tbuckley/cabot-search huggingface dataset:
Malignancy in the Lung: Including Eight Primary Carcinomas With Autopsy Findings
Authors: Henry Monroe Moses
Journal: Annals of Internal Medicine (1931)

Article1 December 1931Malignancy in the Lung: Including Eight Primary Carcinomas With Autopsy FindingsHENRY MONROE MOSES, A.M., M.D., F.A.C.P.HENRY MONROE MOSES, A.M., M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-5-6-765 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptRobert J. Graves, of Dublin, who so clearly described exophthalmic goiter that the condition is still called Graves' Disease, in a clinical lecture1on the Practice of Medicine, delivered nearly ninety years ago, wrote "I shall conclude this lecture with the description of a singular and uncommon disease of the lungs. Rare diseases should not be looked upon as mere matters of curiosity, but should be attentively studied with the view of enabling us to recognize the true nature of similar cases when they again occur." He continues, "The diagnosis of encephaloid tumors of the lungs was, a few years...References1 GRAVES RJ: Clinical lecture on the practise of medicine, Vol. 11, p. 70, 1884, The New Sydenham Society, London. Google Scholar2 MORGAGNI GB: De sedibus et causis morborum per anatomen indagatis, 3v., 1779, Ebroduni in Helvetia. Google Scholar3 ADLER I: Primary malignant growths of lungs and bronchi, p. 17, 1912, Longmans, Green and Company, New York. Google Scholar4 ROSAHN PD: Incidence of primary carcinoma of lung, Am. Jr. Med. Sci., 1930, clxxix, 803-811. CrossrefGoogle Scholar5 DAVIDSON M: Cancer of the lung and other intrathoracic tumors, p. 42, 1930, William Wood and Company, New York. Google Scholar6 EWING J: Neoplastic diseases, p. 857, 1928, W. B. Saunders Company, Philadelphia. Google Scholar7 HAMMAN L: Diseases of the lungs, The Oxford Medicine, Vol. 11, Part 1, Chapter III, p. 82, 1920, Oxford University Press, New York. Google Scholar8 MOSES HM: Primary carcinoma of lung, Am. Jr. Med. Sci., 1925, clxx, 102-118. CrossrefGoogle Scholar9 NORRISLANDIS GWHR: Diseases of the chest and principles of physical diagnosis, p. 340, 1929, W. B. Saunders Company, Philadelphia. Google Scholar10 RIDDLESTURGIS MCCC: Effect of single massive dose of liver extract on patients with pernicious anemia, Am. Jr. Med. Sci., 1930, clxxx, 1-11. CrossrefGoogle Scholar11 STURGISISAACS CCR: Treatment of pernicious anemia with desiccated defatted stomach, Am. Jr. Med. Sci., 1930, clxxx, 597-602. CrossrefGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *From the Medical Service, Kings County Hospital, Brooklyn, N. Y.†Read at a Meeting of the Brooklyn Society of Internal Medicine, November 28, 1930. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1931Volume 5, Issue 6Page: 765-792KeywordsAutopsyHospital medicineLungsMedical services ePublished: 1 December 2008 Issue Published: 1 December 1931 PDF downloadLoading ...
Endofin is a novel component in EGF/EGFR oncogenic signaling
Authors: Weiyi Toy, Yoon Pin Lim
Journal: Clinical Cancer Research (2007)

AACR Centennial Conference: Translational Cancer Medicine-- Nov 4-8, 2007; Singapore

B74 

Epidermal Growth Factor Receptor (EGFR) is a known oncogene and malfunctioning of its receptor endocytosis and/or degradation may result in excessive signaling that could contribute to cancer transformation and tumorigenesis. Previously, we have identified Endofin, an endosomal protein, as one of the novel phosphoproteins from the analysis of an EGF-induced phosphotyrosine proteome using the cICAT-based LC-MS/MS method. Here we demonstrated that Endofin phosphorylation peaks at 30 minutes and starts to decrease after 1 hour. Further studies also showed that the localization of endofin to early endosomes is essential for its phosphorylation. This is indicated by the drastic decrease of Endofin phosphorylation in treated cells with wortmaninn, which prevents Endofin localization through inhibition of PI3P production. In addition, in vivo phosphorylation assay of Endofin FYVE mutant, C753S, resulted in drastic abolishment of phosphorylation, further supporting the notion that localization is crucial for phosphorylation. On the other hand, immunofluorescence staining of cells transfected with Endofin wild-type and phosphorylation site-mutants revealed that phosphorylation is not required for Endofin localization. All these results, taken together, suggest that endofin phosphorylation maybe important for its function at the early endsomes, such as regulation of EGFR endocytosis/degradation, which is a viable strategy in cancer therapeutics.
Letter by de Miguel Castro et al Regarding Article, “Cardiovascular Death and Nonfatal Myocardial Infarction in Acute Coronary Syndrome Patients Receiving Coronary Stenting Are Predicted by Residual Platelet Reactivity to ADP Detected by a Point-of-Care Assay: A 12-Month Follow-Up”
Authors: Antonio de Miguel Castro, Alejandro Diego Nieto, Armando Pérez de Prado
Journal: Circulation (2009)
Abstract 18427: Rotors and Focal Sources for Human Atrial Fibrillation Are Spatially and Temporally Stable
Authors: Vijay Swarup, Tina Baykaner, Junaid Zaman, James Daubert, John Hummel, David E Krummen, John Miller, Geri Tomassoni, Sanjiv Narayan
Journal: Circulation (2014)

Introduction: Several groups now report electrical rotors or focal sources sustaining human atrial fibrillation (AF) after it has been triggered. However, some groups report stable sources while others report transient rotational activity. Hypothesis: We hypothesized that AF rotors would be spatially stable in a large multi center experience, using phase mapping. Methods: We prospectively mapped AF in 277 patients (181 persistent, 61±12 years) at 6 centers in the FIRM-registry, using basket catheters with 64 contact electrodes per atrium. AF was mapped by RhythmView (Topera Inc) before ablation. FIRM uses phase analysis and dynamic physiological analysis of repolarization and conduction. AF propagation movies were interpreted by each operator to assess the stability and dynamics of AF sources in multiple maps over tens of minutes prior to ablation. Results: Sources were identified in 258 of 260 of patients in whom AF was mapped (99%), for 2.8±1.4 sources/patient. Patients showed 1.8±1.1 left atrial and 1.1±0.8 right atrial sources. On FIRM mapping, each source was stable for 4196±6360 cycles, with no difference between patients with paroxysmal vs persistent AF (4290±5847 vs 4150±6604, p=0.78), or right vs left atrial sources (p=0.26) (Figure). Rotors showed precession ('wobble') in ~2 cm2 areas, and spiral arms disorganized (‘fibrillatory conduction)’ beyond a spatial domain that varied around each rotor core for each patient, and between patients. Conclusions: Rotors and focal sources for human AF are stable for thousands of cycles during mapping using FIRM. These data show that AF rotors are distinct from macro-reentry. Notably, rotors precess within small atrial regions, and emanating spiral arms disorganize variably into the fibrillatory milieu in agreement with basic science studies. These results provide a rationale for FIRM-guided ablation at AF sources, and explain why rotors have been difficult to detect using traditional mapping approaches.
Abstract 3594: Tumor microenvironment derived exosomes regulate prostate cancer metabolism
Authors: Hongyun Zhao, Lifeng Yang, Abhinav Achreja, Juan Marini, Donna Peehl, Deepak Nagrath
Journal: Cancer Research (2014)

Abstract Tumor microenvironment is composed of myofibroblasts, extracellular matrix, and many other cells. There are many ways for tumor to communicate with its microenvironment, such as growth factors, cytokines, chemokines and so on. Recent research has indicated that exosomes may serve an important role in communication between tumor and its microenvironment. Exosomes are nanosized particles secreted by cells and contain microRNA, metabolic enzymes, biomarker proteins, and some other functional components. We show a novel regulatory mechanism for modulating metabolism in prostate cancer cells by stromal cells. We found that exosomes from stromal fibroblast cells are uptaken by prostate cancer cells and they release RNAs, enzymes to regulate cancer cells metabolism. Our result shows that exosomes from patient derived fibroblasts enhance glucose uptake, lactate production and pyruvate uptake in prostate cancer cells. We further performed 13C based isotope labeling experiments using glucose and glutamine labeling to study metabolic rewiring induced in cancer cells by stromal exosomes. We found that exosomes downregulated mitochondria metabolism in prostate cancer cells. In summary, stroma derived exosomes enhanced Warburg effect in prostate cancer cells. Our findings can lead to the development of new therapeutics integrating tumor microenvironment and metabolic pathways in tumor cells. Citation Format: Hongyun Zhao, Lifeng Yang, Abhinav Achreja, Juan Marini, Donna Peehl, Deepak Nagrath. Tumor microenvironment derived exosomes regulate prostate cancer metabolism. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3594. doi:10.1158/1538-7445.AM2014-3594
Susceptibility to infection
Authors: Douglas Carnall
Journal: BMJ (2000)

It is interesting why the cystic fibrosis gene should be so common, when the effect of being homozygous for the gene is so devastating. In the late 1980s it was found that heterozygous possession may convey some protection against cholera (www.people.virginia.edu/~rjh9u/cysfib.html), analogous to the effects of the sickle cell gene and malaria.

This week, a …
Abstract PR13: Pancreatic tumor stem cells resistant to inhibition of oncogenic signaling are dependent on mitochondrial function
Authors: Andrea Viale, Piergiorgio Pettazzoni, Costas Lyssiotis, Haoqiang Ying, Nora Sánchez, Matteo Marchesini, Alessandro Carugo, Tessa Green, Sahil Seth, Virginia Giuliani, Timothy Heffernan, Alec Kimmelman, Huamin Wang, Jason Fleming, Lewis Cantley, Ronald DePinho, Giulio Draetta
Journal: Cancer Research (2015)

Abstract Pancreatic ductal adenocarcinoma (PDAC) continues to have a poor prognosis despite extensive characterization of underlying genetic lesions. Although KRAS mutation is a signature driver event required for tumor development and maintenance, all the attempts made to target oncogene-driven signaling pathways have been met with minimal impact on survival and tumors eventually relapse, suggesting that ablation of oncogenic pathways fails to eradicate tumor cells. We used a genetically engineered mouse model of PDAC in which we could control the expression of mutant KRAS in a time- and tissue-specific manner to study the effects of ablating oncogenic signaling on PDAC cells. As previously described (Ying et al. 2012), this model showed rapid tumor growth when KRAS was expressed, followed by robust tumor regression upon oncogene ablation. However a small population of tumor cells survive genetic and pharmacological inactivation of KRAS. These surviving cells are tumor stem cells able to remain in a quiescent state for months before repopulating the original tumor upon reactivation of KRAS signaling. In depth transcriptomic and metabolomic analyses revealed surviving cells have different metabolic features with respect to the bulk of tumor cells, showing a prominent expression of genes governing mitochondrial function, β-oxidation and autophagy, as well as strong reliance on mitochondrial respiration, yet these cells also displayed impaired glycolytic capacity. In accord with their decreased dependence on glycolysis for cellular energetics and their complete absence of glycolytic reserve, these PDAC surviving tumor stem cells show high sensitivity to oxidative phosphorylation inhibitors, which prevented tumor recurrence. Our integrated analysis paves the way for new therapeutic strategies combining KRAS signaling and oxidative phosphorylation inhibition to completely eradicate pancreatic ductal adenocarcinoma. This abstract is also presented as Poster A87. Citation Format: Andrea Viale, Piergiorgio Pettazzoni, Costas Lyssiotis, Haoqiang Ying, Nora Sánchez, Matteo Marchesini, Alessandro Carugo, Tessa Green, Sahil Seth, Virginia Giuliani, Timothy Heffernan, Alec Kimmelman, Huamin Wang, Jason Fleming, Lewis Cantley, Ronald DePinho, Giulio Draetta. Pancreatic tumor stem cells resistant to inhibition of oncogenic signaling are dependent on mitochondrial function. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr PR13.
Amino-Terminal Pro-B-Type Natriuretic Peptide and B-Type Natriuretic Peptide in the General Community
Authors: Lisa C. Costello-Boerrigter, Guido Boerrigter, Margaret M. Redfield, Richard J. Rodeheffer, Lynn H. Urban, Douglas W. Mahoney, Steven J. Jacobsen, Denise M. Heublein, John C. Burnett
Journal: Journal of the American College of Cardiology (2006)
Cases of acute gastroenteritis due to calicivirus in outbreaks: clinical differences by age and aetiological agent
Authors: M.R. Sala, S. Broner, A. Moreno, C. Arias, P. Godoy, S. Minguell, A. Martínez, N. Torner, R. Bartolomé, M. de Simón, S. Guix, A. Domínguez
Journal: Clinical Microbiology and Infection (2013)
Successful Therapy of the Follicular Occlusion Triad in a Young Woman with High Dose Oral Antiandrogens and Minocycline
Authors: P C Goldsmith, Pauline M Dowd
Journal: Journal of the Royal Society of Medicine (1993)

Keywords follicular occlusion triad, hidradenitis suppurativa, dissecting cellulitis of the scalp, acne conglobata, antiandrogens, cyproterone acetate, ethinyl oestradiol
Cervical Cancer Screening Among Women Without a Cervix
Authors: Clay W Richardson
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
Understanding controlled trials: Baseline imbalance in randomised controlled trials
Authors: C. Roberts, D. J Torgerson
Journal: BMJ (1999)

In a controlled trial randomisation ensures that allocation of patients to treatments is left purely to chance. The characteristics of patients that may influence outcome are distributed between treatment groups so that any difference in outcome can be assumed to be due to the intervention. However, imbalance between groups in baseline variables that may influence outcome (such as age or disease severity) can bias statistical tests, a property sometimes referred to as chance bias Observed differences in outcome between groups in a particular trial could by chance be due to characteristics of the patients, not treatments. Some protection against chance bias is given by stratified randomisation or minimisation and by adjusting in the statistical analysis for baseline variables.

In reporting clinical trials it is recommended that prognostic variables should be described for each treatment group.1 This may …
Involvement of Peripheral and Spinal Tumor Necrosis Factor α in Spinal Cord Hyperexcitability During Knee Joint Inflammation in Rats
Authors: Christian König, Maxim Zharsky, Christian Möller, Hans‐Georg Schaible, Andrea Ebersberger
Journal: Arthritis & Rheumatology (2013)

Objective Tumor necrosis factor α (TNFα) is produced not only in peripheral tissues, but also in the spinal cord. The purpose of this study was to address the potential of peripheral and spinal TNFα to induce and maintain spinal hyperexcitability, which is a hallmark of pain states in the joints during rheumatoid arthritis and osteoarthritis. Methods In vivo recordings of the responses of spinal cord neurons to nociceptive knee input under normal conditions and in the presence of experimental knee joint inflammation were obtained in anesthetized rats. TNFα, etanercept, or antibodies to TNF receptors were applied to either the knee joint or the spinal cord surface. Results Injection of TNFα into the knee joint cavity increased the responses of spinal cord neurons to mechanical joint stimulation, and injection of etanercept into the knee joint reduced the inflammation‐evoked spinal activity. These spinal effects closely mirrored the induction and reduction of peripheral sensitization. Responses to joint stimulation were also enhanced by spinal application of TNFα, and spinal application of either etanercept or anti–TNF receptor type I significantly attenuated the generation of inflammation‐evoked spinal hyperexcitability, which is characterized by widespread pain sensitization beyond the inflamed joint. Spinally applied etanercept did not reduce established hyperexcitability in the acute kaolin/carrageenan model. In antigen‐induced arthritis, etanercept decreased spinal responses on day 1, but not on day 3. Conclusion While peripheral TNFα increases spinal responses to joint stimulation, spinal TNFα supports the generation of the full pattern of spinal hyperexcitability. However, established spinal hyperexcitability may be maintained by downstream mechanisms that are independent of spinal TNFα.
Gene therapy of experimental brain tumors using neural progenitor cells
Authors: Sara Benedetti, Barbara Pirola, Bianca Pollo, Lorenzo Magrassi, Maria Grazia Bruzzone, Dorotea Rigamonti, Rossella Galli, Silvia Selleri, Francesco Di Meco, Claudio De Fraja, Angelo Vescovi, Elena Cattaneo, Gaetano Finocchiaro
Journal: Nature Medicine (2000)
More Scrutiny for Dietary Supplements?
Authors: Tracy Hampton
Journal: JAMA (2005)

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
A New, Purified <i>Dermatophagoides farinae</i> Allergen Preparation
Authors: A. Moxnes, S. Dale, E. Andrew, R. Halvorsen
Journal: Allergy (1984)

A purified, standardized and characterized allergen preparation of the house dust mite Dermatophagoides farinae (Df) was evaluated by skin prick test (SPT) and radioallergosorbent test (RAST) in 88 subjects. Skin reactions to the purified Df preparation and a corresponding crude Df preparation were compared. SPT was also performed with a crude Dermatophagoides pteronyssinus (Dpt) preparation to compare reactions obtained with the two mite preparations. By SPT the purified Df allergen preparation was representative of the crude Df preparation (r = 0.78) and the correlation between skin reactions to Df and Dpt was high (r = 0.78). The concordance between results obtained with RAST and SPT techniques with the purified Df preparation was high (84%). The purified D. farinae preparation was well tolerated and is well suited for SPT.
Abstract 15648: Quantitative Evaluation of Mitral Valve Dynamics for Improved Planning of Mitral Valve Repairs
Authors: Ahnryul Choi, Yonghoon Rim, Susan T Laing, David D McPherson, Hyunggun Kim
Journal: Circulation (2014)

Introduction: Mitral valve (MV) repair with ring annuloplasty is the standard surgical technique for the treatment of mitral regurgitation (MR). Long-term studies report MR recurrence in up to 2-4% of repairs. We have developed a novel computational evaluation strategy to determine the biomechanical and physiologic characteristics of MV dynamics prior to and following virtual MV repair to help with optimal surgical planning. Methods: Virtual MV models from patients with large annular dilation and severe MR in the anterolateral region were created using 3D echocardiographic data sets. Two different types of annuloplasty rings were modeled in the simulation: Physio (flat) and Physio II (saddle-shaped). Proper ring size was determined using standard clinical guidelines. Computational simulations of MV function (pre- and post-repair) were performed using dynamic finite element methods. Coaptation ratio (CR) and structural stress distribution across the MVs were determined and compared. Results: Pathologic MVs demonstrated substantial anterolateral malcoaptation (CR=0.34, Fig. 1A). Following virtual ring annuloplasty, there was marked improvement in coaptation (CR=0.65 for Physio, CR=0.62 for Physio II). Pre-repair simulation revealed large stress concentrations over the posterior leaflet (Fig. 1B). Stress concentration decreased by 54% after virtual MV repair. The saddle-shaped Physio II ring demonstrated more evenly distributed stress reduction while the flat ring (Physio) more effectively increased leaflet coaptation. Conclusion: We have quantitatively evaluated patient-specific MV function before and after MV repair using a novel computational simulation protocol. Virtual ring annuloplasty simulation demonstrated sufficient restoration of leaflet coaptation and reduced stress concentration following repair. This simulation strategy has the potential for improved pre-surgical planning and intraoperative evaluation of MV repair.