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Actions of glutamate and serotonin on their respective receptors in the dorsal facial area (DFA) of the medulla are known to regulate common carotid arterial (CCA) blood flow in cats. Less is known about acetylcholine action on its nicotinic receptor (nAChR) subtypes in the DFA for regulation of CCA blood flow and this aspect was investigated.Nicotinic and muscarinic agonists and antagonists were microinjected into the DFA through a three-barrel tubing in anesthetized cats.CCA blood flow was dose-dependently increased by nicotine (a non-selective nAChR agonist) and choline (a selective alpha7-nAChR agonist). These effects of nicotine were attenuated by alpha-bungarotoxin (an alpha7-nAChR antagonist), methyllycaconitine (an alpha7-nAChR antagonist), mecamylamine (a relatively selective alpha3beta4-nAChR antagonist) and dihydro-beta-erythroidine (a relatively selective alpha4beta2-nAChR antagonist). The choline-induced flow increase was attenuated by alpha-bungarotoxin and mecamylamine, but not by dihydro-beta-erythroidine. Muscarinic agonists (muscarine and methacholine) and antagonist (atropine) affected neither the basal nor the nicotine-induced increase in the CCA blood flow.Functional alpha7, alpha4beta2, and alpha3beta4 subunits of the nAChR appear to be present on the DFA neurons. Activations of these receptors increase the CCA blood flow. The present findings do not preclude the presence of other nAChRs subunits. Muscarinic receptors, if any, on the DFA are not involved in regulation of the CCA blood flow. Various subtypes of nAChRs in the DFA may mediate regulation of the CCA and cerebral blood flows.

This study examined the changes in the bacterial community during biodegradation of polycyclic aromatic hydrocarbon (PAH) substrate when N'-N' dimethylformamide (DMF) was added. The microbial populations that biodegrade the PAH substrate were assessed by Fluorescence in-situ hybridization (FISH) and changed from 49.45% Archaea and 49.15% Bacteria to 42.00% Archaea and 51.78% Bacteria when the PAH was supplemented with DMF. Nine microorganisms were classified as Gram-negative alpha-, beta- and gamma-Proteobacteria bacteria during biodegradation of PAH alone by the Biolog system. Incentive eleven microorganisms obtained from the PAH-DMF mixed substrate were found to be beta-, gamma-Proteobacteria bacteria, high G+C Gram-positive bacteria (HGC), low G+C Gram-positive bacteria (LGC) and there was even one Deinococcus-Thermus strain; this indicates greater biodiversity. The numbers in the Pseudomonad group were as high as 10(5)-10(6) CFU ml(-1), suggesting that this group plays an important role in PAH biodegradation. Community-Level Physiological Profiling (CLPP) and physiological characterization were different in the PAH biodegradation process with and without DMF. Utilization of the 95 carbon sources from the Biolog GN2 microtiter plate was greater during PAH biodegradation when PAH is present alone compared to that in the presence of DMF. The range of enzymatic activities during PAH biodegradation was lower in the presence of DMF. These results show that DMF should be used with caution when PAH is a substrate during laboratory or pilot biotreatability studies.

The exact mechanism underlying regional cerebral hypoperfusion in the early phase of Alzheimer's disease (AD) is not understood. We have shown in isolated porcine cerebral arteries that stimulation of sympathetic α7-nicotinic acetylcholine receptors (α7-nAChRs) causes release of nitric oxide in parasympathetic nitrergic nerves and vasodilation. We therefore examined if β-amyloid peptides (Aβs), which play a key role in pathogenesis of AD, blocked sympathetic α7-nAChRs leading to reduced neurogenic nitrergic dilation in isolated porcine basilar arteries, using in vitro tissue bath, calcium image, and patch clamping techniques. The results indicated that Aβ1–40, but not Aβ40–1, blocked relaxation of endothelium-denuded basilar arterial rings induced by nicotine (100μ;mol/L) and choline (1 mmol/L) without affecting that induced by sodium nitroprusside or isoproterenol. In cultured superior cervical ganglion (SCG) cells, Aβ1–40, but not Aβ40–1, blocked choline- and nicotine-induced calcium influx and inward currents. The Aβ blockade of the nitrergic vasodilation and inward currents, but not that of calcium influx, was prevented by acute pretreatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors mevastatin and lovastatin. These results suggest that Aβ1–40 blocks cerebral perivascular sympathetic α7-nAChRs, resulting in the attenuation of cerebral nitrergic neurogenic vasodilation. This effect of Aβ may be responsible in part for cerebral hypoperfusion occurred in the early phase of the AD, which may be prevented by statins most likely because of their effects independent of cholesterol lowering. Statins may offer an alternative strategy in the prevention and treatment of AD.

Thermal immobilization of copper contaminant in a copper-containing solid material collected from local copper smelting and foundry area is investigated in the present work. X-ray absorption spectroscopy (XAS) and X-ray diffraction (XRD) are employed for copper speciation. XAS results indicate that cupric hydroxide is the major copper species in the solid material dried at 105 degrees C. After being subjected to a 500 degrees C thermal process, cupric hydroxide still remains as the main copper species, but some Cu(II) is chemically reduced to Cu(I). More cupric hydroxide is progressively converted to Cu(I) as the sample was heated at 1100 degrees C than that heated at 500 degrees C. The sample heated at 500 degrees C is in its original powder form. However, thermal treatment at 1100 degrees C transforms the powder into a hardened granule-like form that is much bigger in size and difficult to be ground into powders. The sample is sintered with the sparingly soluble cuprous oxide and elemental copper being encapsulated inside. Toxicity characteristic leaching procedure (TCLP) results depict that amount of copper leached from the sample (containing 133,000 mg copper kg-1) heated at 1100 degrees C for 2 h is considerably minor, being 367 mg copper kg-1.

The recent status of the SPring‐8 Taiwan Contract Beamline BL12B2 is reported. The beamline was designed to provide multiple applications for materials and biological researches. It is equipped with four end stations, including an EXAFS station, a Huber 6‐circle diffractometer for X‐ray scattering, a curved image plate for the studies of powder diffraction, and a station for the protein crystallography. The beamline construction was completed in 2000 and it has been in full speed operation since September 2001. To enhance the focusing capacity, the beamline optics has been modified in 2002 and a gain of factor of 10 in photon flux was consequently obtained at protein crystallography station.

A Superconducting Wavelength Shifter (SWLS) insertion device with peak field of 6 Tesla has been installed in the Taiwan Light Source (TLS) storage ring to increase the critical energy of the radiation spectrum from 2 keV to 9 keV. We are constructing three hard X‐ray beamlines BL01A, BL01B and BL01C to utilize the photon source generated by this insertion device. The beamline BL01B is a DCM X‐ray beamline with a toroidal focusing mirror, which provides monochromatic photon beams with energies from 5 keV to 20 keV for X‐ray scattering experiments. At the sample position, the expected photon flux is about 7×1011 photon/sec/200mA with an average energy resolution (ΔE/E) of 1×10−3 and the focused beam size is about 1 mm × 0.4 mm. The beamline BL01C is a standard DCM X‐ray beamline with both collimating and focusing mirrors, which will deliver monochromatic photon beams with energy ranging from 6 keV to 33 keV for EXAFS and powder diffraction. At the sample position, the expected photon flux is 1×1011 photon/sec /200mA with an average energy resolution (ΔE/E) of 1.6×10−4 and the focused beam size is about 0.9 mm × 0.2 mm. The beamline BL01A is a white‐light beamline reserved for other applications. Both BL01A and BL01B beamlines have been constructed and are in commissioning. An average photon flux of 3×1011 photon/sec has been obtained at beamline BL01B.

Nicotine has been shown to induce relaxation via nitric oxide (NO) production with activation of endothelium nitric oxide synthase (eNOS), however the effect of nicotine on lipopolysaccharide/interferon-gamma (LPS/IFN-gamma)-induced NO production and inducible NOS (iNOS) gene expression is still undefined. Here, nicotine alone did not affect the NO and PGE2 production in RAW264.7 and primary peritoneal macrophages. Interestingly, nicotine showed the dose-dependent stimulatory effect on LPS (20 ng/ml)/IFN-gamma (10 ng/ml)-induced NO but not PGE2 production in both cells. Although nicotine stimulates NO production in the presence of LPS/IFN-gamma, LPS at the dose of 20 ng/ml, nicotine showed no obvious inductive effect on the expression of iNOS protein by Western blotting in both cells. However, nicotine significantly stimulates LPS (2.5, 5 ng/ml)/IFN-gamma (10 ng/ml)-induced iNOS expression and NO production in RAW264.7 cells. Cytotoxicity assay showed that nicotine enhanced LPS (20 ng/ml) and IFN-gamma (10 ng/ml)-induced cytotoxicity, which was inhibited by an NOS inhibitor N-nitro-L-arginine (NLA) in RAW264.7 cells. Direct and indirect NOS activity assays indicated that nicotine did not affect NOS activity. And, iNOS protein stability was not changed by nicotine after LPS/IFN-gamma treatment. These data indicates that nicotine may potentiate LPS/IFN-gamma-induced cytotoxic effects by enhancing NO production; enhancing iNOS gene expression induced by LPS/IFN-gamma is involved. A cross-talk between inflammation and smoking was proposed in the present study.

A-type antiferromagnetic (AF) order with a two-dimensional (2D) ferromagnetic short-range fluctuation was observed in the stoichiometric orthorhombic ${\mathrm{La}}_{1\ensuremath{-}x}{\mathrm{Eu}}_{x}{\mathrm{MnO}}_{3+\ensuremath{\delta}}$ system $(0l~xl~1,$ $\ensuremath{\delta}\ensuremath{\sim}0$ with trivalent ${\mathrm{Mn}}^{3+}).$ The observation of strong basal plane ferromagnetic coupling of the A-type AF order with fluctuation above antiferromagnetic N\'eel temperature ${T}_{N}$ strongly indicates a C-type orbital ordering of ${e}_{g}$ electrons at higher temperature throughout the whole system. Anomalous decrease of ${T}_{N}$ from 139 K for ${\mathrm{LaMnO}}_{3},$ to 91 K for ${\mathrm{La}}_{0.5}{\mathrm{Eu}}_{0.5}{\mathrm{MnO}}_{3}$ and down to 42 K for ${\mathrm{EuMnO}}_{3}$ is the result of weaker anisotropic superexchange interaction due to stronger Jahn-Teller lattice distortion in orbital-ordered ${\mathrm{EuMnO}}_{3}$ from power x-ray Rietveld analysis and Mn K-edge x-ray absorption near-edge structure spectroscopic study.

Nonstructural 5A (NS5A) and the second envelope (E2) proteins of hepatitis C virus (HCV) have the potential to block interferon (IFN)-induced RNA-dependent protein kinase (PKR) and may therefore interfere with the response to IFN therapy, but controversy still exists regarding the relevance of this. This study aimed to assess whether mutations in these regions correlated with the response to combination therapy, IFN and ribavirin. Pretreatment parameters were analysed in 57 HCV-1b patients who had received IFN-alpha2b (3 or 5 MU three times weekly) and ribavirin (800-1200 mg per day) for 24 weeks. The amino acid sequences of the NS5A and PKR-eIF2alpha phosphorylation homology domain (E2-PePHD) were deduced from the corresponding coding sequence, which were determinated by direct sequencing of the HCV genome amplified by the polymerase chain reaction. Twenty (36%) patients achieved a sustained virological response (SVR). The mean number of amino acid substitutions in the NS5A-PKR binding domain (2209-2274), interferon sensitivity-determining region (ISDR) (2209-2248), and E2-PePHD sequence (659-670) in patients with and without SVR were 4.53 +/- 3.31 vs 2.83 +/- 1.78 (P = 0.094), 2.45 +/- 2.74 vs 1.03 +/- 1.32 (P = 0.042) and 0.25 +/- 0.70 vs 0.03 +/- 0.17 (P = 0.109), respectively. Patients with a mutant-type (>/= 4) NS5A-ISDR had a higher rate of SVR (six of nine, 67%) than those with wild-type (five of 22, 23%) (P = 0.038). Stepwise multiple logistic regression analysis of the factors (age, gender, viral load, cirrhosis rate, IFN dosage and amino acid substitutions) revealed that the mutation in NS5A-ISDR (>/= 4 vs < 4) was the only independent variable of treatment outcome. Our study showed that NS5A-ISDR mutations were correlated with the SVR to combination therapy in chronic HCV-1b patients in Taiwan.

A procedure for automatic three-dimensional tetrahedral mesh generation is discussed. Points are added according to the Delaunay triangulation. D.F. Watson's (1981) approach is used for mesh generation. The CAD (computer-aided design) package I-DEAS was used to input the solid model and to check the mesh. >

As the chip density grows, wiring circuits on a VLSI chip becomes hard. It is then important to leave feed-through channels in the layouts of cells and macros. One strategy to achieve this goal is to keep wires on their respective wiring grids. This requirement presents a new constraint to the compaction problem of cells and macros. A new efficient algorithm is proposed to solve such a compaction problem on multiple grids. The worst-case time complexity of the algorithm is O((M+1) ( mod V mod + mod E mod )). The algorithm has been implemented in a compactor and applied to the layout designs for both microprocessor chips and ASIC chips. >

The finite-difference-time-domain (FDTD) algorithm is generalized to the curvilinear coordinate system and applied to the problem of electromagnetic scattering from a finite, perfectly conducting cone. The curvilinear FDTD algorithm employs a body-fitted grid for meshing up the computation domain and, consequently, is able to model the geometry of the scatterer with better accuracy than is possible with the staircasing approach conventionally employed in the FDTD algorithm. The problem of plane wave scattering from a conical target is used to illustrate the application of the curvilinear FDTD algorithm developed. >

A unification framework is proposed for three-dimensional shape reconstruction using physically based models. The authors observe that most existing shape-from-X techniques use an observable (e.g., the stereo disparity, intensity, or texture gradient) and a model, which is based on specific domain knowledge (e.g., the triangulation principle, reflectance function, or texture distortion equation) to predict the observable, in 3D shape reconstruction. It is shown that all these observable-prediction-model types of techniques can be incorporated into the framework of energy constraint on a flexible, deformable image frame. Surface reconstruction is achieved through a package wrapping or a shape deformation process based on physics principles. >

It has been suggested in isolated porcine cerebral arteries that stimulation by nicotine of α 7 -nicotinic acetylcholine receptors (α 7 -nAChRs) on sympathetic nerves, but not direct stimulation of parasympathetic nitrergic nerves, caused nitrergic neurogenic dilation. Direct evidence supporting this hypothesis has not been presented. The present study, which used in vitro tissue bath and confocal microscopy techniques, was designed to determine whether choline, a selective agonist for α 7 -nAChRs, induced sympathetic-dependent nitrergic dilation of porcine basilar arterial rings. Choline and several nAChR agonists induced exclusive relaxation of basilar arterial rings without endothelium. The relaxation was blocked by tetrodotoxin, nitro- l -arginine, guanethidine, and β 2 -adrenoceptor antagonists. Furthermore, the relaxation was blocked by methyllycaconitine and α-bungarotoxin (preferential α 7 -nAChR antagonists) and mecamylamine but was not affected by dihydro-β-erythroidine (a preferential α 4 -nAChR antagonist). Confocal microscopic study demonstrated that choline and nicotine induced significant calcium influx in cultured porcine superior cervical ganglionic cells but failed to affect calcium influx in cultured sphenopalatine ganglionic cells, providing direct evidence that choline and nicotine did not act directly on the parasympathetic nitrergic neurons. The increased calcium influx in superior cervical ganglionic cells was attenuated by α-bungarotoxin and methyllycaconitine but not by dihydro-β-erythroidine. These results support our hypothesis that activation of α 7 -nAChRs on cerebral perivascular sympathetic nerves causes calcium influx and the release of norepinephrine, which then act on presynaptic β 2 -adrenoceptors located on the neighboring nitrergic nerve terminals, resulting in NO release and vasodilation. Endogenous choline may play an important role in regulating cerebral sympathetic activity and vascular tone.

Induction of heme oxygenase (HO)-1 during inflammation has been demonstrated in many cell types, but the contribution of inflammatory molecules nitric oxide (NO) and prostaglandin E(2) (PGE(2)) has remained unresolved. Here we show that NO donors including sodium nitroprusside (SNP) and spermine nonoate (SP-NO), and PGE(2) significantly stimulate HO-1 expression in RAW264.7 macrophages, associated with alternative induction on NO and PGE(2) in medium, respectively. NO donors also show the inductive effect on cyclo-oxygenase 2 protein and PGE(2) production. In the presence of lipopolysaccharide and interferon-gamma (LPS/IFN-gamma), HO-1 protein was induced slightly but significantly, and SNP, SP-NO, and PGE(2) enhanced HO-1 protein induced by LPS/IFN-gamma. L-Arginine analogs N-nitro-L-arginine methyl ester (L-NAME) and N-nitro-L-arginine (NLA) significantly block HO-1 protein induced by LPS/IFN-gamma associated with a decrease in NO (not PGE(2)) production. And, NSAIDs aspirin and diclofenase dose dependently inhibited LPS/IFN-gamma-induced HO-1 protein accompanied by suppression of PGE(2) (not NO) production. PD98059 (a specific inhibitor of MEKK), but not SB203580 (a specific inhibitor of p38 kinase), attenuated PGE(2) (not SP-NO) induced HO-1 protein. Under UVC (100 J/m(2)) and UVB (50 J/m(2)) irradiation, PGE(2) or SP-NO treatment prevents cells from UVC or UVB-induced cell death, and HO-1 inhibitor tin protoporphyrin (SnPP) reverses the preventive effects of PGE(2) and SP-NO. The protective activity induced by PGE(2) on UVC or UVB irradiation-induced cell death was blocked by MAPK inhibitor PD98059 (not SB203580). These results demonstrated that inflammatory molecules NO and PGE(2) were potent inducers of HO-1 gene, and protected cells from UV-irradiation-induced cell death through HO-1 induction.

The lithiated transition metal oxide LiVMoO6 has been synthesized by solid state reaction. This is the first report of this compound to be studied as an anode material for use in secondary batteries. The synthesized LiVMoO6 powder has been studied by means of X-ray diffraction (XRD) and X-ray absorption near edge structure (XANES) spectroscopy. The electrochemical characteristics of the prepared electrodes assembled in coin cells were also investigated in terms of half-cell performance. It is observed that the cell exhibits three stages of discharge plateaus. The total discharge capacity, averaged over several test runs, is about 1250 mAh/g. This value is much higher than the capacities exhibited by many kinds of anode materials.

Results of previous pharmacological studies suggested that presynaptic muscarinic M(2) receptors on cerebral perivascular nitric oxidergic (nitrergic) nerves mediated inhibition of nitric oxide release from these nerves. The inhibition was thought to be primarily attributable to a decreased Ca(2+) influx through N-type Ca(2+) channels on nitrergic nerves, but direct evidence supporting this hypothesis was not presented. In the present study, we used cultured rat sphenopalatine ganglion (SPG), a major source of nitrergic nerves to cerebral blood vessels, to investigate the role of muscarinic M(2) receptors in modulating voltage-dependent Ca(2+) channels. SPG neuronal soma and dendrites were immunoreactive for both N-type Ca(2+) channels and muscarinic M(2) receptors, indicating that muscarinic M(2) receptors were colocalized with N-type Ca(2+) channels. Using the whole-cell voltage-clamp technique, we found that voltage-dependent Ca(2+) currents in cultured SPG were largely blocked by omega-conotoxin, an N-type calcium channel antagonist, but were not affected by nifedipine, an L-type calcium antagonist. The Ca(2+) current was inhibited by acetylcholine (ACh) and arecaidine but-2-ynyl ester tosylate (ABET), a preferential muscarinic M(2)-receptor agonist, in a concentration-dependent manner. The inhibition was reversed by atropine and methoctramine (a muscarinic M(2)-receptor antagonist), but was not affected by muscarinic M(1)-, M(3)-, or M(4)-receptor antagonists. Consistent with this, preferential muscarinic M(1)-receptor agonists McN-A-343 and oxotremorine did not affect the Ca(2+) current. Furthermore, pretreatment with pertussis toxin and guanosine 5'-O-(3-thio)triphosphate prevented ACh and ABET inhibition of Ca(2+) currents. These results are consistent with pharmacological findings in the pig basilar arteries and provide direct evidence supporting our hypothesis that M(2)-receptor-mediated inhibition of cerebral nitrergic neurogenic vasodilation is due to a G(i)-protein-mediated suppression of Ca(2+) influx via voltage-dependent N-type Ca(2+) channels on perivascular nerves.

Involvement of nitric oxide (NO) and beta-adrenoceptors in an increase in the cortical cerebral blood flow (CBF) following an intravenous (i.v.) injection of a small dose of nicotine which did not affect the systemic blood pressure in the rats was investigated. I.v. injection of nicotine (30 microg/kg) for 1 min produced a significant increase in CBF lasting for more than 20 min without a significant effect on the systemic blood pressure. I.v. injection of L-N(G)-nitroarginine methylester (30 mg/kg) significantly attenuated nicotine-induced increase in the cortical CBF. The attenuation was reversed by i.v. injection of L-arginine (300 mg/kg), suggesting an intimate role of nitric oxide (NO) in nicotine-induced increase in the cortical CBF. The nicotine-induced increase in the cortical CBF was significantly attenuated by propranolol (10 mg/kg, i.v.) and ICI 118,551 (a beta2-adrenoceptor antagonist, 10 mg/kg, i.v.) but not by metoprolol (a beta1-adrenoceptor antagonist, 10 mg/kg, i.v.). Beta2-adrenoceptors on presynaptic nitrergic nerves may be involved in nicotine-induced NO-mediated increase in the cortical CBF.

The presence of close apposition between the adrenergic and the non-adrenergic or nitrergic nerve terminals in large cerebral arteries in several species is well documented. The axo-axonal distance between these different types of nerve terminals is substantially closer than the synaptic distance between the adventitial nerve terminals and the outermost layer of smooth muscle in the media. This feature suggests that a functional axo-axonal interaction between nerve terminals is more likely to occur than that between the nerve and muscle. Thus, transmitters released from one nerve terminal may modulate release of transmitters from the neighboring nerve terminals, resulting in a neurogenic response. We have reported that nicotine-induced nitric oxide (NO)-mediated neurogenic vasodilation is dependent on intact sympathetic innervation in porcine and cat cerebral arteries. Evidence also has been presented to indicate that nicotine acts on alpha7-nicotinic receptors located on sympathetic nerve terminals, resulting in release of norepinephrine which then diffuses to act on beta2-adrenoceptos located on the neighboring nitrergic nerve terminals to release NO and therefore vasodilation. The predominant facilitatory effect of beta2-adrenoceptors in releasing NO is compromised by presynaptic alpha2-adrenoceptors located on the same nerves. Activation of cerebral sympathetic nerves may cause NO-mediated dilation in large cerebral arteries at the base of the brain.

Short-range-order and long-range-order structures in Ge1 − xSn x /Ge thin films grown by molecular beam epitaxy (MBE) were investigated by using extended x-ray absorption fine structure (EXAFS) and x-ray diffraction (XRD) techniques, respectively. These materials are of great potential for constructing efficient optoelectronic devices. The EXAFS analysis demonstrates that Sn atoms occupy Ge sites in these thin-film samples with Sn concentration up to 20 at.%. The Ge-Sn bonds expected in the substitutional model were also observed in Raman spectra of these samples. The XRD results show that, in the out-of-plane direction, the lattice constants of the films are distinctly larger than that of the Ge substrates. However, such increased lattice parameters were not observed in the in-plane direction. Our x-ray and Raman results have clearly revealed substitutional incorporation of Sn with high concentration in dislocation-free MBE-grown Ge films of practical-device thickness.

Investigation has been made on atomic, electronic structures and magnetic properties of La0.7Sr0.3MnO3 (LSMO) on Si substrate. The effect of different thickness of LSMO and different morphological [flat and nano-pyramid (NP)] of Si substrate are studied in present work. The result of Mn K-edge extended x-ray absorption fine structure indicates the more disorder of local atomic structure of first shell (Mn-O bound) in the thinner LSMO/Si film. The Mn L3,2-edge x-ray absorption near-edge structure shows the presence of Mn2+ ion on the sample. Furthermore, the Mn L3,2-edge x-ray magnetic circular dichroism reveals that the thinner film (LSMO/Si) has highest magnetic moment, in comparison to that of thick LSMO/Si and LSMO/Si-NP samples. This finding suggests that the appearance Mn2+ may play an important role in magnetic behavior of hetero-junction LSMnO/Si and Si-NP.

The electronic and magnetic properties of tetravalent-ion-doped La0.85Zr0.15MnO3 (LZMO) thin films that were epitaxially grown on SrTiO3 (STO) and MgO substrates were studied using temperature-dependent x-ray diffraction (XRD), x-ray absorption near-edge structure, x-ray linear dichroism, and x-ray magnetic circular dichroism at the Mn L3,2- and K-edge. XRD studies reveal that the LZMO thin films have compressive and tensile strains (along the c-axis) on the STO and MgO substrates, respectively. As the temperature is reduced from room temperature to below magnetic transition temperature, the preferentially occupied Mn majority-spin eg orbital changes from the in-plane dx2-y2 to the out-of-plane d3z2-r2 orbital for LZMO/STO, and vice versa for LZMO/MgO. Experimental results suggest that the new hopping path that is mediated by the Mn2+ ions triggers a stronger d3z2-r2 orbital ordering of Mn3+ ions and enhances the ferromagnetic coupling between the Mn spin moments of t2g electrons in LZMO/STO, whereas the ...

We report the effects of Ge partial substitution for Si on local atomic and electronic structures of thermoelectric materials in binary compound cobalt monosilicides (). Correlations between local atomic/electronic structure and thermoelectric properties are investigated by means of X-ray absorption spectroscopy. The spectroscopic results indicate that as Ge is partially substituted onto Si sites at , Co in CoSi1?xGex gains a certain amount of charge in its 3d orbitals. Contrarily, upon further replacing Si with Ge at , the Co 3d orbitals start to lose some of their charge. Notably, thermopower is strongly correlated with charge redistribution in the Co 3d orbital, and the observed charge transfer between Ge and Co is responsible for the variation of Co 3d occupancy number. In addition to Seebeck coefficient, which can be modified by tailoring the Co 3d states, local lattice disorder may also be beneficial in enhancing the thermoelectric properties. Extended X-ray absorption fine structure spectrum results further demonstrate that the lattice phonons can be enhanced by Ge doping, which results in the formation of the disordered Co-Co pair. Improvements in the thermoelectric properties are interpreted based on the variation of local atomic and electronic structure induced by lattice distortion through chemical substitution.

The in-situ X-ray absorption spectroscopy of three tungsten oxide films was performed to study the electronic and atomic structures following repeated cycles of coloration and bleaching processes. The transparent tungsten oxide films become deep blue upon intercalation of Li+ ions in the WO6 octahedra when an external electrical bias was applied. These films reverted to transparent when a reverse external electrical bias was applied. W L3-edge X-ray absorption near-edge structure (XANES) measurements of the nanocrystalline and crystalline tungsten oxide films revealed that the intensity of the white-line feature decreases after coloration and recoverably increases after bleaching owing to the filling and unfilling of the W 5d–O 2p conduction band states. The second derivative of the W L3-edge XANES spectra indicated an increase in structural disordering following repeated cycles of coloration and bleaching. However, the extended X-ray absorption fine structure analysis showed that the nearest-neighbor W–O bond distances in the samples overall remain unchanged by coloration and bleaching. The nanocrystalline tungsten oxide film exhibited more effective recovery (∼97% after first cycle) of the electronic structures than the other two crystalline samples in terms of the filling and unfilling of the W 5d–O 2p conduction band states after repeated coloration and bleaching. These results show that the nanocrystalline tungsten oxide sample has superior electrochromic properties to the crystalline samples.

SummaryTo investigate the role of LFA-1 in the immune defects in DS patients, we analysed lymphocytes from DS patients in LFA-1 expression and LFA-1 mediated cell adhesion. DS patients less than 2 years of age expressed a higher level of LFA-1 when compared with age-matched controls. The difference in LFA-1 expression was much less significant in older DS patients when compared with age-matched children. Although older children (2–15-year-old groups) without DS tend to increase their expression of lymphocyte LFA-1 when compared with younger normal children (0–2 years old), DS patients showed no age-associated increase in lymphocyte LFA-1 expression. Two-colour analysis with CD4/CD8 and LFA-1 in patients and controls showed that proportions of CD4 + lymphocytes were comparable in DS patients and controls, while the proportion of CD8 + lymphocytes was higher in older DS patients. Expression levels of LFA-1 on both CD4 + and CD8 + lymphocytes in younger DS patients were higher when compared with age-matched controls and close to the expression levels in the older DS group. Proportions of memory lymphocytes expressing the CD45RO isoform were higher in both younger and older DS patients when compared with age-matched control groups. Noticeably, the LFA-1 expression levels on CD45RO lymphocytes from younger DS patients were higher than the levels of the controls and declined in the older DS group. We tested lymphocytes (EBV transformed B cells, resting and anti-CD3 stimulated T cells) for cellular adhesion to recombinant ICAM-1 and found that lymphocytes from DS patients were less adhesive, even though their β2 integrin expression was comparable with that of normal controls. These results suggest that more generalized pathological processes, such as early senescence of the immune system or ineffective lymphocyte activation, and subsequent integrin dysfunction may underlie the immune defects in DS patients.

Several natural flavonoids have been demonstrated to perform some beneficial biological activities, however, higher-effective concentrations and poor-absorptive efficacy in body of flavonoids blocked their practical applications. In the present study, we provided evidences to demonstrate that flavonoids rutin, quercetin, and its acetylated product quercetin pentaacetate were able to be used with nitric oxide synthase (NOS) inhibitors (N-nitro-L-arginine (NLA) or N-nitro-L-arginine methyl ester (L-NAME)) in treatment of lipopolysaccharide (LPS) induced nitric oxide (NO) and prostaglandin E2 (PGE2) productions, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expressions in a mouse macrophage cell line (RAW 264.7). The results showed that rutin, quercetin, and quercetin pentaacetate-inhibited LPS-induced NO production in a concentration-dependent manner without obvious cytotoxic effect on cells by MTT assay using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide as an indicator. Decrease of NO production by flavonoids was consistent with the inhibition on LPS-induced iNOS gene expression by western blotting. However, these compounds were unable to block iNOS enzyme activity by direct and indirect measurement on iNOS enzyme activity. Quercetin pentaacetate showed the obvious inhibition on LPS-induced PGE2 production and COX-2 gene expression and the inhibition was not result of suppression on COX-2 enzyme activity. Previous study demonstrated that decrease of NO production by L-arginine analogs effectively stimulated LPS-induced iNOS gene expression, and proposed that stimulatory effects on iNOS protein by NOS inhibitors might be harmful in treating sepsis. In this study, NLA or L-NAME treatment stimulated significantly on LPS-induced iNOS (but not COX-2) protein in RAW 264.7 cells which was inhibited by these three compounds. Quercetin pentaacetate, but not quercetin and rutin, showed the strong inhibitory activity on PGE2 production and COX-2 protein expression in NLA/LPS or L-NAME/LPS co-treated RAW 264.7 cells. These results indicated that combinatorial treatment of L-arginine analogs and flavonoid derivates, such as quercetin pentaacetate, effectively inhibited LPS-induced NO and PGE2 productions, at the same time, inhibited enhanced expressions of iNOS and COX-2 genes.

This study examined whether there is evidence for an association between alcoholism with conduct disorder and alleles of the TaqI A and TaqI B polymorphisms, both individually and as haplotypes, at the dopamine D2 receptor gene (DRD2). We studied 182 Han Chinese subjects, including 34 alcoholics with conduct disorder, 63 alcoholics without conduct disorder, and 85 nonalcoholics. Alcohol dependence and conduct disorder were defined according to DSM-III-R criteria. Significant associations were observed between TaqI A and TaqI B at the DRD2 locus, tested individually and as haplotypes, and alcoholism with conduct disorder. Our results suggested that DRD2 might be associated with conduct disorder or a predisposition to both conduct disorder and alcoholism. However, this needs to be further investigated by examining the differences among conduct disorder with alcoholism, conduct disorder only, and controls for the TaqI A and B system at DRD2.

The electronic structures of five polycrystalline YNi2−xCoxB2C (x=0, 0.05, 0.1, 0.15, and 0.2) borocarbide superconductors were studied by photoemission and photoabsorption spectroscopies and theoretical calculations. The valence-band (VB) photoemission spectrum is compared with the theoretical total and partial density-of-states (DOS) curves. The VB satellite is peaked at a binding energy (EB) of 6 eV. The Ni K-edge x-ray absorption near edge spectra (XANES) are compared with the calculated XANES spectra for these intermetallic compounds. Extended x-ray absorption fine structure (EXAFS) spectra at the Ni and Co K edges are analyzed to yield the structural parameters. The decrease of the superconducting transition temperatures (Tc) with addition of Co dopant in these compounds is due to a decrease of the total DOS at the Fermi level (EF).

Pr doping studies occupy a special place for determining the role played by different cations in evolution of superconductivity in the cuprate perovskites. It is known to quench superconductivity in different systems through different mechanisms that still remain to be firmly established. Reporting of a pure Pr123 superconducting crystal has served to further heighten this debate. Polarized EXAFS measurements have been made on the Pr LIII edge in a Bi2Sr2Ca0.4Pr0.6Cu2O8−Y insulating single crystal to examine the site geometry of the Pr cations and the mechanism of quenching superconductivity in this system. Measurements have been confined to within the ab-plane in E∥a, E∥â 45 and E∥b polarizations. Results show that Pr has a valence of 3+ only, occupies only the Ca sites and hence quenches the itinerant holes rendering the CuO2 planes insulating. No evidence is found of presence of any distortion in the Pr/Ca plane.

We previously reported that nicotine-induced nitric oxide (NO)-mediated cerebral neurogenic vasodilation was dependent on intact sympathetic innervation. We hypothesized that nicotine acted on sympathetic nerve terminals to release norepinephrine (NE), which then acted on adrenoceptors located on the neighboring nitric oxidergic (NOergic) nerve terminals to release NO, resulting in vasodilation. The adrenoceptor subtype in mediating nicotine-induced vasodilation in isolated porcine basilar arterial rings denuded of endothelium was therefore examined pharmacologically and immunohistochemically. Results from using an in vitro tissue bath technique indicated that propranolol and preferential β2-adrenoceptor antagonists (ICI-118,551 and butoxamine), in a concentration-dependent manner, blocked the relaxation induced by nicotine (100 μM) without affecting the relaxation elicited by transmural nerve stimulation (TNS, 8 Hz). In contrast, preferential β1-adrenoceptor antagonists (atenolol and CGP-20712A) did not affect either nicotine- or TNS-induced relaxation. Results of double-labeling studies indicated that β2-adrenoceptor immunoreactivities and NADPH diaphorase reactivities were colocalized in the same nerve fibers in basilar and middle cerebral arteries. These findings suggest that NE, which is released from sympathetic nerves upon application of nicotine, acts on presynaptic β2-adrenoceptors located on the NOergic nerve terminals to release NO, resulting in vasodilation. In addition, nicotine-induced relaxation was enhanced by yohimbine, an α2-adrenoceptor antagonist, which, however, did not affect the relaxation elicited by TNS. Prazosin, an α1-adrenoceptor antagonist, on the other hand, did not have any effect on relaxation induced by either nicotine or TNS. The predominant facilitatory effect of β2-adrenoceptors in releasing NO may be compromised by presynaptic α2-adrenoceptors.

Until two decades ago, chemical transmission from autonomic innervation to vascular effector tissues was thought to be mediated mainly by norepinephrine and acetylcholine. However, it was noted that despite pharmacological blockade of adrenergic receptors, electrical stimulation of sympathetic nerves still evoked residual vasoconstriction in several vascular beds in experimental animals (Folkow and Uvnas,1948 Lundberg and Tatemoto,1982). Direct evidence from examining neuroeffector transmission in isolated vascular preparations using in vitro tissue bath techniques has indicated that contraction and relaxation of isolated blood vessels upon field electrical stimulation of the intramural nerves persist in the presence of adrenoceptor and muscarinic receptor antagonists (Lee and Bevan, 1974 Lee et al., 1975 Lee and Bevan, 1976 Lee and Bevan, 1978 Lee and Bevan, 1980 Von Kugelgen and Starke, 1985 Burnstock and Kennedy, 1986 Morris and Murphy, 1988). These findings, particularly those from in vitro studies using isolated preparations, have led to the evolution of new paradigms for neuroeffector communication in which norepinephrine and acetylcholine are not the respective primary vasoconstrictor and dilator transmitters, for example, in cerebral vascular beds, and a second transmitter substance from each type of nerve is predominant in mediating vasoconstriction and dilation (Lee and Bevan, 1974 Lee et al., 1975 Lee,1986). Accruing evidence has now clearly indicated that several substances other than norepinephrine and acetylcholine are involved in autonomic neurotransmission in various vascular beds (Burnstock, 1972 Su and Lee, 1976; Lee, 1994). Foremost among this has been the discovery of nitric oxide (NO) as a cellular messenger.

An unusual case of solitary breast metastasis from a primary anorectal melanoma in a 59-year-old post-menopausal woman is reported. The course and management of melanotic breast metastases is discussed.

Laparoscopic-assisted resection of colorectal carcinoma is technically feasible. Whether it is beneficial to patients is uncertain. This study reviewed the results of laparoscopic-assisted resection in patients with right-sided colonic adenocarcinoma.We attempted laparoscopic-assisted right to extended right hemicolectomy in 28 patients with right-sided colonic carcinoma (study group). The results were compared with 56 matched patients who underwent conventional open resection in the same period (comparative group).The median follow-up times for the study and comparative groups were 21.4 and 23.5 months, respectively. The operating time was significantly longer (t-test, P0.001), whereas the time to resuming normal diet (Mann-Whitney U-test, P0.001) and the duration of hospital stay (Mann-Whitney U-test, P = 0.002) were significantly less in the study than in the comparative group. The oncological clearance, in terms of the number of lymph nodes removed and the resection margins, the complication rate, the disease-free rate, and the survival rate were comparable in the two groups.We conclude that laparoscopic-assisted resection of right-sided colonic adenocarcinoma has the advantage over open surgery of allowing earlier recovery. However, this is at the expense of a longer operating time.

The clinical and radiographic results of 86 primary total hip arthroplasties performed in 74 patients from 1983 to 1987 with a cemented metal-backed acetabular component and a cemented collared straight femoral stem with a 32-mm head were reviewed at a mean follow-up of 10.1 years. Seven patients (9.2%) underwent acetabular component revision at a mean of 9.0 years after implantation; an additional 24 components (31.6%) demonstrated evidence of radiographic loosening, resulting in a total failure rate of 40.8%. Periacetabular radiolucencies were noted in Charnley zones at the following rates: 34.2% in zone I, 18.4% in zone II, and 27.6% in zone III. In addition, 18.4% and 38.2% of implants demonstrated evidence of migration and excessive polyethylene wear. Excessively vertical cup placement (49 degrees inclination) at the time of initial arthroplasty was statistically correlated with polyethylene wear, implant migration, and fixation failure. A trend of increasing implant failure was also noted with decreasing polyethylene liner thickness. Periacetabular cement mantle thickness was not statistically correlated with subsequent component loosening or failure. Results of Kaplan-Meier survivorship analysis using revision as an endpoint showed 93.6% survivorship at 10 years and 88.4% at 12 years. The mean modified Harris hip scores were 46.9 preoperatively and 81.8 at final follow-up. The significant overall rates of radiographic loosening, migration, polyethylene wear, and implant revision confirm the suspected trend of increasing failure rates of cemented metal-backed acetabular components over time.

The distribution of nitric oxide synthase (NOS)-, choline acetyltransferase (ChAT)-, and vasoactive intestinal polypeptide (VIP)-immunoreactivities, and nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd)-reactivities in the sphenopalatine ganglia (SPG), and perivascular nerves in middle cerebral arteries of the pig was investigated by double-staining techniques using combined immunofluorescence and histochemistry methods. In the SPG, almost all ganglionic cells were NOS-immunoreactive (I) and NADPHd-positive, and both NOS immunoreactivities and NADPHd reactivities were completely co-localized. ChAT-I ganglionic cells accounted for 75%, while VIP-I ganglionic cells represented 42% of all ganglionic cells. Almost all VIP immunoreactivities were co-localized with ChAT immunoreactivities, and all ganglionic cells that were VIP-I and/or ChAT-I were NOS-I and NADPHd-reactive. None of the ganglionic cells in the SPG were immunoreactive to calcitonin gene-related peptide (CGRP). CGRP immunoreactivities, however, were found to surround some ganglionic cells. In middle cerebral arteries, all adventitial NOS-I bundles and fine fibers were coincident with NADPHd fibers. Almost all adventitial ChAT-I bundles and thin fibers, and VIP-I mesh-like fibers stained positively for NADPHd, while the mesh-like NADPHd fine fibers were not ChAT-I. Simultaneous labeling using antibodies against VIP and ChAT further indicated that VIP-I fibers were closer than ChAT-I fibers to the smooth muscle. In rare occasions, perivascular fibers were found to be stained for both ChAT and VIP, showing that most ChAT-I and VIP-I fibers were not coincident. These results suggest that ChAT and VIP are rarely co-localized in perivascular nerves in middle cerebral arteries, and point out that the neurotransmitter and the modulator that are co-localized within the same nerve cell body may distribute totally independently and differently at the terminal level. The present results also indicate that in cerebral perivascular nerves, the combination of nitric oxide (NO) and acetylcholine (ACh), as well as the combination of NO and VIP, are localized in the same nerve with different axons containing either NO plus ACh, or NO plus VIP. These findings support the hypothesis that ACh and VIP may act as modulators in regulating presynaptic release of NO, and therefore, cerebral neurogenic vasodilation, from their respective perivascular cholinergic-nitric oxidergic and VIPergic-nitric oxidergic nerves.

A defect in mitochondrial energy conservation is strongly suggested to be involved in the pathogenesis of Leber's hereditary optic neuropathy (LHON). The authors therefore compared the energy charge in lymphocytes among patients with LHON, their asymptomatic maternal lineages, and normal control subjects.Blood samples were obtained from 7 patients, 10 asymptomatic maternal relatives, and 16 normal subjects. Molecular analysis confirmed that all had the homoplasmic 11,778 point mutation in the mtDNA of their blood cells. The concentrations of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP) were determined by high-performance liquid chromatography. The energy charge was calculated as (ATP + 1/2 ADP)/(ATP + ADP + AMP).The mean energy charges of lymphocytes were 0.871 +/- 0.049 in patients with LHON, 0.884 +/- 0.061 in their asymptomatic maternal relatives, and 0.885 +/- 0.061 in normal controls, respectively. No statistically significant difference was found among the three groups.Although the study did not find the anticipated change in energy charge in peripheral blood cells, this neither confirms nor rejects the notion that a defect in the mitochondrial oxidative phosphorylation system is involved in the pathogenesis of LHON.

Using immunoperoxidase labeling (IPL) and immunofluorescence labeling (IFL) methods, and each followed by NADPH diaphorase (NADPHd) histochemical staining in the same specimen, colocalization of choline acetyltransferase (ChAT) and NADPHd, indicative of nitric oxide synthase (NOS), in cerebral pial arteries and the sphenopalatine ganglia (SPG) of the cat was examined. In addition, retrograde axonal tracing using true blue was performed to determine if cerebral perivascular nerves containing ChAT and NADPHd originate in the SPG. Consistent results were obtained from IPL and IFL methods, indicating that the middle cerebral artery (MCA) and the circle of Willis received dense ChAT-immunoreactive (I) and NADPHd bundles and fine fibers. Almost all ChAT-I fibers and NADPHd fibers were found to be coincident in the arteries examined. A few fine fibers exhibited only NADPHd staining. In the SPG, approximately half of the ganglionic cells were both ChAT-I and NADPHd positive, while the remaining cells were positively only for NADPHd staining. One week after application of true blue on the middle cerebral arteries (MCA), the fluorescent true blue was found in the ganglionic cells of the SPG. Some of the true blue-positive cells contained both ChAT-immunoreactivity and NADPHd staining. These results provide morphological evidence indicating that all ChAT-I fibers in the MCA and the circle of Willis contain NOS, and that these fibers originate in the SPG, although not all NOS-I ganglionic cells in the SPG send fibers to pial vessels. These results also support the hypothesis that acetylcholine (ACh) and nitric oxide (NO) are synthesized and co-released in the same neurons in cerebral perivascular nerves. Based on the reported findings that NO mediates a major component of neurogenic vasodilation, and that ACh acts as a modulator, the present results demonstrate the presence of a cholinergic, nitric oxidergic innervation in cerebral arteries of the cat.

1. Extracts from the leaves of Ginkgo biloba (EGb) and ginsenosides (GS) have been reported to be effective at increasing vascular relaxation. In the present study, the actions of EGb and GS on the vascular functions of porcine basilar arteries were investigated in vitro using tissue bath techniques. 2. Both EGb and GS relaxed the basilar artery in a concentration-dependent and partly endothelium-dependent manner. However, EGb appeared to be more potent than GS. Relaxation induced by transmural nerve stimulation (TNS) was significantly enhanced by EGb (7.5, 15 and 30 micrograms/mL) and GS (20, 40 and 80 micrograms/mL) in both endothelium-intact and -denuded basilar arteries. Enhanced TNS-induced relaxations were abolished by 0.3 mmol/L N-L-arginine. 3. The present study demonstrates that nitric oxide plays a primary role in TNS-induced relaxation as well as in EGb- and GS-enhanced relaxation within the cerebral vasculature. In addition, our data support the potential of these compounds as therapeutic strategies in cerebral ischaemia and other related vascular dysfunctions.

X-ray absorption near edges structure (XANES) spectra of the Diluted Magnetic Semiconductors (DMS) system Zn 1-x M x S (M=Mn, Co) have been measured at the Mn and Co L 3,2 -edge using sample current mode. Analysis of the M L 3,2 -edge XANES spectra for Zn 1-x M x S revealed the presence of a white line feature in each series, whose intensity increased linearly with concentration x. The white line feature is assigned to M 2p 3/2 and 2p 1/2 photoelectron excitations to nonbonding 3d(e) states and to the relatively broadened band of M 3d(t 2 ) - S 3p hybridized antibonding states. The rate of increase of L 3,2 white line intensity with is associated with the difference in the degree of p-d hybridization of states between M 3d and S 3p.

The role of nitric oxide (NO) in endogenous norepinephrine (NE) release in the perfused isolated rat mesenteric vasculature was examined. NE overflow elicited by electrical field stimulation (EFS) at various frequencies was significantly smaller at 24 than at 37 degrees C. The pressor response upon EFS at 8 and 10 Hz, however, was higher at 24 than at 37 degrees C. When production of NO was blocked by N omega-nitro-L-arginine (L-NNA), NE overflow upon EFS at each frequency of stimulation was diminished by 50% at 37 degrees C but remained unchanged at 24 degrees C, whereas the pressor response elicited by EFS became greater at 37 than at 24 degrees C. These effects of L-NNA were reversed by L-arginine, but not by its D-enantiomer. Sodium nitroprusside, an NO donor, increased EFS-elicited NE overflow at 24 degrees C but had no effect at 37 degrees C. These results demonstrate that NE release is NO dependent and NO independent. The NO-dependent mechanism is more sensitive to cooling than the NO-independent mechanism. The increase in EFS-elicited perfusion pressure at 24 degrees C may be due to reduction in synthesis of NO (a potent vasodilator), thus unmasking the effect of NE and other noncatecholamine vasoconstrictors.

Serotonin (5-hydroxytryptamine, 5-HT) has been shown to inhibit the rhythmic constrictions, accompanied by an increase in cAMP synthesis, in porcine pial veins. Since porcine pial veins contain predominant postsynaptic alpha 2-adrenoceptors which are coupled to Gi-protein, the possibility that the inhibitory effect of 5-HT is antagonized by norepinephrine was examined pharmacologically, using tissue bath techniques. The results indicated that norepinephrine (0.1-1 microM) attenuated 5-HT-induced inhibition of rhythmic constriction. This effect of norepinephrine was mimicked by clonidine (an alpha 2-adrenoceptor agonist), but not by methoxamine (an alpha 1-adrenoceptor agonist). Furthermore, the effect of norepinephrine was prevented by yohimbine (an alpha 2-adrenoceptor antagonist) and pertussis toxin, but was not prevented by prazosin (an alpha 1-adrenoceptor antagonist). In parallel studies, the basal concentration of cAMP and that induced by 5-HT in the pial veins were inhibited by norepinephrine (0.3 microM). These results are consistent with the previous findings that 5-HT-induced inhibition of rhythmic constriction in the porcine pial veins is associated with an increase in vascular cAMP synthesis and suggest that norepinephrine attenuates 5-HT-induced inhibition of rhythmic constriction in part by negatively coupling to adenylate cyclase via alpha 2-adrenoceptors.

Polyhydramnios is often associated with fetal anatomical abnormalities; thus chromosome analysis is indicated for fetuses with those indications. However, chromosome analysis for patients with idiopathic polyhydramnios is often overlooked. This is an attempt to evaluate the necessity for chromosome analysis in pregnancies with idiopathic polyhydramnios.Genetic amniocentesis or percutaneous umbilical blood sampling was done in 33 cases with idiopathic polyhydramnios which appeared at 26 to 34 weeks' gestation. To exclude false idiopathic polyhydramniotic cases, a level II sonographic examination was carefully performed for those fetuses with abnormal chromosome. Autopsy ultrasound examination and X-ray examination were done in four neonates with abnormal karyotypes, and the results were compared with prenatal sonographic findings.Seven (21.2%) out of the 33 cases were, surprisingly found to have chromosomal abnormalities. Three out of the seven cases were diagnosed to have fetal anatomical defects, at a repeated level II sono-graphic examination. The incidence of fetal chromosome abnormalities in idiopathic polyhydramnios was 13.3% (4/30). After 7 cases of women older than 34 years and 3 cases with false idiopathic polyhydramnios were excluded, the incidence of chromosomal abnormalities in pregnancies of those under 34 years of age with idiopathic polyhydramnios was 8.3% (2/24).According to the results of this study and other papers, the incidence of chromosomal abnormalities in fetuses with idiopathic polyhydramnios is much higher than that for maternal age specific risk at 34 years of age. Therefore fetal chromosome analysis for pregnancies with idiopathic polyhydramnios is recommended to avoid unnecessary Cesarean sections and deliveries of viable babies with abnormal chromosomes.

1. Ginsenosides, the active ingredients extracted from Panax ginseng, have been shown to promote nitric oxide (NO) release in bovine aortic endothelial cells. Since the endothelial cells and the perivascular nerves in penile corpus cavernosum contain NO synthase and an NO-like substance has been shown to be released from these cells which relaxes corpus cavernosum, the possibility that ginsenosides may relax corpus cavernosum by releasing endogenous NO was examined. 2. With an in vitro tissue superfusion technique, ginsenosides (250, 500 and 750 micrograms ml-1) relaxed corpus cavernosum, concentration-dependently. 3. Using an in vitro tissue bath technique, acetylcholine (ACh)-induced relaxations were increased in the presence of ginsenosides (250 micrograms ml-1). 4. Ginsenosides at 100 micrograms ml-1 significantly enhanced the tetrodotoxin (TTX)-sensitive relaxation of corpus cavernosum elicited by transmural nerve stimulation. 5. The ginsenosides-induced, ACh-induced and ginsenosides-enhanced transmural nerve stimulation-elicited relaxations were significantly attenuated by NG-nitro-L-arginine (100 microM) and oxyhaemoglobin (oxyHb; 5-10 microM), and were enhanced by superoxide dismutase (SOD; 50 u ml-1). 6. The relaxations and their attenuation by NG-nitro-L-arginine and TTX were associated with increase and decrease in tissue cyclic GMP levels, respectively. 7. It is concluded that ginsenosides may release NO from endothelial cells, and enhance NO release from endothelial cells elicited by other vasoactive substances and from perivascular nitrergic nerves in the corpus cavernosum. These endothelial and neurogenic effects of ginsenosides in inducing relaxation of the corpus cavernosum may account for the aphrodisiac effect of Panax ginseng.

Defect engineering techniques have been employed to generate and remove oxygen vacancy defects in nanoparticles of Y2O3:Mn diluted magnetic oxide (DMO). These samples were prepared by thermal decomposition method followed by a series of thermal annealing in oxygen and forming gas. The x-ray absorption analysis reveals that O vacancies surrounding Mn and Y atoms were appreciably increased by forming-gas-annealing and decreased by oxygen-annealing, accompanied by enhanced and reduced saturation magnetization as demonstrated by magnetic measurements, respectively. Our results demonstrate strong correlation between magnetism and O vacancies and therefore strongly support the bound magnetic polaron model for these high-k DMOs.

Memantine, an NMDA receptor antagonist used for treatment of Alzheimer's disease (AD), is known to block the nicotinic acetylcholine receptors (nAChRs) in the central nervous system (CNS). In the present study, we examined by wire myography if memantine inhibited α3β2-nAChRs located on cerebral perivascular sympathetic nerve terminals originating in the superior cervical ganglion (SCG), thus, leading to inhibition of nicotine-induced nitrergic neurogenic dilation of isolated porcine basilar arteries. Memantine concentration-dependently blocked nicotine-induced neurogenic dilation of endothelium-denuded basilar arteries without affecting that induced by transmural nerve stimulation, sodium nitroprusside, or isoproterenol. Furthermore, memantine significantly inhibited nicotine-elicited inward currents in Xenopous oocytes expressing α3β2-, α7- or α4β2-nAChR, and nicotine-induced calcium influx in cultured rat SCG neurons. These results suggest that memantine is a non-specific antagonist for nAChR. By directly inhibiting α3β2-nAChRs located on the sympathetic nerve terminals, memantine blocks nicotine-induced neurogenic vasodilation of the porcine basilar arteries. This effect of memantine is expected to reduce the blood supply to the brain stem and possibly other brain regions, thus, decreasing its clinical efficacy in the treatment of Alzheimer's disease.

Monkey isolated mesenteric arterial rings denuded of endothelium constricted upon transmural nerve stimulation (TNS) in the absence of active muscle tone. The constriction was potentiated by Nω-nitro-l-arginine (3 × 10−5 m), but not by the d-enantiomer (3 × 10−5 m). The potentiation was reversed by l-arginine (3 × 10−4 m). The neurogenic vasoconstriction of mesenteric arteries was also augmented by capsaicin, but to a lesser extent than that induced by Nω-nitro-l-arginine. Indomethacin (10−5 m) did not affect TNS-induced vasoconstriction. These findings suggest that nerve-derived nitric oxide or a related substance may play a greater role than do capsaicin-sensitive vasodilator transmitters in neurogenic regulation of mesenteric arterial tone in the monkey. The transmitter mechanisms for vasodilation in mesenteric circulation vary among species.

The presence of a vasodilator innervation of the cerebral blood vessels from several species is well established. The exact functional role of these nerves and the nature of transmitters for vaso-dilation, however, remain undetermined.