Disruption of Asymmetric Lipid Bilayer Models Mimicking the Outer Membrane of Gram-Negative Bacteria by an Active Plasticin.

The outer membrane (OM) of Gram-negative bacteria is a complex and asymmetric bilayer that antimicrobial peptides must disrupt in order to provoke the cell lysis. The inner and external leaflets of the OM are mainly composed of phospholipids (PL), and lipopolysaccharide (LPS), respectively. Supported lipid bilayers are interesting model systems to mimic the lipid asymmetric scaffold of the OM and determine the quantitative and mechanistic effect of antimicrobial agents, using complementary physicochemical techniques. We report the formation of asymmetric PL/LPS bilayers using the Langmuir-Blodgett/Langmuir-Schaefer technique on two different surfaces (sapphire and mica) with synthetic phospholipids constituting the inner leaflet and bacteria-extracted mutant LPS making up the outer one. The combination of neutron reflectometry and atomic force microscopy techniques allowed the examination of the asymmetric scaffold structure along the normal to the interface and its surface morphology in buffer conditions. Our results allow discrimination of two structurally related peptides, one neutral and inactive, and the other cationic and active. The active cationic plasticin PTCDA1-KF disrupts the asymmetric OM at relevant concentrations through a carpeting scenario characterized by a dramatic removal of lipid molecules from the surface.

Structural analysis of FeO(1 1 1)/Ag(0 0 1): undulation of hexagonal oxide monolayers due to square lattice metal substrates.

Iron oxide monolayers are grown on Ag(0 0 1) via reactive molecular beam epitaxy (metal deposition in oxygen atmosphere). The monolayer shows FeO stoichiometry as concluded from x-ray photoemission spectra. Both low energy electron diffraction as well as scanning tunneling microscopy demonstrate that the FeO layer has a quasi-hexagonal (1 1 1) structure although deposited on a surface with square symmetry. Compared to bulk values, the FeO(1 1 1) monolayer is unidirectionally expanded by 3.4% in [Formula: see text] directions while bulk values are maintained in [Formula: see text] directions. In [Formula: see text] directions, this lattice mismatch between FeO(1 1 1) monolayer and Ag(0 0 1) causes a commensurate undulation of the FeO monolayer where 18 atomic rows of the FeO(1 1 1) monolayer match 17 atomic rows of the Ag(0 0 1) substrate. In [Formula: see text] directions, however, the FeO(1 1 1) monolayer has an incommensurate structure.

[Subacute leukoencephalopathy of the rhombencephalon after pituitary radiotherapy]. / Leucoencéphalopathie subaiguë du rhombencéphale après radiothérapie hypophysaire.

Two patients had early delayed leucoencephalopathy mainly confined to the brainstem after radiotherapy for pituitary tumours. To our knowledge, we report the first MRI description. The patients had somatotroph cell adenomas (associated with prolactin secretion, patient 2). Surgical removal of the adenomas were complete (patient 1) and partial (patient 2). Both underwent pituitary irradiation: patient 1, 55.8 Gy (31 x 1.8 Gy); patient 2, 54 Gy (27 x 2 Gy). Six weeks after completion of radiation, the patients had low vigilance, sleepiness, cerebellar symptoms, optic neuropathy (patient 1), CSF inflammatory reaction. T2-weighted MRI scans showed hypersignal in brainstem, cerebellar peduncles (both patients), temporal lobe white matter (patient 2). T1-weighted images showed hyposignals, pseudonecrotic and contrast-enhanced images in brainstem (patient 1). Both patients responded to intravenous then oral steroid treatment with a progressive and complete clinical recovery. Radiological abnormalities improved with clinical statement. Present characteristics support a demyelinating mechanism of early delayed cerebral radiation injuries.

Trigeminal artery and microemboli to the brain stem. Report of two cases.

The authors report two cases of transient ischemic attacks (TIA's) involving the brain stem. The TIA's were due to microemboli that originated from a carotid bifurcation atherosclerotic plaque and travelled through a persistent trigeminal artery.