Acknowledgement

Distribution by Scientific Domains


Selected Abstracts


ACKNOWLEDGEMENT OF SPECIAL REVIEWERS

JOURNAL OF CONSUMER AFFAIRS, Issue 2 2001
Article first published online: 3 MAR 200
No abstract is available for this article. [source]


REVIEWER ACKNOWLEDGEMENT: Reviewer Acknowledgement

THE JOURNAL OF SEXUAL MEDICINE, Issue 7 2010
Article first published online: 6 JUL 2010
No abstract is available for this article. [source]


Acknowledgement of Referees, 2009

DEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 1 2010
Article first published online: 18 DEC 200
No abstract is available for this article. [source]


Acknowledgement of Reviewers for 2000

EUROPEAN JOURNAL OF NEUROLOGY, Issue 1 2001
Article first published online: 9 OCT 200
[source]


Acknowledgement to referees FEMS Yeast Research Volume 6 [2006]

FEMS YEAST RESEARCH, Issue 8 2006
Article first published online: 9 OCT 200
No abstract is available for this article. [source]


Acknowledgement to Reviewers for Volume 18, 2010

HEALTH & SOCIAL CARE IN THE COMMUNITY, Issue 6 2010
Article first published online: 6 OCT 2010
No abstract is available for this article. [source]


On ACK filtering on a slow reverse channel

INTERNATIONAL JOURNAL OF SATELLITE COMMUNICATIONS AND NETWORKING, Issue 3 2003
Chadi Barakat
Abstract Acknowledgement (ACK) filtering has been proposed as a technique to alleviate the congestion at the input of a slow channel located on the reverse path of a TCP connection. Old ACKs waiting at the input of the slow channel are erased when new ACKs are to be queued. In the literature the case of one-ACK per connection at a time has been studied. In this paper we show that this is too aggressive for short transfers where ACKs arrive in bursts due to the slow start phase, and where the TCP source needs to receive the maximum number of ACKs to increase fast its window. We study first static filtering where a certain ACK queue length is allowed. We show analytically how this length needs to be chosen. We present then some algorithms that adapt the filtering of ACKs as a function of the slow channel utilization rather than the ACK queue length. These algorithms provide a good compromise between reducing the ACK queueing delay and passing a large number of ACKs that guarantee a fast window increase. Copyright © 2003 John Wiley & Sons, Ltd. [source]


Acknowledgement of Guest Reviewers

INTERNATIONAL STUDIES QUARTERLY, Issue 4 2003
Article first published online: 7 NOV 200
First page of article [source]


Erratum: Acknowledgement to Referees

JOURNAL OF APPLIED ECONOMETRICS, Issue 5 2009
Erratum: Acknowledgement to Referees
No abstract is available for this article. [source]


Effects of NGF on different phenotypes and genotypes of cholinergic murine SN56 cells

JOURNAL OF NEUROCHEMISTRY, Issue 2003
H. Bielarczyk
Nerve growth factor (NGF) is important for differentiation and maintenance of septal cholinergic neurons. It caused concentration-dependent increase of choline acetyltransferase (ChAT) activity ([EC50%] 1 ng/mL), acetylcholine (ACh) content and morphologic maturation of SN56TrkA(+)p75(+) but not TrkA(,)p75(+) cells. NGF added with cyclic AMP altered significantly differential effects of the latter neither in TrkA(,) nor TrkA(+). However, when cyclic AMP-predifferentiated cells were treated with NGF alone, it caused suppression of the cholinergic phenotype in both cell lines. Anti-p75 antibodies totally reversed inhibitory effects of NGF on ChAT activity. Differentiation was accompanied by increase whereas its reversal by decrease of intracellular Ca content. These data indicate that NGF may exert opposite effects on phenotype of cholinergic neurons by p75 receptor signaling pathways and changes in intracellular Ca. Acknowledgement: Supported by KBN project 6P05A 01020. [source]


Developmental pattern of synapsin I expression in mouse somatosensory cortex

JOURNAL OF NEUROCHEMISTRY, Issue 2003
M. Liguz-Lecznar
Synapsin I is a member of a synapsin family which are phosphoproteins associated with synaptic vesicles. It is thought to be involved in neuronal development and plasticity. We have shown the existence of two distinct patterns of synapsin I immunostaining in adult mice primary somatosensory cortex (SI). The first consisted of small, dispersed immunoreactive puncta in neuropil. The second is confined to the perikarya and proximal dendrites of the specific class of neurons present in layers IV and VI of SI, probably reflecting the expression of a novel isoform of synapsin I. The aim of this study was to examine the developmental pattern of synapsin I expression in mouse SI cortex. Using immunocytochemistry and Western blot analysis we found that this unique pattern of synapsin I expression in SI appeared between the 2nd and 3rd postnatal week and probably coincides with the increase in the number of synaptic contacts and the development of inhibitory circuits in SI. Acknowledgement: Supported by KBN grant no. 3P04C 008 22. [source]


Protein aggregation in postsynaptic density after transient brain ischemia

JOURNAL OF NEUROCHEMISTRY, Issue 2003
M. Ber, sewicz
Brief cerebral ischemia causes changes in synaptic transmission and in consequence in neuronal function manifested in delayed cell death of CA1 hippocampal region. Postsynaptic density (PSD) is composed by a network of interacting proteins, including scaffolding proteins, neurotransmitter receptors, cytoskeletal proteins and protein kinases. PSD dynamically modulates signal transduction what influence the cell fate. We investigated the composition of the PSD network and effect of ischemia on its complexity. Two experimental procedures were applied. The interaction between PSD-95 and Src, Fyn, Raf-1, paxilin or NMDA receptor subunits were explored using coimmunoprecipitation method. In addition, the effect of ischemia-reperfusion on the density of PSD were evaluated by measurement of is solubility. We find out the decrease in solubility of the PSD-95, NR2A, NR2B and Raf-1. Of interest, the latter was restricted to surviving regions of hippocampus. Acknowledgement:, Financed by PBZ-KBN-002/CD/P05/2000. [source]


NSAIDs protect dopaminergic neurons against 6-OHDA and MPP+ toxicity

JOURNAL OF NEUROCHEMISTRY, Issue 2002
P. Werner
Endogenous and environmental neurotoxins are among the suspected causes of the loss of dopaminergic (DA) neurons in Parkinson's disease (PD). Non-steroidal anti-inflammatory drugs (NSAIDs) reduce inflammation by inhibiting cyclooxygenase (COX)-dependent synthesis of prostaglandins (PG) from arachidonic acid. NSAIDs decrease the incidence of Alzheimer's disease, but little is known about their potential benefit for PD. Therefore, we examined whether NSAIDs could protect DA neurons from neurotoxic insults. NSAIDs can protect DA neurons against excitotoxicity (Casper et al. 2000), and against 6-hydroxydopamine (6-OHDA) toxicity (Carrasco et al. 2001). Here, we compared in primary mesencephalic/DA neuron cultures the effect of NSAIDs on the toxicity of 1-methyl-phenylpyridinium (MPP+) or 6-OHDA. 6-OHDA significantly (*p < 0.0001) increased PG production, whereas MPP+ did not (p < 0.05). We then compared the competitive/unspecific COX inhibitors ibuprofen and naproxen and the noncompetitive/unspecific inhibitor acetylsalicylic acid (ASA, aspirin) for their ability to protect DA neurons against either 6-OHDA or MPP+ toxicity. Interestingly, all three nonselective COX inhibitors protected DA neurons in cultures against both 6-OHDA and MPP+ (p < 0.05), despite the difference in PG induction by 6-OHDA vs. MPP+. The selective COX-2 inhibitor NS398 did protect DA neurons against 5 ,m MPP+ (*p < 0.05), but failed to protect DA neurons against 5 ,m 6-OHDA (p < 0.05). Our results suggest that COX-inhibitors may have neuroprotective benefits unrelated to inhibition of PG synthesis, and that 6-OHDA and MPP+ have partially overlapping mechanisms of neurodegeneration possibly involving COX activity. Acknowledgement:, Supported, in part, by the International Federation for Parkinson's disease, NY, NY. [source]


Neuroprotection with caspase-9 inhbition against in vitro and in vivo trauma

JOURNAL OF NEUROCHEMISTRY, Issue 2002
R. A. Wallis
Objective:, To evaluate the neuroprotective efficacy of the cell-permeable caspase-9 inhibitor, LEHD-CHO, against in vitro and in vivo traumatic neuronal injury. Methods:, The neuroprotective potential of LEHD-CHO was assessed in vitro using rat hippocampal slices. CA1 orthodromic and antidromic population spike (PS) amplitude was monitored before and after fluid percussion injury in slices treated with or without LEHD-CHO. Final recovery of PS amplitude was assessed 95 min after trauma. Studies of in vivo neuroprotection with LEHD-CHO utilized a model of controlled cortical impact (CCI). Rats were given either LEHD-CHO (10 nmol icv) or an equal volume of vehicle at 5 min following CCI. Rats were perfused 24 h after CCI and brains were processed for histological examination. Results:, LEHD-CHO provided significant protection against loss of CA1 evoked response after fluid percussion. The EC50 for LEHD-CHO protection of CA1 orthodromic and antidromic PS amplitude against trauma was 2.1 ,m and 2.3 ,m. Protection extended to preservation of LTP after trauma. In vivo treatment with LEHD-CHO significantly decreased the appearance of eosinophilic cells in the CA1 region after CCI from 131 ± 23 cells in vehicle-treated animals to 24 ± 5 in LEHD-CHO treated animals. Extensive labelling with TUNEL staining was seen in vehicle-treated animals, whereas sections from LEHD-CHO treated animals demonstrated little staining. Conclusions:, These findings indicate that the caspase 9 inhibitor LHED-CHO provides concentration-dependent protection against in vitro CA1 neuronal injury, which extends to protection against in vivo CA1 injury from CCI. They further suggest that inhibition of caspase 9 may be a useful treatment strategy for traumatic brain injury. Acknowledgement:, Supported by VA Research and UCLA BIRC. [source]


Vital signs for vital people: an exploratory study into the role of the Healthcare Assistant in recognising, recording and responding to the acutely ill patient in the general ward setting

JOURNAL OF NURSING MANAGEMENT, Issue 5 2010
JAYNE JAMES RN., Ortho.
james j., butler-williams c., hunt j. & cox h. (2010) Journal of Nursing Management18, 548,555 Vital signs for vital people: an exploratory study into the role of the Healthcare Assistant in recognising, recording and responding to the acutely ill patient in the general ward setting Aim, To examine the contribution of the Healthcare Assistant (HCA) as the recogniser, responder and recorder of acutely ill patients within the general ward setting. Background, Concerns have been highlighted regarding the recognition and management of the acutely ill patient within the general ward setting. The contribution of the HCA role to this process has been given limited attention. Methods, A postal survey of HCAs was piloted and conducted within two district general hospitals. Open and closed questions were used. Results, Results suggest that on a regular basis HCAs are caring for acutely ill patients. Contextual issues and inaccuracies in some aspects of patient assessment were highlighted. It would appear normal communication channels and hierarchies were bypassed when patients' safety was of concern. Educational needs were identified including scenario-based learning and the importance of ensuring mandatory training is current. Conclusions and implications for nursing management, HCAs play a significant role in the detection and monitoring of acutely ill patients. Acknowledgement is needed of the contextual factors in the general ward setting which may influence the quality of this process. The educational needs identified by this study can assist managers to improve clinical supervision and educational input in order to improve the quality of care for acutely ill patients. [source]


Acknowledgement of 2003 Reviewers

LIVER TRANSPLANTATION, Issue 1 2004
You have full text access to this OnlineOpen article
[source]


Acknowledgement of non-editorial board reviewers, 2005

MOLECULAR ORAL MICROBIOLOGY, Issue 6 2005
Article first published online: 14 OCT 200
[source]


2007 Acknowledgement of Reviewers

POLITICS & POLICY, Issue 4 2007
Article first published online: 7 DEC 200
No abstract is available for this article. [source]


REVIEWER ACKNOWLEDGEMENT: Reviewer Acknowledgement

THE JOURNAL OF SEXUAL MEDICINE, Issue 7 2010
Article first published online: 6 JUL 2010
No abstract is available for this article. [source]


Acknowledgements, Author & Subject Indexes

ECOLOGICAL MANAGEMENT & RESTORATION, Issue 3 2002
Article first published online: 20 JAN 200
First page of article [source]


Acknowledgements: Electrophoresis 24/2007

ELECTROPHORESIS, Issue 24 2007
Article first published online: 10 DEC 200
No abstracts. [source]


In vitro1H magnetic resonance spectroscopy differences between meningeoma and astrocytoma

JOURNAL OF NEUROCHEMISTRY, Issue 2003
K. Likav, anová
Tumor transformation of the human brain cells causes different biochemical changes. Here we employed 1H magnetic resonance spectroscopy to compare the presence of low molecular weight metabolites in meningeoma and astrocytoma tumors by measuring perchloric acid extracts of the cells. In 1H spectra of meningeoma we detected high signal from lactate but were unable to detect any signal of NAA and creatine. In contrast, astrocytoma samples revealed significantly higher level of inositol and glycine and significant decrease in glutamate and glutamine compared with meningeoma but no presence of taurine. Our results suggest that 1H MRS can provide useful information about biochemical changes in different types of brain tumors. Acknowledgements: This work was supported by the Grant Category C and Comenius University Grant No. X/2003. [source]


The study of the creatine kinase in rat brain during ischemia by magnetization transfer and biochemical analysis

JOURNAL OF NEUROCHEMISTRY, Issue 2003
D. Dobrota
Various methods are used to study the biochemical changes in the central nervous system under normal and pathological conditions. The magnetization transfer 31P magnetic resonance technique was used here to measure the creatine kinase (CK) reaction rate constant in vivo in rats with cerebral ischemia. The measurements indicated that the rate constant of the CK reaction was significantly reduced in the case of chronic brain ischemia in aged rats. The similar reduction of the creatine kinase activity was found in the ischemic rat brain homogenate measured by biochemical analysis. At the same time, corresponding conventional phosphorus magnetic resonance spectra showed negligible or no change in signal intensities of compounds containing macroergic phosphates. Acknowledgements: This work was supported by the Grant Category C and Comenius University Grant No. X/2003. [source]


Nicotine up-regulates expression of neurotrophic factors and attenuates apoptosis of spinal cord neurons

JOURNAL OF NEUROCHEMISTRY, Issue 2003
R. Garrido
Nicotine may induce neuroprotection in spinal cord injury; however, the mechanisms of these effects are not fully understood. The present study focused on the effects of nicotine on expression of neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and basic fibroblast growth factor (FGF-2) in a model of spinal cord injury. In this model, cultured spinal cord neurons are exposed to 10 mm arachidonic acid (AA). Exposure to AA diminished expression of BDNF and FGF-2; however, pretreatment with nicotine protected against these effects. Mecamylamine and ,-bungarotoxin inhibited nicotine-mediated up-regulation of BDNF and FGF-2. Moreover, nicotine, BDNF and FGF-2 protected against AA-induced apoptosis of spinal cord neurons. These results suggest that AA can induce apoptosis of spinal cord neurons by depletion of neurotrophic factors and that nicotine can protect against these effects through the alpha7 receptor-mediated pathway. Acknowledgements:, Supported by grants from Philip Morris Research Program and KSCHIRT. [source]


Macrophage migration inhibitor factor (MIF) can induce oxidative injury and apoptotic cell death of spinal cord neurons

JOURNAL OF NEUROCHEMISTRY, Issue 2003
M. Toborek
MIF is a cytokine produced by a variety of cells and tissues including the CNS. It can exert a variety of biological functions, such as induction of inflammatory responses and counterregulation of glucocorticoid effects. However, the role of MIF in the pathogenesis of spinal cord trauma is not fully understood. Therefore, the aim of the present study was to evaluate the cellular effects of MIF in cultured spinal cord neurons. A 3-h exposure to MIF significantly enhanced intracellular calcium levels; an effect which was prevented by TMB-8, an antagonist of the IP3 receptor. In addition, MIF treatment increased oxidative stress, decreased viability of spinal cord neurons, increased LDH release and stimulated apoptosis. These results suggest that MIF may play an important role in secondary spinal cord injury. Acknowledgements:, Supported by grants from KSCHIRT and Philip Morris External Research Program. [source]


Characterization of nociceptin binding sites by novel peptide analogs and radioprobes

JOURNAL OF NEUROCHEMISTRY, Issue 2003
S. Benyhe
A number of new synthetic nociceptin ligands were studied in receptor binding and functional tests in rat brain membranes and in cloned systems. Ligand binding experiments were performed with three different radioprobes developed in our lab. The nociceptin derivatives exhibited high affinity in competition experiments. Receptor-mediated G-protein activation was determined in [35S]GTPgS binding assays. Among the new structures examined, Ac-RYYRIK-ol was found to be only a weak stimulator by itself, whereas this compound inhibited receptor-mediated G-protein activation. These data suggest that Ac-RYYRIK-ol is a high affinity peptide antagonist for the nociceptin receptor. Acknowledgements:, Supported by the Hungarian Scientific Research Fund OTKA T-035211, T-033078, T-030841, and the Ministry of Education, NKFP 1/027 Hungary. [source]


Differential activation of C1 complement components in rat spinal cord after sciatic nerve injury

JOURNAL OF NEUROCHEMISTRY, Issue 2003
J. Mika
Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q-associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain. Acknowledgements:, Supported by BMBF01GG9818, SFB297, DFGWE910/8-3, KBN3P05C00623. [source]


Transient forebrain ischemia modulates focal adhesion kinase (FAK)-mediated signal transduction in gerbil hippocampus

JOURNAL OF NEUROCHEMISTRY, Issue 2003
M. Ziemka-Na
Focal adhesion kinase (FAK) is thought to play a major role in conveying survival signals from extracellular matrix (ECM). Phosphorylated FAK may interact with other nonreceptor kinases such as Src, and adaptor molecule Cas, perhaps providing a pathway by which ECM may regulate cell viability. In the present study the expression and tyrosine phosphorylation of FAK, Src and Cas after 5 min of global ischemia were investigated. The primary activation/phosphorylation of FAK, observed during first 6 h after ischemic injury, was followed by its profound down-regulation. At 72 h of reperfusion the level of phosphorylated FAK decrease to about 50% of the control. The decrease of FAK phosphorylation coincides with its proteolytic degradation. Cleavage of FAK coincided temporally with the loss of Src and Cas. Ischemia-induced proteolytic processing of the investigated proteins may lead to the interruption of ECM-derived signals and compromise neuronal survival. Acknowledgements:, Sponsored by SCSR 4P05A 08619 and Med. Res. Ctr. [source]


Agonists specific for the transcription factor PPARdelta accelerate differentiation of oligodendrocytes

JOURNAL OF NEUROCHEMISTRY, Issue 2002
R. P. Skoff
Peroxisome proliferator activated receptors (PPARs) are transcription factors belonging to the nuclear hormone receptor superfamily that regulate key genes involved in lipid metabolism. PPAR, is ubiquitously expressed at low levels in many tissues and its function has remained elusive. However, we have shown that PPAR, is abundantly expressed in oligodendrocytes (Ols), suggesting this receptor plays a critical role in oligodendrocyte differentiation (Granneman et al. 1998 J. Neurosci. Res51, 563). We first investigated the effects of PPAR agonists on proliferation and differentiation of Ols in tissue culture. Primary glial and enriched Ol cultures were treated with ligands that specifically activate PPAR, and PPAR, (Berger et al. 1999 J. Biol. Chem. 274, 6717). PPAR, but not PPAR, agonists increased the size of OL membrane sheets within 24 h of application. The increase in membrane sheet size was mirrored by increases in MBP and PLP mRNA's. In enriched Ol cultures, the number of Ols was increased 70% with the PPAR, agonist but not the PPAR, agonist (Saluja et al. 2001 Glia33, 191). In vivo injections of PPAR, agonist into P2 and P3 mice show an increase of total macroglia in the ventral and dorsal funiculi of the spinal cord of 20,40% compared to controls. Preliminary observations suggest the Ols in agonist treated cultures are larger and more densely stained than controls. Our results show for the first time that a specific ligand for a transcription factor is capable of activating the program of Ol differentiation. Acknowledgements: Supported by NMSS. [source]


The mediterranean fever gene modifies the progression of disability in non-Ashkenazi Jewish multiple sclerosis patients

JOURNAL OF NEUROCHEMISTRY, Issue 2002
Y. Shinar
MS is an autoimmune, CNS demyelinating disease manifested in most patients with progressive disability. The progression rate varies between patients and may depend on modifier, immune related genes. The Mediterranean fever gene, expressed in peripheral blood leukocytes, is responsible for familial Mediterranean fever (FMF), a recessive, periodic autoinflammatory disease prevalent in Semitic populations, and less penetrant in Ashkenazi Jews. We related common, FMF associated MEFV mutations to the progression of disability in Jewish, relapsing remitting (RR) MS patients. The mutations 148Q, 694V, 695R and 726A were identified by enzymatic restriction of PCR-amplified MEFV DNA. The progression to statuses 3 and 6 of the expanded disability status scale (EDSS) was analyzed on survival plots. 35% of 48 non-Ashkenazi patients had one MEFV mutation. Compared to non-carriers (n = 31) the heterozygous cohort (n = 17) represented with an increased fraction reaching both EDSS statuses (p < 0.05), and with a shorter median time to reach both EDSS =,3 (2 years in carriers vs. 10 years in non-carriers, p < 0.01) and EDSS =,6 (6 vs. 23 years, respectively, p < 0.005). 17% of 71 Ashkenazi patients had one MEFV mutation. There was no significant difference in the fraction of disabled or in the progression of disability between Ashkenazi carrier patients and non-carriers. The susceptibility of the non-Ashkenazi group attributed, in part, to the detrimental non-Ashkenazi 694V mutation. The results suggest phenotypic expression of one mutated MEFV gene in non-ashkenazi patients, pertinent to the pathogenesis of disability. Acknowledgements:, Granted by the Israeli Ministry of Science (#6279). [source]