Evaluation of mycobacillin and versicolin as agricultural fungicides. II. Stability in soil.
(9/3424)
The effect of paddy soils on mycobacillin and versicolin was investigated. Soil inactivated mycobacillin as determined by spectral analysis and microbiological assay. Soil can inactive mycobacillin only at or above the threshold concentration (125 approximately 130 mug per 10 mg of soil), the excess being unreacted. No new peak appears in the ultraviolet spectrum (240 approximately 300 nm) while mycobacillin is inactivated. Soil is without any effect on versicolin. (+info)
Analysis of the steps involved in Dengue virus entry into host cells.
(10/3424)
The initial steps of dengue viral entry have been divided into adsorption and penetration using acid glycine treatment to inactivate extracellular virus after attachment to baby hamster kidney (BHK) cells but prior to penetration. First, we showed that virus infection was accomplished within 2 h after adsorption. Second, the assay was used to examine the properties of dengue envelope E protein-specific monoclonal antibodies (MAbs), lectins, and heparin. We found that three MAbs, 17-2, 46-9, and 51-3, may neutralize dengue 2 virus (DEN-2) through inhibition of not only viral attachment but also of penetration. However, one MAb, 56-3.1, interfered specifically with attachment. Therefore, the functional domains of E protein involved in attachment and penetration may be different. Moreover, studies with lectins indicated that carbohydrates, especially alpha-mannose residues, present on the virion glycoproteins may contribute to binding and penetration of the virus into BHK and mosquito C6/36 cells. Finally, virus infectivity was inhibited by heparin through its blocking effects at both virus attachment and penetration. This suggests that cell surface heparan sulfate functions in both viral attachment and penetration of DEN-2 virus. In conclusion, our results further elucidated some aspects of the dengue virus entry process. (+info)
Kinetic evidence for the formation of a Michaelis-Menten-like complex between horseradish peroxidase compound II and di-(N-acetyl-L-tyrosine).
(11/3424)
The formation of a reversible adsorption complex between a dimer of N-acetyl-L-tyrosine [di-(N-acetyl-L-tyrosine), (NAT)2] and horseradish peroxidase (HRP) compound II (CII) was demonstrated using a kinetic approach. A specific KIIm value (0.58 mM) was deduced for this step from stopped-flow measurements. The dimerization of the dipeptide Gly-Tyr was analysed at the steady state and compared with (NAT)2 dimerization [(NAT)2-->(NAT)4]. A saturation of the enzyme was observed for both substrates within their range of solubility. In each case the rate of dimerization reflected the rate-limiting step of compound II reduction to the native HRP (E) (kappcat/Kappm approximately kII-->E). The kappcat values for (Gly-Tyr)2 and (NAT)4 formation were 254 s-1 and 3.6 s-1 respectively. The KappM value of Gly-Tyr was 24 mM. It was observed that the value (0.7 mM) for (NAT)2 was close both to its specific KIIm value for the second step of reduction (CII-->E) and to its thermodynamic dissociation constant (Kd=0.7 mM) with the resting form of the enzyme. As (NAT)2 was a tighter ligand but a poorer substrate than Gly-Tyr, a steady-state kinetic study was performed in the presence of both substrates. A kinetic model which includes an enzyme-substrate adsorption prior to each of the two steps of reduction was derived. This one agreed reasonably well with the experimental data. (+info)
Virus passage through track-etch membranes modified by salinity and a nonionic surfactant.
(12/3424)
Why do viruses sometimes not pass through larger pores in track-etch filters? Increasing the salinity (0.8 to 160 mM Na+) decreased phiX174 and PRD1 passage through track-etch polycarbonate membranes (sodium dodecyl sulfate coated but not polyvinylpyrrolidone coated) and PRD1 passage through polyester membranes. Undiminished passage when 0.1% Tween 80 was added implied that nonionic virus adsorption occurred and indicated that high levels of salinity decreased virus passage by decreasing electrostatic repulsion that prevented adsorption. (+info)
Dextran restores albumin-inhibited surface activity of pulmonary surfactant extract.
(13/3424)
We examined the effect of dextran (molecular weight 71,000) in counteracting the surfactant inhibitory action of plasma albumin. The surface adsorption time of 0.5 mg/ml modified natural surfactant (MNS; porcine lung extract consisting of phospholipids and hydrophobic surfactant proteins) with 7.5 mg/ml albumin decreased from 681 to 143 s by addition of dextran at a concentration of 10 mg/ml (P < 0.01). The minimum surface tension of 2.0 mg/ml MNS with 30 mg/ml albumin decreased from over 21 mN/m to below 3 mN/m when dextran was added at a concentration of 10 mg/ml (P < 0.01). Surfactant-deficient newborn rabbits given 10 ml/kg of a liquid containing 2.0 mg/ml MNS with 30 mg/ml albumin had a mean tidal volume 13 ml/kg (P < 0.05). Although the underlying mechanism remains to be elucidated, we conclude that dextran restores the albumin-inhibited surface activity of MNS. (+info)
Alterations in pulmonary surfactant after rapid arousal from torpor in the marsupial Sminthopsis crassicaudata.
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Torpor in the dunnart, Sminthopsis crassicaudata, alters surfactant lipid composition and surface activity. Here we investigated changes in surfactant composition and surface activity over 1 h after rapid arousal from torpor (15-30 degrees C at 1 degrees C/min). We measured total phospholipid (PL), disaturated PL (DSP), and cholesterol (Chol) content of surfactant lavage and surface activity (measured at both 15 and 37 degrees C in the captive bubble surfactometer). Immediately after arousal, Chol decreased (from 4.1 +/- 0.05 to 2.8 +/- 0.3 mg/g dry lung) and reached warm-active levels by 60 min after arousal. The Chol/DSP and Chol/PL ratios both decreased to warm-active levels 5 min after arousal because PL, DSP, and the DSP/PL ratio remained elevated over the 60 min after arousal. Minimal surface tension and film compressibility at 17 mN/m at 37 degrees C both decreased 5 min after arousal, correlating with rapid changes in surfactant Chol. Therefore, changes in lipids matched changes in surface activity during the postarousal period. (+info)
Longitudinal distribution of chlorine absorption in human airways: comparison of nasal and oral quiet breathing.
(15/3424)
The fraction of an inspired chlorine (Cl2) bolus absorbed during a single breath (Lambda) was measured as a function of bolus penetration (VP) into the respiratory system of five male and five female nonsmokers during both nasal and oral breathing at a quiet respiratory flow of 250 ml/s. The correspondence between VP and specific anatomic landmarks was found for each subject by a combination of acoustic reflection and nitrogen washout measurements. For both nasal and oral breathing, Lambda reached approximately 0. 95 at the distal end of the upper airways and reached 1.00 within the lower conducting airways. The values of a regional mass transfer parameter computed from the Lambda-VP data indicated that the resistance to Cl2 diffusion in the airway mucosa was negligible compared with the diffusion resistance in the respired gas. Changing the peak inhaled Cl2 concentration from 0.5 to 3.0 parts/million did not significantly affect the distribution of Cl2 absorption, suggesting that the underlying mass transport and chemical reaction processes were linear with respect to Cl2 concentration. (+info)
Nonnucleoside pyrrolopyrimidines with a unique mechanism of action against human cytomegalovirus.
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Based upon a prior study which evaluated a series of nonnucleoside pyrrolo[2,3-d]pyrimidines as inhibitors of human cytomegalovirus (HCMV), we have selected three active analogs for detailed study. In an HCMV plaque-reduction assay, compounds 828, 951, and 1028 had 50% inhibitory concentrations (IC(50)s) of 0.4 to 1.0 microM. Similar results were obtained when 828 and 951 were examined by HCMV enzyme-linked immunosorbent assay (IC(50)s = 1.9 and 0.4 microM, respectively) and when 828 was tested in a viral DNA-DNA hybridization assay (IC(50) = 1.3 microM). In yield-reduction assays with a low multiplicity of infection (MOI), all three compounds caused multiple log(10) reductions in virus titer, and the activities of these compounds were comparable to the activity of ganciclovir (GCV; IC(90) = 0.2 microM). In contrast to the reduction of viral titers by GCV, the reduction of viral titers by 828, 951, and 1028 decreased with increasing MOI. Cytotoxicity in human foreskin fibroblasts and KB cells ranged from 32 to >100 microM. In addition, 828 (the only compound tested) was less toxic against human bone marrow progenitor cells than GCV. Time-of-addition and time-of-removal studies established that the three pyrrolopyrimidines inhibited HCMV replication before GCV had an effect on viral DNA synthesis but after viral adsorption. Compound 828 was equally effective against GCV-sensitive and GCV-resistant HCMV clinical isolates. Combination studies with 828 and GCV showed that the effects of the two compounds on HCMV were additive but not synergistic. Taken together, the data indicate that these pyrrolopyrimidines target a viral protein that is required in an MOI-dependent manner and that is expressed early in the HCMV replication cycle. (+info)