bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a novel temperature‐sensitive allele of the CUL1/AXR6 subunit of SCF ubiquitin‐ligases
Authors: Quint Marcel , Ito Hironori , Zhang Wenjing , Gray William M. 
Published: July 2005

SummarySelective protein degradation by the ubiquitin‐proteasome pathway has emerged as a key regulatory mechanism in a wide variety of cellular processes. The selective components of this pathway are the E3 ubiquitin‐ligases which act downstream of the ubiquitin‐activating and ‐conjugating enzymes to identify specific substrates for ubiquitinylation. SCF‐type ubiquitin‐ligases are the most abundant class of E3 enzymes in Arabidopsis. In a genetic screen for enhancers of the tir1‐1 auxin response defect, we identified eta1/axr6‐3, a recessive and temperature‐sensitive mutation in the CUL1 core component of the SCFTIR1 complex. The axr6‐3 mutation interferes with Skp1 binding, thus preventing SCF complex assembly. axr6‐3 displays a pleiotropic phenotype with defects in numerous SCF‐regulated pathways including auxin signaling, jasmonate signaling, flower development, and photomorphogenesis. We used axr6‐3 as a tool for identifying pathways likely to be regulated by SCF‐mediated proteolysis and propose new roles for SCF regulation of the far‐red light/phyA and sugar signaling pathways. The recessive inheritance and the temperature‐sensitive nature of the pleiotropically acting axr6‐3 mutation opens promising possibilities for the identification and investigation of SCF‐regulated pathways in Arabidopsis.
Cell adhesion inArabidopsis thalianais mediated by ECTOPICALLY PARTING CELLS 1 – a glycosyltransferase (GT64) related to the animal exostosins
Authors: Singh Sunil Kumar , Eland Cathlene , Harholt Jesper , Scheller Henrik Vibe , Marchant Alan 
Published: July 2005

SummaryDespite the fact that several hundred glycosyltransferases have been identified from sequencing of plant genomes, the biological functions of only a handful have been established to date. A Poplar glycosyltransferase 64 (GT64) family member that is differentially expressed during the cell division and elongation phases of cambial growth was identified from previously generated transcript profiling of cambium tissues. The predicted Poplar GT64 protein has a closely related Arabidopsis homolog ECTOPICALLY PARTING CELLS (EPC1). Mutation of theEPC1gene, one of three Arabidopsis GT64 family members, results in plants with a dramatically reduced growth habit, defects in vascular formation and reduced cell–cell adhesion properties in hypocotyl and cotyledon tissues. Secondary growth is enhanced inepc1hypocotyl tissues and it is proposed that this results from the abnormal cell–cell adhesion within the cortical parenchyma cell layers. Loss of cell–cell contacts within cotyledon and leaf tissues is also proposed to account for vascular patterning defects and the fragile nature ofepc1tissues. The EPC1 protein thus plays a critical role during plant development in maintaining the integrity of organs via cell–cell adhesion, thereby providing mechanical strength and facilitating the movement of metabolites throughout the plant.
A new seed‐based assay for meiotic recombination in Arabidopsis thaliana
Authors: Melamed‐Bessudo Cathy , Yehuda Elizabeth , Stuitje Antoine R. , Levy Avraham A. 
Published: July 2005

SummaryMeiotic recombination is a fundamental biological process that plays a central role in the evolution and breeding of plants. We have developed a new seed‐based assay for meiotic recombination in Arabidopsis. The assay is based on the transformation of green and red fluorescent markers expressed under a seed‐specific promoter. A total of 74 T‐DNA markers were isolated, sequenced and mapped both physically and genetically. Lines containing red and green markers that map 1–20 cM apart were crossed to produce tester lines with the two markers linked in cis yielding seeds that fluoresced both in red and green. We show that these lines can be used for efficient scoring of recombinant types (red only or green only fluorescing seeds) in a seed population derived from a test cross (backcross) or self‐pollination. Two tester lines that were characterized during several generations of backcross and self‐pollination, one in the background of ecotype Landsberg and one in the ecotype Columbia, are described. We discuss the number of plants and seeds to be scored in order to obtain reliable and reproducible crossing over rate values. This assay offers a relatively high‐throughput method, with the benefit of seed markers (similar to the maize classical genetic markers) combined with the advantages of Arabidopsis. It advances the prospect to better understand the factors that affect the rate of meiotic crossover in plants and to stimulate this process for more efficient breeding and mapping.
Optimization of biometry for intraocular lens implantation using the Zeiss IOLMaster
Authors: Madge Simon N. , Khong C. H. , Lamont Meon , Bansal Atul , Antcliff Richard J. 
Published: July 2005

Abstract.Purpose:  To compare the accuracy of biometry using conventional A‐scan ultrasonography and partial coherence interferometry, and to improve the accuracy of biometry by sequential audit of postoperative refractive error. Methods:  The study was performed in three phases. In phase 1, 20 consecutive patients undergoing routine phacoemulsification underwent biometry using both A‐scan ultrasonography and the Zeiss IOLMaster (ZIOLM). A single experienced optometrist refracted all patients 2 weeks after surgery. The errors between expected and achieved refraction were calculated and compared between the two methods. In phases 2 and 3, a further 22 and 20 patients, respectively, were recruited and only the ZIOLM was used for biometry. The manufacturer's suggested A‐constant was refined and the error between expected and achieved refraction was calculated. Results:  In phase 1, the median unexpected error for the ZIOLM was +0.63 (interquartile range +0.368 to +1.015) and for A‐scan biometry was − 0.24 (interquartile range − 1.335 to +0.802). In phase 1 65% of patients' postoperative refractions were found to be within 1.0 D of emmetropia using the ZIOLM (55% using A‐scan biometry). Refinements to the A‐constant improved this to 95% by phase 3. Conclusion:  An error was identified in IOL power estimation with the ZIOLM, when using the manufacturer's recommended A‐constant (recommended and previously optimized ultrasound A‐constant 118.0; ZIOLM optimized A‐constant 118.6). Serial modifications to the A‐constant were successful in reducing the unexpected error to well within the tolerance limits of published international standards.
Long‐term macular function in eyes with central serous chorioretinopathy
Authors: Baran Nergis V , Gürlü Vuslat P , Esgin Haluk 
Published: July 2005

AbstractBackground:  This study aimed to investigate the long‐term effects of central serous chorioretinopathy (CSCR) on macular function.Methods:  Sixty‐two eyes of 31 patients were included in this study. All patients were diagnosed with unilateral CSCR at the Retina Unit of the Ophthalmology Department, Trakya University Medical Faculty, and had a post‐attack bilateral visual acuity of 6/6 and a follow‐up period of a minimum of 6 months. Visual function was assessed using the Amsler grid, 40‐hue colour discrimination test, visual field examination by means of Octopus automatic perimeter and Cambridge contrast sensitivity tests.Results:  Of the 31 patients, 71% were men and 29% were women, with a mean age of 39.3 ± 7.6 years. The patients had a mean follow‐up period of 50.6 ± 40.5 months after the acute attack. Metamorphopsia was observed in 67.7% of the cases with CSCR. A colour discrimination defect was found in 48.4% of the CSCR eyes and in 54.8% of the fellow eyes. As compared with the fellow eyes, the mean deviation in the central 10° of visual field was significantly higher (t = 2.9, P = 0.007) and the mean contrast sensitivity score was significantly lower (t = −3.2, P = 0.004) in the CSCR eyes.Discussion:  Patients with unilateral CSCR were observed to have long‐term bilateral colour discrimination defects, and eyes with clinical CSCR were determined to have central relative scotoma and loss of contrast sensitivity.
Conjunctival squamous cell carcinoma: atypical presentation of HIV
Authors: De Silva Don Julian , Tumuluri Krishna , Joshi Naresh 
Published: July 2005

AbstractMetastatic squamous cell carcinoma (SCC) of the conjunctiva is uncommon in Western countries. A Nigerian patient who presented with right lower lid swelling treated as a chalazion is described here. She re‐presented 5 months later with widespread metastatic conjunctival SCC and positive HIV serology. Conjunctival SCC may be difficult to distinguish on clinical appearance alone and in an era of increasing global travel, young patients with a history of high ultraviolet‐B radiation exposure and from countries with a high HIV prevalence should be given a low threshold for excision biopsy.
Orbital cellulitis following cataract surgery
Authors: Sharma Vidushi , Benger Ross , Wechsler Alfred W , Kaufman Greg , Burfitt‐Williams Grosvenor CT 
Published: July 2005

AbstractOrbital cellulitis is an extremely uncommon complication following cataract surgery. Herein, a patient who developed orbital cellulitis less than 24 h after undergoing cataract surgery is described. She responded well to systemic antibiotic treatment and ultimately achieved good visual acuity in the affected eye. The most likely mode of pathogen entry in such cases is considered to be the anaesthetic block given before the cataract surgery. It has been suggested that a careful skin antiseptic preparation before the block is given could prevent this occurrence, but such a preparation did not do so in our case.
Scrg1 is induced in TSE and brain injuries, and associated with autophagy
Authors: Dron Michel , Bailly Yannick , Beringue Vincent , Haeberlé Anne‐Marie , Griffond Bernadette , Risold Pierre‐Yves , Tovey Michael G. , Laude Hubert , Dandoy‐Dron Françoise 
Published: July 2005

AbstractWe have previously identified Scrg1, a gene with increased cerebral mRNA levels in transmissible spongiform encephalopathies (TSE) such as scrapie, bovine spongiform encephalopathy and Creutzfeldt–Jakob disease. In this study, Scrg1‐immunoreactive cells, essentially neurons, were shown to be widely distributed throughout the brain of scrapie‐infected mice, while only rare and weakly immunoreactive cells could be detected in the brain of non‐infected normal mice. Induction of the protein was confirmed by Western blot analysis. At the ultrastructural level, Scrg1 protein was associated with dictyosomes of the Golgi apparatus and autophagic vacuoles in the central neurons of the scrapie‐infected mice. These results suggested a role for Scrg1 in the pathological changes observed in TSE. We have generated transgenic mice specifically expressing Scrg1 in neurons. No significant differences in the time course of the disease were detected between transgenic and non‐transgenic mice infected with scrapie prions. However, tight association of Scrg1 with autophagic vacuoles was again observed in brain neurons of infected transgenic mice. High levels of the protein were also detected in degenerating Purkinje cells of Ngsk Prnp0/0 mice overexpressing the Prnd gene coding for doppel, a neurotoxic paralogue of the prion protein. Furthermore, induction of Scrg1 protein was observed in the brain of mice injured by canine distemper virus or gold thioglucose treatment. Taken together, our results indicate that Scrg1 is associated with neurodegenerative processes in TSE, but is not directly linked to dysregulation of prion protein.
Reciprocal interactions between oscillatory activities of different frequencies in the subthalamic region of patients with Parkinson's disease
Authors: Fogelson Noa , Pogosyan Alek , Kühn Andrea A. , Kupsch Andreas , Van Bruggen Gerard , Speelman Hans , Tijssen Marina , Quartarone Angelo , Insola Angelo , Mazzone Paolo , Di Lazzaro Vincenzo , Limousin Patricia , Brown Peter 
Published: July 2005

AbstractSynchronization of neuronal activity evident in the local field potential (LFP) recorded in the subthalamic region of patients with Parkinson's disease occurs at low frequencies (< 30 Hz) and, in some patients following treatment with levodopa, at high frequencies between 65 and 85 Hz. Here we investigate the functional relationship between these different activities by determining whether spontaneous fluctuations in their strength are correlated across time. To this end, we analysed recordings of LFPs from macroelectrodes inserted in the subthalamic area of 16 patients with Parkinson's disease, after treatment with anti‐parkinsonian medication. Time‐evolving autospectra of LFPs with significant 65–85 Hz peaks (from 21 sides) were computed and correlations between frequency components determined over time. LFP activity in the 5–32 Hz band was significantly negatively correlated with that in the 65–85 Hz band in data averaged across all 21 sides, as well as in 15 (71%) of the individual records. Negative correlations were relatively selective for interactions between these frequency bands and occurred over time epochs of as little as 40 s. They occurred about 50 min after levodopa and were recorded concurrently with contralateral levodopa‐induced dyskinesias in all but four cases. Positive correlations were not seen between activities in the 5–32 Hz and 65–85 Hz bands. The spontaneous negative correlations suggest a reciprocal relationship between population synchrony in the high‐ and low‐frequency ranges, and raise the possibility that spontaneous fluctuations in the balance between these activities may contribute to levodopa‐induced dyskinesias.
Minocycline blocks bilirubin neurotoxicity and prevents hyperbilirubinemia‐induced cerebellar hypoplasia in the Gunn rat
Authors: Lin Suizhen , Wei Xing , Bales Kelly R. , Paul Aaron B. C. , Ma Zhizhong , Yan Guangmei , Paul Steven M. , Du Yansheng 
Published: July 2005

AbstractEncephalopathy induced by hyperbilirubinemia in infants has been described in the medical literature for over a century but neither the cellular nor molecular mechanisms underlying bilirubin neurotoxicity are well understood. In this study, we have demonstrated that minocycline potently protects primary cultured rat cerebellar granule neurons against bilirubin neurotoxicity (IC50 ≈ 2 µm) and almost completely blocks cerebellar hypoplasia and the profound loss of Purkinje and granule neurons observed in homozygous Gunn rats, a genetic model of hyperbilirubinemia‐induced neurotoxicity. Minocycline‐treated newborn Gunn rats had nearly equivalent numbers of viable Purkinje and granule neurons in the cerebellum as did control animals. Moreover, minocycline inhibits the bilirubin‐induced phosphorylation of p38 mitogen‐activated protein kinase both in vivo as well as in vitro. Taken together our data demonstrate that minocycline is able to greatly reduce bilirubin‐induced neurotoxicity and suggest that minocycline's neuroprotective effects may be due in part to an inhibition of p38 mitogen‐activated protein kinase activity. Our findings may lead to novel approaches for treating bilirubin‐induced encephalopathy.
Matrix metalloproteinase induction by EMMPRIN in experimental focal cerebral ischemia
Authors: Burggraf Dorothe , Liebetrau Martin , Martens Helge K. , Wunderlich Nathalie , Jäger Gabriele , Dichgans Martin , Hamann Gerhard F. 
Published: July 2005

AbstractFocal cerebral ischemia leads to the gradual disruption of the extracellular matrix. A key role in the turnover of the extracellular matrix is played by the system of matrix metalloproteinases (MMPs). In this study we describe changes of the MMP inducer protein (EMMPRIN) following experimental cerebral ischemia (induced for 3 h and followed by 24 h reperfusion, suture model) in rats. Extracellular EMMPRIN was measured by Western blot of the ischemic and nonischemic basal ganglia and cortex separately. Compared with the contralateral nonischemic area, the ischemic hemisphere showed a significant increase in EMMPRIN: basal ganglia, 158% ± 4% (P < 0.05); cortex, 128% ± 25% (P < 0.05). Immunohistochemistry was used to localize EMMPRIN on cerebral microvessels. EMMPRIN‐positive microvascular structures were quantified by automatic morphometric video‐imaging analysis and a significant increase in the number of cerebral microvessels staining positive for EMMPRIN in the ischemic basal ganglia was shown. The significant loss of microvascular basal lamina antigen collagen type IV in ischemic cortex and basal ganglia was calculated by Western blot. Measured by gelatin zymography, we demonstrated an MMP‐2 and MMP‐9 increase in the ischemic brain regions (P < 0.05). For the first time the MMP activation system EMMPRIN was shown to be relevant in cerebral ischemia. These results raise the possibility that the increased expression of EMMPRIN, the increase in MMPs and the damage of the basal lamina following cerebral ischemia are connected and part of a network of related changes.
Dopamine depletion alters phosphorylation of striatal proteins in a model of Parkinsonism
Authors: Brown Abigail M. , Deutch Ariel Y. , Colbran Roger J. 
Published: July 2005

AbstractNigrostriatal dopamine depletion disrupts striatal medium spiny neuron morphology in Parkinson's disease and modulates striatal synaptic plasticity in animal models of parkinsonism. We demonstrate that long‐term nigrostriatal dopamine depletion in the rat induces evolving changes in the phosphorylation of striatal proteins critical for synaptic plasticity. Dopamine depletion increased the phosphorylation of the alpha isoform of calcium–calmodulin‐dependent protein kinase II (CaMKIIα) at Thr286, a site associated with enhanced autonomous kinase activity, but did not alter total levels of CaMKIIα or other synaptic proteins. Dopamine depletion decreased CaMKIIα levels in postsynaptic density‐enriched fractions without significant changes in other proteins. The activity of protein phosphatase 1 (PP1), a postsynaptic phosphatase that dephosphorylates CaMKII, is regulated by DARPP‐32 (dopamine‐ and cAMP‐regulated phosphoprotein of 32 kDa). Dopamine depletion had no effect on DARPP‐32 phosphorylation at Thr34, but increased DARPP‐32 phosphorylation at Thr75. Levodopa administration reversed the increased phosphorylation of both CaMKIIα and DARPP‐32. Normal ageing increased the levels of PP1(γ1 isoform) but decreased levels of the PP1γ1‐targeting proteins spinophilin and neurabin. Elevated phosphorylations of CaMKIIα and DARPP‐32 were maintained for up to 20 months after dopamine depletion. However, phosphorylation of the CaMKII–PP1 substrate, Ser831in the glutamate receptor GluR1 subunit, was increased only after sustained (9–20 months) dopamine depletion. Interaction of ageing‐related changes in PP1 with the dopamine depletion‐induced changes in CaMKIIα may account for enhanced GluR1 phosphorylation only after long‐term dopamine depletion. These evolving changes may impact striatal synaptic plasticity, Parkinson's disease progression and the changing efficacy and side‐effects associated with dopamine replacement therapy.
Levodopa‐induced dyskinesia in MPTP‐treated macaques is not dependent on the extent and pattern of nigrostrial lesioning
Authors: Guigoni Céline , Dovero Sandra , Aubert Incarnation , Li Qin , Bioulac Bernard H. , Bloch Bertrand , Gurevich Eugenia V. , Gross Christian E. , Bezard Erwan 
Published: July 2005

AbstractThe extent of nigrostriatal denervation is presumed to play a role in the genesis of levodopa‐induced dyskinesia. Yet some parkinsonian patients who have been treated over a long period do not develop dyskinesia, raising the possibility that the pattern of denervation is as important as the extent of lesioning as a risk factor. Here we study the extent and pattern of nigrostriatal denervation in a homogeneous population of parkinsonian macaque monkeys chronically treated with levodopa. Based on the characteristics of the lesioning, non‐dyskinetic animals could not be differentiated from those with dyskinesia. Indeed, the number of tyrosine‐hydroxylase (TH)‐immunopositive neurons in the substantia nigra pars compacta, striatal dopamine transporter (DAT) binding and TH immunostaining, as well as the overall TH striatal content measured by Western blotting were identical. Moreover, the patterns of lesioning assessed by a detailed analysis of the TH‐ and DAT‐immunopositive striatal fibers were comparable in all functional quadrants and at all rostro‐caudal levels considered. These data indicate that neither the extent nor the pattern of nigrostriatal lesioning are sufficient to explain the occurrence of levodopa‐induced dyskinesia.
Spontaneous recurrent network activity in organotypic rat hippocampal slices
Authors: Mohajerani Majid H. , Cherubini Enrico 
Published: July 2005

AbstractOrganotypic hippocampal slices were prepared from postnatal day 4 rats and maintained in culture for >6 weeks. Cultured slices exhibited from 12 days in vitro spontaneous events which closely resembled giant depolarizing potentials (GDPs) recorded in neonatal hippocampal slices. GDP‐like events occurred over the entire hippocampus with a delay of 30–60 ms between two adjacent regions as demonstrated by pair recordings from CA3–CA3, CA3–CA1 and interneurone–CA3 pyramidal cells. As in acute slices, spontaneous recurrent events were generated by the interplay of GABA and glutamate acting on AMPA receptors as they were reversibly blocked by bicuculline and 6,7‐dinitroquinoxaline‐2,3‐dione but not by dl‐2‐amino‐5‐phosphonopentaoic acid. The equilibrium potentials for GABA measured in whole cell and gramicidin‐perforated patch from interconnected interneurones–CA3 pyramidal cells were −70 and −56 mV, respectively. The resting membrane potential estimated from the reversal of N‐methyl‐d‐aspartate‐induced single‐channel currents in cell‐attach experiments was −75 mV. In spite of its depolarizing action, in the majority of cases GABA was still inhibitory as it blocked the firing of principal cells. The increased level of glutamatergic connectivity certainly contributed to network synchronization and to the development of interictal discharges after prolonged exposure to bicuculline. In spite of its inhibitory action, in a minority of cells GABA was still depolarizing and excitatory as it was able to bring principal cells to fire, suggesting that a certain degree of immaturity is still present in cultured slices. This was in line with the transient bicuculline‐induced block of GDPs and with the isoguvacine‐induced increase of GDP frequency.
The intracerebral application of the PPARγ‐ligand pioglitazone confers neuroprotection against focal ischaemia in the rat brain
Authors: Zhao Yi , Patzer Andreas , Gohlke Peter , Herdegen Thomas , Culman Juraj 
Published: July 2005

AbstractThe present study addresses the neuroprotective function of intracerebroventricular (i.c.v.) application of pioglitazone, a selective ligand of the peroxisome proliferator‐activated receptor gamma (PPARγ) in the rat brain after ischaemia. Pioglitazone or vehicle were i.c.v. infused via osmotic minipumps over a 5‐day period before, and 2 days after transient middle cerebral artery occlusion (MCAO) for 90 min. This i.c.v. application of pioglitazone in the brain significantly reduced the infarct size and brain oedema, and attenuated in the peri‐infarct cortical regions the invasion of activated microglia and macrophages. Moreover, pioglitazone improved the recovery of sensory deficits 48 h after MCAO. Our data demonstrate for the first time that it is the activation of intracerebral PPARγ that can confer neuroprotection, anti‐inflammatory and neurological improvement following ischaemic injury.