tbuckley/cabot-search huggingface dataset:
Use of Radiotracer for Sentinel Lymph Node Mapping in Breast Cancer Optimizes Staging Independent of Site of Administration
Authors: Susan B. Kesmodel, Robert J. Canter, Kyla P. Terhune, Todd W. Bauer, Rosemarie Mick, Ernest F. Rosato, Francis R. Spitz, Douglas L. Fraker, Abass Alavi, Brian J. Czerniecki
Journal: Clinical Nuclear Medicine (2006)

In an effort to optimize sentinel lymph node (SLN) mapping for breast cancer, sites of mapping agent administration and types of mapping agents used continue to be evaluated. This study compares SLN mapping using peritumoral (PT) or subareolar (SA) injection of radiolabeled colloid and examines the relative contributions of radiotracer and blue dye to SLN identification.A retrospective review was performed of 456 patients with breast cancer and clinically negative axillae who underwent SLN mapping. Sequential groups of patients were injected with filtered Tc-99m SC, 326 peritumorally (group 1) and 130 subareolarly (group 2). All patients had intraoperative SA injection of 1% isosulfan blue dye.The SLN identification and isotope success rates were 97% and 96% in group 1 and 98% and 98% in group 2, respectively. Eighty-one patients (25%) in group 1 and 44 patients (34%) in group 2 had positive SLNs. Of these patients, 15% from group 1 and 14% from group 2 had only positive nodes detected by radiotracer, and 9 of these patients (6 from group 1 and 3 from group 2) had other nodes identified by both radiotracer and blue dye that were negative for metastases. Six percent of patients with positive SLNs were upstaged because of use of radiotracer.PT and SA injection of radiotracer have comparable success rates for axillary SLN identification. Given that 15% of patients in group 1 and 14% in group 2 had only positive SLNs detected by radiotracer, independent of site of administration, radiotracer remains essential for optimizing breast SLN mapping.
Salm. thompson Gastro-enteritis
Authors: H. A. Wright, J. Norval, A. Orr
Journal: BMJ (1957)

THEOPHYLLINE PLASMA LEVELSBRNmH 69Five patients with cardiac failure showed no appreciable difference in theophylline plasma levels from asthmatics receiving the same compound.I should like to thank Dr. Kenneth Harris for his helpful criticism and for allowing me to study patients under his care.I am most grateful to Dr. Andrew Morland and to Dr.Howard Nicholson for allowing me to study their patients; to Dr. Monica McAllen for her help; and to Mrs. Mclnroy
Individual latex allergen sensitization profiles in spina bifida patients and health care workers using a panel of recombinant latex allergens coupled to immunoCAP
Authors: Monika Raulf-Heimsoth, Peter Rozynek, Maria Lundberg, Reinhold Cremer, Silke Maryska, Thomas Brüning, Hans-Peter Rihs
Journal: Journal of Allergy and Clinical Immunology (2002)
TREATMENT OF CHRONIC ROUND ULCER OF THE STOMACH.
Authors: G. FUETTERER
Journal: JAMA (1902)

Medical men have always had an inherent desire to put therapy on a rational basis. This feeling could not be downed any more than truth itself; knocked down, it would rise again to renewed effort.<i>Cessante causa, cessat effectus</i>, is the never-dying war cry that rings in our ears from generation to generation. Such thought leads me to commence my paper on treatment of ulcer of the stomach with a consideration of its etiology. A normal stomach does not digest its own tissues, neither as a whole, nor in part, and when self-digestion does take place it involves circumscribed portions, showing that there are agents contained in the gastric juice which act in harmony with certain local causes that lessen the resistance of parts of the wall of the stomach, allowing a partial self-digestion, which leads to the formation of a so-called round, peptic, perforating, chronic ulcer of the stomach.
Plasma platelet-activating factor acetylhydrolase activity in human immunodeficiency virus infection and the acquired immunodeficiency syndrome
Authors: W. Khovidhunkit, R.A. Memon, J.K. Shigenaga, M. Pang, M. Schambelan, K. Mulligan, K.R. Feingold, C. Grunfeld
Journal: Metabolism (1999)
Subarachnoid Hemorrhage Diagnosis—Reply
Authors: Jeffrey J. Perry, Marco L. A. Sivilotti, Ian G. Stiell
Journal: JAMA (2014)

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
CXCL10-CXCR3 interactions play an important role in the pathogenesis of acute graft-versus-host disease in the skin following allogeneic stem-cell transplantation
Authors: Karen P. Piper, Claire Horlock, S. John Curnow, Julie Arrazi, Sarah Nicholls, Premini Mahendra, Charles Craddock, Paul A. H. Moss
Journal: Blood (2007)
Abstract 1618: Synergistic growth inhibition of human hepatocellular carcinoma cells by acyclic retinoid and GW4064, a farnesoid X receptor ligand
Authors: Tomohiko Ohno, Masahito Shimizu, Masaya Kubota, Hiroyasu Sakai, Hisataka Moriwaki
Journal: Cancer Research (2012)

Abstract Abnormalities in the expression and function of retinoid X receptor (RXR), a master regulator of the nuclear receptor superfamily, are associated with the development of hepatocellular carcinoma (HCC). Dysfunction of farnesoid X receptor (FXR), one of the nuclear receptors that forms a heterodimer with RXR, also plays a role in liver carcinogenesis. In the present study, we examined the effects of acyclic retinoid (ACR), a synthetic retinoid targeting RXRα, plus GW4064, a ligand for FXR, on the growth of human HCC cells. We found that ACR and GW4064 preferentially inhibited the growth of HLE human HCC cells in comparison with Hc normal hepatocytes. The combination of 1 μM ACR plus 1 μM GW4064 synergistically inhibited the growth of HLE cells by inducing apoptosis and cell cycle arrest in the G0/G1 phase. The combined treatment with these agents acted cooperatively to inhibit the phosphorylation of RXRα, which is regarded as a critical factor for liver carcinogenesis, through inhibition of ERK and Stat3 phosphorylation. This combination also increased the expression levels of p21CIP1 and SHP mRNA, while decreasing the levels of c-myc and cyclin D1 mRNA in HLE cells. In addition, a reporter assay indicated that the FXRE promoter activity was significantly increased by treatment with ACR plus GW4064. Our results suggest that ACR and GW4064 cooperatively inhibit RXRα phosphorylation, modulate the expression of FXR-regulated genes, thus resulting in the growth inhibition of HCC cells. This combination might therefore be effective for the chemoprevention and chemotherapy of HCC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1618. doi:1538-7445.AM2012-1618
Taming the Technology Beast
Authors: Donald M. Berwick
Journal: JAMA (2008)

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
Treatment of Gonorrhea
Authors: Louis J. Lancaster
Journal: JAMA (1971)

<h3>To the Editor.—</h3> An EDITORIAL inThe Journal(<b>216</b>:1472, 1971) voiced great concern about rising incidences of venereal disease in America. If one were to recall the situation in America in the early 1940s one would find great similarities between the situation then and the one we now face. At that time, gonococcal infection was being treated with sulfonamides with poor results. Patients who were supposedly cured continued to have a thin serous discharge for several weeks to months, only to have recurrent infection. Concern was voiced at that time about the methods of stopping the epidemic, but it was only stopped with the advent of penicillin. This was a highly effective treatment at that time, and it stopped the spread of gonorrhea quickly. At the present time, we have an exact situation in America with the exception that the organisms are now resistant to penicillin. I have seen
Statistical Evidence for Miscoding Lesions in Ancient DNA Templates
Authors: Anders J. Hansen, Eske Willerslev, Carsten Wiuf, Tobias Mourier, Peter Arctander
Journal: Molecular Biology and Evolution (2001)

It is generally believed that sequence heterogeneity in PCR products from fossil remains are due to regular DNA polymerase errors as well as miscoding lesions compounded by damage in the template DNA (Paabo 1990; Handt et al. 1994b, 1996; Hoss et al. 1996; Krings et al. 1997). However, it has been difficult to test the frequency with which this assumption holds. First, DNA extractions from fossil remains rarely produce a yield large enough for pre-PCR analysis of postmortem modifications (Hoss et al. 1996). Second, in most cases, it is not possible to determine whether nucleotide misincorporations by the DNA polymerase enzyme during amplification are caused by regular DNA polymerase errors or miscoding lesions in the template DNA sequences (Greenwood et al. 1999). Finally, the error rates of the DNA polymerase enzymes for PCR have proved to be highly unpredictable, making it difficult to account for regular DNA polymerase errors in amplified DNA sequences (Eckert and Kunkel 1991). Here, we present a statistical model for analyzing PCR-mediated base-misincorporations, catalyzed by the commonly used Thermus aquaticus (Taq) polymerase enzyme, in amplification products from fossil remains. The error rate of the Taq polymerase enzyme may vary more than 10-fold (;2 3 1024 to ,1 3 1025 per nucleotide per cycle) according to the precise DNA sequence and the in vitro conditions of DNA synthesis (Eckert and Kunkel 1991). Therefore, the tests of the model rely solely on the relative distribution of the distinct Taq polymerase errors, which, in contrast to the highly variable error rate, is nearly constant and independent of the starting template material and the conditions for the PCR, as shown in table 1. Hence, the tests are not affected by variations in PCR efficiencies and accuracy. The model compares the distribution of the regular Taq polymerase errors with the observed substitutions in amplification products from fossil remains under the hypothesis that any significant differences between the distributions are due to miscoding lesions in the template DNA sequences used for PCR. The model was applied to published multiple clone sequences of the mitochondrial (mt) DNA control region from three differently preserved specimens of Homo representing different ages: a ;600-year-old Hokokam Indian (VC15A) found in a cave in Arizona, southwestern United States (Handt et al. 1996), the ;5,000-
Failure to trigger the oxidative metabolic burst by normal macrophages: possible mechanism for survival of intracellular pathogens.
Authors: C B Wilson, V Tsai, J S Remington
Journal: The Journal of Experimental Medicine (1980)

As previously reported, normal human monocytes (11) and activated mouse macrophages (9) are able to kill or inhibit intracellular replication of Toxoplasma that are not antibody coated, whereas normal human and mouse macrophages are not (7, 9). Each of these types of mononuclear phagocytes is able to kill antibody-coated Toxoplasma. In our studies, phagocytosis of antibody-coated Toxoplasma stimulated the respiratory burst by each of these types of mononuclear phagocytes, whereas phagocytosis of organisms that were not antibody coated stimulated the respiratory burst only by human monocytes and by activated mouse macrophages. Phagocytosis of Toxoplasma did not inhibit production of reactive oxygen metabolites by normal macrophages; rather, it failed to stimulate their production. Killing of Toxoplasma by monocytes from a child with X-linked chronic granulomatous disease and his heterozygote mother was impaired. Thus, reactive oxygen metabolites, perhaps in conjunction with lysosomal contents, appear to be first-line mechanisms whereby mononuclear phagocytes kill this organism. We were not able to determine the exact mechanisms whereby mononuclear phagocytes inhibit the replication of those Toxoplasma that were not killed, although both oxygen-dependent and other nonlysosomal mechanisms may be involved. The differences we observed in oxidative response to phagocytosis of Toxoplasma appear to be one determinant of the antimicrobial activity of these cells and may account for the ability of some intracellular pathogens to survive within phagocytes. These differences may be membrane related. Further studies of Toxoplasma membranes, phagocyte membrane receptors for Toxoplasma, and membrane-related mechanisms for activation of the respiratory burst are needed to define their true basis.
The Immune Response
Authors: Stuart F. Schlossman
Journal: New England Journal of Medicine (1967)

FROM the early days of immunology, immediate hypersensitivity responses, or the antibody-mediated reactions, were separated from and contrasted with the delayed hypersensitivity response, or the cell-mediated reaction. The reasons for this sharp separation were numerous and cogent. The purpose of this presentation is to point out that the 2 types of reactions have some very important basic similarities. They may both be mediated by antibody, and the observed differences merely reflect the locus of the reaction and the chemical and biologic properties of the antibodies involved. Because an extensive literature has now accumulated in this field, I must be both . . .
Understanding the Origins of Diabetes
Authors: Mark Hanson
Journal: JAMA (2014)

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
Educating a New Generation of Doctors to Improve the Health of Populations in Low- and Middle-Income Countries
Authors: Francesca Celletti, Teri A. Reynolds, Anna Wright, Aaron Stoertz, Manuel Dayrit
Journal: PLoS Medicine (2011)

Francesca Celletti and colleagues from WHO argue that a transformation in the scale-up of medical education in low- and middle-income countries is needed, and detail what this might look like.
Common Genetic Variants in <i>NEFL</i> Influence Gene Expression and Neuroblastoma Risk
Authors: Mario Capasso, Sharon Diskin, Flora Cimmino, Giovanni Acierno, Francesca Totaro, Giuseppe Petrosino, Lucia Pezone, Maura Diamond, Lee McDaniel, Hakon Hakonarson, Achille Iolascon, Marcella Devoto, John M. Maris
Journal: Cancer Research (2014)

Abstract The genetic etiology of sporadic neuroblastoma is still largely obscure. In a genome-wide association study, we identified single-nucleotide polymorphisms (SNP) associated with neuroblastoma at the CASC15, BARD1, LMO1, DUSP12, HSD17B12, HACE1, and LIN28B gene loci, but these explain only a small fraction of neuroblastoma heritability. Other neuroblastoma susceptibility genes are likely hidden among signals discarded by the multiple testing corrections. In this study, we evaluated eight additional genes selected as candidates for further study based on proven involvement in neuroblastoma differentiation. SNPs at these candidate genes were tested for association with disease susceptibility in 2,101 cases and 4,202 controls, with the associations found replicated in an independent cohort of 459 cases and 809 controls. Replicated associations were further studied for cis-effect using gene expression, transient overexpression, silencing, and cellular differentiation assays. The neurofilament gene NEFL harbored three SNPs associated with neuroblastoma (rs11994014: Pcombined = 0.0050; OR, 0.88; rs2979704: Pcombined = 0.0072; OR, 0.87; rs1059111: Pcombined = 0.0049; OR, 0.86). The protective allele of rs1059111 correlated with increased NEFL expression. Biologic investigations showed that ectopic overexpression of NEFL inhibited cell growth specifically in neuroblastoma cells carrying the protective allele. NEFL overexpression also enhanced differentiation and impaired the proliferation and anchorage-independent growth of cells with protective allele and basal NEFL expression, while impairing invasiveness and proliferation of cells homozygous for the risk genotype. Clinically, high levels of NEFL expression in primary neuroblastoma specimens were associated with better overall survival (P = 0.03; HR, 0.68). Our results show that common variants of NEFL influence neuroblastoma susceptibility and they establish that NEFL expression influences disease initiation and progression. Cancer Res; 74(23); 6913–24. ©2014 AACR.
Cultured rat hepatic sinusoidal endothelial cells express intercellular adhesion molecule-1 (ICAM-1) by tumor necrosis factor-α or interleukin-1α stimulation
Authors: Hiromasa Ohira, Takato Ueno, Satoshi Shakado, Masaharu Sakamoto, Takuzi Torimura, Sadataka Inuzuka, Michio Sata, Kyuichi Tanikawa
Journal: Journal of Hepatology (1994)
Electrical activity from the sinus node region in conscious dogs.
Authors: R J Hariman, B F Hoffman, R E Naylor
Journal: Circulation Research (1980)

In an attempt to understand the way automatic cells in the sinus node (SN) control the cardiac rhythm, we studied extracellular electrograms recorded from the SN region in conscious dogs. A SN electrode, containing 48 silver terminals arranged 1.5 mm apart, was implanted over the node, and an indifferent electrode was implanted on the superior vena cava. Through terminals of the SN electrode paired with the vena caval electrode, "unipolar" electrograms were recorded at 100 microV/cm and with a time constant of 0.1 second. Low amplitude and low frequency deflections (dV/dt less than or equal to 20 mV/sec) which resulted from electrical activity of the node could be differentiated from the more rapid deflections due to atrial electrical activity. Electrical activity due to the inherent automaticity of what appeared to be groups of automatic cells was recognized as a slow negative-going diastolic slope followed by a slow negative-going, or negative and then positive-going, SN potential. Impulse propagation toward the SN electrode terminal in groups of automatic cells appeared as a slow positive-going deflection interrupting the diastolic slope. Adjacent groups of automatic cells located near the sites of earliest atrial activation discharged asynchronously before the earliest atrial activity; this suggests that multiple groups of automatic cells might initiate atrial activation. In addition to changes in rate and in location of the pacemaking groups of automatic cells, significant beat-to-beat variation in the sinoatrial interval contributed to the changes in atrial rate in "sinus arrhythmia." These studies provide a better understanding of SN function in conscious animals.
Cardiac Sympathetic Denervation Assessed With 123-Iodine Metaiodobenzylguanidine Imaging Predicts Ventricular Arrhythmias in Implantable Cardioverter-Defibrillator Patients
Authors: Mark J. Boogers, C. Jan Willem Borleffs, Maureen M. Henneman, Rutger J. van Bommel, Jan van Ramshorst, Eric Boersma, Petra Dibbets-Schneider, Marcel P. Stokkel, Ernst E. van der Wall, Martin J. Schalij, Jeroen J. Bax
Journal: Journal of the American College of Cardiology (2010)
Tumoricidal activity of human dendritic cells
Authors: Jurjen Tel, Sébastien Anguille, Claire E.J. Waterborg, Evelien L. Smits, Carl G. Figdor, I. Jolanda M. de Vries
Journal: Trends in Immunology (2013)

Dendritic cells (DCs) are a family of professional antigen-presenting cells (APCs) that are able to initiate innate and adaptive immune responses against pathogens and tumor cells. The DC family is heterogeneous and is classically divided into two main subsets, each with its unique phenotypic and functional characteristics: myeloid DCs (mDCs) and plasmacytoid DCs (pDCs). Recent results have provided intriguing evidence that both DC subsets can also function as direct cytotoxic effector cells; in particular, against cancer cells. In this review, we delve into this understudied function of human DCs and discuss why these so-called killer DCs might become important tools in future cancer immunotherapies.