tbuckley/cabot-search huggingface dataset:
CONSERVATION OF HEARING IN INDUSTRY
Authors: C. C. BUNCH
Journal: JAMA (1942)

The consideration of this subject necessitates answers to two questions: 1. Is it generally recognized that hearing losses result from certain industrial hazards? 2. Can anything be done and is anything being done to prevent them?  The first of these must be answered in a qualified negative. Some hazards to hearing are recognized and preventive measures, either direct or indirect, are being taken to eliminate them. Other hazards, because of the peculiar type of hearing loss which they cause, are not being recognized and no concerted action toward conservation has been taken.  Recently an employer was asked what his reaction would be if some one asked permission to test the hearing of his employees. He replied that he preferred to let sleeping dogs lie. A locomotive engineer was asked if he would invite some members of his union to come to the laboratory for hearing tests. No charge was to
Thyroid Hormones in Chronic Renal Failure
Authors: Michael Weissel, H. Krister Stummvoll, Axel Wolf, Heinz Fritzsche
Journal: Annals of Internal Medicine (1977)

Comments and Correction1 May 1977Thyroid Hormones in Chronic Renal FailureMICHAEL WEISSEL, M.D., H. KRISTER STUMMVOLL, M.D., AXEL WOLF, M.D., HEINZ FRITZSCHE, M.D.MICHAEL WEISSEL, M.D.Search for more papers by this author, H. KRISTER STUMMVOLL, M.D.Search for more papers by this author, AXEL WOLF, M.D.Search for more papers by this author, HEINZ FRITZSCHE, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-5-664_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In their recently published paper Spector and associates (1) report on thyroid function and metabolic state in chronic renal failure. In their uremic patients they found low serum 3, 5, 3'-triiodothyronine (T3) and low serum free T3 in contrast to normal free thyroxine (T4) and thyroid-stimulating hormone (TSH) serum levels. Total serum T4 concentrations were in the lower normal range. They point out the similarity of these findings with the results reported for hepatic cirrhosis and various other severe nonthyroidal illnesses in which serum T3 levels are markedly decreased in spite of normal total T4 serum concentrations....References1. SPECTORDAVISHELDERMAN DPJ: Thyroid function and metabolic state in chronic renal failure. Ann Intern Med 85:724-730, 1976 LinkGoogle Scholar2. CHOPRACHOPRASMITH IUS: Reciprocal changes in serum concentrations of 3,3′,5′-triiodothyronine (Reverse T3) and 3,3′, 5′-triiodothyronine (T3) in systemic illnesses. J Clin Endocrinol Metab 41:1043-1049, 1975 CrossrefMedlineGoogle Scholar3. NICODBURGERSTAEHELI PAV: A radioimmunoassay for 3,3′,5′-triiodo-L-thyronine in unextracted serum: method and clinical results. J Clin Endocrinol Metab 42:823-829, 1976 CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThyroid Function in Children on CAPDThyroid Status and Nephron Loss - A study in Patients with Chronic Renal Failure, End Stage Renal Disease and/or on HemodialysisEndocrine System in Acute Renal FailureTSH Response to TRH in Hemodialysis and CAPD PatientsEndocrine and Metabolic Changes Accompanying End-Stage Renal DiseaseThyroidal Status in Uremia - Effects of Hemodialysis and CAPDThyroid function and lipids in patients with chronic renal disease treated by hemodialysis: With comments on the “free thyroxine index” 1 May 1977Volume 86, Issue 5Page: 664-665KeywordsAttentionCirrhosisRenal failureThyroidThyroid hormonesThyroid-stimulating hormoneThyroxineTriiodothyronine Issue Published: 1 May 1977 PDF downloadLoading ...
SP0193 Determinants of disease patterns in vasculitis
Authors: G. Hoffman
Journal: Annals of the Rheumatic Diseases (2013)

Variations in disease patterns are influenced by inborn factors such as genetic background, sex, and ethnicity. It is also clear that acquired life experiences, some of which are common to all (e.g., aging) and some that are unique to individuals (e.g., illnesses, habits, diet, and toxin and environmental exposures), may combine in a stochastic manner to alter tissue and influence vulnerability to injury. Disease vulnerabilities and characteristics are determined not only by who you are at birth, but also by whom you have become. When applied to vascular inflammatory diseases, these variables may be most relevant with regard to regional differences in endothelial cells, subendothelial matrix, vascular smooth muscle, and the response of each to a variety of experiences or injuries. Recovery from injury will, in turn, be dependent on an effective immune response. The response should eliminate the cause of injury and also effectively down-regulate the immune response, so that further injury does not result from the immune response itself. Although it is likely that acquired changes in the vessel wall play a role in determining disease patterns, it is also likely that acquired changes in immune function may be required for disease expression. Certain vasculitides are clearly age- and sex-biased. Age and sex influences may be related to a variety of factors, including changes in hormonal function. To solve the mysteries of disease patterns in vasculitis will require more complete studies of the differences that exist in structure, chemistry, and response to injury of targeted vessels and tissues, compared with sites that are spared. Conducting studies to elucidate gene and protein expression profiles of targeted versus spared sites will be a complex but necessary task. <h3>Disclosure of Interest</h3> None Declared
Development of a novel drug delivery system consisting of an antitumor agent tocopheryl succinate
Authors: Susumu Hama, Satoru Utsumi, Yuki Fukuda, Kayoko Nakayama, Yuriko Okamura, Hiroyuki Tsuchiya, Kenji Fukuzawa, Hedeyoshi Harashima, Kentaro Kogure
Journal: Journal of Controlled Release (2012)
Delayed hypersensitivity due to epidural block with ropivacaine
Authors: John A W Wildsmith
Journal: BMJ (2005)

Managing chronic diseases Palliative care spectrum starts early onEditor-Palliative care does not start when a patient is dying. 1 A whole spectrum of palliation begins from the day of diagnosis of a potentially terminal disease, such as soft tissue sarcoma.Palliation, in the sense of needing to absorb what this means for the patient, becomes even then a medical imperative.The "How long have I got, Doc?" question may not be articulated, but it will be there and needs an empathetic response.Curative treatment is sought, but-with sarcoma-lung metastases signal the end of that phase and the beginning of palliative treatment.The doctor and the patient know the dragon can be disabled but never slain.Palliation is then partnership, working to decide what may be gained at what cost.(This may apply during curative treatment: to take chemotherapy drugs now "just in case," or to keep them for later?)Palliative treatment can be long (in sarcoma up to 20 years or more), or it can be brief.Its ending is not solely a medical judgment.Doctors may decide they can do no more, but active patients use online support groups, seeking new treatment options across the world.Patients may decide to end palliative treatment.Grown weary of painful chemotherapy offering diminishing returns, they may prefer a shorter but better life.Making that choice together is an aspect of palliation.When death is near, palliative care becomes terminal care.If throughout doctors and patients have aligned their understanding of the disease, and have taken decisions jointly, have explored the holistic meaning of disease in life and death, the palliative spectrum may offer healing if not cure.If, however, being palliative begins only when the patient is dying doctors cannot then meet patients, where they are most needed, in the ground of their being and their not being.
Mapping Antibody Epitopes of the Avian H5N1 Influenza Virus
Authors: Hui-Ling Yen, J. S. Malik Peiris
Journal: PLoS Medicine (2009)

JSMP is a co-author of one of the studies, cited as reference [25], discussed in this Perspective.



The authors' research is supported by the Area of Excellence Scheme of the University Grants Committee (Grant AoE/M-12/06), Hong Kong. The funder played no role in the decision to submit this article or in its preparation.



Provenance: Commissioned; not externally peer reviewed
Abstract 4419: The role of ABC transporters in PhIP-induced colon carcinogenesis
Authors: Selvi Durmus, M.A. van der Valk, S.F. Teunissen, Els Wagenaar, Jos Beijnen, Alfred H. Schinkel
Journal: Cancer Research (2012)

Abstract ABC transporters such as BCRP, P-gp, Mrp2 and Mrp3 are thought to protect organisms from xenobiotics, including dietary carcinogens and anticancer drugs. These multidrug transporters reduce the oral uptake, systemic availability and tissue or cellular accumulation of transported substrates by mediating their extrusion from cells and the body in general. Therefore, they could have very important roles in the distribution of carcinogens to certain tissues and cell types, and carcinogen susceptibility. In this study, we aimed to investigate the role of ABC transporters in the tumorigenicity of a dietary carcinogen, PhIP (2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine), which is produced during high-temperature cooking of meat. We have performed a pharmacokinetic experiment in wild-type FVB and ABC transporter knockout strains (Bcrp;Mrp2;Mrp3-/- and Bcrp;Mdr1a/1b;Mrp2-/-) with 200 mg/kg orally administered PhIP and observed that ABC transporters have an impact on the distribution of PhIP metabolites to several organs. There was an accumulation of N-OH-PhIP, a potentially carcinogenic metabolite, in the liver of Bcrp;Mrp2;Mrp3-/- mice and a decrease in the levels of PhIP-5-sulfate, a surrogate marker for DNA exposure to reactive compound, in small intestine of Bcrp;Mrp2;Mrp3-/- and Bcrp;Mdr1a/1b;Mrp2-/- mice compared to wild-type FVB. For carcinogenesis experiments, we used a chemically-induced colon carcinogenesis model where wild-type FVB and ABC transporter compound knock-out mice received a single, oral administration of 200 mg/kg PhIP for initiation and seven days administration of Dextran Sodium Sulfate (DSS) in drinking water for promotion of the tumorigenesis process via colonic inflammation. During the whole experiment, mice were closely checked for their body weight loss, diarrhea and rectal bleeding. Our results showed that PhIP and DSS treatment together induced colonic tumors in all strains over 180 days. No tumor formation could be found in only PhIP-treated, only DSS-treated and negative control groups that received vehicle. Tumor incidence was lower in both knock-outs compared to the wild-type FVB when inflammation levels between the groups were corrected. Our results suggest that these ABC transporters are not protecting the intestinal tract from PhIP-induced carcinogenesis upon oral ingestion in mice, and perhaps even partially enhance PhIP-induced carcinogenesis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4419. doi:1538-7445.AM2012-4419
Intrahepatic cholangiocarcinoma with predominant ductal plate malformation pattern
Authors: Ji-Young Choe, Haeryoung Kim
Journal: Clinical and Molecular Hepatology (2014)

Cholangiocarcinoma arising in the liver can be classified into intrahepatic (or peripheral) cholangiocarcinoma (ICC) or perihilar cholangiocarcinoma, depending on the topographic location of the tumor along the intrahepatic biliary tree.1 Grossly, peripheral ICC usually presents as a mass-forming type, while perihilar ICC may present as mass-forming, periductal infiltrating, or intraductal-growth types. Histologically, ICC is heterogeneous: while the majority of ICC present predominantly as a mucin-producing adenocarcinoma, some tumors take the form of a cholangiolocellular carcinoma (CCC), and others demonstrate mixtures of these components within the tumor.

Recently, Nakanuma et al proposed a new subtype of ICCs resembling the histologic features of ductal plate malformation (DPM).2 DPM is a developmental anomaly in which the fetal ductal plate persists after birth, and is found mainly in congenital or various acquired hepatobiliary diseases.3 ICC with DPM pattern is histologically characterized by irregular and tortuous glandular structures with bridge formation, biliary cell projections into the lumens, and intraluminal tumor cells.2 The histopathologic findings of ICC with predominant DPM pattern are discussed, based on the following case which we recently encountered.
Trial of three-day and ten-day courses of amoxycillin in otitis media.
Authors: D M Chaput de Saintonge, D F Levine, I T Savage, G W Burgess, J Sharp, S R Mayhew, M G Sadler, R Moody, R Griffiths, S Griffiths, G Meadows
Journal: BMJ (1982)

A randomised double-blind controlled trial compared three-day and 10-day courses of amoxycillin (25 mg/kg daily) in children with otitis media. Seventeen doctors from five centres admitted 84 children between the ages of 2 and 10 years. Symptoms and signs were measured on admission to the trial, on day 3, and on day 15. Mother9s observations were recorded daily for 10 days. Audiograms were performed at four and 12 weeks after the end of the trial. The treatment groups showed little difference in the speed of resolution of symptoms and signs, the numbers of primary treatment failures, or the frequency of recurrent ear infections. There were no complications in either group. Most children with otitis media can probably be successfully and safely treated with no more than a three-day course of amoxycillin providing their progress is reviewed about the fifth or sixth day after treatment started. This policy could save over 1 million pounds annually in antibiotic costs.
The Resistance Vasculature.
Authors: C. SALDANHA
Journal: Cardiovascular Research (1993)

Journal Article The Resistance Vasculature. Get access CLYDE SALDANHA CLYDE SALDANHA London, United Kingdom Eds. John Bevan, William Halpern, and Michael Mulvany. (Pp 467; $99.5.) Totowa: Humana Press, 1991. ISBN 0-89603-2 12-4. Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 27, Issue 1, January 1993, Pages 143–144, https://doi.org/10.1093/cvr/27.1.143a Published: 01 January 1993
Infection Prevention in Acute Nonlymphocytic Leukemia
Authors: STEPHEN C. SCHIMPFF
Journal: Annals of Internal Medicine (1975)

Reverse isolation and prophylactic oral nonabsorbable antibiotics were evaluated among 64 consecutive noninfected adults with acute nonlymphocytic leukemia admitted for remission induction. Patients were randomly allocated to laminar air flow room reverse isolation with oral nonabsorbable antibiotics (LAF + A), routine hospital ward care with antibiotics (W + A), or ward care alone (W). The LAF + A patients had a significantly decreased incidence of total infection, bacteremias, pneumonias, rectal abscesses, urinary tract infection, and pharyngitis. Infectious deaths were reduced in the LAF + A group and the time to the first infection or to fatal infection was delayed. The W + A patients who regularly ingested the antibiotics had a reduction in infections similar to that of the LAF + A patients but those who could not tolerate the antibiotics had an incidence of infection comparable to the ward patients. The LAF + A and the W + A patients also had higher complete remission rates and longer median survival than the unprotected ward patients.
Excitatory Projection Neuron Subtypes Control the Distribution of Local Inhibitory Interneurons in the Cerebral Cortex
Authors: Simona Lodato, Caroline Rouaux, Kathleen B. Quast, Chanati Jantrachotechatchawan, Michèle Studer, Takao K. Hensch, Paola Arlotta
Journal: Neuron (2011)
Thymic stromal lymphopoietin–elicited basophil responses promote eosinophilic esophagitis
Authors: Mario Noti, Elia D.Tait Wojno, Brian S. Kim, Mark C. Siracusa, Paul R. Giacomin, Meera G. Nair, Alain J. Benitez, Kathryn R. Ruymann, Amanda B. Muir, David A. Hill, Kudakwashe R. Chikwava, Amin E. Moghaddam, Quentin J. Sattentau, Aneesh Alex, Chao Zhou, Jennifer H. Yearley, Paul Menard-Katcher, Masato Kubo, Kazushige Obata-Ninomiya, Hajime Karasuyama, Michael R. Comeau, Terri Brown-Whitehorn, Rene De Waal Malefyt, Patrick M. Sleiman, Hakon Hakonarson, Antonella Cianferoni, Gary W. Falk, Mei Lun Wang, Jonathan M. Spergel, David Artis
Journal: Nature Medicine (2013)
UNUSUAL FEATURES OF SCABIES ASSOCIATED WITH TOPICAL FLUORINATED STEROIDS
Authors: A. L. MACMILLAN
Journal: British Journal of Dermatology (1972)

Journal Article UNUSUAL FEATURES OF SCABIES ASSOCIATED WITH TOPICAL FLUORINATED STEROIDS Get access A. L. MACMILLAN A. L. MACMILLAN Addenbrooke's Hospital, Cambridge Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 87, Issue 5, 1 November 1972, Pages 496–497, https://doi.org/10.1111/j.1365-2133.1972.tb01597.x Published: 01 November 1972 Article history Accepted: 18 May 1972 Published: 01 November 1972
Conference
Authors: G. Gregoratos, M. D. Cheitlin, A. Conill, A. E. Epstein, C. Fellows, T. B. Ferguson, R. A. Freedman, M. A. Hlatky, Gerald Naccarelli, S. Saksena, R. C. Schlant, M. J. Silka
Journal: Journal of the American College of Cardiology (1998)
Role of β <sub>2</sub> Adrenergic Receptors in Human Atherosclerotic Coronary Arteries
Authors: Emanuele Barbato, Federico Piscione, Jozef Bartunek, Gennaro Galasso, Plinio Cirillo, Giuseppe De Luca, Guido Iaccarino, Bernard De Bruyne, Massimo Chiariello, William Wijns
Journal: Circulation (2005)

Adrenergic regulation of coronary vasomotion is balanced between alpha1-adrenergic-mediated (alpha1-AR) constriction and beta2-adrenergic-mediated (beta2-AR) relaxation. This study aimed at assessing the role of beta2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries.During intracoronary (IC) infusion of increasing doses of the beta2-AR agonist salbutamol (0.15, 0.3, and 0.6 mug/min) and the endothelial vasodilator acetylcholine (1, 3, and 10 microg/min), we measured (1) changes in lumen diameter (LD) by quantitative coronary angiography in 34 normal, 55 mildly atherosclerotic, and 42 stenotic coronary artery segments and (2) changes in average peak velocity (APV) and coronary blood flow (CBF) with the use of Doppler flow wire in 11 normal, 10 mildly atherosclerotic, and 11 stenotic coronary arteries. In 6 of 11 stenotic coronary arteries, the protocol was repeated after an IC bolus (12 microg/kg) of the alpha-adrenergic blocker phentolamine. In 6 of 11 normal coronary arteries, the protocol was repeated after an IC infusion (60 micromol/min) of N(G)-monomethyl-L-arginine (L-NMMA), a nitric oxide inhibitor. Neither salbutamol IC infusion nor acetylcholine significantly changed heart rate or blood pressure, whereas L-NMMA slightly increased blood pressure. In normal coronary arteries, salbutamol increased LD (LD max %: 11+/-2, P<0.05), APV (APV max %: 53+/-17, P<0.05), and CBF (CBF max %: 57+/-17, P<0.05), whereas L-NMMA caused a blunted APV (APV max %: 27+/-6, P<0.05) and CBF (CBF max %: 29+/-6, P<0.05) response to salbutamol. In mildly atherosclerotic coronary arteries, the salbutamol increase in LD (LD max %: 10+/-2, P<0.05), APV (APV max %: 33+/-12, P<0.05), and CBF (CBF max %: 37+/-12, P<0.05) was preserved. In stenotic coronary arteries, salbutamol induced a paradoxical reduction in LD (LD max %: -6+/-2, P<0.05), APV (APV max %: -15+/-9, P<0.05), and CBF (CBF max %: -15+/-6, P<0.05), which was no longer observed after phentolamine. Acetylcholine increased LD (LD max %: 14+/-3, P<0.05), APV (APV max %: 61+/-20, P<0.05), and CBF (CBF max %: 67+/-19, P<0.05) in normal coronary arteries. In mildly atherosclerotic coronary arteries, acetylcholine induced a significant reduction in LD (LD max %: -15+/-2, P<0.05) and no changes in APV (APV max %: -6+/-13, P=NS) and CBF (CBF max %: -10+/-13, P=NS). In stenotic coronary arteries, acetylcholine significantly reduced LD (LD max %: -15+/-3, P<0.05), APV (APV max %: -15+/-9, P<0.05), and CBF (CBF max %: -15+/-6, P<0.05).In severely atherosclerotic coronary arteries, beta2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.
THE TREATMENT OF EMPYEMA OF THE FRONTAL SINUS.
Authors: J. H. BRYAN
Journal: JAMA (1898)

In accepting your invitation to open the discussion on this most important and interesting subject, I feel that I can not do better than first to call your attention to a few of the anatomic peculiarities of the frontal sinuses, in order that the pathology and treatment of chronic suppurative inflammations of these cavities can be the better understood. The size of the frontal sinuses varies greatly in different subjects, and frequently in the same subject the variation is very marked, one cavity occasionally being quite large while the other is many times smaller, or absent altogether. After an examination of 120 skulls made by Herbert Tilley<sup>1</sup>he considers a sinus normal when it measures 28 mm. from the median line outward to about the junction of the inner and middle third of the supraorbital ridge; and in vertical extent measured from the root of the nose from 20
Non‐Hodgkin disease in β‐thalassemia major
Authors: Zaher K. Otrock, Ali I. Shamseddine, Ali T. Taher*
Journal: American Journal of Hematology (2005)

Abstract Thalassemia is a spectrum of diseases characterized by the decrease or absence of globin chains. The occurrence of lymphoma in thalassemia has rarely been reported, and our review of the English literature revealed only four cases. Because anemia is always masked by regular transfusions in thalassemic patients, physicians discover a hidden malignancy late in the course of the disease. We hereby report the case of a thalassemic patient developing non‐Hodgkin disease and discuss the possibility of a link between the two disease entities. This case is intended to alert physicians of the possibility of a malignancy in thalassemia patients. Am. J. Hematol. 81:62–64, 2006. © 2005 Wiley‐Liss, Inc.
δ-Catenin aids angiogenesis
Authors: Amy Maxmen
Journal: The Journal of Experimental Medicine (2010)

![Figure][1] 

Vascular endothelial cells (green) express δ -catenin (red).



By lessening the level of a protein, [DeBusk et al.][2] bring pathological angiogenesis to a halt.

Formerly known only for its effects on neuronal growth, the protein δ-catenin is now found to be highly expressed
Solitary Necrotic Nodule With Larval Infestation in the Liver on F-18 FDG PET/CT
Authors: Chao-Jung Chen, Shih-Cheng Chou, His-Jung Chen, Hong-Yaw Chen
Journal: Clinical Nuclear Medicine (2010)

We present the case of a 64-year-old woman who suffered from occasional right upper abdominal pain for several months. Both abdominal ultrasonography and magnetic resonance imaging showed a hepatic mass of indeterminate nature. F-18 FDG PET/CT showed a solitary hypermetabolic mass in the liver; a malignancy was therefore suspected. Her hepatic tumor was resected; it was a solitary necrotic nodule with larval infestation but no evidence of malignancy.