bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of oral health status of children with epilepsy: A retrospective cohort study
Authors: Morgan Heba Imam , Abou El Fadl Reham Khaled , Kabil Noha Samir , Elagouza Iman 
Published: October 2018

BackgroundEpileptic children are liable to experience oral health problems either due to the disease itself or medications administered to control the condition.AimWe aimed to investigate caries experience, gingival health and oro‐facial traumatic injuries in a sample of epileptic Egyptian children.DesignA retrospective cohort study was conducted from September 2016 to April 2017 using data from medical records in Children Hospital at Ain Shams University. Dental examination was performed for 100 epileptic children and 80 healthy subjects who matched in age, gender, and socio‐economic status. Caries experience was measured using the decayed, missing and filled teeth (DMFT or dmft) index and gingival index (GI) of Loe and Sillness was used to determine gingival health status. Oro‐facial injuries were assessed using the WHO classification of trauma. Quantitative data were presented as mean, SD, and 95% CI values. Qualitative data were presented as frequencies and percentages and the significance level was set at P ≤ 0.05.ResultsThe mean ± SD GI for epileptic children was significantly higher (1.16 ± 0.42) than that of healthy children. (1.01 ± 0.11) Healthy subjects had significantly lower mean dmf index scores 2.2 ± 2.6 compared to epileptic subjects where mean dmf scores were 4.1 ± 2.1. No significant difference, however, was detected between the two groups regarding caries experience in permanent dentition or incidence of oro‐facial injuries.ConclusionsEpileptic children are highly burdened with gingival problems and liable to develop dental caries especially in primary dentition. Oral traumatic injuries, however, are not common complications if seizure attacks are well controlled.
Activation of transient receptor potential vanilloid 3 channel (TRPV3) aggravated pathological cardiac hypertrophy via calcineurin/NFATc3 pathway in rats
Authors: Zhang Qianhui , Qi Hanping , Cao Yonggang , Shi Pilong , Song Chao , Ba Lina , Chen Yunping , Gao Jingquan , Li Shuzhi , Li Baiyan , Sun Hongli 
Published: October 2018

AbstractCardiac hypertrophy is a compensatory response to mechanical stimuli and neurohormonal factors, ultimately progresses to heart failure. The proteins of some transient receptor potential (TRP) channels, Ca2+‐permeable nonselective cation channel, are highly expressed in cardiomyocytes, and associated with the occurrence of cardiac hypertrophy. Transient receptor potential vanilloid 3 (TRPV3) is a member of TRP, however, the functional role of TRPV3 in cardiac hypertrophy remains unclear. TRPV3 was elevated in pathological cardiac hypertrophy, but not in swimming exercise‐induced physiological cardiac hypertrophy in rats. TRPV3 expression was also increased in Ang II–induced cardiomyocyte hypertrophy in vitro, which was remarkably increased by carvacrol (a nonselective TRPV channel agonist), and reduced by ruthenium red (a nonselective TRPV channel antagonist). Interestingly, we found that activated TRPV3 in Ang II–induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated CaMKII protein expression, and enhancing NFATc3 nuclear translocation. However, blocking or knockdown of TRPV3 could inhibit the expressions of calcineurin, phosphorylated CaMKII and NFATc3 protein by Western blot. In conclusion, the activation of TRPV3 aggravated pathological cardiac hypertrophy through calcineurin/NFATc3 signalling pathway and correlated with the protein expression levels of calcineurin, phosphorylated CaMKII and NFATc3, revealing that TRPV3 might be a potential therapeutic target for cardiac hypertrophy.
Dietary material properties shape cranial suture morphology in the mouse calvarium
Authors: Byron Craig , Segreti Meghan , Hawkinson Katelyn , Herman Katelyn , Patel Shivam 
Published: October 2018

AbstractCranial sutures are fibrous connective tissue articulations found between intramembranous bones of the vertebrate cranium. Growth and remodeling of these tissues is partially regulated by biomechanical loading patterns that include stresses related to chewing. Advances in oral processing structure and function of the cranium that enabled mammalian‐style chewing is commonly tied to the origins and evolution of this group. To what degree masticatory overuse or underuse shapes the complexity and ossification around these articulations can be predicted based on prior experimental and comparative work. Here, we report on a mouse model system that has been used to experimentally manipulate dietary material properties in order to investigate cranial suture morphology. Experimental groups were fed diets of contrasting material properties. A masticatory overuse group was fed pelleted rodent chow, nuts with shells, and given access to cotton bedding squares. An underuse group was deprived of cotton bedding as well as diverse textured food, and instead received gelatinized food continuously. Animals were raised from weaning to adulthood on these diets, and sagittal, coronal and lambdoid suture morphology was compared between groups. Predicted intergroup variation was observed in mandibular corpus size and calvarial suture morphology, suggesting that masticatory overuse is associated with jaw and suture growth. The anterior region of the sagittal suture where it intersects with the coronal suture (bregma) showed no effect from the experiment. The posterior sagittal suture where it intersects with the lambdoid sutures (lambda) was more complex in the overuse group. In other words, the posterior calvarium was responsive to dietary material property demands while the anterior calvarium was not. This probably resulted from the different strain magnitudes and/or strain frequencies that occurred during overuse diets with diverse material properties as compared with underuse diets deprived of such enrichment. This work highlights the contrasting pattern of the sutural response to loading differences within the calvarium as a result of diet.
Association between self‐reported bruxism and anger and frustration
Authors: Gouw Simone , de Wijer Anton , Bronkhorst Ewald M. , Kalaykova Stanimira I. , Creugers Nico H. J. 
Published: October 2018

SummaryBackgroundEven though bruxism has been shown to be associated with several psychological factors, few studies have been performed on its relationships with anger and frustration.ObjectiveThis study aimed to determine the association between self‐reported awake and sleep bruxism and anger and frustration.MethodsIn this longitudinal observational study, 55 healthy adult participants with “possible” bruxism reported their experienced level of bruxism and several psychosocial factors and lifestyle factors for 28 consecutive days using a personal logbook. The logbook consisted of a daily diary and a weekly questionnaire composed of Dutch versions of validated questionnaires. The primary outcome data were analysed using multiple regression models.ResultsAn increase in SB of 1 unit (on a scale ranging from 1 to 10) was associated with an increase in the anger‐scale of 0.03 units, and the frustration‐scale of 0.04 units. However, the random intercepts were 0.22 for anger and 0.19 for frustration, meaning that there were major differences between individuals. For awake bruxism (AB), the effects were an increase of 0.04 for anger with a random intercept of 0.21 and an increase of 0.03 for frustration with a random intercept of 0.06. The effects of anger and frustration on both SB and AB were not statistically significant.ConclusionThe association between anger and frustration and self‐reported bruxism is small on group level. In individual cases, anger and frustration and self‐reported bruxism may be co‐existent.
Effects of dietary supplemental methionine source and betaine replacement on the growth performance and activity of mitochondrial respiratory chain enzymes in normal and heat‐stressed broiler chickens
Authors: Sahebi Ala Fatemeh , Hassanabadi Ahmad , Golian Abolghasem 
Published: October 2018

AbstractThis study aimed to evaluate the effects of dietary supplemental methionine (Met) source and betaine (Bet) replacement for Met on performance and activity of mitochondrial respiratory chain enzymes (MRCEs) in normal and heat‐stressed broiler chickens. Total of 1,200‐day‐old Ross 308 chicks were allocated to two houses, each consisted of 12 treatments, five replicates of 10 birds each with 2 × 2×3 × 2 (temperature × Met source × Met level × Bet, respectively) split‐plot factorial arrangement. Met level in the basal diets was 70% requirements (Req) that was increased to the requirement or 130% by supplemental dl‐ or l‐Met. Bet was or was not substituted at the rate of 30% supplemental dl‐ or l‐Met. Feed conversion ratio (FCR) in chicks fed 70% l‐Met was lower than those fed 70% dl‐Met diet during 1–10 days (p = 0.04). Broilers fed diets containing requirement or 130% Met, regardless of its source, showed higher weight gain (WG) than those received 70% Met diet during 11–42 days (p < 0.001). Feed intake (FI) of broilers fed 130% Met diet was decreased compared to other two groups during 11–42 days (p < 0.05). One hundred thirty percent Met requirement diet resulted in lower FCR comparing to other two groups during 11–42 days (p < 0.001). Heat‐stressed birds grew less than those under normal condition (p < 0.05). Broilers fed Req Met diet under normal temperature exhibited higher activities of complexes (Cox) I and III (p < 0.05). Cox I activity in heat‐stressed birds fed Bet + diet was similar to those fed Bet‐diet under normal temperature (p = 0.046). It is concluded that performance and the activities of Cox I and III were increased as the level of Met increased. Bet replacement for 30% supplemental Met resulted in similar consequences comparing to non‐Bet replacement diets on performance, but increased the activity of Cox III. l‐Met was effective than dl‐Met at the cellular level. High ambient temperature depressed performance and MRCE activity.
Label‐free quantitative proteomic analysis of human periodontal ligament stem cells by high‐resolution mass spectrometry
Authors: Han Na‐Young , Hong Ji‐Youn , Park Jong‐Moon , Shin Changsik , Lee Saya , Lee Hookeun , Yun Jeong‐Ho 
Published: October 2018

Background and ObjectivesProteome analysis of periodontal ligament stem cells (PDLSCs) could be used to study the function of PDL tissue. We used a label‐free quantitative proteomic technique to investigate differentially expressed proteins (DEPs) in human PDLSCs (hPDLSCs) compared to human bone marrow mesenchymal stem cells (hBMSCs) and identify proteins specific to hPDLSCs.Material and MethodshPDLSCs (n = 3) and hBMSCs (n = 3) were cultured and harvested for protein extraction and trypsin digestion. The proteomes of both cell types were analyzed by nano‐liquid chromatography/tandem mass spectrometry. DEPs in hPDLSCs compared to hBMSCs were detected by label‐free quantification and evaluated through signal transduction pathway and gene ontology (GO) analysis.ResultsIn total, 690 and 771 proteins were identified from hPDLSCs and hBMSCs, of which 561 proteins were in common and 124 DEPs were found between hPDLSCs and hBMSCs. Fifty‐eight proteins were expressed at significantly higher levels in hPDLSCs, whereas 66 proteins were expressed at lower levels compared to hBMSCs. The more highly expressed proteins were associated with translation and initiating protein synthesis, and lower expressed proteins were related to cell aging and metabolic processes. Proteins unique to hPDLSCs and hBMSCs were associated with translation and metabolic processes, respectively.ConclusionOur results demonstrate evidence of distinct differences in protein expression between hPDLSCs and hBMSCs by using label‐free quantitative proteomic analysis which was the first attempt in this field. DEPs included previously reported hPDLSC marker proteins and novel marker candidates, such as microtubule‐associated protein, CTP synthase 1 and stathmin, which could be the markers for developing periodontal disease diagnostics and therapies.
Periodontal ligament‐associated protein‐1 gets involved in experimental periodontitis
Authors: Yu Xijiao , Liu Hongmei , Liu Shuang , Chen Xue , Zhao Xinyu , Du Yi , Li Shu 
Published: October 2018

Background and ObjectivePeriodontal ligament‐associated protein‐1 (PLAP‐1) is an important regulator of osteogenic differentiation of periodontal ligament cells and plays important role in the homeostasis of periodontal tissues. But the role of PLAP‐1 in periodontitis is poorly understood. Expressions of PLAP‐1 in experimental periodontitis are observed to elucidate whether PLAP‐1 gets involved in the pathogenesis of periodontitis.Material and MethodsWistar rats were randomly allocated to two groups (n = 6/group): Ligation group and Control group. PLAP‐1 expression in experimental periodontitis was assessed by immunohistochemistry and collagen fibers in periodontal ligament were observed using picrosirius red staining. Expressions of PLAP‐1 and CD68 in periodontitis were colocalized by double‐labelled immunofluorescence. To further examine the relationship between PLAP‐1 and osteoclastogenesis in experimental periodontitis, acute periodontal inflammatory infiltration and alveolar bone destruction were induced by administering ligated rats with 10 ng/mL tumor necrosis factor alpha (TNF‐α; ligation + TNF‐α group, n = 6). Alveolar bone loss was observed by micro‐computed tomography (Micro‐CT), and osteoclasts were identified by tartrate‐resistant acid phosphatase staining (TRAP). Expressions of PLAP‐1 in TNF‐α stimulated human periodontal ligament cells were also detected at 24 and 48 hours by western blotting.ResultsPLAP‐1 expression levels in periodontal ligament cells and collagen fibers were lower in the ligation group,compared with the control group. Similarly, TNF‐α decreased PLAP‐1 expression in human periodontal ligament cells in vitro. Degradation or destruction of collagen fibers accompanied the reduced PLAP‐1 expression in the periodontal ligament in the ligation group. Colocalization of PLAP‐1 and CD68 revealed the positive relationship between PLAP‐1 and CD68+ infiltrating cells in periodontitis. More PLAP‐1‐positive inflammatory cells were found in the ligation + TNF‐α group, compared with the ligation + saline group.ConclusionPLAP‐1‐positive inflammatory cells are involved in the pathogenesis of periodontitis. An increase in PLAP‐1‐positive inflammatory cell number contributes periodontal inflammation and alveolar bone loss.
Is dietary melatonin supplementation a viable adjunctive therapy for chronic periodontitis?—A randomized controlled clinical trial
Authors: El‐Sharkawy Hesham , Elmeadawy Samah , Elshinnawi Una , Anees Mohamed 
Published: October 2018

Background and ObjectiveMelatonin is synthesized naturally by pineal gland and responsible for regulation of sleep/waking cycle. It showed appreciated anti‐inflammatory and antioxidant properties. The aim of this randomized clinical trial (RCT) was to assess the additive effect of melatonin supplementation in insomniac individuals with generalized chronic periodontitis (gCP) after scaling and root planing (SRP).Material and MethodsSeventy‐four gCP patients with primary insomnia participated in this 6‐month RCT and randomized into two groups. Melatonin group included 38 patients who were subjected to SRP with a 2‐month regimen of 10 mg oral melatonin capsule once daily before bedtime. In the control group, SRP was performed for 36 participants provided with matching placebo capsules. The primary treatment outcome was the measurement of clinical attachment level gain (CAL gain) after 3 and 6 months of therapy, whereas the measurements of pocket depth reduction (PD reduction), bleeding on probing (BOP %), and the changes in salivary TNF‐α levels and Athens insomnia scale (AIS) scores represented the secondary endpoints.ResultsMelatonin group showed significantly greater CAL gain and PD reduction measurements compared to the control group at 3 and 6 months of therapy, P < 0.01. Likewise, salivary TNF‐α levels and AIS scores were significantly lower in the melatonin group compared to placebo group. BOP% improved significantly in both groups without any difference. However, salivary TNF‐α levels exhibited no correlation with other clinical variables in both melatonin and placebo groups.ConclusionDaily dietary 10 mg of melatonin supplementation might serve as a viable adjunct to SRP that yielded significantly greater CAL gain and PD reduction and lower salivary TNF‐α levels and AIS scores in gCP patients with primary insomnia.
Verse in English from Spenser to Swift
Authors: Carpenter Andrew 
Published: October 2018

AbstractIreland was in turmoil for much of the 17th century as, slowly and painfully, English language and culture gained supremacy over the language and culture of the native Irish. The verse and poetry we have in English from this period was the work of planters, administrators and the Old English, and, on occasions, of Irish speakers seeking to influence the rulers of the country. During recent years, much exciting new work has been undertaken on the verse of the period as research on manuscripts and early printed books has led to a substantial increase in the canon. We now know of over 100 poets active in Ireland between the time of Edmund Spenser and that of Jonathan Swift. In addition, scholars have begun exploring the links between the culture of 17th‐century Ireland and that of Scotland, Wales, and England. This article surveys the work that has been accomplished on the verse and poetry of the period and indicates several areas where further research is needed.
Predictors of nonalcoholic steatohepatitis and significant fibrosis in non‐obese nonalcoholic fatty liver disease
Authors: Kim Donghee , Kim Won , Joo Sae Kyung , Kim Jung Ho , Harrison Stephen A. , Younossi Zobair M. , Ahmed Aijaz 
Published: October 2018

AbstractAimsWe compared (a) demographic and clinical characteristics and (b) determinants of nonalcoholic steatohepatitis and significant fibrosis in non‐obese and obese nonalcoholic fatty liver disease.MethodsA cross‐sectional study of 664 Asian subjects (mean age 53.1 years; men 50.3%) with biopsy‐proven nonalcoholic fatty liver disease and controls was conducted. Subjects were divided by their body mass index into obese (body mass index ≥25 kg/m2) and non‐obese (body mass index <25 kg/m2).ResultsObservations in subjects with non‐obese nonalcoholic fatty liver disease were in between non‐obese controls and subjects with obese nonalcoholic fatty liver disease for body mass index, sagittal abdominal diameter, aminotransferase levels, insulin resistance and abdominal visceral adipose tissue area. There was no significant difference in histology between non‐obese and obese subjects with nonalcoholic fatty liver disease except for lower grade of hepatic steatosis in nonobese nonalcoholic fatty liver disease and higher severity of hepatic fibrosis in nonobese nonalcoholic steatohepatitis. Predictors of nonalcoholic steatohepatitis in nonobese subjects included females (odds ratio 2.49), higher alanine aminotransferase (odds ratio 1.03), lower high‐density lipoprotein cholesterol (odds ratio 0.96), higher prevalence of diabetes (odds ratio 3.65) and higher visceral adipose tissue area (odds ratio 1.63 per standard deviation increase of visceral adipose tissue area) while age (odds ratio 1.04), higher aspartate aminotransferase (odds ratio 1.02), diabetes (odds ratio 2.76) and higher visceral adipose tissue area (odds ratio 1.57 per standard deviation increase) were associated with significant fibrosis in the non‐obese. Sagittal abdominal diameter was independently associated with nonalcoholic steatohepatitis or significant fibrosis among subjects with non‐obese nonalcoholic fatty liver disease.ConclusionWhile there were a few phenotypic differences from obese subjects, non‐obese subjects with nonalcoholic fatty liver disease displayed a similar severity of histological liver damage. Potential factor(s) beyond obesity may play a role as non‐obese nonalcoholic fatty liver disease advances to more severe disease.
Parallel evolution of gene classes, but not genes: Evidence from Hawai'ian honeycreeper populations exposed to avian malaria
Authors: Cassin‐Sackett Loren , Callicrate Taylor E. , Fleischer Robert C. 
Published: October 2018

AbstractAdaptation in nature is ubiquitous, yet characterizing its genomic basis is difficult because population demographics cause correlations with nonadaptive loci. Introduction events provide opportunities to observe adaptation over known spatial and temporal scales, facilitating the identification of genes involved in adaptation. The pathogen causing avian malaria, Plasmodium relictum, was introduced to Hawai'i in the 1930s and elicited extinctions and precipitous population declines in native honeycreepers. After a sharp initial population decline, the Hawai'i ‘amakihi (Chlorodrepanis virens) has evolved tolerance to the parasite at low elevations where P. relictum exists, and can sustain infection without major fitness consequences. High‐elevation, unexposed populations of ‘amakihi display little to no tolerance. To explore the genomic basis of adaptation to P. relictum in low‐elevation ‘amakihi, we genotyped 125 ‘amakihi from the island of Hawai'i via hybridization capture to 40,000 oligonucleotide baits containing SNPs and used the reference ‘amakihi genome to identify genes potentially under selection from malaria. We tested for outlier loci between low‐ and high‐elevation population pairs and identified loci with signatures of selection within low‐elevation populations. In some cases, genes commonly involved in the immune response (e.g., major histocompatibility complex) were associated with malaria presence in the population. We also detected several novel candidate loci that may be implicated in surviving malaria infection (e.g., beta‐defensin, glycoproteins and interleukin‐related genes). Our results suggest that rapid adaptation to pathogens may occur through changes in different immune genes, but in the same classes of genes, across populations.
Update on treatment of immunoglobulin A nephropathy
Authors: Zhang Yue‐Miao , Zhang Hong 
Published: October 2018

ABSTRACTImmunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and the most common cause of end‐stage renal disease in young adults. However, there are still no specific therapies capable of targeting key pathways involved in disease pathogenesis. Recently, many large randomized controlled trials have been reported, such as Supportive Versus Immunosuppressive Therapy for the Treatment of Progressive IgA Nephropathy, Targeted‐release Budesonide Versus Placebo in Patients with IgA Nephropathy and Therapeutic Evaluation of Steroids in IgA Nephropathy Global, which are considered to update the 2012 Kidney Disease: Improving Global Outcomes Guideline. More importantly, with a deeper understanding of the roles of mucosal immunity, B‐cell activation and complement activation in IgAN, the studies of targeting pathogenic pathways are ongoing. In this review, by systemically searching the clinical trials in IgAN on ClinicalTrials.gov (https://clinicaltrials.gov/), we update the evidence for corticosteroids/immunosuppressive therapy in IgAN and explore the promising targeting pathogenic pathway therapeutic options. With better understanding of pathogenesis of IgAN, emerging therapies will soon become a reality in future.