The rabbit brachial plexus as an experimental model--anatomy and surgical approach.

The aim of our study was to analyze the anatomy and surgical approach of the rabbit brachial plexus. The research included 18 rabbits. The rabbit seems to be a good experimental model for spinal nerves injury, especially for the C5 and C6 segments. The anatomical structure of the rabbit's brachial plexus is similar to the human brachial plexus. The structure of the rabbit C5 and C6 segments is analogous to the human structure. The spinal nerves of the C5 and C6 segments in the rabbit are wide and long enough for microsurgical procedures.

Theory of tunneling spectroscopy in a Mn12 single-electron transistor by density-functional theory methods.

We consider tunneling transport through a Mn12 molecular magnet using spin density functional theory. A tractable methodology for constructing many-body wave functions from Kohn-Sham orbitals allows for the determination of spin-dependent matrix elements for use in transport calculations. The tunneling conductance at finite bias is characterized by peaks representing transitions between spin multiplets, separated by an energy on the order of the magnetic anisotropy. The energy splitting of the spin multiplets and the spatial part of their many-body wave functions, describing the orbital degrees of freedom of the excess charge, strongly affect the electronic transport, and can lead to negative differential conductance.

Hyperammonemia and hepatic encephalopathy stimulate rat cerebral synaptic mitochondrial glutamate dehydrogenase activity specifically in the direction of glutamate oxidation.

The effects of hepatic encephalopathy (HE) due to thioacetamide (TAA)-induced liver failure and hyperammonemia (HA) produced by repeated i.p. administration of ammonium acetate on the activity of glutamate dehydrogenase (GlDH) in the direction of glutamate (Glu) synthesis from--(GlDH-NADH) or its oxidation to alpha-ketoglutarate (alpha-KG) (GlDH-NAD), respectively, were examined in non-synaptic and synaptic mitochondria from rat cerebral hemispheres. In non-synaptic mitochondria, HE and HA stimulated the GlDH-NADH activity by, respectively, 33% and 49%, but neither condition affected the GlDH-NAD activity. In synaptic mitochondria, HE and HA decreased the GlDH-NADH activity by, respectively, 31% and 28%, but stimulated the GlDH-NAD activity by as much as 90% (HE) and 100% (HA). Kinetic assays revealed that HA increased the Vmax of the synaptic mitochondrial GLDH-NAD by 105%, without affecting the Km for Glu. The stimulation of GlDH-NAD favors the oxidation of synaptic Glu to alpha-KG, and may represent an adaptive response serving to counteract hyperammonemia-induced decrease of cerebral alpha-KG production in other metabolic pathways.

Electron ionization study of ammonia micro-clusters

An electron impact ion source on a double focusing sector field mass spectrometer was used to investigate ammonia micro-clusters produced by the adiabatic free jet expansion of ammonia gas. The appearance energies for [NH(3)](n)(+), n

Effects of acute hepatic encephalopathy and in vitro treatment with ammonia on glutamate oxidation in bulk-isolated astrocytes and mitochondria of the rat brain.

The metabolism of [1-14C] glutamate to 14CO2 and the glutamate dehydrogenase (GLDH) activity towards alpha-ketoglutarate (alpha-KG) formation were measured in bulk isolated astrocytes derived from control rats and rats with acute hepatic encephalopathy (HE) induced with thioacetamide. In addition, the effects of in vitro treatment of control and HE astrocytes and non-synaptic mitochondria with toxic (3mM) NH4Cl concentration were followed. [1-14C] glutamate oxidation measured as a whole was identical in control and HE astrocytes and was inhibited by ammonia to the same degree in either fraction. In the presence of a glutamate transamination inhibitor--3mM aminooxyacetic acid (AOA), when only the GLDH-mediated part (25% of total) of the glutamate oxidation remained active, the inhibitory effect of ammonia treatment was much more pronounced in HE astrocytes than in control astrocytes. The ability of non-synaptic mitochondria to utilize glutamate to CO2 was not changed in presence of 3mM NH4Cl, whereas a substantial decrease of CO2 production (about 80%) in both the control and HE preparations was observed in the presence of 3mM AOA. GLDH activity was not at all affected by either of the experimental conditions, both in astrocytes and purified non-synaptic mitochondria. Thus, the inhibition of glutamate oxidation in astrocytes by ammonia and the compounded inhibitory effect of HE, ammonia and AOA appeared to be located beyond the glutamate dehydrogenation step within the tricarboxylic acid cycle.

[Synthesis and action of 1-n-hexyl-2-phenyl-3-(n-alkoxymethyl)- and 1-n-hexyl-2-phenyl-3-(6-n-alkylthiomethyl)imidazolium chlorides]. / Synthese und Wirkung von 1-n-Hexyl-2-phenyl-3-(n-alkoxymethyl)-und 1-n-Hexyl-2-phenyl-3-(n-alkylthiomethyl)imidazoliumchloriden.

The synthesis of quaternary imidazolium chlorides was performed by reaction of 1-n-hexyl-2-phenyl-imidazole with chloromethylalkyl ether or chlormethylalkyl sulfide. The antibacterial properties of the compounds obtained was tested on 13 strains of bacteria and fungi. Chlorides with octyl- and decylthiomethyl moiety indicated the best antibacterial activity.

[Effectiveness of new quarternary ammonium chloride compounds against selected bacteria and fungi. XXI. Synthesis of alkoxymethyl-3,4-dimethyl- pyridine and 1-ethyloxymethyl-3-alkylthiomethylimidazole chlorides]. / Badania nad skutecznoscia dzialania nowych czwartorzedowych chlorków amoniowych wobec wybranych szczepów bakterii i grzybów. XXI. Synteza chlorków alkoksymetylo-3,4-dimetylopirydyniowych i chlorków 1-etyloksymetylo-3-alkilotiometyloimidazoliowych.

Syntheses and antibacterial properties of alkoxymethyl-3,4-dimethylpyridinium chlorides and 1-ethyloxymethyl-3-alkylthiomethylimidazolium chlorides are described. Alkoxymetgyl-3,4-dimethylpyridinium chlorides were synthetized by reacting 3,4-dimethylpyridine with chloromethyl alkyl ethers, while 1-ethyloxymethyl-3-alkylthiomethylimidazolium chlorides were obtained in reactions of 1-ethyloxymethylimidazol with chloromethyl alkyl sulfides. Antibacterial properties of the obtained compounds were tested on 13 strains of bacteria and fungi. Strong bacteriostatic activity was found to be displayed by iminium chlorides with octyloxymethyl, decyloxymethyl, octylthiomethyl and decylthiomethyl groups.

Role of the support material on laser desorption/ionization mass spectra.

We report the results of experimental studies on the effects of sample supports in laser desorption/ionization mass spectrometry (LDI-MS). LDI time-of-flight (TOF) mass spectra obtained for C(60) and insulin samples deposited onto standard stainless steel substrate and/or onto some non-metallic materials (glass, scotch tape, floppy disc foil, Teflon foil, photocopy film), all recorded under identical, typical experimental conditions, have been compared with regard to their intensity and quality. The LDI investigations show that compared with stainless steel, glass and floppy disc foil sample supports boost (2-3.5 times) ion yields for C(60)(+) and C(60)(-) ions, respectively. The stainless steel and scotch tape sample supports are the best for the mass resolution of positive ions and the formation of (C(60))(n)(-) (n

Tunneling anisotropic magnetoresistance in Co/AlOx/Au tunnel junctions.

We observe spin-valve-like effects in nanoscaled thermally evaporated Co/AlOx/Au tunnel junctions. The tunneling magnetoresistance is anisotropic and depends on the relative orientation of the magnetization direction of the Co electrode with respect to the current direction. We attribute this effect to a two-step magnetization reversal and an anisotropic density of states resulting from spin-orbit interaction. The results of this study points to future applications of novel spintronics devices involving only one ferromagnetic layer.

Probing spin accumulation in Ni/Au/Ni single-electron transistors with efficient spin injection and detection electrodes.

We have investigated spin accumulation in Ni/Au/Ni single-electron transistors assembled by atomic force microscopy. The fabrication technique is unique in that unconventional hybrid devices can be realized with unprecedented control, including real-time tunable tunnel resistances. A grid of Au disks, 30 nm in diameter and 30 nm thick, is prepared on a SiO2 surface by conventional e-beam writing. Subsequently, 30 nm thick ferromagnetic Ni source, drain, and side-gate electrodes are formed in similar process steps. The width and length of the source and drain electrodes were different to exhibit different coercive switching fields. Tunnel barriers of NiO are realized by sequential Ar and O2 plasma treatment. By use of an atomic force microscope with specially designed software, a single nonmagnetic Au nanodisk is positioned into the 25 nm gap between the source and drain electrodes. The resistance of the device is monitored in real time while the Au disk is manipulated step-by-step with angstrom-level precision. Transport measurements in magnetic field at 1.7 K reveal no clear spin accumulation in the device, which can be attributed to fast spin relaxation in the Au disk. From numerical simulations using the rate-equation approach of orthodox Coulomb blockade theory, we can put an upper bound of a few nanoseconds on the spin-relaxation time for electrons in the Au disk. To confirm the magnetic switching characteristics and spin injection efficiency of the Ni electrodes, we fabricated a test structure consisting of a Ni/NiO/Ni magnetic tunnel junction with asymmetric dimensions of the electrodes similar to those of the single-electron transistors. Magnetoresistance measurements on the test device exhibited clear signs of magnetic reversal and a maximum tunneling magnetoresistance of 10%, from which we deduced a spin polarization of about 22% in the Ni electrodes.

Electron-magnon coupling and nonlinear tunneling transport in magnetic nanoparticles.

We present a theory of single-electron tunneling transport through a ferromagnetic nanoparticle in which particle-hole excitations are coupled to spin collective modes. The model employed to describe the interaction between quasiparticles and collective excitations captures the salient features of a recent microscopic study. Our analysis of nonlinear quantum transport in the regime of weak coupling to the external electrodes is based on a rate-equation formalism for the nonequilibrium occupation probability of the nanoparticle many-body states. For strong electron-boson coupling, we find that the tunneling conductance as a function of bias voltage is characterized by a large and dense set of resonances. Their magnetic field dependence in the large-field regime is linear, with slopes of the same sign. Both features are in agreement with recent tunneling experiments.

Effect of impurities on the matrix-assisted laser desorption/ionization mass spectra of insulin.

The effect of impurity (sodium sulfate Na2SO4; copper sulfate CuSO4; potassium ferrocyanide K4Fe(CN)6; and triammonium citrate (NH4)3C6H5O7) concentration on the positive matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) spectra of insulin is described. 2,5-Dihydroxybenzoic acid was used as a desorption matrix. The estimated maximum concentrations of tested salts for which no insulin signal was observed were determined.

Synthesis and antibiotic activity of 1-cycloalkoxymethyl-4-dimethylaminopyridinium and 1-[(1-alkoxy)ethyl]-4-dimethylaminopyridinium chlorides.

DMAP reacts readily with chloromethylcycloalkyl ethers and alpha-chloroethyl alkyl ethers to give stable (1a-1e) and unstable (2a-2h) pyridinium chlorides. Reaction of these chlorides with NaOH produces the corresponding 4-pyridones. All the chlorides synthesized showed antibiotic activity. Particularly high activity against microbes representing cocci, rods, fungi, and bacilli was shown by 1-cyclododecyloxymethyl-4-dimethylaminopyridinium chloride 1d and 1-[(1-dodecyloxy)ethyl]-4-dimethylaminopyridinium chloride 2f.

[Actions of new iminium compounds on bacteria and fungi. 27. Synthesis of 1-n-decyl-2-phenyl-3-(n-alkylthiomethyl)- and 1-n-decyl-2-phenyl-3-(n-alkoxymethyl)imidazolium chlorides]. / Wirkung neuer Iminiumverbindungen gegen Bakterien und Pilze, 27. Synthese von 1-n-decyl-2-phenyl-3-(n-alkylthiomethyl)- und 1-n-decyl-2-phenyl-3-(n-alkoxymethyl)imidazoliumchloriden.

The imidazolium compounds 1-3 were prepared by quaternization of 1-decyl-2-phenylimidazole with the pertinent chloromethyl-n-alkyl ethers. 1-3 were tested for their antibacterial and antimycotic efficacies.

Changes in the cytoplasmic (lactate dehydrogenase) and plasma membrane (acetylcholinesterase) marker enzymes in the synaptic and nonsynaptic mitochondria derived from rats with moderate hyperammonemia.

The activities of the cytoplasmic and plasma membrane marker enzymes: lactate dehydrogenase (LDH) and acetylcholinesterase (AChE), respectively, were measured in the cerebral homogenates, in the synaptic and nonsynaptic mitochondrial fractions, and in the postmitochondrial supernatants derived from rats in which a 3-d, moderately hyperammonemic condition (no more than 120% increases in blood ammonia) was produced by repeated administration of ammonium acetate (simple hyperammonemia, SHA) or a hepatotoxin, thioacetamide (TAA) (hepatic encephalopathy, HE). As measured in the homogenate and postmitochondrial supernatants, neither of the enzyme activities was affected by SHA or HE. SHA and HE increased the synaptic mitochondrial LDH activity by respectively 53 and 24%, but reduced this enzyme activity in nonsynaptic mitochondria by 19%. Both conditions stimulated the synaptic and nonsynaptic mitochondrial AChE activity by 30-40%. By contrast, the only significant change produced in these fractions by in vitro treatment with a toxic (3 mM) concentration of ammonium chloride was a slight decrease of LDH activity in nonsynaptic mitochondria and postmitochondrial supernatants. It is concluded that moderate hyperammonemia modifies subsequent separation of both cerebral classes of mitochondria from the cytosolic and plasma membrane components. This modification is likely to reflect subtle hyperammonemia-related changes in the physicochemical properties of the two mitochondrial classes and/or other subcellular components.

The two catalytic components of the 2-oxoglutarate dehydrogenase complex in rat cerebral synaptic and nonsynaptic mitochondria: comparison of the response to in vitro treatment with ammonia, hyperammonemia, and hepatic encephalopathy.

The effects of in vitro treatment with ammonium chloride, hepatic encephalopathy (HE) due to thioacetamide (TAA) induced liver failure and chronic hyperammonemia produced by i.p. administration of ammonium acetate on the two components of the multienzyme 2-oxoglutarate dehydrogenase complex (OGDH): 2-oxoglutarate decarboxylase (E1) and lipoamide dehydrogenase (E3), were examined in synaptic and nonsynaptic mitochondria from rat brain. With regard to E1 the response to ammonium ions in vitro (3 mM NH4Cl) was observed in nonsynaptic mitochondria only and was manifested by a 21% decrease of Vmax and a 35% decrease of Km for 2-oxoglutarate (2-OG). By contrast, both in vivo conditions primarily affected the synaptic mitochondrial E1: TAA-induced HE produced an 84% increase of Vmax and a 38% increase of Km for 2-OG. Hyperammonemia elevated Vmax of E1 by 110% and Km for 2-OG by 30%. HE produced no effect at all in nonsynaptic mitochondria while hyperammonemia produced a 35% increase of Vmax and a 30% increase of Km for 2-OG of E1. Both in vivo conditions produced a 20% increase of E3 activity in synaptic mitochondria, but no effect at all in nonsynaptic mitochondria. The preferential sensitivity of E1 to ammonium chloride in vitro in nonsynaptic mitochondria and hyperammonemic conditions in vivo in synaptic mitochondria may play a crucial role in the compartmentation of OGDH responses under analogous conditions. These results confirm the intrinsic differences between the OGDH properties in the synaptic and nonsynaptic brain compartments.