tbuckley/cabot-search huggingface dataset:
Pneumotyphoid.
Journal: JAMA (1922)

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
Novel anticancer therapies for decade ahead may prove to be more specific, less toxic
Authors: A. Skolnick
Journal: JAMA (1990)

ANTIBODIES that lock up tumor cell surface receptors may be another novel way to attack cancer. Mark I. Greene, MD, PhD, and colleagues at the University of Pennsylvania School of Medicine, Philadelphia, have identified antibodies that react with certain cell surface receptors which play an important role in tumor-genesis. "These receptors, when expressed in a particular form or density, can determine the malignant state, Greene told the American Cancer Society seminar in Daytona Beach, Fla. Green and coworkers previously identified a transforming gene from neuroblastomas they called "neu," which encodes the "p185" receptor protein. Greene and colleagues found how a point mutation makes the normal gene product tumorigenic. They have now developed monoclonal antibodies that react with and down-modulate the p185 protein. The down-regulation occurs because the p185 proteins bound to antibodies are absorbed by the cell. This novel approach appears to convert the malignant cell back to a normal
Abstract 4186: An extensive microRNA-mediated network of RNA-RNA interactions regulates established oncogenic pathways in glioblastoma
Authors: Pavel Sumazin, Andrea Califano, Hua sheng Chiu, Xuerui Yang
Journal: Cancer Research (2012)

Abstract By analyzing gene expression data in gliobastoma in combination with matched microRNA profiles, we have uncovered a post-transcriptional regulation layer of surprising magnitude, comprising over 248,000 microRNA -mediated interactions. These include ∼7,000 genes whose transcripts act as microRNA ‘sponges’ and 148 genes that act through alternative, non-sponge interactions. Biochemical analyses in cell lines confirmed that this network regulates established drivers of tumor initiation and subtype, including PTEN, PDGFRA, RB1, VEGFA, STAT3, and RUNX1, suggesting that these interactions mediate crosstalk between canonical oncogenic pathways. RNA silencing of 13 microRNA-mediated PTEN regulators, whose locus deletions are predictive of PTEN expression variability, was sufficient to downregulate PTEN in a 3′ UTR-dependent manner and to increase tumor-cell growth rates. Thus, this microRNA -mediated network provides a mechanistic, experimentally validated rationale for the loss of PTEN expression in a large number of glioma samples with an intact PTEN locus. 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 4186. doi:1538-7445.AM2012-4186
Pathogenesis of disseminated intravascular coagulation in sepsis
Authors: M. Levi
Journal: JAMA (1993)

<h3>Objective.</h3> —To review new insights in the pathogenetic mechanisms involved in the development of disseminated intravascular coagulation (DIC) in septic patients, in order to develop new directions for therapeutic intervention. <h3>Data Sources.</h3> —Articles and published peer-reviewed abstracts on the mechanism of the initiation of DIC in sepsis. <h3>Study Selection.</h3> —Studies selected for detailed review were those reporting specifics about the mechanism of activation of coagulation and fibrinolysis in experimental human and animal models of sepsis. Data extraction guidelines for assessing data quality included validity of the model, quality of the laboratory assessment of activation of coagulation and fibrinolysis, and methodological considerations, such as the presence of control experiments and statistical analysis. <h3>Data Synthesis.</h3> —After the presence of endotoxin in the circulation, significant coagulation activation can be detected. This activation is preceded by an increase in the serum levels of various cytokines, such as tumor necrosis factor and interleukins. Inhibition of the increase in tumor necrosis factor results in inhibition of coagulation activation. Measurement of molecular markers for the activation of coagulation proteins at various levels indicates that the activation of coagulation is mediated by the tissue factor—dependent pathway, which is further confirmed by experiments in which the inhibition of the tissue factor—dependent pathway resulted in complete inhibition of coagulation activation. The activation of coagulation seems to be amplified by impaired function of the protein C—protein S inhibitory pathway. An imbalance between coagulation and fibrinolysis, ultimately leading to plasminogen activator inhibitor type 1—mediated inhibition of fibrinolysis, may further promote the procoagulant state. <h3>Conclusion.</h3> —The increased knowledge of the various pathogenetic mechanisms of coagulation activation and fibrinolysis in sepsis may have therapeutic implications; however, their efficacy needs to be assessed in appropriate clinical trials. (<i>JAMA</i>. 1993;270:975-979)
Roentgen Diagnosis of Diverticulitis
Journal: JAMA (1963)

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
Orthotopic liver transplantation in a patient with Amanita poisoning
Authors: E. S. Woodle
Journal: JAMA (1985)

Orthotopic liver transplantation in patients with acute toxic hepatitis has not, to our knowledge, been reported. Our recent experience with orthotopic liver transplantation in a 3-year-old girl with acute hepatic failure secondary to<i>Amanita</i>poisoning is described. Aspects of<i>Amanita</i>toxin-induced pathophysiology pertinent to orthotopic liver transplantation are discussed. The results in this case provide important implications for patients with fulminant hepatic failure secondary to other hepatotoxic agents in whom liver transplantation is considered. (<i>JAMA</i>1985;253:69-70)
Therapeutic Hypothermia
Authors: Robert M. Smith, John B. Stetson
Journal: New England Journal of Medicine (1961)

THE possible implications of total-body cooling have long interested investigators, clinicians and science-fiction writers. In the confusion of today's literature, it is sometimes difficult to classify authors correctly. Herein, perhaps, lies the excuse for this report, since there are already excellent monographs and reviews,1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 on many separate phases of the subject. Two progress reports have already appeared in the Journal.18 , 19 It is our intention to assess the many forms of therapeutic hypothermia now in vogue and to direct readers to reliable sources. Also, since new concepts are continually developing, it is hoped this review, like a daily newspaper, will . . .
DNA damage response protein checkpoint kinase 2 (CHK2) links chromosomal instability to cellular metabolism in hepatocellular carcinoma (HCC)
Authors: Matteo Lulli, Veronica Ghini, Tommaso Mello, Caecilia Sukowati, Antonio Mazzocca, Paola Turano, Krista Rombouts, Andrea Galli, Vinicio Carloni
Journal: Journal of Hepatology (2020)
THU0121 The interferon type I signature towards prediction of non-response to rituximab in rheumatoid arthritis patients
Authors: H. Raterman, S. Vosslamber, S. de Ridder, M. Nurmohamed, W. Lems, M. Boers, M. van der Wiel, B. Dijkmans, C. Verweij, A. Voskuyl
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> B cell depletion therapy is efficacious in rheumatoid arthritis (RA) patients failing on tumor necrosis factor (TNF) blocking agents. However, approximately 40-50% of rituximab (RTX) treated RA patients have a poor response <h3>Objectives</h3> We investigated whether baseline gene expression levels can discriminate between clinical nonresponders and responders to RTX. <h3>Methods</h3> In 14 consecutive RA patients starting with RTX (test cohort), gene expression profiling on whole peripheral blood RNA was performed by Illumina® HumanHT beadchip microarrays. Supervised cluster analysis (patients ranked on difference in 28 joints disease activity score (DAS28) after 6 months RTX) identified genes expressed differently at baseline in case of nonresponse (both ΔDAS28 &lt;1.2 and EULAR nonresponse). Genes of interest were measured by quantitative real-time PCR and tested for their predictive value using Receiver Operating Characteristics (ROC) curves in an independent validation cohort (n=26). <h3>Results</h3> Genome-wide microarray analysis revealed a marked variation in the peripheral blood cells between RA patients before the start of RTX treatment. Here, we demonstrated that only a cluster consisting of interferon (IFN) type I network genes, represented by a set of IFN type I response genes (IRGs), i.e. <i>LY6E, HERC5, IFI44L, ISG15, MxA, MxB, EPSTI1</i> and <i>RSAD2</i>, was associated with ΔDAS28 and EULAR response outcome (p=0.0074 and p=0.0599, respectively). Based on the 8 IRGs an IFN-score was calculated that reached an AUC of 0.82 to separate non-responders from responders in an independent validation cohort of 26 patients using ROC curves analysis according to ΔDAS28&lt;1.2 criteria. Advanced classifier analysis yielded a 3 IRG-set that reached an AUC of 87%. Comparable findings applied to EULAR nonresponse criteria. <h3>Conclusions</h3> This study demonstrates clinical utility for the use of baseline IRG expression levels as predictive biomarker for nonresponse to RTX in RA. <h3>Disclosure of Interest</h3> H. Raterman: None Declared, S. Vosslamber: None Declared, S. de Ridder: None Declared, M. Nurmohamed Consultant for: Dr. M. Nurmohamed has been a speaker and consultant for BMS, MSD, Roche, Abbott, Pfizer and UCB, W. Lems: None Declared, M. Boers: None Declared, M. van der Wiel: None Declared, B. Dijkmans: None Declared, C. Verweij: None Declared, A. Voskuyl: None Declared
FOUR YEARS' PROGRESS IN PUBLIC HEALTH ORGANIZATION IN OHIO
Journal: JAMA (1921)

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
Announcements
Authors: Chiharu Kubo, Winfried Rief, Susanne Trenkamp, Claudia Auer, Manfred M. Fichter, C.T. Johan Lökk, Bengt B. Arnetz, Thilo Deckersbach, Michael W. Otto, Cary R. Savage, Lee Baer, Michael A. Jenike, A. O'Neill of Tyrone, J.M. Fernandez, P. Bech, Julia M. Foy, John M. Starr, Töres Theorell, Lars Alfredsson, Peter Westerholm, Bengt Falck, L. Grassi, G. Rasconi, A. Pedriali, A. Corridoni, M. Bevilacqua
Journal: Psychotherapy and Psychosomatics (2000)
PTU-095 Bifidobacterium Species Reduce Lipopolysaccharide-induced Small Intestinal Epithelial Cell Shedding<i>in Vivo</i>In A Myd88-dependent Manner And Protect Against Dss-induced Colitis
Authors: K Hughes, C Alcon-Giner, D VanSinderen, L Hall, A Watson
Journal: Gut (2014)

<h3>Introduction</h3> Cell shedding, the process by which intestinal epithelial cells (IECs) are extruded from the small intestinal (SI) villus is known to be elevated in patients with inflammatory bowel disease (IBD) and is correlated with disease relapse. Importantly, there is evidence that the gut bacterial communities (microbiota) influences intestinal epithelial function including gene expression, cell division and energy balance. We thus sought to determine whether specific members of the microbiota, ‘probiotic’ bifidobacterial species, modulate rates of cell shedding and progression of Dextran sodium sulphate (DSS)-mediated colitis. <h3>Methods</h3> C57BL/6 mice (WT) or mice deficient in epithelial Myd88 (Vil-Cre +; Myd88 -/-) (Myd88 KO) were orally gavaged with 1 × 10<sup>9</sup><i>Bifidobacterium breve UCC2003</i>, <i>B. longum</i> NCIMB8809 or PBS (control) in 3x daily doses. To induce SI cell shedding, mice were injected with 1.25 mg kg-1 Lipopolysaccharide (LPS) intrapertioneally. Animals were euthanized 1.5 hr post-LPS and SI tissue sections analysed for cleaved caspase 3 (CC3) by immunohistochemistry to score shedding along the first 50 cell positions from the villus tip. For colitis studies, control mice or mice colonised with <i>B. breve</i> were administered 2% DSS in drinking water for 6 days and euthanized 8 days post-DSS. Disease activity index (DAI) was recorded daily and histology performed on formalin-fixed tissue sections including periodic acid/Schiff (PAS) stain (goblet cell stain). <h3>Results</h3> Mice receiving <i>B. breve</i> and <i>B. longum</i> showed less CC3 +ve shedding cells (3.6% +/-0.6, p &lt; 0.001 and 7.6% +/-2.9, ns, respectively) compared to WT mice (10.6%+/-1.3). Interestingly, the protective effect of <i>B. breve</i> was lost in Myd88 KO mice receiving LPS as numbers of CC3 +ve IECs were the same in mice receiving <i>B. breve</i> or vehicle control (13.3%+/-1.7 vs 10.4%+/1.3; ns), indicating that the protective effect may be mediated by Toll-like receptors. In our colitis model, mice colonised with <i>B. breve</i> had reduced DAI compared to control mice, coupled with a significant increase in numbers of PAS +ve goblet cells per crypt (8.2%+/1.6 vs 16.0%+/-0.6; p = 0.05). <h3>Conclusion</h3> Bifidobacterial species modulate a reduction in rates of cell shedding from the SI villus, potentially via the Myd88 signalling pathway. <i>B. breve</i> is also able to partially ameliorate the adverse effects of DSS-induced colitis through induction of goblet cells. In summary, bifidobacteria, particularly <i>B. breve,</i> may be beneficial as a therapeutic agent for IBD. <h3>Disclosure of Interest</h3> None Declared.
SYPHILITIC SCARS OF THE SPIRIT
Journal: JAMA (1920)

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
Repository Therapy
Authors: Samuel, J. Prigal
Journal: JAMA (1964)

<h3>To the Editor:—</h3> In the past four years, while giving approximately 4,000 injections of emulsified allergens, I have seen only one sterile cyst and two draining abscesses (in one patient), all of which healed spontaneously. However, it is apparent from Dr. Appleman's report and from the observations of others, that the repository procedure as now employed by allergists has limitations. But the picture is not so black as painted by Dr. Appelman. I believe that with proper employment and further improvement, including the use of substitutes for mineral oil, repository injections of allergens will become an established procedure.
Rumination variations
Authors: E. Tucker, J. Wright, M. Fox
Journal: Gut (2011)

<h3>Introduction</h3> Rumination syndrome is the voluntary, albeit subconscious return of gastric content to the mouth. It is socially disabling, often leads to repeated, non-diagnostic investigations and can have significant morbidity. High Resolution Manometry (HRM) with observations after drinking or a test meal is a simple, objective way of establishing the diagnosis. A variety of behaviours and manometric findings are associated with rumination. This study describes how these influence patient presentation and may affect treatment. <h3>Methods</h3> A retrospective review of 20 patients (M = 8, F = 12, age 21–68) referred for HRM with a final diagnosis of rumination was completed. Predominant presenting symptoms included regurgitation (n = 4), vomiting (n = 9), or suspicion of rumination (n = 7). Recurrent belching was also a feature in some (n = 7). In addition to the return of gastric content, patients described typical dyspeptic symptoms (n = 17) and reflux symptoms (n = 3). <h3>Results</h3> HRM revealed normal motility in 14/20, hypotensive in 4/20 and hypertensive in 2/20. Rumination was observed during water swallows in 10, following multiple water swallows in 2 and after a test meal in 8 patients. In patients with dyspepsia, HRM demonstrated classical rumination (‘R waves’) in 10/17 (59%), powerful contraction of abdominal muscles forced gastric content across the lower oesophageal sphincter (LOS). Five patients ruminated following a swallow while the LOS was relaxed, making it easy for gastric content to pass. One ruminated with a closed upper oesophageal sphincter leading to bolus ‘trapping’ and pain, at which point she would induce vomiting. One patient, who had fundoplication as a child, would cough to create the abdominal pressure required to overcome the resistance formed by the wrap. Some patients with prominent belching and dyspepsia (4/7) exhibited supra-gastric belching with rumination. Air was sucked into the oesophagus by creating a negative intra-thoracic pressure and expelled, without passing the LOS. In patients with reflux symptoms (n = 3), all ruminated <i>a few seconds following</i> the appearance of transient LOS relaxation with common cavity (reflux). Unlike classical rumination these events were often high volume, occur after meals, on exertion and in the supine position. <h3>Conclusion</h3> HRM facilitates diagnosis and reveals the behaviour associated with rumination. Ingestion of a test drink and meal increases test sensitivity. Three key ‘rumination variations’ were identified: –Dyspepsia with typical rumination –Dyspepsia with rumination and supra-gastric belching –Reflux related rumination. All may benefit from biofeedback therapy; however, the focus may differ for rumination and supra-gastric belching. Visceral analgesics may ease dyspepsia but proton pump inhibitors or even anti-reflux surgery may be appropriate for reflux related rumination.