Apparatus and Method for Harvesting Carbon Nanotube Arrays

An apparatus is provided for harvesting a carbon nanotube array from a substrate. The apparatus includes a peeler that peels the carbon nanotube array from the substrate and a support that receives the carbon nanotube array peeled from the substrate. In addition the apparatus includes a drawing device that simultaneously draws the carbon nanotube array from the substrate onto the support as the carbon nanotube array is peeled from the substrate. The peeler and drawing device are synchronized in operation so that as a given length of carbon nanotube array is peeled from the substrate, that same given length of carbon nanotube array is drawn onto the support

Thermal Interface Material

A flexible sheet of aligned carbon nanotubes includes an array of aligned nanotubes in a free standing film form not adhered to the synthesis substrate, with a matrix infiltrated interstitially into the nanotube array with access to the nanotube tips from both the top and bottom. That is, the infiltrant is purposely limited from over-filling or coating one or both exterior top and/or bottom surfaces of the array, blocking access to the tips. A typical matrix is a polymer material

High resolution imaging of the M​L​ 2.9 August 2019 earthquake in Lancashire, UK, induced by hydraulic fracturing during Preston New Road PNR-2 operations

Hydraulic fracturing (HF) at Preston New Road (PNR), Lancashire, United Kingdom, in August 2019, induced a number of felt earthquakes. The largest event (⁠ML 2.9) occurred on 26 August 2019, approximately three days after HF operations at the site had stopped. Following this, in November 2019, the United Kingdom Government announced a moratorium on HF for shale gas in England. Here we provide an analysis of the microseismic observations made during this case of HF‐induced fault activation. More than 55,000 microseismic events were detected during operations using a downhole array, the vast majority measuring less than Mw 0. Event locations revealed the growth of hydraulic fractures and their interaction with several preexisting structures. The spatiotemporal distribution of events suggests that a hydraulic pathway was created between the injection points and a nearby northwest–southeast‐striking fault, on which the largest events occurred. The aftershocks of the ML 2.9 event clearly delineate the rupture plane, with their spatial distribution forming a halo of activity around the mainshock rupture area. Across clusters of events, the magnitude distributions are distinctly bimodal, with a lower Gutenberg–Richter b‐value for events above Mw 0, suggesting a break in scaling between events associated with hydraulic fracture propagation, and events associated with activation of the fault. This poses a challenge for mitigation strategies that rely on extrapolating microseismicity observed during injection to forecast future behavior. The activated fault was well oriented for failure in the regional stress field, significantly more so than the fault activated during previous operations at PNR in 2018. The differing orientations within the stress field likely explain why this PNR‐2 fault produced larger events compared with the 2018 sequence, despite receiving a smaller volume of injected fluid. This indicates that fault orientation and in situ stress conditions play a key role in controlling the severity of seismicity induced by HF

A UK Specification for Trusted Research Environments

ObjectivesThe need for Trusted Research Environments (TREs) is clear. Several influential reports have highlighted that personal or sensitive data which have been collected for operational, commercial or governmental reasons need to be managed securely in an environment that encourages best practices.TREs are designed to enable only authorised projects and researchers access to sensitive data whilst minimising risk of data exposure. Yet the TRE landscape has grown organically over at least the last decade resulting in heterogeneous environments, making it harder for data to be discovered, shared and used for public benefit.A baseline specification for TREs is required

Heaviness, health and happiness: a cross-sectional study of 163 066 UK Biobank participants

<b>Background</b><p></p> Obesity is known to increase the risk of many diseases and reduce overall quality of life. This study examines the relationship with self-reported health (SRH) and happiness.<p></p> <b>Methods</b> <p></p>We conducted a cross-sectional study of the 163 066 UK Biobank participants who completed the happiness rating. The association between adiposity and SRH and happiness was examined using logistic regression. SRH was defined as good (excellent, good), or poor (fair, poor). Self-reported happiness was defined as happy (extremely, very, moderately) or unhappy (moderately, very, extremely). <p></p> <b>Results</b> <p></p>Poor health was reported by 44 457 (27.3%) participants. The adjusted ORs for poor health were 3.86, 2.92, 2.60 and 6.41 for the highest, compared with lowest, deciles of Body Mass Index, waist circumference, waist to hip ratio and body fat percent, respectively. The associations were stronger in men (p<0.001). Overall, 7511 (4.6%) participants felt unhappy, and only class III obese participants were more likely to feel unhappy (adjusted OR 1.33, 95% CI 1.15 to 1.53, p<0.001) but the associations differed by sex (p<0.001). Among women, there was a significant association between unhappiness and all levels of obesity. By contrast, only class III obese men had significantly increased risk and overweight and class I obese men were less likely to be unhappy. <p></p> <b>Conclusions</b><p></p>Obesity impacts adversely on happiness as well as health, but the association with unhappiness disappeared after adjustment for self-reported health, indicating this may be mediated by health. Compared with obese men, obese women are less likely to report poor health, but more likely to feel unhappy. <p></p&gt

Gender differences in the association between adiposity and probable major depression: a cross-sectional study of 140,564 UK Biobank participants

<b>Background</b><p></p> Previous studies on the association between adiposity and mood disorder have produced contradictory results, and few have used measurements other than body mass index (BMI). We examined the association between probable major depression and several measurements of adiposity: BMI, waist circumference (WC), waist-hip-ratio (WHR), and body fat percentage (BF%).<p></p> <b>Methods</b><p></p> We conducted a cross-sectional study using baseline data on the sub-group of UK Biobank participants who were assessed for mood disorder. Multivariate logistic regression models were used, adjusting for potential confounders including: demographic and life-style factors, comorbidity and psychotropic medication.<p></p> <b>Results</b><p></p> Of the 140,564 eligible participants, evidence of probable major depression was reported by 30,145 (21.5%). The fully adjusted odds ratios (OR) for obese participants were 1.16 (95% confidence interval (CI) 1.12, 1.20) using BMI, 1.15 (95% CI 1.11, 1.19) using WC, 1.09 (95% CI 1.05, 1.13) using WHR and 1.18 (95% CI 1.12, 1.25) using BF% (all p <0.001). There was a significant interaction between adiposity and gender (p = 0.001). Overweight women were at increased risk of depression with a dose response relationship across the overweight (25.0-29.9 kg/m2), obese I (30.0-34.9 kg/m2), II (35.0-39.9 kg/m2) and III (≥40.0 kg/m2) categories; fully adjusted ORs 1.14, 1.20, 1.29 and 1.48, respectively (all p < 0.001). In contrast, only obese III men had significantly increased risk of depression (OR 1.29, 95% CI 1.08, 1.54, p = 0.006).<p></p> <b>Conclusion</b><p></p> Adiposity was associated with probable major depression, irrespective of the measurement used. The association was stronger in women than men. Physicians managing overweight and obese women should be alert to this increased risk

Rare copy number variants: a point of rarity in genetic risk for bipolar disorder and schizophrenia

Context: Recent studies suggest that copy number variation in the human genome is extensive and may play an important role in susceptibility to disease, including neuropsychiatric disorders such as schizophrenia and autism. The possible involvement of copy number variants (CNVs) in bipolar disorder has received little attention to date. Objectives: To determine whether large (>100 000 base pairs) and rare (found in <1% of the population) CNVs are associated with susceptibility to bipolar disorder and to compare with findings in schizophrenia. Design: A genome-wide survey of large, rare CNVs in a case-control sample using a high-density microarray. Setting: The Wellcome Trust Case Control Consortium. Participants: There were 1697 cases of bipolar disorder and 2806 nonpsychiatric controls. All participants were white UK residents. Main Outcome Measures: Overall load of CNVs and presence of rare CNVs. Results: The burden of CNVs in bipolar disorder was not increased compared with controls and was significantly less than in schizophrenia cases. The CNVs previously implicated in the etiology of schizophrenia were not more common in cases with bipolar disorder. Conclusions: Schizophrenia and bipolar disorder differ with respect to CNV burden in general and association with specific CNVs in particular. Our data are consistent with the possibility that possession of large, rare deletions may modify the phenotype in those at risk of psychosis: those possessing such events are more likely to be diagnosed as having schizophrenia, and those without them are more likely to be diagnosed as having bipolar disorder

The Cerebral Microvasculature in Schizophrenia: A Laser Capture Microdissection Study

BACKGROUND: Previous studies of brain and peripheral tissues in schizophrenia patients have indicated impaired energy supply to the brain. A number of studies have also demonstrated dysfunction of the microvasculature in schizophrenia patients. Together these findings are consistent with a hypothesis of blood-brain barrier dysfunction in schizophrenia. In this study, we have investigated the cerebral vascular endothelium of schizophrenia patients at the level of transcriptomics. METHODOLOGY/PRINCIPAL FINDINGS: We used laser capture microdissection to isolate both microvascular endothelial cells and neurons from post mortem brain tissue from schizophrenia patients and healthy controls. RNA was isolated from these cell populations, amplified, and analysed using two independent microarray platforms, Affymetrix HG133plus2.0 GeneChips and CodeLink Whole Human Genome arrays. In the first instance, we used the dataset to compare the neuronal and endothelial data, in order to demonstrate that the predicted differences between cell types could be detected using this methodology. We then compared neuronal and endothelial data separately between schizophrenic subjects and controls. Analysis of the endothelial samples showed differences in gene expression between schizophrenics and controls which were reproducible in a second microarray platform. Functional profiling revealed that these changes were primarily found in genes relating to inflammatory processes. CONCLUSIONS/SIGNIFICANCE: This study provides preliminary evidence of molecular alterations of the cerebral microvasculature in schizophrenia patients, suggestive of a hypo-inflammatory state in this tissue type. Further investigation of the blood-brain barrier in schizophrenia is warranted

Exome sequencing in bipolar disorder identifies AKAP11 as a risk gene shared with schizophrenia

We report results from the Bipolar Exome (BipEx) collaboration analysis of whole-exome sequencing of 13,933 patients with bipolar disorder (BD) matched with 14,422 controls. We find an excess of ultra-rare protein-truncating variants (PTVs) in patients with BD among genes under strong evolutionary constraint in both major BD subtypes. We find enrichment of ultra-rare PTVs within genes implicated from a recent schizophrenia exome meta-analysis (SCHEMA; 24,248 cases and 97,322 controls) and among binding targets of CHD8. Genes implicated from genome-wide association studies (GWASs) of BD, however, are not significantly enriched for ultra-rare PTVs. Combining gene-level results with SCHEMA, AKAP11 emerges as a definitive risk gene (odds ratio (OR) = 7.06, P = 2.83 × 10-9). At the protein level, AKAP-11 interacts with GSK3B, the hypothesized target of lithium, a primary treatment for BD. Our results lend support to BD's polygenicity, demonstrating a role for rare coding variation as a significant risk factor in BD etiology