Acute myocardial infarction (AMI) and sudden cardiac death (SCD) are among the most serious and catastrophic of acute cardiac disorders, accounting for hundreds of thousands of deaths each year worldwide. Although the incidence of AMI has been decreasing in the US according to the American Heart Association, heart disease is still the leading cause of mortality in adults. In most cases of AMI and in a majority of cases of SCD, the underlying pathology is acute intraluminal coronary thrombus formation within an epicardial coronary artery leading to total or near-total acute coronary occlusion. This article summarizes our current understanding of the pathophysiology of these acute coronary syndromes and briefly discusses new approaches currently being researched in an attempt to define and ultimately reduce their incidence.

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In this 3-part study the distribution of the post-gonococcal stricture has been related to the disposition of mucous glands in paraurethral glands by mapping the distribution of these glands in the human male urethra. Experimental study in the rat has indicated the role of extravasation of urine in the pathogenesis of urethral stricture. Lastly, the ultrastructure of urethral stricture tissue has revealed features that suggest why some strictures are fibrous and others resilient.

This paper presents the fundamental mathematics to determine the minimum crack width detectable with a terrestrial laser scanner in unit-based masonry. Orthogonal offset, interval scan angle, crack orientation, and crack depth are the main parameters. The theoretical work is benchmarked against laboratory tests using 4 samples with predesigned crack widths of 1-7mm scanned at orthogonal distances of 5.0-12.5m and at angles of 0˚-30˚. Results showed that absolute errors of crack width were mostly less than 1.37mm when the orthogonal distance varied 5.0-7.5m but significantly increased for greater distances. Orthogonal distance had a disproportionately negative effect compared to the scan angle.2

Insulin resistance is the main pathologic mechanism that links the constellation of clinical, metabolic and anthropometric traits with increased risk for cardiovascular disease and type II diabetes mellitus. These traits include hyperinsulinemia, impaired glucose intolerance, endothelial dysfunction, dyslipidemia, hypertension, and generalized and upper body fat redistribution. This cluster is often referred to as insulin resistance syndrome. The progression of insulin resistance to diabetes mellitus parallels the progression of endothelial dysfunction to atherosclerosis leading to cardiovascular disease and its complications. In fact, insulin resistance assessed by homeostasis model assessment (HOMA) has shown to be independently predictive of cardiovascular disease in several studies and one unit increase in insulin resistance is associated with a 5.4% increase in cardiovascular disease risk. This review article addresses the role of insulin resistance as a main causal factor in the development of metabolic syndrome and endothelial dysfunction, and its relationship with cardiovascular disease. In addition to this, we review the type of lifestyle modification and pharmacotherapy that could possibly ameliorate the effect of insulin resistance and reverse the disturbances in insulin, glucose and lipid metabolism.