Donor impurity states on structured semiconductor interfaces.
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Biomedical subjects
Publications and source records attributed to H Sun.
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The driving point immittance (impedance or admittance) function is commonly used in electrical characterization of polarized materials and interfaces. The immittance function typically attenuates following a power function dependence on frequency. This fact has been recognized as a macroscopic dynamical property manifested by strongly interacting dielectric, viscoelastic and magnetic materials and interfaces between different conducting substances. Linear interfacial polarization processes which occur at metal electrode-electrolyte interfaces have been represented by the Fractional Power Pole [FPP] function in single or multiple stages. The FPP function is referred to as the Davidson-Cole function in the dielectrics literature. A related function widely used in mathematical modeling of dielectric and viscoelastic polarization dynamics is the Cole-Cole function. The fractional power factor which parametrizes the FPP or the Davidson-Cole function has been shown earlier to equal the logarithmic ratio of the locations of the pole-zero singularities. In this paper we first review a modified form of the singularity decomposition of the FPP function accomplished within a prescribed error range. The distribution spectrum and the corresponding simulation by a cascade R-C network, as opposed to the synthesis by a ladder R-C network, are readily obtained as the next step in the simulation. The method is then applied to decompose the Cole-Cole function; the pole-zero placement of the singularity function is determined and the equivalent cascade R-C network is synthesized.
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With the increasingly stringent standards of image quality in mammography, film processor quality control is especially important. Current methods are not sufficient for ensuring good processing. The authors used a sensitometer and densitometer system to evaluate the performance of 22 processors at 16 mammographic facilities. Standard sensitometric values of two films were established, and processor performance was assessed for variations from these standards. Developer chemistry of each processor was analyzed and correlated with its sensitometric values. Ten processors were retested, and nine were found to be out of calibration. The developer components of hydroquinone, sulfites, bromide, and alkalinity varied the most, and low concentrations of hydroquinone were associated with lower average gradients at two facilities. Use of the sensitometer and densitometer system helps identify out-of-calibration processors, but further study is needed to correlate sensitometric values with developer component values. The authors believe that present quality control would be improved if sensitometric or other tests could be used to identify developer components that are out of calibration.
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The effects of monoclonal antibodies HIP2, APT4 and HI117 on the platelet cytoskeleton were investigated. The results showed that HIP2, APT4 and HI117 could induce an increase of platelet cytoskeleton materials in PRP. The action of HIP2 and APT4 could be obviously inhibited by the calmodulin inhibitor EBB. The inhibition rates of EBB were 76.3% and 48.95%, respectively. But EBB couldn't inhibit the HI117-induced an increase of platelet cytoskeleton materials. EBB could completely inhibit APT4-induced platelet aggregation(100%) and partially inhibit HIP2-induced platelet aggregation (14.26%). It couldn't inhibit HI117-induced platelet aggregation. These McAbs couldn't induce aggregation and actin mobilization in washed platelets in the presence of EDTA. The results indicate that platelet aggregation and the increase of actin induced by these McAbs, in addition to Ca2+, could be related to a factor or factors in the plasma. The Ca(2+)-CM system might play an important role in platelet aggregation and actin mobilization induced by HIP2 and APT4.
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Meiosis-specific double-strand breaks occur at the initiation site for meiotic gene conversion in the yeast ARG4 gene. Here we show that the break fragments end in extensive 3'-overhanging, single-stranded tails. The single-stranded tails very in length, generating a gradient of single-strandedness that parallels the gradient of gene conversion frequencies in ARG4. In strains carrying a rad50S mutation, which blocks meiotic recombination, the extensive single-stranded tails do not form, suggesting that their generation is an obligatory step in meiotic recombination. Using the rad50S mutant, we have mapped the site of the ARG4 break to a small region within the genetically defined recombination initiation site. These results strongly support the double-strand break model of meiotic recombination.
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The interaction between immunoglobulin G (IgG) and ceftriaxone was studied. Using an ultrafiltration method, we performed dose ranging studies at a ceftriaxone concentration range of 1 to 720 micrograms/ml in the presence of various concentrations of human IgG, human serum albumin (HSA), and combinations of IgG and HSA at pH 7.4 and 37 degrees C. The results showed that ceftriaxone binding to IgG was nonlinear and was consistent with the presence of two binding sites that possess different binding capacities and affinities. Except for increased peak percent binding as the IgG concentration increased, the binding characteristics did not change with IgG concentration. Binding to HSA was consistent, with the presence of only one high-affinity binding site. A mathematical model based on the observed data was constructed; this model was used to predict protein binding at various concentrations of drug, IgG, HSA, or combinations of IgG and HSA in buffer and in plasma medium. Correlations between the observed versus the predicted values were excellent in both media. Simulations with the model indicated that patients with hypergammaglobulinemia have an increased potential of being exposed to prolonged subinhibitory concentrations of ceftriaxone if the drug is given once every 24 h.
We have used nonessential circular minichromosomes to monitor sister chromatid exchange during yeast meiosis. Genetic analysis shows that a 64-kb circular minichromosome undergoes sister chromatid exchange during 40% of meioses. This frequency is not reduced by the presence of a homologous linear minichromosome. Furthermore, sister chromatid exchange can be stimulated by the presence of a 12-kb ARG4 DNA fragment, which contains initiation sites for meiotic gene conversion. Using physical analysis, we have directly identified a product of sister chromatid exchange: a head-to-tail dimer form of a circular minichromosome. This dimer form is absent in a rad50S mutant strain, which is deficient in processing of the ends of meiosis-specific double-stranded breaks into single-stranded DNA tails. Our studies suggest that meiotic sister chromatid exchange is stimulated by the same mechanism as meiotic homolog exchange.
The early events of liver allograft rejection in untreated rats were studied in the DA to BN rejection strain combination and compared with DA and BN liver isograft recipients. In the liver allografts, T-cell infiltration first occurred at 2 days after transplantation and localized to the portal triads and subjacent to the terminal hepatic venules (THV), regions rich in intensely Ia + spindle and dendritic-shaped interstitial cells. Double staining showed distinct 'clustering' between donor Ia-positive dendritic-shaped cells and W3/25+ infiltrating lymphocytes, or to a lesser extent, OX8+ cells. The infiltrating mononuclear cells underwent blastogenesis and proliferated in both the triads and THV regions at 3 and 4 days. Donor Ia-positive cells were also noted in the W3/25+ periarterial lymphatic sheath and marginal zone of the recipient spleen 1 day after transplantation. The number of these cells in the spleen peaked at 3 to 4 days, but were no longer detectable by 10 to 12 days. Mitotic activity became evident in these same regions by days 3 and 4. Paracortical blastogenesis (day 2) and proliferation (days 3 and 4) were also noted in the regional lymph nodes of liver allograft recipients, but no donor Ia+ cells were found in the mesenteric nodes or thymus of the allograft recipients. These results demonstrate that sensitization of the recipient lymphoid tissue to liver allografts can occur both peripherally (intragraft) and centrally (spleen and lymph nodes). Passenger leukocytes (donor dendritic cells) are likely the primary stimulators of the rejection reaction. Still, it is probable that other pathways of sensitization exist.
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Reversed-phase high-performance liquid chromatographic assays have been developed to quantitate simultaneously fenoprofen and its major metabolites as well as to distinguish between their R- and S- enantiomers following a single oral dose of 600 mg racemic fenoprofen to healthy volunteers. The compounds are extracted from plasma (after precipitation of plasma protein) or assayed directly in diluted urine samples employing a gradient solution on a C18 column and ultraviolet detection. Two internal standards, ketoprofen and flunoxaprofen, are used to allow measurement of very low (0.05 microgram/ml) and high (70 microgram/ml) concentrations in each sample. R- and S-fenoprofen glucuronides can be separated directly; the 4'-hydroxyfenoprofen conjugates are measured via an indirect method by comparing the concentration of 4'-hydroxyfenoprofen before and after hydrolysis. The R- and S-enantiomers of both parent and 4'-hydroxy metabolite are derivatized with L-leucinamide via an ethyl chloroformate intermediate and subsequently analyzed on a C18 column. Concentrations of metabolites found in plasma were low when compared to parent drug. The S/R ratio of fenoprofen in plasma always exceeds 1 and increases with time after dosage while the S/R ratio of its 4'-hydroxy metabolite remains almost unchanged at 1.1. R-Fenoprofen glucuronide disappears rapidly from plasma as compared to its S-antipode; a less pronounced difference is noted between R- and S-4'-hydroxyfenoprofen conjugates. Fenoprofen is almost completely excreted as its S-acyl glucuronides; the renal clearance of unchanged drug is very low.