bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of Actin Cytoskeleton and Nuclei in Bovine Blastocysts Developed Under Different Culture Conditions Using a Novel Computer Program
Authors: Kuzmany A , Havlicek V , Brem G , Walter I , Besenfelder U 
Published: May 2010

ContentsThis study was performed to investigate the effects, in terms of nuclear material and actin cytoskeleton quantities (fluorescent pixel counts), of four different bovine blastocyst culturing techniques (in vitro, stepwise in vitro‐to‐in vivo, or purely in vivo). Cumulus oocyte complexes from abattoir‐sourced ovaries were matured in vitro and allocated to four groups: IVP‐group embryos developed up to blastocyst stage in vitro. Gamete intra‐fallopian transfer (GIFT)‐group oocytes were co‐incubated with semen for 4 h before transfer to oviducts of heifers. Following in vitro fertilization, cleaved embryos (day 2 of embryo development, day 2–7 group) were transferred into oviducts on day 2. Multiple ovulation embryo transfer (MOET)‐group embryos were obtained by superovulating and inseminating heifers; the heifers’ genital tracts were flushed at day 7 of blastocyst development. Within each group, ten blastocysts were selected to be differentially dyed (for nuclei and actin cytoskeleton) with fluorescent stains. A novel computer program (ColorAnalyzer) provided differential pixel counts representing organelle quantities. Blastocysts developed only in vivo (MOET group) showed significantly more nuclear material than did blastocysts produced by any other technique. In terms of actin cytoskeleton quantity, blastocysts produced by IVP and by day 2–7 transfer did not differ significantly from each other. Gamete intra‐fallopian transfer‐ and MOET‐group embryos showed significantly larger quantities of actin cytoskeleton when compared with any other group and differed significantly from each other. The results of this study indicate that culturing under in vitro conditions, even with part time in vivo techniques, may adversely affect the quantity of blastocyst nuclear material and actin cytoskeleton. The software employed may be useful for culture environment evaluation/developmental competence assessment.
Early Development and Putative Primordial Germ Cells Characterization in Dogs
Authors: Martins DS , Ambrósio CE , Saraiva NZ , Wenceslau CV , Morini AC , Kerkis I , Garcia JM , Miglino MA 
Published: May 2010

ContentsPreviously, three distinct populations of putative primordial germ cells (PGCs), namely gonocytes, intermediate cells and pre‐spermatogonia, have been described in the human foetal testis. According to our knowledge, these PGCs have not been studied in any other species. The aim of our study was to identify similar PGC populations in canine embryos. First, we develop a protocol for canine embryo isolation. Following our protocol, 15 canine embryos at 21–25 days of pregnancy were isolated by ovaryhysterectomy surgery. Our data indicate that dramatic changes occur in canine embryo development and PGCs specification between 21 to 25 days of gestation. At that moment, only two PGC populations with distinct morphology can be identified by histological analyses. Cell population 1 presented round nuclei with prominent nucleolus and a high nuclear to cytoplasm ratio, showing gonocyte morphology. Cell population 2 was often localized at the periphery of the testicular cords and presented typical features of PGC. Both germ cell populations were positively immunostained with anti‐human OCT‐4 antibody. However, at day 25, all cells of population 1 reacted positively with OCT‐4, whereas in population 2, fewer cells were positive for this marker. These two PGCs populations present morphological features similar to gonocytes and intermediate cells from human foetal testis. It is expected that a population of pre‐spermatogonia would be observed at later stages of canine foetus development. We also showed that anti‐human OCT‐4 antibody can be useful to identify canine PGC in vivo.
Risedronate prevents early bone loss and increased bone turnover in the first 6 months of luteinizing hormone‐releasing hormone‐agonist therapy for prostate cancer
Authors: Taxel Pamela , Dowsett Robert , Richter Lee , Fall Pamela , Klepinger Alison , Albertsen Peter 
Published: May 2010

Study Type – Therapy (RCT) Level of Evidence 1bOBJECTIVETo determine whether increased bone loss and bone turnover during the first 6 months of therapy for prostate cancer with luteinizing hormone‐releasing hormone (LHRH)‐agonist therapy could be prevented by bisphosphonate therapy with risedronate 35 mg/week, as prostate cancer is commonly treated with LHRH agonists and this often leads to rapid bone loss within the first 6 months of therapy.PATIENTS AND METHODSA 6‐month randomized, double‐blind, placebo‐controlled trial was conducted, including 40 men aged ≥55 years receiving LHRH‐agonist treatment for 6 months for locally advanced prostate cancer. Bone mineral density (BMD) of the lumbar spine, femoral neck, and total hip was measured every 6 months. In addition, bone turnover markers including N‐telopeptide, serum C‐telopeptide and procollagen peptide, and 25‐OH vitamin D and intact parathyroid hormone were measured at baseline and at 6 months.RESULTSAfter 6 months of LHRH‐agonist therapy, the control group had a significant decline at the spine and hip BMD sites; however, the risedronate group had no bone loss at the hip and an increase at the lumber spine. Markers of bone turnover were increased significantly in the control group but unchanged in the risedronate group.CONCLUSIONSLHRH‐agonist treatment for locally advanced prostate cancer produces increased bone turnover and rapid bone loss within the initial 6 months of therapy, and this can be prevented by weekly risedronate treatment.
Changes in pulse pressure, heart rate and the pulse pressure × heart rate product during squatting in Type 1 diabetes according to age
Authors: Philips J.‐C. , Marchand M. , Scheen A. J. 
Published: May 2010

Diabet. Med. 27, 753–761 (2010)AbstractAims  We assessed changes in pulse pressure and heart rate during a squatting test, as indirect markers of arterial stiffness and cardiovascular autonomic neuropathy, respectively, according to age and sex in patients with Type 1 diabetes mellitus.Methods  We evaluated 160 diabetic patients, divided into four groups of 20 men and 20 women according to age (G1, 20–30 years old; G2, 31–40 years old; G3, 41–50 years old; and G4, 51–60 years old), and 160 non‐diabetic matched control subjects. Each subject underwent a 3 min posture test (standing–squatting–standing) with continuous measurement of arterial blood pressure and heart rate by a Finapres® device. Overall values throughout the test, baseline levels in initial standing position and squatting‐induced changes in pulse pressure, heart rate and the pulse pressure × heart rate product were compared between diabetic patients and healthy control subjects.Results  In the standing position, a greater increase in pulse pressure and lower reduction in heart rate with age led to a significantly higher pulse pressure × heart rate product in diabetic patients compared with control subjects. In the squatting position, a more marked pulse pressure increase in the absence of appropriate reduction in heart rate resulted in a greater rise in the pulse pressure × heart rate product in diabetic patients than in healthy subjects. No major differences were noted between the sexes, with the exception of a stronger relationship between pulse pressure and age in the female population with diabetes. Squatting‐derived indices of cardiovascular autonomic neuropathy were also noted with increasing age in diabetic patients.Conclusions  The marked increase in the pulse pressure × heart rate product (‘pulsatile stress’) according to age, combined with cardiovascular autonomic neuropathy, may contribute to the higher cardiovascular risk of patients with Type 1 diabetes.
Triggering mechanisms of neuroarthropathy following conservative surgery for osteomyelitis
Authors: Aragón‐Sánchez J. , Lázaro‐Martínez J. L. , Hernández‐Herrero M. J. 
Published: May 2010

Diabet. Med. 27, 844–847 (2010)AbstractBackground  The purpose of this study was to raise awareness and stimulate discussion of the possible triggering factors of Charcot neuroarthropathy by presenting the case of one patient who had both undergone surgery and was suffering from osteomyelitis.Case report  We have extracted one case from our data set for a patient who underwent conservative surgery for osteomyelitis and subsequently developed acute Charcot in the midfoot. We present the clinical findings, photographs and X‐ray studies. Preoperative X‐ray showed irregular severe bone destruction in the fourth metatarsal head and a fracture of the fourth metatarsal bone. No signs of midfoot Charcot neuroarthropathy were found in this preoperative X‐ray. The third and fourth metatarsal bones were both removed and the surgical wound was left open to heal by second intention. Histopathological study confirmed osteomyelitis in the bone sample. Twenty‐five days after surgery, the surgical wound showed no signs of infection and healing progressed in a satisfactory way. However, the foot was swollen, erythematous and warm. Skin temperature was two degrees higher than the contralateral foot. X‐ray was taken and acute neuroarthropathy of the tarso‐metatarsal joints was diagnosed.Conclusions  Charcot neuroarthropathy appears to have been triggered by bone infection and/or surgery. We believe that the pivotal factor in the development of acute Charcot neuroarthropathy in this case was the weight bearing in the deformed foot so soon after the operation. Immobilization of the foot is critical as it serves to decrease the inflammation which has a key role in the development of Charcot neuroarthropathy.
The New Political Role of Business in a Globalized World: A Review of a New Perspective on CSR and its Implications for the Firm, Governance, and Democracy
Authors: Scherer Andreas Georg , Palazzo Guido 
Published: May 2010

abstractScholars in management and economics widely share the assumption that business firms focus on profits only, while it is the task of the state system to provide public goods. In this view business firms are conceived of as economic actors, and governments and their state agencies are considered the only political actors. We suggest that, under the conditions of globalization, the strict division of labour between private business and nation‐state governance does not hold any more. Many business firms have started to assume social and political responsibilities that go beyond legal requirements and fill the regulatory vacuum in global governance. Our review of the literature shows that there are a growing number of publications from various disciplines that propose a politicized concept of corporate social responsibility. We consider the implications of this new perspective for theorizing about the business firm, governance, and democracy.
Resampling Strategies for Deforming MLS Surfaces
Authors: Gois João Paulo , Buscaglia Gustavo C. 
Published: May 2010

Abstract Moving‐least‐squares (MLS) surfaces undergoing large deformations need periodic regeneration of the point set (point‐set resampling) so as to keep the point‐set density quasi‐uniform. Previous work by the authors dealt with algebraic MLS surfaces, and proposed a resampling strategy based on defining the new points at the intersections of the MLS surface with a suitable set of rays. That strategy has very low memory requirements and is easy to parallelize. In this article new resampling strategies with reduced CPU‐time cost are explored. The basic idea is to choose as set of rays the lines of a regular, Cartesian grid, and to fully exploit this grid: as data structure for search queries, as spatial structure for traversing the surface in a continuation‐like algorithm, and also as approximation grid for an interpolated version of the MLS surface. It is shown that in this way a very simple and compact resampling technique is obtained, which cuts the resampling cost by half with affordable memory requirements.
Gross muscle morphology and structure in spastic cerebral palsy: a systematic review
Authors: BARRETT ROD S , LICHTWARK GLEN A 
Published: May 2010

Aim  This systematic review and critical evaluation of the literature was conducted to determine how gross muscle morphology and structure are altered in individuals with spastic cerebral palsy (CP).Method  Electronic databases were searched for articles describing studies of muscle morphological and structural properties in individuals with spastic CP. Data describing muscle fascicle length, belly length, fascicle angle, cross‐sectional area, volume, and thickness were extracted and effect sizes were computed for comparisons between individuals with spastic CP and typically developed individuals, between the paretic and non‐paretic side in individuals with hemiplegia for all muscles examined, and across the full spectrum of gross motor function in individuals with spastic CP.Results  The final yield consisted of 15 articles that met the inclusion criteria. The main finding of the review was the consistent evidence for reduced muscle belly length, muscle volume, cross‐sectional area, and muscle thickness in the comparisons between paretic and typically developed muscle and the paretic and non‐paretic muscle across a range of muscles.Interpretation  Given the importance of muscle morphology and structure for generating muscle force, it is likely that the observed alterations that occur secondary to the neural lesion in individuals with spastic CP contribute to muscle weakness and the attendant loss of motor function in spastic CP.
PKC links Gq‐coupled receptors to DAT‐mediated dopamine release
Authors: Opazo Felipe , Schulz Jörg B. , Falkenburger Björn H. 
Published: May 2010

J. Neurochem.(2010)114, 587–596.AbstractThe dopamine transporter (DAT) mediates dopamine uptake in many brain areas and has been suggested to underlie dopamine release in the substantia nigra pars reticulata. This release modulates basal ganglia output and motor performance. It is triggered by glutamatergic subthalamic afferents. We show here that activation of (Gq‐coupled) group I metabotropic glutamate receptors are sufficient to induce dopamine release in rat substantia nigra pars reticulata slices. Release was measured by amperometry and inhibited by a DAT antagonist. In a DAT‐expressing cell line, dopamine release could be induced by activation of Gq‐coupled muscarinic receptors. Release was measured by HPLC and inhibited by a DAT antagonist. In both paradigms, activation of protein kinase C (PKC) was necessary and sufficient for dopamine release, suggesting that Gq‐coupled receptors can induce DAT‐mediated dopamine release through PKC, and providing a physiological role for the known regulation of DAT‐mediated release by PKC. Activation of muscarinic receptors and PKC also induced release from a cell line expressing the norepinephrine transporter, suggesting that transport‐mediated release might be relevant in further brain areas.
Mechanisms underlying striatal vulnerability to 3‐nitropropionic acid
Authors: Herrera‐Mundo Nieves , Sitges María 
Published: May 2010

J. Neurochem.(2010)114, 597–605.AbstractThe striatum is a cerebral structure particularly susceptible to the metabolic challenge exerted by 3‐nitropropionic acid (3‐NPA), a toxin that inhibits the respiratory chain at complex II. The striatum, which receives the nerve endings of the nigro‐striatal pathway, concentrates the largest amount of 3,4‐dihydroxyphenylethylamine or dopamine (DA) in the brain. DA is metabolized to 3,4‐dihydroxyphenylacetic acid (DOPAC) by monoamine oxidase (MAO), an enzyme that contains a redox‐active disulfide in the active site. In striatum isolated nerve endings exposed to 3‐NPAin vitro, DA increased and DOPAC decreased already after 10 min, and after 2 h also an increase in reactive oxygen species and DA‐quinone products formation was detected. These 3‐NPA‐induced effects resulted in an increase in DA release after 2 h. In striatum homogenates from animals presenting motor disturbances in response to 3‐NPAin vivo,the DA metabolites homovanillic acid and DOPAC were increased. It is concluded that in the striatum nerve endings where DA is particularly concentrated, the increase in reactive oxygen species induced by 3‐NPA, oxidizes DA generating DA‐quinones. These DA‐quinones may form adducts with the active site of MAO type A reducing its activity. The DA not metabolized to DOPAC is both, used to unchain generation of more of the harmful DA‐oxidation products and released to the external medium, where is metabolized by the non‐neuronal enzymes MAO type B and catechol‐O‐methyltransferase.
GABA modulates development of cerebellar Purkinje cell dendrites under control of endocannabinoid signaling
Authors: Kawaguchi Koji , Habara Tomomi , Terashima Toshio , Kikkawa Satoshi 
Published: May 2010

J. Neurochem. (2010) 114, 627–638.AbstractPurkinje cells (PCs) are the sole projection neurons in the cerebellar cortex with highly arborized dendrites, on which they receive glutamatergic and GABAergic inputs. Whereas influences of glutamatergic inputs on dendritic development of PCs have been well studied, those of GABA remain elusive. Here we examined effects of GABAergic signaling on dendritogenesis of PCs in dissociated cerebellar cultures. Treatment with GABAA agonists such as muscimol altered Purkinje dendrites to longer and less branched morphology, while GABAA antagonists resulted in shorter dendrites. In contrast, neither a GABAB agonist nor antagonist had major effects on dendritic morphology. Simultaneous addition of a glutamatergic antagonist cocktail or the Trk receptor antagonist K252a did not block muscimol. Furthermore, blockade of endocannabinoid signaling by either AM251 or tetrahydrolipstatin resulted in longer and less branched dendrites similar to those treated with GABAA agonists suggesting upstream regulation by endocannabinoids. Notably, whereas Purkinje dendrites extended in random directions in the presence of muscimol, they oriented to coexisting GABAergic interneurons when treated with AM251. Taken together, our results postulate the hypothesis that GABA released from the cerebellar interneurons modulates dendritogenesis of PCs in an endocannabinoid‐dependent manner in the developing cerebellar cortex.
The major determinant of exendin‐4/glucagon‐like peptide 1 differential affinity at the rat glucagon‐like peptide 1 receptor N‐terminal domain is a hydrogen bond from SER‐32 of exendin‐4
Authors: Mann RJ , Nasr NE , Sinfield JK , Paci E , Donnelly D 
Published: May 2010

BACKGROUND AND PURPOSEExendin‐4 (exenatide, Ex4) is a high‐affinity peptide agonist at the glucagon‐like peptide‐1 receptor (GLP‐1R), which has been approved as a treatment for type 2 diabetes. Part of the drug/hormone binding site was described in the crystal structures of both GLP‐1 and Ex4 bound to the isolated N‐terminal domain (NTD) of GLP‐1R. However, these structures do not account for the large difference in affinity between GLP‐1 and Ex4 at this isolated domain, or for the published role of the C‐terminal extension of Ex4. Our aim was to clarify the pharmacology of GLP‐1R in the context of these new structural data.EXPERIMENTAL APPROACHThe affinities of GLP‐1, Ex4 and various analogues were measured at human and rat GLP‐1R (hGLP‐1R and rGLP‐1R, respectively) and various receptor variants. Molecular dynamics coupled with in silico mutagenesis were used to model and interpret the data.KEY RESULTSThe membrane‐tethered NTD of hGLP‐1R displayed similar affinity for GLP‐1 and Ex4 in sharp contrast to previous studies using the soluble isolated domain. The selectivity at rGLP‐1R for Ex4(9–39) over Ex4(9–30) was due to Ser‐32 in the ligand. While this selectivity was not observed at hGLP‐1R, it was regained when Glu‐68 of hGLP‐1R was mutated to Asp.CONCLUSIONS AND IMPLICATIONSGLP‐1 and Ex4 bind to the NTD of hGLP‐1R with similar affinity. A hydrogen bond between Ser32 of Ex4 and Asp‐68 of rGLP‐1R, which is not formed with Glu‐68 of hGLP‐1R, is responsible for the improved affinity of Ex4 at the rat receptor.
Long‐term outcome of 32 children with encephalopathy with status epilepticus during sleep, or ESES syndrome
Authors: Liukkonen Elina , Kantola‐Sorsa Elisa , Paetau Ritva , Gaily Eija , Peltola Maria , Granström Marja‐Liisa 
Published: May 2010

SummaryPurpose:  To prospectively evaluate the efficacy of drug treatment and long‐term cognitive outcome in children with encephalopathy with status epilepticus during sleep (ESESS).Methods:  Thirty‐two children were diagnosed and prospectively followed up for at least 3 years at our unit between 1991 and 2007. Twenty‐seven children were included in the prospective treatment study with valproate (VPA) and 17 with VPA combined with ethosuximide (ESM). Treatment response of disappearance of electrical status epilepticus during sleep (SES) was documented with overnight EEG recordings. Neuropsychological follow up for at least 5 years was available in 18 patients.Results:  Six children had atypical rolandic (AR) epilepsy, nine Landau‐Kleffner syndrome (LKS), and 17 symptomatic epilepsy. Before ESESS, 20 children were cognitively normal. Prospective treatment with VPA and ESM was effective in 3 of the 17 children (18%) treated. Abolition of SES with drug treatment was observed in 16 patients. In all, 10 children (31%), 4 with AR (67%), 3 with LKS (33%), and 3 with symptomatic etiology (19%), including 9 with treatment response regained the pre‐ESESS cognitive level. Unfavorable cognitive outcome was predicted by younger age at ESESS diagnosis, lower IQ at the time of the diagnosis, and no response to drug treatment when compared with those with favorable cognitive outcome. Eight of the 16 nonresponders underwent epilepsy surgery.Discussion:  Treatment response with VPA combined with ESM was observed more often than with other drug combinations. Most children with ESESS experienced permanent cognitive impairment. Cognitive outcome depends on treatment response on electroencephalography (EEG) and seizures, and on underlying etiology.
Successful epilepsy surgery in a patient with neurosarcoidosis
Authors: Malmgren Kristina , Lycke Jan , Engman Elisabeth , Hedström Anders , Jönsson Lars , Rydenhag Bertil , Nordborg Claes 
Published: May 2010

SummaryThis case concerns a patient with generalized neurosarcoidosis and pharmacoresistant focal epilepsy. Although immunosuppressive therapy resulted in remission of the neurosarcoidosis, seizures continued and were shown to originate from the right temporal lobe (TL). The patient underwent a right anterior temporal lobe resection (TLR) and obtained >90% reduction of seizure frequency.