57 research outputs found
Comparative simulation study of colloidal gels and glasses
Using computer simulations, we identify the mechanisms causing aggregation
and structural arrest of colloidal suspensions interacting with a short-ranged
attraction at moderate and high densities. Two different non-ergodicity
transitions are observed. As the density is increased, a glass transition takes
place, driven by excluded volume effects. In contrast, at moderate densities,
gelation is approached as the strength of the attraction increases. At high
density and interaction strength, both transitions merge, and a logarithmic
decay in the correlation function is observed. All of these features are
correctly predicted by mode coupling theory
Higher order glass-transition singularities in colloidal systems with attractive interactions
The transition from a liquid to a glass in colloidal suspensions of particles
interacting through a hard core plus an attractive square-well potential is
studied within the mode-coupling-theory framework. When the width of the
attractive potential is much shorter than the hard-core diameter, a reentrant
behavior of the liquid-glass line, and a glass-glass-transition line are found
in the temperature-density plane of the model. For small well-width values, the
glass-glass-transition line terminates in a third order bifurcation point, i.e.
in a A_3 (cusp) singularity. On increasing the square-well width, the
glass-glass line disappears, giving rise to a fourth order A_4 (swallow-tail)
singularity at a critical well width. Close to the A_3 and A_4 singularities
the decay of the density correlators shows stretching of huge dynamical
windows, in particular logarithmic time dependence.Comment: 19 pages, 12 figures, Phys. Rev. E, in prin
Dynamic orifice area variations in functional mitral regurgitation: In vivoreproduction and mechanistic insights
Aims: The spinocerebellar ataxia type 2 (SCA2), type 3 (SCA3) and type 7 (SCA7) are clinically characterized by progressive and severe ataxic symptoms, dysarthria, dysphagia, oculomotor impairments, pyramidal and extrapyramidal manifestations and sensory deficits. Although recent clinical studies reported additional disease signs suggesting involvement of the brainstem auditory system, this has never been studied in detail in SCA2, SCA3 or SCA7. Methods: We performed a detailed pathoanatomical investigation of unconventionally thick tissue sections through the auditory brainstem nuclei (that is, nucleus of the inferior colliculus, nuclei of the lateral lemniscus, superior olive, cochlear nuclei) and auditory brainstem fibre tracts (that is, lateral lemniscus, trapezoid body, dorsal acoustic stria, cochlear portion of the vestibulocochlear nerve) of clinically diagnosed and genetically confirmed SCA2, SCA3 and SCA7 patients. Results: Examination of unconventionally thick serial brainstem sections stained for lipofuscin pigment and Nissl material revealed a consistent and widespread involvement of the auditory brainstem nuclei in the SCA2, SCA3 and SCA7 patients studied. Serial brainstem tissue sections stained for myelin showed loss of myelinated fibres in two of the auditory brainstem fibre tracts (that is, lateral lemniscus, trapezoid body) in a subset of patients. Conclusions: The involvement of the auditory brainstem system offers plausible explanations for the auditory impairments detected in some of our and other SCA2, SCA3 and SCA7 patients upon bedside examination or neurophysiological investigation. However, further clinical studies are required to resolve the striking discrepancy between the consistent involvement of the brainstem auditory system observed in this study and the comparatively low frequency of reported auditory impairments in SCA2, SCA3 and SCA7 patients
Nonergodicity transitions in colloidal suspensions with attractive interactions
The colloidal gel and glass transitions are investigated using the idealized
mode coupling theory (MCT) for model systems characterized by short-range
attractive interactions. Results are presented for the adhesive hard sphere and
hard core attractive Yukawa systems. According to MCT, the former system shows
a critical glass transition concentration that increases significantly with
introduction of a weak attraction. For the latter attractive Yukawa system, MCT
predicts low temperature nonergodic states that extend to the critical and
subcritical region. Several features of the MCT nonergodicity transition in
this system agree qualitatively with experimental observations on the colloidal
gel transition, suggesting that the gel transition is caused by a low
temperature extension of the glass transition. The range of the attraction is
shown to govern the way the glass transition line traverses the phase diagram
relative to the critical point, analogous to findings for the fluid-solid
freezing transition.Comment: 11 pages, 7 figures; to be published in Phys. Rev. E (1 May 1999
Agrobacterium-mediated transformation of sorghum: factors that affect transformation efficiency
B-NMR study of a buried Mn &-doped layer in a silicon host
Low temperature growth methods were used to encapsulate a buried Mn Âż-doping layer into a silicon host. A Âż-NMR investigation was performed of the magnetic properties in the temperature range 10-300 K using spin-polarized 8Li+. A depth-dependent broadening and shift of the NMR resonance was detected that is consistent with internal fields distributed at depths of 10-30 nm beneath the surface. At low temperatures, a negative relative shift occurred and the resonance was significantly broadened. At 300 K the line-shape could be described by a single Gaussian line, however, at 10 K the line is best approximated by a two component Lorentzian shape consisting of a broad and narrow component as anticipated for a diluted magnetic alloy. The overall magnitude of the resonance shift at both temperatures is small suggesting a weak interaction between the 8Li+ and the magnetic Mn environment
Huntington's disease (HD):the neuropathology of a multisystem neurodegenerative disorder of the human brain
Huntington's disease (HD) is an autosomal dominantly inherited, and currently untreatable, neuropsychiatric disorder. This progressive and ultimately fatal disease is named after the American physician George Huntington and according to the underlying molecular biological mechanisms is assigned to the human polyglutamine or CAG-repeat diseases. In the present article we give an overview of the currently known neurodegenerative hallmarks of the brains of HD patients. Subsequent to recent pathoanatomical studies the prevailing reductionistic concept of HD as a human neurodegenerative disease, which is primarily and more or less exclusively confined to the striatum (ie, caudate nucleus and putamen) has been abandoned. Many recent studies have improved our neuropathological knowledge of HD; many of the early groundbreaking findings of neuropathological HD research have been rediscovered and confirmed. The results of this investigation have led to the stepwise revision of the simplified pathoanatomical and pathophysiological HD concept and culminated in the implementation of the current concept of HD as a multisystem degenerative disease of the human brain. The multisystem character of the neuropathology of HD is emphasized by a brain distribution pattern of neurodegeneration (i) which apart from the striatum includes the cerebral neo-and allocortex, thalamus, pallidum, brainstem and cerebellum, and which (ii) therefore, shares more similarities with polyglutamine spinocerebellar ataxias than previously thought
Routine monitoring of sodium and phosphorus removal in peritoneal dialysis (PD) patients treated with continuous ambulatory PD (CAPD), automated PD (APD) or combined CAPD plus APD.
Background: Adequate removal of sodium (Na) and phosphorus (P) is of paramount importance for patients with dialysis-dependent kidney disease can easily quantified in peritoneal dialysis (PD) patients. Some studies suggest that automated PD (APD) results in lower Na and P removal. Methods. In this study we retrospectively analysed our data on Na and P removal in PD patients after implementation of a routine monitoring in 2011. Patients were stratified in those treated with continuous ambulatory PD (CAPD, n=24), automated PD (APD, n=23) and APD with one bag change (CAPD+APD, n=10). Until 2015 we collected time-varying data on Na and P removal from each patient (median 5 [interquartile range 4-8] values). Results: Peritoneal Na and P removal (mmol per 24h +/- standard deviation) was 102 +/- 48 and 8 +/- 2 in the CAPD, 90 +/- 46 and 9 +/- 3 in the APD and 126 +/- 39 and 13 +/- 2 in the CAPD+APD group (ANOVA P=0.141 and <0.001). Taking renal excretion into account total Na and P removal (mmol per 24h) was 221 +/- 65 and 16 +/- 5 in the CARD, 189 +/- 58 and 17 +/- 6 in the APD and 183 +/- 38 and 16 +/- 6 in the CAPD+APD group (P=0.107 and 0.764). Over time, peritoneal removal of Na but not that of P increased in all groups. In patients with modifications of PD treatment, Na but not P removal was significantly increased over-time. Conclusions: Overall Na and P removal were similar with different PD modalities. Individualized adjustments of PD prescription including icodextrin use or higher glucose concentration can improve Na removal while P removal is mainly determined by the dialysate volume
Different subcellular localization and trafficking properties of KNOX class 1 homeodomain proteins from rice
Genes of the KN1-like homeobox (KNOX) class 1 encode transcription factors involved in shoot apical meristem development and maintenance. We studied the subcellular localization of Green Fluorescent Protein-tagged rice KNOX proteins (Oskn1-3) after particle bombardment of onion and rice cells and after transformation of Arabidopsis and rice with constitutive and inducible expression constructs. In all test systems, the three rice KNOX proteins showed nuclear and cytoplasmic localization patterns. However, Oskn1 additionally showed in some cells a distribution over punctae moving randomly in the cytosol. Use of an inducible expression system indicated a nuclear presence of Oskn1 in cells of the shoot apical meristem and post-transcriptional down-regulation in early leaf primordia. Arabidopsis and rice test systems were used to study effects of plant hormones and auxin transport inhibition on KNOX protein localization. Application of GA3 or 1-NAA shifted protein localization completely to the cytoplasm and resulted in loss of the punctae formed by Oskn1. Conversely, NPA application induced a complete nuclear localization of the KNOX proteins. To study intercellular movement of the KNOX proteins we set up a novel co-bombardment assay in which trafficking of untagged KNOX proteins was visualized through the co-trafficking of green fluorescent or blue fluorescent marker proteins. In multiple independent experiment
Polyglutamine aggregation in Huntington's disease and spinocerebellar ataxia type 3: similar mechanisms in aggregate formation
AimsPolyglutamine (polyQ) diseases are characterized by the expansion of a polymorphic glutamine sequence in disease-specific proteins and exhibit aggregation of these proteins. This is combated by the cellular protein quality control (PQC) system, consisting of chaperone-mediated refolding as well as proteasomal and lysosomal degradation pathways. Our recent study in the polyQ disease spinocerebellar ataxia type 3 (SCA3) suggested a distinct pattern of protein aggregation and PQC dysregulation. MethodsTo corroborate these findings we have investigated immunohistochemically stained 5m sections from different brain areas of Huntington's disease (HD) and SCA3 patients. ResultsIrrespective of disease and brain region, we observed peri- and intranuclear polyQ protein aggregates. A subset of neurones with intranuclear inclusions bodies exhibited signs of proteasomal dysfunction, up-regulation of HSPA1A and re-distribution of DNAJB1. The extent of the observed effects varied depending on brain area and disease protein. ConclusionsOur results suggest a common sequence, in which formation of cytoplasmic and nuclear inclusions precede proteasomal impairment and induction of the cellular stress response. Clearly, impairment of the PQC is not the primary cause for inclusion formation, but rather a consequence that might contribute to neuronal dysfunction and death. Notably, the inclusion pathology is not directly correlated to the severity of the degeneration in different areas, implying that different populations of neurones respond to polyQ aggregation with varying efficacy and that protein aggregation outside the neuronal perikaryon (e.g. axonal aggregates) or other effects of polyQ aggregation, which are more difficult to visualize, may contribute to neurodegeneration
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