bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adrenocortical carcinoma: Retrospective study of 14 patients experienced at a single institution over 34 years
Authors: Nishida Sachiyo , Itoh Naoki , Sasao Takumi , Masumori Naoya , Taguchi Keisuke , Tsukamoto Taiji 
Published: June 2007

Objective:  To review clinical outcome of patients with adrenocortical carcinoma experienced at a single institute over 34 years.Methods:  The study included 14 patients who were diagnosed as having the disease and were treated at the Department of Urology, Sapporo Medical University Hospital between 1973 and 2006. Their clinical features and outcomes were reviewed.Results:  Of the 14 patients, there were nine men and five women. The median follow‐up period was 13.0 months (range, 1–213). Two patients were classified as having stage II disease, seven as stage III and five as stage IV. The disease was completely removed in eight patients and incompletely in three. Two other patients received exploratory laparotomy only. The remaining one patient had no indication for surgery. The median survival periods were 2 months in patients with stage IV and 108 months in those with stages II and III (P = 0.136). Mitotane treatment in the adjuvant setting did not clearly affect the clinical courses of patients without metastasis. However, the treatment was effective for metastasis that was repeatedly developed as late recurrence in one patient. Three patients with metastasis at diagnosis received combination chemotherapy with etoposide, doxorubicin and cisplatin (EDP) with or without mitotane treatment, to which lung metastasis completely responded in one patient.Conclusions:  Adrenocortical carcinoma is a rare disease but frequently recurs. The best chance of survival may be achieved by early detection and complete surgical removal. There may be patients who possibly benefit from mitotane treatment with or without EDP, although this remains to be conclusively determined.
Sickle‐shaped crack in a round bar under complex Mode I loading
Authors: CARPINTERI A. , BRIGHENTI R. , VANTADORI S. , VIAPPIANI D. 
Published: June 2007

ABSTRACTA sickle‐shaped surface crack in a round bar under complex Mode I loading is considered. First, the stress‐intensity factor (SIF) along the front of the flaw is numerically determined for five elementary Mode I stress distributions (constant, linear, quadratic, cubic and quartic) directly applied on the crack faces. The finite element method and linear elastic fracture mechanics concepts are employed. Then, a numerical procedure to calculate approximate values of SIF for a complex Mode I stress distribution on the crack faces is proposed based on both the power series expansion of the function describing such a stress distribution and the superposition principle. In order to validate the results obtained through the above procedure, a comparison with numerical data available in the literature is made.
The effect of gentamicin sulphate on the fracture properties of a manually mixed bone cement
Authors: BALEANI M. , PERSSON C. , GUANDALINI L. , PIAZZA E. , ERANI P. , SQUARZONI S. , VICECONTI M. 
Published: June 2007

ABSTRACTThis work investigates the effect of adding gentamicin, an antibiotic, on the fracture properties of bone cement.Endurance limit, fatigue crack propagation and fracture toughness were determined for a polymethylmethacrylate‐based cement, containing 10% w/w of barium sulphate as radiopacifying agent, and the same formulation modified by the addition of 4.22% w/w of gentamicin sulphate.The antibiotic does not affect the endurance limit nor the fracture toughness of the material. There are significant differences in the parameters of the Paris' law fitting the crack growth data: once the main crack is nucleated, it initially propagates at a lower rate but thereafter accelerates faster in gentamicin loaded bone cement. Despite this difference, the growth rate for the same stress intensity factor remains of the same order of magnitude in both formulations.The addition of 4.22% w/w of gentamicin sulphate to radiopaque bone cement has a negligible total effect on the fracture properties of the material.
Casein kinase I epsilon gene transfer into the suprachiasmatic nucleus via electroporation lengthens circadian periods of tau mutant hamsters
Authors: Wang Haoran , Ko Caroline H. , Koletar Margaret M. , Ralph Martin R. , Yeomans John 
Published: June 2007

AbstractCircadian activity rhythms in mammals are controlled by the expression and transcriptional regulation of clock genes in the suprachiasmatic nucleus (SCN). The circadian cycle length in hamsters is regulated in part by casein kinase I epsilon (CKIε). A semidominant mutation (C→T, R178C, CKIεtau) appears to act as a dominant‐negative allele to shorten the period of circadian rhythms. We tested this hypothesis in vivo by expressing wild‐type CKIε gene in homozygous tau mutant hamsters. High‐level CKIε+/+ gene transfer and expression (as indicated by green fluorescent protein) were obtained by injecting CKIε‐containing plasmids bilaterally near the SCN, followed by in vivo electroporation. Rhythmicity reappeared 5–7 days after electroporation, with a gradual increase in circadian period over the next 10 days. The circadian period returned to the baseline over the next 20 days. For the five hamsters with clearest gene expression in the SCN, the mean lengthening time was 39.6 min. Period change was not observed in either control tau mutant hamsters electroporated with plasmids lacking the CKIε gene or in wild‐type hamsters with plasmids containing the wild‐type CKIε gene. Therefore, normal periodicity in homozygous CKIεtau hamsters was partially rescued by expression of the wild‐type CKIε gene in the SCN, supporting a competitive and dominant‐negative action of the mutant allele. This study shows that electroporation of wild‐type CKIε gene into the SCN is sufficient for lengthening the shorter circadian period of tau mutant hamsters in a time‐dependent way and supports the conclusion that CKIεtau is the cause of the shorter period.
Two faces of calcium activation after optic nerve trauma: life or death of retinal ganglion cells in vivo depends on calcium dynamics
Authors: Prilloff S. , Noblejas M. I. , Chedhomme V. , Sabel B. A. 
Published: June 2007

AbstractCalcium elevations after neurotrauma are not only implicated in cell death but may contribute to adaptive plasticity. We now wished to resolve this contradiction by following calcium dynamics after optic nerve crush in vivo. Adult rats received no injury (n = 5), unilateral mild (n = 10) or moderate optic nerve crush (n = 10) (ONC), or axotomy (n = 5). Before surgery, retinal ganglion cells (RGCs) were retrogradely labelled with Oregon Green BAPTA‐dextran, a fluorescent calcium marker. Calcium‐related fluorescence intensity (FI) was repeatedly measured in individual RGCs in vivo using the in vivo confocal neuroimaging (ICON) method. Four different RGC types were found. Normal RGCs without FI change were found in sham rats and also in both ONC groups. RGCs with mild damage were seen only after mild ONC, showing an initial calcium depression of 26% at day 4 followed by a 169% increase 15 days after ONC. RGCs with moderate damage were found only after moderate ONC and showed calcium hypoactivation followed by a slower return toward baseline and a delayed calcium increase of 72% above baseline. Sixty to sixty‐five per cent of the RGCs in both ONC groups and all RGCs in the axotomy group died within 6 days following a fast and massive calcium increase of 316% with a concomitant 156% soma size increase. In conclusion rapid calcium elevation leads to cell death, while an initial calcium depression followed by a delayed and moderate calcium hyperactivation is associated with cell survival. We propose that immediate, massive calcium activation is maladaptive whereas delayed and moderate hyperactivation of surviving cells is adaptive. Implications for pharmacotherapy are discussed.
Cellular localization and function of DARPP‐32 in the rodent retina
Authors: Witkovsky Paul , Svenningsson Per , Yan Lily , Bateup Helen , Silver Rae 
Published: June 2007

AbstractThe goal of the present study was to elucidate the role of DARPP‐32 (dopamine‐ and cyclic adenosine 3′‐5′‐monophosphate‐regulated phosphoprotein, 32 kDa) in retinal function. We examined mouse and rat retinas for the presence of DARPP‐32 by immunocytochemistry. In both rodent retinas DARPP‐32 immunoreactivity was localized to horizontal and AII amacrine neurons and to the Mueller glial cells, using immuno‐double labelling. Additional unidentified neurons in the amacrine cell layer also showed DARPP‐32 immunoreactivity. Using mice entrained to a 12–12 h light–dark cycle, we found that exposure to light presented during the dark phase significantly enhanced phosphorylation of DARPP‐32 at threonine (Thr) 34 and phosphorylation of the ionotropic glutamate receptor subunit GluR1 at serine (Ser) 845, as measured by immunoblots. However, light also increased Ser 845‐GluR1 phosphorylation in DARPP‐32‐knockout mice. When a dopamine D1 receptor antagonist was injected into the eye prior to light exposure, phosphorylation of both Thr 34‐DARPP‐32 and Ser 845‐GluR1 was significantly reduced. These data indicate that DARPP‐32 participates in dopamine‐mediated modifications of retinal function. We also tested for a possible circadian rhythm of Thr 34‐ and Thr 75‐DARPP‐32 and Ser 845‐GluR1 expression. No significant circadian rhythm of either DARPP‐32 or GluR1 phosphorylation was found.
Challenging the omnipotence of the suprachiasmatic timekeeper: are circadian oscillators present throughout the mammalian brain?
Authors: Guilding Clare , Piggins Hugh D. 
Published: June 2007

AbstractThe suprachiasmatic nucleus of the hypothalamus (SCN) is the master circadian pacemaker or clock in the mammalian brain. Canonical theory holds that the output from this single, dominant clock is responsible for driving most daily rhythms in physiology and behaviour. However, important recent findings challenge this uniclock model and reveal clock‐like activities in many neural and non‐neural tissues. Thus, in addition to the SCN, a number of areas of the mammalian brain including the olfactory bulb, amygdala, lateral habenula and a variety of nuclei in the hypothalamus, express circadian rhythms in core clock gene expression, hormone output and electrical activity. This review examines the evidence for extra‐SCN circadian oscillators in the mammalian brain and highlights some of the essential properties and key differences between brain oscillators. The demonstration of neural pacemakers outside the SCN has wide‐ranging implications for models of the circadian system at a whole‐organism level.
Human limb‐specific and non‐limb‐specific brain representations during kinesthetic illusory movements of the upper and lower extremities
Authors: Naito Eiichi , Nakashima Tokuro , Kito Tomonori , Aramaki Yu , Okada Tomohisa , Sadato Norihiro 
Published: June 2007

AbstractSensing movements of the upper and lower extremities is important in controlling whole‐body movements. We have shown that kinesthetic illusory hand movements activate motor areas and right‐sided fronto‐parietal cortices. We investigated whether illusions for the upper and lower extremities, i.e. right or left hand or foot, activate the somatotopical sections of motor areas, and if an illusion for each limb engages the right‐sided cortices.We scanned the brain activity of 19 blindfolded right‐handed participants using functional magnetic resonance imaging (fMRI) while they experienced an illusion for each limb elicited by vibrating its tendon at 110 Hz (ILLUSION). As a control, we applied identical stimuli to the skin over a nearby bone, which does not elicit illusions (VIBRATION). The illusory movement (ILLUSION vs. VIBRATION) of each immobile limb activated limb‐specific sections of the contralateral motor cortex (along with somatosensory area 3a), dorsal premotor cortex (PMD), supplementary motor area (SMA), cingulate motor area (CMA), and the ipsilateral cerebellum, which normally participate in execution of movements of the corresponding limb. We found complex non‐limb‐specific representations in rostral parts of the bilateral SMA and CMA, and illusions for all limbs consistently engaged concentrated regions in right‐sided fronto‐parietal cortices and basal ganglia. This study demonstrated complete sets of brain representations related to kinesthetic processing of single‐joint movements of the four human extremities. The kinesthetic function of motor areas suggests their importance in somatic perception of limb movement, and the non‐limb‐specific representations indicate high‐order kinesthetic processing related to human somatic perception of one's own body.
Differential activation of CRF receptor subtypes removes stress‐induced memory deficit and anxiety
Authors: Todorovic Cedomir , Radulovic Jelena , Jahn Olaf , Radulovic Marko , Sherrin Tessi , Hippel Cathrin , Spiess Joachim 
Published: June 2007

AbstractThe objective of this study was to investigate the role of corticotropin‐releasing factor receptors 1 (CRF1) and 2 (CRF2) in anxiety‐like behavior and learning of C57BL/6J mice after exposure to a stressful stimulus. When C57BL/6J mice were exposed to immobilization (1 h) serving as stressful stimulus, context‐ and tone‐dependent fear conditioning were impaired if the training followed immediately after immobilization. The stress‐induced impairment of context‐dependent fear conditioning was prevented by specific blockade of CRF2 of the lateral septum (LS) with anti‐sauvagine‐30. Immobilization did not only affect conditioned fear, but also enhanced, through CRF2 of the LS, anxiety‐like behavior determined with the elevated plus maze. Recovery from stress‐induced anxiety and impairment of context‐dependent fear conditioning was observed after 1 h delay of training and required hippocampal CRF1, as indicated by the finding that this recovery was prevented by blockade of intrahippocampal CRF1. It was concluded that exposure to a stressor initially affected both anxiety‐like behavior and contextual conditioned fear through septal CRF2, while the later activation of hippocampal CRF1 resulted in the return to baseline levels of both processes. Intraventricular injection of mouse urocortin 2, a CRF2‐selective agonist, removed the stress‐induced anxiety and learning impairment, but did not reduce the activation of the hypothalamic pituitary adrenal axis indicative of the hormonal stress response. We propose that the enhanced anxiety is the component of the stress response responsible for the memory deficit.
Mechanism of spontaneous and self‐sustained oscillations in networks connected through axo‐axonal gap junctions
Authors: Maex Reinoud , De Schutter Erik 
Published: June 2007

AbstractElectrical coupling of clusters of neurons via axo‐axonal gap junctions is a candidate mechanism underlying the ultra‐fast (> 100 Hz) oscillations recorded in various in vitro and in vivo normal and pathological conditions [Traub et al. (1999)Neuroscience, 92, 407–426]. The poor characterization of axo‐axonal gap junctions, however, limits experimental verification of this mechanism. We simulated networks of prototype multi‐compartmental neurons in order to identify the parameters constraining the production and frequency of ultra‐fast oscillations. Weak axo‐axonal coupling was found to synchronize networks preferentially at the gamma‐range frequency (30–100 Hz). Networks with strong axo‐axonal coupling were able to produce 200 Hz oscillations, a finding we extended with several new observations. Ultra‐fast oscillations arose spontaneously during dendritic excitation, i.e. in the absence of extrinsic axonal background spikes, as the spike trigger zone concomitantly shifted from soma to axon. The all‐or‐none oscillations could be transitory or self‐sustained, and lasted longer in larger networks. They occurred more likely during low to modest soma firing rates, as strong afterhyperpolarizing currents tended to impair them. The rate of the rhythm was independent of network size and of the level of excitation, but inversely proportional to the distance of the junctions from the soma. As a matter of fact, the resulting axonal firing rate was the highest one at which antidromic spikes would not collide with spikes reflected from the soma. Taken together, the observed model dynamics lends further credibility to axo‐axonal coupling as a mechanism of ultra‐fast oscillations.
Glutamatergic input is coded by spike frequency at the soma and proximal dendrite of AII amacrine cells in the mouse retina
Authors: Tamalu Fuminobu , Watanabe Shu‐Ichi 
Published: June 2007

AbstractIn the mammalian retina, AII amacrine cells play a crucial role in scotopic vision. They transfer rod signals from rod bipolar cells to the cone circuit, and divide these signals into the ON and OFF pathways at the discrete synaptic layers. AII amacrine cells have been reported to generate tetrodotoxin (TTX)‐sensitive repetitive spikes of small amplitude. To investigate the properties of the spikes, we performed whole‐cell patch‐clamping of AII amacrine cells in mouse retinal slices. The spike frequency increased in proportion to the concentration of glutamate puffer‐applied to the arboreal dendrite and to the intensity of the depolarizing current injection. The spike activity was suppressed by L‐2‐amino‐4‐phosphonobutyric acid, a glutamate analogue that hyperpolarizes rod bipolar cells, puffer‐applied to the outer plexiform layer. Therefore, it is most likely that the spike frequency generated by AII amacrine cells is dependent on the excitatory glutamatergic input from rod bipolar cells. Gap junction blockers reduced the range of intensity of input with which spike frequency varies. Application of TTX to the soma and the proximal dendrite of AII amacrine cells blocked the voltage‐gated Na+ current significantly more than application to the arboreal dendrite, indicating that the Na+ channels are mainly localized in these regions. Our results suggest that the intensity of the glutamatergic input from rod bipolar cells is coded by the spike frequency at the soma and the proximal dendrite of AII amacrine cells, raising the possibility that the spikes could contribute to the OFF pathway to enhance release of neurotransmitter.
Homeostatic plasticity in human motor cortex demonstrated by two consecutive sessions of paired associative stimulation
Authors: Müller J. Florian M. , Orekhov Yuriy , Liu Yali , Ziemann Ulf 
Published: June 2007

AbstractLong‐term potentiation (LTP) and long‐term depression (LTD) underlie most models of learning and memory, but neural activity would grow or shrink in an uncontrolled manner, if not guarded by stabilizing mechanisms. The Bienenstock–Cooper–Munro (BCM) rule proposes a sliding threshold for LTP/LTD induction: LTP induction becomes more difficult if neural activity was high previously. Here we tested if this form of homeostatic plasticity applies to the human motor cortex (M1) in vivo by examining the interactions between two consecutive sessions of paired associative stimulation (PAS). PAS consisted of repeated pairs of electrical stimulation of the right median nerve followed by transcranial magnetic stimulation of the left M1. The first PAS session employed an interstimulus interval equalling the individual N20‐latency of the median nerve somatosensory‐evoked cortical potential plus 2 ms, N20‐latency minus 5 ms, or a random alternation between these intervals, to induce an LTP‐like increase in motor‐evoked potential (MEP) amplitudes in the right abductor pollicis brevis muscle (PASLTP), an LTD‐like decrease (PASLTD), or no change (PASControl), respectively. The second PAS session 30 min later was always PASLTP. It induced an moderate LTP‐like effect if conditioned by PASControl, which increased if conditioned by PASLTD, but decreased if conditioned by PASLTP. Effects on MEP amplitude induced by the second PAS session exhibited a negative linear correlation with those in the first PAS session. Because the two PAS sessions activate identical neuronal circuits, we conclude that ‘homosynaptic‐like’ homeostatic mechanisms in accord with the BCM rule contribute to regulating plasticity in human M1.
Ethanol reverses the direction of long‐term synaptic plasticity in the dorsomedial striatum
Authors: Yin Henry H. , Park Brian S. , Adermark Louise , Lovinger David M. 
Published: June 2007

AbstractThe striatum is a critical structure for the control of voluntary behaviour, and striatal synaptic plasticity has been implicated in instrumental learning. As ethanol consumption can cause impairments in cognition, learning, and action selection, it is important to understand the effects of this drug on striatal function. In this study we examined the effects of ethanol on long‐term synaptic plasticity in the dorsomedial striatum (DMS), a striatal subregion that plays a central role in the acquisition and selection of goal‐directed actions. Ethanol was found to impair N‐methyl‐d‐aspartic acid receptor (NMDAR)‐dependent long‐term potentiation (LTP) dose‐dependently in the DMS, and to promote long‐term depression (LTD) at the highest concentration (50 mm) used. These results suggest that ethanol, at a concentration usually associated with mild intoxication, could significantly change experience‐dependent modification of corticostriatal circuits underlying the learning of goal‐directed instrumental actions.
Molecular ecology of nifH genes and transcripts in the eastern Mediterranean Sea
Authors: Man‐Aharonovich Dikla , Kress Nurit , Zeev Edo Bar , Berman‐Frank Ilana , Béjà Oded 
Published: June 2007

SummaryThe eastern Mediterranean Sea is one of the most extreme oligotrophic oceanic regions on earth in terms of nutrient concentrations and primary productivity. Nitrogen fixation has been suggested to contribute to the high N : P molar ratios of ∼28:1 found in this region. Surprisingly, no molecular biological work has been performed in situ to assess whether N2 fixation genes actually occur in the eastern Mediterranean Sea, or to determine which organisms are responsible for this process. In this study, we examined the presence and expression of nitrogenase genes (nifH) in the upper water layer of the eastern Mediterranean. Clone libraries constructed from both DNA and reverse‐transcribed PCR‐amplified mRNA were examined and compared. We observed different nifH genes from diverse microbial groups, such as Cyanobacteria, Proteobacteria and methanogenic Archaea. Interestingly, numerous phylotypes were observed in coastal stations at the DNA level but none were active. However, in far offshore stations, the phylotypes observed at the DNA level were the ones that were actually active. Our preliminary study revealed diverse diazotrophs that possess and express nifH genes, which may support N2 fixation in the eastern Mediterranean Sea.