Abstract-The raised fatty streak (fatty plaque) is the gross term for the lesion intermediate between the juvenile (flat) fatty streak and the raised lesion of atherosclerosis. We measured the percentage of intimal surface involved with flat fatty streaks, raised fatty streaks, and raised lesions in the aortas and right coronary arteries of 2876 autopsied persons aged 15 through 34 years who died of external causes. Raised fatty streaks were present in the abdominal aortas of Ϸ20% of 15-to 19-year-old subjects, and this percentage increased to Ϸ40% for 30-to 34-year-old subjects. Raised fatty streaks were present in the right coronary arteries of Ϸ10% of 15-to 19-year-old subjects, and this percentage increased to Ϸ30% for 30-to 34-year-old subjects. The percent intimal surface involved with raised fatty streaks increased with age in both arteries and was associated with high non-high density lipoprotein (HDL) and low HDL cholesterol concentrations in the abdominal aorta and right coronary artery, with hypertension in the abdominal aorta, with obesity in the right coronary artery of men, and with impaired glucose tolerance in the right coronary artery. Associations of risk factors with raised fatty streaks became evident in subjects in their late teens, whereas associations of risk factors with raised lesions became evident in subjects aged Ͼ25 years. These results are consistent with the putative transitional role of raised fatty streaks and show that coronary heart disease risk factors accelerate atherogenesis in the second decade of life. Thus, long-range prevention of atherosclerosis should begin in childhood or adolescence. (Arterioscler

The percentage of asymptomatic subjects who intermittently shed HSV-1 DNA in tears or saliva was higher than the percentage of subjects with positive ELISA or neutralization antibodies to HSV. Because most HSV transmission occurs during asymptomatic shedding, further knowledge of the prevalence of HSV-1 DNA in tears and saliva is warranted to control its spread. Shedding is simple to study, and its suppression may be an efficient way to evaluate new antivirals in humans.

1. Increased blood or plasma viscosity has been observed in almost all conditions associated with accelerated atherosclerosis. Cognizant of the enlarging body of evidence implicating increased viscosity in atherogenesis, we hypothesize that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity correlate with their association with risk of atherosclerosis. 2. Blood viscometry was performed on samples from 28 healthy, non-fasting adult volunteers using a capillary viscometer. Data were correlated with haematocrit, fibrinogen, serum viscosity, total cholesterol, high-density lipoprotein-cholesterol, triglycerides and calculated low-density lipoprotein-cholesterol. 3. Low-density lipoprotein-cholesterol was more strongly correlated with blood viscosity than was total cholesterol (r = 0.4149, P = 0.0281, compared with r = 0.2790, P = 0.1505). High-density lipoprotein-cholesterol levels were inversely associated with blood viscosity (r = -0.4018, P = 0.0341). 4. To confirm these effects, viscometry was performed on erythrocytes, suspended in saline, which had been incubated in plasma of various low-density lipoprotein/high-density lipoprotein ratios. Viscosity correlated directly with low-density lipoprotein/high-density lipoprotein ratio (n = 23, r = 0.8561, P < 0.01). 5. Low-density lipoprotein receptor occupancy data suggests that these effects on viscosity are mediated by erythrocyte aggregation. 6. These results demonstrate that the effects of low-density lipoprotein and high-density lipoprotein on blood viscosity in healthy subjects correlate with their association with risk of atherosclerosis. These effects on viscosity may play a role in atherogenesis by modulating the dwell or residence time of atherogenic particles in the vicinity of the endothelium.

Lysostaphin is effective in treating experimental endophthalmitis mediated by MRSA.

valuation of the CBD has been performed routinely with ultrasonography for at least 20 years. Within this time period numerous articles have been published describing the changes in caliber of the CBD related to various factors, including hepatobiliary disease, cholelithiasis, 1-3 patient's age, 4-6 and associated renal disease 7 or liver transplantation. 8 Extrinsic factors, such as time of day, 9 respiration, 10 or patient positioning during the examination, 11 also have been shown to affect the caliber of the CBD. The goals of this prospective study were first to determine if a significant change occurs in the diameter of the CBD with aging, in particular after the age of 60 year, and second, if a significant change in duct diameter does occur, to determine what the normal size of the common duct is in this patient population.To achieve these goals, evaluation of a large asymptomatic aging population is necessary. In the most frequently cited report on the effects of aging on CBD size, Wu and colleagues 5 measured the internal diameter of 203 CBD in healthy subjects. Of these

BackgroundThe pathogenesis of vascular disease is complex and as of yet not totally understood. Conventional wisdom suggests that atherosclerotic cardiovascular disease is caused by the accumulation of lipid molecules in the arterial luminal wall. Various therapeutic modalities have been proposed; however, current treatment with cholesterol-lowering drugs has not completely solved this problem. Risk factors aiding in the development of atherosclerotic disease have been long promoted, such as genetics, dyslipidemia, hypertension, smoking, lack of adequate exercise, metabolic syndrome, and obesity. However, 50% of myocardial infarctions occur in subjects without overt hyperlipidemia, and 20% of myocardial infarctions occur in the absence of any classic risk factors [Ridker and Libby, 2011].The reason why the pathogenesis of chronic vascular diseases, including atherosclerosis, hypertension, and the metabolic syndrome, is not fully understood by the mainstream is because the role of blood viscosity has been ignored. Most physicians are aware of acute hyperviscosity syndromes as can be seen in Waldenstrom's macroglobulinemia, polycythemia vera, and leukemia, which require immediate intervention. In these conditions, blood viscosity is in the range of 60 millipoise or greater at a shear rate of 94.5/s. However, chronic lesser elevations of viscosity do occur (roughly, 50-56 millipoise at 94.5/s, normal being 37-49 millipoise at the same shear rate) [Antonova and Velcheva, 1999;Velcheva et al. 2008]. Rosenson and colleagues reported a normal value of 32.6 millipoise at a shear rate of 100/s [Rosenson et al.1996].States of chronic, lower elevations of viscosity are clinically less obvious, and left unappreciated, can ultimately shorten one's lifespan by contributing to cardiovascular disease. In the study of Antonova and Velcheva, viscosities in the range referred to here as 'chronic hyperviscosity' were associated with chronic cerebral infarctions, transient ischemic attacks, and risk factors for stroke [Antonova and Velcheva, 1999]. In Velcheva and colleagues' work, chronic hyperviscosity was associated with transient ischemic attacks and unilateral cerebral infarctions [Velcheva et al. 2008].It should be noted that the reference ranges for blood viscosity are tentative, and work remains in standardizing the reporting and measuring of blood viscosity. Hopefully, a collaboration similar to the Reference Values for Arterial Stiffness'The role of chronic hyperviscosity in vascular disease Gregory Sloop, Ralph E. Holsworth Jr, Joseph J. Weidman and John A. St Cyr Abstract: The pathogenesis of several major cardiovascular diseases, including atherosclerosis, hypertension, and the metabolic syndrome, is not widely understood because the role of blood viscosity is overlooked. Low-density lipoprotein accelerates atherosclerosis by increasing blood viscosity in areas of low flow or shear, predisposing to thrombosis. Atherosclerotic plaques are organized mural thrombi, as proposed by Duguid in the midtwentieth century. High-de...

These studies demonstrate the establishment of Staphylococcus keratitis in the mouse eye. This model should provide for a large range of future studies that are currently unavailable in the rabbit keratitis model, particularly those requiring a genetically altered host or specific immunologic reagents.

Blood viscosity is increased by elevated concentrations of acute phase reactants and hypergammaglobulinemia in inflammation. These increase blood viscosity by increasing plasma viscosity and fostering erythrocyte aggregation. Blood viscosity is also increased by decreased erythrocyte deformability, as occurs in malaria. Increased blood viscosity contributes to the association of acute infections with myocardial infarction (MI), venous thrombosis, and venous thromboembolism. It also increases vascular resistance, which decreases tissue perfusion and activates stretch receptors in the left ventricle, thereby initiating the systemic vascular resistance response. This compensates for the increased vascular resistance by vasodilation, lowering hematocrit, and decreasing intravascular volume. This physiological response causes the anemias associated with malaria, chronic inflammation, and other chronic diseases. Since tissue perfusion is inversely proportional to blood viscosity, anemia may be beneficial as it increases tissue perfusion when erythrocyte aggregating factors or erythrocytes with decreased deformability are present in the blood.