bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protein profiling of human lung telocytes and microvascular endothelial cells using iTRAQ quantitative proteomics
Authors: Zheng Yonghua , Cretoiu Dragos , Yan Guoquan , Cretoiu Sanda Maria , Popescu Laurentiu M. , Fang Hao , Wang Xiangdong 
Published: July 2014

AbstractTelocytes (TCs) are described as a particular type of cells of the interstitial space (www.telocytes.com). Their main characteristics are the very long telopodes with alternating podoms and podomers. Recently, we performed a comparative proteomic analysis of human lung TCs with fibroblasts, demonstrating that TCs are clearly a distinct cell type. Therefore, the present study aims to reinforce this idea by comparing lung TCs with endothelial cells (ECs), since TCs and ECs share immunopositivity for CD34. We applied isobaric tag for relative and absolute quantification (iTRAQ) combined with automated 2‐D nano‐ESI LC‐MS/MS to analyse proteins extracted from TCs and ECs in primary cell cultures. In total, 1609 proteins were identified in cell cultures. 98 proteins (the 5th day), and 82 proteins (10th day) were confidently quantified (screened by two‐sample t‐test, P < 0.05) as up‐ or down‐regulated (fold change >2). We found that in TCs there are 38 up‐regulated proteins at the 5th day and 26 up‐regulated proteins at the 10th day. Bioinformatics analysis using Panther revealed that the 38 proteins associated with TCs represented cellular functions such as intercellular communication (via vesicle mediated transport) and structure morphogenesis, being mainly cytoskeletal proteins and oxidoreductases. In addition, we found 60 up‐regulated proteins in ECs e.g.: cell surface glycoprotein MUC18 (15.54‐fold) and von Willebrand factor (5.74‐fold). The 26 up‐regulated proteins in TCs at 10th day, were also analysed and confirmed the same major cellular functions, while the 56 down‐regulated proteins confirmed again their specificity for ECs. In conclusion, we report here the first extensive comparison of proteins from TCs and ECs using a quantitative proteomics approach. Our data show that TCs are completely different from ECs. Protein expression profile showed that TCs play specific roles in intercellular communication and intercellular signalling. Moreover, they might inhibit the oxidative stress and cellular ageing and may have pro‐proliferative effects through the inhibition of apoptosis. The group of proteins identified in this study needs to be explored further for the role in pathogenesis of lung disease.
Neonatal jaundice and increased risk of attention‐deficit hyperactivity disorder: a population‐based cohort study
Authors: Wei Chang‐Ching , Chang Chun‐Hung , Lin Cheng‐Li , Chang Shih‐Ni , Li Tsai‐Chung , Kao Chia‐Hung 
Published: July 2014

BackgroundPrevious studies have posited conflicting results regarding the relationship between neonatal jaundice and the subsequent risk of attention‐deficit hyperactivity disorder (ADHD). We therefore performed a large population study with a defined neonatal jaundice cohort to investigate the incidence and risk of physician‐diagnosed ADHD in Taiwan.MethodsFrom 2000 to 2004, 24,950 neonatal jaundice cases and 69,964 matched nonjaundice controls were identified. At the end of 2008, the incidence rate and hazard ratios (HRs) of physician‐diagnosed ADHD were calculated.ResultsThe incidence of ADHD was 2.48‐fold greater in the jaundice cohort than in the nonjaundice cohort (3.84 vs. 1.51 per 100,000 person‐years) in the study period. The HR of ADHD was substantially greater for male, preterm, and low‐birth‐weight infants with neonatal jaundice. The risk of developing ADHD in the jaundice cohort was greater after a diagnosis of neonatal jaundice for more than 6 years (HR: 2.64; 95% confidence interval: 2.13–3.28). The risk of ADHD increased for neonates with higher serum bilirubin levels requiring phototherapy and with longer admission days.ConclusionNeonates with jaundice are at high risk for developing physician‐diagnosed ADHD during their growth period. A risk alert regarding neurologic consequences is urgently required after a neonatal jaundice diagnosis. Additional studies should be conducted to clarify the pathogenesis of these relationships.
Partner switching can favour cooperation in a biological market
Authors: Schwagmeyer P. L. 
Published: July 2014

AbstractIntraspecific cooperation and interspecific mutualisms can be promoted by mechanisms that reduce the frequency with which cooperative organisms are exploited by unhelpful partners. One such mechanism consists of changing partners after interacting with an uncooperative individual. I used McNamaraet al.'s (Nature, 451, 2008, 189) partner switching model as a framework to examine whether this mechanism can select for increased cooperative investment by house sparrows (Passer domesticus) collaborating to rear offspring; previous research on this species has shown that substantial cooperative investments by both pair members are required to achieve high pay‐offs from collaborating. I found that the poorer the outcome of a breeding attempt relative to the number of eggs the female invested, the greater the likelihood of partner switching. The incidence of partner switching changed seasonally, with peak switching coinciding with an increase in the number of alternative partners available to females. After females switched partners, their breeding outcomes rose to match those of females that remained with the same partner; this was not the case for males that switched partners. Consistent with the model's prediction, males in stable partnerships achieved over 25% higher than average reproductive success, which was attributable to both persistently good breeding outcomes and their older partners' high fecundity. These results provide empirical support for the hypothesis that partner switching favours increased cooperative investment levels, and they demonstrate that variation in the relative value of by‐product benefits can enhance that process.
Biology and field host range of Ceutorhynchus cardariae, a potential biological control agent for Lepidium draba
Authors: Hinz H. L. , Diaconu A. 
Published: July 2014

AbstractLepidium draba (Brassicaceae) is a clonal herb, originating from Eurasia, which is invasive in North America. A classical biological control project was initiated in 2001, and the gall‐forming weevil Ceutorhynchus cardariae was prioritized as a candidate agent. We studied its biology and field host range between 2003 and 2014 in the laboratory and a common garden in Switzerland and in the field in Romania. Ceutorhynchus cardariae is a univoltine to bivoltine species. In Switzerland, oviposition usually started at the beginning of March and can occur at temperatures as low as 2.5°C. Galls are formed on stems, leaf stalks and midribs of L. draba rosettes and bolting plants. Gall size increased with an increasing number of larvae per gall. The three larval instars feed inside the galls and leave the plant to pupate in the soil once mature. In Switzerland, development from egg to adult took about 12 weeks in spring. Adults emerged from May to July. After a brief feeding period, adults aestivate. From late summer, feeding recommenced and females may oviposit, forming a partial second generation. Eggs and all larval instars can be found in galls throughout winter. The rate of larval ectoparasitism reached 78%, while endoparasitism was low with a maximum of 2.3%. Lepidium draba populations differed in their suitability for development (number of C. cardariae produced), indicating that effectiveness of C. cardariae – in case released – may be variable. In the field, we observed that gall formation by C. cardariae can severely stunt or even kill shoots. Investigations on the field host range of C. cardariae indicated that only the closely related Lepidium campestre may act as an alternative host for the weevil in Europe. Host‐specificity tests are underway to determine its environmental safety before field release in North America is being considered.
Enhanced antiviral treatment efficacy and uptake in preventing the rising burden of hepatitis C‐related liver disease and costs in Australia
Authors: Sievert William , Razavi Homie , Estes Chris , Thompson Alexander J , Zekry Amany , Roberts Stuart K , Dore Gregory J 
Published: July 2014

AbstractBackground and AimChronic hepatitis C virus (HCV) infection is an important cause of advanced liver disease and liver‐related deaths in Australia. Our aim was to describe the burden of HCV infection and consider treatment strategies to reduce HCV‐related morbidity and mortality.MethodsBaseline model parameters were based upon literature review and expert consensus with a focus on Australian data. Three treatment scenarios based on anticipated introduction of improved direct‐acting antiviral regimens were considered to reduce HCV disease burden. Scenario 1 evaluated the impact of increased treatment efficacy alone (to 80–90% by 2016). Scenario 2 evaluated increased efficacy and increased treatment uptake (2550 to 13 500 by 2018) without treatment restriction, while Scenario 3 considered the same increases with treatment limited to ≥ F3 during 2015–2017.ResultsIn 2013, there were an estimated 233 490 people with chronic HCV infection: 13 850 with cirrhosis, 590 with hepatocellular carcinoma (HCC) and 530 liver‐related deaths. If the current HCV treatment setting is unchanged, threefold increases in the number of people with cirrhosis, HCC, and liver disease deaths will be seen by 2030. Scenario 1 resulted in modest impacts on disease burden (4% decrease in HCC, decompensated cirrhosis, and liver deaths) and costs. Scenario 3 had the greatest impact on disease burden (approximately 50% decrease in HCC, decompensated cirrhosis, and liver deaths) and costs, while Scenario 2 had slightly lesser impact.ConclusionsConsiderable increases in the burden of HCV‐related advanced liver disease and its complications will be seen in Australia under current treatment levels and outcomes. Introduction of improved direct‐acting antiviral regimens with enhanced efficacy at current treatment levels will lead to limited impacts on this disease burden. A combination of increased treatment efficacy and greater uptake is required to achieve major reductions in advanced liver disease and related costs.
Addition of docosahexaenoic acid, but not arachidonic acid, activates glutathione and thioredoxin antioxidant systems in murine hippocampal HT22 cells: potential implications in neuroprotection
Authors: Casañas‐Sánchez Verónica , Pérez José A. , Fabelo Noemí , Herrera‐Herrera Antonio V. , Fernández Cecilia , Marín Raquel , González‐Montelongo María C. , Díaz Mario 
Published: July 2014

AbstractDocosahexaenoic acid (DHA, 22:6n‐3) is a major constituent of nerve cell membrane phospholipids. Besides a role in membrane architecture, DHA is a pleiotropic molecule involved in multiple facets of neuronal biology and also in neuroprotection. We show here that supplementation with DHA (but not arachidonic acid) to mouse hippocampal HT22 cells modulates the expression of genes encoding for antioxidant proteins associated with thioredoxin/peroxiredoxin and glutathione/glutaredoxin systems. Thus, within the thioredoxin system, DHA increased Txn1‐2, Trxrd1‐2, Prdx3, and Srxn1 gene expression. Paralleling these changes, DHA increased thioredoxin reductase activity, the main enzyme involved in thioredoxin regeneration. For the glutathione system, the most important change triggered by DHA was the upregulation of Gpx4 gene, encoding for the nuclear, cytosolic and mitochondrial isoforms of phospholipid‐hydroperoxide glutathione peroxidase (PH‐GPx/GPx4, the main enzyme protecting cell membranes against lipid peroxidation), which was followed by a significant increase in total glutathione peroxidase and GPx4 activities. Noticeably, DHA also upregulated a new Gpx4 splicing variant that retained part of the first intronic region. Finally, we demonstrate that DHA treatment, under the same time course, protects HT22 cells from the oxitoxic exposure to amyloid beta (Aβ25–35) peptide. Altogether, our data pinpoint to a role of DHA as Indirect Antioxidant that modulates neuronal defences in neuroprotection.
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DHA improves the antioxidant capacity of cultured hippocampal HT22 cells. We propose that DHA supplementation induces the remodelling of membrane phospholipids, and also triggers a transcriptional program to increase the expression of members of the glutathione and thioredoxin systems. We postulate that this transcriptional effect is mediated by a signal arising from non‐enzymatic oxidation of DHA.
Multiple sphingolipid abnormalities following cerebral microendothelial hypoxia
Authors: Testai Fernando D. , Kilkus John P. , Berdyshev Evgeny , Gorshkova Irina , Natarajan Viswanathan , Dawson Glyn 
Published: July 2014

AbstractHypoxia has been previously shown to inhibit the dihydroceramide (DHC) desaturase, leading to the accumulation of DHC. In this study, we used metabolic labeling with [3H]‐palmitate, HPLC/MS/MS analysis, and specific inhibitors to show numerous sphingolipid changes after oxygen deprivation in cerebral microendothelial cells. The increased DHC, particularly long‐chain forms, was observed in both whole cells and detergent‐resistant membranes. This was reversed by reoxygenation and blocked by the de novo sphingolipid synthesis inhibitor myriocin, but not by the neutral sphingomyelinase inhibitor GW‐4869. Furthermore, oxygen deprivation of microendothelial cells increased levels of dihydro‐sphingosine (DH‐Sph), DH‐sphingosine1‐phosphate (DH‐S1P), DH‐sphingomyelin (DH‐SM), DH‐glucosylceramide (DH‐GlcCer), and S1P levels. In vitro assays revealed no changes in the activity of sphingomyelinases or sphingomyelin synthase, but resulted in reduced S1P lyase activity and 40% increase in glucosylceramide synthase (GCS) activity, which was reversed by reoxygenation. Inhibition of the de novo sphingolipid pathway (myriocin) or GCS (EtPoD4) induced endothelial barrier dysfunction and increased caspase 3‐mediated cell death in response to hypoxia. Our findings suggest that hypoxia induces synthesis of S1P and multiple dihydro‐sphingolipids, including DHC, DH‐SM, DH‐GlcCer, DH‐Sph and DH‐S1P, which may be involved in ameliorating the effects of stroke
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Progressive hypoxia leads to the accumulation of several dihydrosphingolipids in cerebral microendothelial cells. Hypoxia also increases sphingosine‐1‐phosphate and the activity of glucosylceramide (Glc‐Cer) synthase. These changes reverse by inhibiting the de novo sphingolipid synthesis, which worsens hypoxia‐induced endothelial barrier dysfunction and apoptosis, suggesting that the identified sphingolipids may be vasculoprotective.
Association of periodontal status with occlusal force and food acceptability in 70‐year‐old adults: from SONIC Study
Authors: Okada T. , Ikebe K. , Inomata C. , Takeshita H. , Uota M. , Mihara Y. , Matsuda K. , Kitamura M. , Murakami S. , Gondo Y. , Kamide K. , Masui Y. , Takahashi R. , Arai Y. , Maeda Y. 
Published: July 2014

SummaryThis cross‐sectional study aimed to investigate the association of periodontal status with occlusal force and food acceptability. We hypothesised that mastication deteriorated with reduced periodontal support, even when posterior occlusal contacts with natural teeth were maintained and the patients remained clinically asymptomatic. Participants were 482 independently living 69‐71‐year‐olds, classified as Eichner's group A, having no mobile teeth and no periodontal symptoms. The periodontal probing depth (PPD) and restoration status of each tooth were examined. Occlusal force in the intercuspal position was measured with pressure‐sensitive films. Food acceptability was evaluated from the difficulty experienced in chewing apples, grilled beef, and hard rice crackers. Multivariate regression analysis was performed to investigate the association of periodontal status with occlusal force and food acceptability. A P‐value of <0·05 was considered statistically significant. Multiple linear regression analysis showed that occlusal force had significant negative associations with maximal PPD (standardised partial regression coefficient (β) = −0·121) after controlling for gender, handgrip strength, number of teeth, and percentage of restored teeth. Approximately 15% of participants were included in the compromised food acceptability group. Logistic regression analyses showed that compromised food acceptability was significantly associated with PPD, after controlling for gender, number of teeth, and percentage of restored teeth. Periodontal probing depth (PPD) was significantly correlated with occlusal force and self‐rated food acceptability after controlling for the possible confounding factors in septuagenarians, even those with complete posterior occlusal contacts and no tooth mobility.
Podoplanin, E‐cadherin, β‐catenin, and CD44v6 in recurrent ameloblastoma: their distribution patterns and relevance
Authors: Siar Chong Huat , Ishak Ismadi , Ng Kok Han 
Published: July 2014

BackgroundAmeloblastoma is a benign but locally infiltrative odontogenic epithelial neoplasm with a high risk for recurrence. Podoplanin, a lymphatic endothelium marker, putatively promotes collective cell migration and invasiveness in this neoplasm. However, its role in the recurrent ameloblastoma (RA) remains unclear. As morphological, signaling, and genetic differences may exist between primary and recurrent tumors, clarification of their distribution patterns is of relevance.Materials and methodsPodoplanin was examined immunohistochemically in conjunction with E‐cadherin, β‐catenin, and CD44v6 in 25 RA. Immunostaining according to tumor area, cellular type, and location, and relationship of these proteins were analyzed. Findings were compared with 25 unrelated primary ameloblastomas (UPA).ResultsAll four proteins were detected in RA and UPA samples. Expression rates for each protein were not significantly different between these two groups. RA demonstrated significant upregulation of podoplanin at the invasive front (P < 0.05), whereas upregulation of β‐catenin and CD44v6 and downregulation of E‐cadherin at this site were not statistically significant (P > 0.05). Immunolocalization for all four proteins was predominantly membranous and less frequently cytoplasmic. Pre‐ameloblast‐like cells were podoplanin+/CD44v6−, while stellate reticulum‐like cells were podoplanin‐/CD44v6+. Acanthomatous, granular cell, and desmoplastic variants in both RA and UPA were podoplanin−/low but stained weak‐to‐moderate for E‐cadherin, β‐catenin, and CD44v6. Stromal fibroblasts and lymph channels were variably podoplanin‐positive.ConclusionsPodoplanin, β‐catenin, and CD44v6 upregulation at the tumor invasive fronts in RA and UPA supports a differential regulatory role by these molecules in mediating collective cell migration and local invasiveness. E‐cadherin downregulation suggests altered cell adhesion function during tumor progression.
Decreased expression of Kallmann syndrome 1 sequence gene (KAL1) contributes to oral squamous cell carcinoma progression and significantly correlates with poorly differentiated grade
Authors: Liu Jiannan , Cao Wei , Chen Wantao , Xu Liqun , Zhang Chenping 
Published: July 2014

BackgroundKallmann syndrome 1 sequence gene (KAL1) protein is an extracellular matrix associated protein which plays vital roles in neurons development and cell migration. However, its biological functions and clinical implications have yet not been revealed in oral carcinogenesis. The objective of the study was to evaluate the role of KAL1 in oral cancer and determine clinical significance of KAL1 in oral squamous cell carcinomas (OSCCs).MethodsThe expression pattern of KAL1 was examined in a testing cohort including OSCCs (n = 42) and paired adjacent tissues (PATs) (n = 14) by real‐time PCR. The result was further validated in a validating cohort of OSCCs (n = 32). Correlation between clinicopathological parameters and KAL1 mRNA levels was analyzed by Kruskal–Wallis test. In vitro, the effects of KAL1 ablation through siRNA‐mediated knockdown on the proliferation of OSCC cells were determined by CCK‐8, BrdU, and colonies formation assays, respectively. In addition, cell cycle distribution was further evaluated by cytometry.ResultsWe observed that remarkably decreased expression of KAL1 mRNA in two independent cohorts (P = 0.0002 and P = 0.033, respectively). Furthermore, downregulated KAL1 mRNA was significantly associated with worse pathological grade (P = 0.013 and P = 0.035, respectively). Upon KAL1 silencing, the proliferation and colonies formation potentials of OSCC cells were notably promoted by accelerating G1 to M phase transition.ConclusionThese data indicated that KAL1 plays a potential suppressive role on OSCC initiation and progression, and KAL1 gene may serve as an adjuvant biomarker for the identification of pathological grade.
DNA methyltransferase immunohistochemical expression in odontogenic tumours
Authors: Guimarães Douglas Magno , Antunes Daniella Moraes , Duarte Carina Magalhães Esteves , Ferro Leonardo Borges , Nunes Fabio Daumas 
Published: July 2014

BackgroundOdontogenic tumours are a heterogeneous group of lesions formed from tissues that give rise to the tooth. DNA methylation, a covalent addition of a methyl group to the 5‐carbon position of a cytosine nucleotide, is considered an important regulator of gene expression. The addition of the methyl radical is catalysed by DNA methyltransferases (DNMTs). Although some epigenetic studies have been conducted in odontogenic tumours, a study with the three types of DNMTs in several different members of this group is missing. This study analyses the expression of DNMTs in odontogenic tumours.MethodsFormalin‐fixed and paraffin‐embedded tissue samples of 20 ameloblastomas, 10 calcifying cystic odontogenic tumours, 10 calcifying epithelial tumours, 10 adenomatoid odontogenic tumours, 10 keratocystic odontogenic tumours, five ameloblastic fibromas, two ameloblastic fibro‐odontomas, four central odontogenic fibromas, seven peripheral odontogenic fibromas and 10 odontogenic myxomas were included. Immunohistochemical expression of DNMT1, 3A and 3B was assessed using a semi‐quantitative analysis, and also a correlation with p21, p27 and E‐cadherin immunoexpression was made.ResultsDNMT1, 3A and 3B were expressed in the nucleus and/or cytoplasm of all odontogenic tumours. DNMT1 expression was directly correlated with p27 expression in ameloblastomas.ConclusionThe high expression of DNMTs in odontogenic tumour cells suggests methylation as an important mechanism for this group of tumours.