tbuckley/cabot-search huggingface dataset:
ELIMINATION OF COLOR FROM VISUAL HEMOGLOBINOMETRY
Authors: Don H. Duffie
Journal: JAMA (1942)

From their recent studies, involving hundreds of carefully controlled determinations by both physicians and technicians, Karr and Clark<sup>1</sup>conclude that "hemoglobin determinations, as they are done in many laboratories of accredited hospitals with accepted methods, are so inaccurate that they are not only valueless but may well be detrimental to good medical practice." While not every one might have the blunt candor of these investigators, there remains a widely sensed need for a better clinical method of hemoglobin determination than the methods now in use. A method is here described that can be carried out complete in sixty seconds, including two or three readings, readings which in my practice seldom vary as much as 0.4 Gm. (2 per cent) and which can be performed with a relatively inexpensive and reasonably fool-proof photometer that can be folded up and carried in the pocket. The underlying principle of the method is
The Role of Histamine Degradation Gene Polymorphisms in Moderating the Effects of Food Additives on Children's ADHD Symptoms
Authors: Jim Stevenson, Edmund Sonuga-Barke, Donna McCann, Kate Grimshaw, Karen M. Parker, Matthew J. Rose-Zerilli, John W. Holloway, John O. Warner
Journal: American Journal of Psychiatry (2010)

Objective: Food additives can exacerbate ADHD symptoms and cause non-immunoglobulin E-dependent histamine release from circulating basophils. However, children vary in the extent to which their ADHD symptoms are exacerbated by the ingestion of food additives. The authors hypothesized that genetic polymorphisms affecting histamine degradation would explain the diversity of responses to additives. Method: In a double-blind, placebo-controlled crossover trial, challenges involving two food color additive and sodium benzoate (preservative) mixtures in a fruit drink were administered to a general community sample of 3-year-old children (N = 153) and 8/9-year-old children (N = 144). An aggregate ADHD symptom measure (based on teacher and parent blind ratings of behavior, blind direct observation of behavior in the classroom, and—for 8/9-year-old children only—a computerized measure of attention) was the main outcome variable. Results: The adverse effect of food additives on ADHD symptoms was moderated by histamine degradation gene polymorphisms HNMT T939C and HNMT Thr105Ile in 3- and 8/9-year-old children and by a DAT1 polymorphism (short versus long) in 8/9-year-old children only. There was no evidence that polymorphisms in catecholamine genes COMT Val108Met, ADRA2A C1291G, and DRD4-rs7403703 moderated the effect on ADHD symptoms. Conclusions: Histamine may mediate the effects of food additives on ADHD symptoms, and variations in genes influencing the action of histamine may explain the inconsistency between previous studies. Genes influencing a range of neurotransmitter systems and their interplay with environmental factors, such as diet, need to be examined to understand genetic influences on ADHD symptoms.
Understanding spitzoid tumours: new insights from molecular pathology
Authors: P.D. Da Forno, A. Fletcher, J.H. Pringle, G.S. Saldanha
Journal: British Journal of Dermatology (2007)

Journal Article Understanding spitzoid tumours: new insights from molecular pathology Get access P.D. Da Forno, P.D. Da Forno Department of Histopathology, University Hospitals of Leicester NHS Trust, Leicester LE1 5WW, U.K. Correspondence: Philip Da Forno. E‐mail: pddf1@le.ac.uk Search for other works by this author on: Oxford Academic Google Scholar A. Fletcher, A. Fletcher Department of Histopathology, University Hospitals of Leicester NHS Trust, Leicester LE1 5WW, U.K. Search for other works by this author on: Oxford Academic Google Scholar J.H. Pringle, J.H. Pringle Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester LE2 7LX, U.K. Search for other works by this author on: Oxford Academic Google Scholar G.S. Saldanha G.S. Saldanha Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester LE2 7LX, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 158, Issue 1, 1 January 2008, Pages 4–14, https://doi.org/10.1111/j.1365-2133.2007.08207.x Published: 01 January 2008
The Effects of Propranolol on Induction of A-V Nodal Reentrant Paroxysmal Tachycardia
Authors: DELON WU, PABLO DENES, RAMESH DHINGRA, ASHFAQUE KHAN, KENNETH M. ROSEN
Journal: Circulation (1974)

Twelve patients with paroxysmal supraventricular tachycardia (PSVT) were studied before and after administration of 0.1 mg/kg i.v. propranolol. Echo zones for inducing atrioventricular (A-V) nodal reentry were determined using His bundle recording and the atrial extrastimulus technique. After propranolol the echo zone was abolished in two patients, decreased in one, unchanged in five, increased in two. In two patients echo zones appeared only after propranolol. Nine patients had episodes of sustained PSVT prior to propranolol. Following propranolol PSVT persisted in only five. In these five patients propranolol slowed the rate of PSVT. The data were analyzed by plotting A 1 -A 2 and H 1 -H 2 interval curves. On the basis of these curves the patients were separated into those with "dual pathways" and those with "reflection." The effects of propranolol on both conduction patterns are discussed. In summary, the actions of propranolol in PSVT patients were variable. Potentially beneficial effects included slowing of induced PSVT, loss of the ability to sustain PSVT, and decrease or total elimination of echo zones. Potentially deleterious effects included potentiation of the echo phenomenon with either increase or development of echo zones.
Coronary Artery Calcification in Type 2 Diabetes and Insulin Resistance
Authors: James B. Meigs, Martin G. Larson, Ralph B. D’Agostino, Daniel Levy, Melvin E. Clouse, David M. Nathan, Peter W. F. Wilson, Christopher J. O’Donnell
Journal: Diabetes Care (2002)

OBJECTIVE—To assess risk for subclinical coronary atherosclerosis using electron beam- computed tomography in subjects with or without insulin resistance and with normal glucose tolerance (NGT) or impaired glucose tolerance (IGT/impaired fasting glucose [IFG]) or type 2 diabetes. RESEARCH DESIGN AND METHODS—We categorized glucose tolerance by type 2 diabetes therapy (diagnosed diabetes) or with an oral glucose tolerance test (OGTT) (IFG, IGT, and OGTT-detected diabetes) and insulin resistance as an elevated fasting insulin level, in subjects attending the fifth examination (1991–1995) of the Framingham Offspring Study. A representative subset of subjects without clinical atherosclerosis was selected for electron beam computed tomography in 1998–1999 from age- and sex-stratified quintiles of the Framingham risk score. The presence of subclinical atherosclerosis was defined as the upper quartile of the Agatston score distribution (score &amp;gt; 170). We assessed risk for subclinical atherosclerosis using multivariable logistic regression. RESULTS—Of 325 subjects aged 31–73 years, 51% were men, 11.2% had IFG/IGT, and 9.9% had diabetes (2.8% with diagnosed diabetes); 14.5% had insulin resistance. Compared with NGT, subjects with IFG/IGT tended to be more likely (adjusted odds ratio 1.5, 95% CI 0.7–3.4) and those with diabetes were significantly more likely (2.7, 1.2–6.1) to have subclinical coronary atherosclerosis. In age- and sex-adjusted models, subjects with insulin resistance were more likely to have subclinical atherosclerosis than those without insulin resistance (2.1, 1.01–4.2), but further risk factor adjustment weakened this association. In adjusted models including insulin resistance, diabetes remained associated with risk for subclinical atherosclerosis (2.8, 1.2–6.7); diagnosed diabetes (6.0, 1.4–25.2) had a larger effect than OGTT-detected diabetes (2.1, 0.8–5.5). CONCLUSIONS—Individuals with diabetes have an elevated burden of subclinical coronary atherosclerosis. Aggressive clinical atherosclerosis prevention is warranted, especially in diagnosed diabetes.
New Light on the Insulin Controversy
Authors: ROBERT P. HUDSON
Journal: Annals of Internal Medicine (1979)

Editorial Notes1 August 1979New Light on the Insulin ControversyROBERT P. HUDSON, M.D.ROBERT P. HUDSON, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-91-2-311 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe 1923 Nobel Prize in Medicine was awarded for the discovery of insulin to a Canadian surgeon, Frederick G. Banting, and a Scottish physiologist working in Toronto, J. J. R. Macleod. Banting promptly shared his monetary prize equally with Charles Best and Macleod with J. B. Collip. Behind this outward appearance of genial generosity, however, lay a bitterness that was never to be resolved as long as the principals were alive.By the time the prize was announced, Banting was convinced that his rightful role in the discovery of insulin was being stolen by Macleod. During the years each of...References1. MACLEOD J. History of the researches leading to the discovery of insulin. Bull Hist Med. 1978;52:295-312. MedlineGoogle Scholar2. STEVENSON L. Sir Frederick Banting. 2nd ed. Springfield, Illinois: Charles C Thomas; 1947: 101. Google Scholar3. HARRIS S. Banting's Miracle: The Story of the Discoverer of Insulin. Philadelphia: J. B. Lippincott Company; 1946. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Kansas University Medical Center Kansas City, Kansas PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByJohn J.R. Macleod (1876-1935) 70th Anniversary of his deathThe Discovery of InsulinWILLIAM J. STEENROD JR., M.D.The Insulin ControversyROMESH KHARDORI, M.B., M.D. 1 August 1979Volume 91, Issue 2Page: 311-312KeywordsInsulinSurgeons Issue Published: 1 August 1979 Copyright© 1979 American College of PhysiciansPDF DownloadLoading ...
Working Capacity of Women Doctors
Authors: J. Monro
Journal: BMJ (1966)

While many doctors may carry plasma and disposable drip sets, I usually keep these in my surgery and only put them in the car when I am likely to need them.Some of the items carried are seldom needed-for example, I have used the obstetric forceps four times in 13 years in home confinements.No doubt there is equipment missing from my list which one might assume should be there, but in practice I find the equipment is adequate.In my diagnostic bag are: stethoscope, sphygmomanometer, auriscope, ophthalmoscope, spatulae, torch, nasal speculum, Jobson Home ring and probe, patella hammer, foetal stethoscope,
Rheumatic and Metabolic Bone Diseases in the Elderly
Authors: George E. Ehrlich
Journal: JAMA (1982)

This short volume attempts to assist the practicing physician and the physician in training with recognition and management of bone and joint diseases in elderly patients. With an ever enlarging older population, such an emphasis is welcome. However, in many instances, the only difference between the disease in a younger person and in an older person is that one is younger and the other is older. Thus, much of the content of the book would be the same were the title to have been shortened by elimination of its last three words. This is an important distinction, especially in discussing medication, as the metabolism of drugs and the effects on the individual are influenced by changes that accompany aging. Cardiac output tends to be reduced in an elderly person, renal function decreases, and plasma proteins change, thus shifting the equilibrium between concentrations of bound and unbound drugs. Pharmacokinetics reflect these
Oxidative DNA damage accumulation in gastric carcinogenesis
Authors: F Farinati, R Cardin, P Degan, M Rugge, F Di Mario, P Bonvicini, R Naccarato
Journal: Gut (1998)

Background —Gastric carcinogenesis is a multifactorial, multistep process, in which chronic inflammation plays a major role. Aims —In order to ascertain whether free radical mediated oxidative DNA damage is involved in such a process, concentrations of 8-hydroxydeoxyguanosine (8OHdG), a mutagenic/carcinogenic adduct, and thiobarbituric acid reactive substances (TBARS), as an indirect measure of free radical mediated damage, were determined in biopsy specimens from patients undergoing endoscopy. Patients —Eighty eight patients were divided into histological subgroups as follows: 27 with chronic non-atrophic gastritis, 41 with atrophic gastritis, six with gastric cancer, and 14 unaffected controls. Methods —Intestinal metaplasia, Helicobacter pylori infection, and disease activity were semiquantitatively scored. 8OHdG concentrations were assessed by HPLC with electrochemical detection, and TBARS concentrations were fluorimetrically assayed. Results —8OHdG concentrations (mean number of adducts/10 5 dG residues) were significantly higher in chronic atrophic gastritis (p=0.0009). Significantly higher concentrations were also detected in the presence of severe disease activity (p=0.02), intestinal metaplasia (p=0.035), and H pylori infection (p=0.001). TBARS concentrations were also higher in atrophic gastritis, though not significantly so. In a multiple logistic regression analysis, 8OHdG concentrations correlated best with the presence and severity of H pylori infection ( r =0.53, p=0.002). Conclusions —Chronic gastritis is characterised by the accumulation of oxidative DNA damage with mutagenic and carcinogenic potential. H pylori infection is the major determinant for DNA adduct formation.
Alcohol drinking in middle age and subsequent risk of mild cognitive impairment and dementia in old age: a prospective population based study
Authors: Tiia Anttila, Eeva-Liisa Helkala, Matti Viitanen, Ingemar Kåreholt, Laura Fratiglioni, Bengt Winblad, Hilkka Soininen, Jaakko Tuomilehto, Aulikki Nissinen, Miia Kivipelto
Journal: BMJ (2004)

To evaluate the relation between midlife alcohol consumption and mild cognitive impairment and dementia in old age, and the possible modification of this relation by apolipoprotein E.Prospective, population based study.Populations of Kuopio and Joensuu, eastern Finland.Of 1464 men and women aged 65-79 years randomly selected from population based samples studied in 1972 or 1977, 1018 (70%) were re-examined in 1998 (after an average follow up of 23 years).Mild cognitive impairment and dementia in old age.Participants who drank no alcohol at midlife and those who drank alcohol frequently were both twice as likely to have mild cognitive impairment in old age as those participants who drank alcohol infrequently. The risk of dementia related to alcohol drinking was modified by the presence of the apolipoprotein e4 allele. The carriers of apolipoprotein e4 had an increased risk of dementia with increasing alcohol consumption: compared with non-carriers who never drank, the odds ratio for carriers who never drank was 0.6, for infrequent drinkers it was 2.3, and for frequent drinkers was 3.6 (the overall interaction term "drinking frequency(*)apolipoprotein e4" was significant (P = 0.04), as were the interactions "infrequent drinking(*)apolipoprotein e4" (P = 0.02) and "frequent drinking(*)apolipoprotein e4" (P = 0.03)). Non-carriers of apolipoprotein e4 had similar odds ratios for dementia irrespective of alcohol consumption.Alcohol drinking in middle age showed a U shaped relation with risk of mild cognitive impairment in old age. Risk of dementia increased with increasing alcohol consumption only in those individuals carrying the apolipoprotein e4 allele.
Case of Suspected Poisoning by Lobelia Inflata: With the Appearances after Death
Authors: H. Johnson
Journal: BMJ (1858)

such a blade, greater force is required to make it cut itself out.MVforeover, he found that the narrower the knife the less likely was the aqueous humor to escape prematurely.Ulti- mately he adopted an angle selected by Mr. Tyrrell, but reduced the lengthl of the blade.For many years he has had smooth round wooden handles to all of his instruments, and rather later to his cataract knives, cedar handles, fac-similes of all of which may be obtained at Weiss's.(1rigina1 Ponmnunidatirns.
The prolyl isomerase Pin1 acts as a novel molecular switch for TNF-α–induced priming of the NADPH oxidase in human neutrophils
Authors: Tarek Boussetta, Marie-Anne Gougerot-Pocidalo, Gilles Hayem, Silvia Ciappelloni, Houssam Raad, Riad Arabi Derkawi, Odile Bournier, Yolande Kroviarski, Xiao Zhen Zhou, James S. Malter, Ping K. Lu, Aghleb Bartegi, Pham My-Chan Dang, Jamel El-Benna
Journal: Blood (2010)
Abstract 5583: Differential effect of phenethyl isothiocyanate on expression of antioxidant defense genes between normal and cancerous human prostate cells
Authors: Shivendra V. Singh, Anna A. Powolny
Journal: Cancer Research (2011)

Abstract Phenethyl isothiocyanate (PEITC) is a promising cancer chemopreventive constituent of cruciferous vegetables (e.g., watercress) as evidenced by efficacy against chemically-induced cancer in experimental rodents. The PEITC is also empowered to inhibit growth of cultured and xenografted human prostate cancer cells, which correlates with apoptotic and autophagic cell death. We have shown previously that reactive oxygen species (ROS) play a critical role in proapoptotic signal transduction by PEITC in human prostate cancer cells. Interestingly, a representative normal human prostate epithelial cell line (PrEC) is significantly more resistant to PEITC-induced apoptosis compared with cancerous prostate cells including PC-3 and LNCaP. However, the mechanism behind this differential response remains elusive. The present study was undertaken to test a hypothesis that differential sensitivity of normal versus cancerous human prostate cells to PEITC-mediated proapoptotic response is determined by differences in ROS production and/or basal or inducible expression of antioxidant defense genes. The PEITC treatment resulted in ROS production in PC-3 human prostate cancer cells as judged by flow cytometry and fluorescence microscopy using a chemical probe (MItoSOX Red) and EPR using a cell permeable sin probe (1-hydroxy-3-methoxy-carbonyl-2,2,5,5-tetramethylpyrrolidine). These effects were not observed in PrEC cells similarly treated with the PEITC. Basal antioxidant defense gene expression signature was strikingly different between PC-3 and PrEC cells. Moreover, PEITC treatment (2.5 μM, 6 h) caused up-regulation of 29 genes and down-regulation of 2 genes in PC-3 cells. Conversely only 4 genes were up-regulated and 10 genes were down-regulated by a similar PEITC treatment in the PrEC cell line. The results of the present study clearly indicate that differential sensitivity of PC-3 versus PrEC cells to proapoptotic effect of PEITC is likely attributable to both differences in ROS production and basal as well as altered expression of antioxidant defense genes. This investigation was supported by the USPHS grant CA101753-07, awarded by the National Cancer Institute. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 5583. doi:10.1158/1538-7445.AM2011-5583
Double-blind comparison of tolamolol, propranolol, practolol, and placebo in the treatment of angina pectoris.
Authors: G Jackson, L Atkinson, S Oram
Journal: BMJ (1975)

Forty-two patients with angina pectoris have completed a randomized, double-blind trial comparing tolamolol 100 mg and 200 mg with propranolol 80 mg, practolol 100 mg, and placebo, all given three times a day. Tolamolol 200 mg thrice daily was found to be equivalent to propranolol 80 mg thrice daily in anti-anginal efficacy. Anginal attack rates and trinitrin consumption were significantly reduced by all active treatments as compared with the placebo but tolamolol and propranolol were the most effective. Tolamolol 200 mg thrice daily was most effective in reducing blood pressure, while propranolol was most effective in reducing the resting heart rate. All treatments except the placebo significantly increased the amount of exercise which could be performed before angina appeared (exercise work), while tolamolol 200 mg thrice daily significantly reduced Robinson9s index when compared with all other active agents. The degree of S-T segment depression induced by exercise was significantly lessened by both tolamolol and propranolol but not by practolol or placebo. There was no difference in patient preference between tolamolol and propranolol but tolamolol at both dose levels was preferred to practolol. Both tolamolol and propranolol are potent adrenergic beta-receptor antagonists and equal in anti-anginal efficacy but tolamolol has the advantage of being cardioselective. It is superior to practolol.
Effect of oral prednisolone on response to salbutamol and ipratropium bromide aerosols in patients with chronic airflow obstruction.
Authors: P G Curzon, M A Martin, N J Cooke, M F Muers
Journal: Thorax (1983)

We examined the bronchodilator responses to inhalation of salbutamol (200 micrograms) and of ipratropium bromide (40 micrograms) in the morning and in the afternoon before and during a course of oral prednisolone (40 mg daily) in 15 patients with chronic, partly reversible airflow obstruction. Bronchodilatation was assessed by measuring serial peak expiratory flow rates (PEFR) for six hours after aerosol drug administration and calculating the area under the time-response curves. Eleven patients were found to be corticosteroid resistant in not attaining a baseline bronchodilatation of at least 25% during corticosteroid treatment. These patients also failed to show any enhancement of their bronchodilator responses to either salbutamol or ipratropium bromide during prednisolone administration. We therefore conclude that there is no rationale for giving or continuing corticosteroid treatment in known steroid-resistant patients in the hope of nevertheless potentiating their bronchodilator responses to salbutamol or ipratropium bromide.
Diagnostic Devices: Microneedle‐Based Transdermal Sensor for On‐Chip Potentiometric Determination of K<sup>+</sup> (Adv. Healthcare Mater. 6/2014)
Authors: Philip R. Miller, Xiaoyin Xiao, Igal Brener, D. Bruce Burckel, Roger Narayan, Ronen Polsky
Journal: Advanced Healthcare Materials (2014)

A transdermal sensing platform for detection of electrolytes is developed by P. R. Miller, R. Narayan, R. Polsky and colleagues. On page 876, hollow polymer microneedles are integrated with a microfluidic chip for detecting potassium using a solid state ion selective electrode transducer. The device could one day be used as an on body point-of-care medical diagnostic device.