266 research outputs found

    Are the class 18 myosins Myo18A and Myo18B specialist sarcomeric proteins?

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    Initially, the two members of class 18 myosins, Myo18A and Myo18B, appeared to exhibit highly divergent functions, complicating the assignment of class-specific functions. However, the identification of a striated muscle-specific isoform of Myo18A, Myo18Aγ, suggests that class 18 myosins may have evolved to complement the functions of conventional class 2 myosins in sarcomeres. Indeed, both genes, Myo18a and Myo18b, are predominantly expressed in the heart and somites, precursors of skeletal muscle, of developing mouse embryos. Genetic deletion of either gene in mice is embryonic lethal and is associated with the disorganization of cardiac sarcomeres. Moreover, Myo18Aγ and Myo18B localize to sarcomeric A-bands, albeit the motor (head) domains of these unconventional myosins have been both deduced and biochemically demonstrated to exhibit negligible ATPase activity, a hallmark of motor proteins. Instead, Myo18Aγ and Myo18B presumably coassemble with thick filaments and provide structural integrity and/or internal resistance through interactions with F-actin and/or other proteins. In addition, Myo18Aγ and Myo18B may play distinct roles in the assembly of myofibrils, which may arise from actin stress fibers containing the α-isoform of Myo18A, Myo18Aα. The β-isoform of Myo18A, Myo18Aβ, is similar to Myo18Aα, except that it lacks the N-terminal extension, and may serve as a negative regulator through heterodimerization with either Myo18Aα or Myo18Aγ. In this review, we contend that Myo18Aγ and Myo18B are essential for myofibril structure and function in striated muscle cells, while α- and β-isoforms of Myo18A play diverse roles in nonmuscle cells

    Cortical cells are altered by factors including bone morphogenetic protein released from a placental barrier model under altered oxygenation

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    Episodes of hypoxia and hypoxia/reoxygenation during foetal development have been associated with increased risk of neurodevelopmental conditions presenting in later life. The mechanism for this is not understood; however, several authors have suggested that the placenta plays an important role. Previously we found both placentas from a maternal hypoxia model and pre-eclamptic placentas from patients release factors lead to a loss of dendrite complexity in rodent neurons. Here to further explore the nature and origin of these secretions we exposed a simple in vitro model of the placental barrier, consisting of a barrier of human cytotrophoblasts, to hypoxia or hypoxia/reoxygenation. We then exposed cortical cultures from embryonic rat brains to the conditioned media (CM) from below these exposed barriers and examined changes in cell morphology, number, and receptor presentation. The barriers released factors that reduced dendrite and astrocyte process lengths, decreased GABAB1 staining, and increased astrocyte number. The changes in astrocytes required the presence of neurons and were prevented by inhibition of the SMAD pathway and by neutralising Bone Morphogenetic Proteins (BMPs) 2/4. Barriers exposed to hypoxia/reoxygenation also released factors that reduced dendrite lengths but increased GABAB1 staining. Both oxygen changes caused barriers to release factors that decreased GluN1, GABAAα1 staining and increased GluN3a staining. We find that hypoxia in particular will elicit the release of factors that increase astrocyte number and decrease process length as well as causing changes in the intensity of glutamate and GABA receptor staining. There is some evidence that BMPs are released and contribute to these changes

    Metered Cryosprayâ„¢: a novel uniform, controlled, and consistent in vivo application of liquid nitrogen cryogenic spray

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    Typically, wood-based composite materials have been developed through empirical studies. In these products, the constituent wood elements have broad spectrums regarding species, size, and anatomical orientation relative to their own dimensions. To define special strength and stiffness properties during a long-term study, two types of corrugated wood composite panels were developed for possible structural utilization. The constitutional elements of the newly developed products included Appalachian hardwood veneer residues (side clippings) and/or rejected low quality, sliced veneer sheets. The proposed primary usage of these veneer-based panels is in applications where the edgewise loading may cause buckling (e.g., web elements of I-joists, shear-wall and composite beam core materials). This paper describes the development of flat and corrugated panels, including furnish preparations and laboratory-scale manufacturing processes as well as the determination of key mechanical properties. According to the results in parallel to grain direction bending, tension and compression strengths exceeded other structural panels’ similar characteristics, while the rigidities were comparable. Based on the research findings, sliced veneer clipping waste can be transformed into structural panels or used as reinforcement elements in beams and sandwich-type products

    Critical perspectives on ‘consumer involvement’ in health research: epistemological dissonance and the know-do gap

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    Researchers in the area of health and social care (both in Australia and internationally) are encouraged to involve consumers throughout the research process, often on ethical, political and methodological grounds, or simply as ‘good practice’. This paper presents findings from a qualitative study in the UK of researchers’ experiences and views of consumer involvement in health research. Two main themes are presented in the paper. Firstly, we explore the ‘know-do gap’ which relates to the tensions between researchers’ perceptions of the potential benefits of, and their actual practices in relation to, consumer involvement. Secondly, we focus on one of the reasons for this ‘know-do gap’, namely epistemological dissonance. Findings are linked to issues around consumerism in research, lay/professional knowledges, the (re)production of professional and consumer identities and the maintenance of boundaries between consumers and researchers

    The Unusual Infrared Object HDF-N J123656.3+621322

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    We describe an object in the Hubble Deep Field North with very unusual near-infrared properties. It is readily visible in Hubble Space Telescope NICMOS images at 1.6um and from the ground at 2.2um, but is undetected (with signal-to-noise <~ 2) in very deep WFPC2 and NICMOS data from 0.3 to 1.1um. The f_nu flux density drops by a factor >~ 8.3 (97.7% confidence) from 1.6 to 1.1um. The object is compact but may be slightly resolved in the NICMOS 1.6um image. In a low-resolution, near-infrared spectrogram, we find a possible emission line at 1.643um, but a reobservation at higher spectral resolution failed to confirm the line, leaving its reality in doubt. We consider various hypotheses for the nature of this object. Its colors are unlike those of known galactic stars, except perhaps the most extreme carbon stars or Mira variables with thick circumstellar dust shells. It does not appear to be possible to explain its spectral energy distribution as that of a normal galaxy at any redshift without additional opacity from either dust or intergalactic neutral hydrogen. The colors can be matched by those of a dusty galaxy at z >~ 2, by a maximally old elliptical galaxy at z >~ 3 (perhaps with some additional reddening), or by an object at z >~ 10 whose optical and 1.1um light have been suppressed by the intergalactic medium. Under the latter hypothesis, if the luminosity results from stars and not an AGN, the object would resemble a classical, unobscured protogalaxy, with a star formation rate >~ 100 M_sun/yr. Such UV-bright objects are evidently rare at 2 < z < 12.5, however, with a space density several hundred times lower than that of present-day L* galaxies.Comment: Accepted for publication in the Astrophysical Journal. 27 pages, LaTeX, with 7 figures (8 files); citations & references updated + minor format change
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