Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphologic features of graft arteriosclerosis (GA) and other vascular lesions were semiquantitatively evaluated. Five failed cardiac allografts attributable to GA and five other allografts were obtained from nine autopsies and one surgical explanation. The subjects, aged 4.5 to 67 years, had a mean allograft survival of 735 +/- 184 days. A total of 1,174 arterial and 754 venous cross-sections were reviewed. Intimal fibrosis (nine cases, 254 arteries, and 118 veins), fibrofatty plaques (eight cases and 35 arteries), and cellular intima thickening and concentric foam cell lesions (eight cases, 326 arteries, and 20 veins) were seen. Cellular lesions contained T lymphocytes, monocytes, and cells of smooth muscle cell origin detected by staining using the immunoperoxidase technique. Allografts with severe GA had a greater luminal stenosis in epicardial arteries (P less than .05), greater cellular proliferation in large mural arterial lesions (P less than .004), and more foam cell lesions in both arteries (P less than .06) and veins (P less than .03) than other allografts. Medical fibrosis and thinning were present in six allografts. Severity of acute rejection (P less than .01) was correlated with the presence of GA. The morphology and distribution of GA is heterogeneous, with evidence supporting an immune-mediated pathogenesis.
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PMID:Morphology of graft arteriosclerosis in cardiac transplant recipients. 161 76

A case of a basilar bifurcation aneurysm associated with common carotid artery occlusion is reported. A 40-year-old woman was admitted to our hospital with severe headache and nausea. On admission, no neurological abnormality was observed. CT scan showed thin subarachnoid hemorrhage in the basal cistern. Left vertebral angiograms revealed a basilar bifurcation aneurysm located in the high position. Also, the left internal and external carotid arteries were supplied through the anastomotic muscle branches of the left occipital and vertebral artery. The trunk of the left common carotid artery was not visualised from its origin on the aortogram. CT scan at the level of C6 showed thinning of the left common carotid artery and contrast enhancement study indicated occlusion. Neck clipping of the aneurysm was successfully performed by right trans-sylvian approach. Right zygomatic arch was removed to obtain a wider operative field for avoiding further retraction of the brain tissue. The postoperative course was uneventful except transient disorientation for two weeks. It has been well known that internal carotid artery occlusion may be associated with cerebral aneurysm in some cases. However, it seemed to be a rather rare case that the common carotid artery occlusion due to arteriosclerosis was associated with cerebral aneurysm. Hemodynamic factor was positively suggested for aneurysmal formation in this case.
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PMID:[A case of a basilar bifurcation aneurysm associated with common carotid artery occlusion]. 239 17

Atherosclerotic lesions commonly develop at arterial branch sites, which are also the sites of high arterial intramural stress produced by intraluminal pressure. We investigated the effect of reduced intramural stress on the development of atherosclerotic lesions. We exposed the origin of the left renal artery in five rabbits and the aortic bifurcation in another five, lowered the mean arterial pressure to 35 to 45 mm Hg, and poured a dental acrylic liquid around the branch to form a rigid cast. When the rabbits recovered and the arterial pressure increased to normal, the casts prevented the arteries from expanding, thereby maintaining a low intramural stress. These rabbits plus two unoperated, two sham-operated, two with silicone rubber casts placed at similar pressures, and four with casts placed at 95 mm Hg pressure were given a 2% cholesterol-enriched diet for 7 to 11 weeks, and then their arteries were examined. In all rabbits, atherosclerotic lesions developed at the origins of the intercostal, celiac, superior mesenteric, and both renal arteries, and at the aortic bifurcation, with these notable exceptions: no lesions developed at the origins of casted renal arteries or at the casted aortic bifurcations when the cast was placed at a low pressure. Measurements of the diameter and thickness of the aorta in the left renal branch and aortic bifurcation areas, with and without the casts, indicated that there was no significant narrowing of the aortic lumen or thinning of the aorta due to the cast. In conclusion, the inhibition of the development of atherosclerotic lesions appears to be associated with the reduction of arterial intramural stress.
Arteriosclerosis
PMID:Inhibition of atherosclerosis associated with reduction of arterial intramural stress in rabbits. 339 77

The arteries of monkeys given atherogenic diets develop marked intimal thickening and medial thinning, but luminal size apparently changes minimally. The hemodynamic significance of the atherosclerotic changes is therefore uncertain. To evaluate vascular function in atherosclerotic arteries, we studied the hind-limb vessels of adult male rhesus and cynomolgus monkeys to assess the structural and hemodynamic responses to an atherogenic diet given for about 1.5 years or for much longer periods (6.5 years for rhesus and 4.3 years for cynomolgus monkeys). The intimal cross-sectional area greatly increased after the atherogenic diet, but there was no significant luminal narrowing after either the 1.5-year diet or the longer diet periods. The media of atherosclerotic arteries showed focal atrophy and focal thinning after pressure fixation, but the total medial mass was not decreased even after the long diet periods. Hemodynamic studies indicated mild functional impairment in the atherosclerotic vessels; resting resistance increased and vasodilator responses decreased, but adrenergic responses were preserved. Thus, the marked changes that occur in the arterial wall in experimental primate atherosclerosis include adaptations to lesion formation that permit a long prestenotic phase of atherosclerosis in which vascular dysfunction is minimal.
Arteriosclerosis
PMID:Structural and hemodynamic response of peripheral arteries of macaque monkeys to atherogenic diet. 401 7

Transluminal angioplasty has shown promise as a nonoperative treatment of atherosclerotic obstruction. Despite its increasing clinical use and potential importance, little is known of its mechanism and acute effects. To evaluate transluminal angioplasty, three rabbit models of experimental atherosclerosis were developed: Group 1 (n = 20) = high cholesterol diet plus balloon de-endothelialization; Group 2A (n = 12) = high cholesterol diet plus an indwelling catheter; Group 2B (n = 10) = normal diet plus an indwelling catheter. After 6 weeks or 8 weeks, distinct angiographic and pathological lesions in the iliac artery were evident in all groups. Group 1 showed predominant foam cell lesions, while Group 2 showed eccentric mixed fibrous and foam cell or only fibrous lesions. Significant angiographic stenosis was present in 78% of the animals. Angioplasty of the highest grade iliac stenosis resulted in at least a 20% reduction in luminal diameter narrowing in 26 of 37 animals (70%). Histopathological examination 1 day following angioplasty in 17 animals showed two patterns. In Group 1 animals, neointimal fracture and dissection were evident, while in Group 2 animals thinning and stretching of the nonatherosclerotic portion of the vessel walls could be demonstrated. This study demonstrates that the New Zealand rabbit can be used to produce a spectrum of morphologically distinct atherosclerotic lesions that lend themselves to the study of transluminal angioplasty. The immediate consequences of angioplasty, which appear to depend upon the underlying histopathology and widening of the narrowed lumen, are frequently concurrent with intimal fracture, dissection, or thinning of the nonatherosclerotic portion of the vessel wall.
Arteriosclerosis
PMID:Acute effects of transluminal angioplasty in three experimental models of atherosclerosis. 646 20

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

Myocardial ischemia, an uncommon cause of sudden death in dogs, usually results in infarction and fibrosis of the myocardium. Necropsy examination of a 13-year-old German Shepherd dog that died suddenly demonstrated multifocal myocardial thinning and loss in the left and right ventricular free wall and right atrium. Histopathologic examination confirmed the myocardial thinning to be sites of myocyte atrophy and loss, with loose reticulin-positive fibrovascular tissue and adipocytes and little fibrosis. Many intramural coronary arteries were irregularly thickened and partially occluded by segmental intimal and medial deposits of periodic acid-Schiff-positive, Congo red-negative amorphous extracellular material. This finding is consistent with hyaline arteriosclerosis. These vascular lesions likely lead to insufficient perfusion of the affected myocardium and gradual loss of myofibers without the acute necrosis and fibrosis characteristic of infarction.
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PMID:Coronary arteriosclerosis with myocardial atrophy in a 13-year-old dog. 1460 24

Chronic graft dysfunction is the greatest barrier to long-term graft survival, although the immediate outcome in organ transplantation has been greatly improved. Graft arteriosclerosis is a prominent feature of chronic graft dysfunction. Recipient progenitor cells have been shown to participate in neointimal development in graft arteriosclerosis. The present study investigated the role of recipient endothelial cells in the repair and remodeling after a cold preservation injury in an orthotopic cross-sex abdominal aortic allotransplantation model, namely female Wistar to male Sprague-Dawley rats. Grafts were preserved for 48 hours in 4 degrees C University of Wisconsin (UW) solution for a prolonged cold ischemia (PCI) group or preserved for <1 hour in the control group; or for <1 hour in the presence of feeding with cyclosporine (CyA). A direct in situ polymerase chain reaction (ISPCR) for the SRY gene showed SRY-marked endothelial and smooth muscle-like cells in neointima at 2 weeks in the PCI group, at 4 weeks in the control group, and rarely at 3 months in the CyA group. Staining by H&E showed the aortic graft intima to be thicker in the PCI than in the control group at 4 weeks, but thinning thereafter. The SRY-positive cells correlated with intimal thickness in the PCI and the control group (r = .801 and .825; P < .05 and <.05, respectively), but not in the CyA group (r = .247, P > .5). Our data suggest that prolonged cold preservation promotes recipient cell participation in graft arteriosclerosis after endothelium injury. The early neointimal formation via recipient cells incorporated into arteriosclerotic neointima may delay later intimal thickening. In the aortic allotransplantation model, prolonged cold ischemia may be beneficial for long-term graft survival due to early endothelial replacement. We hypothesize that controlled injury to the graft may serve as a new strategy for treatment of intimal thickening.
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PMID:Prolonged cold preservation promotes the recipient's cell participating in neointima formation but delays the later graft arteriosclerosis in rat model. 1580 28

Werner syndrome (WS) is an autosomal recessive premature aging disease manifested by the mimicry of age-related phenotypes such as atherosclerosis, arteriosclerosis, cataracts, osteoporosis, soft tissue calcification, premature thinning, graying, and loss of hair, as well as a high incidence of some types of cancers. The gene product defective in WS, WRN, is a member of the RecQ family of DNA helicases that are widely distributed in nature and believed to play central roles in genomic stability of organisms ranging from prokaryotes to mammals. Interestingly, WRN is a bifunctional protein that is exceptional among RecQ helicases in that it also harbors an exonuclease activity. Furthermore, it preferentially operates on aberrant DNA structures believed to exist in vivo as intermediates in specific DNA transactions such as replication (forked DNA), recombination (Holliday junction, triplex and tetraplex DNA), and repair (partial duplex with single stranded bubble). In addition, WRN has been shown to physically and functionally interact with a variety of DNA-processing proteins, including those that are involved in resolving alternative DNA structures, repair DNA damage, and provide checkpoints for genomic stability. Despite significant research activity and considerable progress in understanding the biochemical and molecular genetic function of WRN, the in vivo molecular pathway(s) of WRN remain elusive. The following review focuses on the recent advances in the biochemistry of WRN and considers the putative in vivo functions of WRN in light of its many protein partners.
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PMID:Current advances in unraveling the function of the Werner syndrome protein. 1594 10

Structural brain imaging studies have shown that obesity is associated with widespread reductions in gray matter (GM) volume. Although the body mass index (BMI) is an easily accessible anthropometric measure, substantial health problems are more related to specific body fat compartments, like visceral adipose tissue (VAT). We investigated cortical thickness measures in a group of 72 healthy subjects (BMI range 20-35 kg/m(2), age range 19-50 years). Multiple regression analyses were performed using VAT and BMI as predictors and age, gender, total surface area and education as confounds. BMI and VAT were independently associated with reductions in cortical thickness in clusters comprising the left lateral occipital area, the left inferior temporal cortex, and the left precentral and inferior parietal area, while the right insula, the left fusiform gyrus and the right inferior temporal area showed a negative correlation with VAT only. In addition, we could show significant reductions in cortical thickness with increasing VAT adjusted for BMI in the left temporal cortex. We were able to detect widespread cortical thinning in a young to middle-aged population related to BMI and VAT; these findings show close resemblance to studies focusing on GM volume differences in diabetic patients. This may point to the influence of VAT related adverse effects, like low-grade inflammation, as a potentially harmful factor on brain integrity already in individuals at risk of developing diabetes, metabolic syndromes and arteriosclerosis.
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PMID:Reduced cortical thickness associated with visceral fat and BMI. 2537 43


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