Prolonged cardiac xenograft survival in guinea pig-to-rat model by a highly active cobra venom factor

A highly active cobra venom factor (CVF) was isolated from the venom of Naja kaouthia by sequential column chromatography. It displays strong anticomplementary activity, and has 1515 U of anti complementary activity per mg protein. A single dose of 0.1 mg/kg CVF given i.v. to rats completely abrogated complement activity for nearly 5 days. Given 0.02 mg/kg of CVF. the complement activity of rats was reduced by more than 96.5% in 6 It. In guinea pig-to-rat heart transplant model, rats treated with a single dose of 0.05 mg/kg CVF had significantly prolonged xenograft survival (56.12 +/- 6.27 h in CVF-treated rats vs. 0.19 +/- 0.07 h in control rats, P < 0.001). (C) 2003 Elsevier Ltd. All rights reserved.

Model reductions for inference: generality of pairwise, binary, and planar factor graphs.

We offer a solution to the problem of efficiently translating algorithms between different types of discrete statistical model. We investigate the expressive power of three classes of model-those with binary variables, with pairwise factors, and with planar topology-as well as their four intersections. We formalize a notion of "simple reduction" for the problem of inferring marginal probabilities and consider whether it is possible to "simply reduce" marginal inference from general discrete factor graphs to factor graphs in each of these seven subclasses. We characterize the reducibility of each class, showing in particular that the class of binary pairwise factor graphs is able to simply reduce only positive models. We also exhibit a continuous "spectral reduction" based on polynomial interpolation, which overcomes this limitation. Experiments assess the performance of standard approximate inference algorithms on the outputs of our reductions.

Characterization of vertical Mo/diamond Schottky barrier diode from non-ideal I-V and C-V measurements based on MIS model

In this study, we investigated non-ideal characteristics of a diamond Schottky barrier diode with Molybdenum (Mo) Schottky metal fabricated by Microwave Plasma Chemical Vapour Deposition (MPCVD) technique. Extraction from forward bias I-V and reverse bias C- 2-V measurements yields ideality factor of 1.3, Schottky barrier height of 1.872 eV, and on-resistance of 32.63 mö·cm2. The deviation of extracted Schottky barrier height from an ideal value of 2.24 eV (considering Mo workfunction of 4.53 eV) indicates Fermi level pinning at the interface. We attributed such non-ideal behavior to the existence of thin interfacial layer and interface states between metal and diamond which forms Metal-Interfacial layer-Semiconductor (MIS) structure. Oxygen surface treatment during fabrication process might have induced them. From forward bias C-V characteristics, the minimum thickness of the interfacial layer is approximately 0.248 nm. Energy distribution profile of the interface state density is then evaluated from the forward bias I-V characteristics based on the MIS model. The interface state density is found to be uniformly distributed with values around 1013 eV - 1·cm- 2. © 2013 Elsevier B.V.

Temperature dependence of effective g factor in diluted magnetic semiconductor (Ga,Mn)As

Time resolved magneto-optic Kerr rotation measurements of optically induced spin quantum beats are performed on heavily doped bulk (Ga,Mn)As diluted magnetic semiconductors (DMS). An effective g-factor of about 0.2-0.3 over a wide range of temperature for both as-grown and annealed (Ga,Mn)As samples is obtained. A larger effective g-factor at lower temperature and an increase of the spin relaxation with increasing in-plane magnetic field are observed and attributed to the stronger p-d exchange interaction between holes and the localized magnetic ion spins, leading to a larger Zeeman splitting and heavy-hole-light-hole mixing. An abnormal dip structure of the g-factor in the vicinity of the Curie temperature suggests that the mean-field model is insufficient to describe the interactions and dynamics of spins in DMS because it neglects the short-range spin correlation effect. (c) 2008 American Institute of Physics.

公用陆面模式（Community Land Model 3.0）简介

IEECAS SKLLQG

Topological structure of the solitons solution in SU(3) Dunne-Jackiw-Pi-Trugenberger model

By using phi-mapping topological current theory and gauge potential decomposition, we discuss the self-dual equation and its solution in the SU(N) Dunne-Jackiw-Pi-Trugenberger model and obtain a new concrete self-dual equation with a 6 function. For the SU(3) case, we obtain a new self-duality solution and find the relationship between the soliton solution and topological number which is determined by the Hopf index and Brouwer degree of phi-mapping. In our solution, the flux of this soliton is naturally quantized.

Elastic Scattering of He-6 + p at 82.3 MeV/nucleon

Differential cross sections for the elastic scattering of halo nucleus He-6 on proton target were measured at 82.3 MeV/u. The experimental results are well reproduced by optical model calculations using global potential KD02 with a reduction of the depth of real volume part by a factor of 0.7. A systematic analysis shows that this behavior might be related to the weakly bound property of unstable nuclei.

STATISTICAL THERMODYNAMICS IN THE FRAMEWORK OF THE LATTICE FLUID MODEL .3. BINARY MIXTURE OF POLYDISPERSE POLYMERS OF SPECIAL DISTRIBUTION WITH STRONG-INTERACTIONS

For a binary mixture of polydisperse polymers with strong interactions, the free energy, the equation of state, the chemical potentials and the spinodal are formulated on the basis of the lattice fluid model. Further, the spinodal curves for the system wi

The effect of concentration and duration of normobaric oxygen in reducing caspase-3 and -9 expression in a rat-model of focal cerebral ischaemia.

The aim of this study was to determine the effect of different concentrations of normobaric oxygen (NBO) on neurological function and the expression of caspase-3 and -9 in a rat model of acute cerebral ischaemia. Sprague-Dawley rats (n=120) were randomly divided into four groups (n=30 per group), including 3 groups given NBO at concentrations of 33%, 45% or 61% and one control group given air (21% oxygen). After 2 h of ischaemic occlusion, each group was further subdivided into six subgroups (n=5) during reperfusion according to the duration (3, 6, 12, 24, 48 or 72 h) and concentration of NBO (33%, 45% or 61%) or air treatment. The Fluorescence Quantitative polymerase chain reaction (PCR) and immunohistochemistry were used to detect caspase-3 and -9 mRNA and protein relative expression respectively. The Neurologic Impairment Score (NIS) was significantly lower in rats given 61% NBO ≥3 h after reperfusion when compared to the control group (P<0.05, Mann–Whitney U). NBO significantly reduced caspase-3 and -9 mRNA and protein expression when compared to the control group at all NBO concentrations and time points (P<0.05, ANOVA). The expression of caspase-3 and -9 was lower in the group given 61% NBO compared any other group, and this difference was statistically significant when compared to the group given 33% NBO for ≥48 h and the control group (both P<0.05, ANOVA). These findings indicate that NBO may inhibit the apoptotic pathway by reducing caspase-3 and -9 expression, thereby promoting neurological functional recovery after stroke.

The development of entrepreneurial culture in a transition economy: an empirical model discussion.

This conceptual paper will focus on the presentation of the model developed from empirical, qualitative research covering 20 years of analysis on the relationship between culture and entrepreneurship in Poland. It is aimed at proposing a comprehensive framework that describes the development of entrepreneurial culture. In this empirical model culture is understood as a set of values and beliefs held by a social group that endorse and are conducive to entrepreneurial behaviour; while entrepreneurial behaviour is treated as an expected outcome and narrowed down to opening the company. The model proves that the differentiation between entrepreneurship (behaviour) and entrepreneurs (who demonstrate this behaviour) needs to be recognised in future research. The case of Poland offers a historical example, which can shed more light on the process of cultural change and the role of entrepreneurship and entrepreneurs in the development of entrepreneurial culture. In the case presented, the behaviour of entrepreneurs has been identified as the key factor leading to further development.

Model-based detection of spiculated lesions in mammograms

R. Zwiggelaar, T.C. Parr, J.E. Schumm. I.W. Hutt, S.M. Astley, C.J. Taylor and C.R.M. Boggis, 'Model-based detection of spiculated lesions in mammograms', Medical Image Analysis 3 (1), 39-62 (1999)

A role for LH in the regulation of expression of mRNAs encoding components of the insulin-like growth factor (IGF) system in the ovine corpus luteum

P.M. Hastie and W. Haresign (2006). A role for LH in the regulation of expression of mRNAs encoding components of the insulin-like growth factor (IGF) system in the ovine corpus luteum. Animal Reproduction Science, 96(1-2), 196-209. Sponsorship: DEFRA RAE2008

The role of glucocorticoid-induced tumour necrosis factor receptor in developing mouse sympathetic neurons

Hereditary sensory autonomic neuropathy IV (HSAN IV) is an autosomal recessive disorder characterised by inability to feel pain and anhidrosis and is a consequence of defective NGF/TrkA signalling and growth of sensory and sympathetic neurons. Glucocortiocoid-induced tumour necrosis factors receptor (GITR), a transmembrane protein, activated by its specific ligand, GITRL, is well known for its role in the regulation of innate and acquired immune system responses. Recently, GITR was found to be required for NGF-dependant and extracellular signal-related kinase 1/2 (ERK1/2)-induced neurite growth and target innervation in the developing sympathetic nervous system (SNS). Given this novel role of GITR, it is possible that strategies targeting GITR have potential therapeutic benefit in promoting neurite growth in autonomic neuropathies such as HSAN IV. Using P1 mouse SCG neurons as a model, in addition to various SCG cell treatments, knock down models and transfection methods, we investigated whether GITR increases the sensitivity of sympathetic neurons to NGF; the region of GITR required for the enhancement of NGF-promoted growth, the signalling pathways downstream of GITR and how extensively GITR is involved in regulating peripheral innervation of the SNS. Results indicate that the region responsible for the growth promoting effects of GITR lies in its juxtamembrane intracellular region (here termed the growth promoting domain (GPD)) of GITR. The GPD of GITR activates ERK1/2 and inhibits nuclear factor kappa B (NF-κB) in an inverse fashion to provide an optimal cellular growth environment for P1 SCG neurons. While deleting the GPD of GITR had no effect on TrkA expression, constitutive phosphorylation of specific sites in the GPD reduced TrkA expression indicating a possible role for GITR in increasing the sensitivity of SCG neurons to NGF by the regulation of these sites, TrkA expression and subsequent NGF/TrkA binding. GITR appears to be heterogeneously required for NGF-promoted target innervation of SCG neurons in some organs, implying additional factors are involved in extensive NGF-target innervation of the SNS. In conclusion, this study answers basic biological questions regarding the molecular mechanism behind the role of GITR in the development of the SNS, and provides a basis for future research if GITR modulation is to be developed as a strategy for promoting axonal growth.

Akt signal transduction dysfunction in the 3xTg-AD mouse model of Alzheimer's disease

Alzheimer’s disease (AD) is an incurable neurodegenerative disorder, accounting for over 60% of all cases of dementia. The primary risk factor for AD is age, however several genetic and environmental factors are also involved. The pathological characteristics of AD include extracellular deposition of the beta-amyloid peptide (Aβ) and intraneuronal accumulation of neurofibrillary tangles (NFTs) made of aggregated paired helical filaments (PHFs) of the hyperphosphorylated tau protein, along with synaptic loss and neuronal death. There are numerous biochemical mechanisms involved in AD pathogenesis, however the reigning hypothesis points to toxic oligomeric Aβ species as the primary causative factor in a cascade of events leading to neuronal stress and dyshomeostasis that initiate abnormal regulation of tau. The insulin and IGF-1 receptors (IR, IGF-1R) are the primary activators of PI3- K/Akt through which they regulate cell growth, development, glucose metabolism, and learning and memory. Work in our lab and others shows increased Akt activity and phosphorylation of its downstream targets in AD brain, along with insulin and insulin-like growth factor-1 signalling (IIS) dysfunction. This is supported by studies of AD models in vivo and in vitro. Our group and others hypothesise that Aβ activates Akt through IIS to initiate a negative feedback mechanism that desensitises neurons to insulin/IGF-1, and sustains activation of Akt. In this study the functions of endogenous Akt, IR, and the insulin receptor substrate (IRS-1) were examined in relationship to Aβ and tau pathology in the 3xTg-AD mouse model, which contains three mutant human transgenes associated with familial AD or dementia. The 3xTg-AD mouse develops Aβ and tau pathology in a spatiotemporal manner that best recapitulates the progression of AD in human brain. Western blotting and immunofluorescent microscopy techniques were utilised in vivo and in vitro, to examine the relationship between IIS, Akt, and AD pathology. I first characterised in detail AD pathology in 3xTg-AD mice, where an age-related accumulation of intraneuronal Aβ and tau was observed in the hippocampal formation, amygdala, and entorhinal cortex, and at late stages (18 months), extracellular amyloid plaques and NFTs, primarily in the subiculum and the CA1 layer of the hippocampal formation. Increased activity of Akt, detected with antibody to phosphoSer473-Akt, was increased in 3xTg-AD mice compared to age-matched non-transgenic mice (non-Tg), and in direct correlation to the accumulation of Aβ and tau in neuronal somatodendritic compartments. Akt phosphorylates tau at residue Ser214 within a highly specific consensus sequence for Akt phosphorylation, and phosphoSer214-tau strongly decreases microtubule (MT) stabilisation by preventing tau-MT binding. PhosphoSer214-tau increased concomitantly with this in the same age-related and region-specific fashion. Polarisation of tau phosphorylation was observed, where PHF-1 (tauSer396/404) and phosphoSer214-tau both appeared early in 3xTg-AD mice in distinct neuronal compartments: PHF-1 in axons, and phosphoSer214-tau in neuronal soma and dendrites. At 18 months, phosphoSer214-tau strongly colocalised with NFTs positive for the PHF- 1 and AT8 (tauSer202/Thr205) phosphoepitopes. IR was decreased with age in 3xTg-AD brain and in comparison to age-matched non-Tg, and this was specific for brain regions containing Aβ, tau, and hyperactive Akt. IRS-1 was similarly decreased, and both proteins showed altered subcellular distribution. Phosphorylation of IRS-1Ser312 is a strong indicator of IIS dysfunction and insulin resistance, and was increased in 3xTg-AD mice with age and in relation to pathology. Of particular note was our observation that abberant IIS and Akt signalling in 3xTg-AD brain related to Aβ and tau pathology on a gross anatomical level, and specifically localised to the brain regions and circuitry of the perforant path. Finally, I conducted a preliminary study of the effects of synthetic Aβ oligomers on embryonic rat hippocampus neuronal cultures to support these results and those in the literature. Taken together, these novel findings provide evidence for IIS and Akt signal transduction dysfunction as the missing link between Aβ and tau pathogenesis, and contribute to the overall understanding of the biochemical mechanisms of AD.