bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interactions between peptidoglycan and the ExeAB complex during assembly of the type II secretin of Aeromonas hydrophila
Authors: Howard S. Peter , Gebhart Carol , Langen Geoffrey R. , Li Gang , Strozen Timothy G. 
Published: December 2005

Summary Aeromonas hydrophila transports extracellular protein toxins via the type II secretion system, an export mechanism comprised of numerous proteins that spans both the inner and outer membranes. Two components of this secretion system, ExeA and ExeB, form a complex in the inner membrane that functions to locate and/or assemble the ExeD secretin in the outer membrane. In the studies reported here, two‐codon insertion mutagenesis of exeA revealed that an insertion at amino acid 495 in the C‐terminal region of ExeA did not alter ExeAB complex formation yet completely abrogated its involvement in ExeD secretin assembly and thus rendered the bacteria secretion negative. In silico analysis of protein motifs with similar amino acid profiles revealed that this amino acid is located within a putative peptidoglycan (PG) binding motif in the periplasmic domain of ExeA. Substitution mutations of three highly conserved amino acids in the motif were constructed. In cells expressing each of these mutants, the ability to assemble the ExeD secretin or secrete aerolysin was lost, while ExeA retained the ability to form a complex with ExeB. In in vivo cross‐linking experiments, wild‐type ExeA could be cross‐linked to PG, whereas the three substitution mutants of ExeA could not. These data indicate that PG binding and/or remodelling plays a role in the function of the ExeAB complex during assembly of the ExeD secretin.
Stem and leaf gas exchange and their responses to fire in a north Australian tropical savanna
Authors: CERNUSAK LUCAS A. , HUTLEY LINDSAY B. , BERINGER JASON , TAPPER NIGEL J. 
Published: December 2005

ABSTRACTWe measured stem CO2 efflux and leaf gas exchange in a tropical savanna ecosystem in northern Australia, and assessed the impact of fire on these processes. Gas exchange of mature leaves that flushed after a fire showed only slight differences from that of mature leaves on unburned trees. Expanding leaves typically showed net losses of CO2 to the atmosphere in both burned and unburned trees, even under saturating irradiance. Fire caused stem CO2 efflux to decline in overstory trees, when measured 8 weeks post‐fire. This decline was thought to have resulted from reduced availability of C substrate for respiration, due to reduced canopy photosynthesis caused by leaf scorching, and to priority allocation of fixed C towards reconstruction of a new canopy. At the ecosystem scale, we estimated the annual above‐ground woody‐tissue CO2 efflux to be 275 g C m−2 ground area year−1 in a non‐fire year, or approximately 13% of the annual gross primary production.We contrasted the canopy physiology of two co‐dominant overstory tree species, one of which has a smooth bark on its branches capable of photosynthetic re‐fixation (Eucalyptus miniata), and the other of which has a thick, rough bark incapable of re‐fixation (Eucalyptus tetrodonta). Eucalyptus miniata supported a larger branch sapwood cross‐sectional area in the crown per unit subtending leaf area, and had higher leaf stomatal conductance and photosynthesis than E. tetrodonta. Re‐fixation by photosynthetic bark reduces the C cost of delivering water to evaporative sites in leaves, because it reduces the net C cost of constructing and maintaining sapwood. We suggest that re‐fixation allowed leaves of E. miniata to photosynthesize at higher rates than those of E. tetrodonta, while the two invested similar amounts of C in the maintenance of branch sapwood.
Abnormal foot function in diabetic patients: the altered onset of Windlass mechanism
Authors: D’Ambrogi E. , Giacomozzi C. , Macellari V. , Uccioli L. 
Published: December 2005

AbstractAim  The aim of this study was to examine foot function in the presence of diabetes‐induced alterations of the anatomical and biomechanical unit formed by the Achilles tendon, plantar fascia and metatarso‐phalangeal joints. More specifically, we focused on the Windlass mechanism, the physiological mechanism which entails stiffening of the foot during propulsion.Methods  Sixty‐one diabetic patients, with or without neuropathy, and 21 healthy volunteers were recruited. The thickness of Achilles tendon and plantar fascia was measured by ultrasound. The main biomechanical parameters of foot–floor interaction during gait were acquired by means of dedicated platforms. The range of motion of the 1st metatarso‐phalangeal joint was measured passively.Results  The plantar fascia (PF) and Achilles tendon (AT) were significantly thickened in diabetic patients [control subjects: PF 2.0 ± 0.5 mm, AT 4.0 ± 0.5 mm; diabetic patients without neuropathy: PF 2.9 ± 1.2 mm (P = 0.002), AT 4.6 ± 1.0 mm (P = 0.016); diabetic patients with neuropathy: PF 3.0 ± 0.8 mm (P < 0.0001), AT 4.9 ± 1.7 mm (P = 0.026)]. Joint mobility was significantly reduced [control subjects: 100.0 ± 10.0°; diabetic patients without neuropathy: 54.0 ± 29.4° (P < 0.0001); diabetic patients with neuropathy: 54.9 ± 17.2° (P < 0.0001)]. Loading times and force integrals under the heel and the metatarsals increased [metatarsal loading time (% stance phase): control subjects 88.2 ± 4.1%; diabetic patients without neuropathy 90.1 ± 4.7% (P = 0.146); diabetic patients with neuropathy 91.7 ± 6.6% (P = 0.048)].Conclusions  Increased thickness of Achilles tendon and plantar fascia, more evident in the presence of neuropathy, may contribute to an overall increase of tensile force and to the occurrence of an early Windlass mechanism, maintained throughout the whole gait cycle. This might play a significant role in the overall alteration of the biomechanics of the foot–ankle complex.
Curriculum authoring tools and inclusive classroom teaching practice: a longitudinal study
Authors: Bain Alan , Parkes Robert John 
Published: December 2005

AbstractThe purpose of this study was to investigate the longitudinal application of a suite of curriculum authoring tools (CATs) to inclusive classroom teaching practice in a secondary school setting. The study sought to establish whether the incorporation of the CATs into the teachers’ curriculum development and implementation covaried with improved implementation integrity of classroom teaching practice over time. A repeated measures design was used to establish whether those teachers with high levels of tool use also recorded higher levels of implementation integrity in their use of specific inclusive teaching practices. The effects of the tools were measured using 578 50‐minute classroom observations gathered over a 2.5‐year period. The results indicated that higher levels of implementation integrity in classroom practice covaried with the extent to which the tools were used for the design and implementation of curriculum.
Effects of circular motion on judgment of rotation direction and depth order in visual motion
Authors: HANADA MITSUHIKO 
Published: December 2005

Abstract:  The rotation direction and depth order of a rotating sphere consisting of random dots often reverses while it is viewed under orthographic projection. However, if a short viewing distance is simulated under perspective projection, the correct rotation direction can be perceived. There are two motion cues for the rotation direction and depth order. One is the speed cue; points with higher velocities are closer to the observer. The other is the vertical motion cue; vertical motion is induced when the dots recede from or approach the observer. It was examined whether circular motion, which does not have any depth information but induces vertical velocities, masks the vertical motion cue. In Experiment 1, the effects of circular motion on the judgment of the rotation direction of a rotating sphere were examined. The magnitude of the two cues (the speed cue and the vertical velocity cue) as well as the angular speed of circular motion was varied. It was found that the performance improved as the vertical velocity increased and that the speed cue had slight effects on the judgment of the rotation direction. It was also found that the performance worsened as the angular speed of the circular motion was increased. In Experiment 2, the effects of circular motion on depth judgment of a rotating half sphere were investigated. The performance worsened as the angular speed of the circular motion increased, as in Experiment 1. These results suggest that the visual system cannot compensate perfectly for circular motion for the judgment of the rotation direction and depth order.
The role of visible persistence for perception of visual bilateral symmetry1
Authors: NIIMI RYOSUKE , WATANABE KATSUMI , YOKOSAWA KAZUHIKO 
Published: December 2005

Abstract:  Although the detection of visual bilateral symmetry has been claimed to be highly efficient, the possible involvement and function of visual memory in such efficient mechanisms has rarely been examined. We hypothesized that symmetry perception is rapid, as it can be achieved from rapidly decaying information of visible persistence. To test this hypothesis, we employed a temporal integration paradigm. A symmetric dot pattern was randomly divided into two asymmetric patterns and presented successively with a blank screen presented between patterns. Observers could detect symmetry when the two patterns were presented close in time (Experiment 1), indicating that observers perceived symmetry presumably utilizing visible persistence. In addition, the inverse‐intensity effect of visible persistence (Di Lollo & Bischof, 1995) was evident in our temporal integration task of symmetry (Experiment 2). The results of the current study clearly demonstrate that the detection of symmetry can be achieved based on the visible persistence. The large capacity and high spatial precision of visible persistence might be adequate for the rapid and spatially global encoding of visual symmetry.
Facilitation of return in voluntary orienting to visual attributes1
Authors: OKUBO MATIA , MUGISHIMA YOSUKE , MISAWA GORO 
Published: December 2005

Abstract:  The present study examined the effects of voluntary and automatic orienting after a relatively long interval in an attentional cueing paradigm. Facilitation of return was observed after the voluntary orienting to a designated color (Experiment 1) and motion direction (Experiment 2), whereas inhibition of return was observed after the automatic orienting to an abrupt stimulus onset (Experiment 1). These results suggest that the voluntary orienting to a visual attribute modulates subsequent processes differently from the automatic orienting to an abrupt onset. In the voluntary orienting to visual attributes, it would be advantageous to return attention to the previously attended location, which is a potential source of information.
Brain‐derived respiring mitochondria exhibit homogeneous, complete and cyclosporin‐sensitive permeability transition
Authors: Hansson Magnus J. , Månsson Roland , Mattiasson Gustav , Ohlsson Jonas , Karlsson Jenny , Keep Marcus F. , Elmér Eskil 
Published: December 2005

AbstractThe mitochondrial permeability transition (mPT) is increasingly implicated in neuronal cell death. In the present study, isolated respiring brain mitochondria were examined for their ability to undergo calcium‐induced mPT and their sensitivity to mPT inhibition by cyclosporin A (CsA). Previous studies have suggested a heterogeneous response to calcium, a limitation of CsA inhibition, and a relative resistance in the ability of respiring brain mitochondria to undergo mPT. Using fluorometric and electron microscopic analyses, we found that virtually the whole population of respiring brain mitochondria readily undergo mPT and swell upon calcium exposure. Further, brain mitochondria were highly sensitive to CsA which potentiated morphological recovery after transient swelling as well as completely blocked mPT induction in the presence of a low concentration of ADP. Using flow cytometry, which allows analysis of individual mitochondria, we demonstrate that both brain and liver mitochondria display homogeneous responses to calcium‐induced mPT. We conclude that the mPT is one likely target for the broad in vivo neuroprotective effects displayed by CsA when allowed to penetrate the blood–brain barrier, and that development of compounds inhibiting mPT may prove beneficial for the treatment of severe brain disease.
Identification of a novel family of G protein‐coupled receptor associated sorting proteins
Authors: Simonin Frederic , Karcher Pascale , Boeuf Julien J.‐M. , Matifas Audrey , Kieffer Brigitte L. 
Published: December 2005

AbstractDuring the past few years several new interacting partners for G protein‐coupled receptors (GPCRs) have been discovered, suggesting that the activity of these receptors is more complex than previously anticipated. Recently, candidate G protein‐coupled receptor associated sorting protein (GASP‐1) has been identified as a novel interacting partner for the delta opioid receptor and has been proposed to determine the degradative fate of this receptor. We show here that GASP‐1 associatesin vitrowith other opioid receptors and that the interaction domain in these receptors is restricted to a small portion of the carboxyl‐terminal tail, corresponding to helix 8 in the three‐dimensional structure of rhodopsin. In addition, we show that GASP‐1 interacts with COOH‐terminus of several other GPCRs from subfamilies A and B and that two conserved residues within the putative helix 8 of these receptors are critical for the interaction with GASP‐1.In situhybridization and northern blot analysis indicate that GASP‐1 mRNA is mainly distributed throughout the central nervous system, consistent with a potential interaction with numerous GPCRsin vivo. Finally, we show that GASP‐1 is a member of a novel family comprising at least 10 members, whose genes are clustered on chromosome X. Another member of the family, GASP‐2, also interacts with the carboxyl‐terminal tail of several GPCRs. Therefore, GASP proteins may represent an important protein family regulating GPCR physiology.
Brain glycogen re‐awakened
Authors: Brown Angus M. 
Published: December 2005

AbstractThe mammalian brain contains glycogen, which is located predominantly in astrocytes, but its function is unclear. A principal role for brain glycogen as an energy reserve, analogous to its role in the periphery, had been universally dismissed based on its relatively low concentration, an assumption apparently reinforced by the limited duration that the brain can function in the absence of glucose. However, during insulin‐induced hypoglycaemia, where brain glucose availability is limited, glycogen content falls first in areas with the highest metabolic rate, suggesting that glycogen provides fuel to support brain function during pathological hypoglycaemia. General anaesthesia results in elevated brain glycogen suggesting quiescent neurones allow glycogen accumulation, and as long ago as the 1950s it was shown that brain glycogen accumulates during sleep, is mobilized upon waking, and that sleep deprivation results in region‐specific decreases in brain glycogen, implying a supportive functional role for brain glycogen in the conscious, awake brain. Interest in brain glycogen has recently been re‐awakened by the first continuous in vivo measurements using NMR spectroscopy, by the general acceptance of metabolic coupling between glia and neurones involving intercellular transfer of energy substrate, and by studies supporting a prominent physiological role for brain glycogen as a provider of supplemental energy substrate during periods of increased tissue energy demand, when ambient normoglycaemic glucose is unable to meet immediate energy requirements.
Methadone increases intracellular calcium in SH‐SY5Y and SH‐EP1‐hα7 cells by activating neuronal nicotinic acetylcholine receptors
Authors: Pakkanen Jukka S. , Nousiainen Heli , Yli‐Kauhaluoma Jari , Kylänlahti Irene , Möykkynen Tommi , Korpi Esa R. , Peng Jian‐Hong , Lukas Ronald J. , Ahtee Liisa , Tuominen Raimo K. 
Published: December 2005

Abstract(–)‐Methadone acts as an agonist at opioid receptors. Both (+)‐ and (–)‐enantiomers of methadone have been suggested to be potent non‐competitive antagonists of α3β4 neuronal nicotinic acetylcholine receptors (nAChRs). In the present study, we have examined interactions of methadone with nAChRs by using receptor binding assays, patch‐clamp recording and calcium fluorometry imaging with SH‐SY5Y cells naturally expressing α7 and α3* nAChR subtypes and SH‐EP1‐hα7 cells heterologously expressing human α7 nAChRs. Methadone potently inhibited binding of [3H]methyllycaconitine to α7 nAChRs and that of [3H]epibatidine to α3* nAChRs. Methadone pretreatment induced up‐regulation of epibatidine binding sites in SH‐SY5Y cells. Using whole‐cell patch‐clamp recording, both isomers of methadone activated cation currents via mecamylamine‐sensitive nAChRs in SH‐SY5Y cells. Nicotine and both (+)‐ and (–)‐methadone evoked increases in [Ca2+]iin both fluo‐3AM loaded cell lines, and these effects were blocked by mecamylamine and by the α7 selective antagonist methyllycaconitine, suggesting effects of methadone as α7‐nAChR agonist. Sensitivity of sustained nicotine and methadone effects to blockade by CdCl2, ryanodine and xestospongin‐c implicates voltage‐operated Ca2+channels and intracellular Ca2+stores as downstream modulators of elevated [Ca2+]i. Collectively, our results suggest that methadone engages in complex and potentially pharmacologically significant interactions with nAChRs.
Structural biology of NCAM homophilic binding and activation of FGFR
Authors: Kiselyov Vladislav V. , Soroka Vladislav , Berezin Vladimir , Bock Elisabeth 
Published: December 2005

SummaryIn this review, we analyse the structural basis of the homophilic interactions of the neural cell adhesion molecule (NCAM) and the NCAM‐mediated activation of the fibroblast growth factor receptor (FGFR). Recent structural evidence suggests that NCAM molecules form cis‐dimers in the cell membrane through a high affinity interaction. These cis‐dimers, in turn, mediate low affinity trans‐interactions between cells via formation of either one‐ or two‐dimensional ‘zippers’. We provide evidence that FGFR is probably activated by NCAM very differently from the way by which it is activated by FGFs, reflecting the different conditions for NCAM–FGFR and FGF–FGFR interactions. The affinity of FGF for FGFR is approximately 106 times higher than that of NCAM for FGFR. Moreover, in the brain NCAM is constantly present on the cell surface in a concentration of about 50 µm, whereas FGFs only appear transiently in the extracellular environment and in concentrations in the nanomolar range. We discuss the structural basis for the regulation of NCAM–FGFR interactions by two molecular ‘switches’, polysialic acid (PSA) and adenosine triphosphate (ATP), which determine whether NCAM acts as a signalling or an adhesion molecule.
A 13 kDa carboxy‐terminal fragment of ApoE stabilizes Abeta hexamers
Authors: Wellnitz Sabine , Friedlein Arno , Bonanni Corinne , Anquez Vivianne , Goepfert Fabienne , Loetscher Hansruedi , Adessi Celine , Czech Christian 
Published: December 2005

AbstractThe pathological role of ApoE4 in Alzheimer's disease (AD) is not fully elucidated yet but there is strong evidence that ApoE is involved in Abeta deposition, which is an early hallmark of AD neuropathology. Overexpression of ApoE in neuroblastoma cells (Neuro2a) leads to the generation of an intracellular 13 kDa carboxy‐terminal fragment of ApoE comparable to fragments seen in brains of AD patients. ApoE4 generates more of this fragment than ApoE2 and E3 suggesting a potential pathological role of these fragments in Alzheimer's disease. Analysis of this intracellular ApoE4 fragment by protease digest followed by MALDI‐TOF mass spectrometry showed the proteolytic cleavage site close to residue 187 of ApoE. We have engineered and expressed the corresponding ApoE fragments in vitro. The recombinant 13 kDa carboxy‐terminal fragment inhibited fibril formation of Abeta; this contrasts with the full‐length ApoE and the corresponding amino‐terminal ApoE fragment. Moreover, we show that the 13 kDa carboxy‐terminal fragment of ApoE stabilizes the formation of Abeta hexamers. Complexes of Abeta with the 13 kDa carboxy‐terminal ApoE fragment show toxicity in PC12 cells comparable to Abeta fibrils. These data suggest that cleavage of ApoE, leading to the generation of this fragment, contributes to the pathogenic effect of ApoE4 in AD.
Integration of G protein signals by extracellular signal‐regulated protein kinases in SK‐N‐MC neuroepithelioma cells
Authors: Chan Anthony S. L. , Yeung Wendy W. S. , Wong Yung H. 
Published: December 2005

AbstractMammalian cells often receive multiple extracellular stimuli under physiological conditions, and the various signaling inputs have to be integrated for the processing of complex biological responses. G protein‐coupled receptors (GPCRs) are critical players in converting extracellular stimuli into intracellular signals. In this report, we examined the integration of different GPCR signals by mitogen‐activated protein kinases (MAPKs) using the SK‐N‐MC human brain neuroepithelioma cells as a neuronal model. Stimulation of the Gi‐coupled neuropeptide Y1and Gq‐coupled muscarinic M1acetylcholine receptors, but not the Gs‐coupled dopamine D1receptor, led to the activation of extracellular signal‐regulated kinase (ERK). All three receptors were also capable of stimulating c‐Jun NH2‐terminal kinases (JNK) and p38 MAPK. The Gi‐mediated ERK activation was completely suppressed upon inhibition of Src tyrosine kinases by PP1, while the Gq‐induced response was suppressed by both PP1 and the Ca2+chelator, BAPTA‐AM. In contrast, activations of JNK and p38 by Gs‐, Gi‐, and Gq‐coupled receptors were sensitive to PP1 and BAPTA‐AM pretreatments. Simultaneous stimulation of Gi‐ and Gq‐coupled receptors resulted in the synergistic activation of ERK, but not JNK or p38 MAPK. The Gi/Gq‐induced synergistic ERK activation was PTX‐sensitive, and appeared to be a co‐operative effect between Ca2+and Src family tyrosine kinases. Enhanced ERK activation was associated with an increase in CREB phosphorylation, while the JNK and p38‐responsive transcription factor ATF‐2 was weakly enhanced upon Gi/Gq‐induction. This report provides evidence that G protein signals can be integrated at the level of MAPK, resulting in differential effects on ERK, JNK and p38 MAPK in SK‐N‐MC cells.
Polarized distribution of nucleoside transporters in rat brain endothelial and choroid plexus epithelial cells
Authors: Redzic Zoran B. , Biringer Jean , Barnes Kay , Baldwin Stephen A. , Al‐Sarraf Hameed , Nicola Pieris A. , Young James D. , Cass Carol E. , Barrand Margery A. , Hladky Stephen B. 
Published: December 2005

AbstractThis study investigated mRNA expression and protein localization of equilibrative and concentrative nucleoside transporters (ENTs, CNTs) in primary cultures of rat brain endothelial cells (RBEC) and rat choroid plexus epithelial cells (RCPEC). Reverse transcriptase PCR analysis revealed that RBEC and RCPEC contained mRNA for rENT1, rENT2 and rCNT2 and for rENT1, rENT2, rCNT2 and rCNT3, respectively. Immunoblotting of membrane fractions of RBEC, fresh RCPEC and primary cultures of RCPEC revealed the presence of rENT1, rENT2 and rCNT2 proteins in all samples. Measurement of [14C]adenosine uptake into cells grown as monolayers on permeable plastic supports revealed a polarized distribution of Na+‐dependent adenosine uptake in that CNT activity was associated exclusively in membranes of RBEC facing the lower chamber (which corresponds to the surface facing the interstitial fluid in situ) and in membranes of RCPEC facing the upper chamber (which corresponds to the surface facing the cerebrospinal fluid in situ). In both RBEC and RCPEC, adenosine uptake from the opposite chambers was Na+‐independent and partially inhibited by nitrobenzylthioinosine, indicating the presence of the equilibrative sensitive transporter rENT1.