Optical Thickness of the Galactic Absorption Layer and Its Ratio of Total to Selective Absorption

As is Well Known, the surface brightness within the galaxies decreases strongly with increasing distance from the center. Therefore, if the diameters of the galaxies are defined by the isophote of a distinct apparent surface brightness, these diameters become smaller and smaller with increasing galactic absorption. The diameters are defined in reference 1 in this manner (by the isophote 26ṃ15/sec2); therefore, the mean surface brightnesses derived in that reference correspond more and more to the inner, brighter parts of the galaxies as the absorption increases. Consequently, in the derivation of the half optical thickness a of the galactic absorption layer from the variation of the mean surface brightnesses S of 113 spiral galaxies with galactic latitude β, the assumption in reference 1, dS/d(csc β) = a, is not correct but has to be replaced by the more complicated formula</jats:p

High-Precision Solar Radiation Data for λλ3300–12500Å

Very precise data on the solar radiation has been obtained by merging: (1) the absolute integrals of the disk-center intensity for 20Å-wide spectral bands, observed in the 1960's by Labs and Neckel (1962, 1963, 1967); (2) the ratios of the mean-to-central intensity following from observations of the center-to-limb variation of (a) all 20Å bands below 6600Å (Neckel and Labs 1984), and (b) the intensities at selected continuum wavelengths (Pierce and Slaughter 1977a, b); and (3) the high-resolution Fourier transform spectra (FTS) obtained by J. Brault at Kitt Peak for the center of the disk and for the irradiance.</jats:p

Relevance of Soft-Tissue Penetration by Levofloxacin for Target Site Bacterial Killing in Patients with Sepsis

Antimicrobial therapy of soft tissue infections in patients with sepsis sometimes lacks efficiency, despite the documented susceptibility of the causative pathogen to the administered antibiotic. In this context, impaired equilibration between the antibiotic concentrations in plasma and those in tissues in critically ill patients has been discussed. To characterize the impact of tissue penetration of anti-infective agents on antimicrobial killing, we used microdialysis to measure the concentration-versus-time profiles of levofloxacin in the interstitial space fluid of skeletal muscle in patients with sepsis. Subsequently, we applied an established dynamic in vivo pharmacokinetic-in vitro pharmacodynamic approach to simulate bacterial killing at the site of infection. The population mean areas under the concentration-time curves (AUCs) for levofloxacin showed that levofloxacin excellently penetrates soft tissues, as indicated by the ratio of the AUC from time zero to 8 h (AUC(0-8)) for muscle tissue (AUC(0-8 muscle)) to the AUC(0-8) for free drug in plasma (AUC(0-8 plasma free)) (AUC(0-8 muscle)/AUC(0-8 plasma free) ratio) of 0.85. The individual values of tissue penetration and maximum concentration (C(max)) in muscle tissue were highly variable. No difference in bacterial killing of a select Staphylococcus aureus strain for which the MIC was 0.5 μg/ml was found between individuals after exposure to dynamically changing concentrations of levofloxacin in plasma and tissue in vitro. In contrast, the decrease in the bacterial counts of Pseudomonas aeruginosa (MIC = 2 μg/ml) varied extensively when the bacteria were exposed to levofloxacin at the concentrations determined from the individual concentration-versus-time profiles obtained in skeletal muscle. The extent of bacterial killing could be predicted by calculating individual C(max)/MIC and AUC(0-8 muscle)/AUC(0-8 plasma free) ratios (R = 0.96 and 0.93, respectively). We have therefore shown in the present study that individual differences in the tissue penetration of levofloxacin may markedly affect target site killing of bacteria for which MICs are close to 2 μg/ml