Contaminant levels were low and associations between contaminant exposure and oxidative stress were weak. Nevertheless, glutathione peroxidase activity

rose with increasing hepatic Se concentrations, levels of thiols declined as Hg and OC/PCB levels rose, and at one of the two study sites levels of lipid peroxidation were elevated with increasing levels of hepatic Hg. These results suggest the possibility E7080 in vivo of a deleterious effect of exposure to contaminants on gull physiology even at low contaminant exposures.”
“Semliki Forest virus (SW) vectors lead to high protein expression in mammalian cells, but expression is transient due to vector cytopathic effects, inhibition of host cell proteins and RNA-based expression. We have used a noncytopathic Idasanutlin supplier SW mutant (ncSFV) RNA vector to generate stable cell lines expressing two human therapeutic proteins: insulin-like growth factor I (IGF-I) and cardiotrophin-1 (CT-1). Therapeutic genes were fused at the carboxy-terminal end of Puromycin N-acetyl-transferase gene by using as a linker the sequence coding for foot-and-mouth disease

virus (FMDV) 2A autoprotease. These cassettes were cloned into the ncSFV vector. Recombinant ncSFV vectors allowed rapid and efficient selection of stable BHK cell lines with puromycin. These cells expressed IGF-I and CT-1 in supernatants at levels reaching 1.4 and 8.61.ig/106 cells/24 hours, respectively. Two cell lines generated with each vector were passaged ten times during 30 days, showing constant levels of protein expression. Recombinant proteins expressed at different passages were functional by in vitro signaling assays. Stability at RNA level was unexpectedly high, showing a very low mutation

rate in the CT-1 sequence, which did not increase at high passages. CT-1 was efficiently purified from supernatants selleckchem of ncSFV cell lines, obtaining a yield of approximately 2 mg/L/24 hours. These results indicate that the ncSFV vector has a great potential for the production of recombinant proteins in mammalian cells.”
“Studies suggested that exposure to agricultural pesticides may affect male fertility. Pyrethroids are widely used pesticides due to their insecticidal potency and low mammalian toxicity. A recombinant yeast assay system incorporating the human -estrogen receptor was used to analyze the estrogenicity of a range of readily available pyrethroid pesticides. The commercial product Ripcord Plus showed estrogenic activity by this assay. To determine whether pyrethroid compounds might exert an effect on male fertility, mouse Sertoli cells were exposed in vitro to the endogenous estrogen, 17-estradiol, and selected estrogenic pyrethroids. Following exposure, transcript levels of the – and -estrogen receptors were assessed.

Immediate treatment efficacy was assessed by contrast enhanced ultrasound 1 day after ablation.

Short-term efficacy was assessed by contrast enhanced computerized tomography and/or contrast enhanced ultrasound at 1, 3 and 6 months, and every 6 months thereafter.

Results: All tumors were completely ablated at a single session and no complications occurred. find more No residual tumor or recurrence was observed at a median followup of 11 months (range 4 to 20). The ablation zone was well defined on contrast enhanced imaging and it gradually shrank with time.

Conclusions: Ultrasound guided percutaneous microwave ablation appears to be a safe and effective technique for small renal cell cancer in select patients.”
“Background: Pulmonary-vein isolation is increasingly being used to treat atrial fibrillation in patients with heart failure.

Methods: In this prospective, multicenter clinical trial, we randomly assigned patients with symptomatic, drug-resistant atrial fibrillation, an ejection fraction of 40% or less, and New York Heart Association

class II or III heart failure to undergo either pulmonary-vein isolation or atrioventricular-node ablation with biventricular pacing. All patients completed the Minnesota Living with Heart Failure questionnaire (scores range from 0 to 105, with a higher score indicating a worse quality of life) and underwent echocardiography and a 6-minute walk test (the composite primary end point). Over a 6-month period, patients were monitored for both symptomatic and asymptomatic episodes of atrial fibrillation.

Results: In all, 41 patients underwent PF-02341066 order pulmonary-vein isolation, and 40 underwent atrioventricular-node ablation with biventricular pacing; none were lost to follow-up at 6 months. The composite primary end point favored the group that underwent pulmonary-vein isolation, with an improved questionnaire score at 6 months (60, vs. 82 in the group that underwent atrioventricular-node ablation with biventricular pacing; P<0.001), a longer 6-minute-walk

distance (340 m vs. 297 m, P<0.001), and a higher ejection fraction (35% vs. 28%, P<0.001). In the group that underwent pulmonary-vein isolation, 88% of patients receiving antiarrhythmic AG-120 solubility dmso drugs and 71% of those not receiving such drugs were free of atrial fibrillation at 6 months. In the group that underwent pulmonary-vein isolation, pulmonary-vein stenosis developed in two patients, pericardial effusion in one, and pulmonary edema in another; in the group that underwent atrioventricular-node ablation with biventricular pacing, lead dislodgment was found in one patient and pneumothorax in another.

Conclusions: Pulmonary-vein isolation was superior to atrioventricular-node ablation with biventricular pacing in patients with heart failure who had drug-refractory atrial fibrillation. (ClinicalTrials.gov number, NCT00599976.).

Melatonin (10 mg/kg, per os) induced a transient enhancement in REM sleep followed by a reduction in REM and SWS sleep and an increase in waking. Ramelteon

(10 mg/kg, per os) provoked a transient increase in REM sleep. Finally, S32006 (10 mg/kg, intraperitoneally), administered at dark phase onset, mimicked the increased SWS provoked by agomelatine, yet diminished REM sleep.

Agomelatine possesses a distinctive EEG profile compared with melatonin, ramelteon, and S32006, possibly reflecting co-joint agonist and antagonist properties at MT(1)/MT(2) and 5-HT(2C) receptors, respectively.”
“Metapolybia wasps live in small societies (around one hundred adults) and rear their young in nests they construct on flat surfaces from plant materials. For processing nest paper, they must gather plant materials and process HKI-272 molecular weight it into pulp with water. selleck kinase inhibitor The water is collected by water foragers and is transferred

to pulp foragers indirectly via a “”common stomach.”" The common stomach, or social crop, is formed by generalist wasps called laborers. These wasps can engage in water exchange, store water in their crops, and may become specialist foragers or builders. We provide an alternative model for regulating task partitioning in construction behavior by using an agent based modeling framework parameterized by our field observations. Our model predicts that assessing colony needs via individual interactions with the common stomach leads to a robust regulation of task partitioning in construction behavior. By using perturbation experiments in our simulations, we show that this emergent task allocation is able to dynamically adapt to perturbations of the environment and to changes in colony-level demands or population structure. The robustness of our model stems from the fact that the common stomach is both a strong buffer and a source of several feedback mechanisms that affect the individual wasps. We show that both

the efficiency and the task fidelity of these colonies are dependent upon colony size. We also demonstrate that the emergence of Selleckchem Cyclosporin A specialist wasps (individuals with high task fidelity) does not require any special initial conditions or reinforcement at the individual level, but it is rather a consequence of colony-level workflow stability. Our model closely mimics the behavior of Metapolybia wasps, demonstrating that a regulation mechanism based on simple pair-wise interactions through a common stomach is a plausible hypothesis for the organization of collective behavior. (C) 2011 Elsevier Ltd. All rights reserved.”
“Eszopiclone and zolpidem are hypnotics that differentially affect sleep and waking states in adult animals. Therefore, it was of interest to compare their effects on the states of sleep and wakefulness in aged animals.

Finally, while the chemokine CX3CL1 behaves as an inverse agonist or inhibitor of constitutive US28 signaling to PLC-beta, we demonstrate that CX3CL1 functions as an agonist with regard to US28-stimulated calcium release. This study is the first to demonstrate that the carboxy terminus of US28 controls US28 signaling in the context of HCMV infection and indicates that chemokines such as CX3CL1 can decrease constitutive US28 signals and yet simultaneously promote nonconstitutive US28 signals.”
“Increasing evidence indicates that sleep deprivation (0) alters responses to pharmacological agents by affecting specific transmitter systems. The present work Selleckchem BI 2536 addressed deficits in passive

avoidance (PA) Navitoclax research buy performance that are seen after SD, and investigated whether treatment with the inverse benzodiazepine agonist beta-CCM could prevent such deficits. Male Wistar rats were deprived of sleep for 96 h using the platform method (SD group), or were sleep deprived and then allowed to recover

sleep for 24 h (SR group). Animals were treated with saline or 0.5 mg/kg beta-CCM before PA training, and were tested 30 min or 24 h later. A separate set of animals was sacrificed for [(3)H]Ro 15-4513 binding analysis. beta-CCM increased PA performance in control animals in both short and long term retention tests, whereas SD and SR animals were unaffected by the drug treatment. Interestingly, [3H]Ro 15-4513 binding was reduced in the entorhinal cortex in both SD and SR groups. These findings suggest that the this website lack of promnesic effects of beta-CCM after SD and SR may be associated with benzodiazepine receptor downregulation in specific brain regions related to memory formation. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Emerging data suggest that a cytotoxic

T-lymphocyte response against a diversity of epitopes confers greater protection against a human immunodeficiency virus/simian immunodeficiency virus infection than does a more focused response. To facilitate the creation of vaccine strategies that will generate cellular immune responses with the greatest breadth, it will be important to understand the mechanisms employed by the immune response to regulate the relative magnitudes of dominant and nondominant epitope-specific cellular immune responses. In this study, we generated dominant Gag p11C- and subdominant Env p41A-specific CD8(+) T-lymphocyte responses in Mamu-A*01(+) rhesus monkeys through vaccination with plasmid DNA and recombinant adenovirus encoding simian-human immunodeficiency virus (SHIV) proteins. Infection of vaccinated Mamu-A*01(+) rhesus monkeys with a SHIV Gag Delta p11C mutant virus generated a significantly increased expansion of the Env p41A-specific CD8(+) T-lymphocyte response in the absence of secondary Gag p11C-specific CD8(+) T-lymphocyte responses.

We measured single-molecule fluorescence trajectories with polarization modulation selleck compound to track the conformation of the

autoinhibitory domain of PMCA pump bound to fluorescently labeled CaM. Interchange of the autoinhibitory domain between associated and dissociated conformations was detected at a physiological Ca2+ concentration of 0.15 mu M, where the enzyme is only partially active, but not at 25 mu M, where the enzyme is fully activated. In previous work we showed that the conformation of the autoinhibitory domain in PMCA-CaM complexes could be monitored by the extent of modulation of single-molecule fluorescence generated with rotating excitation polarization. In the present work, we determined the timescale of association and dissociation STAT inhibitor of the autoinhibitory domain with the catalytic regions of the PMCA. Association of the autoinhibitory domain was rare at a high Ca2+ concentration (25 mM). At a lower Ca2+ concentration (0.15 mM), conformations of the autoinhibitory domain interchanged with a dissociation rate of 0.042 +/- 0.011 sec (-1) and an association rate of 0.023 +/- 0.006 sec(-1). The results indicate that the response time of PMCA upon a reduction in Ca2+ is limited to tens of seconds by autoinhibitory dynamics. This property may reduce the sensitivity of PMCA to transient reductions in intracellular Ca2+. We suggest that the dynamics of the autoinhibitory domain may play a novel role in regulating

PMCA activity.”
“(MHC) class I next molecules with peptides is orchestrated by several assembly factors including the transporter associated with antigen processing (TAP) and tapasin, the endoplasmic reticulum (ER) oxido-reductases

ERp57 and protein disulfide isomerase (PDI), the lectin chaperones calnexin and calreticulin, and the ER aminopeptidase (ERAAP). Typically, MHC class I molecules present endogenous antigens to cytotoxic T lymphocytes (CTLs). However, the initiation of CD8(+) T-cell responses against many pathogens and tumors also requires the presentation of exogenous antigens by MHC class I molecules. We discuss recent developments relating to interactions and mechanisms of function of the various assembly factors and pathways by which exogenous antigens access MHC class I molecules.”
“High temperatures cause a variety of physiological stress responses in insects, including increased generation of reactive oxygen species (ROS), which can cause oxidative damage. This study investigated the effects of thermal stress on ROS generation, the expression of heat shock protein 70 (Hsp70) at the mRNA and protein levels, the activity of antioxidant enzymes (SOD, CAT), and apoptosis in hemocytes of Chilo suppressalis larvae. Results indicated that thermal stress significantly elevated the level of ROS and antioxidant enzyme activity in C. suppressalis larvae. Real-time quantitative PCR showed that hsp70 gene expression was induced by heat stress.

The pathophysiology of cystic fibrosis (CF) lung disease is characterised by abnormal ion and fluid transport across the epithelium and polymorphonuclear (PMN)

leukocyte-dominated inflammatory response. Na+/H+ exchanger regulatory factor 1 (NHERF1) is a protein involved in PKA-dependent activation of CFTR by interacting with CFTR via its PDZ domains and with ezrin via its C-terminal domain. We have previously found that the NHERF1-overexpression dependent rescue CFTR-dependent chloride secretion is due to the re-organisation of the actin cytoskeleton network induced by the formation of the multiprotein complex NHERF1 RhoA ezrin actin. In this this website context, we here studied whether NHERF1 and CFTR

are involved in the organisation and function of TJs. F508del CFBE41o(-) monolayers presented nuclear localisation of zonula occludens (ZO-1) and occludin as well as disorganisation of claudin 1 and junction-associated adhesion molecule 1 as compared with wild-type 16HBE14o(-) monolayers, paralleled by increased permeability to dextrans and PMN transmigration. Overexpression of either NHERF1 or CFTR in CFBE41o(-) cells rescued TJ proteins to their proper intercellular Cyclosporin A location and decreased permeability and PMN transmigration, while this effect was not achieved by overexpressing either NHERF1 deprived of ezrin-binding domain. Further, expression of a phospho-dead ezrin mutant, T567A, increased permeability in both 16HBE14o(-) cells and in a CFBE clone stably overexpressing NHERF1 (CFBE/sNHERF1), whereas a constitutively active form of ezrin, T567D, achieved

FK506 mouse the opposite effect in CFBE41o(-) cells. A dominant-negative form of RhoA (RhoA-N19) also disrupted ZO-1 localisation at the intercellular contacts dislodging it to the nucleus and increased permeability in CFBE/sNHERF1. The inhibitor Y27632 of Rho kinase (ROCK) increased permeability as well. Overall, these data suggest a significant role for the multiprotein complex CFTR-NHERF1-ezrin-actin in maintaining TJ organisation and barrier function, and suggest that the RhoA/ROCK pathway is involved. Laboratory Investigation (2012) 92, 1527-1540; doi:10.1038/labinvest.2012.

3% in MED (P = .14); the mortality rate was 2.0% in ANAT and. 0.8% in MED (P = .79). The 2-year survival free from stroke was MED, 93.6% and ANAT, 98.9% (P = .118); and from restenosis was MED, 91.9%; and ANAT, 91.0% (P = .98). Two-year

overall survival was significantly better in ANAT (84.6%) vs MED (70.1%; P = .026). Four LEE011 price of the seven restenoses in the ANAT group occurred in patients with previous neck radiation. The restenosis rate for radiation-induced (RAD) stenosis treated with CAS was significantly higher at 22.2% (4 of 18) compared with 3.8% (3 of 78) in ANAT group patients without a history of radiation (non-RAD; P = .028). The 2-year restenosis-free survival was 72.7% in the RAD group vs; 95.9% in the non-RAD group (P = .017).

Conclusion: CAS is as technically feasible, safe, and durable in anatomically high-risk patients as in medically high-risk patients, with similar rates of periprocedural stroke and death and late restenosis. However, patients with radiation-induced stenosis appear to be at an increased risk for restenosis. (J Vasc Surg 2009;50:762-8.)”
“Amyloid precursor protein (APP) is strongly related

to the onset of Alzheimer’s disease. It possesses cleavage sites for beta- and gamma-secretases, and the resulting cleaved products (amyloid-beta peptides) are capable of causing neurotoxicity. Such cleavage is promoted by the Swedish PS-341 datasheet and London mutations (APPSwe/Lon) inside the APP gene. Here, we characterized APPSL transgenic

mice (APPSL-Tg) to determine the effects of this mutation. We observed that both the amount of insoluble amyloid-beta and the ratio of amyloid-beta 42/40 increased DNA-PK inhibitor promptly in the brain during 6-16 months of age. Amyloid-beta plaques were observed in whole brain sections at 12 months. In contrast, the spatial memory assessed by the Morris water maze task was already impaired at 3 months, which suggested that the APPSL-Tg mice may represent an early-onset model of familial Alzheimer’s disease. Furthermore, the levels of LAMP-1, a marker protein of lysosome, increased in the brain at 28 months. Such LAMP-1 protein was detected around the amyloid-beta plaques at the hippocampal regions of the APPSL-Tg mice. Our results suggested that the increase in LAMP-1 was enhanced by the accumulation of amyloid-beta occurring during aging. Our findings coincided with the pathological hallmarks of Alzheimer’s disease. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Objective: The PREVENT III (PIII) critical limb ischemia (CLI) risk score is a simple, published tool derived from the PIII randomized clinical trial that can be used for estimating amputation-free survival (AFS) in CLI patients considered for infrainguinal bypass (IB). The current study sought to validate this risk stratification model using data from the prospectively collected Vascular Study Group of Northern New England (VSGNNE).

Striatal monoamine neurotransmitters and striatal as well as liver long chain free fatty acids concentrations were subsequently evaluated in another

group treated i.p. with 20 mg/kg C75. Acute exposure to C75 at 20 mg/kg led to approximately 50% increase in the striatal dopamine levels and a decrease in dopamine turnover for up to 24 h following the injection. The concentration selleck chemical of serotonin remained unchanged. Concentration of saturated fatty acids in the liver and striatum did not change, while striatal unsaturated myristoleic acid (cis-9-tetradecenoic acid) levels were significantly higher as early as 2 h post-injection and remained elevated at 24 h post-injection. These preliminary data suggest a central regulatory role of unsaturated fatty acids under dopaminergic control in the Z-IETD-FMK manufacturer C75-induced anorexia. Pharmacological alterations in

fatty acid metabolism may prove beneficial in the treatment of obesity. Published by Elsevier Ireland Ltd.”
“Purpose: Vesicoureteral reflux familial clustering implies that genetic factors have a key role in reflux pathogenesis. We identified genes that cause this disease and elucidated the biology and genetics of vesicoureteral reflux.

Materials and Methods: There were 166 families and 738 individuals, including 319 parents and 419 offspring. The 166 families had 193 affected sib pairs in whom vesicoureteral reflux was confirmed selleck kinase inhibitor by voiding cystourethrogram. DNA samples were obtained to analyze various candidate genes or regions with a key role in urinary tract development, eg UPK3, UPK2, UPK1B, Chr.10q25.3, KAL1, PAR1 and PAR2. A genome scan was completed in 133 families and the results of genome scan single nucleotide polymorphisms in or closely flanking the candidate genes were investigated. Fine mapping was done to narrow the significant regions and identify potential candidate genes.

Results: Lod scores

based on the model, proposing a single dominant locus with decreased penetrance, were negative at all loci. Marginally significant nonparametric lod scores were seen at several loci, particularly UPK1B and PAR1. A signal of moderate significance was detected at the region centered on 10q 25.2.

Conclusions: Linkage analysis in a large cohort of vesicoureteral reflux families ruled out UPK3, UPK2, UPK1B, KAL, PAR1 and PAR2 as candidate genes for reflux. Results provide evidence supporting genes and regions that may be worth further study as primary vesicoureteral reflux loci.”
“Recent event-related brain potential (ERP) study disentangled an early automatic component and a late top-down controlled component of neural activities to perceived pain of others.

0 mg/kg DOI also reduced accuracy, but the latter concurrently impaired responding. At the lowest dose (0.2 mg/kg), amphetamine increased total trials and rewards without affecting accuracy; 1.0 mg/kg nicotine reduced accuracy without affecting total trials, whereas 10.0 mg/kg SKF38393 had the opposite effect.

Although the possibility for mediating behaviors may exist, the rodent n-back task provides a clinically relevant model of working memory. Amphetamine and MK801 produced selective impairments

without disrupting responding. The cognitive enhancers did not improve working memory, but low doses of amphetamine improved response efficiency. This novel procedure may be useful for examining cognitive deficits and their potential selleck products reversal in animal models of schizophrenia.”
“The mammalian Golgi complex, trans Golgi network (TGN) and

ER-Golgi intermediate compartment (ERGIC) are comprised of membrane cisternae, coated vesicles and membrane tubules, all of which contribute to STI571 membrane trafficking and maintenance of their unique architectures. Recently, a new cast of players was discovered to regulate the Golgi and ERGIC: four unrelated cytoplasmic phospholipase A (PLA) enzymes, cPLA(2)alpha (GIVA cPLA(2)), PAFAH Ib (GVIII PLA(2)), iPLA(2)-beta (GVIA-2 iPLA(2)) and iPLA(1)gamma. These ubiquitously expressed enzymes regulate membrane trafficking from specific Golgi subcompartments, although there is evidence for some functional redundancy between PAFAH Ib and cPLA(2)alpha. Three of these enzymes, PAFAH Ib, cPLA(2)alpha and iPLA(2)-beta, exert effects on Golgi structure and function by inducing the formation of membrane tubules. Maltase We review our current understanding of how PLA enzymes regulate Golgi and ERGIC morphology and function.”
“Astrocytes are implicated

in information processing, signal transmission, and regulation of synaptic plasticity. Aquaporin-4 (AQP4) is the major water channel in adult brain and is primarily expressed in astrocytes. A growing body of evidence indicates that AQP4 is a potential molecular target for the regulation of astrocytic function. However, little is known about the role of AQP4 in synaptic plasticity in the amygdala. Therefore, we evaluated long-term potentiation (LTP) in the lateral amygdala (LA) and associative fear memory of AQP4 knockout (KO) and wild-type mice. We found that AQP4 deficiency impaired LTP in the thalamo-LA pathway and associative fear memory. Furthermore, AQP4 deficiency significantly downregulated glutamate transporter-1 (GLT-1) expression and selectively increased NMDA receptor (NMDAR)-mediated EPSCs in the LA. However, low concentration of NMDAR antagonist reversed the impairment of LIP in KO mice. Upregulating GLT-1 expression by chronic treatment with ceftriaxone also reversed the impairment of LTP and fear memory in KO mice. These findings imply a role for AQP4 in synaptic plasticity and associative fear memory in the amygdala by regulating GLT-1 expression.

The multivalent RGD peptides exhibited rather loose linkages partly including oligo(ethylene glycol) spacers (EG(n)) with different chain lengths. Therefore,

the dependence of multivalent ROD systems with and without EG(n) linkers were investigated on their binding properties to cultured alpha(v)beta(3) integrin-expressing U87MG cells.

Methods: We synthesized a series of di-, tri- and tetravalent rigid scaffolds (terephthalic acid, trimesic acid and adamantane-1,3,5,7-tetracarboxylic acid) conjugated to c(RGDyK) ligands, which were linked contiguously GSK1838705A or separated by the oligo(ethylene glycol) spacers. The inhibition constants of these c(RGDyK) derivatives were determined by competition assays

with (125)I-labeled echistatin.

Results: While c(RGDyK) function is a relative weak competitor against [(125)I]echistatin (Ki, 329 +/- 18 nM) for alpha(v)beta(3) integrin-expressing U87MG cells, RGD dimers improved the competition potency considerably (K 64 23 nM). This effect was even more pronounced with the ROD trimers (K1, 40 +/- 7 nM) and tetramers (K1, check details 26 +/- 9 nM). The introduction of EG(n) spacers and the increase of linker lengths proved to be detrimental since more competitors were needed to compete with [1251]echistatin. The EG(6) group, for example, reduced the inhibition constants by 29% (dimer), 57% (trimer) and 97% (tetramer).

Conclusion: The binding experiments performed with the three forms of multivalent ROD ligands indicate the weakening of competitive potency against [(125)I]echistatin with the introduction of EG(n) spacers. This effect may be related to the decrease of the effective ROD molarity, which becomes most prominent within the tetravalent series. (C) 2010 Elsevier Inc. All rights reserved.”
“In intracellular calcium signaling, calcium buffers has been recognized for their role in reshaping and localizing the calcium concentration profile in the vicinity of the channel, as well as reducing the effective diffusion of free calcium. In

the presence of an excess of endogenous or exogenous buffers, linearization of the reaction-diffusion system describing the calcium-buffer dynamics has C1GALT1 been instrumental in understanding the extent of the microdomain formation and in quantifying the apparent diffusion of the free calcium. In these linearized models, the conclusions are usually drawn from the steady-state solutions upon the opening of the channel. In this work, using the joint Laplace-Fourier method, we give an explicit integral transient solution, as well as, the long-time asymptotic behavior of the linearized calcium-buffer dynamics. The results confirm and emphasize the long stated intuitions on the diffusive character of the calcium-buffer dynamics. Numerical validations of our analytical results will be discussed. (C) 2010 Elsevier Ltd. All rights reserved.