Oral Health and Dental Anxiety in a German Practice-based Sample

Objective Does dental anxiety have an effect on dental and periodontal health? Methods Survey data was collected from n = 200 adults (53 % females, average age 49 years) in a cross-sectional study. Dental anxiety was measured with the modified dental anxiety scale (MDAS, score 1–5, the greater the score, the greater the anxiety). Clinical parameters including probing depth (PD), clinical attachment level (CAL), plaque index (SLI), and bleeding on probing (BoP) as well as the DMFT index were recorded and statistically analyzed. Results Rating of dental anxiety was higher in women than in men (65 vs 35 %). Subjects with higher MDAS values visited the dentist less frequently (p = 0.001) and had more decay (DT 6.7 ± 4.2 vs 1.7 ± 2.4; p \u3c 0.001) but fewer filled teeth than subjects with lower ratings of dental anxiety (FT 7.1 ± 4.5 vs 9.8 ± 5.7; p = 0.042). There were no differences in PD or CAL between subjects with or without dental anxiety, while patients with higher MDAS value showed significantly more BoP (50 ± 19 vs 34 ± 20 %; p = 0.002) than patients with low MDAS scores (no or low dental anxiety). Conclusions Patients with higher ratings of dental anxiety had significantly more caries experience and gingivitis. Therefore, dental anxiety is associated with negative effect on dental and periodontal health. Clinical relevance Identifying patients with high dental anxiety and helping to manage this anxiety has important implications to improve oral health in adults. The MDAS appears to be an easy and efficient tool that can be used to identify patients with dental anxiety in dental practices

Development of reverse phase protein microarrays for the validation of clusterin, a mid-abundant blood biomarker

<p>Abstract</p> <p>Background</p> <p>Many putative disease blood biomarkers discovered in genomic and proteomic studies await validation in large clinically annotated cohorts of patient samples. ELISA assays require large quantities of precious blood samples and are not high-throughput. The reverse phase protein microarray platform has been developed for the high-throughput quantification of protein levels in small amounts of clinical samples.</p> <p>Results</p> <p>In the present study we present the development of reverse-phase protein microarrays (RPPMs) for the measurement of clusterin, a mid-abundant blood biomarker. An experimental protocol was optimized for the printing of serum and plasma on RPPMs using epoxy coated microscope slides and a non-denaturing printing buffer. Using fluorescent-tagged secondary antibodies, we achieved the reproducible detection of clusterin in spotted serum and plasma and reached a limit of detection of 780 ng/mL. Validation studies using both spiked clusterin and clinical samples showed excellent correlations with ELISA measurements of clusterin.</p> <p>Conclusion</p> <p>Serum and plasma spotted in the reverse phase array format allow for reliable and reproducible high-throughput validation of a mid-abundant blood biomarker such as clusterin.</p

PTGER4 expression-modulating polymorphisms in the 5p13.1 region predispose to Crohn's disease and affect NF-κB and XBP1 binding sites.

Genome-wide association studies identified a PTGER4 expression-modulating region on chromosome 5p13.1 as Crohn's disease (CD) susceptibility region. The study aim was to test this association in a large cohort of patients with inflammatory bowel disease (IBD) and to elucidate genotypic and phenotypic interactions with other IBD genes. A total of 7073 patients and controls were genotyped: 844 CD and 471 patients with ulcerative colitis and 1488 controls were analyzed for the single nucleotide polymorphisms (SNPs) rs4495224 and rs7720838 on chromosome 5p13.1. The study included two replication cohorts of North American (CD: n = 684; controls: n = 1440) and of German origin (CD: n = 1098; controls: n = 1048). Genotype-phenotype, epistasis and transcription factor binding analyses were performed. In the discovery cohort, an association of rs4495224 (p = 4.10×10⁻⁵; 0.76 [0.67-0.87]) and of rs7720838 (p = 6.91×10⁻⁴; 0.81 [0.71-0.91]) with susceptibility to CD was demonstrated. These associations were confirmed in both replication cohorts. In silico analysis predicted rs4495224 and rs7720838 as essential parts of binding sites for the transcription factors NF-κB and XBP1 with higher binding scores for carriers of the CD risk alleles, providing an explanation of how these SNPs might contribute to increased PTGER4 expression. There was no association of the PTGER4 SNPs with IBD phenotypes. Epistasis detected between 5p13.1 and ATG16L1 for CD susceptibility in the discovery cohort (p = 5.99×10⁻⁷ for rs7720838 and rs2241880) could not be replicated in both replication cohorts arguing against a major role of this gene-gene interaction in the susceptibility to CD. We confirmed 5p13.1 as a major CD susceptibility locus and demonstrate by in silico analysis rs4495224 and rs7720838 as part of binding sites for NF-κB and XBP1. Further functional studies are necessary to confirm the results of our in silico analysis and to analyze if changes in PTGER4 expression modulate CD susceptibility

Ocular risk management in patients undergoing general anesthesia: an analysis of 39,431 surgeries

OBJECTIVE: This study sought to describe and analyze ocular findings associated with nonocular surgery in patients who underwent general anesthesia. METHODS: The authors retrospectively collected a series of 39,431 surgeries using standardized data forms. RESULTS: Ocular findings were reported in 9 cases (2.3:10,000), which involved patients with a mean age of 58.9±19.5 years. These cases involved patients classified as ASA I (33%), ASA II (55%) or ASA III (11%). General anesthesia with propofol and remifentanil was used in 4 cases, balanced general anesthesia was used in 4 cases, and regional block was used in combination with balanced general anesthesia in one case. Five patients (55%) underwent surgery in the supine position, one patient (11%) underwent surgery in the lithotomy position, two patients (22%) underwent surgery in the prone position, and one patient (11%) underwent surgery in the lateral position. Ocular hyperemia was detected in most (77%) of the 9 cases with ocular findings; pain/burning of the eyes, visual impairment, eye discharge and photophobia were observed in 55%, 11%, 11% and 11%, respectively, of these 9 cases. No cases involved permanent ocular injury or vision loss. CONCLUSION: Ophthalmological findings after surgeries were uncommon, and most of the included patients were relatively healthy. Minor complications, such as dehydration or superficial ocular trauma, should be prevented by following systematic protocols that provide appropriate ocular occlusion with a lubricating ointment and protect the eye with an acrylic occluder. These procedures will refine the quality of anesthesia services and avoid discomfort among patients, surgeons and anesthesia staff

A systematic mapping review of the evolution of the rat Forced Swim Test: Protocols and outcome parameters

As depression is projected to become the leading mental disease burden globally by 2030, understanding the underlying pathology, as well as screening potential anti-depressants with a higher efficacy, faster onset of action, and/or fewer side-effects is essential. A commonly used test for screening novel antidepressants and studying depression-linked aspects in rodents is the Porsolt Forced Swim Test. The present systematic mappping review gives a comprehensive overview of the evolution and of the most prevalently used set-ups of this test in rats, including the choice of animals (strain, sex, and age), technical aspects of protocol and environment, as well as reported outcome measures. Additionally, we provide an accessible list of all existing publications, to support informed decision-making for procedural and technical aspects of the test, to thereby enhance reproducibility and comparability. This should further contribute to reducing the number of unnecessarily replicated experiments, and consequently, reduce the number of animals used in future

Comparative genomics and transcriptomics of lineages I, II, and III strains of Listeria monocytogenes

BACKGROUND: Listeria monocytogenes is a food-borne pathogen that causes infections with a high-mortality rate and has served as an invaluable model for intracellular parasitism. Here, we report complete genome sequences for two L. monocytogenes strains belonging to serotype 4a (L99) and 4b (CLIP80459), and transcriptomes of representative strains from lineages I, II, and III, thereby permitting in-depth comparison of genome- and transcriptome -based data from three lineages of L. monocytogenes. Lineage III, represented by the 4a L99 genome is known to contain strains less virulent for humans. RESULTS: The genome analysis of the weakly pathogenic L99 serotype 4a provides extensive evidence of virulence gene decay, including loss of several important surface proteins. The 4b CLIP80459 genome, unlike the previously sequenced 4b F2365 genome harbours an intact inlB invasion gene. These lineage I strains are characterized by the lack of prophage genes, as they share only a single prophage locus with other L. monocytogenes genomes 1/2a EGD-e and 4a L99. Comparative transcriptome analysis during intracellular growth uncovered adaptive expression level differences in lineages I, II and III of Listeria, notable amongst which was a strong intracellular induction of flagellar genes in strain 4a L99 compared to the other lineages. Furthermore, extensive differences between strains are manifest at levels of metabolic flux control and phosphorylated sugar uptake. Intriguingly, prophage gene expression was found to be a hallmark of intracellular gene expression. Deletion mutants in the single shared prophage locus of lineage II strain EGD-e 1/2a, the lma operon, revealed severe attenuation of virulence in a murine infection model. CONCLUSION: Comparative genomics and transcriptome analysis of L. monocytogenes strains from three lineages implicate prophage genes in intracellular adaptation and indicate that gene loss and decay may have led to the emergence of attenuated lineages

Expanding the clinical spectrum associated with defects in CNTNAP2 and NRXN1

RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.Abstract Background Heterozygous copy-number and missense variants in CNTNAP2 and NRXN1 have repeatedly been associated with a wide spectrum of neuropsychiatric disorders such as developmental language and autism spectrum disorders, epilepsy and schizophrenia. Recently, homozygous or compound heterozygous defects in either gene were reported as causative for severe intellectual disability. Methods 99 patients with severe intellectual disability and resemblance to Pitt-Hopkins syndrome and/or suspected recessive inheritance were screened for mutations in CNTNAP2 and NRXN1. Molecular karyotyping was performed in 45 patients. In 8 further patients with variable intellectual disability and heterozygous deletions in either CNTNAP2 or NRXN1, the remaining allele was sequenced. Results By molecular karyotyping and mutational screening of CNTNAP2 and NRXN1 in a group of severely intellectually disabled patients we identified a heterozygous deletion in NRXN1 in one patient and heterozygous splice-site, frameshift and stop mutations in CNTNAP2 in four patients, respectively. Neither in these patients nor in eight further patients with heterozygous deletions within NRXN1 or CNTNAP2 we could identify a defect on the second allele. One deletion in NRXN1 and one deletion in CNTNAP2 occurred de novo, in another family the deletion was also identified in the mother who had learning difficulties, and in all other tested families one parent was shown to be healthy carrier of the respective deletion or mutation. Conclusions We report on patients with heterozygous defects in CNTNAP2 or NRXN1 associated with severe intellectual disability, which has only been reported for recessive defects before. These results expand the spectrum of phenotypic severity in patients with heterozygous defects in either gene. The large variability between severely affected patients and mildly affected or asymptomatic carrier parents might suggest the presence of a second hit, not necessarily located in the same gene.Peer Reviewe

Aerobic exercise inhibits acute lung injury: from mouse to human evidence Exercise reduced lung injury markers in mouse and in cells

Acute respiratory distress syndrome (ARDS) is defined as hypoxemic respiratory failure with intense pulmonary inflammation, involving hyperactivation of endothelial cells and neutrophils. Given the anti-inflammatory effects of aerobic exercise (AE), this study investigated whether AE performed daily for 5 weeks would inhibit extra-pulmonary LPS-induced ARDS. C57Bl/6 mice were distributed into Control, Exercise, LPS and Exercise+ LPS groups. AE was performed on a treadmill for 5x/week for four weeks before LPS administration. 24hours after the final AE physical test, animals received 100ug of LPS intra-peritoneally. In addition, whole blood cell culture, neutrophils and human endothelial cells were pre-incubated with IL-10, an anti-inflammatory cytokine induced by exercise. AE reduced total protein levels (p<0.01) and neutrophil accumulation in bronchoalveolar lavage (BAL) (p<0.01) and lung parenchyma (p<0.01). AE reduced BAL inflammatory cytokines IL-1 beta, IL-6 and GM-CSF (p<0.001), CXCL1/KC, IL-17, TNF-alpha and IGF-1 (p<0.01). Systemically, AE reduced IL-1 beta, IL-6 and IFN-gamma (p<0.001), CXCL1/KC (p<0.01) and TNF-alpha (p<0.05). AE increased IL-10 levels in serum (p<0.001) and BAL (p<0.001). Furthermore, AE increased superoxide dismutase SOD (p<0.01) and decreased superoxide anion accumulation in the lungs (p<0.01). Lastly, pre-incubation with IL-10 significantly reduced LPS-induced activation of whole blood cells, neutrophils and HUVECs, as observed by reduced production of IL-1 beta, IL-6, IL-8 and TNF-alpha. Our data suggest that AE inhibited LPS-induced lung inflammation by attenuating inflammatory cytokines and oxidative stress markers in mice and human cell culture via enhanced IL-10 production.Sao Paulo Research Foundation (FAPESP) [2012/15165-2]Conselho Nacional de Pesquisa e Desenvolvimento (CNPq) [311335-2015-2]Comissao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [12804/13-4, 1303/13-9]FAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]CAPESNove Julho Univ, Sao Paulo, SP, BrazilBrazilian Inst Teaching & Res Pulm & Exercise Imm, Sao Jose Dos Campos, SP, BrazilFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, BrazilUniv Brasil, Sao Paulo, SP, BrazilUniv Sao Paulo, Sch Med, Dept Pathol LIM 59, Sao Paulo, SP, BrazilUniv Fed Lavras UFLA, Sci Dept Hlth, Lavras, MG, BrazilFed Univ Sao Paulo UNIFESP, Campus Sao Paulo, Sao Paulo, SP, BrazilHarbor UCLA Med Ctr, Div Resp & Crit Care Physiol & Med, Los Angeles Biomed Res Inst, Torrance, CA 90509 USAUniv Tubingen, Inst Clin & Expt Transfus Med IKET, Tubingen, GermanyFed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Santos, SP, BrazilFed Univ Sao Paulo UNIFESP, Campus Sao Paulo, Sao Paulo, SP, BrazilFAPESP [2012/15165-2]CNPq [311335-2015-2]CAPES [12804/13-4, 1303/13-9]FAPESP [2013/24076-6, 2014/23196-0, 2012/14604-8, 2012/25435-7, 2012/24880-7]Web of Scienc

Laser Ablation – Accelerator Mass Spectrometry:a novel approach for rapid radiocarbon analyses of carbonate archives at high spatial resolution

Additional file 5. Immunohistochemistry of SAV-infected heart tissue stained using polyclonal rabbit antiserum targeting PRV σ1 (right panel) and monoclonal murine anti-SAV E2 (left panel). The heart tissue had a SAV Ct-value of 17.1