Lesion development

Figure 1. Effect of twinberry leaf extract infiltrated 24 hours after virus inoculation on TMV starch lesion development on cucumber cotyledons...

Intermittent claudication is a group of symptoms characterized by pain in the calf muscle of one or both legp, caused by walking and relieved by rest. It is a manifestation of peripheral vascular disease, in which atherosclerotic lesions develop in the femoral artery, diminishing blood supply to the lower leg. Cilostazol is used to treat intermittent claudication. 

Schwamm LH, Koroshetz WJ, Sorensen AG, Wang B, Copen WA, Budzik R, Rordorf G, Buonanno FS, Schaefer PW, Gonzalez RG. Time course of lesion development in... 

Potteaux S, Combadiere C, Esposito B, et al. Chemokine receptor CCR1 disruption in bone marrow cells enhances atherosclerotic lesion development and inflammation in mice. Mol Med 2005 11 16-20. 

Reckless J, Metcalfe JC, Grainger DJ (1997) Tamoxifen decreases cholesterol sevenfold and abolishes lipid lesion development in apolipoprotein E knockout mice. Circulation 95 1542-1548... 

Smallpox (variola). The acute clinical symptoms of smallpox resemble other acute viral illnesses, such as influenza, beginning with a 2-4 day nonspecific prodrome of fever and myalgias before rash onset. Several clinical features can help clinicians differentiate varicella (chickenpox) from smallpox. The rash of varicella is most prominent on the trunk and develops in successive groups of lesions over several days, resulting in lesions in various stages of development and resolution. In comparison, the vesicular/pustular rash of smallpox is typically most prominent on the face and extremities, and lesions develop at the same time. 

Schissel, S.L., Jiang, X., Tweedie-Hardman, J., Jeong, T., Camejo, E.H., Najib, J., Rapp, J.H., Williams, K.J. andTabas, I., 1998, Secretory sphingomyelinase, a product ofthe acid sphingomyelinase gene, can hydrolyze atherogenic lipoproteins at neutral pH. Implications for atherosclerotic lesion development. 7. Biol. Chem. 273 2738-2746... 

Symptoms Tree bark shrinks and cracks, often in concentric rings with the central piece of bark falling away. Deep lesions develop on the branches. Swelling can occur around the canker, and young twigs may die back. Cream-colored pustules may be seen in summer red spots are more common in fall. Papery bark can result Canker can ring an entire stem. Fruit skins crack fruits dry and can remain, mummified, on the tree. 

Penciclovir is approved as a topical formulation for the treatment of herpes labialis. In immunocompetent individuals, penciclovir shortens the duration of lesion presence and pain by approximately half a day when it is initiated within an hour of lesion development and applied every 2 hours during waking hours for 4 days. 

Atherosclerosis is a progressive vascular fibroproliferative-inflammatory disease. It is triggered, maintained, and driven by risk factors such as hypercholesterolemia, hyperlipidemia, and hypertonus [28]. The characteristic clinical manifestation of atherosclerosis is the atherosclerotic lesion, developing in the vessel wall (atherosclerotic plaque). 

Raines EW, Ross R. Biology of atherosclerotic plaque formation possible role of growth factors in lesion development and the potential impact of soy. J. Nutr. 125, 624S-630S, 1995. 

A 22-year-old woman presents with a complaint of worsening psoriasis. She has a strong family history of the disease and has had lesions on her scalp and elbows for several years. She recently noted new lesions developing on her knees and the soles of her feet. She has been using topical over-the-counter hydrocortisone cream but admits that this treatment does not seem to help. What therapeutic options are available for the treatment of this chronic disease What risks are involved ... 

Modifying effects of various chemicals on preneoplastic and neoplastic lesion development... 

Pennings M, Meurs I, Ye D, Out R, Hoekstra M, van Berkel T, van Eck M (2006) Regulation of cholesterol homeostasis in macrophages and consequences for atherosclerotic lesion development. FEBS Lett 580(23) 5588-5596... 

The atherosclerotic lesions develop in a complex, chronic process. The first detectable lesion is the so-called fatty streak, an aggregation of lipid-laden macrophage foam cells. The next stage of development is the formation of plaques consisting of a core of lipid and necrotic cell debris covered by a layer of connective tissue and smooth muscle cells. These plaques hinder arterial blood flow and may precipitate clinical events by plaque rupture and thrombus formation. Platelets from the thrombi, activated macrophages, and smooth muscle cells release growth factors and cytokines resulting in an inflammatory-fibroproliferative response that leads to the advanced lesions of atherosclerosis. 

Figure 8.5 Pomegranate by-product (PBP) consumption by E° mice attenuates atherosclerotic lesion development, in association with reduction in macrophage oxidative stress and Ox-LDL uptake. E° mice consumed PBP (17 or 51.5 mg gallic acid equivalents/kilogram/day) for 3 months. Control mice received only water (placebo). At the end of the study, the mice aortas as well as the mice peritoneal macrophages were harvested. (A) Atherosclerotic lesion size determination. (B) Total macrophage peroxide levels were determined by the DCFH-DH assay. (C) For determination of macrophage paraoxonase 2 (PON2) lactonase activity, cells (2 x 10e) were incubated with 1 mmol/L dihydrocoumarin in Tris buffer, and the hydrolysis rate was determined after 10 min of incubation at 25°C. (D) The extent of Ox-LDL (25 pg of protein/ milliliter, labeled with FITC) uptake by the mice macrophages (1 x 10e) was determined by flow cytometry. Results are expressed as mean S.D. of three different determinations. = p < 0.01 versus placebo.

Lesion development the development of a lesion at the site of infection can be monitored by measuring daily the area of dermonecrosis with a caliper and calculated by using the formula ... 

In experimental serum sickness, a fall in serum complement level occurs at the time immune complexes form and inflammatory lesions develop (D6). However, levels of complement do not always reflect activation or consumption by immune complexes. The rate of synthesis of complement proteins may be sufficient to replace the amount being consumed, and several of the complement components are so-called acute-phase reactants, i.e., their levels rise with inflammation. Thus, activation may occur despite normal or even elevated levels in the serum. Turnover studies provide more direct evidence of complement utilization but are technically cumbersome (K4). A simpler approach is the detection of split products of complement components, which provides direct evidence of complement activation, or the examination of effusions for evidence of complement depletion (H31, N7, P7). 

Fig. 4.8. Lesion development in permanent middle cerebral artery (MCA) occlusion in a rat measured by repeated MR diffusion-weighted imaging (DWI). Left column Control condition pre-occlusion in coronal slices from posterior (top) to anterior (bottom). The arrow marks the timepoint of occlusion. Images shown in columns 2 to 7 are DWI (subtraction images) measured 30 to 330 min post-occlusion. Note the lesion growth and the increase in signal intensity within the lesion. (Courtesy Dr. M. Hoehn, Cologne)...

Fig. 4.9. Lesion development in stroke models of permanent focal ischemia (PMCAo) visualized by histology (left) and diffusion-weighted (DW) imaging. [Adapted from Garcia et al. (1993) and Brinker et al. (1999)]...

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