The Effects of Presleep Slow Breathing and Music Listening on Polysomnographic Sleep Measures - a pilot trial

Knowledge on efficient ways to reduce presleep arousal and, therefore, improve sleep, is scanty. We explored the effects of presleep slow breathing and music listening conditions on sleep quality and EEG power spectral density in young adults in a randomized, controlled trial with a crossover design. Participants’ (N = 20, 50% females) sleep was measured on two consecutive nights with polysomnography (40 nights), the other night serving as the control condition. The intervention condition was either a 30-minute slow breathing exercise or music listening (music by Max Richter: Sleep). The intervention and control conditions were placed in a random order. We measured heart rate variability prior to, during and after the intervention condition, and found that both interventions increased immediate heart rate variability. Music listening resulted in decreased N2 sleep, increased frontal beta1 power spectral density, and a trend towards increased N3 sleep was detected. In the slow breathing condition higher central delta power during N3 was observed. While some indices pointed to improved sleep quality in both intervention groups, neither condition had robust effects on sleep quality. These explorative findings warrant further replication in different populations.Peer reviewe

Meta‐Analysis of Genome‐wide Linkage Studies in BMI and Obesity

Objective: The objective was to provide an overall assessment of genetic linkage data of BMI and BMI‐defined obesity using a nonparametric genome scan meta‐analysis. Research Methods and Procedures: We identified 37 published studies containing data on over 31,000 individuals from more than >10,000 families and obtained genome‐wide logarithm of the odds (LOD) scores, non‐parametric linkage (NPL) scores, or maximum likelihood scores (MLS). BMI was analyzed in a pooled set of all studies, as a subgroup of 10 studies that used BMI‐defined obesity, and for subgroups ascertained through type 2 diabetes, hypertension, or subjects of European ancestry. Results: Bins at chromosome 13q13.2‐ q33.1, 12q23‐q24.3 achieved suggestive evidence of linkage to BMI in the pooled analysis and samples ascertained for hypertension. Nominal evidence of linkage to these regions and suggestive evidence for 11q13.3‐22.3 were also observed for BMI‐defined obesity. The FTO obesity gene locus at 16q12.2 also showed nominal evidence for linkage. However, overall distribution of summed rank p values <0.05 is not different from that expected by chance. The strongest evidence was obtained in the families ascertained for hypertension at 9q31.1‐qter and 12p11.21‐q23 (p < 0.01). Conclusion: Despite having substantial statistical power, we did not unequivocally implicate specific loci for BMI or obesity. This may be because genes influencing adiposity are of very small effect, with substantial genetic heterogeneity and variable dependence on environmental factors. However, the observation that the FTO gene maps to one of the highest ranking bins for obesity is interesting and, while not a validation of this approach, indicates that other potential loci identified in this study should be investigated further.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/93663/1/oby.2007.269.pd

Materiaalivalinnat ei-kariologisissa kervikaalisissa kovakudosvaurioissa

Tässä kirjallisuuskatsauksessa käydään läpi ei-kariologisten kervikaalisten kovakudosvaurioiden etiologiaa, milloin nämä vauriot ovat kannattavaa paikata ja millä materiaalilla paikkaus on suositeltavaa tehdä. Tavoitteena on selkeyttää vaurioiden hoitolinjaa sekä sitä, miten vaurioiden syntyä voisi ehkäistä hammaslääkärin toimesta. Ei-kariologisten kervikaalisten kovakudosvaurioiden etiologiassa käsitellään kirjallisuudessa abraasiota, abfraktiota sekä eroosiota. Tutkimuksissa on tultu siihen käsitykseen, että vaurion synty on monitekijäinen sen sijaan, että vain yksi asia vaikuttaisi vaurion syntyyn. Vauriolle altistavia tekijöitä on katsottu olevan ikääntyminen, ruokavalio, kova ja epästabiili purenta sekä hampaiden harjaus. Ei-kariologiset kervikaaliset kovakudosvauriot voivat aiheuttaa potilaalla vihlontaa sekä tyytymättömyyttä estetiikkaan. Vauriot voivat myös ollessaan syviä vaarantaa hampaan pulpaa sekä retentoida plakkia. Nämä ovat kaikki syitä miksi vauriot ovat kannattavaa korjata. Vaurioiden alkuvaiheessa, kun ongelmana on vihlonta tai mahdollisesti estetiikka voidaan hyödyntää fluorilakkausta tai pinnoitusta. Kirjallisuuskatsauksessa on käyty läpi yleisimpiä paikkausmateriaaleja ja näiden ominaisuuksia. Kervikaalisissa vaurioissa paikkausta vaikeuttaa ikenen läheisyys sekä se ettei kiille ympäröi koko kaviteetin reunaa. Riippuen vaurion sijainnista ja suun olosuhteista tämän hetkisessä kirjallisuudessa suositellaan käytettävän ei-kariologisten kervikaalisten kovakudosvaurioiden paikkauksessa yhdistelmämuovia, lasi-ionomeeriä tai resiinimodifioitua lasi-ionomeeriä

Quantitative-Trait-Locus Analysis of Body-Mass Index and of Stature, by Combined Analysis of Genome Scans of Five Finnish Study Groups

In recent years, many genomewide screens have been performed, to identify novel loci predisposing to various complex diseases. Often, only a portion of the collected clinical data from the study subjects is used in the actual analysis of the trait, and much of the phenotypic data is ignored. With proper consent, these data could subsequently be used in studies of common quantitative traits influencing human biology, and such a reanalysis method would be further justified by the nonbiased ascertainment of study individuals. To make our point, we report here a quantitative-trait-locus (QTL) analysis of body-mass index (BMI) and stature (i.e., height), with genotypic data from genome scans of five Finnish study groups. The combined study group was composed of 614 individuals from 247 families. Five study groups were originally ascertained in genetic studies on hypertension, obesity, osteoarthritis, migraine, and familial combined hyperlipidemia. Most of the families are from the Finnish Twin Cohort, which represents a population-wide sample. In each of the five genome scans, ∼350 evenly spaced markers were genotyped on 22 autosomes. In analyzing the genotype data by a variance-component method, we found, on chromosome 7pter (maximum multipoint LOD score of 2.91), evidence for QTLs affecting stature, and a second locus, with suggestive evidence for linkage to stature, was detected on chromosome 9q (maximum multipoint LOD score of 2.61). Encouragingly, the locus on chromosome 7 is supported by the data reported by Hirschhorn et al. (in this issue), who used a similar method. We found no evidence for QTLs affecting BMI