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  • 1
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 84 (1998), S. 6871-6876 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We report on a novel experimental setup using a miniature integrating sphere fitted into a cryostat to measure spectrally resolved the absolute external photoluminescence quantum efficiency ηlum in the temperature range from 6 K to beyond room temperature. Direct access to ηlum is achieved by an uncomplicated method to calibrate the spatially integrated emission spectra absolutely. The fraction of light coupled out of the sphere into the detection system is in good approximation independent of the emitted wavelength and the emission characteristics of the investigated samples, due to their smallness compared with the total sphere area. This fact is proved by theoretical calculations for the sphere throughput and the irradiance within the sphere. To demonstrate the capabilities of this setup, we investigate in high quality ZnSe/ZnMgSSe 10× multiple quantum wells, the temperature dependence of the quantum efficiency, simultaneously for the quantum well and the barrier luminescence. Within a thermal activation model, three processes are found to contribute to the thermal quenching of ηlum of the quantum well luminescence. © 1998 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 114 (2001), S. 4669-4684 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: Combining molecular beam techniques and time-resolved infrared reflection absorption spectroscopy (TR-IRAS) we have studied the kinetics of the CO oxidation reaction on an alumina-supported Pd model catalyst. The Pd particles are deposited by metal evaporation under ultrahigh vacuum (UHV) conditions onto a well-ordered alumina film, prepared on a NiAl(110) single crystal. Particle size, density and structure of the Pd deposits have been characterized in previous studies. In the low temperature region, transient and steady-state experiments have been performed over a wide range of CO and oxygen fluxes by crossing two effusive molecular beams on the sample surface. We determine the steady-state CO2 production rate as a function of the CO fraction in the impinging gas flux. Simultaneously, the occupation of CO adsorption sites under steady-state conditions is monitored by in situ IR spectroscopy. The origin of different types of CO2 transients is discussed. In particular we focus on the transient CO2 production after switching off the CO beam. For the model catalyst investigated, detailed reaction rate measurements in combination with time-resolved IRAS show that the origin of the particular transient behavior of the supported model system is not due to the presence of specific adsorption sites on small particles, as has been proposed previously. Instead, we show that the transient behavior can be semiquantitatively simulated on the basis of a simple kinetic model considering a homogeneous surface, and accounting for the inhibition of the dissociative adsorption of O2 at high CO coverage. Moreover, it is discussed how the inherent heterogeneity of the supported particle system can additionally enhance the observed effect. © 2001 American Institute of Physics.
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  • 3
    Publication Date: 2015-02-13
    Keywords: Acute myocardial infarction
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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  • 4
    Publication Date: 2015-02-27
    Description: Rationale: Inflammation in the setting of acute myocardial infarction (MI) has been linked to risk stratification; however, the release kinetics of inflammatory biomarkers in patients with acute MI has been difficult to establish. Objective: The aim of this study was to determine the kinetics of changes in the levels of several biomarkers specifically linked to inflammation after transcoronary ablation of septal hypertrophy, a procedure that mimics acute MI. Methods and Results: We analyzed release kinetics of C-reactive protein, high-sensitivity C-reactive protein, interleukin-6, soluble CD40 ligand, and peripheral blood leukocyte subsets in patients (n=21) undergoing transcoronary ablation of septal hypertrophy. Blood samples were collected before transcoronary ablation of septal hypertrophy and at various times after transcoronary ablation of septal hypertrophy. Serum levels of C-reactive protein were increased at 24 hours (1.0 mg/dL [interquartile range [IQR], 0.7–1.75] versus 0.2 mg/dL [IQR, 0.1–1.05] at baseline [BL]; P 〈0.001), whereas high-sensitivity C-reactive protein increased as early as 8 hours (2.68 mg/L [IQR, 1.23–11.80] versus 2.17 mg/L [IQR, 1.15–5.06] at BL; P =0.002). Interleukin-6 was significantly increased at 45 minutes (2.59 pg/mL [IQR, 1.69–5.0] versus 1.5 pg/mL [IQR, 1.5–2.21] at BL; P =0.002), and soluble CD40 ligand was significantly decreased at 60 minutes (801.6 pg/mL [IQR, 675.0–1653.5] versus 1750.0 pg/mL [IQR, 1151.0–2783.0] at BL; P =0.016). Elevated counts of polymorphonuclear neutrophils were detectable at 15 minutes, with a significant increase at 2 hours (6415 cells/μL [IQR, 5288–7827] versus 4697 cells/μL [IQR, 2892–5620] at BL; P =0.004). Significant monocytosis was observed at 24 hours (729 cells/μL [IQR, 584–1344] versus 523 cells/μL [IQR, 369–701] at BL; P =0.015). Conclusions: Interleukin-6 and neutrophil granulocytes showed a continuous rise at all prespecified time points after induction of MI. Our results provide valuable additional evidence of the diagnostic value of inflammatory biomarkers in the setting of early acute MI.
    Keywords: Growth factors/cytokines, Ischemic biology - basic studies, Acute myocardial infarction
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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  • 5
    Publication Date: 2012-08-10
    Description: The RNA export adaptor protein Rec, encoded for by the human endogenous retrovirus HERV-K/HML-2 elements, binds to the Rec responsive element (RcRE) located in the 3' untranslated region of HERV-K/HML-2 transcripts. Binding allows the nucleocytoplasmic export of unspliced viral RNA, thereby overcoming host restriction. Chemical probing of the secondary structure of the RcRE corroborated the theory that the RcRE forms a complex folded structure with seven stem-loop regions. Laser-induced liquid beam ion desorption mass spectrometry revealed that Rec forms stable tetramers, which are further stabilized upon RNA binding. The RNA protein complex consists of three Rec tetramers, which bind to multiple sites on the RcRE—preferentially to purine-rich motifs—which represent several low-affinity binding sites. Mutated RcREs, with one to three purine-rich motifs deleted, were still bound and exported by Rec, indicating that the complex folded structure of the RcRE is important for Rec binding. This suggests a binding model where up to three Rec tetramers bind to the complex folded structure of the RcRE and the binding seems to be tightened by recognition of the purine-rich motifs.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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  • 6
    Publication Date: 2014-11-19
    Description: Drosophila C virus (DCV) is a positive-sense RNA virus belonging to the Dicistroviridae family. This natural pathogen of the model organism Drosophila melanogaster is commonly used to investigate antiviral host defense in flies, which involves both RNA interference and inducible responses. Although lethality is used routinely as a readout for the efficiency of the antiviral immune response in these studies, virus-induced pathologies in flies still are poorly understood. Here, we characterize the pathogenesis associated with systemic DCV infection. Comparison of the transcriptome of flies infected with DCV or two other positive-sense RNA viruses, Flock House virus and Sindbis virus, reveals that DCV infection, unlike those of the other two viruses, represses the expression of a large number of genes. Several of these genes are expressed specifically in the midgut and also are repressed by starvation. We show that systemic DCV infection triggers a nutritional stress in Drosophila which results from intestinal obstruction with the accumulation of peritrophic matrix at the entry of the midgut and the accumulation of the food ingested in the crop, a blind muscular food storage organ. The related virus cricket paralysis virus (CrPV), which efficiently grows in Drosophila , does not trigger this pathology. We show that DCV, but not CrPV, infects the smooth muscles surrounding the crop, causing extensive cytopathology and strongly reducing the rate of contractions. We conclude that the pathogenesis associated with systemic DCV infection results from the tropism of the virus for an important organ within the foregut of dipteran insects, the crop. IMPORTANCE DCV is one of the few identified natural viral pathogens affecting the model organism Drosophila melanogaster . As such, it is an important virus for the deciphering of host-virus interactions in insects. We characterize here the pathogenesis associated with DCV infection in flies and show that it results from the tropism of the virus for an essential but poorly characterized organ in the digestive tract, the crop. Our results may have relevance for other members of the Dicistroviridae , some of which are pathogenic to beneficial or pest insect species.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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  • 7
    Publication Date: 2015-01-01
    Description: Rationale: There is mounting evidence of a higher incidence of coronary heart disease in cytomegalovirus-seropositive individuals. Objective: The aim of this study was to investigate whether acute myocardial infarction triggers an inflammatory T-cell response that might lead to accelerated immunosenescence in cytomegalovirus-seropositive patients. Methods and Results: Thirty-four patients with acute myocardial infarction undergoing primary percutaneous coronary intervention were longitudinally studied within 3 months after reperfusion (Cohort A). In addition, 54 patients with acute myocardial infarction and chronic myocardial infarction were analyzed in a cross-sectional study (Cohort B). Cytomegalovirus-seropositive patients demonstrated a greater fall in the concentration of terminally differentiated CD8 effector memory T cells (T EMRA ) in peripheral blood during the first 30 minutes of reperfusion compared with cytomegalovirus-seronegative patients (–192 versus –63 cells/μL; P =0.008), correlating with the expression of programmed cell death-1 before primary percutaneous coronary intervention ( r =0.8; P =0.0002). A significant proportion of T EMRA cells remained depleted for ≥3 months in cytomegalovirus-seropositive patients. Using high-throughput 13-parameter flow cytometry and human leukocyte antigen class I cytomegalovirus-specific dextramers, we confirmed an acute and persistent depletion of terminally differentiated T EMRA and cytomegalovirus-specific CD8 + cells in cytomegalovirus-seropositive patients. Long-term reconstitution of the T EMRA pool in chronic cytomegalovirus-seropositive postmyocardial infarction patients was associated with signs of terminal differentiation including an increase in killer cell lectin-like receptor subfamily G member 1 and shorter telomere length in CD8 + T cells (2225 versus 3397 bp; P 〈0.001). Conclusions: Myocardial ischemia and reperfusion in cytomegalovirus-seropositive patients undergoing primary percutaneous coronary intervention leads to acute loss of antigen-specific, terminally differentiated CD8 T cells, possibly through programmed cell death-1–dependent programmed cell death. Our results suggest that acute myocardial infarction and reperfusion accelerate immunosenescence in cytomegalovirus-seropositive patients.
    Keywords: Pathophysiology, Acute myocardial infarction, Other Research
    Print ISSN: 0009-7330
    Electronic ISSN: 1524-4571
    Topics: Medicine
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  • 8
    Publication Date: 2016-02-27
    Description: Effective treatment of tuberculosis during pregnancy is essential for preventing maternal and fetal mortality, but little is known about the effects of pregnancy on the disposition of antituberculosis drugs. We explored the effects of pregnancy on the pharmacokinetics of rifampin, the key sterilizing drug in tuberculosis treatment, in Tshepiso, a prospective cohort study involving pregnant HIV-infected women with or without tuberculosis in Soweto, South Africa. Participants receiving standard first-line tuberculosis treatment underwent sparse sampling for rifampin at 37 weeks' gestation or delivery and then postpartum. Cord blood was collected when possible. A population pharmacokinetic model was developed to investigate the effects of pregnancy on rifampin pharmacokinetics. Among the 48 participants, median age and weight were 28 years and 67 kg, respectively. A one-compartment model with first-order elimination, transit compartment absorption, and allometric scaling described the data well. Pregnancy reduced rifampin clearance by 14%. The median (interquartile range) model-estimated rifampin area under the concentration-time curve over 24 h (AUC 0–24 ) during pregnancy or intrapartum was 40.8 h · mg/liter (27.1 to 54.2 h · mg/liter) compared to 37.4 h · mg/liter (26.8 to 50.3 h · mg/liter) postpartum. The maximum concentrations were similar during pregnancy and postpartum. Rifampin was detectable in 36% (8/22) of cord blood samples, and 88% (42/48) of the women had successful treatment outcomes. There was one case of perinatal tuberculosis. In conclusion, rifampin clearance is modestly reduced during the last trimester of pregnancy. Exposures are only slightly increased, so dose adjustment during pregnancy is not needed. Rifampin was detected in cord blood samples when delivery occurred soon after dosing. The consequences of exposure to this potent inducer of metabolizing enzymes among HIV-exposed infants are unclear.
    Print ISSN: 0066-4804
    Electronic ISSN: 1098-6596
    Topics: Biology , Medicine
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  • 9
    Publication Date: 2016-02-06
    Description: We developed a counterselectable deletion system for Thermus thermophilus HB27 based on cytosine deaminase (encoded by codA ) from Thermaerobacter marianensis DSM 12885 and the sensitivity of T. thermophilus HB27 to the antimetabolite 5-fluorocytosine (5-FC). The deletion vector comprises the pUC18 origin of replication, a thermostable kanamycin resistance marker functional in T. thermophilus HB27, and codA under the control of a constitutive putative trehalose promoter from T. thermophilus HB27. The functionality of the system was demonstrated by deletion of the bglT gene, encoding a β-glycosidase, and three carotenoid biosynthesis genes, CYP175A1 , crtY , and crtI , from the genome of T. thermophilus HB27.
    Print ISSN: 0099-2240
    Electronic ISSN: 1098-5336
    Topics: Biology
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  • 10
    Publication Date: 2016-05-13
    Description: Antiviral immunity in the model organism Drosophila melanogaster involves the broadly active intrinsic mechanism of RNA interference (RNAi) and virus-specific inducible responses. Here, using a panel of six viruses, we investigated the role of hemocytes and autophagy in the control of viral infections. Injection of latex beads to saturate phagocytosis, or genetic depletion of hemocytes, resulted in decreased survival and increased viral titers following infection with Cricket paralysis virus (CrPV), Flock House virus (FHV), and vesicular stomatitis virus (VSV) but had no impact on Drosophila C virus (DCV), Sindbis virus (SINV), and Invertebrate iridescent virus 6 (IIV6) infection. In the cases of CrPV and FHV, apoptosis was induced in infected cells, which were phagocytosed by hemocytes. In contrast, VSV did not trigger any significant apoptosis but we confirmed that the autophagy gene Atg7 was required for full virus resistance, suggesting that hemocytes use autophagy to recognize the virus. However, this recognition does not depend on the Toll-7 receptor. Autophagy had no impact on DCV, CrPV, SINV, or IIV6 infection and was required for replication of the sixth virus, FHV. Even in the case of VSV, the increases in titers were modest in Atg7 mutant flies, suggesting that autophagy does not play a major role in antiviral immunity in Drosophila . Altogether, our results indicate that, while autophagy plays a minor role, phagocytosis contributes to virus-specific immune responses in insects. IMPORTANCE Phagocytosis and autophagy are two cellular processes that involve lysosomal degradation and participate in Drosophila immunity. Using a panel of RNA and DNA viruses, we have addressed the contribution of phagocytosis and autophagy in the control of viral infections in this model organism. We show that, while autophagy plays a minor role, phagocytosis contributes to virus-specific immune responses in Drosophila . This work brings to the front a novel facet of antiviral host defense in insects, which may have relevance in the control of virus transmission by vector insects or in the resistance of beneficial insects to viral pathogens.
    Print ISSN: 0022-538X
    Electronic ISSN: 1098-5514
    Topics: Medicine
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