520 resultados para Reactivation


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The Holocene vegetation history of the Arabian Peninsula is poorly understood, with few palaeobotanical studies to date. At Awafi, Ras al-Khaimah, UAE, a 3.3 m lake sediment sequence records the vegetation development for the period 8500 cal. yr BP to similar to3000 cal. yr BP. delta(13)C isotope, pollen and phytolith analyses indicate that C3 Pooid grassland with a strong woody element existed during the early Holocene (between 8500 and 6000 cal. yr BP) and became replaced by mixed C3 and C4 grasses with a strong C4 Panicoid tall grass element between 5900 and 5400 cal. yr BP. An intense, arid event Occurred at 4100 cal. yr BP when the lake desiccated and was infilled by Aeolian sand. From 4100 cal. yr BP the vegetation was dominated by C4 Chloridoid types and Cyperaceae, suggesting an incomplete vegetation cover and Aeolian dune reactivation owing to increased regional aridity. These data outline the ecosystem dynamics and carbon cycling in response to palaeomon-soon and north-westerly variability during the Holocene. Copyright (C) 2004 John Wiley Sons, Ltd.

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Lacustrine sediments from southeastern Arabia reveal variations in lake level corresponding to changes in the strength and duration of Indian Ocean Monsoon (IOM) summer rainfall and winter cyclonic rainfall. The late glacial/Holocene transition of the region was characterised by the development of mega-linear dunes. These dunes became stabilised and vegetated during the early Holocene and interdunal lakes formed in response to the incursion of the IOM at approximately 8500 cal yr BP with the development of C3 dominated savanna grasslands. The IOM weakened ca. 6000 cal yr BP with the onset of regional aridity, aeolian sedimentation and dune reactivation and accretion. Despite this reduction in precipitation, the take was maintained by winter dominated rainfall. There was a shift to drier adapted C4 grasslands across the dune field. Lake sediment geochemical analyses record precipitation minima at 8200, 5000 and 4200 cal yr BP that coincide with Bond events in the North Atlantic. A number of these events correspond with changes in cultural periods, suggesting that climate was a key mechanism affecting human occupation and exploitation of this region. (c) 2006 University of Washington. All rights reserved.

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Varicella-zoster virus (VZV) is a member of the Herpesviridae family, primary infection with which causes varicella, more commonly known as chicken pox. Characteristic of members of the alphaherpesvirus subfamily, VZV is neurotropic and establishes latency in sensory neurons. Reactivation of VZV causes herpes zoster, also known as shingles. The most frequent complication following zoster is chronic and often debilitating pain called postherpetic neuralgia (PHN), which can last for months after the disappearance of a rash. During episodes of acute zoster, VZV viremia occurs in some, but not all, patients; however, the effect of the viral load on the disease outcome is not known. Here we describe the development of a highly specific, sensitive, and reproducible real-time PCR assay to investigate the factors that may contribute to the presence and levels of baseline viremia in patients with zoster and to determine the relationship between viremia and the development and persistence of PHN. VZV DNA was detected in the peripheral blood mononuclear cells (PBMCs) of 78% of patients with acute zoster and in 9% of healthy asymptomatic blood donors. The presence of VZV in the PBMCs of patients with acute zoster was independently associated with age and being on antivirals but not with gender, immune status, extent of rash, the age of the rash at the time of blood sampling, having a history of prodromal pain, or the extent of acute pain. Prodromal pain was significantly associated with higher baseline viral loads. Viral load levels were not associated with the development or persistence of PHN at 6, 12, or 26 weeks.

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The E2F transcription factors are instrumental in regulating cell cycle progression and growth, including that in cardiomyocytes, which exit the cell cycle shortly after birth. E2F-6 has been demonstrated to act as a transcriptional repressor; however, its potential role in normal cardiomyocyte proliferation and hypertrophy has not previously been investigated. Here we report the isolation and characterisation of E2F-6 and E2F-6b in rat cardiomyocytes and consider its potential as a target for myocardial regeneration following injury. At the mRNA level, both rat E2F-6 and the alternatively spliced variant, E2F-6b, were expressed in E18 myocytes and levels were maintained throughout development into adulthood. Interestingly, E2F-6 protein expression was down-regulated during myocyte development suggesting that it is regulated post-transcriptionally in these cells. During myocyte hypertrophy, the mRNA expressions of E2F-6 and E2F-6b were not regulated whereas E2F-6 protein was up-regulated significantly. Indeed, E2F-6 protein expression levels closely parallel the developmental withdrawal of myocytes from the cell cycle and the subsequent reactivation of their cell cycle machinery during hypertrophic growth. Furthermore, depletion of E2F-6, using anti-sense technology, results in death of cultured neonatal myocytes. Taken together, abrogation of E2F-6 expression in neonatal cardiomyocytes leads to a significant decrease in their viability, consistent with the notion that E2F-6 might be required for maintaining normal myocyte growth.

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The present study examines whether children reactivate a moved constituent at its gap position and how children's more limited working memory span affects the way they process filler-gap dependencies. 46 5-7 year-old children and 54 adult controls participated in a cross-modal picture priming experiment and underwent a standardized working memory test. The results revealed a statistically significant interaction between the participants' working memory span and antecedent reactivation: High-span children (n = 19) and high-span adults (n = 22) showed evidence of antecedent priming at the gap site, while for low-span children and adults, there was no such effect. The antecedent priming effect in the high-span participants indicates that in both children and adults, dislocated arguments access their antecedents at gap positions. The absence of an antecedent reactivation effect in the low-span participants could mean that these participants required more time to integrate the dislocated constituent and reactivated the filler later during the sentence.

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Alterations to the genetic code – codon reassignments – have occurred many times in life’s history, despite the fact that genomes are coadapted to their genetic codes and therefore alterations are likely to be maladaptive. A potential mechanism for adaptive codon reassignment, which could trigger either a temporary period of codon ambiguity or a permanent genetic code change, is the reactivation of a pseudogene by a nonsense suppressor mutant transfer RNA. I examine the population genetics of each stage of this process and find that pseudogene rescue is plausible and also readily explains some features of extant variability in genetic codes.

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This paper addresses the nature and cause of Specific Language Impairment (SLI) by reviewing recent research in sentence processing of children with SLI compared to typically developing (TD) children and research in infant speech perception. These studies have revealed that children with SLI are sensitive to syntactic, semantic, and real-world information, but do not show sensitivity to grammatical morphemes with low phonetic saliency, and they show longer reaction times than age-matched controls. TD children from the age of 4 show trace reactivation, but some children with SLI fail to show this effect, which resembles the pattern of adults and TD children with low working memory. Finally, findings from the German Language Development (GLAD) Project have revealed that a group of children at risk for SLI had a history of an auditory delay and impaired processing of prosodic information in the first months of their life, which is not detectable later in life. Although this is a single project that needs to be replicated with a larger group of children, it provides preliminary support for accounts of SLI which make an explicit link between an early deficit in the processing of phonology and later language deficits, and the Computational Complexity Hypothesis that argues that the language deficit in children with SLI lies in difficulties integrating different types of information at the interfaces.

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BACKGROUND: Herpes zoster is caused by the reactivation of varicella-zoster virus from sensory neurons. The commonest complication following zoster is chronic pain termed post herpetic neuralgia. OBJECTIVES: To investigate the dynamics of VZV viraemia and viral load following the resolution of zoster and its relationship to PHN development. STUDY DESIGN: Blood samples were collected at baseline, 1 month, 3 months and 6 month from a prospective study of 63 patients with active zoster. Quantification of VZV DNA in whole blood was performed using a real-time PCR assay. RESULTS: During acute zoster, all patients had detectable VZV DNA in their blood. VZV DNA remained detectable in the blood of 91% of patients at 6 months although levels declined significantly (p<0.0001). A history of prodromal symptoms (p=0.005) and severity of pain at baseline (p=0.038) as well as taking antivirals (p=0.046) and being immunocompromised (p=0.043) were associated, with longer time to recovery from PHN. Viral DNA loads were consistently higher in patients with risk factors for PHN and higher viral DNA loads over time were associated with longer time to recovery (p=0.058 overall and 0.038 in immunocompetent). CONCLUSIONS: Based on these observations we hypothesise that VZV replication persists following acute shingles and that higher viral DNA loads contribute to the risk factors for PHN.

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Activated G protein-coupled receptors (GPCRs) are phosphorylated and interact with beta-arrestins, which mediate desensitization and endocytosis. Endothelin-converting enzyme-1 (ECE-1) degrades neuropeptides in endosomes and can promote recycling. Although endocytosis, dephosphorylation, and recycling are accepted mechanisms of receptor resensitization, a large proportion of desensitized receptors can remain at the cell surface. We investigated whether reactivation of noninternalized, desensitized (phosphorylated) receptors mediates resensitization of the substance P (SP) neurokinin 1 receptor (NK(1)R). Herein, we report a novel mechanism of resensitization by which protein phosphatase 2A (PP2A) is recruited to dephosphorylate noninternalized NK(1)R. A desensitizing concentration of SP reduced cell-surface SP binding sites by only 25%, and SP-induced Ca(2+) signals were fully resensitized before cell-surface binding sites started to recover, suggesting resensitization of cell-surface-retained NK(1)R. SP induced association of beta-arrestin1 and PP2A with noninternalized NK(1)R. beta-Arrestin1 small interfering RNA knockdown prevented SP-induced association of cell-surface NK(1)R with PP2A, indicating that beta-arrestin1 mediates this interaction. ECE-1 inhibition, by trapping beta-arrestin1 in endosomes, also impeded SP-induced association of cell-surface NK(1)R with PP2A. Resensitization of NK(1)R signaling required both PP2A and ECE-1 activity. Thus, after stimulation with SP, PP2A interacts with noninternalized NK(1)R and mediates resensitization. PP2A interaction with NK(1)R requires beta-arrestin1. ECE-1 promotes this process by releasing beta-arrestin1 from NK(1)R in endosomes. These findings represent a novel mechanism of PP2A- and ECE-1-dependent resensitization of GPCRs.

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We investigated the on-line processing of unaccusative and unergative sentences in a group of eight Greek-speaking individuals diagnosed with Broca aphasia and a group of language-unimpaired subjects used as the baseline. The processing of unaccusativity refers to the reactivation of the postverbal trace by retrieving the mnemonic representation of the verb’s syntactically defined antecedent provided in the early part of the sentence. Our results demonstrate that the Broca group showed selective reactivation of the antecedent for the unaccusatives. We consider several interpretations for our data, including explanations focusing on the transitivization properties of nonactive and active voice-alternating unaccusatives, the costly procedure claimed to underlie the parsing of active nonvoice-alternating unaccusatives, and the animacy of the antecedent modulating the syntactic choices of the patients.

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[1] Sea ice failure under low-confinement compression is modeled with a linear Coulombic criterion that can describe either fractural failure or frictional granular yield along slip lines. To study the effect of anisotropy we consider a simplified anisotropic sea ice model where the sea ice thickness depends on orientation. Accommodation of arbitrary deformation requires failure along at least two intersecting slip lines, which are determined by finding two maxima of the yield criterion. Due to the anisotropy these slip lines generally differ from the standard, Coulombic slip lines that are symmetrically positioned around the compression direction, and therefore different tractions along these slip lines give rise to a nonsymmetric stress tensor. We assume that the skewsymmetric part of this tensor is counterbalanced by an additional elastic stress in the sea ice field that suppresses floe spin. We consider the case of two leads initially formed in an isotropic ice cover under compression, and address the question of whether these leads will remain active or new slip lines will form under a rotation of the principal compression direction. Decoupled and coupled models of leads are considered and it is shown that for this particular case they both predict lead reactivation in almost the same way. The coupled model must, however, be used in determining the stress as the decoupled model does not resolve the stress asymmetry properly when failure occurs in one lead and at a new slip line.

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Epstein-Barr virus (EBV) is classified as a member in the order herpesvirales, family herpesviridae, subfamily gammaherpesvirinae and the genus lymphocytovirus. The virus is an exclusively human pathogen and thus also termed as human herpesvirus 4 (HHV4). It was the first oncogenic virus recognized and has been incriminated in the causation of tumors of both lymphatic and epithelial nature. It was reported in some previous studies that 95% of the population worldwide are serologically positive to the virus. Clinically, EBV primary infection is almost silent, persisting as a life-long asymptomatic latent infection in B cells although it may be responsible for a transient clinical syndrome called infectious mononucleosis. Following reactivation of the virus from latency due to immunocompromised status, EBV was found to be associated with several tumors. EBV linked to oncogenesis as detected in lymphoid tumors such as Burkitt's lymphoma (BL), Hodgkin's disease (HD), post-transplant lymphoproliferative disorders (PTLD) and T-cell lymphomas (e.g. Peripheral T-cell lymphomas; PTCL and Anaplastic large cell lymphomas; ALCL). It is also linked to epithelial tumors such as nasopharyngeal carcinoma (NPC), gastric carcinomas and oral hairy leukoplakia (OHL). In vitro, EBV many studies have demonstrated its ability to transform B cells into lymphoblastoid cell lines (LCLs). Despite these malignancies showing different clinical and epidemiological patterns when studied, genetic studies have suggested that these EBV- associated transformations were characterized generally by low level of virus gene expression with only the latent virus proteins (LVPs) upregulated in both tumors and LCLs. In this review, we summarize some clinical and epidemiological features of EBV- associated tumors. We also discuss how EBV latent genes may lead to oncogenesis in the different clinical malignancies

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On December 9, 2007, a 4.9 m(b) earthquake occurred in the middle of the Sao Francisco Craton, in a region with no known previous activity larger than 4 m(b). This event reached intensity VII MM (Modified Mercalli) causing the first fatal victim in Brazil. The activity had started in May 25, 2007 with a 3.5 magnitude event and continued for several months, motivating the deployment of a local 6-station network. A three week seismic quiescence was observed before the mainshock. Initial absolute hypocenters were calculated with best fitting velocity models and then relative locations were determined with hypoDD. The aftershock distribution indicates a 3 km long rupture for the mainshock. The fault plane solution, based on P-wave polarities and hypocentral trend, indicates a reverse faulting mechanism on a N30 degrees E striking plane dipping about 40 degrees to the SE. The rupture depth extends from about 0.3 to 1.2 km only. Despite the shallow depth of the mainshock, no surface feature could be correlated with the fault plane. Aeromagnetic data in the epicentral area show short-wavelength lineaments trending NNE-SSW to NE-SW which we interpret as faults and fractures in the craton basement beneath the surface limestone layer. We propose that the Caraibas-Itacarambi seismicity is probably associated with reactivation of these basement fractures and faults under the present E-W compressional stress field in this region of the South American Plate. (c) 2009 Elsevier B.V. All rights reserved.

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During the process of lateral organ development after plant decapitation, cell division and differentiation occur in a balanced manner initiated by specific signaling, which triggers the reentrance into the cell cycle. Here, we investigated short-term variations in the content of some endogenous signals, such as auxin, cytokinins (Cks), and other mitogenic stimuli (sucrose and glutamate), which are likely correlated with the cell cycle reactivation in the axillary bud primordium of pineapple nodal segments. Transcript levels of cell cycle-associated genes, CycD2;1, and histone H2A were analyzed. Nodal segments containing the quiescent axillary meristem cells were cultivated in vitro during 24 h after the apex removal and de-rooting. From the moment of stem apex and root removal, decapitated nodal segment (DNS) explants showed a lower indol-3-acetic acid (IAA) concentration than control explants, and soon after, an increase of endogenous sucrose and iP-type Cks were detected. The decrease of IAA may be the primary signal for cell cycle control early in G1 phase, leading to the upregulation of CycD2;1 gene in the first h. Later, the iP-type Cks and sucrose could have triggered the progression to S-phase since there was an increase in H2A expression at the eighth h. DNS explants revealed substantial increase in Z-type Cks and glutamate from the 12th h, suggesting that these mitogens could also operate in promoting pineapple cell cycle progression. We emphasize that the use of non-synchronized tissue rather than synchronous cell suspension culture makes it more difficult to interpret the results of a dynamic cell division process. However, pineapple nodal segments cultivated in vitro may serve as an interesting model to shed light on apical dominance release and the reentrance of quiescent axillary meristem cells into the cell cycle.

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Background and aims Toxoplasmic retinochoroiditis may recur months or years after the primary infection. Rupture of dormant cysts in the retina is the accepted hypothesis to explain recurrence. Here, the authors present evidence supporting the presence of Toxoplasma gondii in the peripheral blood of immunocompetent patients. Methods Direct observation by light microscopy and by immunofluorescence assay was performed, and results were confirmed by PCR amplification of parasite DNA. Results The authors studied 20 patients from Erechim, Brazil, including acute infected patients, patients with recurrent active toxoplasmic retinochoroiditis, patients with old toxoplasmic retinal scars, and patients with circulating IgG antibodies against T gondii and absence of ocular lesions. Blood samples were analysed, and T gondii was found in the blood of acutely and chronically infected patients regardless of toxoplasmic retinochoroiditis. Conclusions The results indicate that the parasite may circulate in the blood of immunocompetent individuals and that parasitaemia could be associated with the reactivation of the ocular disease.