Sensory Modulation and Sleep Quality among Adults with Learning Disabilities: A Quasi-Experimental Case-Control Design Study

PurposeFollowing the International Classification of Functioning, Disability and Health (ICF) concepts, this study examines body functions such as sensory modulation and sleep quality among adults with learning disabilities (LD).MethodsOne hundred and ten participants, 55 adults with LD and 55 matched controls (mean age 30 years) filled in a socio-demographic questionnaire, the Adults/Adolescents Sensory Profile (AASP), and the Mini Sleep Questionnaire (MSQ). Chi-tests, Mann-Whitney tests, and Kolmogorov-Smirnov tests were conducted to examine group differences related to socio-demographic characteristics and body functions. Correlation and regression analyses were conducted to examine relationships between body functions.ResultsSignificant differences were found between the groups in: (a) unique socio-demographic variables: high-schools attended, family status and number of children; (b) body functions: low registration and sensory sensitivity (p < .001), sensory avoiding (p = .002), sensory seeking (p = .021) and sleep quality (p < .001). Significant correlations were found between AASP subscale scores and the MSQ final score in each group. Regression analysis revealed that for the entire sample (N = 108), low registration accounted for 10.2% of the variance of sleep quality above group membership (p < .001), while in a separate examination of adults with LD (n = 53), low registration accounted for 19.9% of the variance of sleep quality (p < .001).ConclusionsAdults with LD need to be studied through a health-related perspective such as the ICF model to gain further understanding of their unique characteristics and daily needs. Sensory and sleep functions of adults with LD should be further studied in the context of health related quality of life.     

Headaches in overweight children and adolescents referred to a tertiary-care center in Israel

Objective: To assess the association between obesity and primary headaches in children and adolescents. Methods and Procedures: In a prospective study, the short‐questionnaire version based on existing International Headache Society diagnostic criteria was administered. Two hundred and seventy‐three children and adolescents (61% females) aged 9–17 years were assessed. One hundred and sixteen (42.5%) subjects were of normal weight, 45 (16.5%) were at risk for overweight (BMI >85th and <95th percentile for age and gender) and 112 (41%) were overweight (BMI ≥95th percentile). The outcome measures were prevalence of headaches, type of headaches, association between headaches and elevated blood pressure in overweight subjects. Results: Headache was reported in 39 (14.3%) subjects, with a similar rate in females (14.5%) and males (14%). Among 39 subjects with headaches, 20 (17.9%) were overweight, 7 (15.6%) were at risk for overweight and 12 (10.3%) were normal‐weight children. Among females, 7.7% of normal‐weight group suffered from headaches, compared with 14.8% of the at risk for overweight group and 20.3% of the overweight group (P for trend 0.04). Among males, the occurrence of headaches was similar in all three weight groups (P = 0.96). The occurrence of headaches increased from 10.6% among children aged 9–11 years to 21.8% in the 15–18 years age group (P < 0.05). In multivariate analysis, a significant independent risk for headaches was present in overweight females (odds ratio (OR) = 3.93, 95% confidence interval (CI) 1.28–12.1) and in adolescents aged 15–18 years (OR = 2.62, 95% CI 1.07–6.45). Elevated blood pressure was not independently associated with headaches. Of the 15 children with migraine, 12 were either at risk for overweight or overweight. Discussion: Overweight females had an almost fourfold excess risk of headaches when compared with normal‐weight girls.     

Association between Decreased Klotho Blood Levels and Organic Growth Hormone Deficiency in Children with Growth Impairment

Objective

Klotho is an aging-modulating protein expressed mainly in the kidneys and choroid plexus, which can also be shed, released into the circulation and act as a hormone. Klotho deficient mice are smaller compared to their wild-type counterparts and their somatotropes show marked atrophy and reduced number of secretory granules. Recent data also indicated an association between klotho levels and growth hormone (GH) levels in acromegaly. We aimed to study the association between klotho levels and GH deficiency (GHD) in children with growth impairment.

Design

Prospective study comprising 99 children and adolescents (aged 9.0±3.7 years, 49 male) undergoing GH stimulation tests for short stature (height-SDS = −2.1±0.6). Klotho serum levels were measured using an α-klotho ELISA kit.

Results

Klotho levels were significantly lower (p<0.001) among children with organic GHD (n = 11, 727±273 pg/ml) compared to both GH sufficient participants (n = 59, 1497±754 pg/ml) and those with idiopathic GHD (n = 29, 1645±778 pg/ml). The difference between GHS children and children with idiopathic GHD was not significant. Klotho levels positively correlated with IGF-1- standard deviation scores (SDS) (R = 0.45, p<0.001), but were not associated with gender, pubertal status, age or anthropometric measurements.

Conclusions

We have shown, for the first time, an association between low serum klotho levels and organic GHD. If validated by additional studies, serum klotho may serve as novel biomarker of organic GHD.     

Metabolic regulation of protein N-alpha-acetylation by Bcl-xL promotes cell survival

Previous experiments suggest a connection between the N-alpha-acetylation of proteins and sensitivity of cells to apoptotic signals. Here, we describe a biochemical assay to detect the acetylation status of proteins and demonstrate that protein N-alpha-acetylation is regulated by the availability of acetyl-CoA. Because the antiapoptotic protein Bcl-xL is known to influence mitochondrial metabolism, we reasoned that Bcl-xL may provide a link between protein N-alpha-acetylation and apoptosis. Indeed, Bcl-xL overexpression leads to a reduction in levels of acetyl-CoA and N-alpha-acetylated proteins in the cell. This effect is independent of Bax and Bak, the known binding partners of Bcl-xL. Increasing cellular levels of acetyl-CoA by addition of acetate or citrate restores protein N-alpha-acetylation in Bcl-xL-expressing cells and confers sensitivity to apoptotic stimuli. We propose that acetyl-CoA serves as a signaling molecule that couples apoptotic sensitivity to metabolism by regulating protein N-alpha-acetylation.     

Activity and Participation Characteristics of Adults with Learning Disabilities - A Systematic Review

Background

‘Learning disabilities’ (LD) refer to a wide group of neurological disorders caused by deficits in the central nervous system which influence the individual''s ability to maintain-, process or convey information to others in an efficient way. A worldwide discussion about the definitions of LD continues while a conceptual framework for studying the diverse life outcomes of adults with LD is still missing.

Objective

The aim was to review the literature on the activity and participation of adults with LD based on the International Classification of Functioning, Disability and Health (ICF) concepts.

Methods

“PsychInfo”, “Eric” and “PubMed” were searched for relevant literature according to the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). After a three-stage process, 62 articles relevant for domains of activity and participation of adults with LD were included in the review.

Results

Thirty-two articles focused on the domain of major life areas of education, work and employment and twelve articles focused on the domain of learning and applying knowledge. Limitations in activity and participation of the population with LD in these domains are recognized and discussed. Eighteen additional articles demonstrated that adults with LD confront difficulties in various life domains (e.g., communication, interpersonal interactions, mobility, and domestic life), however literature concerning these domains is scarce.

Conclusions

The ICF can be useful for further exploration of activity and participation characteristics of adults with LD in various life domains. Such exploration is required in order to gain a wider perspective of their functional characteristics and daily needs.     

A Cross Modal Performance-Based Measure of Sensory Stimuli Intricacy

We define a new measure of sensory stimuli which has the following properties: It is cross modal, performance based, robust, and well defined. We interpret this measure as the intricacy or complexity of the stimuli, yet its validity is independent of its interpretation. We tested the validity and cross modality of our measure using three olfactory and one visual experiment. In order to test the link between our measure and cognitive performance we also conducted an additional visual experiment. We found that our measure is correlated with the results of the well-established Rapid Serial Visual Presentation masking experiment. Specifically, ranking stimuli according to our measure was correlated at r = 0.75 (p < 0.002) with masking effectiveness. Thus, our novel measure of sensory stimuli provides a new quantitative tool for the study of sensory processing.     

Sequential phosphorylation of insulin receptor substrate-2 by glycogen synthase kinase-3 and c-Jun NH2-terminal kinase plays a role in hepatic insulin signaling

Serine phosphorylation of insulin receptor substrate (IRS) proteins is a potential inhibitory mechanism in insulin signaling. Here we show that IRS-2 is phosphorylated by glycogen synthase kinase (GSK)-3. Phosphorylation by GSK-3 requires prior phosphorylation of its substrates, prompting us to identify the "priming kinase." It was found that the stress activator anisomycin enhanced the ability of GSK-3 to phosphorylate IRS-2. Use of a selective c-Jun NH(2)-terminal kinase (JNK) inhibitor and cells overexpressing JNK implicated JNK as the priming kinase. This allowed us to narrow down the number of potential GSK-3 phosphorylation sites within IRS-2 to four regions that follow the motif SXXXSP. IRS-2 deletion mutants enabled us to localize the GSK-3 and JNK phosphorylation sites to serines 484 and 488, respectively. Mutation at serine 488 reduced JNK phosphorylation of IRS-2, and mutation of each site separately abolished GSK-3 phosphorylation of IRS-2. Treatment of H4IIE liver cells with anisomycin inhibited insulin-induced tyrosine phosphorylation of IRS-2; inhibition was reversed by pretreatment with the JNK and GSK-3 inhibitors. Moreover, overexpression of JNK and GSK-3 in H4IIE cells reduced insulin-induced tyrosine phosphorylation of IRS-2 and its association with the p85 regulatory subunit of phosphatidylinositol 3-kinase. Finally, both GSK-3 and JNK are abnormally upregulated in the diabetic livers of ob/ob mice. Together, our data indicate that IRS-2 is sequentially phosphorylated by JNK and GSK-3 at serines 484/488 and provide evidence for their inhibitory role in hepatic insulin signaling.