tbuckley/cabot-search huggingface dataset:
Is There a Stein--Leventhal Syndrome?
Authors: D. W. T. Roberts, M. Haines
Journal: BMJ (1960)

Two types of L.E. cell factors-transferable and non- transferable-were found in experiments in which plasma from patients with systemic lupus erythematosus was transfused into dogs.Identical results were obtained in human subjects and in dogs with transfusions of transferable and nontransferable L.E. plasma factor.The amount of transfused L.E. plasma appears not to be responsible for the production of two types of L.E. cell factor.
Is Weight Loss a Cure for Type 2 Diabetes?
Authors: John A. Tayek
Journal: Diabetes Care (2002)

It has been estimated that ∼10% of the U.S. population will be diagnosed with type 2 diabetes by the year 2010. Cardiovascular disease accounts for 75% of all related deaths in diabetic patients. While the use of HMG CoA reductase inhibitors has contributed to a marked reduction in mortality in cardiovascular deaths, the benefit in type 2 diabetes has been disappointing. Patients with type 2 diabetes have a sixfold increased risk of a first-time myocardial infarction compared with nondiabetic patients (1). Additionally, diabetic patients have twice the risk of myocardial infarction. As cardiovascular mortality is the leading single cause of death in the U.S. and because patients with type 2 diabetes have a three- to eightfold increased risk of death, new treatment strategies need to be considered for this disease and its prevention (1).

Dixon and O’Brien (2) describe the effects of laparoscopic adjustable gastric band surgery on the development of type 2 diabetes. All patients had severe obesity (BMI ≥35.0 kg/m2). One year after surgery, 64% patients had remission of diabetes. The prevalence of diabetes decreased from 10 to 5.6%. An additional 26% of patients with diabetes had an improvement in their control of diabetes. Gastric band surgery resulted in an average weight loss of 27 kg. HbA1c was reduced from 7.8 to 6.2%. The 1.6% fall in HbA1c was also associated with a 58-mg/dl …
Volumetric, hemodynamic, and excretory characteristics of the liver in acromegaly.
Authors: R Preisig, T Q Morris, J C Shaver, N P Christy
Journal: Journal of Clinical Investigation (1966)

Comprehensive autopsy studies (1, 2) have disclosed that enlargement of the viscera, including the heart, lungs, kidneys, pancreas, adrenals, and particularly the liver, is a prominent and consistent feature of acromegaly.The detailed structural changes responsible for visceromegaly in patients with this disease are poorly understood.Studies of the functional alterations of the hypertrophied organs are few and have been focused almost exclusively on the kidneys.Increased renal plasma flow, glomerular filtration rate, and proximal tu- bular functions have been demonstrated (3-5).It seemed reasonable, therefore, to expect that blood flow and excretory function of the liver might also be augmented.Precise appraisal of liver size by clinical ex- amination alone is difficult; furthermore, evalua- tion of hepatic hyperfunction cannot be made with routine liver function tests.The introduction of methods for measurement of splanchnic blood flow and volume (6, 7) and for estimation of sulfo- bromophthalein (BSP) kinetics (8, 9) has made quantitative determination of hepatic function possible.Correlation of function with hepatic size is feasible owing to the development of tech- niques for quantification of "liver volume" (10).The results of such studies, carried out in 11 pa-
Cognitive Effects of Konzo
Authors: M. J. Friedrich
Journal: JAMA (2013)

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
Incidental Gallbladder Visualization on Nonhepatobiliary Nuclear Medicine Studies
Authors: Ryan D. Niederkohr, I Ross McDougall
Journal: Clinical Nuclear Medicine (2007)

Gallbladder uptake is occasionally encountered with commonly used nonhepatobiliary radiopharmaceuticals. Identification of the biliary tract by a nonhepatobiliary agent can identify disease, such as uptake of labeled white blood cells. However, in most cases, gallbladder uptake of nonhepatobiliary tracers is not due to pathology in these cases. It is important to avoid attributing gallbladder uptake to disease in the gallbladder or adjacent anatomic structures. We present 3 cases of unexpected gallbladder tracer uptake and provide a review of the literature describing incidental gallbladder uptake on nonhepatobiliary nuclear medicine studies. The potential for misdiagnosis and the steps taken to avoid this are discussed.
Grooved Director for Vaginal Hysterectomy.
Authors: E. D. Ferguson
Journal: JAMA (1900)

Troy, N. Y., Nov. 24, 1900. <h3>To the Editor:</h3> It is with pleasure that I acknowledge priority for the director for vaginal hysterectomy in favor of Dr. Joseph Eastman on the statements in the letter to The Journal of November 24, p. 1359. It is only another illustration of the fact that similar ideas and needs often bring identical results. That my oversight of Dr. Eastman's previous publication is at least pardonable is shown by the fact that the "director" was exhibited at three medical meetings in large cities in the state of New York, and privately to several gynecologists of more than national reputation, and in no instance was a hint of previous knowledge given. Having no desire for mere priority, I cheerfully give way to Dr. Eastman, whom I hold in high esteem for his personal worth and professional work.
Some suggested additions to the semantic cognition model
Authors: Jean M. Mandler
Journal: Behavioral and Brain Sciences (2008)

Abstract Rogers &amp; McClelland (R&amp;M) present a powerful account of semantic (conceptual) learning. Their model admirably handles many characteristics of early concept formation, but it also needs to address attentional biases, and distinguish direct input from error-driven learning, and fast versus slow learning. Not distinguishing implicit and explicit knowledge means that the authors also cannot explain why some coherently varying information becomes accessible and other information does not.
Environmental Exposures and ADHD
Authors: Jack Brondum
Journal: Environmental Health Perspectives (2007)

ADHD in those subjects with low ferritin levels.Given that lead exposure may contribute to ADHD and iron deficiency may exacerbate deleterious effects caused by lead, we recommend systematically seeking for iron deficiency in children with ADHD.We also think that controlled studies assessing the potential effectiveness of iron supplementation on ADHD symptoms should be encouraged.Such studies could aid the understanding of the complex pathophysiology underlying ADHD and provide effective therapeutic strategies for this disorder.
Targeting Mutant <i>p53</i> in Human Tumors
Authors: Brian D. Lehmann, Jennifer A. Pietenpol
Journal: Journal of Clinical Oncology (2012)

Article Tools UNDERSTANDING THE PATHWAY Article Tools OPTIONS & TOOLS Export Citation Track Citation Add To Favorites Rights & Permissions COMPANION ARTICLES No companion articles ARTICLE CITATION DOI: 10.1200/JCO.2012.44.0412 Journal of Clinical Oncology - published online before print September 10, 2012 PMID: 22965952 Targeting Mutant p53 in Human Tumors Brian D. LehmannxBrian D. LehmannSearch for articles by this author , Jennifer A. PietenpolxJennifer A. PietenpolSearch for articles by this author Show More Vanderbilt University School of Medicine, Nashville, TN https://doi.org/10.1200/JCO.2012.44.0412 First Page Full Text PDF Figures and Tables © 2012 by American Society of Clinical Oncology
Binding-, intracellular transport-, and biosynthesis-defective mutants of vasopressin type 2 receptor in patients with X-linked nephrogenic diabetes insipidus.
Authors: H Tsukaguchi, H Matsubara, S Taketani, Y Mori, T Seido, M Inada
Journal: Journal of Clinical Investigation (1995)

Nephrogenic diabetes insipidus (NDI) is most often an X-linked disorder in which urine is not concentrated due to renal resistance to arginine vasopressin. We recently identified four vasopressin type 2 receptor gene mutations in unrelated X-linked NDI families, including R143P, delta V278, R202C, and 804insG. All these mutations reduced ligand binding activity to < 10% of the normal without affecting mRNA accumulation. To elucidate whether the receptors are expressed on the cell surface, we analyzed biosynthesis and localization of tagged or untagged receptors stably expressed in Chinese hamster ovary (CHO) cells, using two antibodies directed against distinct termini. Whole-cell and surface labeling studies revealed that the R202C clone had both surface-localized (50-55 kD) and intracellular proteins (40 and 75 kD), similar to the wild-type AVPR2 clone, whereas the R143P and delta V278 clones lacked the surface receptors, despite relatively increased intracellular components. The 804insG mutant cell produced no proteins despite an adequate mRNA level. Immunofluorescence staining confirmed that the R202C mutant reaches the cell surface, whereas the R143P and delta V278 mutants are retained within the cytoplasmic compartment. Thus, R202C, R143P/delta V278, and 804insG result in three distinct phenotypes, that is, a simple binding impairment at the cell surface, blocked intracellular transport, and ineffective biosynthesis or/and accelerated degradation of the receptor, respectively, and therefore are responsible for NDI. This phenotypic classification will help understanding of molecular pathophysiology of this disorder.
Effects of stroke volume and velocity of ejection on end-systolic pressure of canine left ventricle. End-systolic volume clamping.
Authors: H Suga, K Yamakoshi
Journal: Circulation Research (1977)

To study the effects of contraction mode on ventricular end-systolic pressure-volume relationship, we compared the end-systolic pressure of isovolumic contraction with that of ejecting contraction at an identical end-systolic volume. The left ventricle of excised cross-circulated canine hearts was fitted with a water-filled balloon. The balloon was connected to a hydraulic pump that allowed the ventricle to contract to a preset constant end-systolic volume (19-37 ml) from a variable end-diastolic volume. At each of control, enhanced, and depressed levels of contractility, differences of end-systolic pressures of steady state isovolumic and ejecting contractions were evaluated while stroke volume and velocity of ejection were widely varied. The end-systolic pressure in the ejecting contraction tended to decrease by 5-15% from that of the isovolumic beat with increases in either stroke volume to 20-25 ml or peak velocity of ejection to about 800 ml/sec. There was no obvious difference in the results at different levels of contractility. The magnitude of the end-systolic pressure depression due to ejection was, however, relatively small as compared to 4-fold changes in end-systolic pressure due to the changes in contracility. We, therefore, conclude that the ventricular end-systolic pressure-volume relationship is affected slightly by ejection, and that this effect is much smaller than the maximal effect of changing contractility on the end-systolic pressure-volume relationship.
Transforming Admissions: The Gateway to Medicine
Authors: Darrell G. Kirch
Journal: JAMA (2012)

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 5051: MYC-driven models of primitive neuroectodermal tumor are sensitive to inhibitors of glutamine metabolism.
Authors: Sama F. Ahsan, Allison Hanaford, Melanie Weingart, Isabella Taylor, Charles Eberhart, Eric Raabe
Journal: Cancer Research (2013)

Abstract Brain tumors are a diverse group of cancers in which alterations in growth regulation pathways drive tumorigenicity. Histologically similar tumors may have significant differences in underlying molecular pathways and this in turn may have significant implications for the development of targeted treatment. The MYC family of proteins promotes proliferation and an aggressive phenotype in diverse cancers. Primitive Neuroectodermal Tumors (PNETs) are high grade tumors that can arise throughout the neuro-axis. One subset of PNETs is MYC amplified, and some PNETs are known to express LIN28A, a key regulator of MYC. MYC expression in tumors leads to increased reliance on glutamine metabolism (i.e. the Warburg effect). We hypothesized that MYC-driven PNET tumors would up regulate glutamine metabolism and that glutaminase inhibitors would selectively target MYC-driven tumors. We tested this hypothesis using the MYC-positive PNET cell line PFSK as well as MYC-transformed human neural stem cells. The glutamine methabolic inhibitors DON (6-Diazo-5-oxo-L-norleucine) and acivicin were used to disrupt glutamine metabolism in these cells. Using Tetrazolium dye reduction (MTT assay) and Bromodeoxyuridine assays (BrdU) as indicators for cell growth and replication, we found that PFSK growth is inhibited by acivicin at 10 micromolar concentration (MTT activity reduced by 88%, p&amp;lt;0.05, t-test acivicin treated compared to untreated) MYC-negative UW228 cells were resistant to DON and acivicin treatment. Similarly, DON or acivicin inhibited the proliferation of MYC-transformed human neural stem cells. We observed a 75% reduction in BrdU incorporation in MYC transformed cortex neural stem cells using acivicin, (p&amp;lt;0.001, t-test acivicin treated compared to vehicle treated), 60% reduction in cortex MYC cells using DON (p&amp;lt;0.05), and a 48% reduction in hindbrain MYC cells using DON (p&amp;lt;0.01). The growth of control MYC-negative cells was not significantly inhibited by either drug. This data shows that glutaminase inhibition limits cell replication in tissue culture models of MYC-driven PNET. We are currently investigating the mechanism of growth inhibition (e.g. apoptosis versus cell cycle arrest) caused by glutaminase inhibitors. Murine orthotopic xenograft experiments investigating the efficacy of DON and acivicin treatment in MYC-driven PNET are currently underway in our laboratory. Citation Format: Sama F. Ahsan, Allison Hanaford, Melanie Weingart, Isabella Taylor, Charles Eberhart, Eric Raabe. MYC-driven models of primitive neuroectodermal tumor are sensitive to inhibitors of glutamine metabolism. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 5051. doi:10.1158/1538-7445.AM2013-5051
Specific cell-mediated immunity in the laboratory diagnosis of dermatophytic infections
Authors: B.A.J. WALTERS, G.L. BEARDMORE, W.J. HALLIDAY
Journal: British Journal of Dermatology (1976)

The leukocyte adherence inhibition test was used to detect cell-mediated immunity against antigens of the infecting fungi in patients with dermatophytosis. The species-specific diagnosis thus obtained was in all cases consistent with the eventual results of mycological examination. Most of the patients also produced a specific circulating blocking factor, the detection of which may be a useful guide to the success of treatment. Immunological reactivity against Candida albicans was also observed.
National Plan for Pandemic Flu Unveiled
Authors: Mike Mitka
Journal: JAMA (2006)

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
Aminoglutethimide, Alveolar Damage, and Hemorrhage
Authors: DAVID M. RODMAN
Journal: Annals of Internal Medicine (1986)

Letters and Corrections1 October 1986Aminoglutethimide, Alveolar Damage, and HemorrhageDAVID M. RODMAN, M.D., MICHAEL HANLEY, M.D., POLLY PARSONS, M.D.DAVID M. RODMAN, M.D.Search for more papers by this author, MICHAEL HANLEY, M.D.Search for more papers by this author, POLLY PARSONS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-4-633_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Aminoglutethimide is an adrenal and peripheral blocker of steroid metabolism that has seen increasing use as a medical alternative to adrenalectomy. It has proved effective as therapy for patients with metastatic breast and prostate carcinomas, as well as those with functioning adrenal tumors (1). Adverse effects are usually transient and mild; however, serious adverse effects including bone marrow suppression, cholestasis, and systemic lupus erythematosus have been reported (2-4). We report a case of diffuse alveolar damage and hemorrhage associated with this drug.A 47-year-old man with a known islet-cell tumor secreting corticotropin-releasing factor was started on aminoglutethimide,...References1. SANTENWORGULLIPTON RTA. Aminoglutethimide as treatment of postmenopausal women with advanced breast carcinoma. Ann Intern Med. 1982;96:94-101. LinkGoogle Scholar2. BUZDARFRASCHINIBLUMENSCHEIN AGG. Hematologic adverse effects of aminoglutethimide [Letter]. Ann Intern Med. 1984; 100:159. LinkGoogle Scholar3. PERRAULTDOMOVITCH DE. Aminoglutethimide and cholestasis [Letter]. Ann Intern Med. 1984; 100:160. LinkGoogle Scholar4. MCCRAKENBENSONHICKLING MEP. Systemic lupus erythematosus induced by aminoglutethimide. Br Med J. 1980;281:1254. CrossrefMedlineGoogle Scholar5. CooperWhiteMatthay JDR. Drug-induced pulmonary disease: Part 2. Non-cytotoxic drugs. Am Rev Respir Dis. 1986; 133:488-505. MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Colorado Health Science Center Denver, CO 80262 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByPulmonary eosinophilia associated with aminoglutethimideFirst generation aromatase inhibitors ? aminoglutethimide and testololactone 1 October 1986Volume 105, Issue 4Page: 633-633KeywordsAdrenal tumorsAdrenalectomyBone marrowCorticotropin releasing factorDrugsHemorrhageLupus erythematosus Issue Published: 1 October 1986 PDF DownloadLoading ...
Comprehensive metabolomics identifies the alarmin uric acid as a critical signal for the induction of peanut allergy
Authors: J. Kong, K. Chalcraft, T. S. Mandur, R. Jimenez‐Saiz, T. D. Walker, S. Goncharova, M. E. Gordon, L. Naji, K. Flader, M. Larché, D. K. Chu, S. Waserman, B. McCarry, M. Jordana
Journal: Allergy (2015)

Food allergy, in particular peanut allergy, is a growing concern in Western countries. The prevalence of allergy to peanut, which currently stands at 1.4%, nearly tripled between 1997 and 2008. Allergic sensitization is a particularly difficult process to study as it is clinically silent. We sought to identify key pathways and mediators critically involved in the induction of allergic sensitization to peanut.Comprehensive metabolomics analysis with liquid chromatography-mass spectrometry was used to detect metabolite changes in mice (C57BL/6) undergoing sensitization. Loss-of-function and gain-of-function studies were performed in mice subjected to two models of peanut sensitization and anaphylaxis that involved either oral or epicutaneous sensitization. Flow cytometric analyses on dendritic cells (DCs) in vitro and in vivo were used to investigate the mechanisms of immune activation.Elevated levels of uric acid (UA) were detected in mice undergoing sensitization as well as in peanut-allergic children who were not challenged with peanut. In mice, the depletion of UA during sensitization prevented the development of peanut-specific immunoglobulins IgE and IgG1 as well as anaphylaxis while exogenous delivery of UA crystals (monosodium urate, MSU) restored the allergic phenotype. Monosodium urate enhanced CD86 and OX40L expression on DCs, independent of Toll-like receptors 2 and 4, the NLRP3 inflammasome, and IL-1β, via a PI3K signaling pathway.Overproduction of the UA alarmin in the local microenvironment plays a critical role in the induction of peanut-allergic sensitization, likely due to its ability to activate DCs. These finding suggest that cellular damage or tissue injury may be an essential requisite for the development of allergic sensitization to foods.