tbuckley/cabot-search huggingface dataset:
Formaldehyde Sensitivity and Toxicity
Authors: David L. Morris
Journal: JAMA (1981)

<h3>To the Editor.—</h3> Regarding the article, "Toxicology of Urea Formaldehyde and Polyurethane Foam Insulation" inThe Journal(1981;245:243), I have studied the problem in patients I have seen in my allergy practice since 1968. I would define the problem as more that of sensitivity rather than toxicity. The symptoms quoted of dyspnea, headache, rhinitis, eye irritation, cough, and rash are common allergy symptoms. I find that these symptoms correlate well with the degree of exposure and the sensitivity exhibited by the patient to intradermal testing or provocative testing. In cooperation with the University of Wisconsin in La Crosse, we measured levels of formaldehyde in clothing stores, fabric stores, and a biology wet laboratory. We found a level of 0.13 ppm in clothing stores that elevated after new clothing was unpacked. The level in fabric stores averaged 0.60 ppm, and we found 1.7 ppm in the biology wet laboratory. On careful
A Reluctant Doctor Shopper
Authors: Douglas G. MacDonald
Journal: Annals of Internal Medicine (1998)

Letters1 May 1998A Reluctant Doctor ShopperDouglas G. MacDonald, MDDouglas G. MacDonald, MDLahey Hitchcock Clinic-Manchester; Manchester, NH 03104-4125Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-9-199805010-00037 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:If verifiable, Ms. Bingham's conclusion [1] that her physician's misdiagnosis “Endangered my life … and perhaps that of others” is well founded. However, two related issues are not addressed. The first, and least important, is the extent to which physicians “active in both teaching and administration in … leading hospitals” can reasonably be expected to provide adequate availability and triage services to presumably small outpatient practices. Second, although this was not explicitly stated, one would infer from the author's ability and willingness to call her internist at home that there was some degree of friendship or at ...References1. Bingham J. A reluctant doctor shopper. Ann Intern Med. 1997; 127:569-70. Google Scholar Author, Article, and Disclosure InformationAffiliations: Lahey Hitchcock Clinic-Manchester; Manchester, NH 03104-4125 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1998Volume 128, Issue 9Page: 785-786KeywordsOutpatient clinicsTriage Issue Published: 1 May 1998 Copyright & PermissionsCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Diagnosing Osteomyelitis in Patients With Diabetic Neuropathic Osteoarthropathy
Authors: Devasenan Devendra, Kim Farmer, Graham Bruce, Philip Hughes, Gill Vivian, Beverley Anne Millward
Journal: Diabetes Care (2001)

Approximately 15% of diabetic people will develop foot ulcers during their lifetime, and early detection of osteomyelitis is crucial to the management of diabetic foot ulcers (1). Differentiating osteomyelitis from neuropathic osteoarthropathy is clinically difficult, as the symptoms and signs are nonspecific. These patients all present with hot and erythematous feet. At presentation, there is often no change on plain radiographs (2). Many of the imaging findings are also similar, especially in rapidly progressing, noninfected neuro-osteoarthropathy. The most reliable method of establishing infection is to analyze microbiological samples of the lesion. However, this is not always practical and may lead to seeding of …
Abstract 3380: Cancer usurps skeletal muscle as an energy repository
Authors: Yi Luo, Junya Yoneda, Hitoshi Ohmori, Takamitsu Sasaki, Hiroki Kuniyasu
Journal: Cancer Research (2014)

Abstract Cancer cells produce energy through aerobic glycolysis, but contributions of host tissues to cancer energy metabolism is unclear. In this study, we aimed to elucidate the cancer-host energy production relationship, in particular, between cancer energy production and host muscle. During the development and progression of colorectal cancer (CRC), expression of the secreted autophagy-inducing stress protein HMGB1 increased in the muscle of tumor-bearing animals. This effect was associated with decreased expression of pyruvate kinase PKM1 and pyruvate kinase activity in muscle via the HMGB1 receptor RAGE. However, muscle mitochondrial energy production was maintained. In contrast, HMGB1 addition to CRC cells increased lactate fermentation. In the muscle, HMGB1 addition induced autophagy by decreasing levels of active mTOR and increasing autophagy-associated proteins, plasma glutamate and 13C-glutamine incorporation into acetyl-CoA. In a mouse model of colon carcinogenesis, a temporal increase in HMGB1 occurred in serum and colonic mucosa with an increase in autophagy associated with altered plasma free amino acids levels, increased glutamine and decreased PKM1 levels. These differences were abolished by administration of an HMGB1 neutralizing antibody. Similar results were obtained in a mouse xenograft model of human CRC. Taken together, our findings suggest that HMGB1 released during tumorigenesis recruits muscle to supply glutamine to cancer cells as an energy source. Citation Format: Yi Luo, Junya Yoneda, Hitoshi Ohmori, Takamitsu Sasaki, Hiroki Kuniyasu. Cancer usurps skeletal muscle as an energy repository. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3380. doi:10.1158/1538-7445.AM2014-3380
ON THE FUNCTIONS OF THE CHORDA TYMPANI
Authors: W. C. Williamson
Journal: BMJ (1855)

successful treatment adopted in two of the cases, espe- cially the third, rather than any attempt to elucidate the pathology of so troublesome, and sometimes intensely pain- fl affection as herpes zoster, or shingles, must be my ex- &so for offering them for publication.They may, however, serve as examples of the varieties of the disease, as regards pam and constitutional disturbance; there having been scarcely either in the first case, while in the third the pain W said to be of an agonising character.CAS I. A. H., a halthy young lady, aged 5, living at Bixton, was seen by me in December 1849.There was a copious eruption of vesicles, in patches, of the usual ap- pearance, extending from under the right mamma upwards and backwards to the spine.There was little or no pain; and she would scarcely have been aware of the circum- stauce had not another young lady, with whom she had lately been sleeping, been the subject of a similar eruption, but which had been attended with considerable pain in the side previous to its appearance.Beyond a dose of aperient medicine, and a simple dressing, to prevent friction, nothing further was needed.CASE IL In March 1850, I attended a young woman of dark complexion, married, living in Lombard Street, who was attacked with shingles on the inner side of the right thigh.There had been the ordinary heat and darting paia preceding and accompanying the eruption; and when I saw her, there was an irregular and elongated cluster of trans- parent vesiles a few inches above the knee.Purgatives and diaphoretics were prescribed, and saturnine lotion ap- plied to the eruption.The pain, however, continued very severe; and soon some of the vesicles ruptured, coalesced, and began to scab.At the suggestion of a surgeon of great experience, who had previously seen benefit from the appli- cation, the eruption was dressed three times a day with ceratum calaminte spread on lint.She soon experienced relief from this dressing, and continued its use until the scales and crusts had disappeared.CASE III.Mrs. F., aged 40, residing at Kilburn, con- sulted me in September 1855.She is a fair and rather stout woman, of nervous temperament, married, but has never been pregnant.Catamenia regular, scanty.Says she
HEREDOFAMILIAL ANGIOMATOSIS WITH RECURRING EPISTAXIS
Authors: Hyman I. Goldstein
Journal: JAMA (1934)

<h3>To the Editor:—</h3> J. F. Madden of the University of Minnesota Medical School, in his paper on "Generalized Angiomatosis" (The Journal, February 10, p. 442), erroneously states that "hereditary hemorrhagic telangiectasia was first reported by Sutton, in 1864, as internal hemorrhages and telangiectasia of the skin."... Erasmus Wilson, in 1869, called the condition eruptive angiomas. Chiari, in 1883, regarded it as a hemophilia of slight degree; Rendu, in 1896, as juvenile hereditary epistaxis associated with multiple hemorrhagic telangiectasias of the skin and mucous membranes; Ullman, in 1900, as angiomatosis." Since H. Gawen Sutton of the Metropolitan Free Hospital published his paper on "Epistaxis" (<i>M. Mirror</i>, London<b>1:</b>769-781 [Dec.] 1864), I was the first to refer to his work in my publications. Sutton discussed the relation of rheumatic fever and tuberculosis to epistaxis and the connection between epistaxis and hemoptysis. He mentions cases of familial hemoptysis and familial epistaxis. But
OP0051 Differential Methylation Related to Response to Etanercept in Patients with Rheumatoid Arthritis
Authors: A. Webster, D. Plant, S. Eyre, E. Flynn, P. Martin, G. Wilson, A. W. Morgan, J. Isaacs, J. Worthington, A. Barton
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The introduction of biologic drug therapies targeting specific components of the inflammatory response represents a huge advance in the treatment of rheumatoid arthritis (RA). Despite this, up to 40% of patients fail to respond well to these therapies. Ideally, clinicians would like to identify patients who are likely to respond to therapy as early as possible in the disease course, making identification of reliable biomarkers of response an important area of research. Recent studies suggest that epigenetic control of gene expression may be important in RA, we have therefore hypothesized that epigenetic changes such as methylation may provide useful biomarkers of response to biologics. <h3>Objectives</h3> To identify a methylation signature indicative of response to TNF-blockade therapy in patients with RA. <h3>Methods</h3> Patients were recruited from the Biologics in Rheumatoid Arthritis Genetics and Genomics Study Syndicate (BRAGGSS) longitudinal cohort. Patients (n=24) were selected based on having an extreme response phenotype after 3 months of treatment with etanercept; 12 were good responders defined as having an endpoint DAS28&lt;2.6, and 12 were poor responders defined as having an improvement of &lt;0.6 or between 0.6-1.2 with an endpoint DAS28 of &gt;5.1. DNA from each patient, sampled before initiation of etanercept therapy, was bisulfite converted and an epigenome wide association study was conducted using the HumanMethylation450 BeadChip (Illumina). The results were then analysed using the minfi package in R. A detection threshold was applied and probes with a detection p-value of greater than 0.01 were removed. Differentially methylated positions between responders and non responders were identified using the F-test following quantile normalisation. <h3>Results</h3> The fraction of failed probes per sample was less than 0.5%. 9 probes showed significant differences between responders and non-responders to etanercept (p≤10<sup>-4</sup>): cg01037362, cg24725337, cg23704085, cg18631743, cg01379412, cg23881368, cg00011856, cg26282792, cg18772588. Interestingly, cg00011856 (p=9.46x10<sup>-5</sup>) maps 1500bp upstream of the transcription start site of the <i>IGFBP5</i> gene, a known inhibitor of TNF-TNFR1 interactions. The mean beta value for methylation at this CpG site was 0.40 for responders and 0.50 for non-responders. <h3>Conclusions</h3> This is the first methylome wide investigation of treatment response to TNF blockade therapy in RA and, while further well powered studies are required, these preliminary data indicate a possible methylation biomarker of response. <h3>Acknowledgements</h3> This work was supported by the innovative medicines initiative joint undertaking (IMI JU) funded project BeTheCure, (contract number 115142-2). <h3>Disclosure of Interest</h3> None Declared
A Comparison of the Tumor-seeking Agent Tc-99m(V) Dimercaptosuccinic Acid and the Renal Imaging Agent Tc-99m Dimercaptosuccinic Acid in Humans
Authors: HITOYA OHTA, MASAO ISHII, MASAYUKI YOSHIZUMI, KEIGO ENDO, HARUMI SAKAHARA, TETSUO NAKAJIMA, ISAMU YOMODA, HIDESUKE MASUDA, KAZUKO HORIUCHI, NAOTAKA HATA, AKIRA YOKOYAMA, KANJI TORIZUKA
Journal: Clinical Nuclear Medicine (1985)

Being aware of the ideal nuclear properties of Tc-99m, our interest has been focused on the design of the (+5) oxidation state Tc-99m(V) dimercaptosuccinic acid (Tc(V)-DMSA) as a tumor-seeking agent. Tc-99m(V) DMSA holds a TcO4(3-) core and, like PO4(3-), has excellent characteristics for tumor uptake, but has a different distribution than the well-known renal scanning agent, Tc-99m DMSA. The differences in chemical behavior of Tc-99m(V) DMSA and Tc-99m DMSA are discussed. Three cases in which neoplasms were studies with Tc-99m(V) DMSA and Tc-99m DMSA are presented. Tc-99m DMSA and Tc-99m(V) DMSA, having a common ligand and tracer but, with the metal ion core in a different oxidation state, the uptake characteristics are altered markedly.
LUPUS MURINUS.
Authors: ANNE MAGUIRE
Journal: British Journal of Dermatology (1968)

SUMMARY.— The history of the vole type of tubercle bacillus and of the Medical Research Council's trial of vole bacillus vaccine in 1950 is summarized. Fifteen years after this trial 110 vaccinated subjects were re-examined. Seventeen were found to have granulomatous lesions at the vaccination site. The clinical and histological features of the lesions are described. No bacteria could be demonstrated in the lesions histologically or by inoculation of voles. The lesions responded to the administration of antituberculous drugs. The term lupus murinus is proposed for the dermatological lesion induced by primary inoculation with live Mycobacterium tuberculosis var. muris.
The sirtuin family’s role in aging and age-associated pathologies
Authors: Jessica A. Hall, John E. Dominy, Yoonjin Lee, Pere Puigserver
Journal: Journal of Clinical Investigation (2013)

The 7 mammalian sirtuin proteins compose a protective cavalry of enzymes that can be invoked by cells to aid in the defense against a vast array of stressors. The pathologies associated with aging, such as metabolic syndrome, neurodegeneration, and cancer, are either caused by or exacerbated by a lifetime of chronic stress. As such, the activation of sirtuin proteins could provide a therapeutic approach to buffer against chronic stress and ameliorate age-related decline. Here we review experimental evidence both for and against this proposal, as well as the implications that isoform-specific sirtuin activation may have for healthy aging in humans.
Atrial compliance determines the nature of passive atrial stretch and plasma atrial natriuretic factor in the conscious dog
Authors: J. M Stewart, D. J O'Dea, G. C Shapiro, M. B Patel, J. T McIntyre, M. H Gewitz, C. T Hoegler, J. T Shapiro, G. A Zeballos, T. H Hintze
Journal: Cardiovascular Research (1991)

Journal Article Atrial compliance determines the nature of passive atrial stretch and plasma atrial natriuretic factor in the conscious dog Get access Julian M Stewart, Julian M Stewart Correspondence to: Dr Hintze Search for other works by this author on: Oxford Academic PubMed Google Scholar Daniel J O'Dea, Daniel J O'Dea Search for other works by this author on: Oxford Academic PubMed Google Scholar George C Shapiro, George C Shapiro Search for other works by this author on: Oxford Academic PubMed Google Scholar Mrugesh B Patel, Mrugesh B Patel Search for other works by this author on: Oxford Academic PubMed Google Scholar John T McIntyre, John T McIntyre Search for other works by this author on: Oxford Academic PubMed Google Scholar Michael H Gewitz, Michael H Gewitz Search for other works by this author on: Oxford Academic PubMed Google Scholar Carl T Hoegler, Carl T Hoegler Search for other works by this author on: Oxford Academic PubMed Google Scholar Jeffrey T Shapiro, Jeffrey T Shapiro Search for other works by this author on: Oxford Academic PubMed Google Scholar Guillermo A Zeballos, Guillermo A Zeballos Search for other works by this author on: Oxford Academic PubMed Google Scholar Thomas H Hintze Thomas H Hintze Search for other works by this author on: Oxford Academic PubMed Google Scholar Cardiovascular Research, Volume 25, Issue 9, September 1991, Pages 784–792, https://doi.org/10.1093/cvr/25.9.784 Published: 01 September 1991 Article history Received: 24 September 1990 Accepted: 09 May 1991 Published: 01 September 1991
Studies of Platelet 5-Hydroxytryptamine (Serotonin) in Storage Pool Disease and Albinism
Authors: Harvey J. Weiss, Thomas B. Tschopp, John Rogers, Harvey Brand
Journal: Journal of Clinical Investigation (1974)

Platelets in patients with storage pool disease are markedly deficient in a nonmetabolic (storage) pool of ADP that is important in platelet aggregation. They are also deficient in ATP, although to a lesser degree. In seven patients with this disorder, including one with albinism, platelet 5-hydroxytryptamine (5-HT) levels were reduced in proportion to the reduction in ATP (r = 0.94). Their platelets show diminished capacity to absorb [(14)C]5-HT, and the type of defect was similar to that produced in normal platelets by reserpine, a drug known to inhibit the uptake of 5-HT by the platelet dense granules. Storage pool-deficient platelets also converted more [(3)H]5-HT to [(3)H]5-hydroxyindoleacetic acid than did normal platelets, and the platelets in one of two patients studied contained increased amounts of 5-HT metabolites. The above findings, together with those reported previously, support the conclusion that the capacity of the dense granules (which may be either diminished or functionally abnormal) for storing 5-HT is decreased in storage pool disease; as a result, the 5-HT that enters the platelet may be more exposed to monoamine oxidases present on mitochondrial membranes. This diminished storage capacity (for 5-HT) may also explain why preincubating platelet-rich plasma with 5-HT for 45 min without stirring inhibits subsequent platelet aggregation by 5-HT to a greater degree in patients with storage pool disease than in normal subjects. The latter finding is also consistent with the theory that the aggregation of platelets by 5-HT is mediated by the same receptors on the plasma membrane that are involved in its uptake. The diminished release of platelet-bound [(14)C]5-HT by collagen that we found in these patients, as well as findings in previous studies, suggests that the release reaction may also be abnormal in storage pool disease.
Tyrosine Kinase Inhibitor Therapy Induces Remission in a Patient With Refractory <i>EBF1-PDGFRB</i>–Positive Acute Lymphoblastic Leukemia
Authors: Brent W. Weston, Melissa A. Hayden, Kathryn G. Roberts, Susan Bowyer, Johann Hsu, George Fedoriw, Kathleen W. Rao, Charles G. Mullighan
Journal: Journal of Clinical Oncology (2013)
Coronary Artery Disease Risk in Familial Combined Hyperlipidemia and Familial Hypertriglyceridemia
Authors: Paul N. Hopkins, Gerardo Heiss, R. Curtis Ellison, Michael A. Province, James S. Pankow, John H. Eckfeldt, Steven C. Hunt
Journal: Circulation (2003)

Background— Conventional wisdom suggests that a diagnosis of familial combined hyperlipidemia (FCHL) carries a substantially greater risk of premature coronary artery disease (CAD) than a diagnosis of familial hypertriglyceridemia (FHTG). However, no population-based studies have critically addressed this issue. Methods and Results— FCHL and FHTG were diagnosed in 10.2% and 12.3% of 334 random control families and in 16.7% and 20.5% of 293 families with at least one case of premature CAD. The diagnosis of either FCHL or FHTG in an individual was associated with an odds ratio for CAD of 2.0 ( P =0.003 and 0.002, respectively). However, odds ratios for premature CAD associated with both lipid disorders decreased substantially and identically with further adjustment for hypertension, diabetes, and especially HDL cholesterol, triglycerides, or apolipoprotein B. Similar results were found for differences in carotid intima-medial thickness and ankle-brachial index. Metabolic syndrome was identified in 65% of FCHL and 71% of FHTG patients compared with 19% in controls without FCHL or FHTG and was associated with an odds ratio of 3.3 ( P &lt;0.0001). The increased prevalence of the metabolic syndrome alone could account for the elevated CAD risk associated with both FCHL and FHTG. Conclusions— FCHL and FHTG appear more alike than dissimilar. Further, the risk of CAD in FCHL and FHTG was strongly related to features of the metabolic syndrome. These findings suggest that the hypertriglyceridemia in FHTG is not benign and may warrant a change in epidemiological, genetic, and clinical approaches to these lipid disorders.
Interstitial lung disease and leflunomide use
Authors: V Aiyappan
Journal: Thorax (2006)

▴ Suissa S, Hudson M, Ernst P. Leflunomide use and the risk of interstitial lung disease in rheumatoid arthritis. Arthritis Rheum2006;54:1435–9 [OpenUrl][1][CrossRef][2][PubMed][3][Web of Science][4] There have been numerous reports of interstitial lung disease associated with the use of the new disease modifying anti-rheumatic drug leflunomide. This epidemiological study examined the risk of developing interstitial … [1]: {openurl}?query=rft.jtitle%253DArthritis%2Band%2Brheumatism%26rft.stitle%253DArthritis%2BRheum%26rft.aulast%253DSuissa%26rft.auinit1%253DS.%26rft.volume%253D54%26rft.issue%253D5%26rft.spage%253D1435%26rft.epage%253D1439%26rft.atitle%253DLeflunomide%2Buse%2Band%2Bthe%2Brisk%2Bof%2Binterstitial%2Blung%2Bdisease%2Bin%2Brheumatoid%2Barthritis.%26rft_id%253Dinfo%253Adoi%252F10.1002%252Fart.21806%26rft_id%253Dinfo%253Apmid%252F16645972%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [2]: /lookup/external-ref?access_num=10.1002/art.21806&link_type=DOI [3]: /lookup/external-ref?access_num=16645972&link_type=MED&atom=%2Fthoraxjnl%2F61%2F9%2F827.1.atom [4]: /lookup/external-ref?access_num=000237533100011&link_type=ISI
Development of chronic inflammatory demyelinating polyneuropathy in a patient receiving infliximab for psoriasis
Authors: A.C. Foulkes, L. Wheeler, D. Gosal, C.E.M. Griffiths, R.B. Warren
Journal: British Journal of Dermatology (2013)

Journal Article Development of chronic inflammatory demyelinating polyneuropathy in a patient receiving infliximab for psoriasis Get access A.C. Foulkes, A.C. Foulkes The Dermatology Centre Salford Royal NHS Foundation Trust Manchester Academic Health Science Centre University of Manchester Manchester M6 8HD U.K Search for other works by this author on: Oxford Academic Google Scholar L. Wheeler, L. Wheeler The Dermatology Centre Salford Royal NHS Foundation Trust Manchester Academic Health Science Centre University of Manchester Manchester M6 8HD U.K Search for other works by this author on: Oxford Academic Google Scholar D. Gosal, D. Gosal Department of Neurology Salford Royal NHS Foundation Trust Manchester Academic Health Science Centre University of Manchester Manchester M6 8HD U.K Search for other works by this author on: Oxford Academic Google Scholar C.E.M. Griffiths, C.E.M. Griffiths The Dermatology Centre Salford Royal NHS Foundation Trust Manchester Academic Health Science Centre University of Manchester Manchester M6 8HD U.K Search for other works by this author on: Oxford Academic Google Scholar R.B. Warren R.B. Warren The Dermatology Centre Salford Royal NHS Foundation Trust Manchester Academic Health Science Centre University of Manchester Manchester M6 8HD U.K Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 170, Issue 1, 1 January 2014, Pages 206–209, https://doi.org/10.1111/bjd.12572 Published: 01 January 2014