bluuebunny/crossref_metadata_2025_split huggingface dataset:
A reciprocal backcross monosomic analysis of the scab resistant spring wheat (Triticum aestivum L.) cultivar, ‘Frontana’
Authors: Berzonsky W. A. , Gebhard B. L. , Gamotin E. , Leach G. D. , Ali S. 
Published: April 2007

AbstractFusarium head blight (FHB) reduces grain yield of spring wheat and results in deoxynivalenol (DON) production. The resistant spring wheat ‘Frontana’ could be used to diversify and pyramid resistance. A backcross reciprocal monosomic analysis was conducted to identify ‘Frontana’ chromosomes with resistance. Disomic lines, one set containing critical chromosomes from ‘Frontana’ and the other containing chromosomes from susceptible ‘Chris’, were spray‐inoculated and evaluated in separate greenhouse studies (GH‐1 and GH‐2). Measurements were disease severity at 7 and 14 days, visually diseased kernels, kernels/g and DON content. In GH‐2, reciprocal chromosome lines 5B for visually diseased kernels, lines 7B for kernels/g, and lines 4B and 6A for DON content were significantly different. Lines with ‘Frontana’ chromosomes 3A, 6A and 4D reduced visually diseased kernels, kernels/g and DON content in both studies, while ‘Frontana’ chromosomes 2A, 2B, 4B and 7B increased susceptibility, as indicated by an increase in these same measurements in both studies. Genes carried on ‘Frontana’ chromosomes 3A, 6A and 4D could be useful for diversifying and pyramiding sources of FHB resistance.
Patient information preferences among breast and prostate cancer patients
Authors: Sharpley CF , Christie DRH 
Published: April 2007

SummaryPreferences for information about their disease and treatment were collected from 392 patients who had been treated for either breast or prostate cancer an average of 2 years previously. Type of information that they had received, their ratings of its value to them and their preferred format for further information were examined. The most common and most preferred form of information was through doctor interview, followed by educational booklets. Prostate cancer patients preferred videotapes; breast cancer patients tended to prefer individualized approaches including a tour of the department. Effects of age, educational levels, occupational backgrounds and self‐reports for anxiety and depression at the time of the survey and at time of diagnosis were analysed. Prostate cancer patients who were most severely depressed showed a preference for not receiving any information at all, perhaps reflecting a tendency towards withdrawal.
Emergency transcatheter embolization of ruptured hepatocellular carcinomas with tortuous conventional or aberrant hepatic vascular anatomy, or parasitic supply
Authors: Lau KY , Wong WWC , Chan JKW , Kan WK , Leung JLY , Lee ASL , Lee LT , Lee GYK 
Published: April 2007

SummaryEmergency transcatheter embolization is a well‐recognized measure to manage patients with life‐threatening haemoperitoneum due to spontaneous ruptured hepatocellular carcinoma. Traditional embolization technique is to embolize the proper hepatic artery or the segmental hepatic artery by femoral approach using gelfoam pledgets. From 1997 to 2004, in 19 out of 96 embolizations, the embolization technique had to be modified because of tortuous conventional or aberrant hepatic vascular anatomy or parasitic supply to achieve successful embolization.
Impaired hippocampal LTP in inbred mouse strains can be rescued by β‐adrenergic receptor activation
Authors: Schimanski Lesley A. , Ali Declan W. , Baker Glen B. , Nguyen Peter V. 
Published: April 2007

AbstractLong‐term potentiation (LTP), an activity‐dependent enhancement of synaptic strength, and memory can be influenced by neuromodulatory transmitters such as norepinephrine (NE) and also by genetic background. β‐Adrenergic receptor activation can facilitate the expression of hippocampal CA1 LTP induced by weak stimulus patterns, but its influence on LTP induced by stronger stimulus patterns is unclear. We examined neural NE and dopamine (DA) levels, β‐adrenergic receptor expression and hippocampal LTP in genetically diverse inbred mouse strains. Brain tissue levels of NE were significantly lower in strains 129S1/SvImJ (129), BALB/cByJ (BALB) and C3H/HeJ (C3H) than in C57BL/6NCrlBR (B6). Western blot analysis showed that hippocampal β1‐adrenergic receptor expression was similar in strains B6, 129 and C3H, but was increased in BALB. LTP was induced in area CA1 of hippocampal slices by four trains of high‐frequency stimulation (HFS) of the Schaeffer collaterals in the four inbred strains. Two hours after induction, LTP was significantly reduced in strains 129, BALB and C3H compared to B6, correlating with neural NE levels. We rescued hippocampal LTP in strains 129, BALB and C3H to levels seen in B6 by bath application of 1 µm isoproterenol, a β‐adrenergic receptor agonist, during HFS. Propranolol, a β‐adrenergic receptor antagonist, blocked this rescue in 129, BALB and C3H but did not affect LTP in strain B6. Thus, although this form of multitrain LTP does not rely on β‐adrenergic receptor activation, our data show that pharmacological activation of β‐adrenergic receptors during multiple trains of HFS can rescue CA1 LTP in genetically diverse strains with impaired LTP.
Olfactory lateralization in homing pigeons: initial orientation of birds receiving a unilateral olfactory input
Authors: Gagliardo Anna , Pecchia Tommaso , Savini Maria , Odetti Francesca , Ioalè Paolo , Vallortigara Giorgio 
Published: April 2007

AbstractIt has been shown that homing pigeons (Columba livia) rely on olfactory cues to navigate from unfamiliar locations. In fact, the integrity of the olfactory system, from the olfactory mucosa to the piriform cortex, is required for pigeons to navigate over unfamiliar areas. Recently it has been shown that there is a functional asymmetry in the piriform cortex, with the left piriform cortex more involved in the use of the olfactory navigational map than the right piriform cortex. To investigate further the lateralization of the olfactory system in relation to navigational processes in carrier pigeons, we compared their homing performance after either their left or the right nostril was plugged. Contrary to our expectations, we observed an impairment in the initial orientation of the pigeons with their right nostril plugged. However, both groups released with one nostril plugged tended to be poorer than control pigeons in their homing performance. The observed asymmetry in favour of the right nostril might be due to projections from the olfactory bulbs to the contralateral globus pallidum, a structure involved in motor responses.
Social stress induces hypothalamo‐pituitary‐adrenal axis responses in lactating rats bred for high trait anxiety
Authors: Douglas A. J. , Meddle S. L. , Kroemer S. , Muesch W. , Bosch O. J. , Neumann I. D. 
Published: April 2007

AbstractHypothalamo‐pituitary‐adrenal axis responses to various stressors are typically attenuated during lactation, including in rats selectively bred for high or low anxiety. As high‐anxiety dams are more aggressive towards intruders than low‐anxiety dams during maternal defence, we investigated their hypothalamo‐pituitary‐adrenal axis responses to this social stress. Maternal defence induced elevated stress responses in high‐anxiety dams only; nerve‐growth‐factor‐induced gene B mRNA expression in the parvocellular paraventricular nucleus and adrenocorticotropin hormone secretory responses were substantially enhanced after maternal defence. In contrast, secretory responses to a non‐social stress (elevated platform) were not different between high‐ and low‐anxiety dams. Thus, responsiveness of the stress axis in lactation is dependent upon the innate level of anxiety of the dam and, as a consequence, her reactiveness to social threat.
Protein tyrosine phosphatase inhibition reduces degeneration of dopaminergic substantia nigra neurons and projections in 6‐OHDA treated adult rats
Authors: Yang Peng , Dankowski Aygul , Hagg Theo 
Published: April 2007

AbstractThe survival of injured adult dopaminergic substantia nigra pars compacta neurons can be promoted by various neurotrophic factors. Most neurotrophic factor receptors are activated by intracellular tyrosine phosphorylation upon ligand binding and are subsequently inactivated or dephosphorylated by protein tyrosine phosphatases. This raised the possibility that tyrosine phosphatase inhibition might improve neuronal survival. Here, we infused the stable water‐soluble tyrosine phosphatase‐specific inhibitor, peroxovanadium [potassium bisperoxo(1,10‐phenanthroline)oxovanadate (V) (bpV(phen))], for 14 days close to the substantia nigra starting immediately after a unilateral moderate injury by injection of the neurotoxin 6‐hydroxydopamine (6‐OHDA) into the midbrain of adult Sprague–Dawley rats. The dopaminergic nigrostriatal neurons were identified by retrograde tracing with fluorogold 7 days prior to the injury. With infusion of 3 or 10 µm peroxovanadium, 75% of these neurons survived compared to 45% in vehicle‐infused rats. Degeneration of the dopaminergic projections to the neostriatum was also reduced by 10 µm peroxovanadium. Twenty minutes after an acute injection of peroxovanadium into the substantia nigra, increased tyrosine phosphorylation in Western blots of nigral extracts was seen in the same protein bands as after injections of brain‐derived neurotrophic factor (BDNF) or NT‐4. This suggests that peroxovanadium enhances endogenous neurotrophic signalling resulting in improved neuronal survival. The neuroprotective effects of this small molecule protein tyrosine phosphatase inhibitor represent a proof‐of‐principle for a novel treatment strategy in a model for Parkinson's disease.
Empirical tests of the functional significance of amygdala‐based modulation of hippocampal representations: evidence for multiple memory consolidation pathways
Authors: McDonald Robert J. , Lo Queenie , King Amy L. , Wasiak Tamara D. , Hong Nancy S. 
Published: April 2007

AbstractThis series of experiments evaluated the effects of amygdala damage on the acquisition and long‐term retention of variants of the water task, and tested the hypothesis that the amygdala is an essential neural system for consolidation of hippocampal memories. In Experiment 1, rats with large, neurotoxic lesions of the amygdala (AMYG) showed normal acquisition on the standard spatial version of the water task, as well as normal retention and decay rate profiles on the 24‐h and 30‐day retention probes. In Experiment 2, AMYG rats showed normal one‐trial place learning abilities and could retain this one‐trial information over a 24 h delay. Experiment 3 showed that the amygdala lesions used in this study were functionally significant because AMYG rats, from Experiment 2, showed impairments in a discriminative fear conditioning to context paradigm. Experiment 4 was a critical test of the idea that the amygdala is a decisive locus for consolidation of hippocampal memories. AMYG rats were trained to sub‐asymptotic levels of performance on the standard version of the water task. Following each training session, the subjects were given a post‐training peripheral injection of d‐amphetamine. A probe test revealed that normal subjects and AMYG rats showed similar post‐training memory improvement effects. Taken together, the results show that hippocampal memory consolidation processes do not require amygdala modulation. Arguments for an alternative view are presented suggesting that there are multiple memory consolidation pathways, one of which may depend on amygdala neural circuitry.
Dissociable effects of disconnecting amygdala central nucleus from the ventral tegmental area or substantia nigra on learned orienting and incentive motivation
Authors: El‐Amamy Heather , Holland Peter C. 
Published: April 2007

AbstractRecent evidence suggests that the amygdala central nucleus (CeA) and midbrain‐striatal dopamine systems are critically involved in the alteration of attentional and emotional processing of initially neutral stimuli by associative learning. In rats, the acquisition of learned orienting responses (ORs) to visual cues paired with food is impaired by lesions of the CeA, and by lesions that disconnect CeA from the dorsolateral striatum (DLS), a region traditionally implicated in elevated responsiveness to sensory stimuli. Similarly, the acquisition of emotional significance to cues paired with food also depends on the function of CeA and of the ventral striatal nucleus accumbens (ACB), a region often considered crucial to acquired reward and motivation. For example, the ability of a cue previously paired with food to increase the rate of food‐reinforced instrumental responding (Pavlovian‐instrumental transfer, PIT) is eliminated by lesions of the CeA or the accumbens core. In this experiment, we found that lesions that functionally disconnected CeA from the substantia nigra pars compacta (SNc) impaired the acquisition of conditioned orienting to auditory cues paired with food, but had no effect on their ability to enhance instrumental responding, relative to the effects of unilateral lesions of that region. By contrast, lesions that disconnected CeA from the ventral tegmental area (VTA) had no effect on the acquisition of conditioned orienting, but facilitated Pavlovian‐instrumental transfer relative to unilateral midbrain lesions, rescuing that function to sham–lesion control levels. Otherwise, unilateral lesions of either midbrain region impaired transfer. Implications of these results for circuit models of amygdalo–striatal interactions in associative learning are discussed.
Implication of protein kinase C in the orexin‐induced elevation of extracellular dopamine levels and its rewarding effect
Authors: Narita Minoru , Nagumo Yasuyuki , Miyatake Mayumi , Ikegami Daigo , Kurahashi Kana , Suzuki Tsutomu 
Published: April 2007

AbstractIn the present study, we investigated the role of orexinergic systems in the activation of midbrain dopamine neurons. In anin vitrostudy, exposure to either orexin A or orexin B under superfusion conditions produced a transient increase in the intracellular Ca2+concentration through the phospholipase C (PLC)/protein kinase C (PKC) pathway via Gq11α or Gβγ subunits in midbrain cultured neurons, which were shown to be tyrosine hydroxylase (TH)‐positive cells, but not in purified midbrain astrocytes. Here we show thatin vivoinjection with a selective PKC inhibitor chelerythrine chloride or 2‐{8‐[(dimethylamino)methyl]‐6,7,8,9‐tetrahydropyrido[1,2‐a]indol‐3‐yl}‐3‐1‐methyl‐1H‐indol‐3‐ylmaleimide HCl (Ro‐32–0432) into the ventral tegmental area (VTA) significantly suppressed the place preference and increased levels of dopamine in the nucleus accumbens (NAcc) induced by intra‐VTA injection of orexins. These results strongly support the idea that activation of the orexin‐containing neuron in the VTA leads to the direct activation of mesolimbic dopamine neurons through the activation of the PLC/PKC pathway via Gq11α or Gβγ‐subunit activation, which could be associated with the development of its rewarding effect.
Phenylalanine activates the mitochondria‐mediated apoptosis through the RhoA/Rho‐associated kinase pathway in cortical neurons
Authors: Zhang Yongjun , Gu Xuefan , Yuan Xiaobing 
Published: April 2007

AbstractPhenylketonuria (PKU) is caused by deficiency of phenylalanine hydroxylase, resulting in an accumulation of phenylalanine in brain tissue and cerebrospinal fluid of phenylketonuria patients. Phenylketonuria is neuropathologically characterized by neuronal cell loss, white matter abnormalities, dendritic simplification, and synaptic density reduction. The neuropathological effect may be due to the ‘toxicity’ of the high concentration of phenylalanine, while the underlying mechanism remains unclear. In this study, we found that cultured cerebral cortical neurons underwent mitochondria‐mediated apoptosis when exposed to phenylalanine. We further demonstrated that phenylalanine induced RhoA activation. Phenylalanine also promoted myosin light chain (MLC) phosphorylation, which might be the result of the activation of Rho‐associated kinase (ROCK). The RhoA antagonist, C3 transferase (C3), Rho‐associated kinase specific inhibitor, Y‐27632, and the overexpression of either dominant negative RhoA or dominant negative Rho‐associated kinase inhibited phenylalanine‐induced caspase‐3 activation and rescued neurons from apoptosis, indicating that the RhoA/Rho‐associated kinase signalling pathway plays an important role in phenylalanine‐induced neuronal apoptosis.
Dorsolateral cervical spinal injury differentially affects forelimb and hindlimb action in rats
Authors: Muir Gillian D. , Webb Aubrey A. , Kanagal Srikanth , Taylor Laura 
Published: April 2007

AbstractIn experimental spinal injury studies, damage to the dorsal half of the spinal cord is common but the behavioural effects of damage to specific pathways in the dorsal cord have been less well investigated. We performed bilateral transection of the dorsolateral spinal funiculus (DLF) on 12 Long–Evans rats at the third cervical spinal segment. We quantified overground locomotion by measuring ground reaction forces, step timing and step distances as animals moved unrestrained. We also assessed skilled locomotion by measuring footslip errors made while the animals crossed horizontal ladders, and examined paw usage in a cylinder exploration task and during a skilled reaching task. Ground reaction forces revealed that rats with bilateral DLF lesions moved with a symmetrical gait, characterized mainly by altered forces exerted by the hindlimbs, delayed onset of hindlimb stance, and understepping of the hindlimbs relative to the forelimbs. These alterations in overground locomotion were subtle but were nevertheless consistent between animals and persisted throughout the 6‐week recovery period. During ladder crossing, rats with DLF lesions made more footslip errors with the hindlimbs after surgery than before. Spontaneous forelimb usage during exploration was not affected by DLF axotomy but lesioned animals were less successful during skilled reaching. This is the first study which describes preferentially altered hindlimb use during overground locomotion after cervical DLF transections. We discuss these findings in relation to previous work and to the possible contributions of different ascending and descending pathways in the DLF to locomotion and skilled movements in rats.
The extreme C‐terminus of GluRδ2 is essential for induction of long‐term depression in cerebellar slices
Authors: Kohda Kazuhisa , Kakegawa Wataru , Matsuda Shinji , Nakagami Ryoichi , Kakiya Naomasa , Yuzaki Michisuke 
Published: April 2007

AbstractLong‐term depression (LTD) of parallel fibre (PF)–Purkinje cell synapses in the cerebellum is recognized as a cellular substrate of motor learning. Although the δ2 glutamate receptor (GluRδ2) has been shown to be crucial for LTD, the mechanisms by which GluRδ2 functions remain elusive. In this study, we developed a virus vector‐based gene transfer approach to rescue impaired LTD in GluRδ2‐null Purkinje cells in cerebellar slice preparations. We demonstrated that LTD was restored in GluRδ2‐null Purkinje cells transduced with wild‐type but not with mutant GluRδ2, which lacked the PDZ‐ligand domain in the C‐terminus. Immunohistochemical analysis revealed no difference in expression levels or spine localization patterns between virally introduced wild‐type and mutant GluRδ2 proteins. Similarly, LTD was abrogated in Purkinje cells that had been acutely perfused with peptides, hampering the interaction of GluRδ2 with PDZ proteins such as PSD‐93, PTPMEG and S‐SCAM but not with delphilin. Together, these results indicate that PDZ proteins that bind to the C‐terminus of GluRδ2 are not essential for localizing GluRδ2 at synapses but are crucial for conveying signals necessary for the induction of LTD.
Proliferative responses to growth factors decline rapidly during postnatal maturation of mammalian hair cell epithelia
Authors: Gu Rende , Montcouquiol Mireille , Marchionni Mark , Corwin Jeffrey T. 
Published: April 2007

AbstractMillions of lives are affected by hearing and balance deficits that arise as a consequence of sensory hair cell loss. Those deficits affect mammals permanently, but hearing and balance recover in nonmammals after epithelial supporting cells divide and produce replacement hair cells. Hair cells are not effectively replaced in mammals, but balance epithelia cultured from the ears of rodents and adult humans can respond to hair cell loss with low levels of supporting cell proliferation. We have sought to stimulate vestibular proliferation; and we report here that treatment with glial growth factor 2 (rhGGF2) yields a 20‐fold increase in cell proliferation within sheets of pure utricular hair cell epithelium explanted from adult rats into long‐term culture. In epithelia from neonates, substantially greater proliferation responses are evoked by rhGGF2 alone, insulin alone and to a lesser degree by serum even during short‐term cultures, but all these responses progressively decline during the first 2 weeks of postnatal maturation. Thus, sheets of utricular epithelium from newborn rats average > 40% labelling when cultured for 72 h with bromo‐deoxyuridine (BrdU) and either rhGGF2 or insulin. Those from 5‐ and 6‐day‐olds average 8–15%, 12‐day‐olds average < 1% and after 72 h there is little or no labelling in epithelia from 27‐ and 35‐day‐olds. These cells are the mammalian counterparts of the progenitors that produce replacement hair cells in nonmammals, so the postnatal quiescence described here is likely to be responsible for at least part of the mammalian ear's unique vulnerability to permanent sensory deficits.
Changes in neuronal response to ischemia in retinas with genetic alterations of somatostatin receptor expression
Authors: Catalani Elisabetta , Cervia Davide , Martini Davide , Bagnoli Paola , Simonetti Elisa , Timperio Anna Maria , Casini Giovanni 
Published: April 2007

AbstractIschemia is a primary cause of neuronal death in retinal diseases. The repertoire of expressed transmitter receptors would determine the neurons' responses to ischemic damage, and peptidergic receptors may be involved. With a new in vitro model of the ischemic mouse retina, we investigated whether an altered expression of somatostatin receptors could modulate retinal responses to ischemia. We used retinas of somatostatin receptor 1 (sst1) knock out (KO) mice, where sst2 are over‐expressed and over‐functional, and of sst2 KO mice. TUNEL analysis of ischemic retinas showed a marked reduction of cell death in sst1 KO retinas, while there were no differences between wild‐type (WT) and sst2 KO retinas. In addition, caspase‐3 mRNA expression was also reduced in sst1 KO as compared to WT retinas. An immunohistochemical analysis demonstrated that different cell populations responded differently to the ischemic insult, and that the persistence of some immunohistochemical markers was greater in sst1 KO than in WT or in sst2 KO retinas. In particular, rod bipolar cell survival was markedly improved in sst1 KO retinas, while it was dramatically decreased in sst2 KO retinas. Furthermore, consistent with a role of glutamate excitotoxicity in ischemia‐induced neuronal death, retinal glutamate release was observed to increase under ischemic conditions, but this increase was significantly reduced in sst1 KO retinas. These observations demonstrate that an increased presence of functional sst2 protects against retinal ischemia, thus implementing the background for the use of sst2 analogs in therapies of retinal diseases such as glaucoma or diabetic retinopathy.