tbuckley/cabot-search huggingface dataset:
Comment on: Koivikko et al. Autonomic Cardiac Regulation During Spontaneous Nocturnal Hypoglycemia in Patients With Type 1 Diabetes. Diabetes Care 2012;35:1585–1590
Authors: Dario Pitocco, Francesco Zaccardi, Fabio Infusino, Roberto Nerla, Giovanni Ghirlanda, Gaetano A. Lanza
Journal: Diabetes Care (2012)

We read with great interest the article published in Diabetes Care by Koivikko et al. (1) showing that in patients with type 1 diabetes, spontaneous episodes of hypoglycemia are associated with reduced values of heart rate variability (HRV) parameters, indicating sympatho-vagal imbalance toward sympathetic predominance.

The data by Koivikko et al. confirm in type 1 diabetic patients what we already demonstrated—for the first time—in type 2 diabetic patients (2). In our study we performed simultaneous …
Interactions of the advanced glycation end product inhibitor pyridoxamine and the antioxidant α-lipoic acid on insulin resistance in the obese Zucker rat
Authors: Elizabeth A. Muellenbach, Cody J. Diehl, Mary K. Teachey, Katherine A. Lindborg, Tara L. Archuleta, Nicholas B. Harrell, Gaby Andersen, Veronika Somoza, Oliver Hasselwander, Markus Matuschek, Erik J. Henriksen
Journal: Metabolism (2008)
VERY LONG-TERM RESULTS (&gt; 2 YEAR) OF THE VESTASYNC I TRIAL WITH A NOVEL, THIRD-GENERATION, HYDROXYAPATITE POLYMER-FREE SIROLIMUS-ELUTING STENT
Authors: Jose de Ribamar Costa, Alexandre Abizaid, Ricardo Costa, Fausto Feres, Andrea Abizaid, Luiz Fernando Tanajura, Dimytri Siqueira, Rodolfo Staico, Galo Maldonado, Amanda Sousa, J Eduardo Sousa
Journal: Journal of the American College of Cardiology (2010)
Acute and recurrent abdominal pain due to hereditary angio-oedema.
Authors: R P Warin, E R Higgs
Journal: BMJ (1982)

Acute and recurrent abdominal pain due to hereditary angio-oedema Abdominal colic giving rise to recurrent pain or a surgical emergency is often present in patients with hereditary angio-oedema.In some cases the angio-oedema is minimal or may develop later and the cause of the presenting colic may easily be missed.We describe a patient who had suffered from recurrent abdominal pain for 44 years without angio-oedema swellings before hereditary angio-oedema was diagnosed.We also make observations on the incidence and nature of abdominal pain in hereditary angio-oedema based on 20 patients with this condition. PatientsA 58-year-old woman had had attacks of abdominal pain every two to three weeks since the age of 14 and had not been clear of these for more than one to two months.The pains were usually in the central abdomen but occasionally in the groins and iliac fossae.They were colicky, lasted a few hours to one or two days, and at times necessitated bed rest.General weakness, vomiting, and occasional difficulty in micturition occurred with the attacks.
Effects of Adrenergic Blockade on Serum Potassium Changes in Response to Acute Insulin-Induced Hypoglycemia in Nondiabetic Humans
Authors: B Miles Fisher, Ian Thomson, David A Hepburn, Brian M Frier
Journal: Diabetes Care (1991)

Objective To determine the possible role of adrenergic mechanisms in mediating the fall in serum potassium concentration after intravenous injection of insulin. Research Design and Methods Eighteen nondiabetic male volunteers, divided into three groups of six subjects, comprised the study. Hypoglycemia was induced by a bolus of short-acting insulin (0.15 U∕kg body wt). Six subjects were studied in control conditions, six during α-adrenergic blockade with phentolamine, and six during β-adrenergic blockade with propranolol. Results In the control group, there was an immediate fall in serum potassium from 4.0 ± 0.1 to 3.6 ± 0.1 mM at baseline + 15 min. After the onset of acute hypoglycemia, potassium decreased further in the control group, reaching a lowest concentration of 3.3 ± 0.1 mM. In the propranolol group, the late decrease in potassium was inhibited, and there were no further changes in serum potassium. During α-blockade, there was an exaggerated fall to 2.6 ± 0.1 mM at 30 min after the onset of hypoglycemia. Conclusions The later fall in serum potassium, which occurs after the onset of hypoglycemia, is probably mediated by stimulation of β-adrenoreceptors, whereas coincidental stimulation of α-adrenoreceptors opposes this fall in potassium and may prevent the development of severe hypokalemia in response to acute hypoglycemia.
Coronary Care Units
Authors: ELLIOT E. MAZER
Journal: Annals of Internal Medicine (1977)

Comments and Correction1 April 1977Coronary Care UnitsELLIOT E. MAZERELLIOT E. MAZERSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-86-4-504_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: I read with interest the recent paper by Stross and colleagues on the effectiveness of coronary care units in small hospitals (Ann Intern Med85:709-713, 1976). As the sole internist in a small 40-bed hospital located at least an hour from the nearest urban medical center, I was particularly concerned by the finding of increased mortality in units seeing less than 60 patients per year. The authors were able to identify retrospectively some of the factors responsible for this finding and that corrective action had been taken. As we admit only three or four cases of myocardial... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: MC USAF USAF Hospital, Beale (SAC) Beale Air Force Base, CA 95903 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 April 1977Volume 86, Issue 4Page: 504-505KeywordsCardiac care unitMortality Issue Published: 1 April 1977 PDF DownloadLoading ...
Interleukin 6 and liver regeneration
Authors: K L STREETZ
Journal: Gut (2000)

Interleukin 6 and liver regeneration IL-6 and its biological functionThe multifunctional cytokine interleukin 6 (IL-6) was cloned in 1986.Since then, our understanding of its role in the regulatory functions in the immune system has grown steadily.IL-6 is a typical pleiotropic cytokine that acts on various cells.It is commonly produced at local tissue sites and is released in almost all situations of homeostatic perturbation, which include endotoxaemia, trauma, and acute infection.In addition, circulating IL-6, together with tumour necrosis factor (TNF-) and interleukin 1 (IL-1), is required for induction of the acute phase response which comprises fever, corticosteroid release, and hepatic production of acute phase proteins which are mostly protease inhibitors.Overall, induction of the acute phase response by IL-6 has been regarded as part of an attempt to maintain homeostasis.Apart from its role in inflammation, IL-6 induces diVerentiation and development of B cells, T cells, myeloid cells, megakaryocytes, osteoclasts, neural cells, and hepatocytes.IL-6 acts as a growth factor for renal cell carcinoma and Kaposi's sarcoma, and promotes the growth of haematopoietic stem cells.Apart from the cytokine itself, the IL-6 family comprises IL-11, ciliary neurotrophic factor (CNTF), cardiotropin (CT-1), oncostatin M (OSM), leukaemia inhibitory factor (LIF), and the novel neurotrophin 1/B cell stimulating factor 3 (NNT-1/BSF-3), which all share the common signal transducer gp130 as part of their receptors.Except for CNTFR, the IL-6-type cytokine signalling receptors are type I membrane proteins (extracellular N terminus, one transmembrane domain).This receptor family is defined by the presence of at least one cytokine binding molecule (CBM), a set of four conserved tyrosine residues, and a tryptophan-serine-X-tryptophan-serine (W-S-X-S-W) motif, located outside the transmembrane domain.Signal transduction after ligand binding is elicited by homodimerisation of gp130 in the case of IL-6 and IL-11, by heterodimerisation of gp130 and LIFR in the case of LIF, CNTF and CT-1, or by heterodimerisation of gp130 and OSMR in the case of OSM. 1 Thus the molecular mechanism of redundancy between the family members can be explained because all members use at least one gp130 molecule for signal transduction.
Epidemiology and Complications of Escherichia coli O157:H7 Infections
Authors: Nevio Cimolai
Journal: JAMA (1989)

<h3>To the Editor.—</h3> The efforts by Ostroff et al<sup>1</sup>to include<i>Escherichia coli</i>O157:H7 disease as a reportable disease should be commended. The clinical spectrum of enteritis and the incidence of associated hemolytic-uremic syndrome (HUS) certainly make<i>E coli</i>O157:H7 infection at least as important for notification as<i>Shigella</i>-associated disease. Their analysis of risk factors for the progression of enteritis to HUS is also provocative, but the conclusions should be tempered by some of our own recent findings in the same area.<sup>2</sup> The mechanism of acquisition of data is important and is especially so for patients with HUS. These patients are often transferred to tertiary care hospitals from other centers where some form of therapy may have been administered. Documentation of use of antibiotic or antimotility agents may be overlooked by subsequent admitting physicians and therefore such data may not be retrieved retrospectively. This potential problem should
Complete Transposition of Great Vessels
Authors: H. T. Lynch, R. L. Grissom, P. Mooring, A. Krush
Journal: JAMA (1964)

A family has been studied wherein two siblings manifested complete transposition of the great vessels, confirmed at autopsy. Consanguinity was absent and no toxic exposure was found during the prenatal period in either case. All available family members were studied and found to be normal. Only one previous report of this cardiac anomaly in siblings has been found; however, there have been several reports showing complete transposition of the great vessels in one sibling, while another sibling manifested cardiac defects within the spectrum of truncoconal malformations. A genetic fault is postulated as the etiology of some truncoconal malformations, in which a gene effect during embryogenesis, in concert with the intrauterine milieu, produces various anomalies.
Marketing, not evidence based arguments, has probably increased testosterone prescribing
Authors: J. Gorricho, E. Gavilan, J. Gervas
Journal: BMJ (2012)

We strongly disagree with the British Society for Sexual Medicine’s “reflections” on testosterone.1

Firstly, there is no consistent evidence that hormone replacement provides clear health or patient oriented benefits in most men with low testosterone values. The Endocrine Society therefore recommends …
Three dimensional visualisation of velocity profiles in the normal porcine pulmonary trunk
Authors: L. Somod, J M. Hasenkam, W Y. Kim, H. Nygaard, P. K Paulsen
Journal: Cardiovascular Research (1993)

Objective: The aim was to obtain detailed data of velocity profile development in the porcine pulmonary trunk. Methods: Hot film anemometry was used for point blood velocity measurements in the entire cross sectional area one diameter downstream of the normal porcine pulmonary valve. Computerised three dimensional visualisations of the spatial and temporal development of blood velocity profiles were made. Measurement series were conducted under spontaneous and stressed haemodynamic conditions in 16 pigs with a body weight of approximately 90 kg. Results: The velocity profiles revealed consistent temporal and spatial development characteristics. In the systolic acceleration phase the profile was flat, but during peak systole an initially counterclockwise rotation was seen; subsequently the profile turned clockwise and ultimately counterclockwise to become flat during early and late systolic deceleration phases. Conclusions: These skewed, rotating velocity profiles are in conflict with the generally accepted assumption that the velocity profile in the pulmonary trunk is flat. The rotating skewness of the velocity profile in the porcine pulmonary trunk has not been described before. The reason for the rotating velocity profile is obscure. Cardiovascular Research 1993;27:291-295
Sidney Gerrish Hamilton
Authors: V P Smith
Journal: BMJ (2006)

​FormerFormer general practitioner south London (b 1911; q Cambridge/The London Hospital 1937; RNVR, FRCGP), d 10 July 2006.



Figure 1



Sidney Hamilton served with distinction on the ill fated HMS Repulse, saving many lives on the day it was sunk by the Japanese in 1941. He entered general practice in Woolacombe, enthusiastically supported the new NHS, and later moved to Sanderstead. He caught a flu-like illness during the 1953 polio epidemic and recovered, but his wife, Anne, also a general practitioner, became a wheelchair user until her death in 1978. Sidney cared for her and his patients devotedly. He was a founder member of the Royal College of General Practitioners and a pioneer trainer. Before retirement he was medical officer to the British High Commission in Delhi. He was a firm Christian, austere but witty, and a scholar, traveller, and naturalist. He leaves four children and 13 grandchildren.
Preclinical Safety Evaluation of AAV2-sFLT01— A Gene Therapy for Age-related Macular Degeneration
Authors: Timothy K MacLachlan, Michael Lukason, Margaret Collins, Robert Munger, Elisabete Isenberger, Cindy Rogers, Shana Malatos, Elizabeth DuFresne, James Morris, Roberto Calcedo, Gabor Veres, Abraham Scaria, Laura Andrews, Samuel Wadsworth
Journal: Molecular Therapy (2010)

AAV2-sFLT01 is a vector that expresses a modified soluble Flt1 receptor designed to neutralize the proangiogenic activities of vascular endothelial growth factor (VEGF) for treatment of age-related macular degeneration (AMD) via an intravitreal injection. Owing to minimal data available for the intravitreal route of administration for adeno-associated virus (AAV), we initiated a 12-month safety study of AAV2-sFLT01 administered intravitreally at doses of 2.4 × 10(9) vector genomes (vg) and 2.4 × 10(10) vg to cynomolgus monkeys. Expression of sFlt01 protein peaked at ~1-month postadministration and remained relatively constant for the remainder of the study. Electroretinograms, fluorescein angiograms, and tonometry were assessed every 3 months, with no test article-related findings observed in any group. Indirect ophthalmoscopy and slit lamp exams performed monthly revealed a mild to moderate but self-resolving vitreal inflammation in the high-dose group only, which follow-up studies suggest was directed against the AAV2 capsid. Histological evaluation revealed no structural changes in any part of the eye and occasional inflammatory cells in the trabecular meshwork, vitreous and retina in the high-dose group. Biodistribution analysis in rats and monkeys found only trace amounts of vector outside the injected eye. In summary, these studies found AAV2-sFLT01 to be well-tolerated, localized, and capable of long-term expression.
The Leprosy Question.
Authors: Albert S. Ashmead
Journal: JAMA (1897)

New York, Dec. 6, 1897. <h3>To the Editor of Janus, Amsterdam, Netherlands.</h3> —Dr. Ehlers says (<i>Janus</i>, July and August) I attribute to him opinions which he never professed. Whether or not Dr. Ehlers stands for isolation was not the point at issue; it was, should isolation as a principle be promulgated by the Berlin Lepra-Conference? That was the important question. He stood an obstacle to our obtaining official delegates, claiming that governments<i>had always neglected the holy name of hygiene</i>, le saint nom de l'hygiène, in all countries and in all times.<i>It was not, in his opinion, the way that leads to the goal to try to stir up the governments. It is a congress which takes place between known leprologists and not a congress of leprology</i>. Our goal was not so much a congress of leprologists, which I have taken the liberty to call very frequently a congress
Nitric Oxide Inhibits the Positive Inotropic Response to β-Adrenergic Stimulation in Humans With Left Ventricular Dysfunction
Authors: Joshua M. Hare, Evan Loh, Mark A. Creager, Wilson S. Colucci
Journal: Circulation (1995)

Background Nitric oxide (NO) attenuates the contractile response to β-adrenergic stimulation in cultured cardiac myocytes in vitro and in myocardium in vivo. We tested the hypothesis that NO synthesized in the heart inhibits the positive inotropic response to β-adrenergic stimulation in humans with left ventricular (LV) dysfunction. Methods and Results Patients with various degrees of LV dysfunction and free from epicardial coronary artery disease were instrumented with an infusion catheter in the left main coronary artery and a high-fidelity micromanometer-tipped catheter in the LV. Measurements included LV pressure, aortic pressure, heart rate, and LV peak +dP/dt. In eight subjects, dobutamine was infused via the left main coronary artery (25 or 50 μg/min) before and concurrent with intracoronary infusion of the NO synthase inhibitor N G -monomethyl- l -arginine (L-NMMA, 20 μmol/min for 10 minutes). In six other subjects, dobutamine was infused (6, 10, or 15 μg · kg −1 · min −1 ) via a peripheral vein. Intracoronary (n=8) dobutamine infusions increased LV peak +dP/dt by an average of 33±3%. The intracoronary infusion of L-NMMA had no effect on baseline LV peak +dP/dt, LV systolic or end-diastolic pressures, aortic pressure, or heart rate. The intracoronary infusion of L-NMMA, concurrent with a second infusion of dobutamine, potentiated the +dP/dt response to dobutamine by 30±10% ( P &lt;.04 versus dobutamine alone). The intracoronary infusion of L-NMMA likewise potentiated the +dP/dt response to the peripheral infusion of dobutamine by 37±18%. Conclusions Nitric oxide produced in the heart attenuates the positive inotropic response to β-adrenergic stimulation in humans with LV dysfunction. NO may contribute to β-adrenergic hyporesponsiveness in patients with LV dysfunction.
The greek<sup>a</sup>γβ<sup>+</sup>‐hpfh observed in a large black family
Authors: H. J. Huang, T. A. Stoming, H. F. Harris, F. Kutlar, T. H. J. Huisman
Journal: American Journal of Hematology (1987)

Abstract Several members of a Black family with a heterozygosity for an A γGβ + ‐HPFH, shown in 1969 to have relatively low levels of Hb F and a low glycine to alanine ratio in the γ chain of this Hb F, were reinvestigated. Thirteen of 30 available family members in two generations had the heterozygous form of this condition, which was characterized by a decreased level of Hb A 2 , an average Hb F AD value of 13.3%, an equal distribution of Hb F over the red cells, and normal hematological values. The γ chain composition of isolated Hb F was determined by reversed phase high performance liquid chromatography for all 13 heterozygotes and showed an average A γ value of 84.5 %. Hybridization with synthetic oligonucleotides, specific for normal and mutant sequences at positions 111–129 5′ to the A γ globin gene, identified a G ± A base substitution at position 117, similar to that seen in subjects with the Greek A γ‐HPFH. Our data support conclusions by others [15,16,30] that this replacement is causative of the increased A γ chain synthesis in this condition. Haplotype analysis supported the suggestion that the G ± A substitution occurred as an independent event in this Black family.
Postural Fitness: Significance and Variances
Authors: Fred V. Hein
Journal: JAMA (1960)

The authors believe that many disabilities and health problems have their roots in postural deviations. Consequently, they advocate a program of physical education in the schools that includes developmental activities designed to promote good posture and body mechanics. Postural fitness is defined as the capacity to maintain proper segmental relationships in all body movements. As such, it goes beyond sitting, standing, and walking to constitute the best body positioning for functional efficiency in any given activity. The physician, physical educator, school nurse, parents, and others who may be involved are visualized as a team. Together, they can detect needs and plan programs of developmental activities for the child to help adjust irregularities in structural and functional postures. There are definite techniques for detecting such variations, tried procedures for approaching their alleviation, and exercise patterns of proved value to aid in their adjustment. The authors take strong issue with those who
Muscle-specific inactivation of the IGF-I receptor induces compensatory hyperplasia in skeletal muscle
Authors: Ana M. Fernández, Joëlle Dupont, Roger P. Farrar, Sukho Lee, Bethel Stannard, Derek Le Roith
Journal: Journal of Clinical Investigation (2002)

During the development of skeletal muscle, myoblasts withdraw from the cell cycle and differentiate into myotubes. The insulin-like growth factors IGF-I and IGF-II, through their cognate tyrosine kinase receptor (IGF-I receptor), are known to play a role in this process. After withdrawal of myoblasts from the cell cycle, IGF-I promotes muscle differentiation by inducing the expression or activity of myogenic regulatory factors (MyoD, myogenin) and effectors (p21). However, little is known about the intracellular mechanisms by which the IGF-I system regulates these factors during the process of myogenesis. Here we show that MKR mice, which express a dominant negative IGF-I receptor specifically in skeletal muscle, have marked muscle hypoplasia from birth to 3 weeks of age. This hypoplasia occurs concomitantly with a decrease in ERK immunoreactivity levels and decreases in MyoD and myogenin expression. BrdU immunocytochemistry showed a compensatory hyperplasia as MKR mice grew to adulthood. Interestingly, hyperplasia occurred concomitantly with an increase in p38, MyoD, myogenin, and p21 immunoreactivity levels, as well as a decrease in Twist levels. These findings suggest that regulation of these cellular elements by IGF-I may play a role in the development and differentiation of skeletal muscle in vivo.
Geriatric Assessment for the Elderly Patients with Diffuse Large B Cell Lymphoma (DLBCL) and Treatment Outcomes
Authors: Y. Takamatsu, Y. Naito, E. Sato, Y. Ikari, H. Katsuya, T. Goto, A. Shirahashi, T. Tanaka, K. Ishitsuka, K. Tamura
Journal: Annals of Oncology (2013)
Protecting adolescent girls against tetanus
Authors: L. Brabin, J. Kemp, S. M Maxwell, J. Ikimalo, O. K Obunge, N. D Briggs
Journal: BMJ (1995)

An estimated 8 million infants and 2 million children and adults may die from tetanus during the 1990s despite efforts by the World Health Organization (WHO) to eliminate it by 1995. Vaccination to prevent postabortal and maternal tetanus has been neglected. The immunization of preschool children and of pregnant women has omitted adolescent girls, who are therefore at risk. Data collected on 1101 cases of maternal tetanus in developing countries between 1958 and 1990 indicated that 27% were attributed to postabortal and 67% to postpartum sepsis. In southeastern Nigeria where abortion rates are high, a high proportion of girls were also seronegative for tetanus antibodies. Many unvaccinated pregnant women cite the lack of money for obtaining vaccination when obtaining prenatal services. The WHO is promoting vaccination of women of reproductive age by screening their tetanus toxoid status, but adolescents are poorly covered because they are not regular attenders. Expressly targeting girls would be feasible, as it would require 5 injections providing protection for life. Even 4 injections may protect for 20 years if delivered at the end of primary school. Thus a school health service delivering tetanus vaccination may improve the vaccination of adolescent girls. This could be combined with distribution of vitamin A and antihelminthics whereby the response to the vaccine could be improved significantly. In addition, it has also been suggested that a late dose of an acellular pertussis vaccine and a second dose of measles vaccine given in adolescence would reduce the pool of susceptible girls, just as girls have been targeted for rubella vaccination. Implementation of tetanus vaccination would require local schools vaccination days, immunization cards, high potency primary vaccination, and tetanus boosters free of charge with a system to monitor antibody responses.