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 breakdown of passivity and localized corrosion of a Ni-20Cr-10Mo alloy was investigated. The methods employed were potentiodynamic polarization and SEM, and AES and EDX after potentiostatic polarization over a period of 20 hours in the passive and transpassive regions. The 1 micron finished as-cast specimens were polarized in aerated 0.1 M NaCl. The cyclic polarization curves revealed a critical pitting potential of 470 mV (SCE), while the protection potential was 300 mV (SCE). Using the potentiostatic polarization technique, nearly constant corrosion currents appeared, indicating that the whole surface was corroded uniformly. SEM pictures of samples, corroded at 650 mV, showed little pits under the oxide layer and a thinning down of the outer oxide layer. This lead to the opinion that the penetration as well as the adsorption mechanism determine the breakdown of passivity. EDX analysis and AES depth profiles showed an enrichment of Cr and Mo in the oxide. In contrast to oxidized samples, no second layer of Ni was found in the outer oxide region. In the transpassive region the relative amount of Cr and Mo in the oxide layer was higher than the one found in corresponding samples polarized in the passive region. The oxide thickness found was about 5 nm in the passive region (300 mV SCE) and about 250 nm in the transpassive region (650 mV SCE).
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PMID:Scanning electron microscope studies on the breakdown of passivity of a nickel-chromium-molybdenum dental alloy. 365 56

Using sonar microcrystals implanted in conscious dogs, we have characterized left ventricular segmental relaxation (LVSR) by measuring the mean rate to half end-diastolic thinning (RHEDT) and the late diastolic thinning fraction (TF). In protocol 1 (five nonischemic dogs), RHEDT correlated with changes in left ventricular dP/dt (r = .87) and systemic arterial pressure (r = -.80) but not with alterations in heart rate. Only systemic arterial pressure importantly influenced TF (r = -.65). In protocol 2 (21 dogs), LVSR paralleled net systolic segmental wall thickness (NET) during both 2 and 4 hr of coronary occlusion followed by 1 month reperfusion. Both LVSR and NET remained depressed during 2 and 4 hr of coronary occlusion and through 24 hr of reperfusion, but both also gradually improved afterwards. In protocol 3, 31 dogs underwent 4 hr of coronary occlusion with 1 month of reperfusion. Among these animals, 11 dogs (group S4) received saline after 1 hr of occlusion, nine dogs (group P4) received propranolol, and 11 dogs (group D4) received diltiazem. Drug therapy was stopped at 2 hr of reperfusion. In segments with mildly and moderately depressed NET, LVSR was significantly increased in group D4 vs group S4 animals during the diltiazem infusion. Expressed as mean percentage of control value +/- SEM, RHEDT of moderately dysfunctional segments in group D4 compared with group S4 measured 53 +/- 10% vs 25 +/- 5%, respectively, at 2 hr of occlusion of the left anterior descending coronary artery (p = .03), 76 +/- 17% vs 28 +/- 8%, respectively, at 4 hr of occlusion (p = .01), and 74 +/- 11% vs 33 +/- 10%, respectively, at 1 hr of reperfusion (p less than .05). The differences in TF at these same time points were 106 +/- 10% vs 70 +/- 9% (p less than .03), 105 +/- 7% vs 65 +/- 16% (p less than .02), and 106 +/- 11% vs 74 +/- 13% (p less than .05), respectively. The improvement in LVSR occurred independently of changes in NET. The values of LVSR in the diltiazem-treated dogs fell to the levels of groups S4 and P4 within 24 hr of stopping the intervention. Propranolol did not significantly alter LVSR over the short or long term. The increase in LVSR during administration of diltiazem did not appear to be mediated by changes in contractility or regional myocardial blood flow, but were probably mediated in part by afterload reduction and possibly by a reduction in calcium entry into ischemic myocardium.
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PMID:Effect of diltiazem and propranolol on left ventricular segmental relaxation during temporary coronary arterial occlusion and one month reperfusion in conscious dogs. 396 19

The response of ependyma to injury was investigated in rats following placement of bilateral lesions in the floor of the fourth ventricle. Animals were sacrificed from 2-60 days post-operatively and the brains were prepared in the conventional manner for comparative LM, SEM and TEM examination. For LM radioautography, randomly selected lesioned rats received either a single i.p. injection (5 muCi/g BW) or multiple injections (2 muCi/g) of 3H-thymidine prior to sacrifice. Focal disruption of the lining resulted in significant qualitative and quantitative changes in the ependyma at the wound margins. Labelling of normally quiescent ependymal cells occurred from day 2-6 post-operatively, however, the level of turnover was relatively low. Labelling was maximum on day 2 and was greater at the medial than lateral margin of the wound. During the first postoperative week, a gradual increase was observed in the number of ependymal cells per unit length at the margins of the wound concomitant with an abrupt reduction in wound diameter. This was consistent with the assumption that newly formed cells were added to the ependymal sheet at the leading edges of the wound. From 14-60 days after injury, further repair resulted from asymmetrical spreading and thinning of the ependymal sheet in the absence of mitotic activity. Quantitatively, this was reflected in a reduction in cell number at the leading edges of the wound that was most pronounced at the lateral margin. At day 60 neither epithelialization nor wound closure was complete and the normal architecture of the lining had not been fully restored. These results suggest that ependyma in the fourth ventricle of the postnatal rat undergoes a process of only limited repair following injury.
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PMID:Ependymal cells of the rat fourth ventricle: response to injury. 663 67

We investigated the effect of indomethacin, a widely used nonsteroidal antiinflammatory drug, on the healing of myocardial infarction (MI). Experimental MI was produced in anesthetized, open-chest dogs by occluding the left anterior descending coronary artery. Ten dogs received indomethacin, 10 mg/kg i.v., and 11 received saline, 15 minutes and 3 hours after occlusion. After 6 weeks, the dogs were killed and their hearts were subjected to morphologic and biochemical analysis. The average thickness of the transmural scar and the noninfarcted left ventricular wall was measured at multiple sites in formalin-fixed left ventricular slices and the ratio of the thickness of the transmural scar to the noninfarcted wall determined. The average thickness of the noninfarcted wall was 8.80 +/- 0.19 mm (mean +/- SEM) in the control group and 8.44 +/- 0.26 mm in the indomethacin group (NS). The scar thickness was 7.24 +/- 0.64 mm in the control group and 3.56 +/- 0.40 mm in the indomethacin group (p less than 0.001). The ratio of scar to noninfarcted wall thickness was 0.83 +/- 0.07 in the control group and 0.43 +/- 0.04 in the indomethacin group (p less than 0.001). Scars in treated dogs did not differ from controls either by light microscopic histologic analysis or by analysis of hydroxyproline content per unit weight. We conclude that indomethacin results in marked scar thinning when given early after experimental MI.
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PMID:Indomethacin-induced scar thinning after experimental myocardial infarction. 685 Oct 23

The axolotl pronephric duct rudiment is readily accessible to both SEM observation and surgical manipulation. The rudiment segregates from the dorsal part of the lateral mesoderm and then extends caudally along the ventrolateral border of the segmenting comites, eventually contacting the cloacal wall. The marked thinning of the rudiment which accompanies this migration is paralleled by a corresponding reduction in cell number across the duct's diameter and by caudad translocation and elongation of vital dye marks applied to the duct mesoderm. Duct extension thus involves appreciable cell rearrangement. The morphology of duct mesoderm and its substratum (somite and lateral mesoderm) suggests that active locomotion of cells near its tip marshals the duct's caudad elongation. Filopodia and small focal areas of intercellular contact may mediate the adhesions between the cells which must be broken and reformed as the cells rearrange.
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PMID:Amphibian pronephric duct morphogenesis: segregation, cell rearrangement and directed migration of the Ambystoma duct rudiment. 731 Feb 83

The aim of this study was to examine the development of chorionic villous trees during early periods of normal intrauterinal and ectopic (tubal) pregnancies, and to study the structural specializations on the free surface of mature placental villi by scanning and transmission electron microscope (SEM and TEM). In order to study the structures of placental villi between 28 and 34 days old (pc), early, 6-8 week normal and ectopic, and full term human placenta samples were obtained from legal curettage and hysterectomized cases, and spontaneous deliveries, and tissues samples were prepared for SEM and TEM. Three-dimensional configurations of the developing chorionic villous trees were observed as large main villus groups, covered with abundant microvilli of different size and diameters. It appeared that the chorionic villous trees which emerged from the chorionic plate divided gradually into branches of which ramifications originated as buds. These buds gradually grew and were transformed into shoots. The number of developing new villi appeared to increase gradually from 28 days to 9 weeks (pm) of gestation. From the 4th week onwards the massive trophoblastic sprouts were observed on the surface of main chorionic villi which transformed into primary, secondary and tertiary villous trees. When the placental villi formation in ectopic pregnancy was compared with the intra-uterinal pregnancy, an arrested development was remarkable. The configurations of ectopic placental villi seemed to be disparate, such as curved lines or compressed and wrinkled positions so that the three dimensional aspect had been wizened. The ramification and new villi formation seen as in the normal placenta were not only decreased but also infrequent. Some placental villi samples displayed a gradually thinning terminal region. Trophoblastic degenerations were frequently found on the surface of ectopic villi ultrastructurally. According to these results, we comment that in ectopic pregnancy the placental villi formation and development could have been delayed. At term, some specialized structural modifications were observed on the free surface of the mature placental villi. The presence of some dome-like balloonings and many crateriform hollows were the most striking features of the mature intermediate and terminal villi. According to the increasing physiological needs of the growing fetus, these special structures that are related to lung-like and kidney-like functions and named "nephropneumonic-like units", formed in the mature placental barrier. We have observed that these special units were showing a smooth surface similar to an inflated balloon.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The fine structure of normal and ectopic (tubal) human placental villi as revealed by scanning and transmission electron microscopy. 775 46

The quality of bone may be as important as its quantity, influencing bone strength and turnover. Using quantitative BSE (backscattered electron) imaging, we have found changes in the mineral density of bone with age, the proportion of denser bone increasing, and discontinuities occurring in the mineral phase between packets of bone. SEM of resorptive fields showed that severing of trabeculae occurs with deep, vertical excavations; their thinning is by long, narrow, resorption grooves extending from node to node. Grooved regions may become deeper, undercut and burrowing. In vitro, we showed that larger osteoclasts made larger pits. However, the volume of tissue resorbed per nucleus did not increase, and could decrease. Interactions between osteoclasts and autologous osteoblastic cells were observed by time-lapse video microscopy in vitro. Message-mediated contact behaviour, dependent upon the state of activation of both cell types, resulted in changes in the territory of the responding cell. The numbers and sizes of gap junctions between rat parietal bone cells in situ were investigated using confocal fluorescence and reflection microscopy and polyclonal antisera to connexin-43 peptides. The junctions reached approximately 1.3 microns in diameter, with 0.2 microns as the limit of detection. The extent of connectivity and communication may also affect bone quality.
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PMID:Questions of quality and quantity--a morphological view of bone biology. 809 41

Although it is generally accepted that polyurethane-covered breast implants have decreased the incidence of clinical capsular contracture, there remain many unanswered questions regarding the physical and chemical degradation of the polyurethane foam covering itself. We have systematically studied the fibrous capsule and polyurethane foam recovered from human breast "explants" in an effort to characterize more precisely the biodegradation of polyurethane foam in the human body. Seventy-five freshly retrieved polyurethane-covered implants and surrounding capsule from 47 patients have been analyzed. Capsular tissue from several sampling sites around the surface of the implants was digested in a collagenase solution until foam was recovered or all tissue was digested. Additional samples were fixed in 10% formalin. Scanning electron microscopy was used to look for structural changes in the recovered intact foam and to determine the foam strut widths. Fourier transform IR spectroscopy and x-ray photoelectron spectroscopy were used to analyze the chemical composition of the polyurethane. The formalin-preserved capsule samples were examined histologically for further evidence of foam degradation. Of the 75 prostheses analyzed, 36 (48 percent) were removed because of capsular contracture and 10 (13 percent) because of infection or exposure of the prosthesis. The remaining 29 (39 percent) implants were removed for various other reasons. Visibly intact foam was recovered from 36 (48 percent) prostheses after enzymatic digestion of capsule tissue. There was a progressive decline in the ability to recover intact foam as the total implantation time increased. Scanning electron microscopy revealed fractures and fissures in the foam structure and thinning of the polyurethane struts. The mean strut width of control, unimplanted foam was 49 +/- 1.5 microns (+/- SEM). Retrieved foam from implants which developed capsular contracture and the infected implants had strut widths of 30 +/- 3.1 and 32 +/- 3.1 microns, respectively. In implants removed for other reasons, the polyurethane foam strut width was 41.2 +/- 2.3 microns. Despite an inability to recover visibly intact foam from 39 specimens, standard light microscopy of 37 of these same specimens showed residual polyurethane still present in the capsule. Various degrees of scalloping and fracturing of the foam were seen in the histologic sections. There is convincing evidence by scanning electron microscopy and histology that polyurethane is degrading. It was not possible to quantitate accurately the rate of degradation, but factors such as capsular contracture, infection, and time appear to have a role in the biodegradation of polyurethane in the human body. These relationships require further study.
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PMID:Biodegradation of the polyurethane foam covering of breast implants. 823 96

Thinning of the posterior sclera may imply that stretching and/or weakening of the sclera plays a role in axial elongation of myopic eyes. We investigated the elastic stress-strain properties of sclera from developing tree shrew eyes made myopic by monocular deprivation (MD) of form vision. Five days of MD induced a relative myopia (mean +/- SEM) of -5.6 D +/- 0.6 D (retinoscopy) and a vitreous chamber elongation (deprived minus control) of 106 +/- 14 microns, n = 10 (ultrasonography). Posterior scleral test samples (2 mm wide) cut from myopic eyes were significantly thinner than their contralateral eye controls (149 +/- 4 microns versus 164 +/- 4 microns, n = 10, P < 0.01) when measured with a force-controlled micrometer. However, posterior sclera from control eyes was significantly thicker than that from age-matched normal eyes (164 +/- 4 microns versus 149 +/- 3 microns, n = 10, P < 0.01). Under uniaxial tension, posterior scleral samples from myopic eyes failed at 18% lower load (162 g versus 198 g) and extended approximately 25% more than controls at a load corresponding to 20 mm Hg intraocular pressure. These differences were largely accounted for by the differences in scleral thickness. Finite element modelling of tree shrew eyes using the material properties summarised above, implies that simple elastic stretching of the sclera accounts for less than 20% of the observed difference in axial length between myopic and contralateral control eyes.
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PMID:Form deprivation myopia: elastic properties of sclera. 852 54

The aim of this study was to investigate performance of preserved arterial allografts under the protection of a high-dose and a low-dose immunosuppressive regimen, with cyclosporine (CsA). Dog carotid arteries were harvested and stored for 14 days at 4 degrees C in University of Wisconsin organ preservation solution. Segments (6 cm) of carotid artery were orthotopically and bilaterally implanted in mongrel dogs (n = 18). CsA was given in two dosage regimens: 25 mg/kg/day (group I, n = 7) and 10 mg/kg/day (group II, n = 7). The control group received no CsA (group III, n=4). After 3 months of implantation, patency was assessed by angiography. The grafts were excised for investigation of vessel wall and endothelial function and morphology. For assessment of function in vitro, slices of arterial segments were connected as ring preparations to an isometric force transducer and immersed in a 5 ml organ bath (37 degrees C) containing Tyrode's solution. The contractile response was examined by adding 40 mM KCl and phenylephrine (100 microM) to the organ bath; endothelium-dependent relaxation was examined by adding methacholine (100 microM). Morphology was assessed semiquantitatively. The functional responses to KCl, phenylephrine (Phe) and methacho- line (Met) after 14 days of storage in UW, were 30.2 +/- 1.2 mN, 26.9 +/- 1.0 and 45 +/- 1.2% (means +/- SEM, n=9), respectively. Patency after three months of implantation for group I was 100% (14/14), for group II 50% (7/14), and for group III 75% (6/8). In vitro functional responses of preserved arteries, after 3 months of implantation in group I were 58.5 +/- 10.6 mN (KCl), 36.5 +/- 5.8 mN (Phe), and 57.4 +/- 9.7% (Met), respectively. Functions in group II were 1.2 +/- 0.1 mN (KCl, 0.0 mN (Phe), and 0.0% (Met). Grafts in group III showed no function. Measurement of medial thickness showed significant thinning (P <0.05) in groups II and III. Patency and function of arterial allografts under a therapeutic dose of CsA were superior to grafts implanted under low-dose CsA or no immunosuppressive treatment.
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PMID:Experimental arterial allografting under low and therapeutic dosages of cyclosporine for immunosuppression. 861 Apr 6


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