bluuebunny/crossref_metadata_2025 huggingface dataset:
Association between Terror Attacks and Suicide Attempts
Authors: Weizman Tal , Yagil Yaron , Schreiber Shaul
Published: September 2009

Based on Durkheim's ‘Control theory,’ we explored the association between frequency of terror attacks in Israel and the frequency of suicide attempts admitted to the Emergency Room of a major general hospital in Tel‐Aviv (1999–2004). Analysis of the six‐year study period as a whole revealed no significant correlation between the variables, with the exception of one 11‐month segment within it (December 2000–October 2001) that did show a statistically significant positive correlation, and in opposition to Durkeim's hypothesis. It is suggested that suicide attempts as a phenomena should be seen as a product of a multivariate model, in which the social context plays a role as well.
Drug Ingestions in Children 10–14 Years Old: An Old Problem Revisited
Authors: Pomerantz Wendy , Gittelman Michael , Farris Sarah , Frey Lauren
Published: September 2009

To determine changes in rates of drug ingestions in 10–14 year old children in our country, a retrospective chart review of 10–14 year olds hospitalized for drug ingestion between 1993–1995 and 2000–2004 was performed. Odds ratios and Chi‐square were used for analyses. From 1993–1995 there were 92.8 ingestions/100,000 children/year; from 2000–2004 there were 63.3 ingestions/100,000 children/year. More males ingested in 2000–2004 than 1993–1995 (26.3% vs. 14.2% O.R. 2.15 [1.19, 3.92]). More patients took psychiatric medications in 2000–2004 than 1993–1995 (38.9% vs. 27.0%, O.R. 1.72 [1.06, 2.80]). More patients ingested SSRIs in 2000–2004 than 1993–1995; fewer ingested tricyclics. Hospitalization rates for drug ingestions have decreased. There has been a change in drug ingested, and more males are ingesting drugs.
Per Capita Alcohol Consumption and Suicide Rates in the U.S., 1950–2002
Authors: Landberg Jonas
Published: September 2009

The aim of this paper was to estimate how suicide rates in the United States are affected by changes in per capita consumption during the postwar period. The analysis included Annual suicide rates and per capita alcohol consumption data (total and beverage specific) for the period 1950–2002. Gender‐ and age‐specific models were estimated using the Box‐Jenkins technique for time series analysis. No significant estimate was found for males. For females the total alcohol estimate (0.059) was significant at the 10% level whereas the spirits estimate was significant with an effect of 0.152. The results imply that a change in U.S. per capita consumption would result in a change in female suicide rates, whereas the male rates would not be affected.
Ca2+Current versus Ca2+Channel Cooperativity of Exocytosis
Authors: Matveev Victor , Bertram Richard , Sherman Arthur
Published: September 2009

Recently there has been significant interest and progress in the study of spatiotemporal dynamics of Ca2+that triggers exocytosis at a fast chemical synapse, which requires understanding the contribution of individual calcium channels to the release of a single vesicle. Experimental protocols provide insight into this question by probing the sensitivity of exocytosis to Ca2+influx. While varying extracellular or intracellular Ca2+concentration assesses the intrinsic biochemical Ca2+cooperativity of neurotransmitter release, varying the number of open Ca2+channels using pharmacological channel block or the tail current titration probes the cooperativity between individual Ca2+channels in triggering exocytosis. Despite the wide use of these Ca2+sensitivity measurements, their interpretation often relies on heuristic arguments. Here we provide a detailed analysis of the Ca2+sensitivity measures probed by these experimental protocols, present simple expressions for special cases, and demonstrate the distinction between the Ca2+current cooperativity, defined by the relationship between exocytosis rate and the whole-terminal Ca2+current magnitude, and the underlying Ca2+channel cooperativity, defined as the average number of channels involved in the release of a single vesicle. We find simple algebraic expressions that show that the two are different but linearly related. Further, we use three-dimensional computational modeling of buffered Ca2+diffusion to analyze these distinct Ca2+cooperativity measures, and demonstrate the role of endogenous Ca2+buffers on such measures. We show that buffers can either increase or decrease the Ca2+current cooperativity of exocytosis, depending on their concentration and the single-channel Ca2+current.
Spinal Interneuron Axons Spontaneously Regenerate after Spinal Cord Injury in the Adult Feline
Authors: Fenrich Keith K. , Rose P. Ken
Published: September 2009

It is well established that long, descending axons of the adult mammalian spinal cord do not regenerate after a spinal cord injury (SCI). These axons do not regenerate because they do not mount an adequate regenerative response and growth is inhibited at the injury site by growth cone collapsing molecules, such as chondroitin sulfate proteoglycans (CSPGs). However, whether axons of axotomized spinal interneurons regenerate through the inhibitory environment of an SCI site remains unknown. Here, we show that cut axons from adult mammalian spinal interneurons can regenerate through an SCI site and form new synaptic connectionsin vivo. Using morphological and immunohistochemical analyses, we found that after a midsagittal transection of the adult feline spinal cord, axons of propriospinal commissural interneurons can grow across the lesion despite a close proximity of their growth cones to CSPGs. Furthermore, using immunohistochemical and electrophysiological analyses, we found that the regenerated axons conduct action potentials and form functional synaptic connections with motoneurons, thus providing new circuits that cross the transected commissures. Our results show that interneurons of the adult mammalian spinal cord are capable of spontaneous regeneration after injury and suggest that elucidating the mechanisms that allow these axons to regenerate may lead to useful new therapeutic strategies for restoring function after injury to the adult CNS.
Human Microsaccade-Related Visual Brain Responses
Authors: Dimigen Olaf , Valsecchi Matteo , Sommer Werner , Kliegl Reinhold
Published: September 2009

Microsaccades are very small, involuntary flicks in eye position that occur on average once or twice per second during attempted visual fixation. Microsaccades give rise to EMG eye muscle spikes that can distort the spectrum of the scalp EEG and mimic increases in gamma band power. Here we demonstrate that microsaccades are also accompanied by genuine and sizeable cortical activity, manifested in the EEG. In three experiments, high-resolution eye movements were corecorded with the EEG: during sustained fixation of checkerboard and face stimuli and in a standard visual oddball task that required the counting of target stimuli. Results show that microsaccades as small as 0.15° generate a field potential over occipital cortex and midcentral scalp sites 100–140 ms after movement onset, which resembles the visual lambda response evoked by larger voluntary saccades. This challenges the standard assumption of human brain imaging studies that saccade-related brain activity is precluded by fixation, even when fully complied with. Instead, additional cortical potentials from microsaccades were present in 86% of the oddball task trials and of similar amplitude as the visual response to stimulus onset. Furthermore, microsaccade probability varied systematically according to the proportion of target stimuli in the oddball task, causing modulations of late stimulus-locked event-related potential (ERP) components. Microsaccades present an unrecognized source of visual brain signal that is of interest for vision research and may have influenced the data of many ERP and neuroimaging studies.
Silencing the SPCA1 (Secretory Pathway Ca2+-ATPase Isoform 1) Impairs Ca2+Homeostasis in the Golgi and Disturbs Neural Polarity
Authors: Sepúlveda M. Rosario , Vanoevelen Jo , Raeymaekers Luc , Mata Ana M. , Wuytack Frank
Published: September 2009

Neural cell differentiation involves a complex regulatory signal transduction network in which Ca2+ions and the secretory pathway play pivotal roles. The secretory pathway Ca2+-ATPase isoform 1 (SPCA1) is found in the Golgi apparatus where it is actively involved in the transport of Ca2+or Mn2+from the cytosol to the Golgi lumen. Its expression during brain development in different types of neurons has been documented recently, which raises the possibility that SPCA1 contributes to neuronal differentiation. In the present study, we investigated the potential impact of SPCA1 on neuronal polarization both in a cell line and in primary neuronal culture. In N2a neuroblastoma cells, SPCA1 was immunocytochemically localized in the juxtanuclear Golgi. Knockdown of SPCA1 by RNA interference markedly delayed the differentiation in these cells. The cells retarded in differentiation showed increased numbers of neurites of reduced length compared with control cells. Ca2+imaging assays showed that the lack of SPCA1 impaired Golgi Ca2+homeostasis and resulted in disturbed trafficking of different classes of proteins including normally Golgi-localized cameleon GT-YC3.3, bearing a Golgi-specific galactosyltransferase N terminus, and a normally plasma membrane-targeted, glycosyl phosphatidyl inositol-anchored cyan fluorescent protein construct. Also in hippocampal primary neurons, which showed a differential distribution of SPCA1 expression in Golgi stacks depending on differentiation stage, partial silencing of SPCA1 resulted in delayed differentiation, whereas total suppression drastically affected the cell survival. The disturbed overall cellular Ca2+homeostasis and/or the altered targeting of organellar proteins under conditions of SPCA1 knockdown highlight the importance of SPCA1 function for normal neural differentiation.
ConcurrentLpin1andNrcamMouse Mutations Result in Severe Peripheral Neuropathy with Transitory Hindlimb Paralysis
Authors: Douglas Darlene S. , Moran Jennifer L. , Bermingham John R. , Chen Xiang-Jun , Brindley David N. , Soliven Betty , Beier David R. , Popko Brian
Published: September 2009

Peripheral neuropathy is a broad category of disorders with a diverse etiology, grouped together by their common pathogenic effect on the peripheral nervous system (PNS). Because of the heterogeneity observed to be responsible for these disorders, a forward genetics method of gene discovery was used to identify additional affected pathways. In this report, we describe the mutant mouse line 20884, generated byN-ethyl-N-nitrosourea mutagenesis, which is characterized by adult-onset transitory hindlimb paralysis. Linkage mapping revealed that two point mutations are responsible for the phenotype: a partial loss-of-function mutation in the gene for phosphatidate phosphataseLpin1and a truncation mutation in the gene that encodes the neuronal cell adhesion molecule NrCAM. To investigate how the 20884Lpin1andNrcammutations interact to produce the paralysis phenotype, the double mutant and both single mutants were analyzed by quantitative behavioral, histological, and electrophysiological means. TheLpin120884mutant and the double mutant are characterized by similar levels of demyelination and aberrant myelin structures. Nevertheless, the double mutant exhibits more severe electrophysiological abnormalities than theLpin120884mutant. TheNrcam20884mutant is characterized by normal sciatic nerve morphology and a mild electrophysiological defect. Comparison of the double mutant phenotype with the two single mutants does not point to an additive relationship between the two defects; rather, theLpin120884andNrcam20884defects appear to act synergistically to produce the 20884 phenotype. It is proposed that the absence of NrCAM in a demyelinating environment has a deleterious effect, possibly by impairing the process of remyelination.
Differential Expression of Two Distinct Functional Isoforms of Melanopsin (Opn4) in the Mammalian Retina
Authors: Pires Susana S. , Hughes Steven , Turton Michael , Melyan Zare , Peirson Stuart N. , Zheng Lei , Kosmaoglou Maria , Bellingham James , Cheetham Michael E. , Lucas Robert J. , Foster Russell G. , Hankins Mark W. , Halford Stephanie
Published: September 2009

Melanopsin is the photopigment that confers photosensitivity to a subset of retinal ganglion cells (pRGCs) that regulate many non-image-forming tasks such as the detection of light for circadian entrainment. Recent studies have begun to subdivide the pRGCs on the basis of morphology and function, but the origin of these differences is not yet fully understood. Here we report the identification of two isoforms of melanopsin from the mouseOpn4locus, a previously described long isoform (Opn4L) and a novel short isoform (Opn4S) that more closely resembles the sequence and structure of rat and human melanopsins. Both isoforms, Opn4L and Opn4S, are expressed in the ganglion cell layer of the retina, traffic to the plasma membrane and form a functional photopigmentin vitro. Quantitative PCR revealed thatOpn4Sis 40 times more abundant thanOpn4L. The two variants encode predicted proteins of 521 and 466 aa and only differ in the length of their C-terminal tails. Antibodies raised to isoform-specific epitopes identified two discrete populations of melanopsin-expressing RGCs, those that coexpress Opn4L and Opn4S and those that express Opn4L only. Recent evidence suggests that pRGCs show a range of anatomical subtypes, which may reflect the functional diversity reported for mouse Opn4-mediated light responses. The distinct isoforms of Opn4 described in this study provide a potential molecular basis for generating this diversity, and it seems likely that their differential expression plays a role in generating the variety of pRGC light responses found in the mammalian retina.
Reactive Oxygen Species Potentiate the P2X2Receptor Activity through Intracellular Cys430
Authors: Coddou Claudio , Codocedo Juan F. , Li Shuo , Lillo Juan G. , Acuña-Castillo Claudio , Bull Paulina , Stojilkovic Stanko S. , Huidobro-Toro J. Pablo
Published: September 2009

P2X receptor channels (P2XRs) are allosterically modulated by several compounds, mainly acting at the ectodomain of the receptor. Like copper, mercury, a metal that induces oxidative stress in cells, also stimulates the activity of P2X2R and inhibits the activity of P2X4R. However, the mercury modulation is not related to the extracellular residues critical for copper modulation. To identify the site(s) for mercury action, we generated two chimeras using the full size P2X2subunit, termed P2X2a, and a splice variant lacking a 69 residue segment in the C terminal, termed P2X2b, as the donors for intracellular and transmembrane segments and the P2X4subunit as the donor for ectodomain segment of chimeras. The potentiating effect of mercury on ATP-induced current was preserved inXenopusoocytes expressing P2X4/2achimera but was absent in oocytes expressing P2X4/2bchimera. Site-directed mutagenesis experiments revealed that the Cys430residue mediates effects of mercury on the P2X2aR activity. Because mercury could act as an oxidative stress inducer, we also tested whether hydrogen peroxide (H2O2) and mitochondrial stress inducers myxothiazol and rotenone mimicked mercury effects. These experiments, done in both oocytes and human embryonic kidney HEK293 cells, revealed that these compounds potentiated the ATP-evoked P2X2aR and P2X4/2aR currents but not P2X2bR and P2X2a–C430A and P2X2a–C430S mutant currents, whereas antioxidants dithiothreitrol andN-acetylcysteine prevented the H2O2potentiation. Alkylation of Cys430residue with methylmethane-thiosulfonate also abolished the mercury and H2O2potentiation. Altogether, these results are consistent with the hypothesis that the Cys430residue is an intracellular P2X2aR redox sensor.
From Threat to Fear: The Neural Organization of Defensive Fear Systems in Humans
Authors: Mobbs Dean , Marchant Jennifer L. , Hassabis Demis , Seymour Ben , Tan Geoffrey , Gray Marcus , Petrovic Predrag , Dolan Raymond J. , Frith Christopher D.
Published: September 2009

Postencounter and circa-strike defensive contexts represent two adaptive responses to potential and imminent danger. In the context of a predator, the postencounter reflects the initial detection of the potential threat, whereas the circa-strike is associated with direct predatory attack. We used functional magnetic resonance imaging to investigate the neural organization of anticipation and avoidance of artificial predators with high or low probability of capturing the subject across analogous postencounter and circa-strike contexts of threat. Consistent with defense systems models, postencounter threat elicited activity in forebrain areas, including subgenual anterior cingulate cortex (sgACC), hippocampus, and amygdala. Conversely, active avoidance during circa-strike threat increased activity in mid-dorsal ACC and midbrain areas. During the circa-strike condition, subjects showed increased coupling between the midbrain and mid-dorsal ACC and decreased coupling with the sgACC, amygdala, and hippocampus. Greater activity was observed in the right pregenual ACC for high compared with low probability of capture during circa-strike threat. This region showed decreased coupling with the amygdala, insula, and ventromedial prefrontal cortex. Finally, we found that locomotor errors correlated with subjective reports of panic for the high compared with low probability of capture during the circa-strike threat, and these panic-related locomotor errors were correlated with midbrain activity. These findings support models suggesting that higher forebrain areas are involved in early-threat responses, including the assignment and control of fear, whereas imminent danger results in fast, likely “hard-wired,” defensive reactions mediated by the midbrain.
PKMζ Restricts Dendritic Arbor Growth by Filopodial and Branch Stabilization within the Intact and Awake Developing Brain
Authors: Liu Xue Feng , Tari Parisa Karimi , Haas Kurt
Published: September 2009

The molecular mechanisms underlying activity-dependent neural circuit growth and plasticity during early brain development remain poorly understood. Protein kinase Mζ (PKMz), an endogenous constitutively active kinase associated with late-phase long-term synaptic potentiation and memory in the mature brain, is expressed in the embryonicXenopusretinotectal system with heightened levels during peak periods of dendrite growth and synaptogenesis.In vivorapid time-lapse imaging of actively growing tectal neurons and comprehensive three-dimensional tracking of dynamic dendritic growth behavior finds that altered PKMz activity affects morphologic stabilization. Exogenous expression of PKMz within single neurons stabilizes dendritic filopodia by increasing dendritic filopodial lifetimes and decreasing filopodial additions, eliminations, and motility, whereas long-termin vivoimaging demonstrates restricted expansion of the dendritic arbor. Alternatively, blocking endogenous PKMz activity in individual growing tectal neurons with an inhibitory peptide (ζ-inhibitory peptide) destabilizes dendritic filopodia and over long periods promotes excessive arbor expansion. Furthermore, inhibiting endogenous PKMz throughout the tectum decreases colocalization of immunostained presynaptic and postsynaptic markers, SNAP-25 and PSD-95, respectively, suggesting impaired synapse maintenance. Together, these results implicate PKMz activity in restricting dendritic arborization during embryonic brain circuit development through synaptotropic stabilization of dynamic processes.
Similar Neurons, Opposite Adaptations: Psychostimulant Experience Differentially Alters Firing Properties in Accumbens Core versus Shell
Authors: Kourrich Saïd , Thomas Mark J.
Published: September 2009

The principal components of neuronal excitability include synaptic and intrinsic membrane parameters. While recent studies indicate that cocaine exposure can induce widespread changes in synaptic function in the neural circuits for reward, intrinsic firing properties have received much less attention. Using whole-cell recording inex vivobrain slices from cocaine-treated mice, we studied the intrinsic firing characteristics of medium-spiny projection neurons of the nucleus accumbens—a key node in the circuit that controls reward-directed behavior. Our data demonstrate that repeatedin vivococaine (5 × 15 mg/kg, i.p., once daily, 5 d) induces opposite changes in neurons of the two main subdivisions of the accumbens, the shell and the core. While shell neurons exhibit an initial depression in firing capacity (1–3 d abstinence) that persists for at least 2 weeks, core neurons exhibit increased firing capacity during early abstinence (1–3 d) that declines to basal levels within 2 weeks. Shared adaptations between addictive drugs may mediate core processes of addiction. We find that amphetamine exposure (5 × 5 mg/kg, i.p., once daily, 5 d) that induced a similar degree of locomotor sensitization as cocaine also induced an indistinguishable pattern of NAc intrinsic plasticity. Finally, we provided evidence that opposite regulation of A-type potassium current is an important factor in this bidirectional intrinsic plasticity for both cocaine and amphetamine. We propose that a persistent disparity in core/shell excitability might be an important mediator of the changes in reward circuit activity that drive drug-seeking behavior in animal models of addiction.
Parallel Regulation of a Modulator-Activated Current via Distinct Dynamics Underlies Comodulation of Motor Circuit Output
Authors: DeLong Nicholas D. , Kirby Matthew S. , Blitz Dawn M. , Nusbaum Michael P.
Published: September 2009

The cellular mechanisms underlying comodulation of neuronal networks are not elucidated in most systems. We are addressing this issue by determining the mechanism by which a peptide hormone, crustacean cardioactive peptide (CCAP), modulates the biphasic (protraction/retraction) gastric mill (chewing) rhythm driven by the projection neuron MCN1 in the crab stomatogastric ganglion. MCN1 activates this rhythm by slow peptidergic (CabTRP Ia) and fast GABAergic excitation of the reciprocally inhibitory central pattern generator neurons LG (protraction) and Int1 (retraction), respectively. MCN1 synaptic transmission is limited to the retraction phase, because LG inhibits MCN1 during protraction. Bath-applied CCAP also excites both LG and Int1, but selectively prolongs protraction. Here, we use computational modeling and dynamic-clamp manipulations to establish that CCAP prolongs the gastric mill protractor (LG) phase and maintains the retractor (Int1) phase duration by activating the same modulator-activated inward current (IMI) in LG as MCN1-released CabTRP Ia. However, the CCAP-activated current (IMI-CCAP) and MCN1-activated current (IMI-MCN1) exhibit distinct time courses in LG during protraction. This distinction results fromIMI-CCAPbeing regulated only by postsynaptic voltage, whereasIMI-MCN1is also regulated by LG presynaptic inhibition of MCN1. Hence, without CCAP, retraction and protraction duration are determined by the time course ofIMI-MCN1buildup and feedback inhibition-mediated decay, respectively, in LG. WithIMI-CCAPcontinually present, the impact of the feedback inhibition is reduced, prolonging protraction and maintaining retraction duration. Thus, comodulation of rhythmic motor activity can result from convergent activation, via distinct dynamics, of a single voltage-dependent current.
Pathophysiology of Locus Ceruleus Neurons in a Mouse Model of Rett Syndrome
Authors: Taneja Praveen , Ogier Michael , Brooks-Harris Gabriel , Schmid Danielle A. , Katz David M. , Nelson Sacha B.
Published: September 2009

Rett syndrome (RTT) is a neurodevelopmental disorder caused by loss-of-function mutations in the Methyl-CpG-binding protein-2 (MECP2) gene and is characterized by derangements in cognition, behavior, motor control, respiration and autonomic homeostasis, as well as seizures. Deficits in norepinephrine (NE) are thought to contribute to RTT pathogenesis, but little is known about how MeCP2 regulates function of noradrenergic neurons. We therefore characterized morphological, electrical, and neurochemical properties of neurons in the locus ceruleus (LC), the major source of noradrenergic innervation to the central neuraxis, inMecp2mutant mice. We found that MeCP2 null LC neurons are electrically hyperexcitable, smaller in size, and express less of the NE-synthesizing enzyme tyrosine hydroxylase (TH) compared with wild-type neurons. Increased excitability of mutant neurons is associated with reductions in passive membrane conductance and the amplitude of the slow afterhyperpolarization. Studies inMecp2heterozygotes, which are mosaic for the null allele, demonstrated that electrical hyperexcitability and reduced neuronal size are cell-autonomous consequences of MeCP2 loss, whereas reduced TH expression appears to reflect both cell-autonomous and non-autonomous influences. Finally, we found reduced levels of TH and norepinephrine in cingulate cortex, a forebrain target of the LC. Thus, genetic loss of MeCP2 results in a somewhat paradoxical LC neuron phenotype, characterized by both electrical hyperexcitability and reduced indices of noradrenergic function. Given the importance of the LC in modulating activity in brainstem and forebrain networks, we hypothesize that dysregulation of LC function in the absence of MeCP2 plays a key role in the pathophysiology of RTT.
Adenylyl Cyclase Type 5 Contributes to Corticostriatal Plasticity and Striatum-Dependent Learning
Authors: Kheirbek Mazen A. , Britt Jon P. , Beeler Jeff A. , Ishikawa Yoshihiro , McGehee Daniel S. , Zhuang Xiaoxi
Published: September 2009

Dopamine (DA)-dependent corticostriatal plasticity is thought to underlie incremental procedural learning. A primary effector of striatal DA signaling is cAMP, yet its role in corticostriatal plasticity and striatum-dependent learning remains unclear. Here, we show that genetic deletion of a striatum-enriched isoform of adenylyl cyclase, AC5 knock-out (AC5KO), impairs two forms of striatum-dependent learning and corticostriatal synaptic plasticity. AC5KO mice were severely impaired in acquisition of a response strategy in the cross maze, a striatum-dependent task requiring a correct body turn to find a goal arm. In addition, AC5KO mice were impaired in acquisition of a motor skill, as assessed by the accelerated rotarod. Slice electrophysiology revealed a deficit in corticostriatal long-term depression (LTD) after high-frequency stimulation of tissue from AC5KO mice. LTD was rescued by activation of either presynaptic cannabinoid type 1 (CB1) receptors or postsynaptic metabotropic glutamate receptors (mGluRs), suggesting a postsynaptic role of AC5–cAMP, upstream of endocannabinoid release. In striatopallidal-projecting medium spiny neurons, DA D2receptors are negatively coupled to cAMP production, and activation of these receptors is required for endocannabinoid release and corticostriatal LTD. Recordings from striatopallidal neurons indicated that this is mediated by AC5, because coactivation of D2and mGluRs could induce LTD in wild-type but not in AC5KO neurons. To further examine the role of cAMP in corticostriatal plasticity, we elevated cAMP in striatal neurons of wild-type mice via the recording electrode. Under these conditions, corticostriatal LTD was eliminated. Together, these data suggest an AC5–cAMP–endocannabinoid–CB1signaling pathway in corticostriatal plasticity and striatum-dependent learning.
Novel Subtype-Specific Genes Identify Distinct Subpopulations of Callosal Projection Neurons
Authors: Molyneaux Bradley J. , Arlotta Paola , Fame Ryann M. , MacDonald Jessica L. , MacQuarrie Kyle L. , Macklis Jeffrey D.
Published: September 2009

Little is known about the molecular development and heterogeneity of callosal projection neurons (CPN), cortical commissural neurons that connect homotopic regions of the two cerebral hemispheres via the corpus callosum and that are critical for bilateral integration of cortical information. Here we report on the identification of a series of genes that individually and in combination define CPN and novel CPN subpopulations during embryonic and postnatal development. We usedin situhybridization analysis, immunocytochemistry, and retrograde labeling to define the layer-specific and neuron-type-specific distribution of these newly identified CPN genes across different stages of maturation. We demonstrate that a subset of these genes (e.g.,Hspb3andLpl) appear specific to all CPN (in layers II/III and V–VI), whereas others (e.g.,Nectin-3,Plexin-D1, andDkk3) discriminate between CPN of the deep layers and those of the upper layers. Furthermore, the data show that several genes finely subdivide CPN within individual layers and appear to label CPN subpopulations that have not been described previously using anatomical or morphological criteria. The genes identified here likely reflect the existence of distinct programs of gene expression governing the development, maturation, and function of the newly identified subpopulations of CPN. Together, these data define the first set of genes that identify and molecularly subcategorize distinct populations of callosal projection neurons, often located in distinct subdivisions of the canonical cortical laminae.
Should anterior pituitary function be tested during follow-up of all patients presenting at the emergency department because of traumatic brain injury?
Authors: van der Eerden Anke W , Twickler Marcel Th B , Sweep Fred C G J , Beems Tjemme , Hendricks Henk T , Hermus Ad R M M , Vos Pieter E
Published: September 2009

Context

A wide range (15–56%) of prevalences of anterior pituitary insufficiency are reported in patients after traumatic brain injury (TBI). However, different study populations, study designs, and diagnostic procedures were used. No data are available on emergency-department-based cohorts of TBI patients.

Objective

To assess the prevalence of pituitary dysfunction in an emergency-department-based cohort of TBI patients using strict endocrinological diagnostic criteria.

Methods

Of all the patients presenting in the emergency department with TBI over a 2-year period, 516 matched the inclusion criteria. One hundred and seven patients (77 with mild TBI and 30 with moderate/severe TBI) agreed to participate. They were screened for anterior pituitary insufficiency by GHRH–arginine testing, evaluation of fasting morning hormone levels (cortisol, TSH, free thyroxine, FSH, LH, and 17β-estradiol or testosterone), and menstrual history 3–30 months after TBI. Abnormal screening results were defined as low peak GH to GHRH–arginine, or low levels of any of the end-organ hormones with low or normal pituitary hormone levels. Patients with abnormal screening results were extensively evaluated, including additional hormone provocation tests (insulin tolerance test, ACTH stimulation test, and repeated GHRH–arginine test) and assessment of free testosterone levels.

Results

Screening results were abnormal in 15 of 107 patients. In a subsequent extensive endocrine evaluation, anterior pituitary dysfunction was diagnosed in only one patient (partial hypocortisolism).

Conclusion

By applying strict diagnostic criteria to an emergency-department-based cohort of TBI patients, it was shown that anterior pituitary dysfunction is rare (<1%). Routine pituitary screening in unselected patients after TBI is unlikely to be cost-effective.
Geographical correlation between incidence of benign disease and that of cancer of the thyroid among the population of the Rhône-Alpes région of France
Authors: Sassolas Geneviève , Hafdi-Nejjari Zakia , Schott Anne Marie , Bournaud Claire , Peix Jean Louis , Orgiazzi Jacques , Dutrieux-Berger Nicole , Borson-Chazot Françoise , _ _
Published: September 2009

Objective

To analyze, at a population level, the relation between the incidences of benign thyroid diseases in patients submitted to surgery and that of thyroid cancers based on their respective geographical distributions.

Methods

The study included 3169 cases (691 cancers and 2478 benign diseases) operated on in 2002 in the Rhône-Alpes région, which is subdivided into eight départements and 311 cantons.

Results

The total thyroid intervention rate was 54.6/100 000 (23.4 and 86.4), and the annual cancer incidence was 11.9/100 000 (4.7 and 13.8) for men and women respectively. The prevalence of cancer among thyroid surgery was 21.8% and that of cancer discovered in goiters increased with age (44% at 60 years). Intervention rates varied from départment to département. In women, the incidence of microcancers was correlated to the thyroid intervention for benign pathologies rate. In men, the incidence of supracentimetric cancers was related to the TIBR. At the canton level, the relative risk of benign diseases was correlated to that of cancers. TIBR and incidence of cancers were higher in urban cantons than in nonurban ones. The density of endocrinologists influenced the prevalence of cancers among all the cases submitted to surgery.

Conclusion

In the Rhône-Alpes population with high rates of thyroid cancer incidence and of thyroid surgery, a number of correlations were found according to gender and tumor size. However, the general incidence of cancer was not directly related to surgical activity. Geographical variability may be related to the heterogeneous medical and pathological practices.
Dietary omega-3 and -6 polyunsaturated fatty acids affect the composition and development of sheep granulosa cells, oocytes and embryos
Authors: Wonnacott K E , Kwong W Y , Hughes J , Salter A M , Lea R G , Garnsworthy P C , Sinclair K D
Published: September 2009

The evidence that omega-3 (n-3) and -6 (n-6) polyunsaturated fatty acids (PUFAs) have differential effects on ovarian function, oocytes and embryo quality is inconsistent. We report on the effects of n-3 versus n-6 PUFA-enriched diets fed to 36 ewes over a 6-week period, prior to ovarian stimulation and follicular aspiration, on ovarian steroidogenic parameters and embryo quality. Follicle number and size were unaltered by diet, but follicular-fluid progesterone concentrations were greater in n-3 PUFA-fed ewes than in n-6 PUFA-fed ewes. The percentage of saturated FAs (mostly stearic acid) was greater in oocytes than in either granulosa cells or plasma, indicating selective uptake and/orde novosynthesis of saturated FAs at the expense of PUFAs by oocytes. High-density lipoproteins (HDLs) fractionated from sera of these ewes increased granulosa cell proliferation and steroidogenesis relative to the FA-free BSA control during culture, but there was no differential effect of n-3 and n-6 PUFAs on either oestradiol or progesterone production. HDL was ineffective in delivering FAs to embryos during culture, although n-6 PUFA HDL reduced embryo development. All blastocysts, irrespective of the treatment, contained high levels of unsaturated FAs, in particular linoleic acid. Transcripts for HDL and low-density lipoprotein (LDL) receptors (SCARB1andLDLR) and stearoyl-CoA desaturase (SCD) are reported in sheep embryos. HDL reduced the expression of transcripts forLDLRandSCDrelative to the BSA control. The data support a differential effect of n-3 and n-6 PUFAs on ovarian steroidogenesis and pre-implantation development, the latter in the absence of a net uptake of FAs.
Appearing of bone marrow derived stem cells in healthy- and regenerating colonic epithelium
Authors: Valcz Gábor , Krenács Tibor , Sipos Ferenc , Wichmann Barnabás , Tóth Kinga , Leiszter Katalin , Balogh Zsófia , Csizmadia Annamária , Hagymási Krisztina , Műzes Györgyi , Masszi Tamás , Molnár Béla , Tulassay Zsolt
Published: September 2009

A vastagbél gyulladásos folyamataiban kialakuló regenerációban csontvelői eredetű mesenchymalis őssejtek (MSC) is részt vehetnek. Ezek a sejtek a vastagbél hámrétegébe vándorolnak, ahol hámsejtté érnek, vagy megtartva őssejttulajdonságaikat, utódsejteket hoznak létre. Az MSC-sejtek feltehetően a lymphoid aggregátumok területén lépnek ki az erekből, majd innen vándorolnak a környező cryptákba. Vándorlásuk során a szöveti mikrokörnyezet hatására megváltoznak.
Célkitűzés:
Munkánkban a csontvelői őssejtek vastagbélhámba épülésének jellegzetességeit vizsgáltuk egészséges és gyulladásos mintákban. Megvizsgáltuk a lymphoid aggregátumok szerepét is a hámréteg regenerációjában.
Anyagok és módszerek:
Tanulmányunkhoz férfi donor csontvelővel átültetett nők vastagbeléből származó biopsziás mintákat használtunk fel. A mintákon először nemi kromoszómákat mutattunk ki
fluoreszcens in situ hibridizációval
(FISH), majd a metszeteket digitálisan archiváltuk, ez után CD45 és cytokeratin (CK) kettős fluoreszcens immunhisztokémiai (IF) jelölést végeztünk. A metszeteket ismételten digitalizáltuk, a mintákat virtuális mikroszkóp (Mirax Viewer) segítségével párhuzamosan értékeltük.
Eredmények:
A crypták hámrétegébe beépülő Y-FISH-pozitív, CD45-negatív potenciális MSC-sejtek száma lényegességi szintet meghaladó (szignifikáns) emelkedést (p = 0,002; p = 0,003) mutatott (1,075%) a lymphoid aggregátumok környezetében, mind a normális vastagbélszövet (0,027%), mind az enyhe gyulladásos (0,045%) mintákhoz képest.
Következtetés:
Adataink arra utalnak, hogy a szöveti őssejtek kapacitása elégséges a kisfokú gyulladásos folyamatok regenerációjához. Az aspecifikus gyulladás esetében azonban a hámrétegbe beépülő MSC-sejtek száma megnő, ezek funkcionáló hámsejtté érése gyakoribb, mint az utódsejtek létrehozása. Eredményeink azt mutatják, hogy a lymphoid aggregátumok részt vesznek a hám regenerációs folyamataiban.
Adalimumab treatment in infliximab resistant pediatric patient with Crohn’s disease
Authors: Veres Gábor , Putz Réka , Szabó Dolóresz , Molnár Kriszta , Bodánszky Hedvig , Dezsőfi Antal , Arató András
Published: September 2009

Hagyományos kezelésre refrakter, fistulás Crohn-betegek kezelésében a chimer antitumornekrózis-faktor-alfa- (infliximab-) terápia igen hatékony, bár a betegek egy részében infliximabrezisztencia alakulhat ki. A szerzők egy infliximabrezisztens, 12 éves Crohn-beteg fiú esetét ismertetik, akinek luminális gyulladása mellett 3 aktív perianalis fistulája is volt. Teljesen humanizált antitumornekrózis-faktor-alfa- (adalimumab-) kezelést követően a 10. héten a fistulák bezáródtak, a korábbi magas aktivitási index normalizálódott. Validált életminőségi mutatók szintén szignifikánsan javultak. Az eset alapján infliximabrezisztens Crohn-beteg gyermeknél az adalimumabterápia sikerrel alkalmazható.
\documentclass{aastex} \usepackage{amsbsy} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{bm} \usepackage{mathrsfs} \usepackage{pifont} \usepackage{stmaryrd} \usepackage{textcomp} \usepackage{upgreek} \usepackage{portland,xspace} \usepackage{amsmath,amsxtra} \usepackage{bbm} \pagestyle{empty} \DeclareMathSizes{10}{9}{7}{6} \begin{document} \(\mathfrak{B}\) \end{document} -statistical approximation for periodic functions
Authors: Dirik Fadime , Demirci Kamil
Published: September 2009

In this study, using the concept of \documentclass{aastex}
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\end{document}-statistical convergence for sequence of infinite matrices \documentclass{aastex}
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) with \documentclass{aastex}
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\end{document}i
= (
bnk
(
i
)) we prove a Korovkin-type approximation theorem for sequences of positive linear operators defined on
C
* which is the space of all 2π-periodic and continuous functions on ℝ, the set of all real numbers. Also we study the rates of \documentclass{aastex}
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Balancing sets of vectors
Authors: Hegedűs Gábor
Published: September 2009

Let
n
be an arbitrary integer, let
p
be a prime factor of
n
. Denote by
ω1
the
pth
primitive unity root, \documentclass{aastex}
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$$\omega _1 : = e^{\tfrac{{2\pi i}}
{p}}$$
\end{document}.Define
ωi
≔
ω1i

for 0 ≦
i
≦
p
− 1 and
B
≔ {1,
ω1
, …,
ωp
−1
}
n
⊆ ℂ
n
.Denote by
K
(
n; p
) the minimum
k
for which there exist vectors
ν1
, …,
νk
∈
B
such that for any vector
w
∈
B
, there is an
i
, 1 ≦
i
≦
k
, such that
νi
·
w
= 0, where
ν · w
is the usual scalar product of
ν
and
w
.Gröbner basis methods and linear algebra proof gives the lower bound
K
(
n; p
) ≧
n
(
p
− 1).Galvin posed the following problem: Let
m
=
m
(
n
) denote the minimal integer such that there exists subsets
A1
, …,
Am
of {1, …, 4
n
} with |
Ai
| = 2
n
for each 1 ≦
i
≦
n
, such that for any subset
B
⊆ [4
n
] with 2
n
elements there is at least one
i
, 1 ≦
i
≦
m
, with
Ai
∩
B
having
n
elements. We obtain here the result
m
(
p
) ≧
p
in the case of
p
> 3 primes.
Embedding theorems in strong approximation of Fourier series
Authors: Yu Dansheng
Published: September 2009

In this paper, we introduce some new classes of functions and investigate the embedding relations among these classes. Our results generalize the related results of Leindler [3] and Yu-Zhou [9].
On the global attractivity and the solution of recursive sequence
Authors: Elsayed Elsayed
Published: September 2009

In this paper we study the behavior of the difference equation \documentclass{aastex}
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$$x_{n + 1} = ax_{n - 2} + \frac{{bx_n x_{n - 2} }}{{cx_n + dx_{n - 3} }},n = 0,1,...$$
\end{document} where the initial conditions
x−3
,
x−2
,
x−1
,
x0
are arbitrary positive real numbers and
a, b, c, d
are positive constants. Also, we give the solution of some special cases of this equation.
Work-hardening mechanisms of the Ti60Cu14Ni12Sn4Nb10 nanocomposite alloy
Authors: Concustell Amadeu , Sort Jordi , Fornell Jordina , Rossinyol Emma , Suriñach Santiago , Gebert Annett , Eckert Jurgen , Baró M. Dolors
Published: September 2009

The work-hardening mechanisms of the Ti60Cu14Ni12Sn4Nb10 nanocomposite alloy were studied. This material is composed of micrometer-sized dendrites embedded in a nanostructured eutectic matrix and a CuTi2 intermetallic phase. Our study shows that, in the as-quenched state, the nanostructured eutectic matrix behaves softer than the dendrites. During mechanical deformation, both the dendrites and the eutectic matrix harden, whereas the hardness of the CuTi2 intermetallic phase remains unaltered. The high strength of the dendrites is caused by the interplay between solid solution hardening and dislocation networks during plastic flow. Interestingly, the mechanical hardening of the nanoeutectic matrix is also assisted by a martensitic transformation of the NiTi phase. Transmission electron microscopy studies clearly show that the martensitic transformation of this phase is accompanied with grain size refinement, which also plays a role in the deformation-induced mechanical hardening.
Experimental investigation and thermodynamic modeling of the ternary Al–Cu–Fe system
Authors: Chen Hai-Lin , Du Yong , Xu Honghui , Xiong Wei
Published: September 2009

The constitution of the ternary system Al–Cu–Fe in the region above 40 at.% Al at 600 °C is investigated by means of x-ray diffraction, metallography, scanning electron microanalysis, energy dispersive x-ray spectroscopy, and differential thermal analysis. The phase equilibria in the Al-rich corner are clarified by the valuable experimental evidence for the four-phase reaction L + λFe4Al13↔ (Al) + ω at 600.7 °C and experimental findings that the phase αFe4CuAl23was not detected. A thermodynamic model of the Al–Cu–Fe system was then performed over the entire composition range by taking into account the phase diagram data above 560 °C from the literature and the present work. This work challenged the modeling of the considerably complex order–disorder phase transition between bcc_A2 and bcc_B2 phases and the miscibility gap of bcc_B2 phase using the modified sublattice model.
Magnetic tunnel junctions using LaSrMnO ferromagnetic electrodes and PbZrTiO3 piezoelectric barrier
Authors: Pradhan A.K. , Mundle R. , Konda R.B. , Yasar O. , Williams F. , Bahoura M.
Published: September 2009

We report on the fabrication and tunneling characteristics of pulsed-laser deposited LaSrMnO (LSMO)/PbZrTiO(PZT)/LSMO/SrTiO3 magnetic tunnel junctions. The trilayer films show magnetic onset at about 360 K with ferromagnetic hysteresis and uniaxial magnetic behavior at room temperature. The microscopic studies show that the effective barrier thickness is reduced due to the presence of defects in the barrier region. Tunneling magnetoresistance measurements were performed on several samples. Our results suggest that the asymmetric deformation of the barrier potential profile induced by the ferroelectric polarization of PZT influences the tunneling characteristics and can be used for electrically controlled readout in quantum computing schemes.
Grain refinement effect of pulsed magnetic field on solidified microstructure of superalloy IN718
Authors: Ma Xiaoping , Li Yingju , Yang Yuansheng
Published: September 2009

The refinement mechanism of pulsed magnetic field (PMF) was discussed by experimental investigation, and the effects of exciting frequency, exciting voltage, and delay time of PMF on grains refinement of superalloy were studied. The experimental results show that, as exciting frequency or exciting voltage is increased, the grains are refined. However, the grains become coarse when frequency increases further. As delay time of PMF increases, the grain size increases. The refinement effect of PMF is attributed to the detachment of heterogeneous nuclei on the mold wall and subsequently separation of nuclei in the melt. The Joule heat can prolong the continuous nucleation process. However, the refinement effect will be impaired if the Joule heat is strong enough to remelt the detached nuclei.