Filling of light emitting diode via-holes by MOCVD

The growth of epitaxial films on featured substrates has an important device application in junction-confinement, double hetero-structure light emitting diodes. These devices are presently grown by a liquid phase epitaxy process but growth by metalorganic chemical vapor deposition is desirable because of MOCVD's superior surface quality, uniformity, and throughput. This paper describes the effect of growth parameters on AlGaAs films deposited by atmospheric-pressure MOCVD into substrate holes typically made in the fabrication of junction-confinement LEDs. MOCVD growth replicates the substrate features; it does not give a planar surface over the holes. The behavior of epitaxy filling into holes is strongly dependent on growth temperature and total gas flow and largely independent of substrate misorientation and the thickness of the layer grown. Wet-etched holes formed (ll0)-oriented V-groove and dovetail-groove features on the hole circumference. Faceting of the MOCVD growth was seen on the wall with the (111)A feature while smooth growth was seen on the etched (111)B surface. Deceased.     

Constrained optimal control

The explicit form of the optimal control law of a given linear, discrete-time, time-invariant process subject to a quadratic cost criterion is well known. In some applications it is desirable that the state of a controlled dynamic process be nonnegative, given a certain class of initial disturbances. Using the controllable block companion transformation, sufficient conditions on the weighting matrices of the cost criterion are derived to ensure that the closed-loop response of the original process with the standard, unconstrained optimal feedback law will be nonnegative. It is shown that the nondiagonal elements of the transformed weighting matrices can be chosen to ensure nonnegativity     

X-ray tomographic microscopy of fibre-reinforced materials

Aluminium composites containing Al₂O₃ fibres and precipitates of various intermetallic phases are investigated by high-resolution computerized microtomography. Individual fibres 15 μm in diameter and intermetallic phases forming a network with about 15 μm mesh size have been imaged. The capabilities of the method and its further development down 1 μm and less spatial resolution are discussed.     

Reversal of impaired oxidative phosphorylation and calcium overloading in the skeletal muscle mitochondria of CHF-146 dystrophic hamsters

Membrane-mediated excessive intracellular calcium accumulation (EICA) and diminished cellular energy production are the hallmarks of dystrophic pathobiology in Duchenne and Becker muscular dystrophies. We reported reversal of respiratory damage and Ca(2+)-overloading in the in vitro cardiac mitochondria from CHF-146 dystrophic hamsters (DH) with hereditary muscular dystrophy (Bhattacharya et al., 1993). Here we studied respiratory dysfunctions in the skeletal muscle mitochondria from young and old DH, and whether these abnormalities can be reversed by reducing [Ca2+] in the isolation medium, thereby lowering intramitochondrial Ca(2+)-overloading. Age- and sex-matched CHF-148 albino normal hamsters (NH) served as controls. As an index of EICA and cellular degeneration, Ca and Mg levels were assayed in the skeletal muscle and mitochondria. Mitochondria from young and old DH, isolated without EDTA (BE medium), revealed poor coupling of oxidative phosphorylation, diminished stimulated oxygen consumption rate, and lower respiratory control ratio and ADP/O ratios, compared to NH. Incorporation of 10 mM EDTA (Bo medium) in the isolation medium restored mitochondrial functions of the dystrophic organelles to a near-normal level, and reduced Ca(2+)-overloading. The mitochondrial Ca level in DH was significantly higher than in NH, irrespective of the medium. However, compared to Bo medium, the dystrophic organelles isolated in BE medium had lower Ca levels and markedly improved oxidative phosphorylation as seen in NH. Muscle Ca contents in the young and old DH were elevated relative to NH, showing a positive correlation with the increased mitochondrial Ca(2+)-sequestration. Dystrophic muscle also revealed Ca deposition with an abundance of Ca(2+)-positive and necrotic myofibers by light microscopy, and intramitochondrial Ca(2+)-overloading by electron microscopy, respectively. However, Mg levels in the muscle and mitochondria did not alter with age or dystrophy. These data parallel our observations in the heart, and suggest that functional impairments and Ca(2+)-overloading also occur in the skeletal muscle mitochondria of DH, and are indeed reversible if EICA is regulated by slow Ca(2+)-channel blocker therapy (Johnson and Bhattacharya, 1993).     

A study of the mechanism of inhibition of fibrinolysis by activated thrombin-activable fibrinolysis inhibitor

TAFI (thrombin-activable fibrinolysis inhibitor) is a recently described plasma zymogen that, when exposed to the thrombin-thrombomodulin complex, is converted by proteolysis at Arg92 to a basic carboxypeptidase that inhibits fibrinolysis (TAFIa). The studies described here were undertaken to elucidate the molecular basis for the inhibition of fibrinolysis. When TAFIa is included in a clot undergoing fibrinolysis induced by tissue plasminogen activator and plasminogen, the time to achieve lysis is prolonged, and free arginine and lysine are released over time. In addition, TAFIa prevents a 2.5-fold increase in the rate constant for plasminogen activation which occurs when fibrin is modified by plasmin in the early course of fibrin degradation. The effect is specific for the Glu- form of plasminogen. TAFIa prevents or at least attenuates positive feedback expressed through Lys-plasminogen formation during the process of fibrinolysis initiated by tissue plasminogen activator and plasminogen. TAFIa also inhibits plasmin activity in a clot and prolongs fibrinolysis initiated with plasmin. We conclude that TAFIa suppresses fibrinolysis by removing COOH-terminal lysine and arginine residues from fibrin, thereby reducing its cofactor functions in both plasminogen activation and the positive feedback conversion of Glu-plasminogen to Lys-plasminogen. At relatively elevated concentrations, it also directly inhibits plasmin.     

Atrial flutter with 1:1 atrioventricular conduction caused by propafenone

We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beats/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side effect that, although uncommon, should be recognized.     

Neutrophil accumulation is reduced during partial liquid ventilation

OBJECTIVE: This study evaluates the ability of perflubron to inhibit pulmonary neutrophil accumulation during partial liquid ventilation (PLV) in the setting of acute lung injury. DESIGN: Randomized, controlled, nonblinded study. SETTING: Research laboratory at a university. SUBJECTS: Male, Sprague-Dawley rats (n = 120, 506 +/- 42 g). INTERVENTIONS: Animals were divided into eight groups (n = 15 in each group, of which n = 12 for myeloperoxidase content and n = 3 for histologic neutrophil counting): a) GV-CVF group, animals received gas ventilation (GV) with the induction of lung injury using cobra venom factor (CVF); b) PLV-CVF group, animals received partial liquid ventilation before the induction of lung injury; c) PEEP-CVF group, animals received positive end-expiratory pressure (PEEP) before the administration of cobra venom factor; d) CVF-PLV group, animals received partial liquid ventilation after cobra venom factor; e) CVF-PEEP group, animals received PEEP after cobra venom factor; f) PLV only group, animals received partial liquid ventilation only; g) GV only group, animals received gas ventilation only; and h) NVSBA group, nonventilated spontaneous breathing animals. MEASUREMENTS AND MAIN RESULTS: After the experimental period, total lung myeloperoxidase content was significantly decreased in the PLV-CVF (0.29 +/- 0.08, p = .02) and PEEP-CVF (0.34 +/- 0.04, p = .01) groups when compared with the GV-CVF group (0.62 +/- 0.07). When compared with the GV-CVF group, a trend toward a reduction in myeloperoxidase was observed in the CVF-PLV (0.42 +/- 0.05, p = .07) and the CVF-PEEP (0.39 +/- 0.06, p = .07) groups. When compared with the cobra venom factor only group (GV-CVF 47 +/- 2 neutrophils/high-power field), reductions in neutrophil count were observed in all groups (neutrophils/high-power field): PLV-CVF (20 +/- 2, p = .009); PEEP-CVF (24 +/- 1, p = .01); CVF-PLV (30 +/- 2, p = .03); and CVF-PEEP (37 +/- 1, p = .04). CONCLUSION: These data suggest that both partial liquid ventilation and PEEP result in a reduction in neutrophil accumulation in the setting of acute lung injury.     

The transepicondylar axis approximates the optimal flexion axis of the knee

The traditional understanding of knee kinematics holds that no single fixed axis of rotation exists in the knee. In contrast, a recent hypothesis suggests that knee kinematics are better described simply as two simultaneous rotations occurring about fixed axes. Knee flexion and extension occurs about an optimal flexion axis fixed in the femur, whereas tibial internal and external rotations occur about a longitudinal rotation axis fixed in the tibia. No other translations or rotations exist. This hypothesis has been tested. Tibiofemoral kinematics were measured for 15 cadaveric knees undergoing a realistic loadbearing activity (simulated squatting). An optimization technique was used to identify the locations of the optimal flexion and longitudinal rotation axes such that simultaneous rotations about them could best represent the measured kinematics. The optimal flexion axis was compared with the transepicondylar axis defined by bony landmarks. The longitudinal rotation axis was found to pass through the medial joint compartment. The optimal flexion axis passed through the centers of the posterior femoral condyles. No significant difference was found between the optimal flexion and transepicondylar axes. To an average accuracy of better than 3.4 mm in translation, and 2.9 degrees in orientation, knee kinematics were represented successfully by simple rotations about the optimal flexion and longitudinal rotation axes. The optimal flexion axis is fixed in the femur and can be considered the true flexion axis of the knee. The transepicondylar axis axis, which is identified easily by palpation, closely approximates the optimal flexion axis.     

Autoantibodies to small heat shock proteins in glaucoma

PURPOSE: To identify the low-molecular-weight retinal proteins that are the targets of serum autoantibodies in patients with glaucoma and to study the ability of these antibodies to induce retinal apoptosis. METHODS: Serum immunoreactivity against retinal proteins was examined in age-matched groups of 60 patients with normal-pressure glaucoma, 36 patients with high-pressure glaucoma, and a control group of 20 healthy subjects, by means of western blot analysis and enzyme-linked immunosorbent assay. The specificity of the immunoreactivity to small heat shock proteins, including alpha-crystallins and hsp27, was tested by immunoprecipitation of these proteins in retinal fractions. The direct effects of antibodies specific to small heat shock proteins were then studied in isolated intact human retina (ex vivo) and cultured rat retinal cells (in vitro) by immunocytochemistry and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) technique in conjunction with fluorescence microscopy and confocal imaging. RESULTS: Serum immunoreactivity against retinal proteins with low molecular weight in patients with glaucoma was to small heat shock proteins, including alpha-crystallins and hsp27. In addition, patients with normal pressure glaucoma had a higher titer of autoantibodies to small heat shock proteins than did age-matched patients with high-pressure glaucoma or control subjects. It was observed that when antibodies against small heat shock proteins were applied directly to retina tissue or cells, they could trigger cell death through an apoptotic mechanism. CONCLUSIONS: These findings suggest that increased titers of circulating antibodies against retinal small heat shock proteins may have pathogenic significance in some patients with glaucomatous optic neuropathy.     

Absorption and urinary excretion of the coffee diterpenes cafestol and kahweol in healthy ileostomy volunteers

Epidermal growth factor (EGF) has been found to induce enhanced gap junctional intercellular communication (GJIC) in the human kidney epithelial cell line K7. This is in contrast to what is reported for other cell types, which all show decreased GJIC in response to EGF. In the present study it is shown that 12-O-tetradecanoylphorbol-13-acetate (TPA) and EGF induce similar phosphorylation pattern of the gap junction protein connexin43 (Cx43) in K7 cells, although their effects on GJIC are opposite. Tyrosine phosphorylation of a 42 kD protein was observed to be induced concomitantly with phosphorylation of Cx43. EGF was however found to induce only serine phosphorylation of Cx43, indicating that the tyrosine kinase activity of the EGF receptor was not directly affecting the gap junction protein. The 42 kD protein phosphorylated on tyrosine was identified to be a mitogen activated protein (MAP) kinase. Both EGF and TPA was found to activate MAP kinase in these cells. Phosphorylation of Cx43 and enhancement of GJIC in response to EGF occurred with difference in time course. Phosphorylation of Cx43 was completed within 15 min, while the enhanced GJIC appeared 2-3 h later. It is therefore possible that regulation of synthesis or transport of Cx43 is responsible for the increase in GJIC, rather than direct involvement of Cx43 phosphorylation. This is in support of our previous finding that protein synthesis is necessary for EGF induced upregulation of GJIC in K7 cells.