bluuebunny/crossref_metadata_2025_split huggingface dataset:
Self‐Reported Masticatory Dysfunction and Mortality in Community Dwelling Elderly Adults: A 9‐Year Follow‐Up
Authors: Laudisio Alice , Gemma Antonella , Fontana Davide O. , Rivera Chiara , Bandinelli Stefania , Ferrucci Luigi , Incalzi Raffaele Antonelli 
Published: November 2016

ObjectivesTo evaluate the association, if any, between masticatory dysfunction (MD) and mortality in older adults.DesignThe Invecchiare in Chianti (InCHIANTI) Study, a cohort study with 9‐year follow‐up.SettingTuscany, Italy.ParticipantsIndividuals aged 65 and older (N = 1,155).MeasurementsMD was self‐reported; Cox regression was used to assess the association between self‐reported MD and 9‐year all‐cause mortality. This association was also evaluated after stratifying according to use of dentures. Analyses were adjusted for potential confounders, including demographic characteristics, lifestyle habits, comorbidities, nutrient intake, medications, and objective parameters.ResultsFour hundred five (35%) participants reported MD. Over the 9‐year follow‐up, 475 (41%) subjects died. According to Cox regression analysis, self‐reported MD was associated with higher mortality (relative risk (RR) = 1.23, 95% confidence interval (CI) = 1.02–1.48), after adjusting for potential confounders. In participants with self‐reported MD, uncorrected edentulism was the condition associated with the greatest risk of mortality (RR = 2.10, 95% CI = 1.07–4.14); use of dentures seemed to blunt this association (RR = 1.12, 95% CI = 0.87–1.44).ConclusionSelf‐reported MD, chiefly when due to uncorrected edentulism, is associated with 9‐year all‐cause mortality in community‐dwelling elderly adults. Further studies are needed to evaluate whether the timely correction of MD using adequate dentures can increase the survival of older adults.
Interventions for the Management of Denture Stomatitis: A Systematic Review and Meta‐Analysis
Authors: Hilgert Juliana Balbinot , Giordani Jessye Melgarejo do Amaral , de Souza Raphael Freitas , Wendland Eliana Márcia Da Ros , D'Avila Otavio Pereira , Hugo Fernando Neves 
Published: November 2016

ObjectivesTo assess the effectiveness of different interventions for treating or preventing denture stomatitis (DS).DesignSystematic review.SettingRandomized controlled trials (RCTs) comparing any agent or procedure prescribed to treat or prevent DS in adults.ParticipantsOlder adults with denture stomatitis.MeasurementsThere were two main outcomes reported in the trials included in this review: clinical signs of DS and remaining presence of yeast. There were no restrictions regarding language or date of publication. The search period was up to February 2016.ResultsThirty‐five studies were included in the systematic review, with 32 judged as having high risk of bias. Three RCTs compared nystatin with placebo and found a significant effect on the reduction of clinical signs of stomatitis (risk ratio (RR) = 0.51, 95% confidence interval (CI) = 0.36–0.72), four RCTs compared nystatin with placebo and found a significant effect on mycological assessment (RR = 0.61, 95% CI = 0.46–0.80). Five studies of disinfectant agents also showed a significant effect in comparison with an inactive agent (RR = 0.52, 95% CI = 0.30–0.92) in clinical assessment. No evidence was found of an effect of miconazole, amphotericin, or imidazolic drugs. No RCT evaluated the effectiveness of preventive approaches.ConclusionThe results are supportive of the use of nystatin and disinfecting agents in the treatment of DS, but clinicians need to be aware that individual studies had high risk of bias and that the overall quality of the individual reports was judged to be low.
Sp2 is the only glutamine‐rich specificity protein with minor impact on development and differentiation in myelinating glia
Authors: Wegener Amélie , Küspert Melanie , Sock Elisabeth , Philipsen Sjaak , Suske Guntram , Wegner Michael 
Published: November 2016

AbstractOligodendrocytes and Schwann cells are the myelinating glia of the vertebrate nervous system and by generation of myelin sheaths allow rapid saltatory conduction. Previous in vitro work had pointed to a role of the zinc finger containing specificity proteins Sp1 and Sp3 as major regulators of glial differentiation and myelination. Here, we asked whether such a role is also evident in vivo using mice with specific deletions of Sp1 or Sp3 in myelinating glia. We also studied glia‐specific conditional Sp2‐ and constitutive Sp4‐deficient mice to include all related glutamine‐rich Sp factors into our analysis. Surprisingly, we did not detect developmental Schwann cell abnormalities in any of the mutant mice. Oligodendrocyte development and differentiation was also not fundamentally affected as oligodendrocytes were present in all mouse mutants and retained their ability to differentiate and initiate myelin gene expression. The most severe defect we observed was a 50% reduction in Mbp‐ and proteolipid protein 1 (Plp1)‐positive differentiating oligodendrocytes in Sp2 mutants at birth. Unexpectedly, glial development appeared undisturbed even in the joint absence of Sp1 and Sp3. We conclude that Sp2 has a minor effect on the differentiation of myelinating glia, and that glutamine‐rich Sp proteins are not essential regulators of the process.
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The neuronal insulin receptor in its environment
Authors: Gralle Matthias 
Published: November 2016

AbstractInsulin is known mainly for its effects in peripheral tissues, such as the liver, skeletal muscles and adipose tissue, where the activation of the insulin receptor (IR) has both short‐term and long‐term effects. Insulin and the IR are also present in the brain, and since there is evidence that neuronal insulin signaling regulates synaptic plasticity and that it is impaired in disease, this pathway might be the key to protection or reversal of symptoms, especially in Alzheimer's disease. However, there are controversies about the importance of the neuronal IR, partly because biophysical data on its activation and signaling are much less complete than for the peripheral IR. This review briefly summarizes the neuronal IR signaling in health and disease, and then focuses on known differences between the neuronal and peripheral IR with regard to alternative splicing and glycosylation, and lack of data with respect to phosphorylation and membrane subdomain localization. Particularities in the neuronal IR itself and its environment may have consequences for downstream signaling and impact synaptic plasticity. Furthermore, establishing the relative importance of insulin signaling through IR or through hybrids with its homolog, the insulin‐like growth factor 1 receptor, is crucial for evaluating the consequences of brain IR activation. An improved biophysical understanding of the neuronal IR may help predict the consequences of insulin‐targeted interventions.
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Deletion of the vesicular acetylcholine transporter from pedunculopontine/laterodorsal tegmental neurons modifies gait
Authors: Janickova Helena , Rosborough Kaie , Al‐Onaizi Mohammed , Kljakic Ornela , Guzman Monica S. , Gros Robert , Prado Marco A. M. , Prado Vania F. 
Published: November 2016

AbstractPostural instability and gait disturbances, common disabilities in the elderly and frequently present in Parkinson's disease (PD), have been suggested to be related to dysfunctional cholinergic signaling in the brainstem. We investigated how long‐term loss of cholinergic signaling from mesopontine nuclei influence motor behaviors. We selectively eliminated the vesicular acetylcholine transporter (VAChT) in pedunculopontine and laterodorsal tegmental nuclei cholinergic neurons to generate mice with selective mesopontine cholinergic deficiency (VAChTEn1‐Cre‐flox/flox). VAChTEn1‐Cre‐flox/flox mice did not show any gross health or neuromuscular abnormality on metabolic cages, wire‐hang and grip‐force tests. Young VAChTEn1‐Cre‐flox/flox mice (2–5 months‐old) presented motor learning/coordination deficits on the rotarod; moved slower, and had smaller steps on the catwalk, but showed no difference in locomotor activity on the open field. Old VAChTEn1‐Creflox/flox mice (13–16 months‐old) showed more pronounced motor learning/balance deficits on the rotarod, and more pronounced balance deficits on the catwalk. Furthermore, old mutants moved faster than controls, but with similar step length. Additionally, old VAChT‐deficient mice were hyperactive. These results suggest that dysfunction of cholinergic neurons from mesopontine nuclei, which is commonly seen in PD, has causal roles in motor functions. Prevention of mesopontine cholinergic failure may help to prevent/improve postural instability and falls in PD patients.
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Read the Editorial Highlight for this article on page 688.
Multiregional analysis of global 5‐methylcytosine and 5‐hydroxymethylcytosine throughout the progression of Alzheimer's disease
Authors: Ellison Elizabeth M. , Abner Erin L. , Lovell Mark A. 
Published: November 2016

AbstractEpigenetic modifications to cytosine are known to alter transcriptional states and deregulate gene expression in cancer, embryonic development, and most recently in neurodegeneration. To test the hypothesis that global levels of cytosine modification are altered throughout the progression of Alzheimer's disease, 5‐methylcytosine (5‐mC) and 5‐hydroxymethylcytosine (5‐hmC) were quantified using gas chromatography/mass spectrometry (GC/MS) and stable labeled internal standards of cytosine, 5‐mC, and 5‐hmC. Cytosine modifications were quantified in DNA extracted from tissue specimens of four brain regions (cerebellum, inferior parietal lobe, superior and middle temporal gyrus, and hippocampus/parahippocampal gyrus) of cognitively normal control (NC) subjects and subjects with mild cognitive impairment (MCI), preclinical Alzheimer's disease (PCAD), late onset Alzheimer's disease, frontotemporal lobar degeneration (FTLD) and dementia with Lewy bodies (DLB). Repeated measures analyses of the data show significant alterations in 5‐mC and 5‐hmC in early stages of Alzheimer's disease (PCAD and MCI), as well as FTLD and DLB subjects, across multiple regions of the brain. These data suggest alterations in epigenetic regulation of genes may play an early role in the progression of AD as well as other types of neurodegeneration.
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Constitutive regulation of the glutamate/aspartate transporter EAAT1 by Calcium‐Calmodulin‐Dependent Protein Kinase II
Authors: Chawla Aarti R. , Johnson Derrick E. , Zybura Agnes S. , Leeds Benjamin P. , Nelson Ross M. , Hudmon Andy 
Published: November 2016

AbstractGlutamate clearance by astrocytes is an essential part of normal excitatory neurotransmission. Failure to adapt or maintain low levels of glutamate in the central nervous system is associated with multiple acute and chronic neurodegenerative diseases. The primary excitatory amino acid transporters in human astrocytes are EAAT1 and EAAT2 (GLAST and GLT‐1, respectively, in rodents). While the inhibition of calcium/calmodulin‐dependent kinase (CaMKII), a ubiquitously expressed serine/threonine protein kinase, results in diminished glutamate uptake in cultured primary rodent astrocytes (Ashpole et al. 2013), the molecular mechanism underlying this regulation is unknown. Here, we use a heterologous expression model to explore CaMKII regulation of EAAT1 and EAAT2. In transiently transfected HEK293T cells, pharmacological inhibition of CaMKII (using KN‐93 or tat‐CN21) reduces [3H]‐glutamate uptake in EAAT1 without altering EAAT2‐mediated glutamate uptake. While over‐expressing the Thr287Asp mutant to enhance autonomous CaMKII activity had no effect on either EAAT1 or EAAT2‐mediated glutamate uptake, over‐expressing a dominant‐negative version of CaMKII (Asp136Asn) diminished EAAT1 glutamate uptake. SPOTS peptide arrays and recombinant glutathione S‐transferase‐fusion proteins of the intracellular N‐ and C‐termini of EAAT1 identified two potential phosphorylation sites at residues Thr26 and Thr37 in the N‐terminus. Introducing an Ala (a non‐phospho mimetic) at Thr37 diminished EAAT1‐mediated glutamate uptake, suggesting that the phosphorylation state of this residue is important for constitutive EAAT1 function. Our study is the first to identify a glutamate transporter as a direct CaMKII substrate and suggests that CaMKII signaling is a critical driver of constitutive glutamate uptake by EAAT1.
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Life here beyond now: Chronotopes of the ideal life among Iranian transnationals
Authors: Karimzad Farzad 
Published: November 2016

I address how U.S.‐based Iranian transnationals’ migration paths affect their (re)‐construction of chronotopes of the ideal life. Adopting an ethnographically grounded, discourse‐analytic approach, I illustrate how participants with student visas and U.S. Green Cards position themselves differently relative to images of success here [in the U.S.] and lack of success there [in Iran]. I argue that the chronotopes of success here and lack of success there (re)‐constructed by non‐resident Iranian students are prompted by a large‐scale cultural chronotope which pertains to their aspiration to stay in the U.S. This chronotope of ‘life beyond’ is less about a ‘remove from homeland’ and more about an ideal future in the host country. Migrants’ desires and anxieties, I argue, can determine what receives topical prominence in migration chronotopes – as in the case of Iranian educational migrants whose future positionings make temporality topically more prominent than spatiality.
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Risk stratification for locally advanced hepatocellular carcinoma using pretreatment alpha‐foetoprotein and 18F‐fluoro‐2‐deoxyglucose positron emission tomography
Authors: Rhee Woo Joong , Hwang Sang Hyun , Byun Hwa Kyung , Yun Mijin , Han Kwang‐Hyub , Seong Jinsil 
Published: November 2016

AbstractBackground & AimsWe investigated the significance of 18F‐fluoro‐2‐deoxyglucose positron emission tomography (18F‐FDG PET) parameters and alpha‐foetoprotein (AFP) levels in patients with locally advanced hepatocellular carcinoma (LA‐HCC).MethodsWe retrospectively analysed data of 228 patients with LA‐HCC who underwent pretreatment 18F‐FDG PET between January 2003 and December 2013. All patients were treated using liver‐directed therapy involving radiotherapy. The maximum standardized uptake values (SUVs) and tumour‐to‐extratumoural liver SUV ratios were calculated, and pretreatment AFP values were obtained.ResultsPatients were divided into high and low maximum SUV (SUVmax) groups according to a SUV cut‐off of 4.825 determined via receiver‐operating characteristic analysis. High AFP level (>550 ng/mL) and high SUVmax were significant predictors of overall and progression‐free survival. Better treatment responses and longer median progression‐free and overall survival were observed in the low SUVmax group, compared to the high SUVmax group. Similar results were obtained for SUV ratio‐based (cut‐off value: 2.355) and AFP‐based analyses (cut‐off value: 550 ng/mL). Three risk groups were identified using the double biomarkers of SUVmax and AFP value as strong prognosticators predictive of survival outcomes. This risk stratification was identified as a prognosticator of survival outcomes, even after subgroup analyses. Furthermore, in high risk group, significantly high extrahepatic failure was shown while in low risk group, significantly low intrahepatic failure.ConclusionsClinical significance of double biomarkers, SUV and AFP, could be translated into risk stratification for LA‐HCC. It could be a valuable tool for survival outcome prediction.
Vascular cell transcriptomic changes to exercise training differ directionally along and between skeletal muscle arteriolar trees
Authors: Laughlin M. Harold , Yang Hsiao T. , Tharp Darla L. , Rector R. Scott , Padilla Jaume , Bowles Douglas K. 
Published: November 2016

AbstractEXT‐induced arteriolar adaptations in skeletal muscle are heterogeneous because of spatial variations in muscle fiber type composition and fiber recruitment patterns during exercise. The purpose of this report is to summarize a series of experiments conducted to test the hypothesis that changes in vascular gene expression are signaled by alterations in shear stress resulting from increases in blood flow, muscle fiber type composition, and fiber recruitment patterns. We also report results from a follow‐up study of Ankrd23, one gene whose expression was changed by EXT. We expected to see differences in magnitude of changes in gene expression along arteriolar trees and between/among arteriolar trees but similar directional changes. However, transcriptional profiles of arterioles/arteries from OLETF rats exposed to END or SIT reveal that EXT does not lead to similar directional changes in the transcriptome among arteriolar trees of different skeletal muscles or along arteriolar trees within a particular muscle. END caused the most changes in gene expression in 2A arterioles of soleus and white gastrocnemius with little to no changes in the FAs. Ingenuity Pathway Analysis across vessels revealed significant changes in gene expression in 18 pathways. EXT increased expression of some genes (Shc1, desert hedgehog protein (Dhh), adenylate cyclase 4 (Adcy4), G protein‐binding protein, alpha (Gnat1), and Bcl2l1) in all arterioles examined, but decreased expression of ubiquitin D (Ubd) and cAMP response element modulator (Crem). Many contractile and/or structural protein genes were increased by SIT in the gastrocnemius FA, but the same genes exhibited decreased expression in red gastrocnemius arterioles. Ankrd23 mRNA levels increased with increasing branch order in the gastrocnemius arteriolar tree and were increased 19‐fold in gastrocnemius muscle FA by SIT. Follow‐up experiments indicate that Ankrd23 mRNA level was increased 14‐fold in cannulated gastrocnemius FA when intraluminal pressure was increased from 90 and 180 cm H2O for 4 hours. Also, Ankrd23−/− mice exhibit limited ability to form collateral arteries following femoral artery occlusion compared to WT mice (angioscore WT=0.18±0.03; Ankrd23−/−=0.04±0.01). Further research will be required to determine whether Ankrd23 plays an important role in mechanically induced vascular remodeling of the arterial tree in skeletal muscle.
Natural antisense transcripts are linked to the modulation of mitochondrial function and teliospore dormancy in Ustilago maydis
Authors: Ostrowski Lauren A. , Saville Barry J. 
Published: November 2016

SummaryThe basidiomycete smut fungus Ustilago maydis causes common smut of corn. This disease is spread through the production of teliospores, which are thick‐walled dormant structures characterized by low rates of respiration and metabolism. Teliospores are formed when the fungus grows within the plant, and the morphological steps involved in their formation have been described, but the molecular events leading to dormancy are not known. In U. maydis, natural antisense transcripts (NATs) can function to alter gene expression and many NATs have increased levels in the teliospore. One such NAT is as‐ssm1 which is complementary to the gene for the mitochondrial seryl‐tRNA synthetase (ssm1), an enzyme important to mitochondrial function. The disruption of ssm1 leads to cell lysis, indicating it is also essential for cellular viability. To assess the function of as‐ssm1, it was ectopically expressed in haploid cells, where it is not normally present. This expression led to reductions in growth rate, virulence, mitochondrial membrane potential and oxygen consumption. It also resulted in the formation of as‐ssm1/ssm1 double‐stranded RNA and increased ssm1 transcript levels, but no change in Ssm1 protein levels was detected. Together, these findings suggest a role for as‐ssm1 in facilitating teliospore dormancy through dsRNA formation and reduction of mitochondrial function.
cAMP‐independent signal pathways stimulate hyphal morphogenesis in Candida albicans
Authors: Parrino Salvatore M. , Si Haoyu , Naseem Shamoon , Groudan Kevin , Gardin Justin , Konopka James B. 
Published: November 2016

SummaryThe fungal pathogen Candida albicans can transition from budding to hyphal growth, which promotes biofilm formation and invasive growth into tissues. Stimulation of adenylyl cyclase to form cAMP induces hyphal morphogenesis. The failure of cells lacking adenylyl cyclase (cyr1Δ) to form hyphae has suggested that cAMP signaling is essential for hyphal growth. However, cyr1Δ mutants also grow slowly and have defects in morphogenesis, making it unclear whether hyphal inducers must stimulate cAMP, or if normal basal levels of cAMP are required to maintain cellular health needed for hyphal growth. Interestingly, supplementation of cyr1Δ cells with low levels of cAMP enabled them to form hyphae in response to the inducer N‐acetylglucosamine (GlcNAc), suggesting that a basal level of cAMP is sufficient for stimulation. Furthermore, we isolated faster‐growing cyr1Δ pseudorevertant strains that can be induced to form hyphae even though they lack cAMP. The pseudorevertant strains were not induced by CO2, consistent with reports that CO2 directly stimulates adenylyl cyclase. Mutational analysis showed that induction of hyphae in a pseudorevertant strain was independent of RAS1, but was dependent on the EFG1 transcription factor that acts downstream of protein kinase A. Thus, cAMP‐independent signals contribute to the induction of hyphal responses.
Fine‐scale habitat use in Indo‐Pacific humpback dolphins, Sousa chinensis, may be more influenced by fish rather than vessels in the Pearl River Estuary, China
Authors: Pine Matthew K. , Wang Kexiong , Wang Ding 
Published: November 2016

AbstractShifts in habitat use and distribution patterns in dolphins are often concerns that can result from habitat degradation. We investigated how potential changes to a habitat from human activity may alter dolphin distributions within Lingding Bay in the Pearl River Estuary, China, by studying the relationship between fish choruses, vessel presence and Indo‐Pacific humpback dolphin (Sousa chinensis) detection rates. Analyses revealed temporal and spatial variation within fish choruses, vessel presence and dolphin detection rates. After accounting for any temporal autocorrelation, correlations between fish choruses and dolphin detection rates were also found; however, no relationship between fish choruses and vessel presence or dolphin detection rates and vessel presence were observed. Furthermore, fewer dolphins were detected at sites where fish activity was less intense. Thus fish activity, rather than vessels, may be a key factor influencing the distribution of the dolphins within the estuary. These findings emphasize the risk of potential shifts in habitat use for Indo‐Pacific humpback dolphins due to detrimental changes to prey availability and dolphin feeding grounds from human activity, such as overfishing and coastal developments, within the estuary. This is a critical conservation issue for this dolphin population that is facing intense anthropogenic pressure.