bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association of sleep bruxism and dental plaque factors on signs of periodontal disease in children in the mixed dentition
Authors: Restrepo Claudia Cecilia , Tirado Marcela , Jimenez Kelly Juliette 
Published: January 2016

BackgroundPeriodontal disease has a multifactorial etiology; however, dental plaque and possible sleep bruxism (SB) have not been tested together in children as predictors of periodontal disease.AimTo assess the variation of SB, dental biofilm (DBF), gingival index (GI), and plaque index (PI) between localized and generalized pathological probing depth (PPD), crestal bone loss (CBL), and lack of delineation of lamina dura (LD) and to establish the association of DBF, GI, PI and SB with PPD, CBL, and LD in children with mixed dentition.MethodsFifty children were assessed for SB and underwent a clinical and radiographic periodontal examination. anova and three multiple variable analysis were used to analyze the data.ResultsOne‐way anova was found to be statistically significant for SB, between localized and generalized PPD (P = 0.03), CBL (P = 0.01), and LD (P = 0.005) and for DBF between localized and generalized CBL (P = 0.02). The three multiple variable analysis showed statistically and clinically significant associations of DBF with PPD (OR = 3.33); GI (OR = 2.37), and PI (OR = 1.46) with CBL and SB (OR = 7.66) and DBF (OR = 9.87) with LD. PI presented statistically significant association with CBL.ConclusionSignificant associations of SB, DBF, GI, and PI with PD, CBL, and LD and the variations of the same factors between localized and generalized PPD, CBL, and LD suggest the necessity of evaluating SB, DBF, GI, and PI when children are screened in regular dental visits.
Association of salivary gland hypofunction with diabetes mellitus and drugs among the elderly in Karachi, Pakistan
Authors: Lone Muneeb Ahmed , Shaikh Sameer , Lone Maham Muneeb , Afaq Ashar , Lone Mohid Abrar 
Published: January 2016

AbstractAimStudies from Pakistan on salivary dysfunction are lacking, and the Pakistani elderly population is rapidly growing. Among the most common problems in the elderly that could have a deleterious impact on their quality of life are salivary gland hypofunction (SGH), diabetes mellitus (DM), and the intake of drugs with adverse effects on salivary function. In the present study, we aimed to find the association of SGH with DM and drugs among the elderly in Karachi, Pakistan.MethodsThe inclusion criterion was affirmative answers to a series of standardized questions related to the symptoms of dry mouth. A total of 110 individuals were selected from a convenience sample of 200 people aged between 60 and 70 years. Diabetes, drug use, and SGH in the participants were determined by detailed medical and drug history, clinical examination, and sialometry.ResultsSimilar to their international counterparts, the majority of the study participants demonstrated objective evidence of SGH. More importantly SGH was found to be statistically significant with respect to DM and medication (P < 0.05). For participants on medication, the minimum and maximum salivary flow rates were found to be 0.09 mL/min and 0.3 ml/min, respectively, whereas the minimum and maximum salivary flow rates in diabetic participants were 0.01 mL/min and 0.09 mL/min, respectively.ConclusionIn the present study, the majority of elderly participants whose presenting complaint was oral dryness was found to have objective evidence of SGH, with a statistically‐significant association with DM and drugs.
Identification of a binding site of the human immunodeficiency virus envelope protein gp120 to neuronal‐specific tubulin
Authors: Avdoshina Valeria , Taraballi Francesca , Dedoni Simona , Corbo Claudia , Paige Mikell , Saygideğer Kont Yasemin , Üren Aykut , Tasciotti Ennio , Mocchetti Italo 
Published: January 2016

AbstractHuman immunodeficiency virus‐1 (HIV) promotes synaptic simplification and neuronal apoptosis, and causes neurological impairments termed HIV‐associated neurological disorders. HIV‐associated neurotoxicity may be brought about by acute and chronic mechanisms that still remain to be fully characterized. The HIV envelope glycoprotein gp120 causes neuronal degeneration similar to that observed in HIV‐associated neurocognitive disorders subjects. This study was undertaken to discover novel mechanisms of gp120 neurotoxicity that could explain how the envelope protein promotes neurite pruning. Gp120 has been shown to associate with various intracellular organelles as well as microtubules in neurons. We then analyzed lysates of neurons exposed to gp120 with liquid chromatography mass spectrometry for potential protein interactors. We found that one of the proteins interacting with gp120 is tubulin β‐3 (TUBB3), a major component of neuronal microtubules. We then tested the hypothesis that gp120 binds to neuronal microtubules. Using surface plasmon resonance, we confirmed that gp120 binds with high affinity to neuronal‐specific TUBB3. We have also identified the binding site of gp120 to TUBB3. We then designed a small peptide (Helix‐A) that displaced gp120 from binding to TUBB3. To determine whether this peptide could prevent gp120‐mediated neurotoxicity, we cross‐linked Helix‐A to mesoporous silica nanoparticles (Helix‐A nano) to enhance the intracellular delivery of the peptide. We then tested the neuroprotective property of Helix‐A nano against three strains of gp120 in rat cortical neurons. Helix‐A nano prevented gp120‐mediated neurite simplification as well as neuronal loss. These data propose that gp120 binding to TUBB3 could be another mechanism of gp120 neurotoxicity.
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We propose a novel direct mechanism of human immunodeficiency virus neurotoxicity. Our data show that the viral protein gp120 binds to neuronal specific tubulin β‐3 and blocks microtubule transport. Displacing gp120 from binding to tubulin by a small peptide prevents gp120‐mediated neuronal loss. Our study reveals a novel target for developing adjunct therapies against viral infection that promotes neurocognitive disorders.
Smad3 deficiency inhibits dentate gyrus LTP by enhancing GABAA neurotransmission
Authors: Muñoz Mª Dolores , Antolín‐Vallespín Mónica , Tapia‐González Silvia , Sánchez‐Capelo Amelia 
Published: January 2016

AbstractTransforming growth factor‐β signaling through intracellular Smad3 has been implicated in Parkinson's disease (PD) and it fulfills an important role in the neurogenesis and synaptic plasticity that occurs in the adult dentate gyrus (DG). The long‐term potentiation (LTP) induced in the DG by high‐frequency stimulation of the medial perforant pathway is abolished in the DG of Smad3‐deficient mice, but not in the CA1 hippocampal region. Here, we show that NMDA‐ and AMPA‐type glutamate receptors do not participate in the inhibition of LTP associated with Smad3 deficiency. Moreover, there is no difference in the hippocampal GAD65 and GAD67 content, suggesting that GABA biosynthesis remains unaffected. Increased conductance and higher action potential firing thresholds were evident in intracellular recordings of granule cells from Smad3 deficient mice. Interestingly, phasic and tonic GABAA receptor (GABAAR)‐mediated neurotransmission is enhanced in the DG of Smad3‐deficient mice, and LTP induction can be rescued by inhibiting GABAAR with picrotoxin. Hence, Smad3 signaling in the DG appears to be necessary to induce LTP by regulating GABAA neurotransmission, suggesting a central role of this intracellular signaling pathway in the hippocampal brain plasticity related to learning and memory.
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Smad3 deficient mice represent a new and interesting model of Parkinson's disease, displaying hippocampal dysfunctions that include decreased neurogenesis and the failure to induce LTP in the dentate gyrus. Here we show that Smad3 deficiency inhibits LTP induction by enhancing phasic and tonic GABAA receptor‐mediated neurotransmission, while LTP induction can be rescued with a GABAA receptor antagonist. Alteration of GABA neurotransmission is thought to produce hippocampal cognitive dysfunction in Down's syndrome or Alzheimer's disease, and here we provide new insights into the hippocampal changes in an animal model of Parkinson's disease.
Agonist‐induced activation of histamine H3 receptor signals to extracellular signal‐regulated kinases 1 and 2 through PKC‐, PLD‐, and EGFR‐dependent mechanisms
Authors: Lai Xiangru , Ye Lingyan , Liao Yuan , Jin Lili , Ma Qiang , Lu Bing , Sun Yi , Shi Ying , Zhou Naiming 
Published: January 2016

AbstractThe histamine H3 receptor (H3R), abundantly expressed in the central and the peripheral nervous system, has been recognized as a promising target for the treatment of various important CNS diseases including narcolepsy, Alzheimer's disease, and attention deficit hyperactivity disorder. The H3R acts via Gi/o‐proteins to inhibit adenylate cyclase activity and modulate MAPK activity. However, the underlying molecular mechanisms for H3R mediation of the activation of extracellular signal‐regulated kinases 1 and 2 (ERK1/2) remain to be elucidated. In this study, using HEK293 cells stably expressing human H3R and mouse primary cortical neurons endogenously expressing mouse H3R, we found that the H3R‐mediated activation of ERK1/2 was significantly blocked by both the pertussis toxin and the MEK1/2 inhibitor U0126. Upon stimulation by H3R agonist histamine or imetit, H3R was shown to rapidly induce ERK1/2 phosphorylation via PLC/PKC‐, PLDs‐, and epidermal growth factor receptor (EGFR) transactivation‐dependent pathways. Furthermore, it was also indicated that while the βγ‐subunits play a key role in H3R‐activated ERK1/2 phosphorylation, β‐arrestins were not required for ERK1/2 activation. In addition, when the cultured mouse cortical neurons were exposed to oxygen and glucose deprivation conditions (OGD), imetit exhibited neuroprotective properties through the H3R. Treatment of cells with the inhibitor UO126 abolished these protective effects. This suggests a possible neuroprotective role of the H3R‐mediated ERK1/2 pathway under hypoxia conditions. These observations may provide new insights into the pharmacological effects and the physiological functions modulated by the H3R‐mediated activation of ERK1/2.
imageHistamine H3 receptors are abundantly expressed in the brain and play important roles in various CNS physiological functions. However, the underlying mechanisms for H3R‐induced activation of extracellular signal‐regulated kinase (ERK)1/2 remain largely unknown. Here, we provide evidence that upon activation by an agonist, H3Rs trigger ERK1/2 activation via phospholipase C/protein kinase C (PLC/PKC)‐, phospholipase D (PLD)s‐, and matrix metallopeptidase/epidermal growth factor receptor (MMP/EGFR) transactivation‐dependent pathways. Moreover, we demonstrate that H3Rs exhibit a neuroprotective effect on the cultured mouse cortical neurons under hypoxia conditions through the ERK1/2 pathway.
Reports of perceptual distortion of the face are common in patients with different types of chronic oro‐facial pain
Authors: Dagsdóttir L. K. , Skyt I. , Vase L. , Baad‐Hansen L. , Castrillon E. , Svensson P. 
Published: January 2016

SummaryAnecdotally, chronic oro‐facial pain patients may perceive the painful face area as ‘swollen’. Because there are no clinical signs, these self‐reported ‘illusions’ may represent perceptual distortions and can be speculated to contribute to the maintenance of oro‐facial pain. This descriptive study investigated whether chronic oro‐facial pain patients experience perceptual distortions – a kind of body image disruption. Sixty patients were consecutively recruited to fill in questionnaires regarding i) pain experience, ii) self‐reports of perceptual distortion and iii) psychological condition. Perceptual distortions were examined in the total group and in three diagnostic subgroups: i) painful post‐traumatic trigeminal neuropathy (PPTN), ii) painful temporomandibular disorder (TMD) or iii) persistent idiopathic facial pain (PIFP). A large proportion of oro‐facial pain patients reported perceptual distortions of the face (55·0%). In the diagnostic subgroups, perceptual distortions were most pronounced in PPTN patients (81·5%) but with no significant group differences. In the total group of chronic oro‐facial pain patients, the present pain intensity explained 16·9% of the variance in magnitude of the perceptual distortions (R2 = 16·9, F(31) = 6·3, P = 0·017). This study demonstrates that many chronic oro‐facial pain patients may experience perceptual distortions. Future studies may clarify the mechanisms underlying perceptual distortions, which may point towards new complementary strategies for the management of chronic oro‐facial pain.
Mangiferin ameliorates Porphyromonas gingivalis‐induced experimental periodontitis by inhibiting phosphorylation of nuclear factor‐κB and Janus kinase 1–signal transducer and activator of transcription signaling pathways
Authors: Li H. , Wang Q. , Ding Y. , Bao C. , Li W. 
Published: January 2016

Background and ObjectiveMangiferin is a natural polyphenol compound with anti‐inflammatory properties. However, there have been few reports on the effect of mangiferin on periodontitis. Here, we investigated the anti‐inflammatory effects of this compound on experimental periodontitis and the underlying mechanisms.Material and MethodsMice were inoculated with Porphyromonas gingivalis to induce periodontitis, and treated with mangiferin orally (50 mg/kg bodyweight, once a day) for 8 wk. Then, the alveolar bone loss was examined using a scanning electronic microscope. Expression of tumor necrosis factor‐α (TNF‐α) and the phosphorylation levels of nuclear factor‐κB (NF‐κB) and Janus kinase 1–signal transducer and activator of adhesion (JAK1‐STAT) pathways in the gingival epithelium were detected using western blot analysis and immunohistochemical staining.ResultsThe results showed that mice with periodontitis exhibited greater alveolar bone loss, stronger expression of TNF‐α and higher phosphorylation levels of NF‐κB and JAK1–STAT1/3 pathways in gingival epithelia, compared with control mice with no periodontitis. Moreover, treatment with mangiferin could significantly inhibit alveolar bone loss, TNF‐α production and phosphorylation of NF‐κB and JAK1–STAT1/3 pathways in gingival epithelia.ConclusionMangiferin has anti‐inflammatory effects on periodontitis, which is associated with its ability to down‐regulate the phosphorylation of NF‐κB and JAK1–STAT1/3 pathways in gingival epithelia.
Closely coupled evolutionary history of ecto‐ and endosymbionts from two distantly related animal phyla
Authors: Zimmermann Judith , Wentrup Cecilia , Sadowski Miriam , Blazejak Anna , Gruber‐Vodicka Harald R. , Kleiner Manuel , Ott Jörg A. , Cronholm Bodil , De Wit Pierre , Erséus Christer , Dubilier Nicole 
Published: January 2016

AbstractThe level of integration between associated partners can range from ectosymbioses to extracellular and intracellular endosymbioses, and this range has been assumed to reflect a continuum from less intimate to evolutionarily highly stable associations. In this study, we examined the specificity and evolutionary history of marine symbioses in a group of closely related sulphur‐oxidizing bacteria, called Candidatus Thiosymbion, that have established ecto‐ and endosymbioses with two distantly related animal phyla, Nematoda and Annelida. Intriguingly, in the ectosymbiotic associations of stilbonematine nematodes, we observed a high degree of congruence between symbiont and host phylogenies, based on their ribosomal RNA (rRNA) genes. In contrast, for the endosymbioses of gutless phallodriline annelids (oligochaetes), we found only a weak congruence between symbiont and host phylogenies, based on analyses of symbiont 16S rRNA genes and six host genetic markers. The much higher degree of congruence between nematodes and their ectosymbionts compared to those of annelids and their endosymbionts was confirmed by cophylogenetic analyses. These revealed 15 significant codivergence events between stilbonematine nematodes and their ectosymbionts, but only one event between gutless phallodrilines and their endosymbionts. Phylogenetic analyses of 16S rRNA gene sequences from 50 Cand. Thiosymbion species revealed seven well‐supported clades that contained both stilbonematine ectosymbionts and phallodriline endosymbionts. This closely coupled evolutionary history of marine ecto‐ and endosymbionts suggests that switches between symbiotic lifestyles and between the two host phyla occurred multiple times during the evolution of the Cand. Thiosymbion clade, and highlights the remarkable flexibility of these symbiotic bacteria.
Agronomic nitrogen‐use efficiency of rice can be increased by drivingOsNRT2.1expression with theOsNAR2.1promoter
Authors: Chen Jingguang , Zhang Yong , Tan Yawen , Zhang Min , Zhu Longlong , Xu Guohua , Fan Xiaorong 
Published: January 2016

SummaryThe importance of the nitrate () transporter for yield and nitrogen‐use efficiency (NUE) in rice was previously demonstrated using map‐based cloning. In this study, we enhanced the expression of theOsNRT2.1gene, which encodes a high‐affinitytransporter, using a ubiquitin (Ubi) promoter and the‐inducible promoter of theOsNAR2.1gene to driveOsNRT2.1expression in transgenic rice plants. Transgenic lines expressingpUbi:OsNRT2.1orpOsNAR2.1:OsNRT2.1constructs exhibited the increased total biomass including yields of approximately 21% and 38% compared with wild‐type (WT) plants. The agriculturalNUE(ANUE) of thepUbi:OsNRT2.1lines decreased to 83% of that of theWTplants, while theANUEof thepOsNAR2.1:OsNRT2.1lines increased to 128% of that of theWTplants. The dry matter transfer into grain decreased by 68% in thepUbi:OsNRT2.1lines and increased by 46% in thepOsNAR2.1:OsNRT2.1lines relative to theWT. The expression ofOsNRT2.1in shoot and grain showed thatUbienhancedOsNRT2.1expression by 7.5‐fold averagely andOsNAR2.1promoters increased by about 80% higher than theWT. Interestingly, we found that theOsNAR2.1was expressed higher in all the organs ofpUbi:OsNRT2.1lines; however, forpOsNAR2.1:OsNRT2.1lines,OsNAR2.1expression was only increased in root, leaf sheaths and internodes. We show that increased expression ofOsNRT2.1, especially driven byOsNAR2.1promoter, can improve the yield and NUE in rice.
Pepper protein phosphatase type 2C, CaADIP1 and its interacting partner CaRLP1 antagonistically regulate ABA signalling and drought response
Authors: Lim Chae Woo , Lee Sung Chul 
Published: January 2016

AbstractAbscisic acid (ABA) is a key phytohormone that regulates plant growth and developmental processes, including seed germination and stomatal closing. Here, we report the identification and functional characterization of a novel type 2C protein phosphatase, CaADIP1 (Capsicum annuum ABA and Drought‐Induced Protein phosphatase 1). The expression of CaADIP1 was induced in pepper leaves by ABA, drought and NaCl treatments. Arabidopsis plants overexpressing CaADIP1 (CaADIP1‐OX) exhibited an ABA‐hyposensitive and drought‐susceptible phenotype. We used a yeast two‐hybrid screening assay to identify CaRLP1 (Capsicum annuum RCAR‐Like Protein 1), which interacts with CaADIP1 in the cytoplasm and nucleus. In contrast to CaADIP1‐OX plants, CaRLP1‐OX plants displayed an ABA‐hypersensitive and drought‐tolerant phenotype, which was characterized by low levels of transpirational water loss and increased expression of stress‐responsive genes relative to those of wild‐type plants. In CaADIP1‐OX/CaRLP1‐OX double transgenic plants, ectopic expression of the CaRLP1 gene led to strong suppression of CaADIP1‐induced ABA hyposensitivity during the germinative and post‐germinative stages, indicating that CaADIP1 and CaRLP1 act in the same signalling pathway and CaADIP1 functions downstream of CaRLP1. Our results indicate that CaADIP1 and its interacting partner CaRLP1 antagonistically regulate the ABA‐dependent defense signalling response to drought stress.
WD40‐REPEAT 5a functions in drought stress tolerance by regulating nitric oxide accumulation in Arabidopsis
Authors: Liu Wen‐Cheng , Li Yun‐Hui , Yuan Hong‐Mei , Zhang Bing‐Lei , Zhai Shuang , Lu Ying‐Tang 
Published: January 2016

AbstractNitric oxide (NO) generation by NO synthase (NOS) in guard cells plays a vital role in stomatal closure for adaptive plant response to drought stress. However, the mechanism underlying the regulation of NOS activity in plants is unclear. Here, by screening yeast deletion mutants with decreased NO accumulation and NOS‐like activity when subjected to H2O2 stress, we identified TUP1 as a novel regulator of NOS‐like activity in yeast. Arabidopsis WD40‐REPEAT 5a (WDR5a), a homolog of yeast TUP1, complemented H2O2‐induced NO accumulation of a yeast mutant Δtup1, suggesting the conserved role of WDR5a in regulating NO accumulation and NOS‐like activity. This note was further confirmed by using an Arabidopsis RNAi line wdr5a‐1 and two T‐DNA insertion mutants of WDR5a with reduced WDR5a expression, in which both H2O2‐induced NO accumulation and stomatal closure were repressed. This was because H2O2‐induced NOS‐like activity was inhibited in the mutants compared with that of the wild type. Furthermore, these wdr5a mutants were more sensitive to drought stress as they had reduced stomatal closure and decreased expression of drought‐related genes. Together, our results revealed that WDR5a functions as a novel factor to modulate NOS‐like activity for changes of NO accumulation and stomatal closure in drought stress tolerance.
Campylorrhinus lateralis, Bilateral microphthalmia and odontoma temporalis in an Oldenburg Foal
Authors: Casteleyn C , Cornillie P , Tüllmann V , Van Cruchten S , Van Ginneken C 
Published: January 2016

ContentsAn Oldenburg colt with wry nose was autopsied after having lived for only 30 min. It presented cyanotic oral mucosae, underdeveloped eyes and a right‐sided temporal osseous mass. The applicable nomenclature for the defects is discussed, and the potential etiopathogenesis is explored by describing the normal embryonic development of the affected body parts.
Successful eradication of invasive Scopulariopsis brumptii in a liver transplant recipient
Authors: Pate M.J. , Hemmige V. , Woc‐Colburn L. , Restrepo A. 
Published: January 2016

AbstractTen months after orthotopic liver transplant, a 53‐year‐old male patient developed cough and fever. Imaging revealed diffuse ground‐glass opacities involving all lobes, and subsequent bronchoscopic washings revealed Scopulariopsis brumptii infection. The patient initially had significant clinical deterioration requiring intubation and extracorporeal membrane oxygenation. However, combination antifungal therapy, including posaconazole and terbinafine, eventually proved successful in eradicating the infection.