tbuckley/cabot-search huggingface dataset:
Myeloma Solstice
Authors: Ronald Pies
Journal: JAMA (2015)

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
"Journal of Medical Genetics"
Journal: BMJ (1964)

Noonan syndrome is a genetic autosomal dominant disorder characterized by facial dysmorphy, short stature, delayed puberty and congenital heart defects.The first gene implicated in this syndrome is PTPN11, encoding protein tyrosine phosphatase SHP-2.Several studies worldwide have identified missense mutations in this gene in patients with Noonan syndrome.Our objective focused on mutations screening of PTPN11 on a Senegalese population with Noonan syndrome.Six patients clinically diagnosed with Noonan syndrome were included in this study.DNA was extracted from whole blood by phenol chloroform.Mutation screening was performed by bidirectional sequencing of amplified polymerase chain reaction (PCR) products of PTPN11 exons frequently mutated in Noonan syndrome.This study identified in two patients, a c.923A˃C mutation in exon 8, predicting Asn308Thr (N308T) on SHP-2 protein.This is the first time that this mutation is described in Noonan syndrome in Africa, while codon 308 was reported as a hot spot mutation site in other populations.Frequently reported amino acid substitutions were Asn308Asp and Asn308Ser.All these mutations affected the protein tyrosine phosphatase domain (PTP) of SHP-2 protein exerting a gain of function which would likely explain observed phenotypes in patients.
T cell reactivity in neonates from an East and a West German city - results of the LISA study
Authors: I. Lehmann, A. Thoelke, M. Weiss, U. Schlink, R. Schulz, U. Diez, G. Sierig, F. Emmrich, B. Jacob, P. Belcredi, G. Bolte, J. Heinrich, O. Herbarth, H.E. Wichmann, M. Borte
Journal: Allergy (2002)
OP0183 Long-Term Outcome of Rheumatoid Arthritis Defined According to the 2010-Classification Criteria
Authors: J. A. B. Van Nies, L. E. Burgers, L. Y. Ho, D. P. C. de Rooy, T. W. J. Huizinga, A. H. M. van der Helm-van Mil
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The 2010 ACR/EULAR-criteria for RA have been thoroughly studied for the test characteristic but it is unclear whether ‘2010-RA’ has a different phenotype than ‘1987-RA’ when assessing the severity of the disease course. <h3>Objectives</h3> Therefore this study compared two long-term disease outcomes in patients classified according to the 2010 ACR/EULAR-criteria and according to the 1987 ACR criteria for RA. <h3>Methods</h3> 1502 early arthritis patients that had no other diagnoses than RA or UA were studied on fulfilling the 1987-ACR-criteria, 2010-criteria or both. The severity of joint damage was studied with yearly radiographs over 7-years. Achieving DMARD-free sustained remission was assessed over 10-years follow-up. Multivariate normal regression and Cox-proportional hazard regression were used, adjusting for age, gender and treatment. <h3>Results</h3> 550 patients fulfilled the 1987-criteria, 788 patients the 2010-criteria and 489 both criteria sets. Patients fulfilling the 2010-criteria developed less severe radiological joint damage (p=0.023) and achieved DMARD-free sustained remission more often (HR=1.17 (0.93-1.49)) than patients fulfilling the 1987-critera, though the latter was not statistically significant. All 1987+2010-patients were ACPA-negative. When also applying the radiologic criterion of the 2010-criteria half of the 1987+2010- patients became 2010-criteria positive, but results on the long-term outcome remained similar. <h3>Image/graph</h3> <h3>Conclusions</h3> ‘2010-RA’ has a milder disease course than ‘1987-RA’. This may have important implications for basic scientific studies and clinical trials in RA. <h3>Disclosure of Interest</h3> None Declared
Abstract 77: The Role of Vinculin in Cardiomyocyte Adhesion and Mechanical Continuity
Authors: Chelsea D Merkel, Adam V Kwiatkowski
Journal: Circulation Research (2017)

Cardiomyocytes are joined end-to-end by a complex adhesive structure known as the intercalated disc (ICD). The ICD is composed of mechanical and electrical junctional complexes including the adherens junction (AJ). The core of the AJ is the cadherin/catenin complex, which links the actin cytoskeletons of neighboring cells to provide mechanical continuity. Myofibrils – the contractile machinery of the heart – are coupled to the ICD, presumably through the AJ; however, this mechanical linkage is poorly defined. Tension applied to the AJ is sensed in part through alpha-catenin, which connects the cadherin/catenin complex to actin. Force alters the conformation of alpha-catenin to reveal binding sites for actin-binding ligands, including vinculin and afadin, which are both found at the ICD. We investigated the role of alpha-catenin and its ligands in linking the AJ to actin in cardiomyocytes. Using a Förester resonance energy transfer tension-sensing module inserted into N-cadherin, we found that N-cadherin is under tension at the ICD. We then measured protein mobility of EGFP-tagged N-cadherin and found that N-cadherin dynamics were reduced at sites of myofibril integration, suggesting that myofibrils stabilize N-cadherin. To examine the composition of AJs in cardiomyocytes, we used immunofluorescence and found that vinculin and afadin were preferentially recruited to myofibril integration sites at the ICD. To further examine the linkage between AJs and myofibrils, we built a series of EGFP-tagged N-cadherin:alpha-catenin fusion constructs to delineate the individual and combined roles of alpha-catenin, vinculin and afadin. A constitutively active alpha-catenin increased vinculin recruitment and decreased the mobility of the N-cadherin fusion, suggesting that vinculin recruitment stabilizes the AJ. In contrast, restricting the AJ-actin interface to afadin reduced stability, indicating afadin alone cannot replace vinculin in linking AJs to the myofibril network. Together, our data support a model in which alpha-catenin, vinculin and afadin cooperate to anchor myofibrils at the ICD to provide mechanical continuity between cells.
Colorectal Stenting
Authors: M. Keymling
Journal: Endoscopy (2003)

Intestinal stenting is a procedure that is rapidly coming into more widespread use. It is reported to be a safe and highly effective alternative in patients with unresectable intestinal obstruction. Recent reports show the value of this procedure in colorectal obstruction, as it is relatively safe and can avoid the need for high-risk emergency laparotomy and resection in two sessions. New stents can be inserted in a one-step procedure, with delivery through the scope during the initial diagnostic endoscopy. If examinations show that curative treatment is not possible, resection can be completely avoided, so that the initial stent already forms part of the palliative strategy. Although stents are expensive, the procedure appears to be cost-effective, since emergency surgery can be avoided in patients with acute bowel obstruction, and in those with advanced disease no resection of the colon is necessary.
Which Radioiodine?
Authors: Earle M. Chapman
Journal: New England Journal of Medicine (1971)

Radioactive iodine is entering its fourth decade as a therapeutic agent that is supplementing surgery to reduce the amount of hyperplastic thyroid but with the expectation of leaving enough tissue to provide normal hormone production. Since the introduction of radioiodine there have been concerns that it might cause thyroid carcinoma, leukemia or genetic mutations in children born of treated parents. Hypothyroidism as a result of overtreatment was first produced in 1946.1 The long-range follow-up studies supported by the Bureau of Radiologic Health of the United States Public Health Service2 , 3 have produced convincing evidence from thousands of treated patients that an . . .
Activities of the Federation of the State Medical Boards of the United States, Inc.
Authors: M. H. Crabb
Journal: JAMA (1970)

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
Abstract P369: Left Ventricular Hypertrophy and Coronary Heart Disease Risk Reclassification in Blacks and Whites: The Atherosclerosis Risk in Communities (ARIC) Study
Authors: Tochi Okwuosa, Elsayed Z Soliman, Alvaro Alonso, Kim A Williams, Faye Lopez, Keith C Ferdinand
Journal: Circulation (2013)

Introduction: Left ventricular hypertrophy (LVH) is more prevalent in blacks than whites, and is a major independent predictor of coronary heart disease (CHD)/CVD survival in blacks. We evaluated the ability of LVH to predict CHD outcomes beyond traditional cardiovascular risk factors in blacks, compared with whites from a large community-based cohort. Methods: Data were analyzed on 14,489 participants (mean age 54 +/- 5.7 years, 43.5% men, and 26% black) within the ARIC cohort, with baseline (1987-1989) electrocardiograms (ECG), followed through 2009. Risk estimates for incident CHD were assessed using the 10-year Framingham Risk Score (FRS). Model 1 was the Framingham base model, while model 2 included the base model plus LVH by any of 11 traditional ECG-LVH criteria (Table). Net reclassification improvement (NRI) was calculated, and the distribution of risk was compared using model 2 vs. model 1. Results: There were 690 (4.8%) 10-year and 1515 (10.5%) 20-year CHD events. LVH defined by any criteria was associated with CHD events in the entire cohort [HR (95% CI): 1.42 (1.20-1.7)]. LVH defined by the Framingham ECG score and LV strain criteria were the criteria most associated with CHD overall. LVH by Framingham ECG score was most associated with CHD in blacks [HR (95%CI): 2.53 (1.65-3.89)], while LV strain showed the strongest association with CHD in whites [1.73 (1.18-2.56)]. No statistically significant improvement in NRI or C-statistic was observed in model 2 [C-statistic (95% CI): 0.779 (0.763-0.794), NRI = 0.006 (p = 0.41)], compared with the base model [0.777 (0.762-0.792)]; and no racial interactions were observed. Findings were unchanged when the base model was replaced with the 10 and 20-year ARIC risk model (includes diabetes) for CHD. Conclusions: In this cohort of black and white men and women, LVH (defined by ECG) was significantly associated with CHD after adjustment for FRS; but did not significantly improve CHD risk prediction beyond the FRS. No significant black-white differences in risk prediction were observed. Table. Reclassification of Coronary Heart Disease by the addition of each Criterion for Left Ventricular Hypertrophy, based on a 10-year Framingham Risk Model * Base model factors in age, gender, current smoking, diabetes, systolic blood pressure, diastolic blood pressure, HDL cholesterol and total cholesterol as separate variables. * NRI categorized as &lt;10%, 10-20% and &gt;20%. Abbreviations: NRI = Net Reclassification Index, IDI = Integrated Discrimination Index, HR = Hazard Ratio, CI = Confidence Interval
Radiation and Cancer: Three Reports
Journal: JAMA (1966)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
Die Leitungsbahnen des Schmerzgefühls und die chirurgische Behandlung der Schmerzzustände.
Journal: JAMA (1927)

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
Coloscopie double ballon (CDB): le moyen le plus efficace d'atteindre le caecum après une coloscopie incomplète
Authors: G Gay, M Delvaux, I Fassler, M Frédéric
Journal: Endoscopy (2009)

Introduction: La technique de progression utilisée pour l'entéroscopie double ballon s'est révélée utile pour la réalisation de coloscopies difficiles, notamment chez des patients multiopérés. Le but de cette étude était d'évaluer l'intérêt de cette technique de CDB, utilisant un nouveau coloscope (EC-450B15. Fujinon Optical Co. Ltd., Saitama, Japon) pour réaliser une coloscopie complète chez des patients dont la coloscopie classique avait été incomplète en raison de difficultés de progression.
Monitoring
Authors: V. Néve, R. Logier, Y. Riou, L. Storme, A. Martinot, F. Leclerc, V. L. Montgomery, L. Tortorolo, G. Polidori, G. Vento, E. Zecca, C. Romagnoli, A. C. P. Ferreira, W. B. Carvalho, B. I. Kopelman, A. Peltenazzo, E. Baraldi, P. Biban, F. Zaglia, N. Azzolin, R. Van Asperen, A. Flemmer, E. Stehr, G. Simbruner
Journal: Intensive Care Medicine (1996)
Dementia care
Authors: David G Smithard
Journal: Journal of the Royal Society of Medicine (1998)

This is particularly pertinent in view of the growing belief that dysmorphophobia, or body dysmorphic disorder, is underdiagnosed: some have suggested that as many as 12% of psychiatric outpatients suffer from this disorder'.Screening instruments for clinicians or patients to fill out include the Body Dysmorphic Disorder Questionnaire'
Retraction: ‘Number needed to treat with 4‐factor prothrombin complex concentrate for urgent warfarin reversal’ by Andrew Chua, Vishal Patel, Allison Perrin, Lee Stern, Jenifer Ehreth, Laurel Omert, Christopher Hood, Julie Farley, Michael McGlynn and Liping Huang
Journal: American Journal of Hematology (2017)

Abstract The above abstract from the THSNA 2016 Summit Abstract Proceedings, first published online in the American Journal of Hematology on 20 July 2016 in Wiley OnlineLibrary ( www.onlinelibrary.wiley.com ), and in Volume 91, Issue 9, p. E427, has been retracted by agreement between the authors, the journal Editor‐in‐Chief, Carlo Brugnara, and Wiley Periodicals, Inc. The retraction has been agreed due to concerns from the submitting authors that the abstract was inadvertently submitted prior to receiving approval from all authors and proper review of data analytics, thereby rendering it incomplete. Reference 2016 . Am. J. Hematol. , 91 : E427 . https://doi.org/ 10.1002/ajh.24471
New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter
Authors: D. Peteiro-Gonzalez, J. Lee, J. Rodriguez-Fontan, I. Castro-Piedras, J. Cameselle-Teijeiro, A. Beiras, S. B. Bravo, C. V. Alvarez, D. M. Hardy, H. M. Targovnik, P. Arvan, J. Lado-Abeal
Journal: Endocrine Reviews (2010)

Thyroglobulin (TG) gene mutations cause congenital hypothyroidism (CH) with goiter. A founder effect has been proposed for some frequent mutations. Mutated proteins have a defect in intracellular transport causing intracellular retention with ultrastructural changes that resemble an endoplasmic reticulum storage disease. To reveal new aspects of thyroglobulin pathophysiology through clinical, cellular, molecular, and genetic studies in a family presenting with CH due to TG mutations from Galicia, an iodine-deficient area of Spain. The included clinical evaluation of family members, DNA sequencing for TG gene mutation and haplotyping analysis, ultrastructural analysis of thyroid tissue specimens from affected subjects, analysis of effects of mutations found on TG gene transcription, and in vitro studies of cellular production and secretion of mutated proteins. Locations included primary care and university hospitals. Family members with CH, mental retardation, and goiter were compound heterozygous for c.886C→T (p.R277X) and g.IVS35+1delG. For c.886C→T, a founder effect cannot be excluded, and its transcription was hardly detectable. g.IVS35+1delG caused an in-frame deletion in exon 35 and produced a protein that, although synthesized, could not be secreted. Ultrastructural analyses showed morphological changes consistent with an endoplasmic reticulum storage disease. The shorter thyroglobulin resulting from the novel g.IVS35+1delG was retained within the endoplasmic reticulum of thyrocytes, and together with p.R227X caused severe hypothyroidism with goiter. p.R277X, the most commonly described TG mutation, is caused by a TG exon-7 highly mutation-prone region, and the possibility that some cases were introduced to South America from Galicia cannot be excluded.
Medical Courtesy.
Authors: None R. A. H.
Journal: JAMA (1898)

Clarksburg, W. Va., Dec. 21, 1897. <h3>To the Editor:</h3> —In case a physician who is in good standing in his State medical society moves his location to a town in a neighboring county of the same State, in accordance with social or professional ethics, who is expected to first extend courtesies in the way of friendly calls, the new-comer or his older established professional brethren? Very respectfully, <h3>Answer:</h3> Where a physician moves into a neighborhood, courtesy demands that his brother practitioners should call on him within a reasonable time and give him the right hand of fellowship.
SCIDOT-26. THE ROLE OF TUMOR-DERIVED GRANULOCYTE MACROPHAGE COLONY STIMULATING FACTOR (GM-CSF/CSF2) IN REGULATION OF MICROGLIA-DEPENDENT INVASION IN GLIOMAS
Authors: Katarzyna Poleszak, Maria Pasierbinska, Aleksandra Ellert-Miklaszewska, Bartosz Wojtas, Kamil Wojnicki, Bozena Kaminska
Journal: Neuro-Oncology (2019)

Abstract Brain resident immune cells (microglia) and peripheral macrophages accumulate in malignant gliomas and constitute for 30–50% of the tumor mass. These immune cells are polarized by factors released by glioma and become the pro-invasive, immunosuppressive cells that support tumor progression. We have previously found that tumor-derived granulocyte macrophage colony stimulating factor (GM-CSF/Csf-2) is a crucial factor controlling accumulation of microglia and macrophages in murine gliomas. The analysis of TCGA dataset revealed overexpression of the CSF2 gene (encoding GM-CSF) in a set of mesenchymal glioblastomas (most aggressive WHO grade IV gliomas) and its association with high immune gene expression. To study the role of GM-CSF in microglia-stimulated glioma invasion, we used a co-culture system, which mimics microglia interactions with tumor cells. We silenced the expression of CSF2 in glioma cells and found reduced microglia-dependent invasion of glioma cells. To translate those results into clinically relevant setting, we designed and tested humanized short peptides interfering with binding of GM-CSF to its receptor. Selected peptide effectively inhibited binding of GM-CSF to its receptor as demonstrated with different methods. We selected the non-cytotoxic peptides that potently blocked microglia-dependent glioma invasion in cell co-cultures. Blocking GM-CSF-receptor signaling pathway with a neutralizing antibody against a GM-CSF receptor also inhibited microglia-dependent invasion of glioma cells. Altogether, our results demonstrate that glioma-derived GM-CSF supports pro-tumorigenic polarization of microglia turning them into cells that facilitate glioma growth and shape the immune microenvironment. The study was supported by grant 2014/15/B/NZ3/04704 from The National Science Centre, Poland.