In situ studies of precipitate formationin Al-Pb monotectic solidification by X-ray transmission microscopy

Al-1.5 wt pct Pb monotectic alloys were unidirectionally solidified. X-ray transmission microscope (XTM) observations, both during and after solidification, revealed various new morphological/compositional features in the melt and solid. In the melt, nonuniform lead-rich interfacial segregation layers and droplets were observed to form well ahead of the interface. In the solid, periodic striae formed at translation/solidification velocities as low as 6 × 10⁻⁶ m/s. The striae shape does not replicate that of the interface. The striae spacing decreases from 4 to 2 × 10⁻⁴ m with an increasing solidification rate between 6 and 16 × 10⁻⁶ m/s. High resolution postsolidification XTM examination reveals that these striae consist of Pb-rich particles of 2 to 3 × 10⁻⁶ m diameter. At translation/solidification velocities below 6 × 10⁻⁶ m/s, Pb incorporation into the solid occurs in the form of continuous fibers and strings of particles of about 5 × 10⁻⁶ m diameter. Bands, parallel to the interface, in which these fibers were aligned in the solidification direction, alternated with bands of poor fiber alignment. The width of these bands is comparable to the striae spacings obtained at the high solidification rates.     

In situ studies of grain growth in thin metal films

Grain growth in thin films of aluminum has been studied using in situ transmission electron microscopy and a heating stage. Videotapes taken during grain growth were analyzed with the intent of searching for the predominant local rearrangement processes responsible for growth. Evolution of a soap froth can be decomposed into only two elementary local topology rearranging events. We have found numerous exceptions to prevailing theories that compare grain growth in thin films to the evolution of such froths. These observations suggest that a more complete picture of grain growth is necessary and that such a theory must include more complex local rearrangement processes.     

In situ studies of ion irradiation effects in an electron microscope

The High-Voltage Electron Microscope (HVEM)-Accelerator Facility at Argonne National Laboratory (ANL) has been used to gain insight into the process of collapse of displacement cascades to vacancy loops in metals (Ni, Cu, Fe, Ni-Si, and Ni-Al) and the crystalline-amorphous transition produced in GaAs by ion implantation. This paper is based on a presentation made in the symposium “Irradiation-Enhanced Materials Science and Engineering” presented as part of the ASM INTERNATIONAL 75th Anniversary celebration at the 1988 World Materials Congress in Chicago, IL, September 25-29, 1988, under the auspices of the Nuclear Materials Committee of TMS-AIME and ASM-MSD. KODAK is a trademark of Eastman Kodak Corporation, Rochester, NY. PHILIPS is a trademark of Philips Instruments Corporation, Mahwah, NJ.     

Deformation anisotropy induced by presence of physical fields

An attempt is made to develop an internally consistent theory of plastic flow with anisotropic hardening induced by physical fields of arbitrary structure. Standard theories of plastic flow based on the assumption that the deformation anisotropy is induced by presence of plastic strain, strain rate and temperature. It is worth to be noted that the presence of plastic anisotropy may be induced by influence of another physical fields, like radiation, magnetic fields and so on.     

Enhancement of human platelet aggregation and secretion induced by rapamycin

BACKGROUND: Rapamycin is a new immunosuppressive drug of the macrolide type. Despite binding to one of the FK-binding proteins as the initial step in intracellular action, further effects differ from those of the other fungally derived macrolides, cyclosporine and tacrolimus. We have previously demonstrated an enhancement of agonist-mediated platelet activation by cyclosporine and tacrolimus which was associated with increased phosphorylation of two intracellular platelet proteins, p20 and p40. Because rapamycin utilizes the same class of binding proteins as tacrolimus, but its action is not associated with the inhibition of calcineurin, we postulated that if the stimulatory effect of cyclosporine or tacrolimus was due to calcineurin inhibition, rapamycin should not affect platelets in a similar fashion. METHODS: Normal, washed human platelets were treated with various concentrations of rapamycin (from ng to microg/ml), and pre-incubated at 37 degrees C with rapamycin for various periods (1-30 min). Several platelet functional parameters were measured in samples treated with rapamycin and these parameters were compared with control platelet samples treated with the vehicle for the same period. Platelet aggregations following exposure to ADP or to the thrombin equivalent, TRAP-6, were measured as changes in optical transmission in a Chronolog lumi-aggregometer. Each experiment was repeated at three or more times and the mean results were used for statistical comparison. RESULTS: Rapamycin-treated platelets demonstrated an increase in their dose- and time-dependent sensitivity to ADP, resulting in a significantly enhanced primary wave of ADP-induced platelet aggregation followed by a secondary wave of aggregation, indicative of granule secretion. Furthermore, rapamycin-treated platelets showed significantly enhanced sensitivity to TRAP-6 as demonstrated by an increase in the initial velocity of aggregation, an increase in their maximal extent of aggregation and an enhancement of granular ATP secretion. Concentrations of rapamycin in the ng range, as well as short pre-incubation times (within min), were sufficient to cause significant enhancement of agonist-induced platelet aggregation and secretion (P < 0.001) as compared with their vehicle controls. CONCLUSIONS: Rapamycin significantly potentiates agonist-induced platelet aggregation in a time- and dose-dependent manner. As these findings are similar to those observed with the other fungal macrolides, we hypothesize that inhibition of calcineurin may not be necessary for the increase in intracellular protein phosphorylation observed following exposure of platelets to cyclosporine or tacrolimus. Whether the rapamycin-induced enhancement of sensitivity to agonists and platelet hyperaggregability explains the thrombocytopenia observed in patients when high doses of rapamycin are administered in the clinical setting, and whether these effects are synergistic with cyclosporine, are questions which remain to be investigated.     

In vivo and in vitro studies of the inhibitory effect of propofol on human platelet aggregation

BACKGROUND: The inhibitory effects of propofol on platelet aggregation are controversial because the fat emulsion used as the solvent for propofol may affect platelet function. The effects of propofol on platelet intracellular calcium ion concentration and on aggregation were investigated. METHODS: Platelet aggregation was measured in 10 patients who received an intravenous infusion of propofol. Intralipos, the propofol solvent, was infused in 10 healthy volunteers and platelet aggregation were measured. The in vitro effects of propofol and Intralipos on platelets were also investigated. The inhibitory effects of various concentrations of propofol were studied. The effects of propofol on the changes in intracellular calcium level using a fluorescent dye, fura-2, were also observed. Template bleeding time was measured to determine the effect of propofol in clinical use. RESULTS: Platelet aggregation was significantly inhibited by infusion of propofol, although bleeding time was not prolonged. Intralipos did not inhibit platelets either in vivo or in vitro. Propofol significantly inhibited platelet aggregation in vitro and at 5.81 +/- 2.73 microg/ml but not at 2.08 +/- 1.14 microg/ml. The increase of intracellular calcium concentration was inhibited both in influx and discharge of calcium. CONCLUSIONS: Propofol inhibited platelet aggregation both in vivo and in vitro. Inhibition of platelet aggregation appeared to be caused by propofol itself and not by the fat emulsion. This inhibitory effect was also supported by the suppressed influx and discharge of calcium. No change in the bleeding time suggests that this inhibitory effect does not impair hemostasis clinically.     

Organ culture of craniopharyngioma and its cellular effects induced by colloidal chromic phosphate

Since a marked clinical improvement has been reported following chromic phosphate treatment in recurrent craniopharyngioma, we have attempted to study the in vitro cellular changes of two craniopharyngiomas maintained in organ culture system and subsequently treated with colloidal chronic phosphate. When incubated for 24 and 48 hours respectively, at a concentration of 10 muCi/ml. of colloidal 32P, only vacuolar degeneration and hyperchromasia of the tumor cells have been observed. When incubated with 50 muCi/ml. for 24 hours, further cellular degeneration and focal necrosis begin to appear. Up to 48 hours after 50 muCi/ml. obvious necrosis and extensive degeneration become apparent. Autoradiography confirms the fact that radioactive material is absorbed by the tumor cells. Brain tumors when maintained in an organ culture system may serve as a useful model for the evaluation of the effects of various chemotherapeutic and radiotherapeutic agents in vitro.     

Calculation of electric fields induced near metal implants by magnetic resonance imaging switched-gradient magnetic fields

Electric (E) fields induced near metal implants by MRI switched-gradient magnetic fields are calculated by a new equivalent-circuit numerical technique. Induced E-field results are found for a metallic spinal-fusion implant consisting of two thin wires connected to the metallic case of a current generator as well as for its subsections: a bare U-shaped wire, an insulated U-shaped wire, a cut insulated wire, and a generator. The presence of the metallic implants perturbs the E field significantly. Near the ends of the bare U-shaped wire, the E field is 89.7 times larger than in the absence of the wire. The greatest E field concentration occurs near the ends of the cut insulated wire, where the E field is 196.7 times greater than in the absence of the wire. In all cases, the perturbation of the induced E field by the implanted wire is highly localized within a few diameters of the wire.     

In situ detection of apoptosis at sites of chronic bacterially induced inflammation in human gingiva

Apoptosis is a key phenomenon in the regulation of the life span of terminally differentiated leukocytes. Human gingiva represents an established model to study immune responses to bacterial infection. In this investigation, we used the TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) technique to evaluate presence and topographic location of apoptosis-associated DNA damage in human gingival biopsies along with the expression of the p53 and Bcl-2 apoptosis-regulating proteins. Qualitative data analysis showed high densities of cells expressing DNA damage and p53 both within the epithelial attachment to the tooth and in the perivascular infiltrate (infiltrated connective tissue [ICT]) immediately underlying the site of chronic bacterial aggression. Topographic consistency between DNA damage- and p53-positive cells was consistently observed. Quantitative analysis of the ICT showed mean densities of DNA damage- and p53-positive cells of 345 +/- 278 and 403 +/- 182 cells/mm2, respectively. Numerical consistency was confirmed by multivariate regression analysis: densities of DNA damage-positive cells were significantly predicted by densities of p53-positive cells (P = 0. 001, r2 = 0.84). In the ICT, cells displaying biotinylated DNA nicks were 3.8% +/- 2.7% of total cellularity, while p53- and Bcl-2-positive cells represented 4.4% +/- 1.7% and 15.4% +/- 6.7% of total cells, respectively. It is suggested that p53 expression associated with DNA damage is a prevalent phenomenon in chronically inflamed human gingiva, and that apoptosis may be a relevant process for the maintenance of local immune homeostasis at sites of chronic bacterial challenge in vivo.