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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The forming surfaces of enamel of rat incisors were examined by scanning electron microscope one hour after injection of either 5 mg/100 g body weight of sodium fluoride or 12 mg/100 g body weight of cobalt chloride. The cell debris from the surfaces of the separated incisors was either gently wiped off with soft facial tissues or chemically removed by treating with NaOH, NaOCl or trypsin. Best results to remove cell debris were obtained from 0.25% trypsin treatment. SEM studies revealed that the surface of the normal secretory enamel was characteristic in appearance with well-developed smooth prism outlines. In fluoride specimens the prism outlines were feathery in appearance, laced with protruding spine-shaped clusters of mineral crystals. In the case of cobalt treatment, prism outlines were less uniform and in some areas they were incomplete. The calcium concentration of surface enamel was significantly lower in the cobalt-treated specimens than those from control and fluoride-treated animals. The Ca:Mg ratio was also lower in cobalt-treated specimens as compared to control and fluoride-treated ones.
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PMID:Effect of fluoride and cobalt on forming enamel: scanning electron microscope and X-ray microanalysis study. 320 Nov 97

A knee simulator was used to study the wear of carbon fiber reinforced UHMWPE (Poly Two) (Poly Two is a registered trademark of Zimmer, USA) tibial and patellar components against Ti-6A1-4V, titanium nitride (TiN)-coated Ti-6A1-4V, and cobalt-chromium-molybdenum femoral components. The prostheses tested were regular sized Miller-Galante total knees mounted on 316L stainless steel fixtures using bone cement. An environmental chamber surrounded the knee and maintained bovine serum lubricant at 37 degrees C. The specimens were tested using consecutive blocks of 464 level walking steps, 8 ascending stairs and 8 descending stairs for a total of 100,000 steps. The wear mechanisms found on the tibial components were scratching, carbon-fiber associated damage, surface deformation, pitting, minor abrasion, and delamination. Three forms of carbon fiber associated damage were identified; fibers pulled from the surface, broken fibers, and UHMWPE removed from the surface fibers. The SEM evaluation revealed a pit forming mechanism. No correlation was found between femoral component material and tibial surface damage. Visual examination of the femoral components revealed no signs of wear or scratching on the cobalt-chromium-molybdenum or TiN-coated Ti-6A1-4V components. There were, however, many light surface scratches on the uncoated Ti-6A1-4V components, which were also observed in a supplementary test of an uncoated Ti-6A1-4V component tested with a conventional polyethylene tibial component.
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PMID:Component wear of total knee prostheses using Ti-6A1-4V, titanium nitride coated Ti-6A1-4V, and cobalt-chromium-molybdenum femoral components. 322 Aug 40

Disks of four cobalt-chromium alloys were electrolytically etched and bonded together using a microfilled restorative resin. The bonds of the resin to two of the tested alloys, Bondi-loy and Vitallium, showed tensile strengths of approximately 18 MPa. The bonds were significantly stronger than those obtained using the other two alloys, Dentitan and Novarex. The tensile bond strengths of etched Dentitan and Novarex were 5.3 and 7.5 MPa respectively. The etched and debonded surfaces were studied in SEM.
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PMID:Resin bond to electrolytically etched cobalt-chromium alloys. 355 Oct 39

Polymorphonuclear leucocytes released LTD4-dipeptidase activity in a time-, calcium-, and cell number-dependent fashion. The LTD4-dipeptidase released from polymorphonuclear leucocytes (PMN) by incubation with calcium (0.91 mM) was detectable up to a cell concentration of 1 X 10(6)/ml and increased with higher concentrations. Maximal LTD4-dipeptidase activity within the extracellular environment was detected after 15 min of incubation (2 X 10(7)/ml) in the presence of 2-4.5 mM calcium or after 30 min, when stimulation was carried out with 0.91 mM calcium. The activity of the released LTD4-dipeptidase was modulated by various metal ions and other compounds. The addition of Mn2+, Co2+, and Zn2+ (final concentration 1 mM) enhanced the LTD4-dipeptidase activity, while Cu2+ led to a complete inhibition. In the absence of exogenous calcium EDTA inhibited LTD4-dipeptidase. Calcium up to a concentration of 5 and 10 mM decreased the dipeptidase activity. The LTD4-dipeptidase is not affected by bestatin, leupeptin, or N-ethyl-maleinimide (NEM). The Km of LTD4-dipeptidase for LTD4 was 0.95 +/- 0.2 microM and Vmax was 737.5 +/- 112.5 pmol/min X mg protein (n = 3 +/- SEM). The highest LTD4-dipeptidase activity was obtained at physiological pH values. LTD4-dipeptidase activity can also be released from other cell types, but the enzyme activity from human PMN exceeded that of other cells (e.g. human lymphocytes/monocytes and basophils (LMB) and human lung cell suspension).
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PMID:Release and functional characterization of the leukotriene D4-metabolizing enzyme (dipeptidase) from human polymorphonuclear leucocytes. 356 17

In order to assess whether pulsed electromagnetic fields influence the rate of corrosion of orthopaedic metal implants, an alloy, called MP-35N, was exposed for 3 wk to a pulsed electromagnetic field. The results demonstrated that while there was a progressive release of the major constituents of MP-35N, i.e. cobalt (32.5%), nickel (36%), and chromium (20%), with time, corrosion was not significantly higher in the presence of the pulsed electromagnetic field when compared to that of the non-exposed pins. There was a significantly higher release of cobalt by the control pins after 5, 10, and 15 d incubation when compared with the pulsed pins. These findings were confirmed by SEM which demonstrated progressive surface corrosion with time and that the extent of corrosion was similar for both the control and pulsed pins. These results suggest that pulsed electromagnetic fields have no effect in promoting the surface corrosion of orthopaedic metallic implants.
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PMID:The effect of pulsed electromagnetic fields on the corrosion of a chromium-cobalt-nickel alloy orthopaedic implant. 374 57

Considerable evidence suggests that Ca2+ modulates endothelial cell metabolic and morphologic responses to mediators of inflammation. We have used the fluorescent Ca2+ indicator, quin2, to monitor endothelial cell cytosolic free Ca2+, [Ca2+]i, in cultured human umbilical vein endothelial cells. Histamine stimulated an increase in [Ca2+]i from a resting level of 111 +/- 4 nM (mean +/- SEM, n = 10) to micromolar levels; maximal and half-maximal responses were elicited by 10(-4) M and 5 X 10(-6) M histamine, respectively. The rise in [Ca2+]i occurred with no detectable latency, attained peak values 15-30 s after addition of stimulus, and decayed to a sustained elevation of [Ca2+]i two- to threefold resting. H1 receptor specificity was demonstrated for the histamine-stimulated changes in [Ca2+]i. Experiments in Ca2+-free medium and in the presence of pyrilamine or the Ca2+ entry blockers Co2+ or Mn2+, indicated that Ca2+ mobilization from intracellular pools accounts for the initial rise, whereas influx of extracellular Ca2+ and continued H1 receptor occupancy are required for sustained elevation of [Ca2+]i. Ionomycin-sensitive intracellular Ca2+ stores were completely depleted by 4 min of exposure to 5 X 10(-6) M histamine. Verapamil or depolarization of endothelial cells in 120 mM K+ did not alter resting or histamine-stimulated [Ca2+]i, suggesting that histamine-elicited changes are not mediated by Ca2+ influx through voltage-gated channels. Endothelial cells grown on polycarbonate filters restricted the diffusion of a trypan blue-albumin complex; histamine (through an H1-selective effect) promoted trypan blue-albumin diffusion with a concentration dependency similar to that for the histamine-elicited rise in [Ca2+]i. Exposure of endothelial cells to histamine (10(-5) M) or ionomycin (10(-7) M) was associated with a decline in endothelial F-actin (relative F-actin content, 0.76 +/- 0.07 vs. 1.00 +/- 0.05; histamine vs. control, P less than 0.05; relative F-actin content, 0.72 +/- 0.06 vs. 1.00 +/- 0.05; ionomycin vs. control, P less than 0.01). The data support a role for cytosolic calcium in the regulation of endothelial shape change and vessel wall permeability in response to histamine.
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PMID:Histamine type I receptor occupancy increases endothelial cytosolic calcium, reduces F-actin, and promotes albumin diffusion across cultured endothelial monolayers. 378 1

When uptake of L-[14C]ascorbic acid ([14C]AA) to various organs in guinea-pigs was studied after intracardiac injection, the adenohypophysis, pars intermedia, and the neurohypophysis had an uptake per milligramme protein which was about half of the uptake to the adrenals. Adrenal uptake was 20 +/- 2.8 pmol mg-1 protein microCi-1 injected. The uptake to the different parts of the hypophysis was considerably higher than the uptake to pancreas, liver, kidney, spleen and other organs. When isolated nerve endings (neurosecretosomes) from ox neurohypophyses were incubated with a medium containing labelled dehydroascorbic acid ([14C]DHA), the uptake was much slower than when the medium contained labelled ascorbic acid. The uptake of [14C]DHA showed a linear dependence on concentration, and was not influenced by addition of Mg2+ and ATP. Addition of Mg2+ + ATP, omission of Ca2+ and Mg2+ or exchange of Na+ in the medium with K+ had no effect on the uptake of ascorbic acid. When isolated secretory granules from ox neurohypophyses were incubated with a medium containing [14C]DHA, uptake was considerably faster than the uptake when they were incubated in a medium containing [14C]AA. The uptake of dehydroascorbic acid was linear with the concentration in the medium and was not changed by addition of Mg2+ ATP. Addition of 10 mM NH4Cl or exchange of 120 mM K+ in the incubation medium with Na+ did not change the uptake of dehydroascorbic acid. The contents of copper, zinc, iron and cobalt were determined in isolated nerve endings (A) and membranes (B) as well as in lysate (C) from isolated neurosecretory granules. The results (in nmol mg-1 protein) were for Cu: (A): 0.25 +/- 0.01 (SEM), (B): 0.67 +/- 0.16, (C): 0.22 +/- 0.06; for Zn: (A): 0.53 +/- 0.13, (B): 6.97 +/- 0.75, (C): 1.8 +/- 0.53; and for Fe: (A): 15.6 +/- 1.9, (B): 6.92 +/- 0.32, (C): 3.15 +/- 0.43. In all preparations the cobalt content was below the detection limit (less than 5 pmol mg-1 protein).
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PMID:Uptake of dehydroascorbic acid and ascorbic acid to isolated nerve terminals and secretory granules from ox neurohypophyses. 381 87

Intracellular recordings were obtained from sympathetic preganglionic neurons of the intermedio-lateral nucleus of the adult cat in slices of upper thoracic spinal cord maintained in vitro. The neurons were identified by their antidromic responses to stimulation of various ipsilateral sites. Sites from which antidromic responses could be evoked were the white ramus, the ventral root, the ventral root exit zone, the white matter between the latter and the outer edge of the tip of the ventral horn, the lateral edge of the ventral horn. Resting membrane potential was --61.3 +/- 1.6 mV (mean +/- SEM), input resistance 67.5 +/- 3.7 M omega, time constant 11.5 +/- 1.2 ms. The amplitude of the action potential generated by antidromic or direct stimulation was 77.4 +/- 2.3 mV. Threshold for direct spikes was 18.2 +/- 1.8 mV. The action potential had an average duration of 3.03 +/- 0.16 ms. It showed a prominent "hump" on the falling phase. The action potential had a tetrodotoxin (TTX)-sensitive and a TTX-resistant component. The latter was abolished by cobalt. Tetraethylammonium, cesium and barium prolonged the action potential duration which acquired a plateau-shape. A prolonged after-hyperpolarization (AHP) followed the sympathetic preganglionic neuron spike. Following a single spike, AHP duration and peak amplitude were 2.8 +/- 0.3 s and 16.6 +/- 0.7 mV, respectively. The AHP was abolished by cesium or barium, but enhanced by tetraethylammonium. An AHP followed the TTX-resistant spike. EPSPs and IPSPs could be generated by focal stimulation. The EPSP triggered spikes when threshold (15.0 +/- 2.0 mV) was reached.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Electrophysiological properties of sympathetic preganglionic neurons in the cat spinal cord in vitro. 396 Jul 3

The nature of the metal-tissue interface following the implantation of five pure metals, lead, copper, nickel, aluminium and cobalt, in rats has been observed by scanning electron microscopy. The general conclusion, derived from light microscopy that the tissue response to pure metals is characteristic of and specific to individual pure metals has been confirmed in this study. However, far more detailed observations of factors such as the extent of metallic corrosion, the distribution of red blood cells, platelets and other cells in the capsule and adherent to the metal surface, have been possible with SEM.
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PMID:Scanning electron microscopy of the metal-tissue interface. II. Observations with lead, copper, nickel, aluminium, and cobalt. 711 61

To study the cellular basis for FSH-stimulated dose-dependent graded increases in intracellular Ca2+ concentrations in populations of Sertoli cells, we investigated the effects of FSH on free Ca2+ ion concentrations ([Ca2+]i) in individual rat Sertoli cells using the Ca(2+)-sensitive dye fura-2/AM and digital fluorescent videomicroscopy. Ovine or rat FSH elicited a hormone-specific rise in [Ca2+]i within 20-140 sec, with a peak level 2.7 +/- 0.9-fold greater than the basal value (mean +/- SEM; n = 8) lasting for 4-16 min. The amplitude and kinetics of the FSH-induced [Ca2+]i signal were not dose dependent. Instead, increasing doses of FSH recruited a higher percentage of responding cells. Chelation of extracellular Ca2+ or cotreatment with verapamil or cobalt abolished FSH-induced [Ca2+]i increases. Furthermore, in the presence of extracellular Mn2+, direct evidence for FSH-mediated Ca2+ influx was obtained from the quench of fura-2 fluorescence. Induced Ca2+ increases were mimicked by forskolin or protein kinase-A type I activators [8-(6-amino-hexyl)amino-cAMP and N6-benzoyl-cAMP (N6B)]. However, the cAMP analogs, 8-bromo-cAMP, N6,2'-O-dibutyryl cAMP, or protein kinase-A type II activators (8-thiomethyl-cAMP and N6B), induced [Ca2+]i increases even in the absence of extracellular Ca2+, and the time course of the [Ca2+]i rise induced by cAMP analogs was more rapid than that induced by FSH. Similarly, the uninhibited rise in [Ca2+]i induced by FSH in pertussis toxin-pretreated Sertoli cells suggests that PT-sensitive G-proteins are not involved in the action of FSH on [Ca2+]i. In summary, we demonstrate that FSH evokes sustained [Ca2+]i increases in single Sertoli cells in a nongraded fashion and recruits increasing numbers of responding cells in a dose-dependent fashion. We also provide explicit evidence that FSH induces Ca2+ influx. Mimicry of the FSH-induced [Ca2+]i rise by certain cAMP analogs [8-(6-amino-hexyl)amino-cAMP and N6B; protein kinase-A type I activator] or forskolin suggests that Ca2+ may be part of a dual pathway of cAMP-initiated intracellular signaling.
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PMID:Cellular basis for follicle-stimulating hormone-stimulated calcium signaling in single rat Sertoli cells: possible dissociation from effects of adenosine 3',5'-monophosphate. 813 59


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