tbuckley/cabot-search huggingface dataset:
Remarks on Animal Vaccination
Authors: E. Warlomont
Journal: BMJ (1879)

<h3>Abstract</h3> In a prospective cohort study involving 12,413 Health Care Workers (HCW), we assessed immunogenicity, vaccine-effectiveness (VE) and safety of the third BNT162b2 vaccine dose. One month after third dose, anti-RBD-IgG were induced 1.7-folds compared to one month after the second. A significant increase in avidity from 61.1% (95%CI:56.1-66.7) to 96.3% (95%CI:94.2-98.5) resulted in a 6.1-folds neutralizing antibodies induction. Linear mixed model demonstrated that the third dose elicited a greater response among HCW≥60 or those with ≥two comorbidities who had a lower response following the second dose. VE of the third dose relative to two doses was 85.6% (95% CI, 79.2-90.1%). No serious adverse effects were reported. These results suggest that the third dose is superior to the second dose in both quantity and quality of IgG-antibodies and safely boosts protection from SARS-CoV-2 infection by generating high avidity antibodies to levels that are not significantly different between healthy and vulnerable populations.
Immediate vs delayed catheterization and angioplasty following thrombolytic therapy for acute myocardial infarction. TIMI II A results. The TIMI Research Group
Journal: JAMA (1988)

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
JAMA Reference Directories
Journal: JAMA (1980)

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
Playing God
Authors: Michael A. LaCombe
Journal: Annals of Internal Medicine (1992)

On Being A Doctor15 January 1992Playing GodMichael A. LaCombe, MDMichael A. LaCombe, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-116-2-161 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptWhy she called me first I never figured out. Maybe she had more brains than I gave her credit for. All she had said was,My husband has passed away, Doctor. Can you come over?That was it: flat monotone, no emotion, just matter-of-fact. Now I'm one of those old-fashioned doctors who still makes house calls on certain occasions, and this was definitely one of those occasions. I could feel it in the pit of my stomach. I grabbed my clothes, got dressed in the bathroom so as not to wake my wife, brushed the snow from the car, and... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Oxford Hills Medical Group Norway, ME 04268 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByAversion to playing God and moral condemnation of technology and scienceNarrative Means to Humanistic EndsA community-based approach to the medical humanities"Playing God" as an Act of HopeMichael T. Kovalchik, MDPlaying God—RevisitedDaniel C. Citron, MDReflections on "Playing God"Christine K. Cassel, MD 15 January 1992Volume 116, Issue 2Page: 161-162KeywordsBrainEmotionsStomach Issue Published: 15 January 1992 Copyright© 1992 American College of PhysiciansPDF DownloadLoading ...
Pulse Paradoxes
Authors: Glen C. Cayler
Journal: JAMA (1974)

<h3>To the Editor.—</h3> Having been for many years a paradox watcher, especially of "paradoxes of pulsus paradoxus," I feel compelled to comment on the EDITORIAL of your senior editor, Samuel Vaisrub, MD, on "Pulsus Paradoxus Pulmonale" (228:1030, 1974). First, an inspiratory fall in peak systolic pressure is not a paradox (that is, it is not contrary to nature), but a
Meeting Mania
Authors: A B Bergman
Journal: New England Journal of Medicine (1994)

With health care reform rising to the top of our nation's political agenda, the burgeoning costs of the nonclinical aspects of patient care are finally coming under scrutiny1. Most of the focus is properly being directed toward paperwork, malpractice, and unnecessary services. Less attention is being devoted to a more insidious and pervasive requirement for physicians: attendance at meetings, the frequency of which appears to be increasing at a logarithmic rate.Meeting mania, a rampant phenomenon of the 1990s, occurs in all fields of endeavor, wherever people in white collars or power suits congregate. “Sorry, he/she is in a . . .
Changes in bone density with lactation
Authors: M. Sowers
Journal: JAMA (1993)

<h3>Objective.</h3> —To test the a priori hypotheses that significant bone loss occurs in lactation of greater than 5 months' duration and that bone mass returns to baseline levels when breast-feeding ceases. <h3>Design.</h3> —Prospective cohort study design of 12 months' duration. <h3>Setting.</h3> —General community setting with recruitment occurring at birthing education classes. <h3>Participants.</h3> —Volunteer sample of 98 healthy women of white (n=95) and Asian (n=3) origin, aged 20 to 40 years, and 0 to 1 parity prior to parturition, grouped according to lactation duration: 0 through 1, 2 through 5, and 6 or more months. <h3>Main Outcome Measures.</h3> —Bone mineral density (BMD) of the proximal femur was measured by dual-energy x-ray densitometry at 2 weeks (baseline), 2 months, 4 months, 6 months, and 12 months following parturition, and BMD of the lumbar spine was measured at baseline, 6 months, and 12 months after parturition. <h3>Results.</h3> —Women with lactation duration of 6 months or longer had mean BMD losses of 5.1% and 4.8% at the lumbar spine and femoral neck, respectively, comparing baseline values with those at 6 months post partum. Women who breast-fed 0 through 1 month lost no BMD at either bone site. Bone loss in women who breast-fed 6 months or longer was not explained by differences in age, diet, body size, or physical activity. Among women who breast-fed 6 months or longer, there was evidence of return to baseline levels of the lumbar spine at 12 months after parturition. The BMD of the lumbar spine of those women who continued to breast-feed more than 9 months had increased but was still significantly lower than baseline. <h3>Conclusion.</h3> —Extended lactation (≥70% of energy intake is provided for ≥6 months) is associated with bone loss; however, there is evidence of return to baseline BMD measurement at 12 months after parturition. (<i>JAMA</i>. 1993;269:3130-3135)
Fix
Authors: Brenda Butka
Journal: Annals of Internal Medicine (2015)

Ad Libitum3 March 2015FixBrenda Butka, MDBrenda Butka, MDFrom Nashville, Tennessee.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/M14-2334 Audio Reading - “Fix” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "Fix," by B. Butka. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail he comes into the clinicdragging his oxygen behindwife riding shotgun off to the rightslack in his chair, twitchinghe is asking how will he livehow can he breatheair is a precious commodityinside and outlooks to me for answersdata, rescue, salvationthis should not be his fatesuccessful, in this latecentury, hasn't science conqueredeverything, isn'tthere always a fix? Author, Article, and Disclosure InformationAuthors: Brenda Butka, MDAffiliations: From Nashville, Tennessee.Current Author Address: Brenda Butka, MD; e-mail, brenda.butka@vanderbilt.edu PreviousarticleNextarticle Advertisement Audio Reading - “Fix” Audio. Michael A. LaCombe, MD, Annals Associate Editor, reads "Fix," by B. Butka. Your browser does not support the audio element. Audio player progress bar Step backward in current audio track Play current audio trackPause current audio track Step forward in current audio track Mute current audio trackUnmute current audio track 00:00/ FiguresReferencesRelatedDetails Metrics 3 March 2015Volume 162, Issue 5 Page: 344 Keywords Firearm injuries Oxygen ePublished: 3 March 2015 Issue Published: 3 March 2015 Copyright & PermissionsCopyright © 2015 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Abstract 17473: Obesity is Associated With Impaired Left Atrial Function in Young Patients With Recent Onset Atrial Fibrillation
Authors: Dinant N Oemrawsingh, Rob A Vermond, Ernaldo G Marcos, Anne H Hobbelt, Yoran M Hummel, Joost P van Melle, Yuri Blaauw, Isabelle C van Gelder, Michiel Rienstra
Journal: Circulation (2015)

Introduction: Obesity is a risk factor for atrial fibrillation (AF), and reduction of weight has been shown to reduce the burden of AF. However, the exact underlying pathogenesis is unknown. Hypothesis: We hypothesize that obesity is related with impaired left atrial function, measured with echocardiographic strain analysis, in young patients (&lt;60 years) with recent onset AF (AF history&lt; 3 years). Methods: We studied 94 patients of the Phenotyping young-onset AF patients study, all with sinus rhythm during echocardiography. Detailed clinical and echocardiographic information was collected. Three strain-patterns (reservoir, activation, and conduit strain) representing left atrial functional phases were measured. Results: Of the 94 patients, 32 were obese and 62 were non-obese (34±3 kg/m2 vs. 25±2 kg/m2, p&lt;0.001). Mean age was 50±9 years and 34% were women. No significant differences in cardiovascular conditions and risk factors were found, except for diabetes mellitus (13% vs. 2%, p=0.026), and metabolic syndrome (56% vs. 8%, p&lt;0.001), both more common in obese patients. Left atrial volume index (mean 30±8ml/m2), and left ventricular mass index and ejection fraction were not significantly different between both groups. However, the left atrial reservoir (27±8 vs. 33±10%, p=0.008) and conduit strain (16±6 vs. 20±8%, p=0.011) were significantly reduced in obese patients, the left atrial activation strain was not (p=0.118). Using linear regression analysis adjusting for significant baseline differences, the association between reservoir strain (beta=-0.304, p=0.013), and conduit strain (beta=-0.246, p=0.045) and obesity remained significant. The correlation between BMI and left atrial function are shown in the figure. Conclusions: In young patients with recent onset AF, obesity is associated with impaired left atrial function, in absence of dilatation. Left atrial dysfunction may be the first sign of atrial remodeling in obese AF patients.
Operating Room Procedure for Nurses and Internes
Journal: JAMA (1934)

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 LB-155: A new syngeneic MYCN-overexpressing neuroblastoma mouse model and MYCN-DNA vaccine
Authors: Alexander Stermann, Nicole Huebener, Holger N. Lode
Journal: Cancer Research (2011)

Abstract High-level expression of MycN caused by amplification of the gene characterizes the malignant phenotype of neuroblastoma. Recent studies suggest that MYCN is a suitable target for immunotherapy, but up to now, a syngeneic NB mouse model over expressing MYCN is not available to examine immunotherapeutic strategies in vivo. Here, we report the development of a tetracycline inducible MYCN expressing murine NB cell line syngeneic to A/J mice and a MYCN-DNA vaccine. For this purpose, the murine NB cell line C1300, syngeneic to A/J mice, was stably transfected with a tetracycline inducible MYCN expression vector. Stable transfection was verified by real-time PCR and Western-Blot, revealing high expression levels of MYCN RNA and protein, respectively. Furthermore, a MYCN-DNA vaccine, based on epitopes encoding for three peptides from the murine MYCN protein sequence with high affinity to the A/J mouse MHC class I allele H2-Kk, was designed and tested in vivo for its ability to induce an antigen-specific immune response. Lymphocytes isolated from A/J mice vaccinated with the MYCN vaccine effectively lysed C1300-MYCN +tet cells in cytotoxicity assays in contrast to wild type C1300 cells and lymphocytes from control mice. Lymphocytes from minigene vaccinated mice produced significantly higher amounts of IFN-γ after stimulation with irradiated C1300 cells than lymphocytes from control mice. Interestingly, vaccine induced cytotoxic T lymphocytes also kill parental C1300 tumor cells which show low MYCN expression. We expect that this effect will be enhanced when MYCN-over expressing C1300 cells are employed in a similar cytotoxicity assay which will be reported at the meeting. In summary, we report the development of a new MYCN-DNA vaccine and a murine tetracycline inducible MYCN NB cell line providing an useful syngeneic mouse model for in vivo evaluation of MYCN directed immunotherapeutic strategies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr LB-155. doi:10.1158/1538-7445.AM2011-LB-155
Involvement of phosphatidylinositol 3-kinase (PI3-K) in regulation of endocytotic-transcytotic pathways and bile secretion II Dpt. Gastro, Univ. Rome; Dpt. Med. I, H.S. Raffaele, Milan; Joslin Diabetes CTR., Boston (USA); Dpt. Gastro, Univ. Ancona, Italy
Journal: Hepatology (1995)
Evaluation of the efficacies of methylphenidate and biofeedback treatments in giggle incontinence: One-year follow-up study
Authors: A. Hacıislamoğlu, M. Ekşi, D.N. Özlü, A.H. Yavuzsan, İ. Evren, S. Karadağ, H. Polat, T. Kargı, A.İ. Taşçı
Journal: European Urology (2021)
Secretion of cytokines and growth factors into autosomal dominant polycystic kidney disease liver cyst fluid
Authors: Matthew T. Nichols, Elsa Gidey, Tom Matzakos, Rolf Dahl, Greg Stiegmann, Raj J. Shah, Jared J. Grantham, J. Gregory Fitz, R. Brian Doctor
Journal: Hepatology (2004)

The principal extrarenal manifestation of autosomal dominant polycystic kidney disease (ADPKD) involves formation of liver cysts derived from intrahepatic bile ducts. Autocrine and paracrine factors secreted into the cyst would be positioned to modulate the rate of hepatic cyst growth. The aim of this study was to identify potential growth factors present in human ADPKD liver cyst fluid. Cytokine array and enzyme-linked immunosorbent assay analysis of human ADPKD liver cyst fluid detected epithelial neutrophil attractant 78, interleukin (IL)-6 (503 ± 121 pg/mL); and IL-8 (4,488 ± 355 pg/mL); and elevated levels of vascular endothelial growth factor compared with non-ADPKD bile (849 ± 144 pg/mL vs. 270 pg/mL maximum concentration). ADPKD liver cyst cell cultures also released IL-8 and vascular endothelial growth factor, suggesting that cystic epithelial cells themselves are capable of secreting these factors. Western blotting of cultured cyst cells and immunostaining of intact cysts demonstrate that cysteine-X-cysteine receptor 2, an epithelial neutrophil attractant 78 and IL-8 receptor, is expressed at the apical domain of cyst lining epithelial cells. Suggesting the cystic epithelial cells may exist in hypoxic conditions, electron microscopy of the ADPKD liver cyst epithelium revealed morphological features similar to those observed in ischemic bile ducts. These features include elongation, altered structure, and diminished abundance of apical microvilli. In conclusion, IL-8, epithelial neutrophil attractant 78, IL-6, and vascular endothelial growth factor may serve as autocrine and paracrine factors to direct errant growth of ADPKD liver cyst epithelia. Interruption of these signaling pathways may provide therapeutic targets for inhibiting liver cyst expansion. (Hepatology 2004;40:836–846).
Lack of vitamin D and other stories . . .
Journal: BMJ (2013)

Lack of vitamin D and other stories . . .Homo sapiens probably reached Ulm in southern Germany around 40 000 years ago, when the area offered plenty of good mammoth hunting on the steppe between the Alpine ice mass immediately to the south and the endless glacier that covered Europe from about Hamburg northwards.The human population of Ulm has changed a great deal since then, but one ancient feature remains-Ulmians, like most people in Europe, are bad at making vitamin D. In a study of 1418 older people living in southern Germany, researchers investigated the seasonal differences in vitamin D levels (Age and Ageing 2013; doi:10.1093/ageing/aft042).They found that proportions of vitamin D deficiency, insufficiency, and sufficiency were 78.8%, 19.2%, and 1.9% in March 2009, respectively.Corresponding proportions in August 2009 were 16.1%, 63.4%, and 20.5%, respectively.Now that their supply of mammoth liver has dried up, the people of Ulm may need to look to other sources to remedy their lack of vitamin D.
Incorrect Signature
Journal: JAMA (1984)

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
Clostridium Welchii Conjunctivitis
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
Malpractice Suits
Authors: Alan Y. Medvin
Journal: JAMA (1978)

<h3>To the Editor.—</h3> I am an attorney who specializes in the trial of medical malpractice cases. I am a member of the Medical Malpractice Committee of the New Jersey Branch of the Association of Trial Lawyers of America. In addition, I happen to subscribe to<i>JAMA</i>to attempt to keep abreast of recent developments in medicine. After reading the letter of Adolph Wolferman, MD (239:494, 1978), I feel compelled to respond. Dr Wolferman demonstrates unfamiliarity with the handling of a medical malpractice claim. He is under the misconception that initiation of a malpractice action is "an investment without risk for lawyer and patient alike." The fact is that a malpractice case is by far the riskiest type of legal action undertaken today. The malpractice action, properly prepared, generally involves the expenditure of thousands of dollars plus enumerable hours. These factors all dictate that a medical malpractice attorney very carefully screen