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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral type 1 and genital type 2 Herpesvirus hominis (HVH) strains demonstrate distinctive biological properties in primary chick embryo cells (PCE) cultivated in microtest plates. With this procedure four reference strains of known types and 106 clinical isolates were differentiated as type 1 or 2. The type 1 strains showed low efficiency of infection and either no cytopathic effect (CPE) or only an incomplete CPE characterized by uniform thinning of the cell sheet in test wells. Type 2 strains had a high efficiency of infection and with CPE characterized by patchy plaque-like lesions readily distinguished from CPE of type 1 strains. A 96% correlation (27/28) between the PCE microtyping and kinetic neutralization tests and a 94% correlation (60/64) between the PCE microtyping and immunofluorescence test was obtained. The microplate PCE test is a simple, clear-cut, and reliable procedure for the typing of HVH.
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PMID:A chick-embyo cell microtest for typing of Herpesvirus hominis (38531). 16 69

From observations on 454 coronary arteries from subjects ranging in age from prematurely newborn to 90 years, six structural patterns of medial smooth muscle are interpreted as representing, or related to, the proliferation and/or migration of medial smooth muscle into intima. By measuring the extent of inner medial circumference occupied by four of the six patterns, it was possible to calculate a numerical value designated the medial proliferatice and / or migratory activity (MP-MA) of each artery. During the first three decades, nonatherosclerotic diffuse intimal thickening was the characteristic intimal process, and during this phase of the arterial maturation span, the MP-MA of the arteries was significantly related to the degree of intimal thickening. Following a peak MP-MA level by the end of the third decade, there was a progressive decrease in the MP-MA level as the incidence and severity of atherosclerotic intimal thickening increased. At advanced stages of atherosclerotic intimal thickening, which were associated with thinning of adjacent media, intimal-medial structural patterns indicating a relationship between medial smooth muscle proliferative activity and the expanding atherosclerotic plaque were also apparent. The observations support the concept that the movement of medial smooth muscle into intima is a critical step preceding and during the evolution of the atherosclerotic plaque.
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PMID:Structural changes within the media of coronary arteries related to intimal thickening. 33 34

Clinical experience with 5 patients who had complications of atherosclerosis within the aorta at the site of the obliterated ductus arteriosus suggested the occurrence of clinically significant preferential atherosclerosis at this location. To examine this hypothesis, the clinical findings in these patients (4 with saccular aneurysm and 1 with systemic emboli from an ulcerated plaque at this location) were correlated with postmortem examination of the aortic isthmus in 40 consecutive cadavers. The point of ductal closure was the area of most severe atheromatous involvement in 32 of the 40 cadavers, and 25 of the 40 specimens demonstrated ulcerated plaques at this location. Microscopical examination consistently demonstrated intimal irregularity or disruption and thinning of the aortic media in this area. These studies indicate that preferential atherosclerosis occurs at the aortic end of the obliterated ducts arteriosus and that these atherosclerotic changes can be a clinically significant development.
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PMID:Preferential atherosclerosis at the aortic junction of the ligamentum arteriosum: clinical significance and pathological correlation. 93 39

The surfactant delmopinol, which is a new antiplaque agent with a low anti-microbial profile, was tested for its effects on the viscosity of bacterial extracellular glucans. Glucans were isolated from Streptococcus mutans broth supernatants incubated with 0.15 M sucrose in 50 mM sodium phosphate buffer at pH 6. The viscosity was measured in a shear rate range from 15 to 230 reciprocal seconds. The viscosity of the water-soluble glucan was found to be independent of shear rate whereas the water-insoluble glucan showed a strong shear thinning. The addition of delmopinol to preformed glucans did not affect the viscosity nor the shear rate dependence of the glucans. However, when present during synthesis of the polysaccharides, delmopinol was found to reduce the viscosity of both water-soluble and water-insoluble glucans by approximately 50% at the shear rates investigated. The reduction in viscosity for the water-soluble glucans was obtained at a delmopinol concentration of 0.32 mM (0.01%) and for the water-insoluble glucans at 3.2 mM delmopinol. The observed reduction of viscosity of glucans indicates that the in vivo stability of plaque matrix after delmopinol treatment would be lowered, which may lead to a reduction of plaque cohesion and thus facilitate mechanical plaque removal.
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PMID:Effect of delmopinol on the viscosity of extracellular glucans produced by Streptococcus mutans. 142 43

Idiopathic retroperitoneal fibrosis leading to obstructive uropathy is a rare disease in our country, so a typical case deserves presentation. The patient is a 56-year-old female to have a clinical manifestation of obstructive uropathy. Retrograde pyelogram permitted 5 Fr. ureteral catheter to pass the stenotic segment. At the mean-time, there was hydronephrosis, medial deviation and gradual thinning and pointing of the middle segment of the ureter (classic triad). Computed tomography revealed that retroperitoneal soft tissue plaque enveloped aorta, inferior vena cava, and bilateral ureters. The patient received ureterolysis with ureter intraperitonealization and lateralization. The plaque was pathologically proved fibrosis. Renal function became normal postoperatively.
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PMID:[Idiopathic retroperitoneal fibrosis causing obstructive uropathy: a case report]. 165 31

Restenosis is the most important problem limiting the success of coronary angioplasty. Clinically, restenosis is seen in approximately one-third of patients undergoing percutaneous transluminal coronary angioplasty. Several clinical and angiographic risk factors have been identified which may contribute to the development of restenosis. Histopathologic studies indicate that restenosis is characterized by intimal proliferation of smooth muscle cells in a loose connective tissue matrix. These intimal lesions are associated predominantly with the nonatheromatous portion of the vessel wall. Thinning of the media of the plaque-free wall and marked fragmentation of the internal elastic lamina are also seen. Traumatic injury of the vessel wall during angioplasty probably triggers a series of cellular and subcellular events which may ultimately lead to myointimal proliferation and restenosis. Although the exact mechanism by which this occurs is unknown, several factors may enhance smooth muscle cell growth and therefore may play a role in the development of restenosis. These include platelet deposition, mechanical stretching of the media, inflammation of the vessel wall, the activity of growth factors, and alterations in vessel geometry. These possible mechanisms of restenosis suggest several potential ways to limit the proliferative response to vascular injury. Anticoagulants and platelet antagonists, direct inhibitors of smooth muscle proliferation, anti-inflammatory agents, growth factor inhibitors, and new devices which improve final vessel geometry are currently being tested as methods to curb restenosis. Unfortunately, no treatment has yet been shown to reduce significantly the rate of restenosis following angioplasty. The problem of restenosis will most likely be solved by better understanding of the basic molecular and biologic phenomena involved in vascular injury and repair.
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PMID:Restenosis following coronary angioplasty. 195 87

To determine whether aneurysms form in experimental diet-induced atherosclerosis, we reviewed our experience with cynomolgus monkeys (n = 268) and rhesus monkeys (n = 175) fed an atherogenic diet for various lengths of time. Many animals in long-term experiments were fed "regression" diets and cholestyramine to lower cholesterol levels after lesions were established. No aneurysms were found in animals on normal diet. There were no aneurysms in 252 animals fed an atherogenic diet with or without regression for 12 months or less. However, aneurysms formed in 13% of cynomolgus monkeys (4 of 31) and 1% (1 of 107) rhesus monkeys on an atherogenic regimen for 16 to 24 months. Four of the five animals with aneurysms were on a regression diet and cholestyramine for 4 to 12 months. The fifth was fed the atherogenic diet for 20 months without subsequent regression. Aneurysms were prominent and involved the thoracic and abdominal aorta, innominate artery, carotid arteries, iliac and femoral arteries, and formed in areas most involved with plaque formation in both species. Histologic evidence was found of thinning of the media and atrophy with loss of normal architecture. The higher incidence of aneurysms in cynomolgus monkeys was associated with greater media destruction than was noted in the rhesus. These data support the thesis that aneurysm formation is a manifestation of atherosclerosis. In primate atherosclerosis, aneurysms form only after prolonged exposure to the atherogenic regimen, even in the presence of declining serum cholesterol levels. Matrix fibers in plaques may provide structural support to the aortic wall where there is underlying atrophy of the media. With time or declining serum cholesterol levels or both, plaques may atrophy leaving an aortic wall too thin to support increasing mural tension, leading to aneurysmal enlargement.
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PMID:Aneurysm formation in experimental atherosclerosis: relationship to plaque evolution. 239 95

The effects of topical chemotherapy of 1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) on the lesions of mycosis fungoides were evaluated in 7 patients, ranging in age from 44 to 79 years old. Either 0.2% or 0.4% concentration of ACNU, in ointment and ethanol was used. 0.4% ACNU ethanol solution was effective in bringing the plaque lesions under satisfactory control with a complete clearance. ACNU was painted two to three times a week with a maximum dose of 50mg. Irritation and erosion of the applied areas were the major side effects, which were however, controlled by topical steroid ointment. No serious side effects of marrow and liver function were found even when ACNU was applied as long as 40 months (total ACNU dose: 16 gm). Histologically the cleared lesions revealed the thinning of epidermis, almost complete loss of lymphocytic infiltrates and fibrosis of dermis which was density infiltrated by lymphocytes prior to the ACNU therapy. Thus, topical chemotherapy of ACNU appears to be encouraged for modifying the plaque lesions of mycosis fungoides.
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PMID:[Topical application of ACNU for the treatment of mycosis fungoides]. 696 47

The majority of coronary artery blood flow occurs in diastole; however, systolic epicardial coronary artery expansion has been described. With the advent of intravascular ultrasound, precise measurements of arterial structures with excellent spacial and temporal resolution are now readily available. However, the effect of dynamic expansion of the coronary arteries on routine intravascular ultrasound measurements has not been assessed. The purpose of this study was to determine in vivo the presence, timing, and extent of dynamic changes in the coronary arteries and saphenous vein grafts and to assess their implications for intravascular ultrasound measurements. Intravascular ultrasound images were obtained with simultaneous electrocardiographic monitoring in 202 coronary artery and 50 saphenous vein graft sites in 32 patients with varying plaque burden and morphologic features. Arterial, luminal, and plaque area were measured at end-diastole and early, mid-, and end-systole. Coronary luminal diameter increased 2.1%; luminal area increased 8.1%; arterial area increased 3.7%; and plaque area decreased 4.9% during mid and late systole (p < 0.01). There was no detectable cyclic change in saphenous vein graft dimensions. In coronary arteries there was significant systolic expansion of the artery and lumen and systolic thinning of the plaque. The magnitude of dynamic luminal area change was greater than the variability in measurement and thus warrants gating to the cardiac cycle. The lack of dynamic change in saphenous vein grafts and the relatively small dynamic change in luminal diameter and arterial and plaque areas suggest nominal utility in gating these measurements to the cardiac cycle.
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PMID:Dynamic expansion of the coronary arteries: implications for intravascular ultrasound measurements. 761 Nov 22

Sclerotic involvement of abdominal aorta and lower limb arteries is related to 2 types of fundamental lesions: atherosclerosis and arteriosclerosis. Atherosclerosis is a focal intimal thickening (plaque) of large- and medium-sized arteries, which combines atheroma (lipid deposition) and fibrosis. Plaque rupture is the crucial event in the progression of atherosclerosis, directly causing most acute thrombotic events, and contributing in great part to plaque expansion. Arteriosclerosis is a diffuse fibrosis of the arterial wall with thickening of the intima, and thinning of the media. Two forms of arteriosclerosis probably exist with distinct mechanisms and consequences. Obliterating arteriosclerosis mainly involves leg arteries (causing poor distal run-off) and appears to be essentially enhanced by ageing, diabetes and chronic renal insufficiency. Dilating arteriosclerosis involves large arteries where it provokes aneurysm formation; it is related to ageing, but seems also to be dependent upon an inborn dystrophy of arterial connective tissue. These 3 components of sclerotic arterial diseases of the lower limbs are often combined in the same individual.
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PMID:[Description and mechanisms of sclerotic arterial diseases of the lower limbs]. 772 5


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