A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (me/cfs) and sickness behavior

It is of importance whether myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a variant of sickness behavior. The latter is induced by acute infections/injury being principally mediated through proinflammatory cytokines. Sickness is a beneficial behavioral response that serves to enhance recovery, conserves energy and plays a role in the resolution of inflammation. There are behavioral/symptomatic similarities (for example, fatigue, malaise, hyperalgesia) and dissimilarities (gastrointestinal symptoms, anorexia and weight loss) between sickness and ME/CFS. While sickness is an adaptive response induced by proinflammatory cytokines, ME/CFS is a chronic, disabling disorder, where the pathophysiology is related to activation of immunoinflammatory and oxidative pathways and autoimmune responses. While sickness behavior is a state of energy conservation, which plays a role in combating pathogens, ME/CFS is a chronic disease underpinned by a state of energy depletion. While sickness is an acute response to infection/injury, the trigger factors in ME/CFS are less well defined and encompass acute and chronic infections, as well as inflammatory or autoimmune diseases. It is concluded that sickness behavior and ME/CFS are two different conditions

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

Meeting abstrac

Tractography of developing white matter of the internal capsule and corpus callosum in very preterm infants

To investigate in preterm infants associations between Diffusion Tensor Imaging (DTI) parameters of the posterior limb of the internal capsule (PLIC) and corpus callosum (CC) and age, white matter (WM) injury and clinical factors. In 84 preterm infants DTI was performed between 40-62 weeks postmenstrual age on 3 T MR. Fractional anisotropy (FA), apparent diffusion coefficient (ADC) values and fibre lengths through the PLIC and the genu and splenium were determined. WM injury was categorised as normal/mildly, moderately and severely abnormal. Associations between DTI parameters and age, WM injury and clinical factors were analysed. A positive association existed between FA and age at imaging for fibres through the PLIC (r = 0.48 p < 0.001) and splenium (r = 0.24 p < 0.01). A negative association existed between ADC and age at imaging for fibres through the PLIC (r = -0.65 p < 0.001), splenium (r = -0.35 p < 0.001) and genu (r = -0.53 p < 0.001). No association was found between DTI parameters and gestational age, degree of WM injury or categorical clinical factors. These results indicate that in our cohort of very preterm infants, at this young age, the development of the PLIC and CC is ongoing and independent of the degree of prematurity or WM injury.Neuro Imaging Researc

How accurate is an LCD screen version of the Pelli–Robson test?

Purpose: To evaluate the accuracy and repeatability of a computer-generated Pelli–Robson test displayed on liquid crystal display (LCD) systems compared to a standard Pelli–Robson chart. Methods: Two different randomized crossover experiments were carried out for two different LCD systems for 32 subjects: 6 females and 10 males (40.5 ± 13.0 years) and 9 females and 7 males (27.8 ± 12.2 years), respectively, in the first and second experiment. Two repeated measurements were taken with the printed Pelli–Robson test and with the LCDs at 1 and 3 m. To test LCD reliability, measurements were repeated after 1 week. Results: In Experiment 1, contrast sensitivity (CS) measured with LCD1 resulted significantly higher than Pelli–Robson both at 1 and at 3 m of about 0.20 log 1/C in both eyes (p < 0.01). Bland–Altman plots showed a proportional bias for LCD1 measures. LCD1 measurements showed reasonable repeatability: ICC was 0.83 and 0.65 at 1 and 3 m, respectively. In Experiment 2, CS measured with LCD2 resulted significantly lower than Pelli–Robson both at 1 and at 3 m of about 0.10 log 1/C in both eyes (p < 0.01). Bland–Altman plots did not show any proportional bias for LCD2 measures. LCD2 measurements showed sufficient repeatability: ICC resulted 0.51 and 0.65 at 1 and 3 m, respectively. Conclusions: Computer-generated versions of Pelli–Robson test, displayed on LCD systems, do not provide accurate results compared to classic Pelli–Robson printed version. Clinicians should consider that Pelli–Robson computer-generated versions could be non-interchangeable to the printed version

Lack of the Long Pentraxin PTX3 Promotes Autoimmune Lung Disease but not Glomerulonephritis in Murine Systemic Lupus Erythematosus

The long pentraxin PTX3 has multiple roles in innate immunity. For example, PTX3 regulates C1q binding to pathogens and dead cells and regulates their uptake by phagocytes. It also inhibits P-selectin-mediated recruitment of leukocytes. Both of these mechanisms are known to be involved in autoimmunity and autoimmune tissue injury, e.g. in systemic lupus erythematosus, but a contribution of PTX3 is hypothetical. To evaluate a potential immunoregulatory role of PTX3 in autoimmunity we crossed Ptx3-deficient mice with Fas-deficient (lpr) C57BL/6 (B6) mice with mild lupus-like autoimmunity. PTX3 was found to be increasingly expressed in kidneys and lungs of B6lpr along disease progression. Lack of PTX3 impaired the phagocytic uptake of apoptotic T cells into peritoneal macrophages and selectively expanded CD4/CD8 double negative T cells while other immune cell subsets and lupus autoantibody production remained unaffected. Lack of PTX3 also aggravated autoimmune lung disease, i.e. peribronchial and perivascular CD3+ T cell and macrophage infiltrates of B6lpr mice. In contrast, histomorphological and functional parameters of lupus nephritis remained unaffected by the Ptx3 genotype. Together, PTX3 specifically suppresses autoimmune lung disease that is associated with systemic lupus erythematosus. Vice versa, loss-of-function mutations in the Ptx3 gene might represent a genetic risk factor for pulmonary (but not renal) manifestations of systemic lupus or other autoimmune diseases

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale(1-3). Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter(4); identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation(5,6); analyses timings and patterns of tumour evolution(7); describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity(8,9); and evaluates a range of more-specialized features of cancer genomes(8,10-18).Peer reviewe

Recent progress in iron oxide based photoanodes for solar water splitting

Solar assisted water splitting in a PEC is an attractive concept to store solar energy as hydrogen fuel but the effective efficiency of the process is too low for it to be a serious contender for commercialization. The most important component of the PEC to achieve efficient water splitting is a photo active anode that could effectively absorb photons and deliver holes for the oxygen evolution reaction. Hematite has many attributes that make it a good candidate material for a photoanode but it also has some deficiencies. This article reviews the state-of-the-art hematite-based photoanodes, with special emphasis on attempts made by researchers to overcome its drawbacks. The numerous research reports are categorized under distinct strategies such as nanostructuring, elemental doping, surface passivation, cocatalyst application, conducting template incorporation and heterostructures which are possible pathways to improve the performance of hematite. The scientific understandings of the operating mechanisms for each strategy are systematically presented and discussed, and the improvements achieved by different approaches are compared. Some cutting-edge strategies, such as heterojunctions, could be important and hematite based heterostructures are discussed. A developing interest in an emerging material, Fe2TiO5 is also discussed and some of the important benefits of this material are presented. Finally, the importance of scaling up the technology is discussed and attention is drawn to some possible challenges on scaling up. The paper concludes with some future technology directions and prospects for hematite-based photoanodes