Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0851184 (
thinning
)
11,252
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
To clarify the mechanism of ulcer formation of atherosclerotic plaques in human carotid arteries, autopsy investigations were performed on eight patients who had died of cerebral infarction due to recent carotid thrombosis. Eleven control patients who had carotid atherosclerosis without thrombosis were also investigated. Histological changes of the arteries in serial sections were reconstructed three-dimensionally. Each artery with occlusive thrombosis was found to have an intimal ulcer at the head of the thrombus on the proximal slope near the base of the thickened atheromatous
plaque
at the carotid sinus. Most ulcers formed obliquely or longitudinally, were parallel to the vessel axis, had a fusiform shape, and measured 7 +/- 2 x 3 +/- 1 mm (mean +/- s.d.). The ulcers arose by marginal separation of the innermost layer from the underlying layer of the stratified intima. An underlying atheroma developed along the borders of these intimal layers reaching the subendothelium, with
thinning
of the intimal cap to less than 150 microns. The process of ulceration may be generated by vessel injury induced by hemodynamic forces, such as tensile forces and shear stress. The ulcer may extend along the fragile region where the wall may exhibit uneven compliance due to differences in the tissue structures of each intimal layer. Furthermore, macrophages may play a key role in ulcer formation.
...
PMID:Three-dimensional analysis of human carotid atherosclerotic ulcer associated with recent thrombotic occlusion. 783 75
Unstable plaques are undergoing thrombosis which, in most instances, is due to fissuring and rupture of the
plaque
cap. This process (deep intimal injury) is a complication of plaques with a lipid-rich core. The cap tear allows blood to enter the core from the lumen, leading initially to intraplaque thrombosis and, subsequently, in some cases intraluminal thrombosis. Cap tears reflect the interplay between the force exerted on the tissue and its inherent mechanical strength. Factors which elevate and concentrate circumferential wall stress on the cap during systole include an increasing proportion of the total
plaque
volume occupied by the lipid core,
thinning
of the cap and a loss of internal collagen struts within the core. Factors which lead to an inherent reduction in the mechanical strength of cap tissue include a reduction in collagen and glycosaminoglycan concentrations, an increase in the number and density of macrophages, and a concomitant reduction in smooth muscle cells in the cap tissue. It is therefore possible to define a vulnerable
plaque
as one in which the lipid core is disproportionately large, the cap thin, and in which monocytes preponderate over smooth muscle cells.
...
PMID:Lipid and cellular constituents of unstable human aortic plaques. 794 74
The coral derived hydroxyapatite sphere is a popular, integrated orbital implant designed to provide improved motility of the ocular prosthesis following enucleation. Although the implant has rapidly become widely used by ophthalmologists, little information is available regarding the problems of this technique in a large series of cases. Experience with 250 consecutive cases of hydroxyapatite orbital implant use was reviewed and the problems of the implants and their management investigated specifically. The reasons for enucleation included uveal melanoma (157 cases), retinoblastoma (70 cases), blind painful eye (22 cases), and intraocular medulloepithelioma (one case). Earlier treatment to the eye was performed before enucleation in 47 cases and included repair of ruptured globe (17 cases),
plaque
radiotherapy (18 cases), external beam radiotherapy (six cases), and others (six cases). During a mean of 23 months' follow up (range 6-40 months), there have been no recognisable cases of orbital haemorrhage related to the implant, and no cases of implant extrusion or implant migration. There was one case of presumed orbital infection (culture negative) that resolved with intravenous antibiotics and the implant was retained within the orbit. Other problems included conjunctival
thinning
in eight cases managed by observation and prosthesis adjustment, and conjunctival erosion in four cases managed by combinations of scleral patch graft, conjunctival flap, and prosthesis adjustment. The conjunctival erosion was caused by a poorly fitting prosthesis in three cases and wound dehiscence in one case. The problem rate in eyes receiving prior radiotherapy or surgery was not increased. The hydroxyapatite integrated orbital implant is a well tolerated motility implant without the high rate of extrusion and infection seen with other motility implants. The prosthesis fit may contribute to the tolerance of the implant.
...
PMID:Problems with the hydroxyapatite orbital implant: experience with 250 consecutive cases. 794 52
The coral-derived hydroxyapatite sphere is a popular, new integrated orbital implant designed to provide improved motility of the ocular prosthesis following enucleation. Although the implant has rapidly become widely used by ophthalmologists, there is little information available regarding the complications of this technique in a large series of cases. We report our results on our initial 250 consecutive cases of hydroxyapatite implantation for eyes enucleated primarily for intraocular neoplasms, with specific emphasis on the complication an their management. The reasons for enucleation included uveal melanoma (157 cases), retinoblastoma (70 cases), blind painful eye (22 cases), and intraocular medulloepithelioma (1 case). Prior treatment to the eye was performed before enucleation in 47 cases and included repair of ruptured globe (17 cases),
plaque
radiotherapy (18 cases), external beam radiotherapy (6 cases), and others (6 cases). During a mean of 23 months follow-up (range, 6 to 42 months), there have been no recognizable cases of orbital hemorrhage related to the implant and no cases of implant extrusion or implant migration. There was one case of presumed orbital infection (culture-negative) that resolved with intravenous antibiotics, and the implant was retained within the orbit. Other problems included conjunctival
thinning
in eight cases managed by observation and prosthesis adjustment and conjunctival erosion in four cases managed by combinations of scleral patch graft, conjunctival flap, and prosthesis adjustment. The conjunctival erosion was caused by a poorly fitting prosthesis in three cases and wound dehiscence in one case. The complication rate in eyes receiving prior radiotherapy or surgery was not increased. The hydroxyapatite integrated orbital implant is a well-tolerated motility implant without the high rate of extrusion and infection seen with other motility implants.
...
PMID:Lack of complications of the hydroxyapatite orbital implant in 250 consecutive cases. 814 Jun 90
Rupture of
plaque
is an important factor in the initiation of acute myocardial infarction. Plaque rupture is related to stress distribution in atheroma, but morphological alteration in coronary atheroma
plaque
in vivo is little understood. Atheroma
plaque
was observed during the cardiac cycle using 3.5 or 2.8 F, 30 MHz intracoronary ultrasound (ICUS) in seven patients with coronary artery disease. Coronary ostial pressure (P) measurements were simultaneously performed. Seven of the eccentric stenotic sites were analyzed. Intima-medial thickness (Th) and regional radius of curvature (R) at the middle and lateral portions of the atheroma were measured. Delta Th and % delta Th were calculated from change in thickness from end-diastole to peak systole. These parameters of the middle portion were compared with those of the lateral portion. The lateral % delta Th was 20.1 +/- 13.6% (delta Th 0.13 +/- 0.08 mm; 0.69 to 0.56 mm), and was significantly greater than the middle % delta Th [5.8 +/- 6.6% (delta Th 0.06 +/- 0.08 mm; 1.24 to 1.18 mm), p < 0.05]. Regional radius of curvature did not significantly differ. Wall stress calculated as P x R/Th was greater at the lateral portion (peak systole 3.7 x 10(5) dynes/cm2, end-diastole 1.9 x 10(5) dynes/cm2) than at the middle portion (peak systole 1.4 x 10(5) dynes/cm2, end-diastole 0.9 x 10(5) dynes/cm2). The change in stress from end-diastole to peak systole at the lateral portion was significantly greater (1.8 x 10(5) dynes/cm2) than that at the middle portion (0.5 x 10(5) dynes/cm2). The change in stress during the cardiac cycle, caused by the increase in intracoronary pressure, was greater at the lateral than at the middle of the
plaque
. This imbalanced distribution of stress may result in greater
thinning
of
plaque
at the lateral portion. Therefore, the distortion of
plaque
may be a mechanism for atheroma rupture at the lateral portion.
...
PMID:[Cyclic alteration in atheroma plaque morphology observed by intracoronary ultrasound: initiation mechanism of acute myocardial infarction]. 886 81
Ferromagnetic (FM) hyperthermia has previously been evaluated in a rabbit tumour model of ocular melanoma. To study the effect of focal heating in normal rabbit eyes, FM seeds were implanted into a 14-mm episcleral
plaque
an heated to operating temperatures of 48 or 58 degrees C. Thermal induction was performed by placing rabbits in a uniform, oscillating (11 kHz) magnetic field operating at 1200 W and as H-field strength of 265 A/m. Eyes were heated for 60 min with continuous scleral temperature monitoring. Hyperthermic effects were monitored by direct opthalmic examination, fundus photography, serial electroretinography and histopathology. Intraocular temperatures were mapped with direct fiberoptic thermometry. All treatment effects were confined to the area covered by the episcleral
plaque
. Direct ophthalmoscopic examination revealed early retinal whitening during heat induction followed by localized exudative retinal detachments, limited to the area of the retinal surface overlying the
plaque
, that resolved spontaneously. Serial electroretinography was virtually indistinguishable between the 48 and 54 degrees C temperature groups. We noted a minimal alteration in a- and b-wave amplitudes with no changes in implicit times. Histopathology at 3 weeks post-treatment documented chorioretinal scarring overlying the thermal
plaque
treatment zone. No evidence of heamorrhage infection, cataract or scleral
thinning
was noted. This study documents the apparent focal containment of thermal effects with FM heating utilizing operating temperatures ad high as 54 degrees C for 60 min, and discloses no evidence of diffuse ocular toxicity.
...
PMID:Ferromagnetic hyperthermia: functional and histopathologic effects on normal rabbit ocular tissue. 927 71
To investigate the mechanism of
plaque
rupture, we carried out morphologic and quantitative assessments of ruptured
plaque
with a 30-MHz intravascular ultrasound catheter before coronary intervention. Plaque rupture, defined as an echolucent intraplaque area communicating with arterial lumen, was noted in all of 22 patients with coronary artery disease examined in the study. The
plaque
was eccentric in 16 patients (73%) and in 10 of these 16 patients there was a tear at the margin of the
plaque
(63%). Calcification was noted in only 6 patients (22%). Plaque area ranged from 8.7 to 44.1 mm2. The ruptured area ranged widely, from 1.0 to 14.0 mm2, and the percent ruptured area also ranged widely, from 3.9% to 50.9%. Fibrous cap was recognized in 20 patients. The thickness of the fibrous cap ranged from 0.1 to 0.6 mm (mean, 0.36 mm) and
thinning
of the fibrous cap was noted in 16 patients (80%). From these results, we conclude that intravascular ultrasound can provide detailed observations of
plaque
rupture consistent with pathologic studies. Accordingly, it is a suitable method for evaluation of
plaque
rupture in vivo. Plaque weakness, due to the presence of atheromatous core, thin fibrous cap, and no calcification, seems to be the major determinant of
plaque
rupture. In addition, the great variation in cap thickness and ruptured area suggests the role of other triggers, such as mechanical and hemodynamic stress, in
plaque
rupture.
...
PMID:Assessment of plaque rupture by intravascular ultrasound. 947 76
Coronary artery diseases may categorized into asymptomatic disease, angina pectoris, myocardial infarction, chronic heart failure, and sudden coronary death. Unstable angina, acute myocardial infarction, and sudden cardiac death are known as the acute coronary syndromes. Coronary atheroma is unstable in the patients with acute coronary syndromes. Stable plaques will be unstable when dynamic alterations occur. The alterations are
plaque
rupture,
plaque
hemorrhage, coronary thrombosis and vasospasm. They act each other. We analysed the histopathology of coronary arteries who died of acute myocardial infarction in 85 cases. It showed that the risk factors of
plaque
rupture are clusters of form cells, eccentric
plaque
with soft lipid rich core, and
thinning
of fibrous cap in atheroma. Most of these cases ruptured at edge of the atheroma.
...
PMID:[Pathogenesis of acute coronary syndromes]. 978 Jul 33
Senescence is the effect of the immune system incapacity to see "self" and "non-self"; timo-involution induced down-regulation of immunoregulatory -T and B-lymphocytes. Immunosenescence mutations in oral cavity are examined. Even the oral ecosystem presents disorders in quality and quantity of the bacterial
plaque
and a different immune response. Age senescence is particularly evident in the masticatory apparatus, in fact the dental tissues have remarkable morpho-structural physiological changes; the epithelial, connective and osseous tissues of the periodontium have structural age changes related to the collagen synthesis and physical properties, with an increase of the stroma and a decrease of cell population. The osseous tissue presents cellular atrophy, sclerosis, osteoporosis and is undergoing a continuous structural remodelling; the oral mucous membranes show a
thinning
of epithelium and an increase of the stroma related to the parenchyma. Specific individual changes could be appraised in the involution of stomatognathic apparatus, more than an indefinite reduction of the performances.
...
PMID:[Changes in the biological and immunologic parameters in the oral cavity of the aged. Review]. 979 66
Coronary atherosclerosis is by far the most frequent cause of ischemic heart disease and
plaque
disruption with superimposed thrombosis is the main cause of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden coronary death. Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why, after years of indolent growth, it suddenly becomes complicated by life-threatening thrombosis. Therefore, we have to focus on
plaque
composition and vulnerability to rupture and
plaque
thrombogenicity rather than on
plaque
size and stenosis severity. The risk for
plaque
disruption depends more on
plaque
vulnerability (
plaque
type) than on degree of stenosis (
plaque
size). Lipid-rich and soft plaques are more vulnerable and prone to rupture than collagen-rich and hard plaques. They are also highly thrombogenic after disruption because of high content of tissue factor. There seems to be three major determinants of a
plaque
's vulnerability to rupture: 1) the size and consistency of the lipid-rich atheromatous core, 2) the thickness of the fibrous cap covering the core, and 3) ongoing inflammation and repair processes within the fibrous cap. Lipid accumulation, cap
thinning
, lack of smooth muscle cells (smc), and macrophage-related inflammation destabilize plaques, making them vulnerable to rupture. In contrast, smc-related healing and repair processes stabilize plaques, protecting them against disruption. Plaque size or stenosis severity tell nothing about a
plaque
's vulnerability. Many vulnerable plaques are invisible angiographically due to their small size and compensatory vascular remodeling.
...
PMID:Plaque pathology and coronary thrombosis in the pathogenesis of acute coronary syndromes. 1038 96
<< Previous
1
2
3
4
5
6
7
8
9
10
Next >>