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

Ion etching and thinning using ionized argon beams have been used to prepare surfaces and thin sections of human and animal compact cortical bone for examination in both scanning and transmission modes of the electron microscope. Using these techniques the mineral component in bone is revealed as a continuous, vermiform microskeleton composed of spheroidal segments approximately 0.1 micrometer in diameter. Electron diffraction and micro-analysis have confirmed that the mineral segments contain calcium and phosphate ions arranged in a poorly crystallised form of hydroxyapatite.
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PMID:The spatial arrangement of bone mineral as revealed by ion bombardment. 732 18

Eggshell thinning in ducks was induced by administration of p,p'-DDE in the diet (40 mg/kg food) for 45 days. This treatment resulted in a 19% reduction of the Eggshell Index (EI). Shells from calcifying eggs obtained at the time of slaughter showed a 36% reduction of EI. Prostaglandin synthesis by a homogenate of eggshell gland mucosa from p,p'-DDE-treated ducks was reduced by 24%. HCO3(-)-stimulated ATPase activity by a homogenate of eggshell gland mucosa from p,p'-DDE-treated ducks was not significantly changed. The calcium content of eggshell gland mucosa was increased to 127% in p,p'-DDE-treated ducks. p,p'-DDE-treated ducks showed profound changes in the shell gland luminal content of several ions. Calcium (-43%), sodium (-15%), potassium (-15%), bicarbonate (-33%) and chloride (-29%) were all significantly reduced in p,p'-DDE-treated ducks. The content of phosphate was unchanged. These findings are discussed in relation to a proposed mechanism for p,p'-DDE-induced eggshell thinning that involves inhibition of prostaglandin synthesis in eggshell gland mucosa.
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PMID:Changes in the levels of different ions in the eggshell gland lumen following p,p'-DDE-induced eggshell thinning in ducks. 788 10

The effects of high toxic doses of the anticancer drugs, etoposide and its phosphate derivative, BMY-40481, on the nervous system of female CD-1 mice were examined by light microscopy (LM) and transmission electron microscopy. Mice were euthanatized 4 wk following a single iv injection of either 0, 50, 100, or 150 mg/kg of BMY-40481 or 44 or 88 mg/kg of etoposide. Mice treated with 100 or 150 mg/kg of BMY-40481 or 88 mg/kg of etoposide had clinical symptomology of progressive ataxia, impaired righting reflex, and splaying and paresis of fore- and hindlimbs at day 8. Similar, dose-related LM changes were observed with both drugs at all doses and consisted of degeneration of dorsal root ganglion cells and axonal degeneration of their distal and proximal processes in peripheral nerves, dorsal spinal roots, and dorsal funiculi of spinal cord. Axonal degeneration was characterized by LM as shrinkage, swelling, and fragmentation of axon cylinders accompanied by secondary demyelination. Degenerative changes in ganglion cell bodies included eccentric nuclei, cytoplasmic vacuolation, central chromatolysis, and peripheral clumping of Nissl's bodies. Ultrastructurally, ganglion cell bodies had focally extensive dilation of the rough endoplasmic reticulum, mitochondrial swelling, increased numbers of phagolysosomes and prominent aggregations of microfilaments (globular filamentous bodies). Ultrastructural axonal changes occurred primarily in large, myelinated fibers and consisted of axonal swelling or loss, thinning of myelin sheaths, and a decrease in the number of organelles. This is the first report of etoposide-related sensory neuropathy in laboratory rats, a model that my be useful for the study of etoposide-related peripheral neuropathy in humans.
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PMID:Etoposide- and BMY-40481-induced sensory neuropathy in mice. 789 82

Sprague-Dawley rats were given 42 mg/kg xylazine intramuscularly, and lungs were lavaged with phosphate-buffered saline 3, 6, and 12 hr later. Total protein, lactate dehydrogenase (LDH), xanthine oxidase (XO), tumor necrosis factor (TNF), and interleukin 1 (IL-1) were measured in bronchoalveolar lavage fluid (BALF). Protein concentration, LDH, XO, and TNF levels were increased (p < 0.05) in the BALF from xylazine-treated rats as compared to controls. IL-1 level was unchanged at 3 and 6 hr and was reduced (p < 0.05) at 12 hr. Another group of rats was given 42 mg/kg xylazine intramuscularly, and lungs were fixed 0.5 and 12 hr later. Histologically, severe pulmonary edema (PE) involving the alveoli and perivascular stroma was observed. Fibrin, increased numbers of eosinophils, and macrophages with foamy cytoplasm were present in the alveoli of all treated animals. Ultrastructurally, endothelial damage, characterized by thinning, detachment from basement membranes, or bleb formation, was observed. The lesions were similar in both xylazine groups, differing mainly in severity with the 12-hr group having more severe lesions than the 0.5-hr group. To determine whether endothelial injury is caused by direct toxicity of xylazine, bovine pulmonary artery endothelial cells (BPAECs) were incubated with xylazine (0.3, 3, and 30 micrograms) for 0.5 or 3 hr. Xylazine did not have any effects on BPAECs, as indicated by phase-contrast microscopy and dye-exclusion viability assay. These results indicate that xylazine-induced PE is due to increased permeability resulting from endothelial injury, which is not caused by direct effect of xylazine on pulmonary endothelium. While oxygen radicals and TNF are possibly involved, IL-1 does not appear to play a role in xylazine-induced PE.
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PMID:Biochemical and morphological alterations in xylazine-induced pulmonary edema. 805 3

We investigated the temporal relationship of the emergence of biochemical abnormalities to the development of behavioral dysfunction to identify the central factors of ischemic neurological disorders in developing brains. To induce early ischemia, bilateral carotid artery occlusion (BCAO) was surgically performed on 21 cats at the second week of age. BCAO produces histopathological damage, including neuronal loss and thinning of white matter. 31P magnetic resonance spectroscopy was used to monitor brain oxidative metabolism, neuronal membrane growth, and myelination of the prefrontal cortex in the first 3 months. Neurological development was monitored by conducting 25 tests of reflex, motor, sensory, and integrated behavioral function. At 1 month, phosphodiester (PDE) levels, a component of membranes and myelin, were low in animals showing complete ligation. At 2 months, the growth of PDE was low (1/4 to 1/2 of normal) in BCAO animals, whereas normal animals demonstrated a 23% increase. Phosphocreatine (PCr) levels, indicated by PCr/ATP and PCr/inorganic phosphate ratios, were retarded at 2 months in completely ligated animals (1/4 of normal). Neurologically, the completely ligated animals showed retardation of general development. The retardation was most pronounced for integrative functions, including visual function, and became more pronounced later in development. The time course of emergence of the retardation generally coincided with emergence of abnormalities in phosphorous compounds. The simultaneous occurrence of several biochemical and functional abnormalities in development following early ischemic insult suggests a causal relationship between membrane and mitochondrial development and neurological function.
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PMID:Consequences of reduced cerebral blood flow in brain development. II. Retardation of neurological outcome and phosphorus metabolism. 828 31

Postnatal formation of alveoli can be largely prevented by glucocorticoid treatment, which accelerates alveolar wall thinning and inhibits outgrowth of new interalveolar septa. Since a double capillary network is a prerequisite for interalveolar wall formation, we hypothesized that glucocorticoid treatment inhibited alveolar formation, indirectly, by inducing precocious microvascular maturation. Between 4 and 60 days we followed up qualitatively and quantitatively the effects of 2 weeks (days 2-15) of daily Decadron (Dexamethasone phosphate) injections on the lung structure. Glucocorticoid induced only small changes in body weight or lung volume. However, during the first 2 weeks, it accelerated alveolar wall thinning and microvascular maturation and partly suppressed the outgrowth of new interalveolar septa. In Decadron-treated rats, the interstitial tissue mass was significantly reduced during the first 2 weeks, and a larger alveolar surface area was endowed with a capillary monolayer on days 10 and 13. One week after drug withdrawal, the trend towards precocious maturation of the lung was reversed. Lipofibroblasts reappeared, and inter-airspace septa regressed towards a more immature state. We found indications of a second burst of alveolization by resumption of secondary septa formation. The late sequelae of Decadron treatment (day 60) were manifested as an 'emphysematous' condition of the lungs, with larger and fewer airspaces, the delayed alveolization being insufficient to compensate for the initial deficit.
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PMID:Influence of postnatally administered glucocorticoids on rat lung growth. 858 Feb 14

Calcium phosphate ceramic coatings with a hydroxyapatite chemistry applied on the surface of dental implants eliminate the need for initial mechanical retention and decrease the time necessary for bonding the implants to the bone. Hydroxyapatite-coated implants retrieved from patients were found to be compatible and to have bonded strongly to the bone, but the coatings showed thinning because of partial or total loss of coating material. This study compared the behavior in bone of newly developed fluorapatite and heat-treated hydroxyapatite coatings, with the clinically used hydroxyapatite coatings used as controls in experimental studies in dogs. The biologic responses to fluorapatite and heat-treated hydroxyapatite coatings were the same as those to hydroxyapatite coatings, and bone condensation around all coatings was histologically evident. However, the coating thickness of the fluorapatite and heat-treated hydroxyapatite coatings remained stable with only minor changes during the observation period of 24 months.
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PMID:Behavior of calcium phosphate coatings with different chemistries in bone. 863 37

Type X collagen has been implicated in the morphogenetic events of endochondral ossification (EO), including the calcification of hypertrophic cartilage and trabeculae prior to their replacement by bone and marrow. Recently, transgenic mice, which expressed a truncated collagen X protein, were reported to exhibit morphologic alterations in all tissues arising through EO. Specifically, the growth plates were compressed within the zone of cartilage hypertrophy, and the number and size of calcified trabeculae were reduced. The condition in the mouse is comparable to Schmid metaphyseal chondrodysplasia in humans for which, to date, 20 defined type X collagen mutations have been reported. The transgenic mouse showed no alterations in mineralization by conventional histology, however, it did show a decrease in newly formed bony trabeculae, and a thinning of periosteal bones. Fourier transform infrared (FTIR) spectroscopy has previously been shown to provide quantitative and qualitative information about the relative amount of mineral and carbonate present, mineral composition, and crystal perfection. To determine whether the expression of abnormal collagen X molecules had an effect on mineral properties, the "quality" of mineral crystals was analyzed in thin sections of tibia from day 17 and day 25 genotypically negative (normal) and positive (mutant) mice from several independent transgenic mouse lines showing varying degrees of the mutant phenotype, by means of Fourier transform infrared microscopic analysis (FTIRM). The results indicate definite differences between normal and transgenic mice calcified cartilage mineral, both in the amount present and the "quality" of the crystals. Calcified cartilage mineral from transgenic mice exhibited less crystallinity and higher acidic phosphate content than the corresponding mineral from normal specimens.
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PMID:Fourier transform infrared microspectroscopic analysis identifies alterations in mineral properties in bones from mice transgenic for type X collagen. 885 59

We present a quantitative analysis of the effects of hydrophobic matching and membrane-mediated protein-protein interactions exhibited by gramicidin embedded in dimyristoylphosphatidylcholine (DMPC) and dilauroylphosphatidylcholine (DLPC) bilayers (Harroun et al., 1999. Biophys. J. 76:937-945). Incorporating gramicidin, at 1:10 peptide/lipid molar ratio, decreases the phosphate-to-phosphate (PtP) peak separation in the DMPC bilayer from 35.3 A without gramicidin to 32.7 A. In contrast, the same molar ratio of gramicidin in DLPC increases the PtP from 30.8 A to 32.1 A. Concurrently, x-ray in-plane scattering showed that the most probable nearest-neighbor separation between gramicidin channels was 26.8 A in DLPC, but reduced to 23.3 A in DMPC. In this paper we review the idea of hydrophobic matching in which the lipid bilayer deforms to match the hydrophobic surface of the embedded proteins. We use a simple elasticity theory, including thickness compression, tension, and splay terms to describe the membrane deformation. The energy of membrane deformation is compared with the energy cost of hydrophobic mismatch. We discuss the boundary conditions between a gramicidin channel and the lipid bilayer. We used a numerical method to solve the problem of membrane deformation profile in the presence of a high density of gramicidin channels and ran computer simulations of 81 gramicidin channels to find the equilibrium distributions of the channels in the plane of the bilayer. The simulations contain four parameters: bilayer thickness compressibility 1/B, bilayer bending rigidity Kc, the channel-bilayer mismatch Do, and the slope of the interface at the lipid-protein boundary s. B, Kc, and Do were experimentally measured; the only free parameter is s. The value of s is determined by the requirement that the theory produces the experimental values of bilayer thinning by gramicidin and the shift in the peak position of the in-plane scattering due to membrane-mediated channel-channel interactions. We show that both hydrophobic matching and membrane-mediated interactions can be understood by the simple elasticity theory.
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PMID:Theoretical analysis of hydrophobic matching and membrane-mediated interactions in lipid bilayers containing gramicidin. 1035 42

This study represents the first report of the physical and chemical changes occurring in coatings of failed hydroxyapatite (HA)-coated titanium implants obtained from a comprehensive, multicenter human dental implant study. A total of 53 retrieved samples were obtained and compared with unimplanted controls with the same manufacturer and similar manufacture dates. Forty-five retrieved implants were examined for surface characteristics and bulk composition. Implants were staged based on implantation history: stage 1 (implants retrieved between surgical placement and surgical uncovering), stage 2 (implants retrieved at surgical uncovering and evaluation), stage 3 (implants retrieved between surgical uncovering evaluation and occlusal loading), and stage 4 (implants retrieved after occlusal loading). Scanning electron microscopy showed progressive coating thinning with implantation time. At later stages, bare Ti metal was detected by energy-dispersive X-ray analysis and electron spectroscopy for chemical analysis. Increases in Ti and Al (2-7.5 atm % each) were detected at the apical ends of all stage 4 samples. In unimplanted coatings, X-ray diffraction analysis demonstrated the presence of amorphous calcium phosphate, beta-tricalcium phosphate, tetracalcium phosphate, and calcium oxide in addition to large hydroxyapatite crystals (c axis size, D002 = 429 +/- 13 A; a axis size, D300 = 402 +/- 11 A, a/c aspect ratio 0.92). The nonapatitic phases disappeared with increased implantation time, although there was a persistence of amorphous calcium phosphate. Bulk coating chemical analysis showed that Ca/P ratios for implant controls (1.81 +/- 0.01) were greater than stoichiometric HA (1.67) and decreased for implant stages 3 and 4 (1.69 +/- 0.09 and 1.67 +/- 0.09, respectively), explained by the dissolution of the non apatitic phases. Crystal sizes also changed with implantation times, being smaller than the control at all but stage 4. Fourier transform infrared analyses agreed with these results, and also indicated the accumulation of bone (protein and carbonate-apatite) in the retrieved coatings. The accumulation of bone was not stage dependent. These findings indicate that there was some biointegration with the surrounding bone, but the greatest changes occurred with the HA coating materials, their loss, and chemical change.
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PMID:Physicochemical study of plasma-sprayed hydroxyapatite-coated implants in humans. 1142 92


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