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

The thickness of the left ventricular free wall and internal chamber diameter were continuously measured by pairs of ultrasonic crystals together with left ventricular pressure in normal conscious dogs. During the resting state, wall thickness decreased abruptly with the onset of atrial contraction from 10.5 mm to an average end-diastolic valueof9.8 mm. In contrast to most previous studies, there was no change in wall thickness during isovolumic systole, and with ejection the wall thickened by 31.3 percent of end-diastolic wall thickness. Atrial pacing, phenylephrine, isoproterenol and propranolol produced significant changes in chamber size with reciprocal changes in wall thickness. In addition, changes in the extent and velocity of left ventricular chamber shortening in the minor equator were associated with comparable reciprocal changes in the extent and velocity of free wall thickening (correlation coefficients 0.97 to 0.99). During acute coronary occlusion, progressive reductions in the extent and velocity of regional wall shortening with partial ischemia were associated with comparable changes in systolic wall thickening characteristics (r = 0.96 and 0.95), and holosystolic elongation in fully ischemic areas was associated with holosystolic wall thinning. During chronic pressure overload, despite wall thickening, the relation between chamber shortening and wall thickening were retained and direct computation of dynamic wall stress variations was possible. These measurements allowed precise definition of the dynamics of the left ventricular wall during normal and abnormal cardiac states. The demonstration that in the absence of regional dysfunction analysis of wall thickness in a single region of ventricular free wall can be used to describe myocardial and overall left ventricular function, as well as regional function in the presence of ischemia, constitutes a new approach to the assessment of cardiac function that has potential for echocardiographic applications.
Am J Cardiol 1976 Dec
PMID:Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog. 13 93

A bent-limb syndrome in lambs raised in total confinement was characterized by curvature of the forelimbs. Radiographic findings included flaring of the affected long bone and thinning of the growth plate. The main histologic change was endochondral dysplasia of the long bone. In feed samples, all trace minerals analyzed were within recommended concentrations except iron, which was much higher (400 ppm dry matter) than the normal requirement of lambs (70 ppm). All mineral concentrations in serum were normal except those of inorganic phosphorus and iron, which were higher. Results of soft tissue and bone mineral analyses were normal. Altering the ratio of calcium and phosphorus did not affect the incidence of disease, but intramuscular administration of massive doses of vitamin D3 and reducing the amount of dietary iron had a prophylactic effect. The increase in serum phosphorus was probably related to the dietary excess of iron, which probably decreased vitamin D metabolite formation in the kidney, which in turn could be prevented by massive doses of vitamin D3.
J Am Vet Med Assoc 1978 Dec 15
PMID:Bent-limb syndrome in lambs raised in total confinement. 21 16

Previous studies have attributed changes in the retinal surface over or adjacent to large superficial retinal vessels to a variety of conditions, the most common being 'anomalous vitreoretinal attachments.' The fundamental nature of the lesions and their pathogenesis, however, has remained controversial. The present study was undertaken to categorize the ultrastructural alterations of the vitreoretinal juncture over retinal vessels in the posterior fundus of man, and to clarify the relationship of these fundamental changes to clinically significant lesions in this region. Results show no difference in vitreoretinal, or more specifically vitreolaminar attachments over vessels when compared with adjacent regions. The cause of the more significant anomalies, notably surface breaks and their sequelae, is apparently multifactorial and related to a sequence of events. Initially three events predispose to or cause small surface breaks: developmental thinning of the inner limiting lamina; subsurface retinal degeneration; and transmigrating macrophages. These small surface breaks, when complicated by vitreous incarceration or by simple epiretinal membrane formation, can during posterior vitreous detachment cause peeling of the retinal surface, and the resulting large surface breaks may in turn provoke more complex proliferative lesions of the vitreoretinal juncture.
Albrecht Von Graefes Arch Klin Exp Ophthalmol 1977 Dec 31
PMID:Vitreoretinal juncture over retinal vessels. 30 81

A 15-year-old girl with familial dysautonomia had acute corneal ulcerations while on a respiratory during a dysautonomic crisis. Within 18 days she developed irritating corneal ring calcifications. Subsequent corneal perforation in the left eye was treated successfully with a lamellar graft, followed later by a penetrating graft in the right eye under local anesthesia. Four days postoperatively, the patient died during a vomiting crisis. Neuropathologic studies showed marked cell reduction in the superior cervical and trigeminal ganglia, but slight in the ciliary. The foveas appeared immature and macular ganglion cells were mildly reduced. The corneal button and lamellar grafted cornea had severe thinning and superficial calcification. Keratoplasty in familial dysautonomia is considered hazardous because of the continual threat of vomiting crises, but with sufficient care may be worthwhile for corneal perforation or advanced corneal scarring.
Am J Ophthalmol 1979 Dec
PMID:Corneal transplantation in familial dysautonomia. 39 Oct 49

The thickness of left patellar articular cartilages after formalin fixation was studied in a series of autopsies on 82 subjects aged 25-96 years. For each specimen the minimal uncalcified cartilage thickness in a transverse patellar slab was determined separately for a 'lateral' segment and a 'central and medial' segment. In the women the cartilage from subjects more than 50 years old showed progressive thinning with increasing age. This was due to lesions causing disintegration of the tissue and not to matrix shrinkage. It had a strong potential to progress to full-thickness cartilage loss in the older women, and to give an appearance indistinguishable from osteoarthrosis as seen in surgical excision specimens. This progression towards patellofemoral osteoarthrosis in the elderly affects the female population generally, and not just a special subgroup; however, the incidence of clinical symptoms from this cause is not known. In men progressive thinning with age of patellar cartilage in subjects more than 50 years old was less severe, especially so in the case of the 'lateral' segment; a site of full-thickness uncalcified cartilage loss on the left patella at autopsy was seen only occasionally in the older men.
Ann Rheum Dis 1977 Dec
PMID:Effect of age on thickness of adult patellar articular cartilage. 59 49

Fifteen corneal buttons were removed at keratoplasty from patients with keratoconus who had previously undergone thermokeratoplasty (TKP). The buttons were studied with light microscopy, in an attempt to analyze the type of changes produced by TKP. The principal histologic findings in patients with retarded epithelial healing (8 of 15) included epithelial thinning, bullous keratopathy, thickening of the epithelial basement membrane, and frequent destruction of Bowman's membrane. More severely affected patients showed asceptic stromal necrosis and fibrinous iritis with hypopyon. A poor visual result in patients with normal epithelial healing (7 of 15) was caused by superficial stromal scarring or persistent inflammatory infiltrate. Vascularization was seen in only one patient.
Arch Ophthalmol 1976 Dec
PMID:Alterations in corneal morphology following thermokeratoplasty. 79 73

The pathogenesis of acute gastric mucosal lesions produced by distension of the rat stomach was studied. One hour of distension with 0.1 N HCl, but not saline, produced lesions in the glandular stomach in all rats. Histologic studies revealed marked thinning of the mucosa plus thrombus formation in the ulcerated area. Gastric distension with 8 ml HCl (per 100 g body weight) produced severe lesions, 4 ml minimal lesions and 2 ml no lesions. Intragastric pressure in the 8-ml group remained above 110 mm H2O for the first 10 min. Distension with 8 ml acid/100 g body weight for just 10 min resulted in significant lesion formation. Acid distension did not cause generalized disruption of the gastric mucosal barrier to H+ back-diffusion. It appears that an intragastric pressure of over 110 mm H2O for 10 min damages the mucosa by pressure (with thinning) and ischemia (with thrombosis), resulting in decreased resistance to acid peptic digestion and consequent acute lesion formation.
Am J Dig Dis 1977 Dec
PMID:Mucosal lesions due to gastric distension in the rat. 93 Sep 7

Colonic diverticulosis is a common cause of acute severe rectal hemorrhage. The precise site of bleeding, etiology, and pathogenesis have not been previously identified. Arteriographic, microangiographic, and detailed histologic observations in 10 cases of massively bleeding colonic diverticulosis demonstrated strikingly consistent changes related to the characteristic angioarchitecture of colonic diverticula. These changes included: (1) asymmetric rupture of the vas rectum toward the lumen of the diverticulum precisely at its dome or its antimesenteric margin; (2) conspicuous eccentric intimal thickening of the vas rectum, often with thinning of the media and duplication of the internal elastic lamina at and near the bleeding point; and (3) general absence of diverticulitis. Comparison with control colonic diverticula suggests that traumatic factors arising within the diverticular or colonic lumen induce asymmetric intimal proliferation and segmental weakening of the associated vas rectum, predisposing to rupture and massive bleeding.
AJR Am J Roentgenol 1976 Dec
PMID:Pathogenesis of massively bleeding colonic diverticulosis: new observations. 108 23

A TEM specimen preparation method is described, with the aid of which electron transparent foils can be obtained across the external surface of a specimen. After careful pre-treatment, steel specimens have been electrolytically coated with nickel. Conventional thinning in a plane cutting the substrate-coating interface, gave thin foils displaying the internal structure as a function of depth under the initial free surface. The method has also been applied to minute metal particles, of dimensions too small to allow manipulating and foil preparation by conventional methods. Image examples are shown, and the applicability of the method is discussed.
Ultramicroscopy 1975 Dec
PMID:A specimen preparation technique for transmission electron microscopy of surface layers. 123 23

Atomic-scale computer models were developed for how cecropin peptides may assemble in membranes to form two types of ion channels. The models are based on experimental data and physiochemical principles. Initially, cecropin peptides, in a helix-bend-helix motif, were arranged as antiparallel dimers to position conserved residues of adjacent monomers in contact. The dimers were postulated to bind to the membrane with the NH2-terminal helices sunken into the head-group layer and the COOH-terminal helices spanning the hydrophobic core. This causes a thinning of the top lipid layer of the membrane. A collection of the membrane bound dimers were then used to form the type I channel structure, with the pore formed by the transmembrane COOH-terminal helices. Type I channels were then assembled into a hexagonal lattice to explain the large number of peptides that bind to the bacterium. A concerted conformational change of a type I channel leads to the larger type II channel, in which the pore is formed by the NH2-terminal helices. By having the dimers move together, the NH2-terminal helices are inserted into the hydrophobic core without having to desolvate the charged residues. It is also shown how this could bring lipid head-groups into the pore lining.
Biophys J 1992 Dec
PMID:Modeling the ion channel structure of cecropin. 128 47


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