Kerr effect of charged dipolar macromolecules without condensed counterions in conducting solution.

The theoretical treatment of the Kerr constant of rigid, dipolar, conducting ellipsoidal macromolecules of O'Konski and Krause (1970. J. Phys. Chem. 74:3243) has been extended to very low ionic strength solutions for charged macromolecules. The O'Konski and Krause theoretical treatment postulated a surface conductivity directly on the surface of each macromolecule. For charged macromolecules, this surface conductivity was generally assumed to be caused by movement of condensed counterions on the macromolecules. In the present work, it has been assumed that, at very low ionic strength, the average counterion is at the Debye characteristic distance from the surface of each charged macromolecule and contributes to surface conductivity at that distance, with no additional surface conductivity on the true surface of the macromolecule. Essentially, these considerations change the calculated interaction energy of the macromolecule with an externally applied electric field via a change in both the internal field components and in the reaction field of the macromolecular dipole. The new interaction energy is used to calculate the orientation distribution function of the macromolecules in solution and this distribution function can, in principle, be used to calculate the steady state electric linear or circular dichroism, electric light scattering, anisotropy of conductivity, etc., using the appropriate theoretical treatment for each of these quantities.     

Chromosome analyses of children after ecological lead exposure

In the present work chromosome analysis was performed in a group of 30 children living in a town with a lead plant. Due to the emission of the smelter the individual lead uptake through food, drinking water and inhalation was increased. They were selected out of 1600 children whose blood lead level, delta-aminolevulinic acid dehydratase activity in the erythrocytes and erythrocyte porphyrine level was measured. In the investigated group of children the values of these parameters showed to be indicative for a significant lead exposure. A total of 10,000 cells was scored after 48 h culture time. Despite a significantly increased lead load as compared with two groups of 10 children from a suburb and the isle of Helgoland there was neither evidence for a higher number of cells with structural chromosome aberrations, nor for an increased aberration yield.     

Mechanism of action of antipruritic drugs.

Astemizole and terfenadine, two potent non-sedative H1 antihistamines, had no effect on itch measured objectively as nocturnal scratching and subjectively on a 10 cm line. Trimeprazine, however, a more sedative but less potent H1 antihistamine, was antipruritic, as was nitrazepam, a sedative benzodiazepine. We concluded (a) that antipruritic drugs act centrally by a property related to sedation; (b) H1 receptor antagonists have a peripheral antipruritic action only when itch is due to histamine release, as in the wealing disorders. Thus the new nonsedative H1 antihistamines have no place in the treatment of itch from other causes.     

Inhibition of soluble guanylate cyclase activity by citrate

Soluble guanylate cyclase activity from guinea pig heart is inhibited by increasing concentrations of sodium citrate. The Ki value was found to be 2.83 +/- 0.05 mM in the presence of 3 mM Mn2+ and 0.6 mM GTP. Citrate acts by lowering Vmax and increasing the apparent values of Km for GTP and K0.5 for Mn2+ and Mg2+. The soluble guanylate cyclase, activated by sodium nitroprusside, was also inhibited by citrate. This inhibitory action of citrate was not restricted to soluble guanylate cyclase activity of the heart and has been demonstrated also in the supernatant of lung, liver, diencephalon and in the homogenate of blood platelets. Since citrate is known to be an important intermediate of metabolism, its intracellular concentration may be also of relevance for guanylate cyclase activity.     

Evolutionary changes in non-histone chromosomal proteins within the Drosophila melanogaster group revealed by monoclonal antibodies

Monoclonal antibodies directed against nonhistone chromosomal proteins of D. melanogaster were tested for crossreactivity with the homologous antigens of various Drosophila species. — By indirect immunofluorescence it could be shown that three antibodies react only with polytene chromosomes of species of the D. melanogaster subgroup, and only much less with chromosomes of other species of Drosophila. — With chromosomes of various other species of the Sophophora or Drosophila radiations only a reaction at background level could be observed. — The results suggest that the three antibodies react with different antigenic determinants of a single protein whose conformation changed rather fast during evolution of the Drosophilidae.     

Studies on facial temperature rise and involvement of serotonin in the respiratory stimulation by CRH.

Following an intravenous injection of 100 micrograms hCRH a facial flushing can frequently be observed along with respiratory stimulation. Both effects can be mediated by a common transmitter. Serotonin is well known to produce facial flush as well as to modulate respiration. In order to clarify is serotonin is a common mediator for facial flush and respiratory stimulation after i.v. application of hCRH, we studied the time course of facial skin temperatures and respiratory stimulation after intravenous injection of 100 micrograms hCRH in 10 healthy subjects. Furthermore, we measured respiratory stimulation after i.v. administration of 100 micrograms hCRH in 10 healthy subjects pretreated with the serotonin antagonist cyproheptadine. Facial skin temperatures reached maximum levels 9 min after CRH administration and remained raised for more than 60 min. Respiratory stimulation occurred within the first minute after CRH administration and reached a maximum during the second minute, but could no longer be observed after 10 min. Serum serotonin levels did not change after CRH stimulation in doses up to 3 micrograms/kg body weight), and cyproheptadine did not abolish the respiratory stimulation effect of hCRH in a dosage sufficient to suppress CRH.-induced cortisol secretion.     

Retinol-induced modification of the extracellular matrix of endothelial cells: Its role in growth control

Summary The growth of the endothelial cell (EC) is tightly regulated throughout the body. Many factors have been implicated in modulating EC growth including diffusible compounds, cell-to-cell interactions, and the extracellular matrix (ECM). Retinol, or vitamin A alcohol, has recently been shown to inhibit the growth of bovine capillary ECs, in vitro. Retinoids are known to modify ECM in other cell systems, and pure ECM components have been shown to effect EC growth rates. We, therefore, examined the role of the matrix in the retinol-induced inhibition of ECs. Cell-free matrices from control and vitamin A-treated ECs were prepared by removing cells with EGTA treatment after 7 d of culture. Matrix proteins were analyzed by solubilizing the matrices in 5M quanidine-HCl and performing Western blot analysis using specific antibodies to matrix proteins. In isolating the ECM, we observed that retinol-treated cultures of ECs were resistant to EGTA removal; retinol-treated ECs required twice the exposure time to EGTA to detach from their matrix than did controls cells. Western blot analysis of matrix proteins derived from control and retinol-treated EC cultures demonstrated a 1.6-fold increase in lamininβ chains and a 2.5-fold increase in fibronectin in the ECM of retinol-treated EC compared to control cell matrix. Functional properties of these matrices were assessed by plating control and Day 6 retinol-treated ECs onto the matrices and measuring attachment and growth by determining cell numbers at 24, 72, and 144 h. These studies revealed that control cells attached in greatest numbers to a control matrix whereas retinol-treated ECs preferentially attached to a matrix derived from retinol-treated cells. Furthermore, control ECs which grew rapidly on a control matrix were growth inhibited on a retinol-derived matrix. These data indicate that vitamin A treatment of ECs effects both their phenotype and influences the composition and the functional properties of their underlying ECM. These studies also demonstrate that alterations of the matrix are at least in part responsible for the growth inhibition of EC by retinol.     

Mycoplasma pneumoniae cytadherence phase-variable protein HMW3 is a component of the attachment organelle.

The subcellular location of the phase-variable cytadherence-accessory protein HMW3 in Mycoplasma pneumoniae has been examined by biochemical and immunoelectron microscopic techniques. Analysis by Western blot (immunoblot) with HMW3-specific antiserum established the presence of this protein within the M. pneumoniae Triton X-100-insoluble fraction or triton shell. Immunogold labeling of Triton-extracted mycoplasmas with affinity-purified antibodies localized HMW3 to the terminal knob on the rodlike extensions of the triton shell, a location that would correspond to the adherence organelle in whole mycoplasmas. Treatment of triton shells with KI resulted in the selective removal of the adherence-accessory proteins HMW1 to HMW4. Analysis of these triton shells by transmission electron microscopy revealed dramatic ultrastructural changes in the filamentous network and core structure. Immunogold labeling of KI-extracted shells reflected the removal of HMW3 from the disrupted tip structure. An examination of ultrathin sections of wild-type cells by transmission electron microscopy following labeling with HMW3-specific antibodies provided further evidence for the nonrandom distribution of HMW3 and its localization to the terminal portion of filamentous cell extensions. Most colloidal gold molecules were associated with the cell interior, but limited peripheral labeling of the terminal region was also observed. Postfixation antibody labeling of whole cells suggested limited exposure of HMW3 on the mycoplasma surface at the tip structure. However, prefixation antibody labeling failed to indicate surface exposure, raising some uncertainty regarding the relationship of HMW3 with the mycoplasma membrane.