bluuebunny/crossref_metadata_2025_split huggingface dataset:
Overexpression of the plasma membrane‐localized NDR1 protein results in enhanced bacterial disease resistance in Arabidopsis thaliana
Authors: Peter Coppinger  , Repetti Peter P. , Day Brad , Dahlbeck Douglas , Mehlert Angela , Staskawicz Brian J. 
Published: September 2004

SummaryPrevious studies have established that mutations in the NDR1 gene in Arabidopsis thaliana suppress the resistance response of three resistance proteins, RPS2, RPM1, and RPS5, to Pseudomonas syringae pv. tomato (Pst) strain DC3000 containing the cognate effector genes, avrRpt2, avrRpm1, and avrpPhB, respectively. NDR1 is a plasma membrane (PM)‐localized protein, and undergoes several post‐translational modifications including carboxy‐terminal processing and N‐linked glycosylation. Expression of NDR1 under the NDR1 native promoter complements the ndr1‐1 mutation, while overexpression of NDR1 results in enhanced resistance to virulent Pst. Sequence analysis and mass spectrometry suggest that NDR1 is localized to the PM via a C‐terminal glycosylphosphatidyl‐inositol (GPI) anchor. GPI modification would potentially place NDR1 on the outer surface of the PM, perhaps allowing NDR1 to act as a transducer of pathogen signals and/or interact directly with the pathogen.
Phosphoinositide‐specific phospholipase C is involved in cytokinin and gravity responses in the moss Physcomitrella patens
Authors: Repp Alexander , Mikami Koji , Mittmann Franz , Hartmann Elmar 
Published: September 2004

SummaryThe phosphoinositide signalling pathway is important in plant responses to extracellular and intracellular signals. To elucidate the physiological functions of phosphoinositide‐specific phopspholipase C, PI‐PLC, targeted knockout mutants of PpPLC1, a gene encoding a PI‐PLC from the moss Physcomitrella patens, were generated via homologous recombination. Protonemal filaments of the plc1 lines show a dramatic reduction in gametophore formation relative to wild type: this was accompanied by a loss of sensitivity to cytokinin. Moreover, plc1 appeared paler than the wild type, the result of an altered differentiation of chloroplasts and reduced chlorophyll levels compared with wild type filaments. In addition, the protonemal filaments of plc1 have a strongly reduced ability to grow negatively gravitropically in the dark. These effects imply a significant role for PpPLC1 in cytokinin signalling and gravitropism.
Growth, nutrient utilization and parameters of mineral metabolism in Nile tilapia Oreochromis niloticus (Linnaeus, 1758) fed plant‐based diets with graded levels of microbial phytase
Authors: Portz L. , Liebert F. 
Published: September 2004

SummaryDiets with graded levels of the experimental microbial phytase SP1002 (0, 500, 1000, 2000 and 4000 FTU/kg) were fed to juvenile Nile tilapia (average BW = 68.8 g) for 60 days (n = 4). A digestibility trial ran parallel to the growth trial using 0.3 g TiO2/100 g as an indigestible marker. The efficiency of phytase supplementation was evaluated by parameters of growth response, crude protein and mineral utilization (using body composition data), apparent nutrient digestibility, mineral content in scale and vertebra and inorganic phosphorus in blood plasma. Data were submitted to anova and Tukey‐test using SAS‐program. Significant improvements (p < 0.01) were found for growth, FCR and SGR, mainly for diets with 1000 and 2000 FTU/kg phytase supplementation. Protein utilization was significantly increased and maximized between 1000 and 2000 FTU/kg. Phosphorus utilization increased significantly up to 4000 FTU/kg. Digestibility of protein and phosphorus was also significantly improved. Phosphorus concentration in the blood, vertebra and scale increased significantly after phytase addition. Similarly, calcium and magnesium concentration in vertebra and scale were increased. Generally, phytase supplementation between 1000 and 2000 FTU/kg resulted in growth rates and mineralization parameters similar to a control diet with inorganic phosphorus.
Macronutrient digestibility, nitrogen balance, plasma indicators of protein metabolism and mineral absorption in horses fed a ration rich in sugar beet pulp
Authors: Olsman A. F. S. , Huurdeman C. M. , Jansen W. L. , Haaksma J. , van Oldruitenborgh‐Oosterbaan M. M. Sloet , Beynen A. C. 
Published: September 2004

SummaryIn a cross‐over study with six mature horses, the effect of iso‐energetic replacement of dietary glucose by beet pulp on macronutrient digestibility, nitrogen metabolism and mineral absorption was studied. The test ration contained 25% beet pulp in the total dietary dry matter. Beet pulp feeding significantly lowered crude fat and non‐structural carbohydrate digestibility, but had no significant effect on digestibility of other macronutrients, faecal and urinary nitrogen excretion and the faecal to urinary nitrogen excretion quotient. However, on the beet pulp diet, plasma ammonia and creatinin concentrations were significantly lower than on the glucose diet. No diet effect on magnesium absorption was observed. It is suggested that dietary beet pulp stimulates the conversion of ammonia into urea.
Additional dietary zinc for weaning piglets is associated with elevated concentrations of serum IGF‐I
Authors: Carlson D. , Poulsen H. D. , Vestergaard M. 
Published: September 2004

SummaryTwo experiments were performed in order to study how weaning and post‐weaning dietary zinc level affect serum IGF‐I. Further, whether the growth‐enhancing effect of 2500 ppm of dietary zinc (Zn2500) and/or 175 ppm of dietary copper (Cu175) in post‐weaning diets is associated with elevated serum IGF‐I levels in piglets was studied. Experiment 1 included 54 piglets (six litters of nine piglets). One piglet from every litter was assigned to a control group (blood sampled 1 day before weaning). At weaning the remaining eight piglets from every litter were allocated randomly to four dietary treatments with increasing zinc inclusions (Zn100, Zn250, Zn1000, Zn2500). In exp. 2, 48 piglets (six litters of eight piglets) were allocated to four dietary treatments (Zn100, Zn100Cu175, Zn2500, Zn2500Cu175). All piglets in exp. 1 were blood sampled at −1, 1–2, 5–6 or 14–15 days after weaning and in exp. 2 blood samples were taken from all pigs 5–7 days after weaning. Feed intake was recorded per pen (two piglets) and weight gain was recorded for every piglet. Just after weaning feed intake was very low, piglets lost weight and serum IGF‐I decreased in exp. 1. However, the piglets fed 2500 ppm of zinc reached pre‐weaning levels of serum IGF‐I at 14–15 days post‐weaning, whereas piglets receiving lower zinc levels showed no changes in serum IGF‐I. In exp. 2, additional dietary zinc in weaning diets for piglets was found to be associated with increased feed intake, improved growth rate and increased serum IGF‐I. High levels of dietary copper did not affect any of these measurements. Zinc‐induced rise in serum IGF‐I was partly due to increased feed intake. After correcting for differences in feed intake, zinc significantly increased serum IGF‐I. However, to completely separate effects of feed intake from effects of zinc status, pair‐feeding should be considered in future studies.
The selenium requirement of the puppy
Authors: Wedekind K. J. , Yu S. , Combs G. F. 
Published: September 2004

SummaryCurrent selenium (Se) recommendations for the puppy are based on extrapolation from other species (0.11 mg Se/kg diet). The purpose of this study was to experimentally determine the Se requirement in puppies. Thirty beagle puppies (average = 8.8 weeks old) were utilized in a randomized complete block design with age, litter and gender used as blocking criteria. Puppies were fed a low Se (0.04 mg Se/kg diet) torula yeast‐based diet for 14 days (pre‐test period) after which this same diet was supplemented with five levels of Na2SeO3for 21 days (experimental period) to construct a response curve (0, 0.13, 0.26, 0.39 or 0.52 mg Se/kg diet). Response variables included Se concentrations and Se‐dependent glutathione peroxidase activities (GSHpx) in serum as well as serum total triiodothyronine (TT3), serum total thyroxine (TT4) and serum free T4(FT4). No significant changes in food intake and body weight gain occurred, and no clinical signs of Se deficiency were observed. A breakpoint for serum GSHpx could not be determined in our study due to analytical difficulties. A broken‐line, two‐slope response in serum Se occurred with a breakpoint at 0.17 mg Se/kg diet. When Se from the basal diet was added to this estimate, the breakpoint for serum Se equated to 0.21 mg Se/kg diet. TT3increased linearly with increasing Se intake, whereas TT4was unchanged. However, the ratio of TT4 : TT3decreased linearly in response to supplemental Se. In summary, although we estimated the selenium requirement for the puppy based on serum Se, our 0.21 mg Se/kg diet estimate is higher than that seen for adult dogs, kittens, rats or poultry (0.13, 0.15, 0.15 and 0.15 mg Se/kg diet respectively). This difference may be due to the fact that GSHpx was used as the biomarker of Se status.
12‐Lipoxygenase plays a key role in cell death caused by glutathione depletion and arachidonic acid in rat oligodendrocytes
Authors: Wang Hong , Li Jianrong , Follett Pamela L. , Zhang Yumin , Cotanche Douglas A. , Jensen Frances E. , Volpe Joseph J. , Rosenberg Paul A. 
Published: September 2004

AbstractOxidative injury to premyelinating oligodendrocytes (preOLs) in developing white matter has been implicated in the pathogenesis of periventricular leukomalacia, the lesion underlying most cases of cerebral palsy in premature infants. In this study, we investigated the pathways of OL death induced by intracellular glutathione (GSH) depletion. We found that the lipoxygenase (LOX) inhibitors AA‐861 and BMD‐122 (N‐benzyl‐N‐hydroxy‐5‐phenylpentamide; BHPP), but not the cyclooxygenase (COX) inhibitor indomethacin, fully protected the cells from GSH depletion caused by cystine deprivation. Arachidonic acid (AA), the substrate for 12‐LOX, potentiated the toxicity of mild cystine deprivation and at higher concentration was itself toxic. This toxicity was also blocked by 12‐LOX inhibitors. Consistent with a role for 12‐LOX in the cell death pathway, 12‐LOX activity increased following cystine deprivation in OLs. Blocking 12‐LOX with AA‐861 effectively inhibited the accumulation of reactive oxygen species (ROS) induced by cystine deprivation. These data suggest that, in OLs, intracellular GSH depletion leads to activation of 12‐LOX, ROS accumulation and cell death. Mature OLs were more resistant than preOLs to cystine deprivation. The difference in sensitivity was not due to a difference in 12‐LOX activity but rather appeared to be related to the presence of stronger antioxidant defense mechanisms in mature OLs. These results suggest that 12‐LOX activation plays a key role in oxidative stress‐induced OL death.
Haemorrhage‐evoked decompensation and recompensation mediated by distinct projections from rostral and caudal midline medulla in the rat
Authors: Heslop David J. , Bandler Richard , Keay Kevin A. 
Published: September 2004

AbstractThe haemodynamic response to blood loss consists of three phases: (i) an initial compensatory phase during which resting arterial pressure is maintained; (ii) a decompensatory phase characterized by a sudden, life‐threatening hypotension and bradycardia; and (iii) if blood loss ceases, a recompensatory phase during which arterial pressure returns to normal. Previous research indicates that topographically distinct, rostral and caudal parts of the caudal midline medulla (CMM) contain neurons that differentially regulate the timing and magnitude of each of the three phases. Specifically, decompensation depends critically on the integrity of the rostral CMM; whereas compensation and recompensation depend upon the integrity of the caudal CMM. This study aimed to determine, using retrograde and anterograde tracing techniques, if the rostral and caudal CMM gave rise to different sets of projections to the major cardiovascular region of the ventrolateral medulla (VLM) and spinal cord. It was found that rostral and caudal CMM each have projections of varying density to the region containing bulbospinal (presympathetic) motor neurons in the rostral VLM and preganglionic sympathetic motor neurons in the intermediolateral cell column of the spinal cord. Via these projections vasomotor tone and hence arterial pressure can be regulated. More strikingly: (i) consistent with a role in mediating bradycardia during decompensation, the rostral CMM projects uniquely to VLM regions containing vagal cardiac motor neurons; and (ii) consistent with its role in mediating recompensation, the caudal CMM projects uniquely onto tyrosine hydroxylase‐containing, caudal VLM (A1) neurons whose activity mediates vasopressin release, on which recompensation depends.
Tyrosine hydroxylase‐positive neurons intrinsic to the human striatum express the transcription factorNurr1
Authors: Cossette Martine , Parent André , Lévesque Daniel 
Published: September 2004

AbstractThe putative dopaminergic (DA) neurons intrinsic to human striatum were studied to determine their similarity with DA neurons of the substantia nigra pars compacta (SNpc). The comparison was based on morphological features and on the presence or absence ofNurr1, an orphan receptor of the nuclear receptor family that is essential for the expression of DA phenotype by developing SNpc neurons. Immunohistochemistry for the neuronal nuclear protein (NeuN; a neuronal marker) andin situhybridization for tyrosine hydroxylase (TH) and/orNurr1were applied topost‐mortemtissue obtained from seven normal individuals. On one hand, the TH‐positive multipolar neurons in the human striatum, which were subdivided into three groups according to their size and pattern of dendritic arborization, were found to be morphologically similar to TH‐positive neurons of the SNpc. The distribution frequency of striatal TH‐positive neurons, according to their diameter, closely matches the frequency observed for multipolar TH‐positive cells in the SNpc. On the other hand, the proportion of neurons expressingNurr1and TH mRNA transcripts on single striatal section was similar to the proportion of TH‐immunoreactive neurons observed on adjacent sections. More importantly, in each striatum analysed, virtually all cells that stained for TH also expressed NeuN andNurr1. This study provides novel data that confirm the existence of DA neurons intrinsic to the human striatum. It also provides the first evidence for the existence of striking morphological and chemical similarities between the DA neurons present at striatal level and those that populate the SNpc.
Locomotor and oculomotor impairment associated with cerebellar dysgenesis in Zic3‐deficient (Bent tail) mutant mice
Authors: Aruga Jun , Ogura Hiroo , Shutoh Fumihiro , Ogawa Miyuki , Franke Barbara , Nagao Soichi , Mikoshiba Katsuhiko 
Published: September 2004

AbstractWe examined the adult neural phenotypes of the Bent tail mutant mouse. The Bent tail mutant mouse was recently shown to lack a submicroscopic part of the X chromosome containing the Zic3 gene, which encodes a zinc‐finger protein controlling vertebrate neural development. While nearly one‐fourth of hemizygous Bent tail (Bn/Y, Zic3‐deficient) mice developed neural tube defects in their midbrain and hindbrain region, the other Bn/Y mice showed apparently normal behaviour in a C57BL/6 genetic background. A battery of behavioural and eye movement tests revealed impaired spontaneous locomotor activity, reduction of muscle tone and impairments of vestibuloocular and optokinetic eye movements in these mice. Morphological examination of the mutant brain showed a significant reduction in the cell numbers in the cerebellar anterior lobe and paraflocculus–flocculus complex. Our results indicate that the cerebellar dysgenesis characterized by subregional hypoplasia affects the locomotor activity, muscle tone and eye movement control of the mice. These findings may have some clinical implications in relation to disorders characterized by cerebellar dysgenesis, such as Joubert syndrome.
Single‐pulse transcranial magnetic stimulation over the frontal eye field can facilitate and inhibit saccade triggering
Authors: Nyffeler Thomas , Bucher Oliver , Pflugshaupt Tobias , Von Wartburg Roman , Wurtz Pascal , Hess Christian W. , Müri René M. 
Published: September 2004

AbstractThe aim of this study was to investigate the effect of single‐pulse transcranial magnetic stimulation on the triggering of saccades. The right frontal eye field was stimulated during modified gap and overlap paradigms with flashed presentation of the lateral visual target of 80 ms. In order to examine possible facilitating or inhibitory effects on saccade triggering, three different time intervals of stimulation were chosen, i.e. simultaneously with onset of the target, during the presentation and after target end. Stimulation applied simultaneously with target onset significantly decreased the latency of contralateral saccades in the gap but not in the overlap paradigm. Stimulation after target end significantly increased saccade latency for both sides in the gap paradigm and for the contralateral side in the overlap paradigm. Stimulation during presentation had no effect in either paradigm. The results show that, depending on the time interval and the paradigm tested, a facilitation or inhibition of saccade triggering can be achieved. The results are discussed in a context of two probable transcranial magnetic stimulation effects, a direct interference with the frontal eye field on the one hand and a remote interference with the superior colliculus on the other hand.
Presynaptic muscarinic acetylcholine receptors suppress GABAergic synaptic transmission in the intermediate grey layer of mouse superior colliculus
Authors: Li Fengxia , Endo Toshiaki , Isa Tadashi 
Published: September 2004

AbstractThe intermediate grey layer (the stratum griseum intermediale; SGI) of the superior colliculus (SC) receives cholinergic inputs from the parabrachial region of the brainstem. It has been shown that cholinergic inputs activate nicotinic acetylcholine (nACh) receptors on projection neurons in the SGI. Therefore, it has been suggested that they facilitate the initiation of orienting behaviours. In this study, we investigated the effect of muscarinic acetylcholine (mACh) receptor activation on GABAergic synaptic transmission to SGI neurons using the whole‐cell patch‐clamp recording technique in slice preparations from mice. The GABAA receptor‐mediated inhibitory postsynaptic currents (IPSCs) evoked in SGI neurons by focal electrical stimulation were suppressed by bath application of 10 µm muscarine chloride. During muscarine application, both the paired‐pulse facilitation index and the coefficient of variation of IPSCs increased; however, the current responses induced by a transient pressure application of 1 mm GABA were not affected by muscarine. Muscarine reduced frequencies of miniature IPSCs (mIPSCs) while the amplitudes of mIPSCs remained unchanged. These results suggestd that mAChR‐mediated inhibition of IPSCs was of presynaptic origin. The suppressant effect of muscarine was antagonized by an M1 receptor antagonist, pirenzepine dihydrochloride (1 µm), and a relatively specific M3 receptor antagonist, 4‐DAMP methiodide (50 nm). By contrast, an M2 receptor antagonist, methoctramine tetrahydrochloride (10 µm), was ineffective. These results suggest that the cholinergic inputs suppress GABAergic synaptic transmission to the SGI neurons at the presynaptic site via activation of M1 and, possibly, M3 receptors. This may be an additional mechanism by which cholinergic inputs can facilitate tectofugal command generation.
Cascades of response vectors of olfactory receptor neurons in Xenopus laevis tadpoles
Authors: Schild Detlev , Manzini Ivan 
Published: September 2004

AbstractOlfactory receptor neurons (ORNs) of Xenopus laevis tadpoles respond to water‐born stimuli such as amino acids. Their sensitivity spectra with respect to amino acids have recently been shown to become more selective over ontogenetic stages [Manzini & Schild (2004) J. Gen. Physiol., 123, 99–107]. In this paper, we undertake a theoretical analysis of this data set and determine the correlational relationships among odorant responses represented as binary response vectors. We first show that, on the one hand, the number of 204 ORN classes (out of 283 recorded ORNs) cannot be explained by a random expression pattern of olfactory receptors (ORs). On the other hand, this number does not appear to be reconcilable with the idea that individual ORNs express one type of OR each. The covariance matrix of stimulus responses shows that the responses to some stimuli are correlated to those of others. Furthermore, the response vectors show positive as well as negative correlations among each other. While the positive correlations can partly be explained by the differing response frequencies to the odorants used, the negative ones cannot. Finally, we analyse the similarity among responses using the Hamming distance as a distance measure, the result being that most response vectors differ from others by small Hamming distances. Such vectors are shown to form pattern cascades, possibly reflecting a decreasing number of ORs being expressed over ontogenetic stages.
A disaccharide derived from chondroitin sulphate proteoglycan promotes central nervous system repair in rats and mice†
Authors: Rolls Asya , Avidan Hila , Cahalon Liora , Schori Hadas , Bakalash Sharon , Litvak Vladimir , Lev Sima , Lider Ofer , Schwartz Michal 
Published: September 2004

AbstractChondroitin sulphate proteoglycan (CSPG) inhibits axonal regeneration in the central nervous system (CNS) and its local degradation promotes repair. We postulated that the enzymatic degradation of CSPG generates reparative products. Here we show that an enzymatic degradation product of CSPG, a specific disaccharide (CSPG‐DS), promoted CNS recovery by modulating both neuronal and microglial behaviour. In neurons, acting via a mechanism that involves the PKCα and PYK2 intracellular signalling pathways, CSPG‐DS induced neurite outgrowth and protected against neuronal toxicity and axonal collapse in vitro. In microglia, via a mechanism that involves ERK1/2 and PYK2, CSPG‐DS evoked a response that allowed these cells to manifest a neuroprotective phenotype ex vivo. In vivo, systemically or locally injected CSPG‐DS protected neurons in mice subjected to glutamate or aggregated β‐amyloid intoxication. Our results suggest that treatment with CSPG‐DS might provide a way to promote post‐traumatic recovery, via multiple cellular targets.