tbuckley/cabot-search huggingface dataset:
Inhaled nitric oxide therapy in neonates and children: reaching a European consensus
Authors: Duncan J. Macrae, David Field, Jean-Christophe Mercier, Jens Møller, Tom Stiris, Paolo Biban, Paul Cornick, Allan Goldman, Sylvia Göthberg, Lars E. Gustafsson, Jürg Hammer, Per-Arne Lönnqvist, Manuel Sanchez-Luna, Gunnar Sedin, Nim Subhedar
Journal: Intensive Care Medicine (2004)
CEREBELLAR VASOREACTIVITY IN STROKE PATIENTS WITH CROSSED CEREBELLAR DIACHISIS ASSESSED BY ACETAZOLAMIDE AND Tc-99m HMPAO SPECT
Authors: S E Kim, B-W Yoon, H I Yang, D S Lee, J-K Chung, J K Roh, M C Lee, C-S Koh
Journal: Clinical Nuclear Medicine (1993)

Kim, S E; Yoon, B-W; Yang, H I; Lee, D S; Chung, J-K; Roh, J K; Lee, M C; Koh, C-S Author Information
PSYCHIATRIC DISORDERS AND MYXEDEMA
Authors: FERRIS N. PITTS, SAMUEL B. GUZE
Journal: American Journal of Psychiatry (1961)

A brief survey of the literature on psychiatric symptoms in myxedema is followed by 3 case reports demonstrating that "Myxedema Madness" may present as seemingly specific organic or functional psychoses, and that psychiatric care may prove vital in the management of these patients. The successful use of EST in psychiatric symptoms resistent to thyroid substitution in myxedema is reported. The further evaluation of EST in this circumstance is suggested.
Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group.
Authors: A B Newman, D S Siscovick, T A Manolio, J Polak, L P Fried, N O Borhani, S K Wolfson
Journal: Circulation (1993)

Peripheral arterial disease measured noninvasively by the ankle-arm index (AAI) is common in older adults, largely asymptomatic, and associated with clinically manifest cardiovascular disease (CVD). The criteria for an abnormal AAI have varied in previous studies. To determine whether there is an inverse dose-response relation between the AAI and clinical CVD, subclinical disease, and risk factors, we examined the relation of the AAI to cardiovascular risk factors, other noninvasive measures of subclinical atherosclerosis using carotid ultrasound, echocardiography and electrocardiography, and clinical CVD.The AAI was measured in 5084 participants > or = 65 years old at the baseline examination of the Cardiovascular Health Study. All subjects had detailed assessment of prevalent CVD, measures of cardiovascular risk factors, and noninvasive measures of disease. Participants were stratified by baseline clinical CVD status and AAI (< 0.8, > or = 0.8 to < 0.9, > or = 0.9 to < 1.0, > or = 1.0 to < 1.5). Analyses tested for a dose-response relation of the AAI with clinical CVD, risk factors, and subclinical disease. The cumulative frequency of a low AAI was 7.4% of participants < 0.8, 12.4% < 0.9, and 23.6% < 1.0. participants with an AAI < 0.8 were more than twice as likely as those with an AAI of 1.0 to 1.5 to have a history of myocardial infarction, angina, congestive heart failure, stroke, or transient ischemic attack (all P < .01). In participants free of clinical CVD at baseline, the AAI was inversely related to history of hypertension, history of diabetes, and smoking, as well as systolic blood pressure, serum creatinine, fasting glucose, fasting insulin, measures of pulmonary function, and fibrinogen level (all P < .01). Risk factor associations with the AAI were similar in men and women free of CVD except for serum total and low-density lipoprotein cholesterol, which were inversely associated with AAI level only in women. Risk factors associated with an AAI of < 1.0 in multivariate analysis included smoking (odds ratio [OR], 2.55), history of diabetes (OR, 3.84), increasing age (OR, 1.54), and nonwhite race (OR, 2.36). In the 3372 participants free of clinical CVD, other noninvasive measures of subclinical CVD, including carotid stenosis by duplex scanning, segmental wall motion abnormalities by echocardiogram, and major ECG abnormalities were inversely related to the AAI (all P < .01).There was an inverse dose-response relation of the AAI with CVD risk factors and subclinical and clinical CVD among older adults. The lower the AAI, the greater the increase in CVD risk; however, even those with modest, asymptomatic reductions in the AAI (0.8 to 1.0) appear to be at increased risk of CVD.
Superoxide generation and reversal of acetylcholine-induced cerebral arteriolar dilation after acute hypertension.
Authors: E P Wei, H A Kontos, C W Christman, D S DeWitt, J T Povlishock
Journal: Circulation Research (1985)

The appearance of superoxide anion radical in cerebral extracellular space during and after acute hypertension induced by intravenous norepinephrine was investigated in anesthetized cats equipped with cranial windows. Superoxide was detected by demonstrating the presence of superoxide dismutase-inhibitable reduction of nitroblue tetrazolium. The superoxide dismutase-inhibitable rate of reduction of nitroblue tetrazolium was 4.1 +/- 1.61 nM/min per cm2 during hypertension and 4.55 +/- 0.62 nM/min per cm2 one hour after hypertension had subsided. During norepinephrine administration in the absence of hypertension, the superoxide dismutase-inhibitable rate of reduction of nitroblue tetrazolium was 0.44 +/- 0.17 nM/min per cm2. The reduction of nitroblue tetrazolium during hypertension was also inhibited by prior treatment of the brain surface with phenylglyoxal at pH 10, to induce irreversible inhibition of the anion channel. The results show that acute hypertension is associated with the generation of superoxide which enters the extracellular space of the brain via the anion channel. Following hypertension, the sustained vasodilation caused by acute hypertension was inhibited significantly by topical application of superoxide dismutase and catalase, showing that it was due in part to superoxide and other radicals derived from it. The vasodilator response of cerebral arterioles to topical acetylcholine was converted to vasoconstriction following acute hypertension, and restored to vasodilation following topical application of superoxide dismutase and catalase. The results show that superoxide and other radicals generated after acute hypertension interfere with acetylcholine-induced endothelium-dependent vasodilation, probably because they destroy the endothelium-derived relaxant factor.
PREVALENCE AND RISK FACTORS FOR ACUTE OCCLUSIVE ARTERIAL INJURY FOLLOWING PEDIATRIC CARDIAC CATHETERIZATION IN THE MODERN ERA AT A LARGE VOLUME CENTER
Authors: Andrew C. Glatz, Diana Geisser, Ann L. McCarthy, Kaitlyn Daniels, Matthew Gillespie, Brian Hanna, Samir S. Shah, Jonathan Rome
Journal: Journal of the American College of Cardiology (2012)
Amyloid vascular disease: cord-like thickening of mucocutaneous arteries, intermittent claudication and angina in a case with underlying myelomatosis
Authors: S. M. BREATHNACH, G. C. WELLS
Journal: British Journal of Dermatology (1980)

SUMMARY A patient with established myelomatosis and an IgG paraproteinaemia presented with intermittent claudication. Indurated cord-like structures were noted on the dorsum of the right hand and the buccal surface of the lower lip, and biopsy of the hand lesion revealed massive amyloid deposition within the wall of an artery. Cord-like thickening of mucocutaneous arteries as a presenting sign of systemic amyloidosis in the absence of glossomegaly or other cutaneous lesions has not been reported previously. The presence of intermittent claudication and angina suggested that amyloid involvement of large arteries was extensively distributed.
Lymphokine-activated killer cell phenomenon. II. Precursor phenotype is serologically distinct from peripheral T lymphocytes, memory cytotoxic thymus-derived lymphocytes, and natural killer cells
Authors: EA Grimm, KM Ramsey, A Mazumder, DJ Wilson, JY Djeu, SA Rosenberg
Journal: The Journal of Experimental Medicine (1983)

Culture of human peripheral blood lymphocytes (PBL) in partially purified and lectin-free interleukin 2 results in the generation of cytotoxic effector cells which have the unique property of lysing natural killer (NK)-resistant fresh human tumor cells. We have termed these effector cells "lymphokine- activated killer" cells (LAK). LAK are generated from both normal and cancer patients' PBL and are able to lyse both autologous and allogeneic tumor cells from all histologic tumor types tested. Our previous studies suggested that the LAK phenomenon was distinct from either the cytotoxic thymus-derived lymphocyte (CTL) or NK systems based on a variety of criteria. This study reports that the cell type involved is also distinct, as determined by phenotypic characteristics. The LAK effector cell phenotype was analyzed in parallel with alloimmune CTL, and LAK were found to be similarly susceptible to the monoclonal anti-T cell antibodies OKT-3 or OKT-8 plus complement. In contrast the LAK precursor was not susceptible to the OKT-3 or Leu-1 antibodies plus complement, while the ability to generate alloimmune CTL was totally obliterated when tested using the same PBL responder population; in fact, generation of LAK was found to be augmented five- to sixfold, clearly suggesting that LAK precursor cells are not T lymphocytes as defined by these antibodies. LAK precursors were found to be abundant in NK cell-enriched Percoll gradient fractions, which had been depleted of the 29 degrees C E- rosetting "high affinity" T cells. However, LAK precursors were found to be distinct from the majority of NK cells since lysis of fresh PBL with the monoclonal antibodies OKM-1, Leu-7, or OKT-11 significantly depleted or totally eliminated NK activity, while subsequent activation of the remaining cells generated high levels of LAK and in some cases augmented levels of LAK. LAK precursors were found to be distributed in the thymus, bone marrow, spleen, lymph node, and thoracic duct in addition to the PBL. Therefore, while the cell(s) responsible for activation and expression of LAK activity have some common features with the classic T cell-mediated CTL and NK cell systems, the LAK precursor cells are clearly distinct as determined by phenotype analysis using monoclonal antibodies and complement, and at present must be classified as a "null" cell.
Vitamin D modulates aromatase expression in human macrophages and downregulates proinflammatory cytokine production via ERK/MAPK signaling.
Authors: B Villaggio, S Soldano, M Cutolo
Journal: Annals of the Rheumatic Diseases (2012)

<h3>Background and objectives</h3> Vitamin D<sub>3</sub> (calcitriol) was found to downregulate innate immune response in human macrophages and showing immune-modulatory effects1. Gender-linked differences in serum levels of sex hormones and their peripheral metabolites play an important role in the neuroendocrine immune/inflammatory response also in monocyte/macrophage cells2. This in vitro study evaluated the effects of calcitriol on the expression and the activity of the aromatase involved in estrogen production in cultures of human macrophages and its possible ability to modulate the production of the proinflammatory cytokines (IL-1β, IL-6 and tumour necrosis factor α (TNFα)) involved in the innate immunity response. <h3>Materials and methods</h3> Cultures of human THP-1 were activated to macrophages by interferon γ (IFNγ) (500 U/ml) and treated for 24 h with calcitriol (10<sup>−8</sup>M) and 17β-estradiol (E<sub>2</sub>, 10<sup>−8</sup>M) alone and in combination.Untreated macrophages (THP-1-activated) were used as controls (cnt). P450-aromatase synthesis was evaluated by immunocytochemistry (ICC) and western blotting (WB), whereas the expression of the related CYP19A1 gene was quantified by Real-Time PCR (RT-PCR). IL-1β, IL-6 and TNFα synthesis was analysed by enzyme immunoassay (ELISA) and WB. The signal transduction pathway of mitogen activated proteins ERK1/2 was evaluated by WB. <h3>Results</h3> P450-aromatase synthesis and related CYP19A1 mRNA expression were found significantly downregulated by calcitriol in presence of E<sub>2</sub> (p&lt;0.001 vs E<sub>2</sub>-treated cells). The IL-1β, IL-6 and TNFα production decreased in the THP-1-activated macrophages treated with calcitriol with and without E<sub>2</sub> (p&lt;0.001 in calcitriol alone vs cnt and in calcitriol/E<sub>2</sub> vs E<sub>2</sub> for all cytokines). The data were obtained by ELISA and confirmed by WB. Interestingly, calcitriol decreased ERK1/2 phosphorilation both alone (vs cnt) and in presence of E2 (vs E2-treated cells) reducing the ERK pathway activation, as observed by WB. <h3>Conclusions</h3> Our data suggest that calcitriol downregulated the aromatase expression, involved in the production of estrogens, and decreased proinflammatory cytokine production by human macrophages. These downregulatory effects of calcitriol were found to correlate with the reduction in phosphorilation of ERK pathway. These results suggest a possible role of calcitriol on innate immunity of human macrophage that drive the inflammatory processes in RA and its anti-inflammatory and immunosuppressive intracrine activity.
The Oxford Medical Companion
Authors: C. R Scriver
Journal: BMJ (1995)

Ed John Walton, Jeremiah A Barondess, Stephen Lock Oxford University Press, £40, pp 1038 ISBN 0 19 262355 9

The first edition of the Oxford Medical Companion was published in two volumes to positive reviews in, among others, the Lancet, New England Journal of Medicine, Nature, and Times Literary Supplement. The BMJ did not review it. The first edition provided definitions and facts (over 5000 entries); was a dictionary of brief international medical biographies (none of the 1000-odd subjects …
Fate of nonflow-limiting dissections after treatment with iridium-192 therapy: results from the GAMMA I and II trials
Authors: Kazuyuki Shirai, Alexandra J. Lansky, Costantino Costantini-Ortiz, Maria Corral, Nishe Dave, Lubbe F. Dieter, Peter B. Berger, Kartik Desai, Martin B. Leon
Journal: Journal of the American College of Cardiology (2002)
The Plot Against the Patient
Authors: G. L. Fite
Journal: JAMA (1967)

Here we go again. The a cappella choir of<i>The Plot</i>sings<i>l'allegro</i>about the modern barber surgeons who conspire against the patient for the sake of his money and without sincere regard for his health. The ending,<i>il penseroso</i>, is the plea for the total welfare state in medicine. Ho hum. For more than 300 pages the book repeats all the shoddy history of the American Medical Association, the private health insurance scandal, the shocking sink tests run by the best hospitals, and the burial of the hospital's and the physician's mistakes. The situation is dreadful, including the "huge publications projects centered about the<i>AMA Journal...</i>" In lucid English this book has quoted condemnatory records of the past generation or more, indicting American medicine, and occasionally praising foreign medicine as better than that in the United States. Taking the book at its face value, it is necessary to conclude
Regulation of B cell lymphomagenesis by a malignant Qal+ inducer T cell clone.
Authors: C L Reinisch, A P Sing, E R Bacon, R B Corley, R K Gershon
Journal: The Journal of Experimental Medicine (1984)

A series of Thy-1.2+ Ly-1+ Qa-1+ malignant T cell clones have been isolated from murine sarcoma virus-murine leukemia-Moloney (MSV-MuLV-M)-induced B cell lymphomas or from MSV-MuLV-M-infected B6 mice. These T cell clones enhance both antigen-independent and -dependent lymphocyte differentiation and function. They also induce the differentiation of granulocytes and erythrocytes in the stem cell compartment, a function that parallels the immunopathology of the disease in vivo. The malignant T cell appears to sustain B lymphoma growth in vivo by releasing a factor (BCGF) that promotes B cell proliferation.
831-5 Increased thermal heterogeneity of the culprit lesion is prolonged in patients with recent myocardial infarction: The role of inflammation
Authors: Konstantinos Toutouzas, Sophia Vaina, John Mitropoulos, Eleftherios Tsiamis, Manolis Vavuranakis, Konstantinos Tsioufis, Christos Pitsavos, Irini Bosinakou, Christodoulos Stefanadis
Journal: Journal of the American College of Cardiology (2004)
Environmental medicine in Germany--a review.
Authors: Hans Joachim Seidel
Journal: Environmental Health Perspectives (2002)

In this review I describe the development of environmental medicine as a specialized field of clinical medicine in Germany. New scientific societies were founded, based on traditions of public hygiene and occupational medicine, as a reaction to environmental issues concerning human health. Environmental medicine issues were also addressed by independent "critical" physicians. The first institutions to accept patients were centers for environmental medicine affiliated with research institutions and/or with the public health service. Medical professional organizations, particularly the German General Medical Council, described the need for and formulated conditions for additional qualification for doctors in environmental medicine, including a 200-hr course. This course and a qualifying exam were passed by about 3,000 doctors, mainly from the public health service and from occupational medicine. Unfortunately, few general physicians in primary outpatient care were similarly trained. To date, no representative study has been conducted on environmental patients, but I include in this review a typical list of patients' complaints. I also summarize research activities typical for environmental medicine in Germany. Present problems concern accounting systems and, for example, diagnosis and treatment of patients with multiple chemical sensitivities (MCS). A coordinated research program on MCS has been started.
Erratum to “Amniotic liquid derived stem cells as reservoir of secreted angiogenic factors capable of stimulating neo-arteriogenesis in an ischemic model” [Biomaterials 32 (2011) 3689–3699]
Authors: Teodelinda Mirabella, Michele Cilli, Sebastiano Carlone, Ranieri Cancedda, Chiara Gentili
Journal: Biomaterials (2012)
Review: Blood pressure–lowering treatments reduce CV morbidity and mortality in patients receiving dialysis
Authors: John Harnett
Journal: Annals of Internal Medicine (2009)

Source Citation Heerspink HJ, Ninomiya T, Zoungas S, et al. Effect of lowering blood pressure on cardiovascular events and mortality in patients on dialysis: a systematic review and meta-analysis of randomised controlled trials. Lancet. 2009;373:1009-15. 19249092
IL-28B/IFN-λ3 Drives Granzyme B Loading and Significantly Increases CTL Killing Activity in Macaques
Authors: Matthew P Morrow, Jian Yan, Panyupa Pankhong, Devon J Shedlock, Mark G Lewis, Kendra Talbott, Roberta Toporovski, Amir S Khan, Niranjan Y Sardesai, David B Weiner
Journal: Molecular Therapy (2010)

Type III/lambda interferons (IFNs) were discovered less than a decade ago and are still in the process of being characterized. Although previous studies have focused on the function of IFN-lambda 3 (also known as interleukin (IL)-28B) in a small animal model, it is unknown whether these functions would translate to a larger, more relevant model. Thus in the present study, we have used DNA vaccination as a method of studying the influence of IFN-lambda 3 on adaptive immune responses in rhesus macaques. Results of our study show for the first time that IFN-lambda 3 has significant influence on antigen-specific CD8(+) T-cell function, especially in regards to cytotoxicity. Peripheral CD8(+) T cells from animals that were administered IFN-lambda 3 showed substantially increased cytotoxic responses as gauged by CD107a and granzyme B coexpression as well as perforin release. Moreover, CD8(+) T cells isolated from the mesenteric lymph nodes (MLN) of animals receiving IFN-lambda 3 loaded significant amounts of granzyme B upon extended antigenic stimulation and induced significantly more granzyme B-mediated cell death of peptide pulsed targets. These data suggest that IFN-lambda 3 is a potent effector of the immune system with special emphasis on CD8(+) T-cell killing functions which warrants further study as a possible immunoadjuvant.
Tricuspid Atresia With Atrial Septal Defect, Ventricular Septal Defect, and Right Ventricular Hypoplasia Demonstrated by Multidetector Computed Tomography
Authors: Teruhito Mochizuki, Takashi Ohtani, Hiroshi Higashino, Yoshifumi Sugawara, Takaharu Tsuda, Michihito Sekiya, Masao Miyagawa, Kenji Ohmoto, Junpei Ikezoe
Journal: Circulation (2000)
Review: Tiotropium does not increase risk for cardiovascular events in chronic obstructive pulmonary disease
Authors: Matthew B. Stanbrook
Journal: Annals of Internal Medicine (2010)

ACP Journal Club20 July 2010Review: Tiotropium does not increase risk for cardiovascular events in chronic obstructive pulmonary diseaseMatthew B. Stanbrook, MD, PhDMatthew B. Stanbrook, MD, PhDUniversity Health Network, University of Toronto, Toronto, Ontario, Canada (M.B.S.)Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-153-2-201007200-02002 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationCelli B, Decramer M, Leimer I, et al. Cardiovascular safety of tiotropium in patients with COPD. Chest. 2010;137:20-30. https://pubmed.ncbi.nlm.nih.gov/19592475Clinical Impact RatingsGIM/FP/GP: Cardiology: Pulmonology: References1 Singh S, Loke YK, Furberg CD. Inhaled anticholinergics and risk of major adverse cardiovascular events in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis. JAMA. 2008;300:1439-50. [PMID: 18812535] Google Scholar2 Tashkin DP, Celli B, Senn S, et al. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med. 2008;359:1543-54. [PMID: 18836213] Google Scholar3 Lee TA, Pickard AS, Au DH, Bartle B, Weiss KB. Risk for death associated with medications for recently diagnosed chronic obstructive pulmonary disease. Ann Intern Med. 2008;149:380-90. [PMID: 18794557] Google Scholar4 Global Initiative for Chronic Obstructive Lung Disease. Global strategy for diagnosis, management and prevention of COPD. December 2009. www.goldcopd.org/Guidelineitem.asp?l1=2&l2=1&intId=2003 (accessed 7 May 2010). Google Scholar Author, Article, and Disclosure InformationAuthors: Matthew B. Stanbrook, MD, PhDAffiliations: University Health Network, University of Toronto, Toronto, Ontario, Canada (M.B.S.)This article was published at Annals.org on 6 July 2010. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetailsSee AlsoRecent use of ipratropium bromide increased risk for cardiovascular events in chronic obstructive pulmonary disease Matthew B. Stanbrook Metrics 20 July 2010Volume 153, Issue 2Page: JC1-2KeywordsAdverse eventsBronchodilatorsCardiovascular disease riskChronic obstructive pulmonary diseaseDatabasesMyocardial infarctionPulmonary medicineSafetySafety studiesThorax ePublished: 20 July 2010 Issue Published: 20 July 2010 Copyright & PermissionsCopyright © 2010 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
LIPOIDS AS THE GROWTH-INHIBITING FACTOR IN SERUM
Authors: Lillian E. Baker, Alexis Carrel
Journal: The Journal of Experimental Medicine (1925)

The growth-inhibiting action of serum has been shown to be due largely to the lipoids. Serum from which the lipoids have been removed is much less inhibiting to the growth of fibroblasts in vitro than is the original serum, and only slightly more inhibiting than Tyrode solution. The lipoids extracted from the serum are toxic and more inhibiting to the growth of fibroblasts than the original serum. Lipoids extracted from chicken brain, chicken liver, egg, and embryonic tissue have likewise an inhibiting action.