tbuckley/cabot-search huggingface dataset:
The following articles for this Special Issue were published before this collection was released. They can be found in their respective issues or online.
Journal: Medicinal Research Reviews (2021)

Volume 41, Number 2 Mitochondria as a promising target for developing novel agents for treating Alzheimer's disease Elena F. Shevtsova, Andrey V. Maltsev, Darya V. Vinogradova, Pavel N. Shevtsov, and Sergey O. Bachurin https://doi.org/10.1002/med.21715 Activation of transcription factor Nrf2 to counteract mitochondrial dysfunction in Parkinson's disease Claudia Bento‐Pereira and Albena T. Dinkova‐Kostova https://doi.org/10.1002/med.21714 Mitochondria and lipid peroxidation in the mechanism of neurodegeneration: Finding ways for prevention Plamena R. Angelova, Noemi Esteras, and Andrey Y. Abramov https://doi.org/10.1002/med.21712 Pharmacotranscriptomics of peptide drugs with neuroprotective properties Lyudmila V. Dergunova, Ivan B. Filippenkov, Svetlana A. Limborska, and Nikolai F. Myasoedov https://doi.org/10.1002/med.21704
Hypertension
Authors: Dorothea Loofbourow, Robert S. Palmer
Journal: New England Journal of Medicine (1950)

Neurohumoral SystemIn view of recent work and interest in the pressor amines, it seems worthwhile to review the most probable mechanism regarding the formation of those substances. If epinephrine is formed from tyrosine, as has been suggested86 and if nor-epinephrine is the precursor of epinephrine,86, 87 the steps might be as shown in Figure 1.The first two reactions are known to take place in the body; the product is a primary amine. The last steps are possible, but the exact reaction is not known; both 3 and 3′ can occur. It is also possible to have both methylation and demethylation, . . .
A REPORT OF FOUR RECENT CASES OF THORACOPLASTY
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
Mast Cell Degranulation in Rat Uvea
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 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
THE CAUSE OF SCARLET FEVER.
Journal: JAMA (1904)

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
The merits of geriatric consultation
Authors: E. W. Campion
Journal: JAMA (1987)

Consultation entails anticipation. The valued consultant brings the experience and expertise needed to anticipate complications as well as to discover elusive diagnoses. To benefit the patient, the consultant's wisdom must result in clear communication and reasonable compliance, both of which may be sizable challenges in themselves.<sup>1,2</sup> An ambitious goal of the consultant geriatrician is to avert the ills that can befall the hospitalized elderly. However, specific complications remain very difficult to anticipate. Only a minority of the major complications were anticipated in Becker and colleagues'<sup>3</sup>well-designed study appearing in this issue ofThe Journal: infection-related (10%), procedural (14%), trauma-related (28%), and medication-related (39%). None of the ten falls were predicted. In this study age alone seems once again to predict little except birth year. The art of averting complications is still imprecise. Effective interventions require more accurate clinical prediction. The powerful, though retrospective, wisdom of multivariate analysis will
An autopsy study of cancer patients. I. Accuracy of the clinical diagnoses (1955 to 1965) Boston City Hospital
Authors: F. W. Bauer
Journal: JAMA (1972)

At the Boston City Hospital between 1955 and 1965 one fourth of all autopsies involved cancer patients. Forty percent of these 2,734 patients had serious clinical errors for diagnosing cancer, and 63% of patients with these errors died from cancer. Twenty-six percent of all patients reviewed had clinically undiagnosed cancer, and 45% of these neoplasms were fatal. Nonmalignant diseases caused death in 24% of all cancer patients reviewed. Generally, errors in clinical diagnoses of cancer were most common with the most common cancers. Cancer patients were almost a decade older than control patients without cancer.
Environmental Chemical Exposures and Risk of Herpes Zoster
Authors: Volker Arndt, Marilyn F. Vine, Kristen Weigle
Journal: Environmental Health Perspectives (1999)

This study investigated whether residence in Aberdeen, North Carolina, the location of the Aberdeen pesticides dumps site (a national priority list Superfund site containing organochlorine pesticides, volatile organic compounds, and metals), is associated with immune suppression as indicated by a higher incidence of herpes zoster and recent occurrences of other common infectious diseases. Study participants included 1,642 residents, 18-64 years of age, who responded to a telephone survey concerning potential occupational and recreational exposures to pesticides and other chemicals, lifetime history of herpes zoster (shingles), and the recent occurrence of other common infectious diseases. Stratified and logistic regression analyses were used to compare the cumulative incidence of herpes zoster among Aberdeen residents and residents of nearby communities. There was little evidence of an overall increased risk of herpes zoster among Aberdeen residents during the period 1951-1994 [relative risk (RR), 1.3; 95% confidence interval (CI), 0.8-2.1]. However, an elevated risk of herpes zoster was noted consistently among Aberdeen residents of younger ages as compared to residents of the nearby communities. The RR was 2.0 (CI, 1.0-4.0) among those 18-40 years of age and was not affected by controlling for potential confounders. The RR of herpes zoster was also consistently elevated in all age groups for the period before 1985. No differences were noted between residents of Aberdeen and those of the nearby communities with respect to the recent occurrence of other common infectious diseases. These results support the plausibility of an association between exposure to the Aberdeen pesticides dumps site and immune suppression and the potential use of herpes zoster as a marker of immune suppression in studies of environmental chemical exposures.
Correction: A Randomized Controlled Trial of a 6-Month Low-Carbohydrate Intervention on Disease Progression in Men with Recurrent Prostate Cancer: Carbohydrate and Prostate Study 2 (CAPS2)
Authors: Stephen J. Freedland, Jenifer Allen, Aubrey Jarman, Taofik Oyekunle, Andrew J. Armstrong, Judd W. Moul, Howard M. Sandler, Edwin Posadas, Dana Levin, Emily Wiggins, Lauren E. Howard, Yuan Wu, Pao-Hwa Lin
Journal: Clinical Cancer Research (2021)

In the original version of [this article][1] ([1][2]), 1 of the control patients was mistakenly coded as a patient in the intervention arm (low-carbohydrate diet) during data entry. This error has been corrected in the latest online HTML and PDF versions of this article. The authors regret this
A Revolution in Bread
Journal: JAMA (2011)

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 210: αMyHC-mCherry-LC3 Transgenic Mice is a New and Useful Tool to Examine the Role of Autophagy in Cardiomyocytes
Authors: Mai Terada, Kiyoshi Nobori, Yoshiko Munehisa, Manabu Kakizaki, Takayoshi Ohba, Takashi Koyama, Yoichiro Takahashi, Masaru Ishida, Kenji Iino, Toshimitsu Kosaka, Hiroyuki Watanabe, Hitoshi Hasegawa, Hiroshi Ito
Journal: Circulation (2008)

Autophagy is an intracellular process in which proteins and organelles are transported in double-membrane vesicles called autophagosomes through the cytoplasm to lysosomes for degradation. The autophagosome acquires hydrolytic enzymes by fusing with the lysosome to generate an autolysosome. Constitutive autophagy in the heart under baseline conditions is a homeostatic mechanism for maintaining cardiomyocyte size and global cardiac structure and function. Upregulation of autophagy in various heart diseases, including cardiac hypertrophy and heart failure, is an adaptive response for protecting cells from hemodynamic stress. However, the detailed roles of autophagy in the heart remain unclear. LC3 is localized on the autophagosome membrane. Exogenously expressed GFP fused to LC3 (GFP-LC3) serves as an ideal molecular marker for autophagosome. Transgenic mice expressing GFP-LC3 (CAG-GFP-LC3) have been used to detect autophagy systemically. However, CAG-GFP-LC3 mice cannot distinguish autophagy-positive cardiomyocytes from other cells such as fibroblasts and smooth muscles in the heart and cannot detect autolysosome because GFP-LC3 loses fluorescence due to lysosomal acidic and degradative conditions. To resolve these problems, we have generated transgenic mice (αMyHC-mCherry-LC3) expressing mCherry fused to LC3 under the control of αmyosin heavy chain promoter instead of CAG promoter to detect autophagy only in cardiomyocytes. mCherry is an improved-monomeric red-fluorescence protein and does not lose fluorescence under acidic condition. Thus, αMyHC-mCherry-LC3 mice can detect not only autophagosome before fusion with lysosome but also autophagosome after fusion with lysosome. Moreover, we have crossed αMyHC-mCherry-LC3 mice with CAG-GFP-LC3 mice. Green signals showed autophagosome in non-cardiomyocytes. On the other hand, red signals showed autolysosome and double positive signals showed autophagosome in cardiacmyocytes. In conclusion, we have generated αMyHC-mCherry-LC3 mice to detect both autophagosome and autolysosome. The double transgenic mice cannot only detect autophagosome and autolysosome but also distinguish between them. This is an innovative method to examine the role of autophagy in cardiomyocytes.
Circulating cell-free DNA as predictor of treatment failure after neoadjuvant chemoradiotherapy before surgery in patients with locally advanced rectal cancer
Authors: J.V. Schou, B.S. Sørensen, F.O. Larsen, R. Abrantes, A. Boysen, J.S. Johansen, B. Vittrup Jensen, D. Nielsen, K-L. Spindler
Journal: Annals of Oncology (2017)
NEUROLOGY
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
Evaluation de l’impact du système d’endoscopie, de la haute définition et de la chromo-endoscopie virtuelle sur la coloscopie de routine: un essai randomisé
Journal: Endoscopy (2019)

Plusieurs modalités d’imagerie, telle que l’endoscopie haute résolution et la chromo-endoscopie virtuelle, ont été développées dans le but d’améliorer la détection de lésions muqueuses. Le but de cette étude était d’évaluer leur impact sur la détection de polypes coliques au cours de la coloscopie dans un centre hospitalier tertiaire.
Role of Proto-Oncogene Activation in Carcinogenesis
Authors: Marshall W. Anderson, Steven H. Reynolds, Ming You, Robert M. Maronpot
Journal: Environmental Health Perspectives (1992)

The accumulation of genetic damage in the forms of activated proto-oncogenes and inactivated tumor-suppressor genes is the driving force in the evolution of a normal cell to a malignant cell. For example, both the activation of ras oncogenes and the inactivation of several suppressor genes, including p53, have been observed in the development of human colon and lung tumors. Point mutations in key codons can activate ras proto-oncogenes and inactivate the p53 suppressor gene. Thus, several critical genes for tumorigenesis are potential targets for carcinogens and radiation that can induce point mutations at low doses. The ras proto-oncogenes are targets for many genotoxic carcinogens. Activation of the ras gene is an early event--probably the "initiating" step--in the development of many chemical-induced rodent tumors. ras Oncogenes are observed in more human tumors and at a higher frequency than any other oncogene, and activation of the proto-oncogene may occur at various stages of the carcinogenic process. Numerous proto-oncogenes other than the ras genes have been shown to be activated in human tumors and to a lesser extent in rodent tumors. Mechanisms that induce aberrant expression of proto-oncogenes are gene amplification and chromosomal translocation or gene rearrangement. Amplification of proto-oncogenes and possibly gene overexpression during the absence of gene amplification occur in the development of many human tumors. For a specific tumor type, amplification of any one proto-oncogene may occur at a low frequency, but the frequency of tumors in which at least one proto-oncogene is amplified can be much higher. Proto-oncogene amplification is usually associated with late stages of tumor progression; however, amplified HER2/neu has been observed in early clinical stages of mammary neoplasia. Activation of proto-oncogenes by chromosomal translocation has been detected at a high frequency in several hematopoietic tumors. Non-ras genes have been detected by DNA transfection assays in both human and rodent tumors. For example, ret and trk genes were found to be activated by gene rearrangements in human papillary thyroid carcinomas. Several potentially new types of oncogenes have also been detected by DNA transfection assays. The etiology of the genetic alterations observed in most human tumors is unclear at present. Examples of ras gene activation and those documented for mutations in the p53 gene demonstrate that exogenous conditions can induce oncogenic mutants of normal genes. The genetic alterations observed in most human tumors are probably generated by both spontaneous events and exogenous conditions.
Book Review An Index of Treatment . By various authors. Edited by Sir Robert Hutchison, Bart., M.D., LL.D., F.R.C.P., assisted by Reginald Hilton, MA., M.D., F.R.C.P. Twelfth edition, revised. 8°, cloth, 996 pp., with 148 illustrations. Baltimore: Williams &amp; Wilkins Company, 1940. $12.00.
Journal: New England Journal of Medicine (1941)
THE TECHNICAL EXPOSITION
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
Prevalence of the Metabolic Syndrome Among Patients Receiving Clozapine
Authors: J Steven Lamberti, David Olson, John F Crilly, Telva Olivares, Geoffrey C Williams, Xin Tu, Wan Tang, Karen Wiener, Steven Dvorin, Marci B Dietz
Journal: American Journal of Psychiatry (2006)

Objective: This study compared the prevalence of the metabolic syndrome among outpatients with schizophrenia and schizoaffective disorder receiving clozapine with a matched comparison group from the National Health and Nutrition Examination Survey. Method: Ninety-three outpatients and a matched group of 2,701 comparison subjects were compared according to National Cholesterol Education Program criteria. Outpatient data were obtained through physical assessments, laboratory testing, and reviews of medical records. Results: The prevalence of the metabolic syndrome was significantly higher among clozapine patients (53.8%) than among the comparison group (20.7%). For clozapine patients, logistic regression analysis revealed significant associations with age, body mass index, and duration of clozapine treatment. Only age and body mass index were associated with the prevalence of metabolic syndrome in both groups. Conclusions: Patients receiving clozapine are at significantly increased risk for developing the metabolic syndrome. Psychiatrists and other providers should consider performing regular physical health monitoring to prevent long-term adverse health consequences.
MEDICAL ERRORS IN FICTION.
Journal: JAMA (1904)

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