bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Association of the Arabidopsis Actin-Related Protein2/3 Complex with Cell Membranes Is Linked to Its Assembly Status But Not Its Activation
Authors: Kotchoni Simeon O. , Zakharova Taya , Mallery Eileen L. , Le Jie , El-Assal Salah El-Din , Szymanski Daniel B. 
Published: October 2009

AbstractIn growing plant cells, the combined activities of the cytoskeleton, endomembrane, and cell wall biosynthetic systems organize the cytoplasm and define the architecture and growth properties of the cell. These biosynthetic machineries efficiently synthesize, deliver, and recycle the raw materials that support cell expansion. The precise roles of the actin cytoskeleton in these processes are unclear. Certainly, bundles of actin filaments position organelles and are a substrate for long-distance intracellular transport, but the functional linkages between dynamic actin filament arrays and the cell growth machinery are poorly understood. The Arabidopsis (Arabidopsis thaliana) “distorted group” mutants have defined protein complexes that appear to generate and convert small GTPase signals into an Actin-Related Protein2/3 (ARP2/3)-dependent actin filament nucleation response. However, direct biochemical knowledge about Arabidopsis ARP2/3 and its cellular distribution is lacking. In this paper, we provide biochemical evidence for a plant ARP2/3. The plant complex utilizes a conserved assembly mechanism. ARPC4 is the most critical core subunit that controls the assembly and steady-state levels of the complex. ARP2/3 in other systems is believed to be mostly a soluble complex that is locally recruited and activated. Unexpectedly, we find that Arabidopsis ARP2/3 interacts strongly with cell membranes. Membrane binding is linked to complex assembly status and not to the extent to which it is activated. Mutant analyses implicate ARP2 as an important subunit for membrane association.
Multiple Biochemical and Morphological Factors Underlie the Production of Methylketones in Tomato Trichomes
Authors: Ben-Israel Imri , Yu Geng , Austin Michael B. , Bhuiyan Nazmul , Auldridge Michele , Nguyen Thuong , Schauvinhold Ines , Noel Joseph P. , Pichersky Eran , Fridman Eyal 
Published: October 2009

Abstract
Genetic analysis of interspecific populations derived from crosses between the wild tomato species Solanum habrochaites f. sp. glabratum, which synthesizes and accumulates insecticidal methylketones (MK), mostly 2-undecanone and 2-tridecanone, in glandular trichomes, and cultivated tomato (Solanum lycopersicum), which does not, demonstrated that several genetic loci contribute to MK metabolism in the wild species. A strong correlation was found between the shape of the glandular trichomes and their MK content, and significant associations were seen between allelic states of three genes and the amount of MK produced by the plant. Two genes belong to the fatty acid biosynthetic pathway, and the third is the previously identified Methylketone Synthase1 (MKS1) that mediates conversion to MK of β-ketoacyl intermediates. Comparative transcriptome analysis of the glandular trichomes of F2 progeny grouped into low- and high-MK-containing plants identified several additional genes whose transcripts were either more or less abundant in the high-MK bulk. In particular, a wild species-specific transcript for a gene that we named MKS2, encoding a protein with some similarity to a well-characterized bacterial thioesterase, was approximately 300-fold more highly expressed in F2 plants with high MK content than in those with low MK content. Genetic analysis in the segregating population showed that MKS2's significant contribution to MK accumulation is mediated by an epistatic relationship with MKS1. Furthermore, heterologous expression of MKS2 in Escherichia coli resulted in the production of methylketones in this host.
Correlation of vertical electrical sounding and electrical borehole log data for groundwater exploration
Authors: Hodlur G.K. , Dhakate Ratnakar 
Published: October 2009

ABSTRACTWe have correlated the longitudinal unit conductance CL obtained from interpreted vertical electrical sounding data with the formation resistivity Rt and the formation resistivity factor F, obtained by carrying out electrical borehole logging. Interpreted geophysical data of eleven soundings and two electrical borehole log records are used for the analysis. The geophysical data used were acquired in a sedimentary basin. The study area is called Lower Maner Basin located in the province of Andhra Pradesh, India. Vertical electrical soundings were carried out using a Schlumberger configuration with half current electrode separation varying from 600–1000 m. For logging the two boreholes, a Widco logger‐model 3200 PLS was used. True formation resistivity Rt was calculated from a resistivity log. Formation resistivity factor F was also calculated at various depths using Rt values. An appreciable inverse relation exists between the correlated parameters. The borehole resistivity Rt and the formation resistivity factor F decrease with the increase in the longitudinal unit conductance CL. We have shown the use of such a relation in computing borehole resistivity Rt and formation resistivity factor F at sites that posses only vertical electrical sounding data, with a fair degree of accuracy. Validation of the correlation is satisfactory. Scope for updating the correlation is discussed. Significance and applications of the relation for exploration of groundwater, namely to update the vertical electrical sounding data interpretation by translating the vertical electrical sounding data into electrical borehole log parameters, to facilitate correlations studies and to estimate the porosity (φ), permeability (K) and water saturation Sw of water bearing zones are discussed.
Preoperative stoma siting and education by stomatherapists of colorectal cancer patients: a descriptive study in twelve Spanish colorectal surgical units
Authors: Millan Monica , Tegido Montse , Biondo Sebastiano , García‐Granero Eduardo 
Published: October 2009

AbstractObjective  Patients with colorectal cancer who need a stoma should undergo preoperative marking of the stoma site and education by a trained stomatherapist. This study examined the care received by ostomy patients with colorectal cancer in Spanish colorectal surgery units, to assess its quality and to detect areas for improvement.Method  A prospective study was conducted in twelve Spanish colorectal surgery units in Spain including patients visited by the stomatherapist after surgery for colorectal cancer. Each patient answered a questionnaire about their stoma care.Results  Between September 2007 and May 2008, 270 patients were included, (63% colostomies, 37% ileostomies). Of whom; 75% had elective and 25% emergency surgery. Stomatherapist marked the stoma site in 45,6% of patients (0% emergency created stomas and 58,8% elective). However, patients who saw a stoma therapist preoperatively presented significantly lower rates of stoma complications (p < 0.001) and anxiety (p < 0.001) compared to those who did not postoperatively.Conclusions  The study has demonstrated the importance of preoperative stomatherapy assessment.
Irradiation to the immature brain attenuates neurogenesis and exacerbates subsequent hypoxic‐ischemic brain injury in the adult
Authors: Zhu Changlian , Huang Zhiheng , Gao Jianfeng , Zhang Yu , Wang Xiaoyang , Karlsson Niklas , Li Qian , Lannering Birgitta , Björk‐Eriksson Thomas , Georg Kuhn H. , Blomgren Klas 
Published: October 2009

AbstractCranial radiotherapy is common in pediatric oncology. Our purpose was to investigate if irradiation (IR) to the immature brain would increase the susceptibility to hypoxic‐ischemic injury in adulthood. The left hemisphere of postnatal day 10 (P10) mice was irradiated with 8 Gy and subjected to hypoxia‐ischemia (HI) on P60. Brain injury, neurogenesis and inflammation were evaluated 30 days after HI. IR alone caused significant hemispheric tissue loss, or lack of growth (2.8 ± 0.42 mm3, p < 0.001). Tissue loss after HI (18.2 ± 5.8 mm3, p < 0.05) was synergistically increased if preceded by IR (32.0 ± 3.5 mm3, p < 0.05). Infarct volume (5.1 ± 1.6 mm3) nearly doubled if HI was preceded by IR (9.8 ± 1.2 mm3, p < 0.05). Pathological scoring revealed that IR aggravated hippocampal, cortical and striatal, but not thalamic, injury. Hippocampal neurogenesis decreased > 50% after IR but was unchanged by HI alone. The number of newly formed microglia was three times higher after IR + HI than after HI alone. In summary, IR to the immature brain produced long‐lasting changes, including decreased hippocampal neurogenesis, subsequently rendering the adult brain more susceptible to HI, resulting in larger infarcts, increased hemispheric tissue loss and more inflammation than in non‐irradiated brains.
Glycogen synthase kinase 3β in the nucleus accumbens core mediates cocaine‐induced behavioral sensitization
Authors: Xu Chun‐mei , Wang Jun , Wu Ping , Zhu Wei‐li , Li Qian‐qian , Xue Yan‐xue , Zhai Hai‐fen , Shi Jie , Lu Lin 
Published: October 2009

AbstractGlycogen synthase kinase 3β (GSK‐3β) is a ubiquitous serine/threonine protein kinase involved in a number of signaling pathways. Previous studies have demonstrated a role for GSK‐3β in the synaptic plasticity underlying dopamine‐associated behaviors and diseases. Drug sensitization is produced by repeated exposure to the drug and is thought to reflect neuroadaptations that contribute to addiction. However, the role of GSK‐3β in cocaine‐induced behavior sensitization has not been examined. The present study investigated the effects of chronic cocaine exposure on GSK‐3β activity in the nucleus accumbens (NAc) and determined whether changes in GSK‐3β activity in the NAc are associated with cocaine‐induced locomotor sensitization. We also explored whether blockade of GSK‐3β activity in the NAc inhibits the initiation and expression of cocaine‐induced locomotor sensitization in rats using systemic or brain region‐specific administration of the GSK‐3β inhibitors lithium chloride (LiCl) and SB216763. GSK‐3β activity in the NAc core, but not NAc shell, increased after chronic cocaine (10 mg/kg, i.p.) administration. The initiation and expression of cocaine‐induced locomotor sensitization was attenuated by systemic administration of LiCl (100 mg/kg, i.p.) or direct infusion of SB216763 (1 ng/side) into the NAc core, but not NAc shell. Collectively, these results indicate that GSK‐3β activity in the NAc core, but not NAc shell, mediates the initiation and expression of cocaine‐induced locomotor sensitization, suggesting that GSK‐3β may be a potential target for the treatment of cocaine addiction.
The microtubule interacting drug candidate NAP protects against kainic acid toxicity in a rat model of epilepsy
Authors: Zemlyak Ilona , Manley Nathan , Vulih‐Shultzman Inna , Cutler Andrew B. , Graber Kevin , Sapolsky Robert M. , Gozes Illana 
Published: October 2009

AbstractNAP (NAPVSIPQ, generic name, davunetide), a neuroprotective peptide in clinical development for neuroprotection against Alzheimer’s disease and other neurodegenerative indications, has been recently shown to provide protection against kainic acid excitotoxicity in hippocampal neuronal cultures.In vivo, kainic acid toxicity models status epilepticus that is associated with hippocampal cell death. Kainic acid toxicity has been previously suggested to involve the microtubule cytoskeleton and NAP is a microtubule‐interacting drug candidate. In the current study, kainic acid‐treated rats showed epileptic seizures and neuronal death. Injection of NAP into the dentate gyrus partially protected against kainic acid‐induced CA3 neuron death. Microarray analysis (composed of > 31 000 probe sets, analyzing over 30 000 transcripts and variants from over 25 000 well‐substantiated rat genes) in the kainic acid‐injured rat brain revealed multiple changes in gene expression, which were prevented, in part, by NAP treatment. Selected transcripts were further verified by reverse transcription coupled with quantitative real‐time polymerase chain reaction. Importantly, among the transcripts regulated by NAP were key genes associated with proconvulsant properties and with long‐lasting changes that underlie the epileptic state, including activin A receptor (associated with apoptosis), neurotensin (associated with proper neurotransmission) and the Wolfram syndrome 1 homolog (human, associated with neurodegeneration). These data suggest that NAP may provide neuroprotection in one of the most serious neurological conditions, epilepsy.
Regulation of striatal nitric oxide synthesis by local dopamine and glutamate interactions
Authors: Park Diana J. , West Anthony R. 
Published: October 2009

AbstractNitric oxide (NO) is a key neuromodulator of corticostriatal synaptic transmission. We have shown previously that dopamine (DA) D1/5 receptor stimulation facilitates neuronal NO synthase (nNOS) activity in the intact striatum. To study the impact of local manipulations of D1/5 and glutamatergic NMDA receptors on striatal nNOS activity, we combined the techniques ofin vivoamperometry and reverse microdialysis. Striatal NO efflux was monitored proximal to the microdialysis probe in urethane‐anesthetized rats during local infusion of vehicle or drug. NO efflux elicited by systemic administration of SKF‐81297 was blocked following intrastriatal infusion of: (i) the D1/5 receptor antagonist SCH‐23390, (ii) the nNOS inhibitor 7‐nitroindazole, (iii) the non‐specific ionotropic glutamate receptor antagonist kynurenic acid, and (iv) the selective NMDA receptor antagonist 3‐phosphonopropyl‐piperazine‐2‐carboxylic acid. Glycine co‐perfusion did not affect SKF‐81297‐induced NO efflux. Furthermore, intrastriatal infusion of SKF‐81297 potentiated NO efflux evoked during electrical stimulation of the motor cortex. The facilitatory effects of cortical stimulation and SKF‐81297 were both blocked by intrastriatal infusion of SCH‐23390, indicating that striatal D1/5 receptor activation is necessary for the activation of nNOS by corticostriatal afferents. These studies demonstrate for the first time that reciprocal DA‐glutamate interactions play a critical role in stimulating striatal nNOS activity.
Vitamin‐regulated cytokines and growth factors in the CNS and elsewhere
Authors: Scalabrino Giuseppe 
Published: October 2009

AbstractThere is a growing awareness that natural vitamins (with the only exception of pantothenic acid) positively or negatively modulate the synthesis of some cytokines and growth factors in the CNS, and various mammalian cells and organs. As natural vitamins are micronutrients in the human diet, studying their effects can be considered a part of nutritional genomics or nutrigenomics. A given vitamin selectively modifies the synthesis of only a few cytokines and/or growth factors, although the same cytokine and/or growth factor may be regulated by more than one vitamin. These effects seem to be independent of the effects of vitamins as coenzymes and/or reducing agents, and seem to occur mainly at genomic and/or epigenetic level, and/or by modulating NF‐κB activity. Although most of the studies reviewed here have been based on cultured cell lines, but their findings have been confirmed by some keyin vivostudies. The CNS seems to be particularly involved and is severely affected by most avitaminoses, especially in the case of vitamin B12. However, the vitamin‐induced changes in cytokine and growth factor synthesis may initiate a cascade of events that can affect the function, differentiation, and morphology of the cells and/or structures not only in the CNS, but also elsewhere because most natural vitamins, cytokines, and growth factors cross the blood–brain barrier. As cytokines are essential to CNS‐immune and CNS‐hormone system communications, natural vitamins also interact with these circuits. Further studies of such vitamin‐mediated effects could lead to vitamins being used for the treatment of diseases which, although not true avitaminoses, involve an imbalance in cytokine and/or growth factor synthesis.
Thrombin potentiatesd‐aspartate efflux from cultured astrocytes under conditions of K+homeostasis disruption
Authors: Vázquez‐Juárez Erika , Hernández‐Benítez Reyna , López‐Domínguez Alejandra , Pasantes‐Morales Herminia 
Published: October 2009

AbstractThrombin levels increase in brain during ischemia and hemorrhagic episodes, and may contribute to excitotoxic neural damage. This study examined the effect of thrombin on glutamate efflux from rat cortical cultured astrocytes using3H‐d‐aspartate as radiotracer. The glutamate efflux was initiated by addition of 100 mM K+plus 1 mM ouabain (K/O) to replicate extracellular and intracellular ionic changes that occur during cerebral ischemia. Upon exposure to K/O, astrocytes swelled slowly and progressively with no evidence of volume regulation. The K/O‐induced swelling was inhibited by 65% with bumetanide and 25% with BaCl2, suggesting contribution of Na+/K+/Cl−co‐transporter and Kir channels. K/O‐elicited3H‐d‐aspartate that consisted of two phases. The first transient component of the release corresponded to 13.5% of total3H‐d‐aspartate loaded. It was markedly reduced (61%) by the glutamate transporter blocker DL‐threo‐b‐Benzyloxyaspartic acid and weakly inhibited (21%) by the volume‐sensitive anion channel blocker 4‐[(2‐Butyl‐6,7dichloro‐2‐cyclopentyl‐2,3‐dihidro‐1oxo‐1H‐inden‐5‐yl)oxy] butanoic acid (DCPIB). During the second sustained phase of release, cells lost 45% of loaded of3H‐d‐aspartate via a mechanism that was insensitive to DL‐threo‐b‐Benzyloxyaspartic acid but nearly completely suppressed by DCPIB. Thrombin (5 U/mL) had only marginal effects on the first phase but strongly potentiated (more than two‐fold)3H‐d‐aspartate efflux in the second phase. The effect of thrombin effect was proportional to cell swelling and completely suppressed by DCPIB. Overall our data showed that under K/O swelling conditions, thrombin potently enhance glutamate release via volume‐sensitive anion channel. Similar mechanisms may contribute to brain damage in neural pathologies which are associated with cell swelling, glutamate efflux and increased thrombin levels.
PRIMARY CARBON AND NITROGEN METABOLIC GENE EXPRESSION IN THE DIATOMTHALASSIOSIRA PSEUDONANA(BACILLARIOPHYCEAE): DIEL PERIODICITY AND EFFECTS OF INORGANIC CARBON AND NITROGEN1
Authors: Granum Espen , Roberts Karen , Raven John A. , Leegood Richard C. 
Published: October 2009

Diel periodicity and effects of inorganic carbon (Ci) and NO3−on the expression of 11 key genes for primary carbon and nitrogen metabolism, including potential C4photosynthesis, in the marine diatomThalassiosira pseudonanaHasle et Heimdal were investigated. Target gene transcripts were measured by quantitative reverse transcriptase–PCR, and some of the gene‐encoded proteins were analyzed by Western blotting. The diatom was grown with a 12 h photoperiod at two different Ciconcentrations maintained by air‐equilibration with either 380 μL · L−1(near‐ambient) or 100 μL · L−1(low) CO2. Transcripts of the principal Ciand NO3−assimilatory genes RUBISCO LSU (rbcL) and nitrate reductase displayed very strong diel oscillations with peaks at the end of the scotophase. Considerable diel periodicities were also exhibited by the β‐carboxylase genes phosphoenolpyruvate carboxylase (PEPC1andPEPC2) and phosphoenolpyruvate carboxykinase (PEPCK), and the Benson–Calvin cycle gene sedoheptulose–bisphosphatase (SBPase), with peaks during mid‐ to late scotophase. In accordance with the transcripts, there were substantial diel periodicities in PEPC1, PEPC2, PEPCK, and especially rbcL proteins, although they peaked during early to mid‐photophase. Inorganic carbon had some transient effects on the β‐carboxylase transcripts, and glycine decarboxylase P subunit was highly up‐regulated by low Ciconcentration, indicating increased capacity for photorespiration. Nitrogen‐starved cells had reduced amounts of carbon metabolic gene transcripts, but thePEPC1,PEPC2,PEPCK, andrbcL transcripts increased rapidly when NO3−was replenished. The results suggest that the β‐carboxylases inT. pseudonanaplay key anaplerotic roles but show no clear support for C4photosynthesis.
Neurotrophic factors promote cholinergic differentiation in human embryonic stem cell‐derived neurons
Authors: Nilbratt Mats , Porras Omar , Marutle Amelia , Hovatta Outi , Nordberg Agneta 
Published: October 2009

AbstractCholinergic neurotransmission is essential for many important functions in the brain, including cognitive mechanisms. Here we demonstrate that human embryonic stem (hES) cells differentiate into a population of neuronal cells that express the cholinergic enzyme choline acetyltransferase and homeobox proteins specifying neuronal progenitors of ventral telencephalic lineage. These differentiated cells express transcripts for cholinergic α3, α4 and α7 nicotinic acetylcholine (ACh) receptor subunits and for M1, M2 and M3 muscarinic acetylcholine receptor (mAChR) subtypes. Stimulation with brain‐derived neurotrophic factor, neurotrophin‐3, ciliary neurotrophic factor and nerve growth factor increases the proportion of cholinergic neurons. These cholinergic receptors also mediate ACh‐evoked increase in cytosolic calcium levels, and this response was unaffected by extracellular calcium removal and was abolished by the mAChR antagonist scopolamine. Our findings demonstrate expression of functional cholinergic receptors on hES cell‐derived neurons, which may provide a source of expandable cells to facilitate screening of novel cholinergic drugs and useful for evaluating cell transplantation in animal models of cholinergic dysfunction.
The actin filament cross‐linker L‐plastin confers resistance to TNF‐α in MCF‐7 breast cancer cells in a phosphorylation‐dependent manner
Authors: Janji Bassam , Vallar Laurent , Tanoury Ziad Al , Bernardin François , Vetter Guillaume , Schaffner‐Reckinger Elisabeth , Berchem Guy , Friederich Evelyne , Chouaib Salem 
Published: October 2009

AbstractWe used a tumour necrosis factor (TNF)‐α resistant breast adenocarcinoma MCF‐7 cell line to investigate the involvement of the actin cytoskeleton in the mechanism of cell resistance to this cytokine. We found that TNF resistance correlates with the loss of cell epithelial properties and the gain of a mesenchymal phenotype, reminiscent of an epithelial‐to‐mesenchymal transition (EMT). Morphological changes were associated with a profound reorganization of the actin cytoskeleton and with a change in the repertoire of expressed actin cytoskeleton genes and EMT markers, as revealed by DNA microarray‐based expression profiling. L‐plastin, an F‐actin cross‐linking and stabilizing protein, was identified as one of the most significantly up‐regulated genes in TNF‐resistant cells. Knockdown of L‐plastin in these cells revealed its crucial role in conferring TNF resistance. Importantly, overexpression of wild‐type L‐plastin in TNF‐sensitive MCF‐7 cells was sufficient to protect them against TNF‐mediated cell death. Furthermore, we found that this effect is dependent on serine‐5 phosphorylation of L‐plastin and that non‐conventional protein kinase C isoforms and the ceramide pathway may regulate its phosphorylation state. The protective role of L‐plastin was not restricted to TNF‐α resistant MCF‐7 cells because a correlation between the expression of L‐plastin and the resistance to TNF‐α was observed in other breast cancer cell lines. Together, our study discloses a novel unexpected role of the actin bundling protein L‐plastin as a cell protective protein against TNF‐cytotoxicity.