The impact of water on slip system activity in olivine and the formation of bimodal crystallographic preferred orientations

Crystallographic preferred orientations (CPOs) in olivine are widely used to infer the mechanisms, conditions, and kinematics of deformation of mantle rocks. Recent experiments on water-saturated olivine were the first to produce a complex CPO characterised by bimodal orientation distributions of both [100] and [001] axes and inferred to form by combined activity of (001)[100], (100)[001], and (010)[100] slip. This result potentially provides a new microstructural indicator of deformation in the presence of elevated concentrations of intracrystalline hydrous point defects and has implications for the interpretation of seismic anisotropy. Here, we document a previously unexplained natural example of this CPO type in a xenolith from Lesotho and demonstrate that it too may be explained by elevated concentrations of hydrous point defects. We test and confirm the hypothesis that combined (001)[100], (100)[001], and (010)[100] slip were responsible for formation of this CPO by (1) using high-angular resolution electron backscatter diffraction to precisely characterise the dislocation types present in both the experimental and natural samples and (2) employing visco-plastic self-consistent simulations of CPO evolution to assess the ability of these slip systems to generate the observed CPO. Finally, we utilise calculations based on effective-medium theory to predict the anisotropy of seismic wave velocities arising from the CPO of the xenolith. Maxima in S-wave velocities and anisotropy are parallel to both the shear direction and shear plane normal, whereas maxima in P-wave velocities are oblique to both, adding complexity to interpretation of deformation kinematics from seismic anisotropy.D. Wallis, L.N. Hansen, and A.J. Wilkinson acknowledge support from the Natural Environment Research Council Grant NE/M000966/1. M. Tasaka acknowledges support through a JSPS Research Fellowship for Young Scientists (26-4879) and the Japan Society for the Promotion of Science (16K17832). D.L. Kohlstedt acknowledges support through NASA Grant NNX15AL53G. K.M. Kumamoto acknowledges support through NSF Division of Earth Science grants 1255620 and 1625032

Export of functional Streptomyces coelicolor alditol oxidase to the periplasm or cell surface of Escherichia coli and its application in whole-cell biocatalysis

Streptomyces coelicolor A3(2) alditol oxidase (AldO) is a soluble monomeric flavoprotein in which the flavin cofactor is covalently linked to the polypeptide chain. AldO displays high reactivity towards different polyols such as xylitol and sorbitol. These characteristics make AldO industrially relevant, but full biotechnological exploitation of this enzyme is at present restricted by laborious and costly purification steps. To eliminate the need for enzyme purification, this study describes a whole-cell AldO biocatalyst system. To this end, we have directed AldO to the periplasm or cell surface of Escherichia coli. For periplasmic export, AldO was fused to endogenous E. coli signal sequences known to direct their passenger proteins into the SecB, signal recognition particle (SRP), or Twin-arginine translocation (Tat) pathway. In addition, AldO was fused to an ice nucleation protein (INP)-based anchoring motif for surface display. The results show that Tat-exported AldO and INP-surface-displayed AldO are active. The Tat-based system was successfully employed in converting xylitol by whole cells, whereas the use of the INP-based system was most likely restricted by lipopolysaccharide LPS in wild-type cells. It is anticipated that these whole-cell systems will be a valuable tool for further biological and industrial exploitation of AldO and other cofactor-containing enzymes.

Expression of RECK and matrix metalloproteinase-2 in ameloblastoma

<p>Abstract</p> <p>Background</p> <p>Ameloblastoma is a frequent odontogenic benign tumor characterized by local invasiveness, high risk of recurrence and occasional metastasis and malignant transformation. Matrix metalloproteinase-2 (MMP-2) promotes tumor invasion and progression by destroying the extracellular matrix (ECM) and basement membrane. For this proteolytic activity, the endogenous inhibitor is reversion-inducing cysteine rich protein with Kazal motifs (RECK). The aim of this study was to characterize the relationship between RECK and MMP-2 expression and the clinical manifestation of ameloblastoma.</p> <p>Methods</p> <p>Immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) were employed to detect the protein and mRNA expression of RECK and MMP-2 in keratocystic odontogenic tumor (KCOT), ameloblastoma and ameloblastic carcinoma.</p> <p>Results</p> <p>RECK protein expression was significantly reduced in KCOT (87.5%), ameloblastoma (56.5%) and ameloblastic carcinoma (0%) (P < 0.01), and was significantly lower in recurrent ameloblastoma compared with primary ameloblastoma (P < 0.01), but did not differ by histological type of ameloblastoma. MMP-2 protein expression was significantly higher in ameloblastoma and ameloblastic carcinoma compared with KCOT (P < 0.01). RECK mRNA expression was significantly lower in ameloblastoma than in KCOT (P < 0.01), lower in recurrent ameloblastoma than in primary ameloblastoma, and was negative in ameloblastic carcinoma. MMP-2 mRNA expression was significantly higher in ameloblastoma compared with KCOT (P < 0.01), but was no different in recurrent ameloblastoma versus primary ameloblastoma. RECK protein expression was negatively associated with MMP-2 protein expression in ameloblastoma (r = -0.431, P < 0.01).</p> <p>Conclusion</p> <p>Low or no RECK expression and increased MMP-2 expression may be associated with negative clinical findings in ameloblastoma. RECK may participate in the invasion, recurrence and malignant transformation of ameloblastoma by regulating MMP-2 at the post-transcriptional level.</p

Dependence of CMI Growth Rates on Electron Velocity Distributions and Perturbation by Solitary Waves

We calculate growth rates and corresponding gains for RX and LO mode radiation associated with the cyclotron maser instability for parameterized horseshoe electron velocity distributions. The velocity distribution function was modeled to closely fit the electron distribution functions observed in the auroral cavity. We systematically varied the model parameters as well as the propagation direction to study the dependence of growth rates on model parameters. The growth rate depends strongly on loss cone opening angle, which must be less than $90^{o}$ for significant CMI growth. The growth rate is sharply peaked for perpendicular radiation ($k_{\parallel} = 0$), with a full-width at half-maximum $1.7^{o}$, in good agreement with observed k-vector orientations and numerical simulations. The fractional bandwidth varied between 10$^{-4}$ and 10$^{-2}$, depending most strongly on propagation direction. This range encompasses nearly all observed fractional AKR burst bandwidths. We find excellent agreement between the computed RX mode emergent intensities and observed AKR intensities assuming convective growth length $L_c\approx$20-40 km and group speed 0.15$c$. The only computed LO mode growth rates compatible observed LO mode radiation levels occurred for number densities more than 100 times the average energetic electron densities measured in auroral cavities. This implies that LO mode radiation is not produced directly by the CMI mechanism but more likely results from mode conversion of RX mode radiation. We find that perturbation of the model velocity distribution by large ion solitary waves (ion holes) can enhance the growth rate by a factor of 2-4. This will result in a gain enhancement more than 40 dB depending on the convective growth length within the structure. Similar enhancements may be caused by EMIC waves.Comment: 21 pages, 11 figures. J. Geophys. Res. 2007 (accepted

Asteroseismology of red giants & galactic archaeology

Red-giant stars are low- to intermediate-mass ($M \lesssim 10$~M$_{\odot}$) stars that have exhausted hydrogen in the core. These extended, cool and hence red stars are key targets for stellar evolution studies as well as galactic studies for several reasons: a) many stars go through a red-giant phase; b) red giants are intrinsically bright; c) large stellar internal structure changes as well as changes in surface chemical abundances take place over relatively short time; d) red-giant stars exhibit global intrinsic oscillations. Due to their large number and intrinsic brightness it is possible to observe many of these stars up to large distances. Furthermore, the global intrinsic oscillations provide a means to discern red-giant stars in the pre-helium core burning from the ones in the helium core burning phase and provide an estimate of stellar ages, a key ingredient for galactic studies. In this lecture I will first discuss some physical phenomena that play a role in red-giant stars and several phases of red-giant evolution. Then, I will provide some details about asteroseismology -- the study of the internal structure of stars through their intrinsic oscillations -- of red-giant stars. I will conclude by discussing galactic archaeology -- the study of the formation and evolution of the Milky Way by reconstructing its past from its current constituents -- and the role red-giant stars can play in that.Comment: Lecture presented at the IVth Azores International Advanced School in Space Sciences on "Asteroseismology and Exoplanets: Listening to the Stars and Searching for New Worlds" (arXiv:1709.00645), which took place in Horta, Azores Islands, Portugal in July 201

Hsp90 governs dispersion and drug resistance of fungal biofilms

Fungal biofilms are a major cause of human mortality and are recalcitrant to most treatments due to intrinsic drug resistance. These complex communities of multiple cell types form on indwelling medical devices and their eradication often requires surgical removal of infected devices. Here we implicate the molecular chaperone Hsp90 as a key regulator of biofilm dispersion and drug resistance. We previously established that in the leading human fungal pathogen, Candida albicans, Hsp90 enables the emergence and maintenance of drug resistance in planktonic conditions by stabilizing the protein phosphatase calcineurin and MAPK Mkc1. Hsp90 also regulates temperature-dependent C. albicans morphogenesis through repression of cAMP-PKA signalling. Here we demonstrate that genetic depletion of Hsp90 reduced C. albicans biofilm growth and maturation in vitro and impaired dispersal of biofilm cells. Further, compromising Hsp90 function in vitro abrogated resistance of C. albicans biofilms to the most widely deployed class of antifungal drugs, the azoles. Depletion of Hsp90 led to reduction of calcineurin and Mkc1 in planktonic but not biofilm conditions, suggesting that Hsp90 regulates drug resistance through different mechanisms in these distinct cellular states. Reduction of Hsp90 levels led to a marked decrease in matrix glucan levels, providing a compelling mechanism through which Hsp90 might regulate biofilm azole resistance. Impairment of Hsp90 function genetically or pharmacologically transformed fluconazole from ineffectual to highly effective in eradicating biofilms in a rat venous catheter infection model. Finally, inhibition of Hsp90 reduced resistance of biofilms of the most lethal mould, Aspergillus fumigatus, to the newest class of antifungals to reach the clinic, the echinocandins. Thus, we establish a novel mechanism regulating biofilm drug resistance and dispersion and that targeting Hsp90 provides a much-needed strategy for improving clinical outcome in the treatment of biofilm infections

Metastatic colorectal cancer to a primary thyroid cancer

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