University of Western Australia

About: University of Western Australia is a education organization based out in Perth, Western Australia, Australia. It is known for research contribution in the topics: Population & Poison control. The organization has 29613 authors who have published 87405 publications receiving 3064466 citations. The organization is also known as: UWA & University of WA.

Function of nutrients: micronutrients

Abstract: Publisher Summary This chapter focuses on the functions of iron, manganese, copper, zinc, nickel, molybdenum, boron, and chlorine in plants and describes the effects of their deficiency and toxicity. Iron (Fe) plays a crucial role in redox systems in cells and in various enzymes. In dicotyledonous and monocotyledonous plant species, Fe deficiency is associated with the formation of rhizodermal transfer cells, which is a part of a their strategy to enhance iron uptake. Manganese (Mn) and copper (Cu) are important for redox systems, as activators of various enzymes including those involved in the detoxification of superoxide radicals, and for the synthesis of lignin. In dicotyledonous plants, intercostal chlorosis of the younger leaves is the most distinct symptom of Mn deficiency, whereas in cereals, greenish grey spots on the older leaves are the major symptoms. Stunted growth, distortion of young leaves, chlorosis/ necrosis starting at the apical meristem extending down to the leaf margins, bleaching of young leaves, and/or “summer dieback” in trees are typical visible symptoms of Cu deficiency. Zinc (Zn) plays a role in the detoxification of superoxide radicals, membrane integrity, as well as the synthesis of proteins and the phytohormone IAA. Nickel (Ni) is involved in N metabolism as a metal component of the enzyme urease, whereas molybdenum (Mo) helps in N metabolism by acting as a metal component of the nitrogenase (N2 fixation) and nitrate reductase enzymes. Boron (B) is crucial for cell wall and membrane integrity, whereas chlorine plays a role in osmoregulation and stomata movement.

Familial Hypercholesterolaemia in Children and Adolescents: Gaining Decades of Life by Optimizing Detection and Treatment

Abstract: Familial hypercholesterolaemia (FH) is a common genetic cause of premature coronary heart disease (CHD). Globally, one baby is born with FH every minute. If diagnosed and treated early in childhood, individuals with FH can have normal life expectancy. This consensus paper aims to improve awareness of the need for early detection and management of FH children. Familial hypercholesterolaemia is diagnosed either on phenotypic criteria, i.e. an elevated low-density lipoprotein cholesterol (LDL-C) level plus a family history of elevated LDL-C, premature coronary artery disease and/or genetic diagnosis, or positive genetic testing. Childhood is the optimal period for discrimination between FH and non-FH using LDL-C screening. An LDL-C ≥5 mmol/L (190 mg/dL), or an LDL-C ≥4 mmol/L (160 mg/dL) with family history of premature CHD and/or high baseline cholesterol in one parent, make the phenotypic diagnosis. If a parent has a genetic defect, the LDL-C cut-off for the child is ≥3.5 mmol/L (130 mg/dL). We recommend cascade screening of families using a combined phenotypic and genotypic strategy. In children, testing is recommended from age 5 years, or earlier if homozygous FH is suspected. A healthy lifestyle and statin treatment (from age 8 to 10 years) are the cornerstones of management of heterozygous FH. Target LDL-C is 10 years, or ideally 50% reduction from baseline if 8–10 years, especially with very high LDL-C, elevated lipoprotein(a), a family history of premature CHD or other cardiovascular risk factors, balanced against the long-term risk of treatment side effects. Identifying FH early and optimally lowering LDL-C over the lifespan reduces cumulative LDL-C burden and offers health and socioeconomic benefits. To drive policy change for timely detection and management, we call for further studies in the young. Increased awareness, early identification, and optimal treatment from childhood are critical to adding decades of healthy life for children and adolescents with FH.

Evolution of halophytes: multiple origins of salt tolerance in land plants

Abstract: The evolution of salt tolerance is interesting for several reasons. First, since salt-tolerant plants (halophytes) employ several different mechanisms to deal with salt, the evolution of salt tolerance represents a fascinating case study in the evolution of a complex trait. Second, the diversity of mechanisms employed by halophytes, based on processes common to all plants, sheds light on the way that a plant’s physiology can become adapted to deal with extreme conditions. Third, as the amount of salt-affected land increases around the globe, understanding the origins of the diversity of halophytes should provide a basis for the use of novel species in bioremediation and conservation. In this review we pose the question, how many times has salt tolerance evolved since the emergence of the land plants some 450–470 million years ago? We summarise the physiological mechanisms underlying salt-tolerance and provide an overview of the number and diversity of salt-tolerant terrestrial angiosperms (defined as plants that survive to complete their life cycle in at least 200 mM salt). We consider the evolution of halophytes using information from fossils and phylogenies. Finally, we discuss the potential for halophytes to contribute to agriculture and land management and ask why, when there are naturally occurring halophytes, it is proving to be difficult to breed salt-tolerant crops.