tbuckley/cabot-search huggingface dataset:
A Novel Method of Expressing Left Ventricular Mass Relative to Body Size in Children
Authors: Bethany J. Foster, Andrew S. Mackie, Mark Mitsnefes, Huma Ali, Silvia Mamber, Steven D. Colan
Journal: Circulation (2008)

Background— Left ventricular (LV) hypertrophy (LVH) in children is widely defined as a left ventricular mass index (LVMI, g/m 2.7 ) &gt;95th percentile. However, LVMI increases with decreasing height in young children; thus, the 95th percentile LVMI will depend on the height distribution of the reference population. The objective of this study was to compare the performance of a novel method of expressing LV mass relative to body size (centile curves) with the LVMI method. Methods and Results— LV mass was estimated by M-mode echocardiography in 440 healthy nonobese reference children (birth to 21 years) and 239 children at risk for LVH; the LVMI was calculated for all children. Three samples of 270 children, each with different height distributions, were drawn from the reference population. A sample-specific 95th percentile LVMI was determined for each reference sample. At-risk children were classified as having LVH or not based on each sample-specific 95th percentile. Four LV mass-for-height centile curves were constructed with the Cole lambda-mu-sigma method and data from each reference sample. At-risk children were each assigned an LV mass-for-height percentile with these curves and were reclassified as having LVH if LV mass-for-height was &gt;95th percentile. The centile method provided a stable estimate of the proportion of at-risk children with LVH regardless of reference group, whereas proportion estimates varied significantly depending on the reference population when the LVMI method was used. Conclusions— LV mass-for-height centile curves are superior to LVMI as a method of normalizing LV mass to body size in children.
Some Effects of Stenosis of the Terminal Common Bile Duct on the Biliary Tract and Liver
Authors: John V. Pikula, J. Englebert Dunphy
Journal: New England Journal of Medicine (1959)

TWO hundred and one years ago an English physician, Thomas Coe,1 made the following observation: "When by any means the bile is stopped or retarded so as to stagnate long, either in the gall bladder or ducts, especially if before the stoppage it was unusually thick and viscid or abounded more than ordinarily with earthy particles it is readily formed into biliary concretions or gallstones of various kinds." A hundred and forty years later William Hunter2 agreed that stagnation was important but considered a "catarrhal condition" also necessary to form "irritant products" that might act as nuclei for stones. Harvey . . .
Editorial: The many faces of bromocriptine
Authors: S. Vaisurb
Journal: JAMA (1976)

In 1676, Dodart observed that ergot inhibited lactation (<i>Journal des Savants</i>, 1676, p 76). Thus, we need not be astonished that 300 years later, bromocriptine (2-bromergokriptine, CB154), a semisynthetic ergot alkaloid free of the cardiovascular and oxytocic actions of its progenitor, has proved successful in suppressing puerperal lactation without producing undesirable side effects.<sup>1</sup> What comes as a surprise is the potential usefulness of bromocriptine in a variety of clinical conditions. Originally thought to be a stimulant to secretion of the hypothalamic prolactin-release inhibiting factor, the drug itself has since been shown to be such a factor. It acts directly on the pituitary cells by activating their dopamine receptors.<sup>2</sup>Because this dopaminergic action is not confined to prolactin-secreting cells, the drug (it has yet to be approved by the FDA) is being tried in the treatment of various disorders—galactorrhea, infertility, acromegaly, parkinsonism—that are susceptible to direct or indirect effects
γ-Glutamyltransferase in Hypernephroma
Authors: Lisa J. Cardo
Journal: JAMA (1991)

<h3>To the Editor. —</h3> Renal cell carcinoma is known to be associated with reversible hepatic dysfunction accompanied by hepatosplenomegaly in the absence of metastatic disease to the liver or spleen.<sup>1,2</sup>The syndrome has been reported to cause elevations in the levels of serum alkaline phosphatase, serum bilirubin, aspartate aminotransferase, alanine aminotransferase, and serum L-lactate dehydrogenase. A patient recently presented with the syndrome and elevation of the serum γ-glutamyl-transferase (GGT) level, a test that was introduced subsequent to previously reported cases. <h3>Report of a Case.—</h3> A 69-year-old woman with a history (18 years ago) of renal cell carcinoma and left nephrectomy came to the emergency department complaining of severe epigastric pain, weight loss, and early satiety. There was no history of alcohol abuse, drug or medication use, blood transfusion, or recent travel. Physical examination revealed an epigastric mass and splenomegaly. Serum chemistry values were as follows: L-lactate dehydrogenase, 375 U/L;
The calcium-sensing receptor is required for normal calcium homeostasis independent of parathyroid hormone
Authors: Claudine H. Kos, Andrew C. Karaplis, Ji-Bin Peng, Matthias A. Hediger, David Goltzman, Khalid S. Mohammad, Theresa A. Guise, Martin R. Pollak
Journal: Journal of Clinical Investigation (2003)

The extracellular calcium-sensing receptor (CaR; alternate gene names, CaR or Casr) is a membrane-spanning G protein–coupled receptor. CaR is highly expressed in the parathyroid gland, and is activated by extracellular calcium (Ca2+o). Mice homozygous for null mutations in the CaR gene (CaR–/–) die shortly after birth because of the effects of severe hyperparathyroidism and hypercalcemia. A wide variety of functions have been attributed to CaR. However, the lethal CaR-deficient phenotype has made it difficult to dissect the direct effect of CaR deficiency from the secondary effects of hyperparathyroidism and hypercalcemia. We therefore generated parathyroid hormone–deficient (PTH-deficient) CaR–/– mice (Pth–/–CaR–/–) by intercrossing mice heterozygous for the null CaR allele with mice heterozygous for a null Pth allele. We show that genetic ablation of PTH is sufficient to rescue the lethal CaR–/– phenotype. Pth–/–CaR–/– mice survive to adulthood with no obvious difference in size or appearance relative to control Pth–/– littermates. Histologic examination of most organs did not reveal abnormalities. These Pth–/–CaR–/– mice exhibit a much wider range of values for serum calcium and renal excretion of calcium than we observe in control littermates, despite the absence of any circulating PTH. Thus, CaR is necessary for the fine regulation of serum calcium levels and renal calcium excretion independent of its effect on PTH secretion.
Amoxil and Talpen.
Authors: E T Knudsen
Journal: BMJ (1977)

diazepoxide is also reported to have caused non-urticarial reactions.8In most cases the abnormalities resolved after the offending agent was discontinued.However, rechallenge in some instances with the aetiological agent at a later date was rapidly followed by reappearance of the allergic reactions noted earlier.This brief review clearly establishes the fact that, although hypersensitivity reactions to diazepam and other benzodiazepines are rare, they are far from being undocumented.
Dissecting out the mechanism of cardioprotection by endogenous erthyropoietin using genetic engineering
Authors: S DAVIDSON, D YELLON
Journal: Cardiovascular Research (2006)

See article by Tada et al.  [2]  (pages 466–477) in this issue. 

Erythropoietin (EPO), as the name suggests, was first discovered as a cytokine for red blood cells, but as is so often the case, turns out to have other highly interesting physiological effects. It is produced primarily in the kidneys, and its synthesis increases in response to a decrease in blood oxygen levels. In 1989, the use of recombinant EPO was approved for the treatment of anemia resulting from chronic renal failure. Anemia also occurs quite frequently in patients with chronic heart failure, and may be an independent risk factor for adverse outcomes [1]. Preliminary data suggests that treatment with EPO may improve symptoms in these patients [1]. However, exciting developments in recent years indicate that erythroid progenitors are not the only cells that express the EPO receptor (EpoR), and EPO may have direct effects on other cell types. Functional EpoR pathways have been observed in cardiomyocytes, neurons, and other cell types.

In a report in this issue of Cardiovascular Research , Tada and colleagues have used a powerful genetic approach to evaluate the importance of the endogenous EpoR signalling pathway in myocardial ischemia and reperfusion [2]. They made use of EpoR knockout mice that had been transgenically re-engineered to re-express EpoR under the control of the GATA-1 promoter, and therefore solely in the hematopoietic cell lineage. These … 

* Corresponding author. Tel.: +44 207 380 9591; fax: +44 207 388 5095. Email address: d.yellon{at}ucl.ac.uk
The role of RhoA kinase inhibition in human placenta-derived multipotent cells on neural phenotype and cell survival
Authors: Chih-Hsiang Wang, Chia-Ching Wu, Shan-Hui Hsu, Jun-Yang Liou, Yu-Wei Li, Kenneth K. Wu, Yiu-Kay Lai, B. Linju Yen
Journal: Biomaterials (2013)
Anomalous Pulmonary Venous Drainage
Authors: SYED M. MOHIUDDIN, HUGH S. LEVIN, VINCENT RUNCO, RICHARD W. BOOTH
Journal: Circulation (1966)

An anomaly of pulmonary venous drainage in an 8-year-old child is described whereby all four pulmonary veins emptied into a common chamber which in turn communicated with both the left atrium and the inferior vena cava. The venous anomaly and an accompanying atrial septal defect were demonstrated by selective cineangiocardiography. Ligation of the vein at the level of the right diaphragm, thus rerouting the entire pulmonary venous return through the alternate pathway to the left atrium, was tolerated without difficulty. The embryology, diagnosis, and surgical management of the anomaly are discussed.
Diltiazem at reperfusion reduces neutrophil accumulation and infarct size in dogs with ischaemic myocardium
Authors: G. Rousseau, G. St-Jean, J.-G. Latour, Y. Merhi, S. Nattel, D. Waters
Journal: Cardiovascular Research (1991)

The aim was to demonstrate the ability of diltiazem to protect the ischaemic myocardium in the course of coronary reperfusion, and to establish if an interaction with neutrophils is implied.Ischaemia was induced by occluding the left anterior descending coronary artery for 90 min followed by 6 h of reperfusion with a residual critical stenosis left in place. Three groups were studied: group 1 (control) received a saline perfusion; group 2 was given a bolus injection of 400 micrograms.kg-1 of diltiazem 10 min before reperfusion, followed by 4 micrograms.kg-1.min-1 perfusion until termination of experiment; group 3 was made neutropenic by injecting a neutrophil antiserum produced in rabbits and was then treated with diltiazem, as in the second group.60 mongrel dogs of either sex were allocated at random into one of the three groups the day before the experiment.Diltiazem plasma concentrations ranged from 68.6(SEM 10.0) to 102.5(15.2) micrograms.litre-1 during the study. Transmural collateral blood flow, measured with 153Gd microspheres 15 min after occlusion, and area at risk, evaluated by Evans blue perfusion, did not differ among the three groups. Infarct size, estimated by triphenyltetrazolium staining of heart slices and expressed as a percentage of area at risk, was less (p less than 0.05) in the diltiazem [20.5(5.2)%] and diltiazem plus neutropenia [17.6(5.4)%] groups compared to controls [39.8(6.9)%] but neutropenia added no significant benefit to diltiazem alone. The animals treated with diltiazem alone had lower serum creatine kinase levels than controls, at 5719(891) v 14,333(2885) IU.litre-1, p less than 0.05. The neutrophilia seen in controls was virtually absent in diltiazem dogs. Myocardial neutrophil accumulation estimated by scintigraphy of 111In labelled autologous neutrophils was much less in diltiazem than in control dogs, at 3948(1228) v 11,021(2081) 111In-neutrophil.g-1 of infarct, p less than 0.02.Diltiazem given during reperfusion reduces infarct size by a mechanism that includes an inhibition of neutrophil accumulation in the post-ischaemic myocardium.
Structural Determinants of the Capacity of Heparin to Inhibit the Formation of the Human Amplification C3 Convertase
Authors: Michel D. Kazatchkine, Douglas T. Fearon, Dean D. Metcalfe, Robert D. Rosenberg, K. Frank Austen
Journal: Journal of Clinical Investigation (1981)

The ability of heparin glycosaminoglycan to prevent formation of the properdin-stabilized amplification C3 convertase is independent of antithrombin binding activity and requires substitution of the amino sugar and a degree of oxygen (O)-sulfation which could be on the uronic acid or the amino sugar. Preparations of heparin glycosaminoglycan isolated by different techniques from different species (rat, human, and porcine) exhibited an equivalent capacity to inhibit generation of the amplification C3 convertase. Hyaluronic acid, which is devoid of O-sulfation, had no inhibitory activity; chondroitin 4-sulfate of rat and whale origins, chondroitin 6-sulfate of rat and shark origins, and dermatan sulfate from porcine skin are O-sulfated on the galactosamine and had minimal activity. Porcine heparin glycosaminoglycan, isolated on the basis of affinity for antithrombin III, had no greater anticomplementary activity than porcine glycosaminoglycan, which failed to bind antithrombin III and had essentially no anticoagulant activity. Nitrogen (N)-desulfation of porcine heparin reduced anticomplementary activity to the level of the other sulfated mucopolysaccharides, and both N-resulfation and N-acetylation restored the original activities, thereby indicating a requirement for N-substitution, but not N-sulfation. N-resulfation of N-desulfated and O-desulfated heparin did not restore any activity, thus indicating that O-sulfation and N-substitution represent independent, critical structural requirements for the anticomplementary activity of heparin glycosaminoglycan. Inasmuch as N-desulfated-N-acetylated heparin had no anticoagulant activity, the nature of the N-substitution completely distinguishes the plasma-protein effector pathway that is inhibited.
Body surface map patterns of altered depolarization and repolarization in right bundle branch block.
Authors: G S Sohi, N C Flowers
Journal: Circulation (1980)

Surface maps from 14 patients with right bundle branch block were analyzed throughout depolarization and repolarization. The abnormalities in depolarization found in all the subjects were 1) epicardial breakthrough that was delayed and shifted to the left, and 2) development of right upper anterior positivity during the midportion of depolarization. In eight patients, this positivity manifested as multiple peaks, suggesting a fragmented spread of depolarization. We believe these findings result not only from the delayed engagement of the right ventricle by the conduction process, but also from its nonuniform and dyssynchronous spread. The recovery phase displayed five abnormal patterns: 1) simultaneous negativity on the right and positivity on the left of the midline in six patients; 2) only negativity on the right of the midline in four; 3) only positive potentials in the left upper chest in two; 4) only negative potentials on the left side of the midline in one; and 5) negative potentials spread diffusely over the precordium in one. The different degrees of this altered repolarization, we believe, depend upon the degrees of altered sequence of activation of the heart in addition to the changes produced by the underlying disease process.
Book: Humanitarian Crises: The Medical and Public Health Response
Authors: D. Summerfield
Journal: BMJ (2000)

Eds Jennifer Leaning, Susan M Briggs, Lincoln C Chen Harvard University Press, £27.95, pp 379 ISBN 0 674 15515 7 Rating: ![Graphic][1]</img> ![Graphic][2]</img> ![Graphic][3]</img> ![Graphic][4]</img> Call me a misery, but the passing of the 20th century—in which war and genocide claimed over 150 million people—might more properly have been marked by a requiem mass than by all the razzmatazz. Between 25 and 40 wars were active at any one time in the 1980s and 1990s, almost all “internal” and principally targeting civilians and their ways of life. Most of the arms used in these wars came from members of the United Nations Security Council, an apt commentary … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif [3]: /embed/inline-graphic-3.gif [4]: /embed/inline-graphic-4.gif
Effects of spontaneous myocardial oscillation on cardiac function: direct observation of the epicardial fluorescence image in calcium overloaded isolated hamster hearts
Authors: T. Shinozaki, N. Ishide, M. Satoh, K. Shirato
Journal: Cardiovascular Research (1996)

Calcium overload induces spontaneous cyclic calcium release from the sarcoplasmic reticulum, leading to spontaneous myocardial oscillation. This study was designed to elucidate (1) the effect of the myocardial oscillation on changes in ventricular performance and (2) how these changes relate to the strength of the diastolic spontaneous myocardial oscillation and the spatial extent--that is, in how extensive an area of the epicardium it occurred.the isovolumic pressure of the left ventricle and epicardial fura 2 fluorescence in isolated hamster hearts were simultaneously observed at various calcium concentrations ([Ca2+]o). Endothelial cells and pericytes of the capillaries, preferentially stained by fura 2, were passively oscillated by surrounding myocytes during diastole at concentrations greater than 1 mmol/l of [Ca2+]o. The strength of the myocardial oscillation was evaluated as the root mean square (RMS) of fluctuation in the distance between endothelial cells or pericytes. The spatial extent of the myocardial oscillation was estimated as the appearance rate, defined as the ratio of the number of microscopic fields showing the capillary oscillation, to the total number of examined fields.Up to 4 mmol/l of [Ca2+]o, developed pressure and maximum rate of pressure rise significantly increased in a manner dependent on [Ca2+]o, but a further increase in [Ca2+]o significantly decreased these parameters. In the presence of ryanodine (2.5 mumol/l), developed pressure and maximum rate of pressure rise monotonously increased in a manner dependent on [Ca2+]o. Although the oscillation was never observed at 1 mmol/l of [Ca2+]o (appearance rate = 0%), it occurred in some of the microscopic fields at 2 and 4 mmol/l (appearance rate = 19.5 and 56.3%, respectively) and occurred in all microscopic fields at concentrations greater than 4 mmol/l (appearance rate = 100%). Ryanodine, which completely eliminated the capillary oscillation, inhibited the increase of both RMS and end-diastolic pressure by an increase in [Ca2+]o.Our data suggest that the myocardial oscillation impairs systolic and diastolic function in intact ventricle, and that these effects are associated with the spatial extent and the strength of the myocardial oscillation.
ADDITIONAL COMMUNICATIONS CONCERNING A REMEDY FOR TUBERCULOSIS.
Authors: R. KOCH
Journal: JAMA (1891)

The following translation of Mr. Doctor McDill represents perfectly the original treatise. PROF. EHRLICHforPROF. KOCH. Berlin, Jan. 17, 1891. Since the publication, two months ago, (see<i>Deutsche Med. Wochenschr</i>., No. 46 a) of my experiments with a new method of cure for tuberculosis, many physicians have obtained the remedy and have thereby been enabled to become acquanted with its properties by personal experiences. As far as I review the publications which have appeared, together with the communications to me by letter on this subject, my statements have, upon the whole, found full corroboration. It may be considered as generally accepted that the remedy has a specific action upon tuberculous tissue and that it consequently can be utilized as a very subtle and reliable reagent for the bringing to light of the hidden, and the diagnosing of the doubtful tuberculosis processes. Also regarding the curative effect of the
Monitoring circulating epithelial tumor cells (CETCs) during primary systemic chemotherapy including trastuzumab for early prediction of outcome in patients with Her2/neu-positive tumors
Authors: M. Gajda, O. Camara, S. Oppel, T. Kroll, C. Jörke, S. Krauspe, U. Hammer, C. Rabenstein, M. Untch, I.B. Runnebaum, K. Pachmann
Journal: Annals of Oncology (2008)
Premature coronary deaths in Asians
Authors: A. Ascherio, E. Cho, K. Walsh, F. M Sacks, W. C Willett, A. Faruqui
Journal: BMJ (1996)

children becomes concentrated in large, tertiary paediatric intensive care units.1 Training junior doctors in more than just the basic sldlls of resuscitation will be easier in centres with a high throughput of patients, and ultimately this will enable a higher standard of care to be delivered in local hospitals, where most of these doctors will eventually work.T SAJJANHAR Feliow in paediatric intensive care MJMARSH Consultant in psediatric intensive care I A MURDOCH Consultant in paediatric intensive care Guy's Hospital, London SE1
MICROELECTROPHORESIS OF BLOOD PLATELETS AND THE EFFECTS OF DEXTRAN*†
Authors: S. William Ross, Richard V. Ebert
Journal: Journal of Clinical Investigation (1959)

The intravenous administration of dextran has previously been shown to produce a bleeding tendency in laboratory animals and in humans. Extensive studies concerning the hemostatic defect have yielded much useful information. Carbone, Furth, Scott and Crosby (1) found that the major abnormality consisted of a prolongation of the bleeding time. In seven of 11 patients given 1,500 to 6,500 ml. of dextran intravenously over a five day period the bleeding time was prolonged over 30 minutes. The concentration of platelets, clotting time, fibrinogen level, clot retraction time and prothrombin consumption test were not significantly affected by dextran. The prothrombin time was slightly abnormal. It appears unlikely that this finding explains the hemostatic defect because of the inconstancy and mild degree of the change. Adelson, Crosby and Roeder (2) found that smaller amounts of dextran were required to produce a prolonged bleeding time in dogs made thrombocytopenic by irradiation than in normal dogs. Comparable volumes of gelatin in the thrombocytopenic dogs did not prolong the
USE OF GENTIAN VIOLET IN THRUSH
Authors: Harold K. Faber
Journal: JAMA (1925)

<h3>To the Editor:</h3> —Through a regrettable inadvertence in preparing our clinical note on the gentian violet treatment of thrush (The Journal, September 19, p. 900) we failed to mention the work of Churchman, whose priority in the experimental and clinical study of gentian violet is, of course, well known. We have found, since submitting our manuscript, that Churchman in 1921 (Further Studies of the Behavior of Bacteria Toward Gentian Violet,<i>J. Exper. Med.</i><b>33</b>:569 [May] 1921) reported that "in a plain agar plate... strokes of stained gram-negative organisms, for example<i>Bacillus subtilis</i>and<i>Oidium albicans</i>, will not grow at all" and showed photographs illustrating the point. While our own study was made in ignorance of these observations, we take pleasure in acknowledging them now. It is, of course, gratifying to us to find experimental support for our clinical impressions.
The critical role of histone H2A-deubiquitinase Mysm1 in hematopoiesis and lymphocyte differentiation
Authors: Anastasia Nijnik, Simon Clare, Christine Hale, Claire Raisen, Rebecca E. McIntyre, Kosuke Yusa, Aaron R. Everitt, Lynda Mottram, Christine Podrini, Mark Lucas, Jeanne Estabel, David Goulding, Niels Adams, Ramiro Ramirez-Solis, Jacqui K. White, David J. Adams, Robert E. W. Hancock, Gordon Dougan
Journal: Blood (2011)