CT dose reduction factors in the thousands using X-ray phase contrast

Phase-contrast X-ray imaging can improve the visibility of weakly absorbing objects (e.g. soft tissues) by an order of magnitude or more compared to conventional radiographs. Previously, it has been shown that combining phase retrieval with computed tomography (CT) can increase the signal-to-noise ratio (SNR) by up to two orders of magnitude over conventional CT at the same radiation dose, without loss of image quality. Our experiments reveal that as radiation dose decreases, the relative improvement in SNR increases. We discovered this enhancement can be traded for a reduction in dose greater than the square of the gain in SNR. Upon reducing the dose 300 fold, the phase-retrieved SNR was still almost 10 times larger than the absorption contrast data. This reveals the potential for dose reduction factors in the tens of thousands without loss in image quality, which would have a profound impact on medical and industrial imaging applications

Did Medicaid Expansion Close African American-white Health Care Disparities Nationwide? A Scoping Review

Objectives: To investigate the impact of the Affordable Care Act’s (ACA) Medicaid expansion on African Americanwhite disparities in health coverage, access to healthcare, receipt of treatment, and health outcomes. Design: A search of research reports, following the PRISMA-ScR guidelines, identified twenty-six national studies investigating changes in health care disparities between African American and white non-disabled, non-elderly adults before and after ACA Medicaid expansion, comparing states that did and did not expand Medicaid. Analysis examined research design and findings. Results: Whether Medicaid eligibility expansion reduced African American-white health coverage disparities remains an open question: Absolute disparities in coverage appear to have declined in expansion states, although exceptions have been reported. African American disparities in health access, treatment, or health outcomes showed little evidence of change for the general population. Conclusions: Future research addressing key weaknesses in existing research may help to uncover sources of continuing disparities and clarify the impact of future Medicaid expansion on African American health care disparities

PiFM and XPS Studies of Porous TiO2 Films for the Photocatalytic Decomposition of Polystyrene

The rate of photocatalytic oxidation of polystyrene over 0.1 wt% copper-doped TiO2 catalyst spin coated onto a flat substrate is investigated as a function of the catalyst deposition spin speed and, hence, film thickness. Photoinduced force microscopy and photoelectron spectroscopy show no evidence of any products of the photocatalytic oxidation remaining on the surface after reaction. The oxidation reaction shows no discernible dependence on spin speed; it is close to zero order in polystyrene concentration and exhibits a ½ life almost 50 times greater than the equivalent photocatalytic oxidation of stearic acid on the same catalysts. No difference between the rate of decay of the aliphatic and aromatic hydrogens of the polymer was observed, suggesting that once a polymer chain begins oxidising, subsequent steps are relatively rapid. This is consistent with the rate-determining step being dependent on the extent of coordination to the surface, which is much more favourable with stearic acid because of its carboxylic group

The role of Cu and film thickness on the photocatalytic activity of mesoporous spin coated TiO2 films

Most practical applications of photocatalysts will involve coatings on an inert support; here we have examined how copper doping of spin coated porous TiO2 films affects their physical characteristics and photocatalytic activity. The photocatalytic degradation of stearic acid was used as a measure of photocatalytic activity for catalysts spin coated from a sol-gel onto glass with 0, 0.1, 0.5, 1, 2.5 and 5 wt% copper introduced into the catalyst lattice before gelation. The effects of spin coating speed on film thickness, structure and band gap were studied and the nature of the copper incorporated into the films examined with XPS and XANES measurements. Increased spin coating speeds reduces the thickness of the deposited films from ∼ 50 μm to ∼ 20 μm until a spin speed of ∼ 3000 rpm at which point non-Newtonian behaviour of the gels prevents further reductions in film thickness. A larger effect on film thickness is the presence of the added copper nitrate which results in thinner films. After calcining, XANES shows the bulk of the copper to be in a Cu(II) state but at the surface of the thinnest, most active films XPS shows only Cu(I). Photocatalytic activity is much more strongly affected by the presence of the copper than the thickness of the films with 0.1 wt% Cu catalysts as much as 10 times more active than the undoped catalysts. Increasing the copper content, however, reduces activity until at ∼ 5 wt% activity is lower than for the pure TiO2 films

Service user experiences of REFOCUS: a process evaluation of a pro-recovery complex intervention

Purpose: Policy is increasingly focused on implementing a recovery-orientation within mental health services, yet the subjective experience of individuals receiving a pro-recovery intervention is under-studied. The aim of this study was to explore the service user experience of receiving a complex, pro-recovery intervention (REFOCUS), which aimed to encourage the use of recovery-supporting tools and support recovery-promoting relationships. Methods: Interviews (n=24) and two focus groups (n=13) were conducted as part of a process evaluation and included purposive sample of service users who received the complex, pro-recovery intervention within the REFOCUS randomised controlled trial (ISRCTN02507940). Thematic analysis was used to analyse the data. Results: Participants reported that the intervention supported the development of an open and collaborative relationship with staff, with new conversations around values, strengths and goals. This was experienced as hope-inspiring and empowering. However, others described how the recovery tools were used without context, meaning participants were unclear of their purpose and did not see their benefit. During the interviews, some individuals struggled to report any new tasks or conversations occurring during the intervention. Conclusion: Recovery-supporting tools can support the development of a recovery-promoting relationship, which can contribute to positive outcomes for individuals. The tools should be used, in a collaborative and flexible manner. Information exchanged around values, strengths and goals should be used in care-planning. As some service users struggled to report their experience of the intervention, alternative evaluation approaches need to be considered if the service user experience is to be fully captured

Intentional injury reported by young people in the Federated States of Micronesia, Kingdom of Tonga and Vanuatu

<p>Abstract</p> <p>Background</p> <p>Intentional injury presents a threat to the physical and psychological well being of young people, especially in developing countries, which carry the greatest part of the global injury burden. While the importance of this problem is recognized, there are limited population data in low and middle income countries that can guide public health action. The present study investigates the prevalence and distribution of intentional injury among young people in three Pacific Island societies, and examines behavioural and psychosocial factors related to risk of intentional injury.</p> <p>Methods</p> <p>Population surveys were conducted with <b>s</b>tudents aged 11–17 years in Pohnpei State in the Federated States of Micronesia (n = 1495), the Kingdom of Tonga (n = 2808) and Vanuatu (n = 4474). Surveys measured self-reported injury and intentional injury, sources of intentional injury, and the range of behavioural, psychological, educational and social variables that may be related to injury risk.</p> <p>Results</p> <p>Among boys and girls aged 14–17 years the respective period prevalence of intentional injury was 62% and 56% in Pohnpei, 58% and 41% in Tonga, and 33% and 24% in Vanuatu. The prevalence of intentional injury declined with age in Tonga and Vanuatu, but there was little evidence of an age-trend in Pohnpei. Across the three societies, the major sources of intentional injury among boys were 'other persons' followed by boyfriends/girlfriends and fathers. Mothers, boyfriends/girlfriends and other persons were primary sources of injury among girls. An intentional injury was reported more often by those who had been bullied (OR 1.40–1.66, P < 0.05), by regular smokers in Tonga and Vanuatu (OR 1.52–2.21, P < 0.05), and illicit drug users in Pohnpei and Vanuatu (OR 1.87–1.92, P < 0.05).</p> <p>Conclusion</p> <p>Intentional injury was reported extensively in these three populations. Interventions directed towards the school environment and which take into account the role of bullying and drug use need to be considered.</p

SARS-CoV-2 breakthrough infections among vaccinated individuals with rheumatic disease : Results from the COVID-19 Global Rheumatology Alliance provider registry

Funding Information: members of the COVID-19 Global Rheumatology Alliance and do not necessarily represent the views of the American College of Rheumatology (ACR), EULAR, the UK National Health Service (NHS), the National Institute for Health Research (NIHR), the UK Department of Health or any other organisation. Competing interests KLH reports she has received non-personal speaker’s fees from AbbVie and grant income from BMS, UCB and Pfizer, all unrelated to this manuscript; KLH is supported by the NIHR Manchester Biomedical Research Centre. LG reports personal consultant fees from AbbVie, Amgen, BMS, Biogen, Celgene, Gilead, Janssen, Lilly, Novartis, Pfizer, Samsung Bioepis, Sanofi-Aventis and UCB, and grants from Amgen, Lilly, Janssen, Pfizer, Sandoz, Sanofi and Galapagos, all unrelated to this manuscript. AS reports research grants from a consortium of 14 companies (among them AbbVie, BMS, Celltrion, Fresenius Funding Information: Kabi, Gilead/Galapagos, Lilly, Mylan/Viatris, Hexal, MSD, Pfizer, Roche, Samsung, Sanofi-Aventis and UCB) supporting the German RABBIT register and personal fees from lectures for AbbVie, MSD, Roche, BMS, Lilly and Pfizer, all unrelated to this manuscript. LC has not received fees or personal grants from any laboratory, but her institute works by contract for laboratories among other institutions, such as AbbVie Spain, Eisai, Gebro Pharma, Merck Sharp & Dohme España, Novartis Farmaceutica, Pfizer, Roche Farma, Sanofi-Aventis, Astellas Pharma, Actelion Pharmaceuticals España, Grünenthal and UCB Pharma. EF-M reports personal consultant fees from Boehringer Ingelheim Portugal and that LPCDR received support for specific activities: grants from AbbVie, Novartis, Janssen-Cilag, Lilly Portugal, Sanofi, Grünenthal, MSD, Celgene, Medac, Pharmakern and GAfPA; grants and non-financial support from Pfizer; and non-financial support from Grünenthal, outside the submitted work. IB reports personal consultant fees from AbbVie, Novartis, Pfizer and Janssen, all unrelated to this manuscript. JZ reports speaker fees from AbbVie, Novartis and Janssen/Johnson & Johnson, all unrelated to this manuscript. GR-C reports personal consultant fees from Eli Lilly and Novartis, all unrelated to this manuscript. JS is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant numbers: R01 AR077607, P30 AR070253 and P30 AR072577), and the R Bruce and Joan M Mickey Research Scholar Fund. JS has received research support from Amgen and Bristol Myers Squibb and performed consultancy for Bristol Myers Squibb, Gilead, Inova, Janssen and Optum, unrelated to this work. LW receives speaker’s bureau fees from Aurinia Pharma, unrelated to this manuscript. SB reports no competing interests related to this work. He reports non-branded consulting fees for AbbVie, Horizon and Novartis (all <$10 000). MGM has no competing interests related to this work. She serves as a patient consultant for BMS, BI JNJ and Aurinia (all <$10 000). RG reports no competing interests related to this work. Outside of this work she reports personal and/or speaking fees from AbbVie, Janssen, Novartis, Pfizer and Cornerstones and travel assistance from Pfizer (all <$10 000). JH reports no competing interests related to this work. He is supported by grants from the Rheumatology Research Foundation and has salary support from the Childhood Arthritis and Rheumatology Research Alliance. He has performed consulting for Novartis, Sobi and Biogen, all unrelated to this work (<$10 000). ESi reports non-financial support from Canadian Arthritis Patient Alliance, outside the submitted work. PS reports personal fees from the American College of Rheumatology/Wiley Publishing, outside the submitted work. ZW reports grant support from Bristol Myers Squibb and Principia/Sanofi and performed consultancy for Viela Bio and MedPace, outside the submitted work. His work is supported by grants from the National Institutes of Health. PMM has received consulting/speaker’s fees from AbbVie, BMS, Celgene, Eli Lilly, Galapagos, Janssen, MSD, Novartis, Orphazyme, Pfizer, Roche and UCB, all unrelated to this study. PMM is supported by the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre (BRC). PCR reports no competing interests related to this work. Outside of this work PCR reports personal fees from AbbVie, Atom Bioscience, Eli Lilly, Gilead, GlaxoSmithKline, Janssen, Kukdong, Novartis, UCB, Roche and Pfizer; meeting attendance support from BMS, Pfizer and UCB; and grant funding from Janssen, Novartis, Pfizer and UCB Pharma (all <$10 000). JY reports no competing interests related to this work. Her work is supported by grants from the National Institutes of Health (K24 AR074534 and P30 AR070155). Outside of this work, she has received research grants or performed consulting for Gilead, BMS Foundation, Pfizer, Aurinia and AstraZeneca. Funding Information: Twitter Jean Liew @rheum_cat, Loreto Carmona @carmona_loreto, Pedro M Machado @pedrommcmachado and Philip C Robinson @philipcrobinson Contributors All authors contributed to the study design, data collection, interpretation of results and review/approval of the final submitted manuscript. JL and MG are guarantors for this manuscript. Funding MG reports grants from the National Institutes of Health, NIAMS, outside the submitted work. KLH is supported by the NIHR Manchester Biomedical Research Centre. JS is supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grant numbers: R01 AR077607, P30 AR070253 and P30 AR072577), and the R Bruce and Joan M Mickey Research Scholar Fund. JH is supported by grants from the Rheumatology Research Foundation. ZW is supported by grants from the National Institutes of Health. PMM is supported by the National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre (BRC). JY is supported by grants from the National Institutes of Health (K24 AR074534 and P30 AR070155). Publisher Copyright: ©Objective. While COVID-19 vaccination prevents severe infections, poor immunogenicity in immunocompromised people threatens vaccine effectiveness. We analysed the clinical characteristics of patients with rheumatic disease who developed breakthrough COVID-19 after vaccination against SARS-CoV-2.  Methods. We included people partially or fully vaccinated against SARS-CoV-2 who developed COVID-19 between 5 January and 30 September 2021 and were reported to the Global Rheumatology Alliance registry. Breakthrough infections were defined as occurring ≥14 days after completion of the vaccination series, specifically 14 days after the second dose in a two-dose series or 14 days after a single-dose vaccine. We analysed patients' demographic and clinical characteristics and COVID-19 symptoms and outcomes. Results SARS-CoV-2 infection was reported in 197 partially or fully vaccinated people with rheumatic disease (mean age 54 years, 77% female, 56% white). The majority (n=140/197, 71%) received messenger RNA vaccines. Among the fully vaccinated (n=87), infection occurred a mean of 112 (±60) days after the second vaccine dose. Among those fully vaccinated and hospitalised (n=22, age range 36-83 years), nine had used B cell-depleting therapy (BCDT), with six as monotherapy, at the time of vaccination. Three were on mycophenolate. The majority (n=14/22, 64%) were not taking systemic glucocorticoids. Eight patients had pre-existing lung disease and five patients died. Conclusion. More than half of fully vaccinated individuals with breakthrough infections requiring hospitalisation were on BCDT or mycophenolate. Further risk mitigation strategies are likely needed to protect this selected high-risk population.publishersversionPeer reviewe

Camurati-Engelmann Disease: Unique Variant Featuring a Novel Mutation in TGFβ1 Encoding Transforming Growth Factor Beta 1 and a Missense Change in TNFSF11 Encoding RANK Ligand

We report a 32-year-old man and his 59-year-old mother with a unique and extensive variant of Camurati-Engelmann disease (CED) featuring histopathological changes of osteomalacia and alterations within TGFβ1 and TNFSF11 encoding TGFβ1 and RANKL, respectively. He suffered leg pain and weakness since childhood and reportedly grew until his late 20s, reaching 7 feet in height. He had deafness, perforated nasal septum, torus palatinus, disproportionately long limbs with knock-knees, low muscle mass, and pseudoclubbing. Radiographs revealed generalized skeletal abnormalities, including wide bones and cortical and trabecular bone thickening in keeping with CED, except that long bone ends were also affected. Lumbar spine and hip BMD Z-scores were + 7.7 and + 4.4, respectively. Biochemical markers of bone turnover were elevated. Hypocalciuria accompanied low serum 25-hydroxyvitamin D (25[OH]D) levels. Pituitary hypogonadism and low serum insulin-like growth factor (IGF)-1 were present. Karyotype was normal. Despite vitamin D repletion, iliac crest histology revealed severe osteomalacia. Exon 1 of TNFRSF11A (RANK), exons 2, 3, and 4 of LRP5, and all coding exons and adjacent mRNA splice junctions of TNFRSF11B (OPG), SQSTM1 (sequestosome 1), and TNSALP (tissue nonspecific alkaline phosphatase) were intact. His asymptomatic and less dysmorphic 5′11″ mother, also with low serum 25(OH)D, had milder clinical, radiological, biochemical, and histopathological findings. Both individuals were heterozygous for a novel 12-bp duplication (c.27_38dup, p.L10_L13dup) in exon 1 of TGFβ1, predicting four additional leucine residues in the latency-associated-peptide segment of TGFβ1, consistent with CED. The son was also homozygous for a single base transversion in TNFSF11, predicting a nonconservative amino acid change (c.107C > G, p.Pro36Arg) in the intracellular domain of RANKL that was heterozygous in his nonconsanguineous parents. This TNFSF11 variant was not found in the SNP Database, nor in published TNFSF11 association studies, but it occurred in four of the 134 TNFSF11 alleles (3.0%) we tested randomly among individuals without CED. Perhaps the unique phenotype of this CED family is conditioned by altered RANKL activity. © 2011 American Society for Bone and Mineral Research

Genome-wide association studies of autoimmune vitiligo identify 23 new risk loci and highlight key pathways and regulatory variants

Vitiligo is an autoimmune disease in which depigmented skin results from the destruction of melanocytes1, with epidemiological association with other autoimmune diseases2. In previous linkage and genome-wide association studies (GWAS1 and GWAS2), we identified 27 vitiligo susceptibility loci in patients of European ancestry. We carried out a third GWAS (GWAS3) in European-ancestry subjects, with augmented GWAS1 and GWAS2 controls, genome-wide imputation, and meta-analysis of all three GWAS, followed by an independent replication. The combined analyses, with 4,680 cases and 39,586 controls, identified 23 new significantly associated loci and 7 suggestive loci. Most encode immune and apoptotic regulators, with some also associated with other autoimmune diseases, as well as several melanocyte regulators. Bioinformatic analyses indicate a predominance of causal regulatory variation, some of which corresponds to expression quantitative trait loci (eQTLs) at these loci. Together, the identified genes provide a framework for the genetic architecture and pathobiology of vitiligo, highlight relationships with other autoimmune diseases and melanoma, and offer potential targets for treatment