Do sleep disturbances and psychotic-like experiences in adolescence share genetic and environmental influences?

Sleep disturbances regularly co-occur with clinical psychotic disorders and dimensions of psychotic-like experiences (PLEs). One possible explanation for this, which has yet to be tested, is that similar genetic or environmental influences underlie sleep disturbances and vulnerability to PLEs. We conducted a twin study to test this possibility in relation to sleep disturbances and six specific PLEs in adolescence in the general population. Approximately 5,000 16-year-old twin pairs completed the Pittsburgh Sleep Quality Index and Insomnia Severity Index. PLEs were assessed using the Specific PLEs Questionnaire, comprising five self-report subscales (Paranoia, Hallucinations, Cognitive Disorganization, Grandiosity, and Anhedonia) and one parent-report subscale (Negative Symptoms). The associations between these measures were tested using structural equation twin model fitting. Paranoia, Hallucinations, and Cognitive Disorganization displayed moderate and significant correlations with both sleep measures (0.32–.42), while Negative Symptoms, Anhedonia, and Grandiosity showed lower correlations (0.01–0.17). Genetic and environmental influences significantly overlapped across PLEs (Paranoia, Hallucinations, Cognitive Disorganization) and both types of sleep disturbance (mean genetic and nonshared environmental correlations = 0.54 and 0.24, respectively). These estimates reduced, yet remained significant, after controlling for negative affect. The association between PLEs with sleep disturbances in adolescence is partly due to genetic and environmental influences that are common to them both. These findings indicate that the known neurobiology of sleep disturbance may provide clues regarding the causes of PLEs in adolescence

Sc2Ga2CuO7: A possible quantum spin liquid near the percolation threshold

Sc2Ga2CuO7 (SGCO) crystallizes in a hexagonal structure (space group: P63/mmc), which can be seen as an alternating stacking of single and double triangular layers. Combining neutron, x-ray, and resonant x-ray diffraction we establish that the single triangular layers are mainly populated by non-magnetic Ga3+ ions (85% Ga and 15% Cu), while the bi-layers have comparable population of Cu2+ and Ga3+ ions (43% Cu and 57% Ga). Our susceptibility measurements in the temperature range 1.8 - 400 K give no indication of any spin-freezing or magnetic long-range order (LRO).We infer an effective paramagnetic moment μeff = 1.79±0.09 μB and a Curie-Weiss temperature �CW of about −44 K, suggesting antiferromagnetic interactions between the Cu2+(S = 1/2) ions. Low-temperature neutron powder diffraction data showed no evidence for LRO down to 1.5 K. In our specific heat data as well, no anomalies were found down to 0.35 K, in the field range 0-140 kOe. The magnetic specific heat, Cm, exhibits a broad maximum at around 2.5 K followed by a nearly power law Cm/ T� behavior at lower temperatures, with � increasing from 0.3 to 1.9 as a function of field for fields upto 90 kOe and then remaining at 1.9 for fields upto 140 kOe. Our results point to a disordered ground state in SGCO

Cross talk between adipose tissue and placenta in obese and gestational diabetes mellitus pregnancies via exosomes

Obesity is an important public health issue worldwide, where it is commonly associated with the development of metabolic disorders, especially insulin resistance (IR). Maternal obesity is associated with an increased risk of pregnancy complications, especially gestational diabetes mellitus (GDM). Metabolism is a vital process for energy production and the maintenance of essential cellular functions. Excess energy storage is predominantly regulated by the adipose tissue. Primarily made up of adipocytes, adipose tissue acts as the body’s major energy reservoir. The role of adipose tissue, however, is not restricted to a “bag of fat.” The adipose tissue is an endocrine organ, secreting various adipokines, enzymes, growth factors, and hormones that take part in glucose and lipid metabolism. In obesity, the greater portion of the adipose tissue comprises fat, and there is increased pro-inflammatory cytokine secretion, macrophage infiltration, and reduced insulin sensitivity. Obesity contributes to systemic IR and its associated metabolic complications. Similar to adipose tissue, the placenta is also an endocrine organ. During pregnancy, the placenta secretes various molecules to maintain pregnancy physiology. In addition, the placenta plays an important role in metabolism and exchange of nutrients between mother and fetus. Inflammation at the placenta may contribute to the severity of maternal IR and her likelihood of developing GDM and may also mediate the adverse consequences of obesity and GDM on the fetus. Interestingly, studies on maternal insulin sensitivity and secretion of placental hormones have not shown a positive correlation between these phenomena. Recently, a great interest in the field of extracellular vesicles (EVs) has been observed in the literature. EVs are produced by a wide range of cells and are present in all biological fluids. EVs are involved in cell-to-cell communication. Recent evidence points to an association between adipose tissue-derived EVs and metabolic syndrome in obesity. In this review, we will discuss the changes in human placenta and adipose tissue in GDM and obesity and summarize the findings regarding the role of adipose tissue and placenta-derived EVs, with an emphasis on exosomes in obesity, and the contribution of obesity to the development of GDM

Coexpression analysis of large cancer datasets provides insight into the cellular phenotypes of the tumour microenvironment

Background: Biopsies taken from individual tumours exhibit extensive differences in their cellular composition due to the inherent heterogeneity of cancers and vagaries of sample collection. As a result genes expressed in specific cell types, or associated with certain biological processes are detected at widely variable levels across samples in transcriptomic analyses. This heterogeneity also means that the level of expression of genes expressed specifically in a given cell type or process, will vary in line with the number of those cells within samples or activity of the pathway, and will therefore be correlated in their expression.Results: Using a novel 3D network-based approach we have analysed six large human cancer microarray datasets derived from more than 1,000 individuals. Based upon this analysis, and without needing to isolate the individual cells, we have defined a broad spectrum of cell-type and pathway-specific gene signatures present in cancer expression data which were also found to be largely conserved in a number of independent datasets.Conclusions: The conserved signature of the tumour-associated macrophage is shown to be largely-independent of tumour cell type. All stromal cell signatures have some degree of correlation with each other, since they must all be inversely correlated with the tumour component. However, viewed in the context of established tumours, the interactions between stromal components appear to be multifactorial given the level of one component e.g. vasculature, does not correlate tightly with another, such as the macrophage

Magnetic excitations of the charge stripe electrons below half doping in La2−xSrxNiO4 (x = 0.45, 0.4)

The low energy magnetic excitation spectrum of charge stripe ordered La2−xSrxNiO4, x = 0.4 and x = 0.45 were studied by neutron scattering. Two excitation modes are observed in both materials, one from the ordered magnetic moments, and a second mode consistent with pseudo-onedimensional antiferromagnetic excitations of the charge stripe electrons (q-1D). The dispersion of the q-1D excitation follows the same relation as in x = 1/3 composition, with even spectral weight in the two counter-propagating branches of the x = 0.4, however in the x = 0.45 only one dispersion branch has any measurable spectral weight. The evolution of the q-1D excitations on doping to the checkerboard charge ordered phase is discussed

Predictors of hospital surface contamination with Extended-spectrum β-lactamase-producing Escherichia coli and Klebsiella pneumoniae: patient and organism factors

BACKGROUND: The role of the hospital environment in transmission of ESBL-Klebsiella pneumoniae (ESBL-KP) and ESBL-Escherichia coli (ESBL-EC) is poorly defined. Recent data however suggest that in the hospital setting, ESBL-KP is more transmissible than ESBL-EC. We sought therefore to measure the difference in hospital contamination rates between the two species and to identify key risk factors for contamination of the hospital environment with these organisms. METHODS: We systematically sampled 8 surfaces in the rooms and bathrooms of adult patients colonized or infected with ESBL-EC or ESBL-KP throughout their hospital stay. Data were collected on factors potentially affecting contamination rates. Environmental contamination was defined as recovery of an ESBL-producing organism matching the source patient’s isolate. Multivariate logistic regression analysis was performed at the level of the patient visit using generalized estimating equations to identify independent predictors of environmental contamination. RESULTS: 24 patients (11 with ESBL-KP, 11 ESBL-EC and 2 with both organisms) had 1104 swabs collected during 138 visits. The overall contamination rate was 3.4% (38/1104) and was significantly higher for ESBL-KP than ESBL-EC (5.4% versus 0.4%; p < 0.0001). After multivariate analysis, environmental contamination was found to be negatively associated with carbapenem exposure (OR 0.06 [95% CI 0.01-0.61]; p = 0.017) and positively associated with the presence of an indwelling urinary catheter (OR 6.12 [95% CI 1.23-30.37]; p = 0.027) and ESBL-KP in the source patient (OR 26.23 [95% CI 2.70-254.67]; p = 0.005). CONCLUSIONS: Contamination of the hospital environment with ESBL-producing Enterobacteriaceae (ESBL-E) is inversely associated with carbapenem exposure. Predictors of hospital contamination with ESBL-E include: indwelling urinary catheters and ESBL-KP. Rooms of patients with ESBL-KP have substantially higher contamination rates than those with ESBL-EC. This finding may help explain the apparently higher transmissibility of ESBL-KP in the hospital setting

Coordinated dynamic gene expression changes in the central nucleus of the amygdala during alcohol withdrawal.

BACKGROUND: Chronic alcohol use causes widespread changes in the cellular biology of the amygdala\u27s central nucleus (CeA), a GABAergic center that integrates autonomic physiology with the emotional aspects of motivation and learning. While alcohol-induced neurochemical changes play a role in dependence and drinking behavior, little is known about the CeA\u27s dynamic changes during withdrawal, a period of emotional and physiologic disturbance. METHODS: We used a qRT-PCR platform to measure 139 transcripts in 92 rat CeA samples from control (N = 33), chronically alcohol exposed (N = 26), and withdrawn rats (t = 4, 8, 18, 32, and 48 hours; N = 5, 10, 7, 6, 5). This focused transcript set allowed us to identify significant dynamic expression patterns during the first 48 hours of withdrawal and propose potential regulatory mechanisms. RESULTS: Chronic alcohol exposure causes a limited number of small magnitude expression changes. In contrast, withdrawal results in a greater number of large changes within 4 hours of removal of the alcohol diet. Sixty-five of the 139 measured transcripts (47%) showed differential regulation during withdrawal. Over the 48-hour period, dynamic changes in the expression of γ-aminobutyric acid type A (GABA(A) ), ionotropic glutamate and neuropeptide system-related G-protein-coupled receptor subunits, and the Ras/Raf signaling pathway were seen as well as downstream transcription factors (TFs) and epigenetic regulators. Four temporally correlated gene clusters were identified with shared functional roles including NMDA receptors, MAPKKK and chemokine signaling cascades, and mediators of long-term potentiation, among others. Cluster promoter regions shared overrepresented binding sites for multiple TFs including Cebp, Usf-1, Smad3, Ap-2, and c-Ets, suggesting a potential regulatory role. CONCLUSIONS: During alcohol withdrawal, the CeA experiences rapid changes in mRNA expression of these functionally related transcripts that were not predicted by measurement during chronic exposure. This study provides new insight into dynamic expression changes during alcohol withdrawal and suggests novel regulatory relationships that potentially impact the aspects of emotional modulation