tbuckley/cabot-search huggingface dataset:
Council on Physical Therapy
Journal: JAMA (1931)

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
Myoglobin sustains cardiac function during ischemia and facilitates oxygen diffusion in the beating heart Marc W. Merx, Ulrich Fl�gel, Axel G�decke, Ulrich K. M. Decking, J�rgen Schrader. Institut f�r Herz- und Kreislaufphysiologie, Heinrich Heine Universit�t, D�sseldorf, Germany
Journal: Journal of the American College of Cardiology (2001)
The transcription factor KLF14 regulates macrophage glycolysis and immune function by inhibiting HK2 in sepsis
Authors: Yuan Yuan, Guangjian Fan, Yuqi Liu, Lu Liu, Tong Zhang, Pengfei Liu, Qing Tu, Xinyi Zhang, Shiyuan Luo, Liangfang Yao, Feng Chen, Jingbao Li
Journal: Cellular and Molecular Immunology (2022)

Abstract Sepsis is a heterogeneous syndrome induced by a dysregulated host response to infection. Glycolysis plays a role in maintaining the immune function of macrophages, which is crucial for severely septic patients. However, how the pathways that link glycolysis and macrophages are regulated is still largely unknown. Here, we provide evidence to support the function of KLF14, a novel Krüppel-like transcription factor, in the regulation of glycolysis and the immune function of macrophages during sepsis. KLF14 deletion led to significantly increased mortality in lethal models of murine endotoxemia and sepsis. Mechanistically, KLF14 decreased glycolysis and the secretion of inflammatory cytokines by macrophages by inhibiting the transcription of HK2. In addition, we confirmed that the expression of KLF14 was upregulated in septic patients. Furthermore, pharmacological activation of KLF14 conferred protection against sepsis in mice. These findings uncover a key role of KLF14 in modulating the inflammatory signaling pathway and shed light on the development of KLF14-targeted therapeutics for sepsis.
Prevention of schistosomiasis
Authors: A. Karstorp
Journal: JAMA (1984)

<h3>To the Editor.—</h3> Istre et al<sup>1</sup>describe in<i>JAMA</i>a small outbreak of acute schistosomiasis among a group of adventurers rafting in Ethiopia. Being one of the "adventurers" (I like that expression!) and experienced in tropical medicine, I have a few comments. As the authors say, we were aware that the Omo and Mui rivers were infected with schistosomiasis. We therefore planned a "schistosoma checkup" three months after returning from the trip to reveal even very light infections. This time the symptoms appeared very quickly, however. The problem with white water rafting is that you get all wet every time you pass a rapid (which we did every 15 to 20 minutes) and partially wet every time you land the raft and carry it ashore. Under these conditions, normal precautions such as brisk towel drying are not realistic. It might be better to use an oily body lotion frequently
Cell of Origin Influences Pancreatic Cancer Subtype
Authors: Brittany M. Flowers, Hang Xu, Abigail S. Mulligan, Kathryn J. Hanson, Jose A. Seoane, Hannes Vogel, Christina Curtis, Laura D. Wood, Laura D. Attardi
Journal: Cancer Discovery (2021)

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a deadly disease with a 5-year survival rate of approximately 9%. An improved understanding of PDAC initiation and progression is paramount for discovering strategies to better detect and combat this disease. Although transcriptomic analyses have uncovered distinct molecular subtypes of human PDAC, the factors that influence subtype development remain unclear. Here, we interrogate the impact of cell of origin and different Trp53 alleles on tumor evolution, using a panel of tractable genetically engineered mouse models. Oncogenic KRAS expression, coupled with Trp53 deletion or point mutation, drives PDAC from both acinar and ductal cells. Gene-expression analysis reveals further that ductal cell–derived and acinar cell–derived tumor signatures are enriched in basal-like and classical subtypes of human PDAC, respectively. These findings highlight cell of origin as one factor that influences PDAC molecular subtypes and provide insight into the fundamental impact that the very earliest events in carcinogenesis can have on cancer evolution. Significance: Although human PDAC has been classified into different molecular subtypes, the etiology of these distinct subtypes remains unclear. Using mouse genetics, we reveal that cell of origin is an important determinant of PDAC molecular subtype. Deciphering the biology underlying pancreatic cancer subtypes may reveal meaningful distinctions that could improve clinical intervention. This article is highlighted in the In This Issue feature, p. 521
Intravascular ultrasound predictors of late recurrence after stent implantation in small coronary arteries Alexandre Abizaid, Gary S. Mintz, Andrea S. Abizaid, Roxana Mehran, George Dangas, Augusto Pichard, Lowell Salter, Izat Hijazi, Rajshekar Narasimaiah, Alexandra J. Lansky, Gregg W. Stone, Martin B. Leon. Cardiovascular Research Foundation, New York, NY, Washington Hospital Center, Washington, DC
Journal: Journal of the American College of Cardiology (2001)
Genomic landscape in small intestine cancer from real-world data (RWD) of clinical genomic testing.
Authors: Hiroyuki Takeda, Hiroyuki Yamamoto, Ritsuko Oikawa, Kumiko Umemoto, Ayako Doi, Yoshiki Horie, Takuro Mizukami, Takashi Ogura, Naoki Izawa, Jay A. Moore, Ethan Sokol, Yu Sunakawa
Journal: Journal of Clinical Oncology (2022)

642 Background: Panel-based comprehensive genomic profiling (CGP) is used in clinical practice worldwide, however, large aggregated RWD of patients with advanced small intestine cancer have not been characterized. In particular, there has been limited data regarding examining CGP in pediatric/ Adolescent and Young Adult (AYA) small intestine cancer. For patient subgroups, it is unclear what clinically relevant alterations co-occur. Here, we investigated the genomic landscape of small intestine cancer patients, stratified by sub-group to help refine and discover new targets for improved cancer therapies in advanced small intestine cancer. Methods: This is a collaborative biomarker study using RWD paired with CGP testing (Foundation Medicine, Inc.). Hybrid capture was carried out on up to 395 cancer-related genes and select introns from up to 31 genes frequently rearranged in cancer. One thousand three hundred sixty-four patients were available for analyses and were stratified by age (≥40/ &lt; 40), MSI status, tumor mutational burden (TMB) status (High ≥10/Low &lt; 10Muts/Mb), and select gene alterations. Using a chi-square test with Yate’s correction, frequencies of alterations were analyzed according to clinical or genomic background. Results: Genes with frequent alterations including mutation, amplification, and rearrangement/fusion were TP53 (59.8%), KRAS (54.8%), APC (27.7%), CDKN2A (22.4%), and SMAD4 (20.2%). Genomic profiling according to age, MSI, and TMB status is shown in the following table. In pediatric/AYA patients, frequency of APC alterations was significantly low ( P&lt; 0.001). In KRAS mutated tumors, codon 12 most abundant mutations were G12D (31.1%) followed by G12V (22.3%), G12C (6.2%), and G12R (5.1%), while G13D (13.8%) was the predominant mutation in codon 13. In TMB-High tumors, which were detected in 12% of patients, the mutation rate of KRAS was modestly lower compared to TMB-Low tumors (42.3% vs. 53.3%). Frequent genes with amplification were MYC (6.7%), MDM2 (5.9%), GATA6 (5.5%), CCND1 (3.4%), FGF19 (3.3%), and ERBB2 (2.3%). The number of any gene amplification was lower in MSI-High compared to TMB-High population. Conclusions: RWD from clinical panel testing revealed the genomic landscape in small intestine cancer and differences in CGP according to clinical or genomic background. These findings would provide insight on the direction of the future development of the treatment in advanced small intestine cancer.[Table: see text]
ESGE Newsletter
Journal: Endoscopy (2012)

The UEG week is traditionally one of the annual highlights for the ESGE, as this is a unique platform to provide a full range of educational activities to a large audience. We would like to encourage all those visiting the UEGW to make as much use as possible of the lectures and training sessions held in the ESGE Learning Area from the opening weekend of the congress and throughout the congress week. There is always something going on and registration is not required apart from the hands-on training sessions on biologic models on Saturday and Sunday. The activities are open to all delegates of the congress and can be visited repeatedly.
COVID-19 and the US health insurance conundrum
Authors: None The Lancet Oncology
Journal: The Lancet Oncology (2020)

The devastating effects of the COVID-19 pandemic go far beyond public health; with many industries on hold and unemployment increasing worldwide, the global economy is approaching the deepest recession in living memory. In the USA, where health insurance is largely provided by employers and more than 30 million people have filed for unemployment in the past 2 months, such a recession could cause an unprecedented surge in uninsured or underinsured people. Indeed, an analysis published on May 4, 2020, has estimated that if unemployment in the USA reaches 20%, 25–43 million people could lose their health insurance.
Is cancer prevention better than cure?
Authors: E. J. Freireich
Journal: JAMA (1979)

Some members of Congress are urging that the fight against cancer be shifted from treatment to prevention. This is an appealing concept, especially when coupled with the widely held notion that virtually all cancers are caused by environmental factors and that lends credence to the conclusion that we should abandon treatment as the major approach to solving the cancer problem and invest all of our financial and intellectual resources in a cancer prevention campaign. While attractive on the surface, the prevention strategy has serious limitations. We know that the process of developing a cancer generally requires long periods of exposure to causative agents, and, therefore, prevention will have to be consistently applied for long periods, perhaps decades, to be effective. Moreover, even among those persons most heavily exposed to cancer-causing agents, such as cigarette smokers, the risk of the development of cancer is still fairly low. These limitations have important
Error in the Results Section
Authors: Srishti Saha, Piyush Nathani, Arjun Gupta
Journal: JAMA Internal Medicine (2021)

Cindy N. Roy, PhD; Peter J. Snyder, MD; Alisa J. Stephens-Shields, PhD; Andrew S. Artz, MD, MS; Shalender Bhasin, MD; Harvey J. Cohen, MD; John T. Farrar, MD, PhD; Thomas M. Gill, MD; Bret Zeldow, MS; David Cella, PhD; Elizabeth Barrett-Connor, MD; Jane A. Cauley, DrPH; Jill P. Crandall, MD; Glenn R. Cunningham, MD; Kristine E. Ensrud, MD, MPH; Cora E. Lewis, MD, MPH; Alvin M. Matsumoto, MD; Mark E. Molitch, MD; Marco Pahor, MD; Ronald S. Swerdloff, MD; Denise Cifelli, MS; Xiaoling Hou, MS; Susan M. Resnick, PhD; Jeremy D. Walston, MD; Stephen Anton, PhD; Shehzad Basaria, MD; Susan J. Diem, MD, MPH; Christina Wang, MD; Stanley L. Schrier, MD; Susan S. Ellenberg, PhD
I Have Reason to Believe.
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 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
WHAT CONSTITUTES A SATISFACTORY DRUG?
Journal: JAMA (1925)

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
Cardiac Energy Metabolism in Heart Failure
Authors: Gary D. Lopaschuk, Qutuba G. Karwi, Rong Tian, Adam R. Wende, E. Dale Abel
Journal: Circulation Research (2021)

Alterations in cardiac energy metabolism contribute to the severity of heart failure. However, the energy metabolic changes that occur in heart failure are complex and are dependent not only on the severity and type of heart failure present but also on the co-existence of common comorbidities such as obesity and type 2 diabetes. The failing heart faces an energy deficit, primarily because of a decrease in mitochondrial oxidative capacity. This is partly compensated for by an increase in ATP production from glycolysis. The relative contribution of the different fuels for mitochondrial ATP production also changes, including a decrease in glucose and amino acid oxidation, and an increase in ketone oxidation. The oxidation of fatty acids by the heart increases or decreases, depending on the type of heart failure. For instance, in heart failure associated with diabetes and obesity, myocardial fatty acid oxidation increases, while in heart failure associated with hypertension or ischemia, myocardial fatty acid oxidation decreases. Combined, these energy metabolic changes result in the failing heart becoming less efficient (ie, a decrease in cardiac work/O 2 consumed). The alterations in both glycolysis and mitochondrial oxidative metabolism in the failing heart are due to both transcriptional changes in key enzymes involved in these metabolic pathways, as well as alterations in NAD redox state (NAD + and nicotinamide adenine dinucleotide levels) and metabolite signaling that contribute to posttranslational epigenetic changes in the control of expression of genes encoding energy metabolic enzymes. Alterations in the fate of glucose, beyond flux through glycolysis or glucose oxidation, also contribute to the pathology of heart failure. Of importance, pharmacological targeting of the energy metabolic pathways has emerged as a novel therapeutic approach to improving cardiac efficiency, decreasing the energy deficit and improving cardiac function in the failing heart.
Estrogen induces a favorable modulation of coronary blood flow and vasomotor responses during atrial pacing in postmenopausal women Ioannis Kallikazaros, Constantinos Tsioufis, Panayiotis Zambaras, Christodoulos Stefanadis, Anastasios Spanos, Kostas Tzioumis, Pavlos Toutouzas. HIPPOKRATION HOSPITAL, ATHENS, Greece
Journal: Journal of the American College of Cardiology (2001)
First Aid in Illness and Injury.
Journal: JAMA (1897)

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
Questions and Answers
Authors: Vernon L. Nickel
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
Outbreak of Severe Acute Respiratory Syndrome—Worldwide, 2003
Journal: JAMA (2003)

Since late February 2003, CDC has been supporting the World Health Organization (WHO) in the investigation of a multicountry outbreak of atypical pneumonia of unknown etiology. The illness is being referred to as severe acute respiratory syndrome (SARS). This report describes the scope of the outbreak, preliminary case definition, and interim infection control guidance for the United States.
Viral Hepatitis
Authors: Joseph D. Boggs
Journal: JAMA (1970)

MS-1 serum, previously shown to produce hepatitis in infants, produced hepatitis in three of ten adult male volunteers when 0.05 ml of infectious serum was introduced orally. One plasma sample, taken before the period of rising transaminase levels from one of the volunteers who developed hepatitis, did not produce hepatitis when passed to ten volunteers. However, plasma obtained at the time of maximum transaminase levels from another of the men produced hepatitis in five of ten volunteers. When acute-phase plasma from two of the volunteers was inoculated and passed in a serially cloned line of Detroit-6 cells, cytopathic effects occurred. No cytopathogenic agents were present in the plasma of the same volunteers before inoculation, or in the cell controls carried in parallel with each passage. These findings call for continued work with hepatitis virus in tissue culture.