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Adequately powered prospective studies with long-term follow-up are needed to confirm our findings.

Our results suggest that DSM-5 can be used for the initial diagnosis ASD to initiate early intervention for children with this condition in resource-limited set-ups. Adequately powered prospective studies with long-term follow-up are needed to confirm our findings.The susceptibility of children to coronavirus disease-19 (COVID-19) and transmission of COVID-19 from children to others is a relatively unexplored area. The aim of this study was to understand the transmission dynamics of Severe Acute Respiratory Syndrome Coronavirus 2 in children. This was a retrospective observational study where a total of 19 paediatric index cases (including a set of twins) with COVID-19 and 42 primary contacts (adults-36, paediatric-6) from the immediate family members were included. All the index cases and four of the five positive contacts were asymptomatic. Despite adults staying with positive children in the same vehicle, same room in the quarantine centre and the same ward, only four of the parents became positive.

Sleep disorders affect over half of mild traumatic brain injury (mTBI) patients. Despite evidence linking sleep and neurodegeneration, longitudinal TBI-related dementia studies have not considered sleep. We hypothesized that poor sleepers with mTBI would have elevated markers of neurodegeneration and lower cognitive function compared to mTBI good sleepers and controls. Our objective was to compare biomarkers of neurodegeneration and cognitive function with sleep quality in warfighters with chronic mTBI.

In an observational warfighters cohort (n=138 mTBI, 44 controls), the Pittsburgh Sleep Quality Index (PSQI) was compared with plasma biomarkers of neurodegeneration and cognitive scores collected an average of 8 years after injury.

In the mTBI cohort, poor sleepers (PSQI≥10, n = 86) had elevated plasma neurofilament light (NfL, x̅ = 11.86 vs. 7.91 pg/mL, p=0.0007, d=0.63) and lower executive function scores by the categorical fluency (x̅ = 18.0 vs 21.0, p=0.0005, d= -0.65) and stop-go tests (x̅ = 30.1 vs 31.1, p=0.024, d = -0.37). These findings were not observed in controls (n = 44). PSQI predicted NfL (Beta=0.22, p=0.00002) and tau (Beta=0.14, p=0.007), but not amyloid β42. Poor sleepers showed higher obstructive sleep apnea (OSA) risk by STOP-BANG scores (x̅ = 3.8 vs 2.7, p=0.0005), raising the possibility that the PSQI might be partly secondary to OSA.

Poor sleep is linked to neurodegeneration and select measures of executive function in mTBI patients. This supports implementation of validated sleep measures in longitudinal studies investigating pathobiological mechanisms of TBI related neurodegeneration, which could have therapeutic implications.

Poor sleep is linked to neurodegeneration and select measures of executive function in mTBI patients. see more This supports implementation of validated sleep measures in longitudinal studies investigating pathobiological mechanisms of TBI related neurodegeneration, which could have therapeutic implications.Epidemiological studies support a strong link between organ fibrosis and epithelial cancers. Moreover, clinical and experimental investigations consistently indicate that these diseases intertwine and share strikingly overlapping features. As a deregulated response to injury occurring in all body tissues, fibrosis is characterized by activation of fibroblasts and immune cells, contributing to progressive deposition of extracellular matrix (ECM) and inflammation. Cancers are driven by genetic alterations resulting in dysregulated cell survival, proliferation and dissemination. However, non-cancerous components of tumour tissues including fibroblasts, inflammatory cells and ECM play key roles in oncogenesis and cancer progression by providing a pro-mutagenic environment where cancer cells can develop, favouring their survival, expansion and invasiveness. Additional commonalities of fibrosis and cancer are also represented by overproduction of growth factors, like transforming growth factor β, epithelial-to-mesenchymal transition, high oxidative stress, Hippo pathway dysfunctions and enhanced cellular senescence. Here, we review advances in the analysis of cellular and molecular mechanisms involved in the pathogenesis of both organ fibrosis and cancer, with particular reference to chronic kidney diseases and renal cell cancers. Most importantly, improved understanding of common features is contributing to the development of innovative treatment strategies targeting shared mechanisms.Acquired thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease characterized by thrombotic microangiopathy leading to end-organ damage. The standard of care (SOC) treatment is therapeutic plasma exchange (TPE) alongside immunomodulation with steroids, with increasing use of rituximab ± other immunomodulatory agents. The addition of caplacizumab, a nanobody targeting von Willebrand factor, was shown to accelerate platelet count recovery and reduce TPE treatments and hospital length of stay in TTP patients treated in 2 major randomized clinical trials. The addition of caplacizumab to SOC also led to increased bleeding from transient reductions in von Willebrand factor and increased relapse rates. Using data from the 2 clinical trials of caplacizumab, we performed the first-ever cost-effectiveness analysis in TTP. Over a 5-year period, the projected incremental cost-effectiveness ratio (ICER) in our Markov model was $1 482 260, significantly above the accepted 2019 US willingness-to-pay threshold of $195 300. One-way sensitivity analyses showed the utility of the well state and the cost of caplacizumab to have the largest effects on ICER, with a reduction in caplacizumab cost demonstrating the single greatest impact on lowering the ICER. In a probabilistic sensitivity analysis, SOC was favored over caplacizumab in 100% of 10 000 iterations. Our data indicate that the addition of caplacizumab to SOC in treatment of acquired TTP is not cost effective because of the high cost of the medication and its failure to improve relapse rates. The potential impact of caplacizumab on health system cost using longer term follow-up data merits further study.