We report on the first measurement of the F_{2} structure function of the neutron from the semi-inclusive scattering of electrons from deuterium, with low-momentum protons detected in the backward hemisphere. Restricting the momentum of the spectator protons to ≲100  MeV/c and their angles to ≳100° relative to the momentum transfer allows an interpretation of the process in terms of scattering from nearly on-shell neutrons. The F_{2}^{n} data collected cover the nucleon-resonance and deep-inelastic regions over a wide range of Bjorken x for 0.65<Q^{2}<4.52  GeV^{2}, with uncertainties from nuclear corrections estimated to be less than a few percent. These measurements provide the first determination of the neutron to proton structure function ratio F_{2}^{n}/F_{2}^{p} at 0.2≲x≲0.8 with little uncertainty due to nuclear effects.

OBJECTIVES: Sox2 is a major transcription factor and the transforming growth factor-α (TGF-α)/EGFR autocrine loop is a hallmark of prostate cancer progression. In this study, we have evaluated the effects and potential mechanisms of Sox2 on cell proliferation and apoptosis, and investigated effects of TGF-α on expression of Sox2 on androgen-independent human prostate cancer cells. MATERIALS AND METHODS: Expression of Sox2 has been determined by RT-PCR, western blot analysis and immunocytochemistry, using RNAi and over-expression strategy to study functions of Sox2 in DU145 and PC-3 cells. Changes in level of proliferation, cell cycle and apoptosis profiles were measured by MTT, colony-forming, bromodeoxyuridine incorporation assays, cell cycle and annexin V analysis. RESULTS: Sox2 was expressed in six human prostate cancer cell lines, and its inhibition reduced cell proliferation and induced apoptosis in DU145 cells. We have shown that knock-down of Sox2 inhibited G(1) to S phase transition concomitantly with down-regulation of cyclin E and up-regulation of p27 proteins. Conversely, over-expression of Sox2 led to the opposite effect in PC-3 cells but its inhibition induced apoptosis by down-regulation of survivin in DU145 cells. We also found that TGF-α up-regulated Sox2 and survivin protein expression via the EGFR/PI3K/AKT pathway. CONCLUSIONS: Sox2 expression is necessary for cell proliferation and evasion of apoptosis in prostate cancer cells and TGF-α could regulate Sox2 and survivin expression by activating the EGFR/PI3K/AKT pathway.

The parity-violating cross-section asymmetry in the elastic scattering of polarized electrons from unpolarized protons has been measured at a four-momentum transfer squared Q^{2}=0.624  GeV^{2} and beam energy E_{b}=3.48  GeV to be A_{PV}=-23.80±0.78(stat)±0.36(syst) parts per million. This result is consistent with zero contribution of strange quarks to the combination of electric and magnetic form factors G_{E}^{s}+0.517G_{M}^{s}=0.003±0.010(stat)±0.004(syst)±0.009(ff), where the third error is due to the limits of precision on the electromagnetic form factors and radiative corrections. With this measurement, the world data on strange contributions to nucleon form factors are seen to be consistent with zero and not more than a few percent of the proton form factors.

AIM Aim of this study was to evaluate the clinical efficacy of three-dimensional contrast-enhanced magnetic resonance angiography (3D CE-MRA); at 3.0T scanner in the classification of peripheral arterial occlusive disease (PAOD). METHODS Thirty-five patients diagnosed of PAOD underwent 3D CE-MRA, 30 cases underwent digital subtracted angiography (DSA) successfully, and 12 cases underwent surgery. RESULTS The vascular tree from the distal aorta to the lower limbs was well demonstrated. The extent and grade of disease seen in 3D CE-MRA closely matched those seen in DSA and/or surgery. Compared to the results of DSA and/or surgery, the common coincidence of 3D CE-MRA in diagnosing PAOD was 96.89%(780/805), the coincidence in diagnosing mild, moderate, severe stenosis and occlusion was 90.48%(76/84), 87.14%(61/70), 95.77%(68/71), and 98.29%(115/117) respectively, the rate of overestimate in mild, moderate, and severe stenosis was 5.95%(5/84), 10%(7/70), and 2.82%(2/71) respectively, the rate of underestimate in mild, moderate, severe stenosis and occlusion was 3.57%(3/84), 2.86%(2/70), 1.41%(1/71) and 1.74%(2/115) respectively. CONCLUSION 3D CE-MRA at 3.0T scanner is of great value in the accurate assessment of the classification of PAOD; it is a reliable and promising new technique.

Real time protein signaling in a complex medium may provide a promising way for high-throughput protein analysis, but it is largely unmet due to the challenge of signal transduction and the interferences of nonspecific binding and high background. Our recent work indicates that a fluorescent aptamer can display a protein binding-induced reduction of fluorescence anisotropy (FA)(Zhang, D.; Lu, M.; Wang, H. J. Am. Chem. Soc.2011, 133, 9188-9191), which is exclusively different from a traditionally simplified concept hinting a molecular size increase-induced FA increase. Inspired by this unexpected observation, we describe a novel FA reduction approach for protein signaling. The feasibility of this approach is demonstrated through the assays of a blood protein human α-thrombin and an oncoprotein human platelet-derived growth factor B-chain (PDGF-BB) using two screened fluorescent aptamers, respectively. By the developed FA reduction method, the spiked human α-thrombin in diluted serum can be detected at the concentration as low as 250 pM. In contrast, in a traditional molecular size-dependent FA assay, the thrombin spiked in diluted serum cannot induce reliable FA change even at a 256-fold higher concentration (64 nM). The results clearly show that the FA reduction approach has a dramatically enhanced specificity against target protein and high sensitivity in complex medium and is applicable to the no-separation based detection of proteins in biological matrixes.

We report the first measurement of the double-spin asymmetry A_{LT} for charged pion electroproduction in semi-inclusive deep-inelastic electron scattering on a transversely polarized ^{3}He target. The kinematics focused on the valence quark region, 0.16<x<0.35 with 1.4<Q^{2}<2.7  GeV^{2}. The corresponding neutron A_{LT} asymmetries were extracted from the measured ^{3}He asymmetries and proton over ^{3}He cross section ratios using the effective polarization approximation. These new data probe the transverse momentum dependent parton distribution function g_{1T}^{q} and therefore provide access to quark spin-orbit correlations. Our results indicate a positive azimuthal asymmetry for π^{-} production on ^{3}He and the neutron, while our π^{+} asymmetries are consistent with zero.

Evidence from basic molecular biology has noted a critical role of GSK-3 in Alzheimer's disease (AD) pathogenesis such as beta-amyloid (Aβ) production and accumulation, the formation of neurofibrillary tangle (NFT), and neuronal degeneration. Aβ generation and deposition represents a key feature and is generated from APP by the sequential actions of two proteolytic enzymes: β-secretase and γ-secretase. GSK-3 could play a critical role in Aβ production via enhancing β-secretase activity. GSK-3 not only modulates APP processing in the process of Aβ generation, but regulates Aβ production by interfering with APP cleavage at the γ-secretase complex step since the APP and PS1 (a component of γ-secretase complex) are substrates of GSK-3 as well. GSK-3 may downregulate α-secretase through PKC and ADAMs which are the substrates of GSK-3 contributing to Aβ production. Meanwhile, Aβ accumulation can induce GSK-3 activation through Aβ-mediated neuroinflammation and oxidative stress. Considering that active GSK-3 and some common GSK-3-shared factors induce the hyperphosphorylation of tau and neurofibrillary lesions, GSK-3 is a possible linking between amyloid plaques and NFT pathology. Additionally, GSK-3 could disrupt acetylcholine activity, and accelerate axon degeneration and failures in axonal transport, and lead to cognitive impairment in AD. Preclinical and clinical studies have supported that GSK-3β inhibitors could be useful in the treatment of AD. Thus, an effective measure to inhibit GSK-3 activity may be a very attractive drug target in AD.

Nested PCR amplicons of ribosomal RNA genes have been used to identify individuals within assemblages of arbuscular mycorrhizal (AM) fungi in roots and to estimate their relative abundance. Microscopy has also been used to identify their relative abundance in roots, but only at low resolution, usually the genus level. We evaluated the robustness of using nested PCR amplicons of ribosomal RNA genes to estimate the relative abundance of undefined AM fungi in uniformly aged roots in comparison to visual estimates. The relative abundance of AM fungi was assessed as per cent root length colonised by morphotypes and relative sequence type abundance in clone libraries. Plants were grown in coastal soil to obtain assemblages of unknown AM fungi at two times (spring and autumn). Relative abundance of dominant genera of AM fungi in roots (Archaeospora and Glomus) based on an analysis of ribosomal RNA genes did not consistently correspond with relative abundance of morphotypes. This microscopic vs. molecular genetic comparison supports previous conclusions that there can be limitations in using nested PCR amplicons for quantifying the relative abundance of AM fungi in roots, with a sampling bias likely to be of significance. Both molecular genetic and morphological methods are used to estimate relative abundance of AM fungi as a precursor to understanding mycorrhizal function in field soils, but they are rarely verified using alternative approaches although this may be necessary.

A Gram-positive, obligately anaerobic, slender to flexible rod-shaped, and motile bacterium, strain SC/BZ-SP2T, was isolated from a mixed alkaline water and sediment of Soap Lake, Washington State, USA. Strain SC/BZ-SP2T formed salmon to pink, was alkaliphilic, and grew at pH35 7.5-10.5 with an optimum at pH 9.7. Growth occurred at temperatures of 8-40°C (optimum at 35-37°C) and at the total Na+ ions concentrations of 0.35-1.38 M (optimum at 0.44-0.69 M). This organism utilized L-arabinose, D-ribose, D-xylose, D-fructose, D-mannose, D-galactose, D-cellobiose, maltose, sucrose, trehalose, sorbitol, xylan, malate, and yeast extract as the carbon and energy sources. Best growth was observed with L-arabinose, D-cellobiose, maltose, and trehalose. Major fermentation products of beech wood xylan were propionate and acetate. The dominant fatty acids were iso-C15:0, anteiso-C15:0, iso-C17:0 3OH, C17:0 3OH and C15:0 3OH. Cell-wall sugars included ribose, xylose, galactose and glucose. Thiosulfate and sulfite could be reduced to sulfide. The genomic DNA G+C content of strain SC/BZ-SP2T was 39.5 ± 0.9 mol%. Phylogenetic analyses based on 16S rRNA gene sequence comparisons indicated that strain SC/BZ-SP2T belongs to the family Marinilabiaceae in the order Bacteroidales of the class Bacteroidia. The most closely related species were Alkaliflexus imshenetskii Z-7010T (91.8% 16S rRNA gene sequence similarity), Marinilabilia salmonicolor Cy s1T (91.0%) and Anaerophaga thermohalophila Fru22T (90.4%). On the basis of phenotypic, chemotaxonomic and phylogenetic features, strain SC/BZ-SP2T should be placed in family Marinilabiaceae as a novel genus and species. The name Alkalitalea saponilacus gen. nov. sp. nov. is proposed with SC/BZ-SP2T (=ATCC BAA-2172T =DSMZ 24412T) as the type strain.

The metabotropic glutamate receptor 5 (mGluR5) is closely relative to the proliferation, survival, and differentiation of neural progenitor cells (NPCs). This study primarily examined the mGluR5 expression of NPCs in subventricular zone (SVZ) and the effects of mGluR5 on neurogenesis to intracerebral hemorrhage (ICH) rat. The experiment was designated as the following:(1) The ICH model was established by collagenase infusion into the right striatum of the rats, and the brain tissue was collected to assess the expression of mGluR5 in SVZ NPCs.(2) The rat brains were sampled for immunostaining of doublecortin (DCX) and 5-bromo-2'-deoxyuridine (BrdU) to examine the effects of the (R,S)-2-chloro-5-hydroxyphenylglycine (CHPG) on neurogenesis.(3) Behavioral testing was carried out to evaluate the effects of CHPG on neurofunctional recovery. The results of Western blot analysis showed that mGluR5 levels in the ipsilateral SVZ increased as early as at 3 days after ICH, peaked at 14 days. The change of mGluR5 mRNA level in the ipsilateral SVZ was generally similar to the pattern of Western blot analysis. The immunostaining also demonstrated that some nestin-positive cells were co-expressed with mGluR5. The injection of CHPG into ipsilateral ventricle increased DCX levels both in the ipsilateral striatum (STR) and the peri-lesion area of the striatum (PLA). Meanwhile, a significant difference in behavioral score was presented at 28 days after ICH between the CHPG-treated rats and the vehicle-treated or the non-treated rats. Our results demonstrated for the first time that the increased expression of mGluR5 in SVZ NPCs occurred in ICH rat. The CHPG promoted the neurogenesis and improved neurofunctional symptom induced by ICH. These results suggested that the increased expression of mGluR5 on NPCs in SVZ may play an important role in neurogenesis in ICH rat.