The Epidemiology of Insomnia and Sleep Duration Across Mental and Physical Health: The SHoT Study

Objective: Numerous epidemiological studies have been conducted to examine the prevalence and comorbidities of insomnia and document sleep duration, but a common limitation in many studies is the lack of use of agreed-upon definitions of insomnia, as well as insufficient statistical power to examine comorbid mental and physical disorders/conditions. Aim: To examine the prevalence of insomnia operationalized according to formal DSM-5 criteria and differences in mean sleep duration across a wide range of mental and physical disorders, examining men and women separately. Materials and Methods: Data stem from the SHoT study (Students’ Health and Wellbeing Study), a national survey of all college and university students in Norway. In all, 162,512 students aged 18–35 received an invitation to participate, of whom 50,054 students completed the internet-based survey (attendance rate: 30.8%). Insomnia was defined according to the Diagnostic and Statistical Manual of Mental Disorders (5th ed.) criteria and sleep duration was calculated separately for weekdays and weekends. Self-reported mental and physical disorders/conditions were assessed using a pre-defined list modified to fit this age group. Pearson chi-squared tests were used to examine the prevalence of insomnia across the various mental and physical disorders/conditions in men and women separately, and log-link binomial regression analysis were used to calculate effect-sizes, adjusting for age. Results: The prevalence of insomnia in both sexes was significantly higher across all mental disorders compared with a healthy reference group. Among females, the prevalence of insomnia ranged from 61.3% for comorbid depression (adj. RR = 2.49, 95% CI: 2.40) to 83.3% for comorbid schizophrenia (adj. RR = 3.37, 95% CI: 2.61–4.35). For males, the insomnia prevalence ranged from 32.3% for comorbid autism/Asperger (adj. RR = 2.02, 95% CI: 1.39–2.92) to 74.2% for comorbid eating disorder (adj. RR = 4.51, 95% CI: 3.87–5.27). The overall prevalence of insomnia was also significantly higher across most physical conditions compared with the healthy reference group, although generally lower compared to the mental disorders. For females, the insomnia prevalence ranged from 25% for comorbid multiple sclerosis (not significant) to 65.4% for comorbid chronic fatigue syndrome/ME (adj. RR = 2.66, 95% CI: 2.44–2.89). For males, the insomnia prevalence ranged from 20% for both comorbid cancer and diabetes (not significant) to 74.2% for comorbid fibromyalgia (adj. RR = 4.35, 95% CI: 2.96–6.39). Similar patterns were observed for sleep duration, with a significantly shorter sleep duration for across many physical disorders, but especially mental disorders. Conclusion: Insomnia and short sleep duration are strongly associated with a range of different disorders and conditions. Insomnia is most strongly associated with mental disorders, and physical conditions characterized by some level of psychological or psychosomatic properties.publishedVersio

Are book publications disappearing from scholarly communication in the social sciences and humanities?

In the social sciences and humanities book publishing takes a prominent role, both in terms of communicating with international peers and with a broader intelligentsia (Hicks, 2004; Verleysen & Engels, 2014). Empirical evidence regarding the evolution of the share of scholarly book publications in the total volume of scholarly publications in a given country is rare. In this study we intend to fill this gap with an analysis of the comprehensive coverage data on the share of peer reviewed book publications (book chapters, edited volumes and monographs) that are available from Flanders and Slovenia for the period 2004 to 2015. We supplement these data with data on peer reviewed book chapters and monographs from Norway for the period 2005-2015 as well as data on all types of peer reviewed book publishing for the period 2009 to 2014 for Poland and 2011 to 2015 for Finland

Ghrelin receptor in GtoPdb v.2021.3

The ghrelin receptor (nomenclature as agreed by the NC-IUPHAR Subcommittee for the Ghrelin receptor [19]) is activated by a 28 amino-acid peptide originally isolated from rat stomach, where it is cleaved from a 117 amino-acid precursor (GHRL, Q9UBU3). The human gene encoding the precursor peptide has 83% sequence homology to rat prepro-ghrelin, although the mature peptides from rat and human differ by only two amino acids [74]. Alternative splicing results in the formation of a second peptide, [des-Gln14]ghrelin with equipotent biological activity [49]. A unique post-translational modification (octanoylation of Ser3, catalysed by ghrelin Ο-acyltransferase (MBOAT4, Q96T53) [133] occurs in both peptides, essential for full activity in binding to ghrelin receptors in the hypothalamus and pituitary, and for the release of growth hormone from the pituitary [58]. Structure activity studies showed the first five N-terminal amino acids to be the minimum required for binding [4], and receptor mutagenesis has indicated overlap of the ghrelin binding site with those for small molecule agonists and allosteric modulators of ghrelin function [44]. An endogenous antagonist and inverse agonist called Liver enriched antimicrobial peptide 2 (Leap2), expressed primarily in hepatocytes and in enterocytes of the proximal intestine [35, 68] inhibits ghrelin receptor-induced GH secretion and food intake [35]. The secretion of Leap2 and ghrelin is inversely regulated under various metabolic conditions [71]. In cell systems, the ghrelin receptor is constitutively active [45], but this is abolished by a naturally occurring mutation (A204E) that results in decreased cell surface receptor expression and is associated with familial short stature [93]

Ghrelin receptor in GtoPdb v.2023.1

The ghrelin receptor (nomenclature as agreed by the NC-IUPHAR Subcommittee for the Ghrelin receptor [19]) is activated by a 28 amino-acid peptide originally isolated from rat stomach, where it is cleaved from a 117 amino-acid precursor (GHRL, Q9UBU3). The human gene encoding the precursor peptide has 83% sequence homology to rat prepro-ghrelin, although the mature peptides from rat and human differ by only two amino acids [75]. Alternative splicing results in the formation of a second peptide, [des-Gln14]ghrelin with equipotent biological activity [50]. A unique post-translational modification (octanoylation of Ser3, catalysed by ghrelin Ο-acyltransferase (MBOAT4, Q96T53) [134] occurs in both peptides, essential for full activity in binding to ghrelin receptors in the hypothalamus and pituitary, and for the release of growth hormone from the pituitary [59]. Structure activity studies showed the first five N-terminal amino acids to be the minimum required for binding [4], and receptor mutagenesis has indicated overlap of the ghrelin binding site with those for small molecule agonists and allosteric modulators of ghrelin function [45]. An endogenous antagonist and inverse agonist called Liver enriched antimicrobial peptide 2 (Leap2), expressed primarily in hepatocytes and in enterocytes of the proximal intestine [36, 69] inhibits ghrelin receptor-induced GH secretion and food intake [36]. The secretion of Leap2 and ghrelin is inversely regulated under various metabolic conditions [72]. In cell systems, the ghrelin receptor is constitutively active [46], but this is abolished by a naturally occurring mutation (A204E) that results in decreased cell surface receptor expression and is associated with familial short stature [94]

Ghrelin receptor (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

The ghrelin receptor (nomenclature as agreed by the NC-IUPHAR Subcommittee for the Ghrelin receptor [18]) is activated by a 28 amino-acid peptide originally isolated from rat stomach, where it is cleaved from a 117 amino-acid precursor (GHRL, Q9UBU3). The human gene encoding the precursor peptide has 83% sequence homology to rat prepro-ghrelin, although the mature peptides from rat and human differ by only two amino acids [70]. Alternative splicing results in the formation of a second peptide, [des-Gln14]ghrelin with equipotent biological activity [48]. A unique post-translational modification (octanoylation of Ser3, catalysed by ghrelin Ο-acyltransferase (MBOAT4, Q96T53) [127] occurs in both peptides, essential for full activity in binding to ghrelin receptors in the hypothalamus and pituitary, and for the release of growth hormone from the pituitary [56]. Structure activity studies showed the first five N-terminal amino acids to be the minimum required for binding [4], and receptor mutagenesis has indicated overlap of the ghrelin binding site with those for small molecule agonists and allosteric modulators of ghrelin function [43]. In cell systems, the ghrelin receptor is constitutively active [44], but this is abolished by a naturally occurring mutation (A204E) that results in decreased cell surface receptor expression and is associated with familial short stature [88]

Trajectories and stability of self-reported short sleep duration from adolescence to adulthood

The trajectories and stability of self-reported sleep duration recorded at ages 13, 15, and 23 years on reported sleep duration at age 30 years among 1105 students (55% male) who participated in the Norwegian Longitudinal Health and Behaviour Study were examined. Questionnaire data were used to obtain demographic and sleep variables. Dichotomised short sleep duration was based on normative values and set as ≤8.5 h (age 13 years), ≤8 h (age 15 years) and ≤7 h (ages 23 and 30 years). Results indicated a significant overall reduction in total sleep duration (h per night) across age groups. Sleep duration (continuous) at age 15 and 23 years (whole group) was moderately but positively correlated with sleep duration at age 30 years (P < 0.01). When split by sex, at age 15 years, this association was present among females only (P < 0.01); however, at age 23 years, this association was present in both male and females (both P < 0.001). Categorical short sleep at age 23 years (whole group) was associated with short sleep at age 30 years (unadjusted odds ratio = 3.67, 95% confidence interval 2.36-5.69). Following sex stratification, this effect was significant for both males (unadjusted odds ratio = 3.77, 95% confidence interval: 2.22-6.42) and females (unadjusted odds ratio = 2.71, 95% confidence interval: 1.46-5.04). No associations were noted for categorical short sleep at ages 13 or 15 years, and subsequent short sleep at 30 years. Habitual short sleep duration during middle adulthood is not sustained from the time of early adolescence. Rather, these trends appear to be formed during early adulthood

Are book publications disappearing from scholarly communication in the social sciences and humanities?

© 2018, Tim C.E. Engels, Andreja Istenič Starčič, Emanuel Kulczycki, Janne Pölönen and Gunnar Sivertsen. Purpose: The purpose of this paper is to analyze the evolution in terms of shares of scholarly book publications in the social sciences and humanities (SSH) in five European countries, i.e. Flanders (Belgium), Finland, Norway, Poland and Slovenia. In addition to aggregate results for the whole of the social sciences and the humanities, the authors focus on two well-established fields, namely, economics & business and history. Design/methodology/approach: Comprehensive coverage databases of SSH scholarly output have been set up in Flanders (VABB-SHW), Finland (VIRTA), Norway (NSI), Poland (PBN) and Slovenia (COBISS). These systems allow to trace the shares of monographs and book chapters among the total volume of scholarly publications in each of these countries. Findings: As expected, the shares of scholarly monographs and book chapters in the humanities and in the social sciences differ considerably between fields of science and between the five countries studied. In economics & business and in history, the results show similar field-based variations as well as country variations. Most year-to-year and overall variation is rather limited. The data presented illustrate that book publishing is not disappearing from an SSH. Research limitations/implications: The results presented in this paper illustrate that the polish scholarly evaluation system has influenced scholarly publication patterns considerably, while in the other countries the variations are manifested only slightly. The authors conclude that generalizations like “performance-based research funding systems (PRFS) are bad for book publishing” are flawed. Research evaluation systems need to take book publishing fully into account because of the crucial epistemic and social roles it serves in an SSH. Originality/value: The authors present data on monographs and book chapters from five comprehensive coverage databases in Europe and analyze the data in view of the debates regarding the perceived detrimental effects of research evaluation systems on scholarly book publishing. The authors show that there is little reason to suspect a dramatic decline of scholarly book publishing in an SSH

Near-normalization of glycaemic control with glucagon-like peptide-1 receptor agonist treatment combined with exercise in patients with type 2 diabetes

AIMS: To investigate the effects of exercise in combination with a glucagon‐like peptide‐1 receptor agonist (GLP‐1RA), liraglutide, or placebo for the treatment of type 2 diabetes. METHODS: Thirty‐three overweight, dysregulated and sedentary patients with type 2 diabetes were randomly allocated to 16 weeks of either exercise and liraglutide or exercise and placebo. Both groups had three supervised 60‐minute training sessions per week including spinning and resistance training. RESULTS: Glycated haemoglobin (HbA1c) levels dropped by a mean ± standard deviation of 2.0% ± 1.2% (from 8.2% ± 1.4%) in the exercise plus liraglutide group vs 0.3% ± 0.9% (from 8.0% ± 1.2%) in the exercise plus placebo group ( P < .001), and body weight was reduced more with liraglutide (−3.4 ± 2.9 kg vs −1.6 ± 2.3 kg; P < .001). Compared with baseline, similar reductions were seen in body fat (exercise plus liraglutide: −2.5% ± 1.4% [ P < .001]; exercise plus placebo: −2.2% ± 1.9% [ P < .001]) and similar increases were observed in maximum oxygen uptake (exercise plus liraglutide: 0.5 ± 0.5 L O(2)/min [ P < .001]; exercise plus placebo: 0.4 ± 0.4 L O(2)/min [ P = .002]). Greater reductions in fasting plasma glucose (−3.4 ± 2.3 mM vs −0.3 ± 2.6 mM, P < .001) and systolic blood pressure (−5.4 ± 7.4 mm Hg vs −0.6 ± 11.1 mm Hg, P < .01) were seen with exercise plus liraglutide vs exercise plus placebo. The two groups experienced similar increases in quality of life during the intervention. CONCLUSIONS: In obese patients with type 2 diabetes, exercise combined with GLP‐1RA treatment near‐normalized HbA1c levels and caused a robust weight loss when compared with placebo. These results suggest that a combination of exercise and GLP‐1RA treatment is effective in type 2 diabetes

Semi-automated assignment of vegetation survey plotswithin anapriori classification of vegetation types

Assignment of large numbers of vegetation plots to a priori vegetation classifications is increasingly being required to support natural resource management, monitoring and conservation at regional scales. Several automated systems have been developed that use quantitative synoptic tables and algorithm-based plot-to-type assignment. However, where synoptic tables do not exist, and qualitative species lists characterise vegetation type classifications, existing systems may not apply. In these situations, vegetation experts may resort to manual assignment processes that can be slow, subjective and fraught with difficulties. This study combines repeatable and objective quantitative analyses, with new software, to deliver a semi-automated plot-to-type assignment process appropriate for a priori classifications based on qualitative species lists. The flexible semi-automated assignment program (SAAP) calculates a quantitative goodness-of-fit score between plots and types, based on the species that characterise each a priori vegetation type, and the species that characterise groups of plots derived from quantitative analyses. We applied the SAAP to a case-study of 630 native vascular plant species from 930 plots, and an a priori classification of 99 vegetation types. We varied vegetation data set transforms [cover per cent (0–100%), cover score (0–6) and presence–absence (1, 0)] and analysis settings and tested the degree to which the SAAP provided plot-to-type assignment concordant with manual expert assignment. Results provided clear evidence supporting the choice of particular data set transformations and analysis settings to maximise concordance. The SAAP allocated up to 50% of plots to the same expert-assigned vegetation type, and more than 70% of plots to an expert-assigned vegetation type ranked in the top five by the SAAP. When coupled with repeatable and objective quantitative analyses, the SAAP provides vegetation experts with a new semi-automated and quantitative decision support tool to assist with the assignment of vegetation plots within a priori vegetation classifications defined by characteristic species lists