tbuckley/cabot-search huggingface dataset:
Science and the Modern World. Lowell Lectures, 1925.
Authors: Alfred North Whitehead
Journal: JAMA (1926)

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 1818: ERBB3/HER2 signaling limits the effectiveness of EGFR blockade in head and neck and colorectal cancer models
Authors: Li Zhang, Carla Castanaro, Bo Luan, Katie Yang, Amy Fan, John Rudge, Nicholas Papadopoulos, Gavin Thurston, Christopher Daly
Journal: Cancer Research (2014)

Abstract Introduction: EGFR blocking antibodies are approved for the treatment of colorectal cancer (CRC) and head and neck squamous cell carcinoma (HNSCC). However, responses to single agent EGFR blocking antibodies are relatively infrequent and transient. Thus, there is a clear need for agents that can enhance the benefit of EGFR blockade. While ERBB3 signaling has been proposed to limit the effectiveness of EGFR inhibitors, the underlying molecular mechanisms are not fully understood. In this report, we employ blocking antibodies against ERBB3 (REGN1400) and EGFR (REGN955), as well as a HER2 blocking antibody, to investigate the role of ERBB3 in modulating the response to EGFR inhibition. Experimental procedures and results: We show that EGFR and ERBB3 are co-activated in multiple HNSCC cell lines and that combined blockade of EGFR and ERBB3 inhibits the growth of these cell lines more effectively than blockade of either receptor alone. Western blotting analysis shows that REGN955 strongly inhibits activation of ERK, but not Akt, while REGN1400 strongly inhibits activation of Akt, but not ERK, consistent with the more potent effect of the combination on cell growth. In addition, using a colorectal cancer cell line with low endogenous ERBB3 activity, we show that neuregulin 1 treatment significantly increases ERBB3 phosphorylation and reverses the inhibitory effect of REGN955 on cell growth. To further understand the mechanism of ERBB3 activation, we employed a HER2 blocking antibody to show that ERBB3 phosphorylation in HNSCC and CRC cells is strictly dependent on association with HER2, but not EGFR, and that neuregulin 1 activates ERBB3/HER2 signaling to reverse the effect of EGFR blockade on CRC cell growth. Finally, while REGN1400 and REGN955 as single agents slowed the growth of HNSCC and CRC xenografts, the combination of REGN1400 plus REGN955 caused significant tumor regression. Summary and conclusion: Our findings demonstrate that ERBB3 partners with HER2 to activate the Akt survival pathway and to limit the effect of EGFR blockade on the growth of HNSCC and CRC cell lines and tumor xenografts. These findings suggest that REGN1400, which is currently in a Phase 1 clinical trial, could provide clinical benefit when combined with EGFR blocking antibodies. Citation Format: Li Zhang, Carla Castanaro, Bo Luan, Katie Yang, Amy Fan, John Rudge, Nicholas Papadopoulos, Gavin Thurston, Christopher Daly. ERBB3/HER2 signaling limits the effectiveness of EGFR blockade in head and neck and colorectal cancer models. [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 1818. doi:10.1158/1538-7445.AM2014-1818
The Deubiquitylase MATH-33 Controls DAF-16 Stability and Function in Metabolism and Longevity
Authors: Thomas Heimbucher, Zheng Liu, Carine Bossard, Richard McCloskey, Andrea C. Carrano, Christian G. Riedel, Bogdan Tanasa, Christian Klammt, Bryan R. Fonslow, Celine E. Riera, Bjorn F. Lillemeier, Kenneth Kemphues, John R. Yates, Clodagh O’Shea, Tony Hunter, Andrew Dillin
Journal: Cell Metabolism (2015)
Cancer statistics, 2011
Authors: Rebecca Siegel, Elizabeth Ward, Otis Brawley, Ahmedin Jemal
Journal: CA A Cancer Journal for Clinicians (2011)

Each year, the American Cancer Society estimates the numbers of new cancer cases and deaths expected in the United States in the current year and compiles the most recent data on cancer incidence, mortality, and survival based on incidence data from the National Cancer Institute, the Centers for Disease Control and Prevention, and the North American Association of Central Cancer Registries and mortality data from the National Center for Health Statistics. A total of 1,596,670 new cancer cases and 571,950 deaths from cancer are projected to occur in the United States in 2011. Overall cancer incidence rates were stable in men in the most recent time period after decreasing by 1.9% per year from 2001 to 2005; in women, incidence rates have been declining by 0.6% annually since 1998. Overall cancer death rates decreased in all racial/ethnic groups in both men and women from 1998 through 2007, with the exception of American Indian/Alaska Native women, in whom rates were stable. African American and Hispanic men showed the largest annual decreases in cancer death rates during this time period (2.6% and 2.5%, respectively). Lung cancer death rates showed a significant decline in women after continuously increasing since the 1930s. The reduction in the overall cancer death rates since 1990 in men and 1991 in women translates to the avoidance of about 898,000 deaths from cancer. However, this progress has not benefitted all segments of the population equally; cancer death rates for individuals with the least education are more than twice those of the most educated. The elimination of educational and racial disparities could potentially have avoided about 37% (60,370) of the premature cancer deaths among individuals aged 25 to 64 years in 2007 alone. Further progress can be accelerated by applying existing cancer control knowledge across all segments of the population with an emphasis on those groups in the lowest socioeconomic bracket. CA Cancer J Clin 2011. © 2011 American Cancer Society.
Stimulating Muscle Growth
Authors: Tracy Hampton
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
Targeted disruption of cd39/ATP diphosphohydrolase results in disordered hemostasis and thromboregulation
Authors: Keiichi Enjyoji, Jean Sévigny, Yuan Lin, Paul S. Frenette, Patricia D. Christie, Jan Schulte Am Esch, Masato Imai, Jay M. Edelberg, Helen Rayburn, Miroslaw Lech, David L. Beeler, Eva Csizmadia, Denisa D. Wagner, Simon C. Robson, Robert D. Rosenberg
Journal: Nature Medicine (1999)
Diagnosis and disease severity assessment of epidermolysis bullosa acquisita by ELISA for anti-type VII collagen autoantibodies: an Italian multicentre study
Authors: A.V. Marzano, E. Cozzani, D. Fanoni, O. De Pità, C. Vassallo, E. Berti, A. Parodi, C. Crosti, M. Cugno
Journal: British Journal of Dermatology (2012)

Journal Article Diagnosis and disease severity assessment of epidermolysis bullosa acquisita by ELISA for anti‐type VII collagen autoantibodies: an Italian multicentre study Get access A.V. Marzano, A.V. Marzano Unità di Dermatologia, Dipartimento di Fisiopatologia e dei Trapianti, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda – Ospedale Maggiore Policlinico, Via Pace 9, 20122, Milano, Italy Angelo V. Marzano. E‐mail: angelovalerio.marzano@policlinico.mi.it Search for other works by this author on: Oxford Academic Google Scholar E. Cozzani, E. Cozzani Section of Dermatology, University of Genoa Medical School, Viale Benedetto XV 7, 16132, Genoa, Italy Search for other works by this author on: Oxford Academic Google Scholar D. Fanoni, D. Fanoni Unità di Dermatologia, Dipartimento di Fisiopatologia e dei Trapianti, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda – Ospedale Maggiore Policlinico, Via Pace 9, 20122, Milano, Italy Search for other works by this author on: Oxford Academic Google Scholar O. De Pità, O. De Pità Laboratory of Immunology and Allergology, Istituto Dermopatico dell'Immacolata, IDI‐IRCCS, Via dei Monti di Creda 104, Roma, Italy Search for other works by this author on: Oxford Academic Google Scholar C. Vassallo, C. Vassallo Institute of Dermatology, University of Pavia and Foundation IRCCS Policlinico S. Matteo, Vialle Camillo Golgi 19, 27100, Pavia, Italy Search for other works by this author on: Oxford Academic Google Scholar E. Berti, E. Berti Unità di Dermatologia, Dipartimento di Fisiopatologia e dei Trapianti, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda – Ospedale Maggiore Policlinico, Via Pace 9, 20122, Milano, Italy Search for other works by this author on: Oxford Academic Google Scholar A. Parodi, A. Parodi Section of Dermatology, University of Genoa Medical School, Viale Benedetto XV 7, 16132, Genoa, Italy Search for other works by this author on: Oxford Academic Google Scholar C. Crosti, C. Crosti Unità di Dermatologia, Dipartimento di Fisiopatologia e dei Trapianti, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda – Ospedale Maggiore Policlinico, Via Pace 9, 20122, Milano, Italy Search for other works by this author on: Oxford Academic Google Scholar M. Cugno M. Cugno Unità di Medicina Interna, Dipartimento di Fisiopatologia e dei Trapianti, Università degli Studi di Milano, Fondazione IRCCS Ca' Granda – Ospedale Maggiore Policlinico, Via Pace 9, 20122, Milano, Italy Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 168, Issue 1, 1 January 2013, Pages 80–84, https://doi.org/10.1111/bjd.12011 Published: 01 January 2013 Article history Accepted: 12 August 2012 Published: 01 January 2013
Increased frequency and severity of viral infections during infancy is associated with recurrent wheezing in the first three years of life*1
Authors: D.F.G. Da Silva, K.A. Roberg, C.J. Tisler, E.L. Anderson, H.J. Hiemke, T.E. Pappas, P.A. Shult, C.J. Kirk, R.E. Gangnon, Z. Li, M.D. Evans, J.E. Gern, R.F. Lemanske
Journal: Journal of Allergy and Clinical Immunology (2004)
S92 Cognitive function &amp; cerebral white matter tract microstructure in COPD
Authors: J. W. Dodd, M. Van Den Broek, P. W. Jones, R. A. Charlton
Journal: Thorax (2011)

<h3>Rationale</h3> There is evidence to suggest that COPD leads to cognitive impairment in patients both with and without hypoxaemia1; but the pathogenesis remains poorly understood. Also relevant to potential brain pathology in COPD are common vascular comorbidities including hypertension, diabetes and older age. Diffusion tensor imaging (DTI) is a novel MRI technique sensitive to subtle changes in white matter due to vascular damage. This is the first study to investigate white matter microstructure and tract pathology in COPD. <h3>Methods</h3> Participants (n=50) completed a full cognitive assessment (including executive function, working memory, episodic memory, processing speed, visuospatial ability) and 3T MRI scan. We compare 25 stable non-exacerbating COPD and 25 age-matched healthy controls. Volumes of grey matter (GMV), white matter (WMV), and white matter lesions (LV), were calculated. DTI data was analysed using tract based spatial statistics (TBSS).2 <h3>Results</h3> There are significant group differences between COPD patients and controls on all cognitive measures except episodic memory (executive function: F=15.39, p&lt;0.001; working memory: F=5.94, p=0.019; episodic memory: F=3.91, p=0.054; processing speed: F=11.64, p=0.001; visuospatial ability: F=10.10, p=0.003). COPD patients did not differ from healthy controls on measures of normalised GMV (t=0.229, p=0.820) or WMV (t=−0.727, p=0.471). Normalised Lesion Volume was significantly greater in patients vs controls (t=−2.27, p=0.029). DTI-TBSS revealed lower fractional anisotropy (FA) and higher mean diffusivity (MD) values throughout the brain in COPD patients vs Control subjects. Group differences in white matter integrity were observed throughout the temporal, frontal, parietal and occipital lobes and amounted to 60% of the total FA skeleton. See Abstract S92 figure 1. <h3>Conclusion</h3> This is the first paper to demonstrate that white matter integrity throughout the brain is significantly compromised in patients with COPD compared to age-matched Controls. This damage to white matter is also demonstrated by the significant group differences in white matter lesion load. No differences between patients and Controls were observed in brain volume, suggesting that group differences may be related to white matter integrity rather than atrophy.
Abstract 1469: Segregation of Copper-dependent Transcription Factor and Copper Chaperone Function of Antioxidant-1 in Wound Healing
Authors: Ha Won Kim, Jay Yang, Lydia Finney, Stefan Vogt, Ronald D McKinney, Traci A Wilgus, Luisa A DiPietro, Masuko Ushio-Fukai, Tohru Fukai
Journal: Circulation (2008)

Copper plays an essential role in cell growth involved in wound repair and angiogenesis; however, underlying molecular mechanism remains unclear. We recently have found that the copper binding protein antioxidant-1 (Atox1), previously appreciated as a copper chaperone for secretory copper enzymes at the transGolgi network (TGN), mediates copper-induced cell proliferation in cultured fibroblasts. The role of Atox1 in wound healing in vivo is unknown. Using mouse wound healing model, here we show that Atox1 is highly induced at BrdU-positive nuclei in hair follicles and epidermis in wounding tissues where copper is accumulated, as assessed by X-ray fluorescence microscopy and by ICP-mass spectrometry (2.1-fold increase) as compared to non-wounding skin. Confocal microscopy and cell fractionation analysis demonstrate that Atox1 is predominantly found in cytosol in basal state. Copper or PKC activator PMA promotes translocation of Atox1 to nucleus as well as Atox1 threonine phosphorylation in a time-dependent manner. These copper-induced effects on Atox1 are prevented by a specific PKC inhibitor GF109203X. Luciferase reporter gene assays show that copper increases cyclin D1 promoter by 2.8±0.2 fold, which is blocked by the mutation of Atox1 responsive elements in the promoter and by GF109203X. Gel shift and ChIP assays demonstrate that Atox1 directly binds to the Atox1 responsive element including DNA segment in the cyclin D1 promoter. Atox1 knockout (KO) mice show a marked delay in the rate of wound closure (7.1 day) as compared to wild-type (WT) mice (11.2 day), which is associated with decrease in a number of BrdU-positive proliferating cells and cyclin D1 protein expression. All these defective responses in Atox1 KO mice are rescued by lentivirus-mediated re-expression of nuclear targeted Atox1 and Atox1-WT, but not TGN-targeted Atox1. In summary, copper-dependent transcription factor function of Atox1, but not copper chaperone function, plays a major role in wound healing in vivo through PKC-dependent phosphorylation and binding to the cyclin D1 promoter involved in cell proliferation. These findings provide novel insight into Atox1 as a potential therapeutic target for wound repair process or angiogenesis in response to injury.
A Man in His 40s With Headache, Lethargy, and Altered Mental Status
Authors: Kathleen E. McKee, Mark R. Etherton, Scott B. Lovitch, Anoopum S. Gupta, Douglas S. Micalizzi, Travis Tierney, Martha Wadleigh, Henrikas Vaitkevicus
Journal: JAMA Neurology (2015)

A man in his 40s presented with 1 month of worsening confusion, fatigue, and headache. Results from laboratory analyses were notable for a complete white blood cell count of 17 000/μL (31% blast cells), a platelet count of 76 000/μL, and a hemoglobin level of 16.6 g/dL. Imaging studies revealed a large mixed-attenuation subdural collection in the right frontal region with prominent mass effect. The patient underwent an emergency neurosurgical procedure. The differential diagnosis, pathologic findings, and diagnosis are discussed.
Efforts Grow to Keep Mentally Ill Out of Jails
Authors: Lynne Lamberg
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
Abstract 18709: Myostatin Expression is Markedly Increased after Biventricular Mechanical Support in Congenital Heart Disease
Authors: Isaac George, Larry T Bish, Simon Maybaum, Yoshifumi Naka, H L Sweeney, Jonathan Chen
Journal: Circulation (2010)

Purpose: Myostatin directly inhibits skeletal muscle proliferation and development; however, its role in cardiac muscle and function in early congenital heart disease (CHD) is unknown. We studied m...
Metabolic syndrome in people with schizophrenia: a review
Authors: MARC DE HERT, VINCENT SCHREURS, DAVY VANCAMPFORT, RUUD VAN WINKEL
Journal: World Psychiatry (2009)

Metabolic syndrome and other cardiovascular risk factors are highly prevalent in people with schizophrenia. Patients are at risk for premature mortality and overall have limited access to physical health care. In part these cardio-metabolic risk factors are attributable to unhealthy lifestyle, including poor diet and sedentary behaviour. But over recent years it has become apparent that antipsychotic agents can have a negative impact on some of the modifiable risk factors. The psychiatrist needs to be aware of the potential metabolic side effects of antipsychotic medication and to include them in the risk/benefit assessment when choosing a specific antipsychotic. He should also be responsible for the implementation of the necessary screening assessments and referral for treatment of any physical illness. Multidisciplinary assessment of psychiatric and medical conditions is needed. The somatic treatments offered to people with severe and enduring mental illness should be at par with general health care in the non-psychiatrically ill population.
Victorian medicine: Our grandfather's patient
Authors: G. R. S. Grogono, B. J. S. Grogono
Journal: BMJ (1999)

The casebook of our grandfather, Dr Russell Steele of Reigate, has a graphic account of rabies in a young boy.

“On July 4th 1876, shortly after 7 o'clock in the morning, the patient, a little boy called Alfred Cox (aged 91/2 years), the son of the stationmaster at Bletchworth, was playing with a strange dog which had bites about its muzzle, and was bitten several times by it on the right hand and leg. He was brought to me soon afterwards, when I cauterised the wounds freely with linear caustic. He came to see me twice afterwards to have the wounds dressed with water dressing, after which they healed up. Six weeks and three days from …
Brief Report: In Search of a Candidate Pathogen for Giant Cell Arteritis: Sequencing‐Based Characterization of the Giant Cell Arteritis Microbiome
Authors: Ami S. Bhatt, Veronica E. Manzo, Chandra Sekhar Pedamallu, Fujiko Duke, Diana Cai, Don C. Bienfang, Robert F. Padera, Matthew Meyerson, William P. Docken
Journal: Arthritis & Rheumatology (2014)

Objective To characterize the microbiome of the temporal artery in patients with giant cell arteritis (GCA), and to apply an unbiased and comprehensive shotgun sequencing‐based approach to determine whether there is an enrichment of candidate pathogens in the affected tissue. Methods Temporal artery biopsy specimens were collected from patients at a single institution over a period of 4 years, and unbiased DNA sequencing was performed on 17 formalin‐fixed, paraffin‐embedded specimens. Twelve of the 17 patients fulfilled the clinical and histopathologic criteria for GCA, and the other 5 patients served as controls. Using PathSeq software, human DNA sequences were computationally subtracted, and the remaining non‐human DNA sequences were taxonomically classified using a comprehensive microbial sequence database. The relative abundance of microbes was inferred based on read counts assigned to each organism. Comparison of the microbial diversity between GCA cases and controls was carried out using hierarchical clustering and linear discriminant analysis of effect size. Results Propionibacterium acnes and Escherichia coli were the most abundant microorganisms in 16 of the 17 samples, and Moraxella catarrhalis was the most abundant organism in 1 control sample. Pathogens previously described to be correlated with GCA were not differentially abundant in cases compared to controls. There was not a significant burden of likely pathogenic viruses. Conclusion DNA sequencing of temporal artery biopsy specimens from GCA cases, in comparison with non‐GCA controls, showed no evidence of previously identified candidate GCA pathogens. A single pathogen was not clearly and consistently associated with GCA in this case series.