THE DESIGN AND ANALYSIS OF EXPERIMENTS. By Oscar Kempthorne. New York, John Wiley and Sons, Inc., 1952. 631 pp. $8.50. This book by a teacher of statistics (as well as a consultant for \"experimenters\") is a comprehensive study of the philosophical background for the statistical design of experiment. It is necessary to have some facility with algebraic notation and manipulation to be able to use the volume intelligently. The problems are presented from the theoretical point of view, without such practical examples as would be helpful for those not acquainted with mathematics. The mathematical justification for the techniques is given. As a somewhat advanced treatment of the design and analysis of experiments, this volume will be interesting and helpful for many who approach statistics theoretically as well as practically. With emphasis on the \"why,\" and with description given broadly, the author relates the subject matter to the general theory of statistics and to the general problem of experimental inference. MARGARET J. ROBERTSON

The Design and Analysis of Experiments

Global strategy for asthma management and prevention

ecent research has shown that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis. Immune cells dominate early atherosclerotic lesions, their effector molecules accelerate progression of the lesions, and activation of inflammation can elicit acute coronary syndromes. This review highlights the role of inflammation in the pathogenesis of atherosclerotic CAD. It will recount the evidence that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree. A decade ago, the treatment of hypercholesterolemia and hypertension was expected to eliminate CAD by the end of the 20th century. Lately, however, that optimistic prediction has needed revision. Cardiovascular diseases are expected to be the main cause of death globally within the next 15 years owing to a rapidly increasing prevalence in developing countries and eastern Europe and the rising incidence of obesity and diabetes in the Western world. 1 Cardiovascular diseases cause 38 percent of all deaths in North America and are the most common cause of death in European men under 65 years of age and the second most common cause in women. These facts force us to revisit cardiovascular disease and consider new strategies for prediction, prevention, and treatment.

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Inflammation, Atherosclerosis, and Coronary Artery Disease

ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation : The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC).

/pdf/2015-esc-guidelines-for-the-management-of-acute-coronary-6did6h5nxk.pdf

2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC)

ACCF
: American College of Cardiology Foundation
ACS
: acute coronary syndrome
AHA
: American Heart Association
CAD
: coronary artery disease
CABG
: coronary artery bypass grafting
CKMB
: creatine kinase MB isoform
cTn
: cardiac troponin
CT
: computed tomography
CV
: coefficient of variation
ECG
: electrocardiogram
ESC
: European Society of Cardiology
FDG
: fluorodeoxyglucose
h
: hour(s)
HF
: heart failure
LBBB
: left bundle branch block
LV
: left ventricle
LVH
: left ventricular hypertrophy
MI
: myocardial infarction
mIBG
: meta-iodo-benzylguanidine
min
: minute(s)
MONICA
: Multinational MONItoring of trends and determinants in CArdiovascular disease)
MPS
: myocardial perfusion scintigraphy
MRI
: magnetic resonance imaging
mV
: millivolt(s)
ng/L
: nanogram(s) per litre
Non-Q MI
: non-Q wave myocardial infarction
NSTEMI
: non-ST-elevation myocardial infarction
PCI
: percutaneous coronary intervention
PET
: positron emission tomography
pg/mL
: pictogram(s) per millilitre
Q wave MI
: Q wave myocardial infarction
RBBB
: right bundle branch block
sec
: second(s)
SPECT
: single photon emission computed tomography
STEMI
: ST elevation myocardial infarction
ST–T
: ST-segment –T wave
URL
: upper reference limit
WHF
: World Heart Federation
WHO
: World Health Organization

Myocardial infarction (MI) can be recognised by clinical features, including electrocardiographic (ECG) findings, elevated values of biochemical markers (biomarkers) of myocardial necrosis, and by imaging, or may be defined by pathology. It is a major cause of death and disability worldwide. MI may be the first manifestation of coronary artery disease (CAD) or it may occur, repeatedly, in patients with established disease. Information on MI rates can provide useful information regarding the burden of CAD within and across populations, especially if standardized data are collected in a manner that …

/pdf/third-universal-definition-of-myocardial-infarction-1nbq846anm.pdf

Third universal definition of myocardial infarction

Eight patients with homozygous sickle cell anemia, 15 heterozygotes, and eight control individuals were investigated with respect to plasma concentrations of the inflammatory markers lysozyme and myeloperoxidase and the complement activation marker C3d The patients showed significantly increased levels of myeloperoxidase and C3d, but not lysozyme, compared with the heterozygotes and the controls The heterozygotes were also significantly different from the controls with regard to C3d concentration The concentrations of myeloperoxidase and C3d in plasma showed a significant inverse correlation with the hemoglobin concentration Myeloperoxidase and C3d showed a significant positive correlation This suggests a role for the neutrophil and the complement system in the pathophysiology of sickle cell disease

Increased in vivo activation of neutrophils and complement in sickle cell disease

Human neutrophil lipocalin in fMLP-activated whole blood as a diagnostic means to distinguish between acute bacterial and viral infections

The function of alveolar macrophages (AM phi s) was studied in terms of the secretion of various chemotactic factors. Human AM phi s were obtained by BAL from healthy non-smokers and smokers. One of the chemotactic factors was LTB4, an arachidonic acid metabolite of the lipoxygenase pathway. The amount of LTB4 was determined in culture medium, in cell homogenate and in BAL-fluid. The total chemotactic activity for neutrophils was measured in culture medium and in BAL-fluid. AM phi s from smokers showed an impaired secretion of LTB4. The spontaneous secretion in vitro was inhibited by 90% (p less than 0.05) and the stimulated one was blocked by 84% (p less than 0.05). This impairment was not followed by a decrease in total chemotactic activity, indicating the existence of other chemotactic factors than LTB4. Preliminary characterization of the chemotactic activity by gel filtration demonstrated at least four different chemotactic factors. Budesonide inhibited both the release of LTB4 and the total chemotactic activity in medium from stimulated AM phi s.

Human alveolar macrophages from smokers have an impaired capacity to secrete LTB4 but not other chemotactic factors.

Three eosinophil proteins, eosinophil cationic protein (ECP), eosinophil protein-X (EPX), and eosinophil-derived neurotoxin (EDN), have neurotoxic properties. EDN and EPX may be identical. ECP is by far the most potent neurotoxic eosinophil-derived protein. The damaging effect of the three proteins have been claimed to be selective. This selectivity can, at least in part, be explained by way of the experimental injections. Several observations are in favour of a selectivity through accumulation. Immunocytochemical localization of intraventricular injected ECP supports this hypothesis and indicates furthermore that ECP has an immediate reactivity towards and possible toxic effect against nervous tissue in general.

Eosinophils and cellular injury: the Gordon phenomenon as a model.

The ferritin level in serum was investigated in 9 patients with myocardial infarction, all with a history of chest pain of less than 4 hours before admission. A significant rise in serum ferritin level was found in 8 patients. The rise was generally smaller than that seen in acute infection and not significantly correlated to the size of infarction, as estimated from changes in serum levels of myoglobin, ASAT and LDH. The rise started after a mean of 30 hours, the peak being reached within a week (M 4.3 days). Serum ferritin then fell to 120--300% (M 190) of the initial level, where it remained. An initial rise in serum iron levels was unexpectedly seen within 12 hours in 7 patients.

Per Venge

Papers

Increased in vivo activation of neutrophils and complement in sickle cell disease

Human neutrophil lipocalin in fMLP-activated whole blood as a diagnostic means to distinguish between acute bacterial and viral infections

Human alveolar macrophages from smokers have an impaired capacity to secrete LTB4 but not other chemotactic factors.

Eosinophils and cellular injury: the Gordon phenomenon as a model.

Serum Ferritin during Inflammation A Study on Myocardial Infarction