tbuckley/cabot-search huggingface dataset:
THE HOSPITAL DIETARY
Journal: JAMA (1927)

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Obstetrics
Authors: Benjamin Tenney
Journal: New England Journal of Medicine (1950)

IN REVIEWING the literature of the past two years, one cannot say, truthfully, that there has been any marked change in any obstetric problem or treatment. Further light has been thrown on many controversial issues, but none have been definitely settled. The pregnant woman has become the source of inspiration and material to endocrinologists, general practitioners, chemists, physiologists, dietitians and numerous others. Many interesting observations have been made, but few of any clinical application. It still remains the responsibility of the obstetrician to carry his patient through a healthy pregnancy and to deliver her of a healthy child. With this . . .
Abstract 316: Adap1 Prevents Cardiomyocyte Hypertrophy by Interfering with Integrin Signaling
Authors: Hugo Giguere, Audrey-Ann Dumont, Jonathan Berthiaume, Gino Laberge, Mannix Auger-Messier
Journal: Circulation Research (2017)

The Arf GTPase activating protein with dual PH domains 1 (Adap1), a putative regulator of the small G protein ADP-ribosylation factor 6 (Arf6), might be expressed to some extent in the heart. Although Arf6 roles in cardiomyocytes are not well defined, this small G protein was shown to alter surface expression of integrins in other cell types. Considering the importance of integrins on cellular mechanisms of adhesion and spreading, we hypothesized that Adap1 might impact cardiomyocyte hypertrophy by regulating integrin signaling . In order to determine the role of Adap1 in cardiomyocytes, we analyzed its cardiac expression in Sprague Dawley rats. Comparatively to its high mRNA expression in the brain, we showed that Adap1 transcript is expressed at relatively low levels in the heart of adult and neonatal rats. However, Western blot detection of Adap1 showed that it is well expressed in the whole heart of adult and neonatal rats at levels reaching 13% and 17% relative to the brain, respectively. Moreover, Adap1 was 3-fold more abundant in isolated rat neonatal ventricular cardiomyocyte (RNVC) comparatively to partially enriched non-cardiomyocyte cells. Adenoviral-mediated overexpression of ADAP1 partially prevented the increase in cell surface area of cultured RNVCs in response to increasing serum concentrations. Interestingly, ADAP1 overexpression completely blocked constitutively active mutant Mek1- and phenylephrine-induced hypertrophy of RNVCs. In these conditions, ADAP1 did not impair the Mek1ca-induced fetal gene program in RNVCs, suggesting that its anti-hypertrophic effect was not mediated by transcriptional regulation. In fact, cell surface biotin labeling indicated that ADAP1 significantly reduced the localization of integrin β1 at the membrane of RNVCs without changing its total expression. Strikingly, integrin β1 was almost completely absent from the surface of RNVCs overexpressing both ADAP1 and Mek1ca. These findings demonstrate for the first time that Adap1 expressed in cardiomyocytes interferes with the surface expression of integrin β1, thereby slowing the development of hypertrophy in vitro. Further in vivo studies are needed to characterize the anti-hypertrophic function of Adap1 in response to pathological stresses.
Pulse
Journal: JAMA (1997)

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
Injuries and Illnesses Among New York City Fire Department Rescue Workers After Responding to the World Trade Center Attacks
Journal: JAMA (2002)

Within minutes of the terrorist attacks on September 11, 2001, the Fire Department of New York City (FDNY) operated a continuous rescue/recovery effort at the World Trade Center (WTC) site. Medical officers of FDNY Bureau of Health Services (FDNY-BHS) responded to provide emergency medical services (see box). The collapse of the WTC towers and several adjacent structures resulted in a vast, physically dangerous disaster zone. The height of the WTC towers produced extraordinary forces during their collapse, pulverizing considerable portions of the buildings' structural components and exposing first responders and civilians to substantial amounts of airborne particulate matter. Fires burned continuously under the debris until mid-December 2001. Because of ongoing fire activity and the large numbers of civilians and rescue workers who were killed during the attacks, approximately 11,000 FDNY firefighters and many emergency medical service (EMS) personnel worked on or directly adjacent to the rubble and incurred substantial exposures (Figure). This report describes morbidity and mortality in FDNY rescue workers during the 11-month period after the WTC attacks and documents a substantial increase in respiratory and stress-related illness compared with the time period before the WTC attacks. These findings demonstrate the need to provide acute and long-term medical monitoring, treatment, and counseling to FDNY rescue workers exposed to this disaster and to solve supply, compliance, and supervision problems so that respiratory protection can be rapidly provided at future disasters.
Author Index
Authors: Y. Ago, M. Sugita, H. Teshima, T. Nakagawa, Caroline B. Thomas, Joyce McDougall, M. von Rad, F. Lolas, Louise Demers-Desrosiers, Graeme Taylor, Kenneth Doody, H. Warnes, Réjean Fontaine, Denis Boisvert, A.H. Crisp, A.V. Bhat, Adolph-Ernst Meyer, R.A. Ramsay, A.J. Krakowski, Z. Rydzynski, M. Jarosz, F. Engelsmann, J. Ananth, K. Köhle, E. Gaus, C. Simons, C. Westphale, Yujiro Ikemi, Akira Ikemi, Hellmuth Freyberger, Lutz Besser, Adam J. Krakowski, J. Bastiaans, Chase Patterson Kimball, John C. Nemiah, Louis A. Gottschalk, David R. Hawkins, J. Binder, A. Dobler-Mikola, J. Angst, Giovanni A. Fava, Issy Pilowsky, Alessandra Pierfederici, Manuela Bernardi, Dorothy Pathak, G.H.B. Baker, H.B.M. Murphy, Finn Askevold, Albert J. Silverman, Michael Plaut, Stanford B. Friedman, Ronald Grossarth-Maticek, Dusan T. Kanazir, Peter Schmidt, Hermann Vetter
Journal: Psychotherapy and Psychosomatics (1982)
Fundamental Immunology
Authors: Philip C. Anderson
Journal: JAMA (1994)

The first great revolution in immunology is credited to Louis Pasteur. Among the many achievements stemming from that early period is the elimination of smallpox from the entire world in 1977, a century later. The second great revolution, beginning with immunochemistry in the 1940s, is ongoing. Perhaps our counterparts a century from now will be pleased with the outcome. This elegant textbook explains what is going on in immunology today and where it may lead us. Could any outcome, a century from now, be as impressive as the elimination of smallpox? The editor, Dr William Paul, is a physician and a scientist at the National Institute of Allergy and Infectious Diseases. Recently he was appointed director of AIDS research, an important and prestigious office. Dr Paul has a fine national reputation as a senior lecturer and teacher of remarkable fluency and clarity. He and his coworkers have devised not a
TRAINING SCHOOLS FOR MALE NURSES.
Journal: JAMA (1992)

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
Men’s Health
Authors: Cynthia L. Henderson, Patrick A. Griffith
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
Physiology PhDs
Journal: JAMA (1977)

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
STEM-23. INHIBITING PROTEIN PHOSPHATASE 2A INCREASES THE ANTITUMOR EFFECT OF PROTEIN ARGININE METHYLTRANSFERASE 5 INHIBITION IN MODELS OF GLIOBLASTOMA
Authors: Yeshavanth Kumar Banasavadi Siddegowda, Hannah Sur, Yoshihiro Otani, Guruprasad Rachaiah, Sriya Namagiri, Ashis Chowdhury, Cole Lewis, Toshihiko Shimizu, Arunakumar Gangaplara, Xiang Wang, Amélie Vézina, Dragan Maric, Sadhana Jackson, Yuanqing Yan, Zhuang Zhengping, Abhik Ray-Chaudhury, Sachin Kumar, Prashant Chittiboina, John Heiss, Ji Young Yoo, Balveen Kaur
Journal: Neuro-Oncology (2020)

Abstract BACKGROUND: Despite multi-model therapy of maximal surgical resection, radiation, chemotherapy, and tumor treating fields, median survival of Glioblastoma (GBM) patients is less than two years. Protein Arginine Methyltransferase 5 (PRMT5) catalyzes the symmetric di-methylation of arginine residues and is overexpressed in GBM. Inhibition of PRMT5 causes senescence of immature GBM tumor cells. LB100, first-in-class small molecule inhibitor of Protein Phosphatase 2A (PP2A) can sensitize therapy-resistant tumor cells. Here, we tested the anti-GBM effect of concurrent PRMT5 and PP2A inhibition. Methods: Patient-derived primary GBM neurospheres (GBMNS), transfected with PRMT5 target-specific siRNA were treated with LB100 and subjected to in vitro assays including PP2A activity and western blot. The intracranial mouse xenograft model was used to test the in vivo antitumor efficacy of combination treatment. Results: We found that PRMT5-depletion increased PP2A activity in GBMNS. LB100 treatment significantly reduced the viability of PRMT5-depleted GBMNS compared to PRMT5 intact GBMNS. LB100 enhanced the G1 cell cycle arrest induced by PRMT5-depletion. Combination therapy also increased the expression of phospho-MLKL. Necrostatin-1 rescued PRMT5-depleted cells from the cytotoxic effects of LB100, indicating that necroptosis caused the enhanced cytotoxicity of combination therapy. In the in vivo mouse tumor xenograft model, LB100 treatment combined with transient depletion of PRMT5 significantly decreased tumor size and prolonged mice survival, while LB100 treatment alone had no survival benefit. Conclusion: Overall, combined PRMT5 and PP2A inhibition had significantly greater antitumor effects than PRMT5 inhibition alone.
The art of medicine
Authors: E Tullo
Journal: BMJ (2006)

atrial fibrillation and may decrease the risk of low bone density in postmenopausal women. 24 25 Once the decision has been made to treat subclinical hyperthyroidism, the goal of therapy is to normalise serum TSH values, preferably by using small doses of thionamides or, less advisably, definitive therapy with 131 I. When should general practitioners refer?Because patients with thyrotoxicosis usually present to general practitioners rather than to specialists, it is essential for all medical practitioners to recognise typical signs and symptoms and to know how to initiate a diagnostic work-up.In most cases, once thyrotoxicosis has been detected, patients should be referred to an endocrinologist for management.w13 Coordination of care between general practitioners and endocrinologists is essential in order to provide optimal and cost effective care for patients with thyrotoxicosis. ConclusionsThyrotoxicosis can be readily diagnosed on the basis of serum thyroid function tests in patients with typical signs or symptoms.Several effective forms of therapy for thyrotoxicosis exist, all of which have advantages and disadvantages.The choice of treatment depends on the cause and severity of the thyrotoxicosis, as well as on patients' preferences.Box 2 gives information on unanswered research questions and ongoing clinical trials.
DNA Adducts and Carcinogenicity of Nitro-Polycyclic Aromatic Hydrocarbons
Authors: Peter P. Fu, Diogenes Herreno-Saenz, Linda S. Von Tungeln, Jack O. Lay, Yu-Sen Wu, J-S. Lai, Frederick E. Evans
Journal: Environmental Health Perspectives (1994)

We have been interested in the structure-activity relationships of nitro-polycyclic aromatic hydrocarbons (nitro-PAHs), and have focused on the corre- lation of structural and electronic features with biological activities, including mutagenicity and tumorigenicity.In our studies, we have emphasized 1-, 2-, 3-, and 6-nitrobenzo[a]pyrenes (nitro-B[a]Ps) and related compounds, all of which are derived from the potent carcinogen benzo[alpyrene.While 1-, 2-, and 3-nitro-B[a]P are potent mutagens in Salmonella, 6-nitro-B[a]P is a weak mutagen.In vitro metabolism of 1-and 3-nitro-B[a]P has been found to generate multiple pathways for mutagenic activation.The formation of the corresponding trans-7,8-dihydrodiols and 7,8,9,1 0-tetrahy- drotetrols suggests that 1-and 3-nitro-B[a]P trans-7,8-diol-9,1 0-epoxides are ultimate metabolites of the parent nitro-B[a]Ps.We have isolated a DNA adduct from the reaction between 3-nitro-B[a]P trans-7,8-diol-anti9,10-epoxide and calf thymus DNA, and identified it as 10-(deoxyguanosin-N2-yl)- 7,8,9-trihydroxy-7,8,9,10-tetrahydro-3-nitro-B[a]P.The same adduct was identified from in vitro metabolism of [3H]3-nitro-B[a]P by rat liver micro- somes in the presence of calf thymus DNA.A DNA adduct of 3-nitro-B[a]P formed from reaction of N-hydroxy-3-amino-B[a]P, prepared in situ with calf thymus DNA was also isolated.This adduct was identified as 6-(deoxyguanosin-N2-yl)-3-amino-B[a]P.The same adduct was obtained from incu- bating DNA with 3-nitro-B[a]P in the presence of the mammalian nitroreductase, xanthine oxidase, and hypoxanthine.These data indicate that a mammalian nitroreductase can metabolize 3-nitro-B[a]P to an activated derivative that reacts with DNA to give a novel adduct distant from the site of nitrenium ion formation.Similar DNA adducts were obtained from ring-oxidation and nitroreduction of 1-nitro-B[aIP.Metabolism of 6-nitro-B[a]P resulted in a different pattern, and DNA adducts have not been detected from chemical or biologic activation.Based on these results, together with the other findings, we have proposed that orientation of the nitro functional group is a critical structural feature that can affect metabolism, DNA binding, mutagenicity, and tumorigenicity of nitro-PAHs.Additional data from the derivatives of the nitro-B[a]Ps support this hypothesis.-
Role of Insulin-Like Growth Factor-Binding Protein 5 (IGFBP5) in Organismal and Pancreatic β-Cell Growth
Authors: Catherine E. Gleason, Yun Ning, Tara P. Cominski, Rana Gupta, Klaus H. Kaestner, John E. Pintar, Morris J. Birnbaum
Journal: Endocrine Reviews (2009)

Abstract A family of IGF-binding proteins (IGFBP) exerts biological actions both dependent on and independent of IGF-I. A major effector of the insulin/IGF-I signaling pathway, the serine/threonine protein kinase Akt, mediates cellular processes such as glucose uptake, protein synthesis, cell survival, and growth. IGF-I is required for normal organismal growth, and in the pancreatic β-cell, the insulin/IGF-I signaling pathway is critical for normal and adaptive maintenance of β-cell mass. Expression of myrAkt1, an activated form of Akt, in the endocrine pancreas drives β-cell expansion through dramatic increases in both islet and β-cell size and number. Herein we present a comparative expression profiling of myrAkt1 transgenic islets that demonstrates the increased abundance of transcripts encoding proteins associated with growth, suppression of apoptosis, RNA processing, and metabolism. Although IGFBP5 is identified as a gene induced by Akt1 activation in the β-cell, Igfbp5 expression is not necessary for myrAkt1 to augment β-cell size or mass in vivo. However, in the absence of Igfbp5, mice demonstrate an increase in size and mild glucose intolerance. This is accentuated during diet-induced obesity, when Igfbp5-deficient mice have increased adiposity compared with wild-type mice on the same diet. These studies reveal a novel role for Igfbp5 in the control of growth and metabolism.
Hygienic Measures and Experiences in the Flood Catastrophe in Hamburg in February, 1962
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