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Notes: Experimental results show that the exchange coupling field (Hex) of NiFe/FeMn for Ta/NiFe/FeMn/Ta multilayers is higher than that for spin-valve multilayers Ta/NiFe/Cu/NiFe/FeMn/Ta. In order to find out the reason, the composition and chemical states at the surface of Ta(12 nm)/NiFe(7 nm), Ta(12 nm)/NiFe(7 nm)/Cu(4 nm), and Ta(12 nm)/NiFe(7 nm)/Cu(3 nm)/NiFe(5 nm) were studied using x-ray photoelectron spectroscopy. The results show that no elements from lower layers float out or segregate to the surface in the first and second samples. However, Cu atoms segregate to the surface of Ta(12 nm)/NiFe(7 nm)/Cu(3 nm)/NiFe(5 nm) multilayers, i.e., Cu atoms segregate to the NiFe/FeMn interface for Ta/NiFe/Cu/NiFe/FeMn/Ta multilayers. We believe that the presence of Cu atoms at the interface of NiFe/FeMn is one of the important factors which causes the exchange coupling field (Hex) of Ta/NiFe/Cu/NiFe/FeMn/Ta to be weaker than that of Ta/NiFe/FeMn/Ta. © 2002 American Institute of Physics.

Notes: 1 The aim of this study was to investigate the co-localization of histamine and dopamine-β-hydroxylase in the superior cervical ganglion of guinea-pig and release of histamine from cardiac sympathetic terminals in guinea-pig isolated atrium. 2 Histidine decarboxylase (a histamine-synthesizing enzyme) mRNA signals were detected in the neurones of superior cervical ganglion of guinea-pig by in situ hybridization. The results of double-labelled immunofluorescence further confirmed the co-localization of histamine and dopamine-β-hydroxylase in the large principle neurons and small intensely fluorescent cells in the superior cervical ganglion. The immunoreactivities of both histamine and dopamine-β-hydroxylase were significantly attenuated after 6-hydroxydopamine-induced lesion of sympathetic nerves. 3 The refractory electrical field stimulation caused the release of histamine from cardiac sympathetic terminals of guinea-pig isolated atria (112.14 ± 40.34 ng ml−1), which was significantly attenuated to 35 ± 15.57 ng ml−1 by reserpine pretreatment. Following administering compound 48/80, a mast cell degranulator, electrical field stimulation induced a dramatic increase of endogenous histamine release from isolated atria (303.57 ±72.93 ng ml−1). When compound 48/80 was added to the reserpine-treated atria, the release of histamine induced by field stimulation was decreased to 207.14 ± 76.39 ng ml−1. 4 These results provide novel evidence that histamine co-exists with noradrenaline in sympathetic nerves and might act as a neurotransmitter to modulate sympathetic neurotransmission.

Notes: Dyschromatosis symmetrica hereditaria (DSH) is a pigmentary genodermatosis of autosomal dominant inheritance characterized by a mixture of hyperpigmented and hypopigmented macules distributed on the dorsal aspects of the hands and feet. It is caused by mutations of the RNA-specific adenosine deaminase gene. We report the identification of a Chinese family with a three-generation pedigree of DSH, in whom a novel tyrosine substitution mutation in DSRAD was demonstrated: a heterozygous nucleotide A→G transition at position 2879 in exon 10 of the DSRAD gene was detected.

Notes: Marie Unna hereditary hypotrichosis (MUHH) is a rare autosomal dominant disorder with progressive hair loss starting in early childhood and aggravating at puberty. Several studies have mapped the MUHH gene to chromosome 8p21. Here we report a Chinese MUHH family with variable phenotypes. All affected individuals have anomalies affecting both hair density and hair shafts. Major clinical characteristics, disease history and histological examination support the diagnosis of MUHH, but the features of scarring in this kindred are modest and none of the patients have vertex hair loss, which is in contrast with typical MUHH. We now report genotyping and linkage analysis using 11 polymorphic microsatellite markers spanning the MUHH locus at 8p. Two-point linkage analysis using these markers revealed significant exclusion of this locus (log of the odds scores 〈 − 2) at θ = 0 indicating that there is a range of clinical presentations in MUHH, and that more than one genetic locus is responsible for the disorder.

Notes: Haplotype associations of the major histocompatibility complex (MHC) with psoriasis vulgaris (PV) have been demonstrated in different racial or ethnic populations. The objective of this study was to demonstrate the different haplotype associations of the MHC in Chinese patients with psoriasis according to the type of onset and their sex. One hundred and thirty-eight patients with PV and 149 normal control subjects without psoriasis were typed for HLA-A, -B, -C, -DQA1, -DQB1 and -DRB1 by using the PCR with sequence-specific primers. The results showed: (i) HLA-A*26 (26.1% vs. 12.1%, Pc 〈 1 × 10−5), -B*27 (17.03% vs. 1.01%, Pc 〈 1 × 10−7), -Cw*0602 (15.58% vs. 5.03%, Pc 〈 1 × 10−2), -DQA1*0104 (19.93% vs. 9.40%, Pc 〈 1 × 10−3), -DQA1*0201 (22.40% vs. 10.74%, Pc 〈 1 × 10−3), -DQB1*0303 (18.12% vs. 9.73%, Pc 〈 1 × 10−7), and -DRB1*0701/02 (26.09% vs. 9.73%, Pc 〈 1 × 10−7) were significantly increased in PV patients, while HLA-B*57, -DQB1*0201 were slightly increased in PV patients. HLA-Cw*0304 (5.07% vs. 14.43%, Pc 〈 1 × 10−3), -DQA1*0501 (5.79% vs. 14.09%, Pc 〈 0.05) were found to be negatively associated with PV, but HLA-A*2 (2.54% vs. 6.38%, Pc 〈 0.5) was decreased in PV patients without statistical significance. (ii) HLA-A*26-B*27 [P 〈 0.0001, odds ratio (OR) = 48.38], -A*26-Cw*0602 (P 〈 0.0001, OR = 11.84), -B*27-Cw*0602 (P 〈 0.0001, OR = undefined), -DRB1*0701/02-B*27 (P 〈 0.0001, OR = 22.62), -DRB1*0701/02-DQA1*0104 (P 〈 0.0002, OR = 3.59), -DRB1*0701/02-DQB1*0303 (P 〈 0.0001, OR = 5.63), -DQA1*0201-DQB1*0303 (P 〈 0.0002, OR = 7.77), -A*26-B*27-Cw*0602 (P 〈 0.0004, OR = undefined), -A*26-DRB1*0701/02-DQA1*0201-DQB1*0303 (P 〈 0.01, OR = undefined) were identified as risk haplotypes for patients with PV in China. (iii) HLA-A*26 -B*27 (P 〈 0.0001, OR = 58.47), -DQA1*0201-DQB1*0303 (P 〈 0.0001, OR = 8.62), -DRB1*0701/02 -DQA1*0104 (P 〈 0.0002, OR = 4.13), -DRB1*0701/02-DQB1*0303 (P 〈 0.0001, OR = 6.68) and -A*26-DRB1*0701-DQA1*0201 -DQB1*0303 (P 〈 0.006, OR = undefined) were only significantly associated with type I psoriasis compared with controls, while others showed no differences in either type I or type II psoriasis. (iv) These associated haplotypes with PV were not different by sex, except that the frequency of DRB1*0701/02-DQB1*0303 (P 〈 0.0001, OR = 10.14) was higher in male patients with psoriasis. To summarize, this study demonstrated a differential association of HLA and identified some special risk haplotypes in Chinese patients with PV compared with other ethnic or racial populations.

Notes: Summary Dystrophic epidermolysis bullosa (DEB) is caused by mutations in the COL7A1 gene encoding type VII collagen, the major component of anchoring fibrils. The characteristic genetic lesion in dominant DEB (DDEB) is a glycine substitution in the collagenous domain of the protein. In this study, we identified a Chinese family with a four-generation pedigree of DDEB, in whom a novel glycine substitution mutation in COL7A1 was demonstrated. A heterozygous nucleotide G→A transition at position 6208 in exon 74 of COL7A1 was detected, which resulted in a glycine to arginine substitution (G2070R) in the triple-helical domain of type VII collagen. This substitution was not found in 110 unrelated normal alleles. This report emphasizes the predominance of glycine substitution mutations in DDEB and contributes to the expanding database on COL7A1 mutations.

Notes: We present a physical model to calculate the direct tunneling hole current through ultrathin gate oxides from the inversion layer of metal–oxide–semiconductor field-effect transistors. A parametric self-consistency method utilizing the triangular well approximation is used for the electrostatics of the inversion layer. For hole quantization in the inversion layer, an improved one-band effective mass approximation, which is a good approximation to the rigorous six-band effective mass theory, is used to account for the band-mixing effect. The tunneling probability is calculated by a modified Wentzel–Kramers–Brilliouin (WKB) approximation, which takes the reflections near the Si/SiO2 interfaces into account. It is found that the parabolic dispersion in the SiO2 band gap used in the WKB approximation is only applicable for hole tunneling in oxides thinner than about 2 nm and for low gate voltage. A more reasonable Freeman–Dahlke hole dispersion form with significantly improved fitting to all experimental data for different oxide thickness and gate voltage range is adopted and discussed. © 2002 American Institute of Physics.

Notes: Dysregulated stimulation of microglia, the resident macrophages in the brain, can lead to excessive induction of inflammatory agents and subsequently damage to neurons. Fibrillar β-amyloid peptide (fAβ), a major component of senile plaques in Alzheimer's disease (AD) brain, is known to induce microglial-mediated neurotoxicity under certain conditions. Microglial ‘priming’ by macrophage colony stimulatory factor (MCSF) or interferon-gamma (IFNγ) appears to be required for this fAβ-induced microglia mediated neurotoxicity in vitro. We report here that while both MCSF and IFNγ induce microglial-mediated fAβ neurotoxicity, their mechanisms of toxicity differ. The enhancement of neurotoxicity by IFNγ or MCSF is not due to enhanced Aβ ingestion by microglia or to the direct effect of proinflammatory cytokine production. The neurotoxicity resulting from IFNγ/fAβ treatment was blocked by pretreatment with nitric oxide synthase inhibitor l-N-5-(1-iminoethyl) ornithine hydrochloride (l-NIO), consistent with a role for nitric oxide in the IFNγ-mediated toxicity mechanism. In contrast, no induction of nitric oxide production was detected for microglia treated with MCSF/fAβ. Furthermore, inhibiting the generation of reactive oxygen species (ROS) using the specific NADPH oxidase inhibitor apocynin reversed fAβ/MCSF-induced neurotoxicity while l-NIO had little effect. As MCSF is endogenously expressed within the brain, and both its level and that of the MCSF receptor are dramatically increased in the AD brain, the neurotoxicity resulting from ROS release by fAβ/MCSF coactivated microglia may be a more appropriate model for assessing fAβ-induced microglial-mediated neuropathology in AD.

Notes: High-resolution x-ray photoelectron spectroscopy (XPS) was applied to characterize the electronic structures for a series of high-k materials (HfO2)x(Al2O3)1−x grown on (100) Si substrate with different HfO2 mole fraction x. Al 2p, Hf 4f, O 1s core levels spectra, valence band spectra, and O 1s energy loss all show continuous changes with x in (HfO2)x(Al2O3)1−x. These data are used to estimate the energy gap (Eg) for (HfO2)x(Al2O3)1−x, the valence band offset (ΔEν) and the conduction band offset (ΔEc) between (HfO2)x(Al2O3)1−x and the (100) Si substrate. Our XPS results demonstrate that the values of Eg, ΔEν, and ΔEc for (HfO2)x(Al2O3)1−x change linearly with x. © 2002 American Institute of Physics.

Notes: Ta/Ni81Fe19 and Ni81Fe19/Ta structures are commonly used in the magnetic multilayers with giant magnetoresistance. For a Ta/Ni81Fe19/Ta fundamental structure, Ta seed and Ta cap layers resulted in a loss of moment equivalent to a magnetically dead layer of thickness 1.6±0.2 nm. In order to find out the reason, the composition and chemical states at the interface regions of Ta/Ni81Fe19 and Ni81Fe19/Ta were studied using the x-ray photoelectron spectroscopy and peak decomposition technique. The results show that there are thermodynamically favorable reactions at the Ta/Ni81Fe19 and Ni81Fe19/Ta interfaces: 2Ta+Ni=NiTa2. However, the thickness of a magnetically dead layer was significantly reduced by the insertion of a small amount of Bi in the Ta/Ni81Fe19/Ta structure. This result indicates that a surfactant Bi can suppress the interface reaction in multilayers. © 2002 American Institute of Physics.