tbuckley/cabot-search huggingface dataset:
Metabolic Interrelationships between Arsenic and Selenium
Authors: Orville A. Levander
Journal: Environmental Health Perspectives (1977)

In 1938, Moxon discovered that arsenic protected against selenium toxicity. Since that time it has been shown that this protective effect of arsenic against selenium poisoning can be demonstrated in many different animal species under a wide variety of conditions. Antagonistic effects between arsenic and selenium have also been noted in teratologic experiments. Early metabolic studies showed that arsenic inhibited the expiration of volatile selenium compounds by rats injected with acutely toxic doses of both elements. This was puzzling since pulmonary excretion had long been regarded as a means by which animals could rid themselves of excess selenium. However, later work demonstrated that arsenic increased the biliary excretion of selenium. Not only did arsenic stimulate the excretion of selenium in the bile, but selenium also stimulated the excretion of arsenic in the bile. This increased biliary excretion of selenium caused by arsenic provides a reasonable rationale for the ability of arsenic to counteract the toxicity of selenium, although the chemical mechanism by which arsenic does this is not certain. The most satisfactory explanation is that these two elements react in the liver to form a detoxication conjugate which is then excreted into the bile. This is consistent with the fact that both arsenic and selenium each increase the biliary excretion of the other. Several other metabolic interactions between arsenic and selenium have been demonstrated in vitro, but their physiological significance is not clear. Although arsenic decreased selenium toxicity under most conditions, there is a pronounced synergistic toxicity between arsenic and two methylated selenium metabolites, trimethylselenonium ion or dimethyl selenide. The ecological consequences of these synergisms are largely unexplored, although it is likely that selenium methylation occurs in the environment. All attempts to promote or prevent selenium deficiency diseases in animals by feeding arsenic have been unsuccessful. Over 30 years ago it was suggested that industrial hygienists use arsenic as a tonic to prevent or cure selenium poisoning in workers exposed to this hazard. Organic arsenical feed additives were tried as partial antidotes against selenium poisoning in livestock raised in seleniferous agricultural areas but were not found to be practical.
AUTOLYSIS.
Authors: P. A. LEVENE
Journal: JAMA (1906)

Before concluding the review of the products resulting from proteid cleavage in the process of autolysis mention has to be made of the formation of plasteins. From the foregoing discussion it is apparent that great activity has been displayed in the study of degradation of the proteid molecule within the body and in the test tube, and an attempt has been made to explain the bearing the work had on our understanding of various physiologic functions. However, there was one great problem which inspired many workers in their labors and which remains unsolved by them. This was to discover a process by which proteid, the chief tissue component, could be constructed out of its simple components, and also to discover the mechanism which the organism employs to build up tissue proteid out of those fragments which are formed in the digestive tract. It has been stated before that the first
Animal Studies Help Evaluate Role of Normal Intestinal Flora
Journal: JAMA (1964)

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
Public Health Informatics: How Information-Age Technology Can Strengthen Public Health
Authors: A. Friede
Journal: Annual Review of Public Health (1995)

The combination of the burgeoning interest in health, health care reform and the advent of the Information Age, represents a challenge and an opportunity for public health. If public health's effectiveness and profile are to grow, practitioners and researchers will need reliable, timely informati6n with which to make information-driven decisions, better ways to communicate, and improved tools to analyze and present new knowledge. "Public Health Informatics" (PHI) is the science of applying Information- Age technology to serve the specialized needs of public health. In this paper we define Public Health Informatics, outline specific benefits that may accrue from its widespread application, and discuss why and how an academic discipline of public health informatics should be developed. Finally, we make specific recommendations for actions that government and academia can take to assure that public health professionals have the systems, tools, and training to use PHI to advance the mission of public health.
The Allen &amp;amp; Hanburys Athletic Drug Reference
Journal: JAMA (1991)

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
TCT-825 In-Vivo Long Term Evaluation of a Novel Mitral Valve Regurgitation Therapy: Experience in a Preclinical Large Animal Model
Authors: Athanasios Peppas, Jon Wilson, Yanping Cheng, Christopher Seguin, Masahiko Shibuya, Greg L. Kaluza, Juan Granada
Journal: Journal of the American College of Cardiology (2013)
Formaldehyde toxicity
Authors: J. R. Bender
Journal: JAMA (1982)

<h3>To the Editor.—</h3> The article on formaldehyde by Harris et al (1981; 245:243) reflects a severely restricted point of view. The article is further complicated because the citations do not correspond with the text, and the references cited have not been accurately reviewed. For example, in the Gofmekler<sup>1</sup>study, the actual number of offspring in the formaldehyde-exposed rats was higher than controls (208, 235, and 135 for 0.8, 0.01, and 0 ppm formaldehyde, respectively). Marks et al<sup>2</sup>has demonstrated that oral formaldehyde, even in toxic doses, does not produce statistically significant teratogenic effects in the fetuses of surviving dams. Harris et al apparently "confirmed" that formaldehyde can cause sensitization and airway obstruction based on the article by Schoenberg and Mitchell<sup>3</sup>—a cross-sectional study that lacked appropriate controls, included small numbers of exposed subjects, and did not exclude the contribution of parent resins, phenol, and acrylic breakdown products.
CORRECTION
Journal: American Journal of Psychiatry (2018)

rTMS especially over the left DLPFC on the cortico-striatothalamo-cortical circuitry (Figure 1B through 1E).To our knowledge, this case report, a retrospective analysis of rTMS treatment administered as part of routine clinical care, is the first to use ASL-guided rTMS over the left DLPFC in OCD.By providing a quantitative index of CBF during a brief and noninvasive resting state measurement, ASL might be well-suited for clinical applications involving rTMS.Although we found reduced symptom severity and CBF in OCD-related regions, we cannot rule out possible carry-on effects of the proceeding presupplementary motor area rTMS because of the uncontrolled design of the study.Therefore, further research is required to determine the optimal stimulation site and duration.
Intraperitoneal administration of broad-spectrum antibiotics in patients with renal failure
Authors: R. J. Bulger
Journal: JAMA (1965)

Broad-spectrum antibiotics (cephalothin, ampicillin, tetracycline, and two forms of chloramphenicol) were administered intraperitoneally during peritoneal dialysis to patients with essentially no renal function. Significant serum levels were obtained with all drugs tested except chloramphenicol succinate. Despite continuing intraperitoneal administration for 18 to 32 hours, all drugs except tetracycline demonstrated a leveling off of serum levels. The dangers of administration of tetracycline during peritoneal dialysis are emphasized. The dynamics of peritoneal absorption, pharmacology, and toxicity are discussed and recommendations are made regarding choice and dosage of appropriate antibiotics.
Abstract LB-074: Priming the tumor microenvironment with epigenetic modifiers to overcome resistance to immune checkpoint inhibitors
Authors: Tessa J. Knox, Eva Sahakian, Debarati Banik, Melissa Hadley, Erica Palmer, Jennifer Kim, Satish Noonepalle, John Powers, Maria Gracia-Hernandez, Vasco Oliveira, Fengdong Cheng, Jie Chen, Cyril Barinka, Javier Pinilla-Ibarz, Norman Lee, Alan Kozikowski, Alejandro Villagra
Journal: Cancer Research (2019)

Abstract Histone deacetylases (HDACs) are involved in diverse cellular regulatory mechanisms including functions outside the chromatin environment. Several publications have demonstrated that selective HDAC inhibitors (HDACi) can influence tumor immunogenicity and the functional activity of specific immune cells. In particular, the selective inhibition of HDAC6 has been reported to decrease tumor growth in several malignancies. However, there is still no clarity about the cellular components mediating this effect. In this study, we evaluated the immunological modulation of the HDAC6i Nexturastat A in combination with anti-PD-1 checkpoint blockade therapy and the use of this HDAC6i as a priming agent to facilitate the transition of the tumor microenvironment from “cold” to “hot” in order to more specifically augment immune check-point blockade therapies. This combination of Nexturastat A and anti-PD-1 therapy demonstrated a significant reduction of tumor growth in syngeneic melanoma tumor animal models. Additionally, we observed a complete neutralization of the up-regulation of PD-L1 and other immunosuppressive pathways induced by the treatment with anti-PD-1 blockade. This combination also showed that the pre-treatment with selective HDAC6i induced major changes in the tumor microenvironment such as enhanced infiltration of immune cells, increased central and effector T cell memory, and a significant reduction of pro-tumorigenic M2 macrophages. The evaluation of the effect of HDAC6i on individual immune components suggest that the in vivo anti-tumor activity of HDAC6i is mediated by its effect on tumor cells and tumor associated macrophages, and not directly over T cells. Overall, our results indicate that selective HDAC6i could be used as immunological priming agents to sensitize immunologically “cold” tumors and subsequently improve ongoing immune check-point blockade therapies. Note: This abstract was not presented at the meeting. Citation Format: Tessa J. Knox, Eva Sahakian, Debarati Banik, Melissa Hadley, Erica Palmer, Jennifer Kim, Satish Noonepalle, John Powers, Maria Gracia-Hernandez, Vasco Oliveira, Fengdong Cheng, Jie Chen, Cyril Barinka, Javier Pinilla-Ibarz, Norman Lee, Alan Kozikowski, Alejandro Villagra. Priming the tumor microenvironment with epigenetic modifiers to overcome resistance to immune checkpoint inhibitors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr LB-074.
Activated Endothelial Cells Induce Apoptosis in Leukemic Cells by Endothelial Interleukin-8
Authors: Yasuhito Terui, Masayuki Ikeda, Hiroshi Tomizuka, Tadashi Kasahara, Tetsuya Ohtsuki, Masaya Uwai, Masaki Mori, Takehito Itoh, Miyuki Tanaka, Muneo Yamada, Seiichi Shimamura, Yukihito Ishizaka, Kazuma Ikeda, Keiya Ozawa, Yasusada Miura, Kiyohiko Hatake
Journal: Blood (1998)
Abstract 476: MEK inhibitors for treatment of oligodendroglioma
Authors: Nazanin Majd, Soon Young Park, Marisela Martinez de Kraatz, Veerakumar Balasubramaniyan, Mittal Sandeep, Jian Hu, Jihye Paik, John de Groot
Journal: Cancer Research (2019)

Abstract Oligodendroglioma (OD) is defined by the 2016 WHO classification as IDH mutant gliomas with 1p19q co-deletion. Although ODs are sensitive to chemotherapy, they eventually recur leading to functional deficits and ultimately death. CIC gene mutations, located on chromosome 19q are seen in 60% of 1p19q co-deleted OD and have been linked to worse survival. Despite our growing knowledge of the molecular characteristics of OD, all recurrent OD patients are treated similarly mainly using radiation and/or poorly tolerated cytotoxic chemotherapy with modest benefit. There is therefore an urgent unmet medical need to understand the molecular consequence of recurrent mutations in OD in order to improve patient outcomes. CIC gene mutations result in truncated, degraded or non-functional CIC protein, disrupting CIC protein repressor functions. This leads to upregulation of ETS-Pea3 family of transcription factors which are known oncogenes in a variety of solid cancers. MAPK signaling pathway has been shown to directly activate ETS family of proteins in drosophila. However, the link between MAPK signaling, ETS proteins and CIC in OD is elusive. Here, we propose a model of aggressiveness in CIC mutant OD in which these cells are dependent on MAPK axis for activation of their augmented ETS proteins (i.e ETV1, ETV4) and therefore are sensitive to MAPK inhibition. To test our model, we evaluated mRNA and protein expression of ETS family of proteins in CIC mutant and CIC wild-type mouse OD cell lines and show that ETV1 and ETV4 have elevated protein and mRNA expression in CIC mutant OD cells, respectively. Consistent with our hypothesis, two different MEK inhibitors, trametinib and pimasertib, reduce cell viability of OD cell lines with greater reduction in CIC mutant than wild-type cells. As proof of concept, we demonstrate that CIC mutant cells have increased pERK expression when compared with CIC wild-type cells indicating that MAPK pathway is more active in CIC mutant cells. Overall, we were able to show that MEK inhibitors have anti-tumor effects in OD cell lines, with greater sensitivity seen in CIC mutant cells. This work lays the foundation for repurposing the widely clinically used MEK inhibitors for treatment oligodendroglioma patients with CIC mutation. Citation Format: Nazanin Majd, Soon Young Park, Marisela Martinez de Kraatz, Veerakumar Balasubramaniyan, Mittal Sandeep, Jian Hu, Jihye Paik, John de Groot. MEK inhibitors for treatment of oligodendroglioma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 476.
Carcinogen Regulation
Authors: David P. Rall
Journal: JAMA (1982)

<h3>To the Editor.—</h3> I agree with much of what was written in the article entitled "Carcinogen Regulation" (1981; 246:253). On the same subject, may I recommend "Assessment of Technologies for Determining Cancer Risks From the Environment" (Office of Technology Assessment, June 1981), which strongly endorses the continued need for animal testing. One point requires clarification. The cost of long-term bioassays is estimated at between $250 and $750 million a year (100 to 300 a year times $250,000 per test). In fact, the total amount spent on long-term animal bioassays is considerably less. At the National Toxicology Program (NTP), where most of this testing is done in the federal government, we spend about $40 million. Because the NTP is including special studies (hematology, urinalysis, and assessments of damage to kidney, liver, lungs, and the immune and nervous systems), these broadened bioassays will provide scientists with more toxicological information than a simple
Use of cholesterol measurements in childhood for the prediction of adult hypercholesterolemia. The Muscatine Study
Authors: R. M. Lauer
Journal: JAMA (1990)

This article describes the validity and utility of screening tests for total cholesterol levels in school-age children to predict those who, when adults, will have cholesterol levels that the National Cholesterol Education Program suggests need continuing surveillance and intervention. Two thousand three hundred sixty-seven children aged 8 to 18 years were examined on several occasions and were followed up to ages 20 to 30 years. Of children with cholesterol concentrations exceeding the 75th percentile on two occasions, 75% of girls and 56% of boys would not qualify for intervention as adults by the National Cholesterol Education Program criteria. Of children with cholesterol levels exceeding the 90th percentile on two occasions, 57% of girls and 30% of boys would not qualify for intervention as adults. Because the efficacy, safety, acceptability, and cost of treatment for high cholesterol concentrations in childhood is evolving, the need for universal screening of childhood cholesterol levels must be considered carefully in view of the number of children with high levels of cholesterol who, as adults, do not meet the criteria for intervention suggested by the National Cholesterol Education Program. (<i>JAMA</i>. 1990;264:3034-3038)
Novel Mode of Bleeding.
Journal: JAMA (1883)

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
Abstracts
Journal: Annals of the Rheumatic Diseases (1971)

This paper describes a brother and sister seen at the Department of Medicine of the State University of New York.Both patients had rheumatoid arthritis and died of myasthenia gravis.Rheumatoid arthritis was diagnosed in the brother at the age of 52 years and treated with prednisolone and corticotrophin; 6 months later he developed fatigue, ptosis, and weakness which responded to treatment with anticholinesterases.He continued to work to the age of 58, but thereafter his myasthenic symptoms increased.His clinical state shortly before his death at age 61 is recorded, together with the findings at a post mortem examination.The sister developed myasthenia at age 29 and rheumatoid arthritis at age 40; the myasthenia initially responded to neostigmine, but sub- sequently became resistant and there was no improvement after thymectomy.She died at the age of 44 years and a post mortem is reported.In the family a brother had a history suggestive of myasthenia, a second brother had rheumatoid arthritis, and two other siblings had neither disease.The familial occurrence of each disease is discussed and the relevant literature cited.The results of sero- logical tests in these two conditions are evaluated.
THE REPORT OF A CASE OF FATTY URINE ACCOMPANYING AN ABSCESS IN THE RIGHT ILIAC FOSSA—RECOVERY
Journal: JAMA (1991)

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 MEDICAL STUDENTS MUST BE DEFERRED
Journal: JAMA (1941)

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