ac.uk Search for other works by this author on: Oxford Academic Google Scholar G. Lowe, G. Lowe Ninewells Hospital and Medical School, Photobiology Unit, Department of Dermatology, Dundee DD1 9SY, U.K. E‐mail: a.kerr@dundee.ac.uk Search for other works by this author on: Oxford Academic Google Scholar J. Ferguson J. Ferguson Ninewells Hospital and Medical School, Photobiology Unit, Department of Dermatology, Dundee DD1 9SY, U.K. E‐mail: a.kerr@dundee.ac.uk Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 162, Issue 6, 1 June 2010, Pages 1406–1408, https://doi.org/10.1111/j.1365-2133.2010.09717.x Published: 01 June 2010
Trastuzamab antibody drug conjugates demonstrate robust <i>in vitro</i> antitumor activity in HER2 amplified breast cancer cell lines
Authors: Sankar Mohan, Carol O'Brien, Heidi Savage, Gail Phillips, Howard Stern, Mark Lackner, Ajay Pandita
Journal: Clinical Cancer Research (2010)

Abstract Breast cancer is a heterogeneous disease with molecular subtypes characterized by distinct histopathology and gene expression signatures. HER2 oncogene amplification and over-expression is a defining feature of the HER2-amplified subtype of breast cancer. Currently, assays for detecting gene amplification and protein over-expression are used as diagnostic assays for the selection of patients for HER2-targeted therapies. In the present study, we compared the sensitivity of several HER2-targeted therapies across a panel of 31 breast cancer cell lines and correlated the sensitivity of the cell lines with HER2 positivity, as determined by IHC, qPCR and FISH. The agents utilized for the cell line screening were trastuzamab (Herceptin), two trastuzamab antibody-drug conjugates (ADCs) that employ an anti-mitotic agent, and a small molecule inhibitor of HER2 kinase activity. HER2 testing revealed 32% of the cell lines to be positive for HER2 by qPCR and FISH, and 90% of these demonstrated gene amplification in the form of clusters, as detected by FISH, or more than 10 copies as detected by qPCR. Several of the cell lines exhibited polysomy for chromosome 17 with accompanying extra copies of HER2 but did not meet the criteria for HER2 amplification. The HER2 IHC assay revealed 10 cell lines to be positive (2+, 3+) by IHC, with 8 exhibiting high-level expression (3+). The agents tested were more efficacious in the HER2-amplified cell lines, with wideranging activity observed in response to the ADCs. Cell lines exhibiting polysomy for HER2 and 1+ expression by IHC were less responsive to any of the agents tested. Consistent with previous reports, many of the cell lines resistant to trastuzamab or the small molecule HER2 inhibitor exhibited deregulation of the PI-3 kinase pathway illustrated by mutations in the PIK3CA gene or loss of PTEN protein expression. Interestingly, the majority of these resistant cell lines were sensitive to ADCs. In summary, our study demonstrates a high sensitivity to ADCs in breast cancer cell lines harboring high-level amplification of the HER2 gene and suggests these agents may overcome in vitro resistance conferred by activation of the PI-3 kinase pathway.
140. Hydrodynamics-Based Transfection of the Liver: Entrance into Hepatocytes of DNA That Causes Expression, Takes Place Very Early after Injection
Authors: Amir S. Khan, Louis C. Smith, Ronald V. Abruzzese, Kathleen K. Cummings, Melissa A. Pope, Patricia A. Brown, Ruxandra Draghia-Akli
Journal: Molecular Therapy (2004)
Comparative ompA gene sequence analysis of Rickettsia felis-like bacteria detected in Haemaphysalis sulcata ticks and isolated in the mosquito C6/36 cell line
Authors: M. Gracner, T. Avsic-Zupanc, V. Punda-Polic, J. Dolinsek, D. Bouyer, D.H. Walker, J.E. Zavala-Castro, N. Bradaric, P.A. Crocquet-Valdes, D. Duh
Journal: Clinical Microbiology and Infection (2009)
Statistics Notes: Time to event (survival) data
Authors: D. G Altman, J M. Bland
Journal: BMJ (1998)

In many medical studies an outcome of interest is the time to an event. Such events may be adverse, such as death or recurrence of a tumour; positive, such as conception or discharge from hospital; or neutral, such as cessation of breast feeding. It is conventional to talk about survival data and survival analysis, regardless of the nature of the event. Similar data also arise when measuring the time to complete a task, such as walking 50 metres.

The distinguishing feature of survival data is that at the end of the follow up period the event will probably not have occurred for all patients. For these patients the survival time is said to be censored, indicating that the observation period was cut off before the event occurred. We do not know when (or, indeed, whether) the patient will experience the event, only that he or she has not done so by the end of the observation period.

Censoring may also occur in other ways. Patients may be lost to follow up during the study, or they may experience a “competing” event which makes further follow up impossible. For example, patients being followed …
Who's kicking who?
Authors: Nigel Hawkes
Journal: BMJ (2006)

Are you clear what a primary care trust does or how payment by results works?To help, we asked a health journalist to explain the numerous changes in the English health service and their implications Sometimes it helps to take a different point of view.Doctors puzzled by what is happening to the National Health Service in England do not have the time or the inclination to wade through the blizzard of documents that issue from the Department of Health.Doing so would not guarantee understanding, anyway.What follows is an idiot's guide to the new look NHS in England, written from a different perspective.Lenin famously asked, "Who whom?"What he meant was, "Who has the power over whom?Who is the master, and who the servant?"Seen in this light, the English NHS reforms become more understandable.As they move the pieces about the chess board, ministers talk grandly about "strengthening the architecture of the NHS," but what really matters is who does the kicking and who is kicked.
Abstract 17581: Evidence for Circulating Stem Cells Derived from the Human Heart and Their Therapeutic Potential
Authors: Han-Mo Yang, Ju-Young Kim, Hyun-Jai Cho, Joo-Eun Lee, So-Jung Lim, Sooryeonhwa Jin, Kyung-Woo Park, Sahmin Lee, Hae-Young Lee, Hyun-Jae Kang, Byung-Hee Oh, Young-Bae Park, Hyo-Soo Kim
Journal: Circulation (2014)

Introduction and Hypothesis: Many studies have shown resident cardiac stem cells in myocardium as well as epicardial progenitor cells in epicardium. However, the presence of stem cells in the endocardium has not been elucidated. In this study, we identified circulating multipotent stem cells from human peripheral blood. Furthermore, we investigated the origin and the therapeutic potential of these cells. Methods and Results: We identified a new population of cells from human peripheral blood mononuclear cells, which were quite different from previously reported stem cells. Newly identified cells expressed genes such as Oct3/4, KLF4, Nanog, and c-Myc. Moreover, FACS analysis precluded the possibility that these cells might be hematopoietic stem cells. To investigate the origin of these cells, we collected peripheral blood from patients undergoing bone marrow, liver, heart, or kidney transplantation. After culturing these cells, we could confirm that these stem cells were derived from the human heart by identifying the HLA types or the STR (short tandem repeat) profiles. In addition, we demonstrated that Nuclear Factor of Activated T-cells (NFAT)-positive and CD31-positive circulating cells in peripheral blood were derived from NFAT-positive cells in the endocardium. These cells had multipotency, indicating the ability of differentiation not only into mesodermal lineages, but also into ectodermal or endodermal lineages. When injected into the mouse heart in vivo , these stem cells were differentiated into multiple lineages, resulting in the improvement of the heart function. We established more than 200 cell lines from peripheral blood of patients with coronary artery diseases, cardiomyopathies, hematologic diseases, liver diseases, and kidney diseases. Conclusions: We demonstrated the existence of novel circulating multipotent stem cells in human peripheral blood, which express NFAT. Interestingly, these cells are derived from the tissue-resident stem cells of the endocardium of the human heart. Our findings suggest that these stem cells obtainable from peripheral blood could be a promising tool for heart regeneration.
Investigation of survivin gene polymorphism in non-small cell lung cancer patients (NSCLC)
Authors: Engin Aynaci, Ender Coskunpinar, Ayse Eren, Onur Kum, Yasemin Müsteri Oltulu, Nergiz Akkaya, Akif Turna, Aysun Aynaci, Ilhan Yaylim, Pinar Yildiz
Journal: European Respiratory Journal (2012)

INTRODUCTION - AIM

Survivin gene is one of the first reported inhibitors of apoptosis proteins (IAPs), which is an important family of proteins that regulate apoptosis. A common polymorphism at the survivin gene promoter (-31 G/C) has been shown to influence survivin expression and the risk for cancer development. Purpose of this study reports, relation between Turkish population who have survivin polymorphism and NSCLC also; its relevant with diseases's development and prognosis.

METHODS

146 NSCLC cases and 98 healthy control cases who were diagnosed at Yedikule Chest Diseases and Chest Surgery, Training and Research Hospital third clinic were included in this study. Pulmonary function test and routine biochemical analysis were done for all voluntaries. PCR-RFLP technique was used for genotyping.

RESULT

Genotype distrubition of Survivin gene's -31G/C region were detected (n=146) %77.4 GG (n=113), %.18.5 GC (n=27), %4.1 CC (n=6); at patient group and (n=98) % 6.1 GG (n=56), %47.5 GC (n=34), % 46.4 CC (n=8) (*p=0,003), at control group; -644T/C region were detected (n=146) %40.4 TT (n=59), %.48.6 TC (n=71), %11.0 CC (n=16); at patient group and (n=98) % 55.1 TT (n=54), %40.8 TC (n=40), % 4.1 CC (n=4) (*p=0,031), at control group; -625G/C region were detected (n=146) %49.3 GG (n=72), %.39.1 GC (n=57), %11.6 CC (n=17); at patient group and (n=98) % 57.1 GG (n=56), %32.7 GC (n=32), % 10.2 CC (n=10) (p=0,484) at control group.

CONCLUSION

These results show that Survivin gene -31 G/C polymorphism causes predisposition to lung cancer development in Turkish population.
Washing the Car
Authors: Gary Stein
Journal: JAMA (2004)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Diabetes Group Warns Vascular Complication Is Underdiagnosed and Undertreated
Authors: Mike Mitka
Journal: JAMA (2004)

PERIPHERAL ARTERIAL DISEASE (PAD) in individuals with diabetes is underdiagnosed and undertreated, leading to increased risk of mortality and morbidity, said researchers in a consensus statement issued by the American Diabetes Association (ADA). The researchers warned that PAD can lead to amputations of the lower limbs and is associated with an increased risk of cardiovascular and cerebrovascular disease in all patients (Diabetes Care.2003;26:3333-3341). In patients with diabetes, the risks associated with PAD are even higher, said Peter Sheehan, MD, director of the Diabetes Foot and Ankle Center at the New York University School of Medicine. “PAD in diabetes is different than PAD with other conditions,” said Sheehan, who chaired the ADA panel that issued the consensus statement. “It’s different for diabetes because of biology, clinical presentation, and treatment.” PAD is atherosclerotic occlusive disease in the legs and feet. While the most common symptom is intermittent claudication (calf pain during exercise with relief after stopping), the disease is also a marker for systemic vascular disease.