Erratum to: One-year follow-up of mud-bath therapy in patients with bilateral knee osteoarthritis: a randomized, single-blind controlled trial

The online version of the original article can be found at http://dx.doi.org/ 10.1007/s00484-14-0943-0

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Retrospective evaluation of patient profiling and effectiveness of apremilast in an Italian multicentric cohort of psoriatic arthritis patients

We aimed to evaluate the baseline characteristics, the reasons for prescription, and the effectiveness/safety profile of real-life apremilast for the treatment of psoriatic arthritis (PsA)

Fauna parasitária de tambaqui Colossoma macropomum (Characidae) cultivado em tanque-rede no estado do Amapá, Amazônia oriental Parasitic fauna of tambaqui Colossoma macropomum(Characidae) farmed in cages in the State of Amapá, eastern Amazon

O objetivo principal deste trabalho foi estudar a parasitofauna e a relação hospedeiro- parasito em tambaqui Colossoma macropomum cultivados em tanques-rede no Rio Matapi, município de Santana, estado do Amapá, região da Amazônia oriental, Brasil. Foram examinados 60 tambaquis, dos quais 96,7% estavam parasitados por protozoários Ichthyophthirius multifiliis (Ciliophora) e Piscinoodinium pillulare (Dinoflagellida), monogenoideas Mymarotheciun boegeri e Anacanthorus spathulatus (Dactylogyridae) e sanguessugas Glossiiphonidae gen. sp. (Hirudinea). Os maiores níveis de parasitismo foram causados por protozoários I. multifiliis e P. pillulare e os menores por sanguessugas Glossiiphonidae gen. sp. Porém, os índices de infestação não tiveram efeitos na saúde dos peixes hospedeiros, uma vez que o fator de condição relativo (Kn) não foi estatisticamente (p<0,05) correlacionado com a intensidade desses parasitos. Este foi o primeiro relato da ocorrência de I. multifiliis e P. pillulare em C. macropomum cultivados em tanques-rede na Amazônia brasileira.<br>The purpose of this paper was to evaluate the parasitic fauna and the host-parasite relationship in Colossoma macropomum farmed in cages of Matapi River, municipally of Santana, State of Amapá, in eastern Amazon, Brazil. Of 60 specimens of tambaqui examined, 96.7% were parasitized by protozoans Ichthyophthirius multifiliis (Ciliophora) and Piscinoodinium pillulare (Dinoflagellida), monogenoideans Mymarotheciun boegeri and Anacanthorus spathulatus (Dactylogyridae), and leeches Glossiphoniidae gen. sp. (Hirudinea). The higher infestation levels were caused by protozoans I. multifiliis and P. pillulare, while the lower infestation levels were caused by leeches. No effects of parasitic infestation rates on fish health were observed. The relative condition factor (Kn) was not correlated with the intensity of parasites found. This was the first record of I. multifiliis and P. pillulare in C. macropomum farmed in cages in the Brazilian Amazon

Whole-genome sequencing reveals host factors underlying critical COVID-19

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes-including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)-in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease