Analisis Kandungan Merkuri (Hg) dan Kadar Klorofil Lamun Enhalus Acoroides Di Perairan Marlosso dan Nametek Kabupaten Buru Provinsi Maluku

Seagrass is a type of vegetation that is able to live and develop well in coastal areas and is a habitat for several types of marine animals,such as sea cucumbers, sea urchins, starfish and sea urchins. Seagrass is an organism that is susceptible to pollution of the coastal environment such as mercury (Hg) so that it has an impact on the chlorophyll content of seagrass leaves. This study aims to determine the content of heavy metal Hg and its relationship with the chlorophyll content of seagrass Enhalus acoroides in the waters of Marlosso and Nametek in Buru District Maluku Province. The study was conducted in May 2018 and laboratory analysis was conducted in June 2018. Samples were taken at two stations namely Nametek Beach and Muos Sungai Marlosso. The results showed that the content of heavy metal Hg in roots> rhizoma> seagrass leaves. The content of heavy metals and seagrass chlorophyll content has a negative correlation where the Hg metal has a correlation of (r = - 0.97) and indicates that the higher the content of heavy metals will reduce the seagrass chlorophyll conten

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