Universal iron supplementation: the best strategy to tackle childhood anaemia in malaria-endemic countries?

Iron deficiency presents a major public health concern in many malaria-endemic regions, and both conditions affect young children most severely. Daily iron supplementation is the standard public health intervention recommended to alleviate rates of iron deficiency in children, but there is controversy over whether universal supplementation could increase the incidence and severity of malaria infection. Current evidence suggests that iron supplementation of deficient individuals is safe and effective in high-transmission settings when accompanied by malaria prevention strategies. However, low-resource settings often struggle to effectively control the spread of malaria, and it remains unclear whether supplementation of iron replete individuals could increase their risk of malaria and other infections. This review explores the evidence for and against universal iron supplementation programmes, and alternative strategies that could be used to alleviate iron deficiency in malaria-endemic areas, while minimising potential harm.

Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.

Although the link between DNA damage and aging is well accepted, the role of different DNA repair proteins on functional/physiological aging is not well-defined. Here, using Caenorhabditis elegans, we systematically examined the effect of three DNA repair genes involved in key genome stability pathways. We assayed multiple health proxies including molecular, functional and resilience measures to define healthspan. Loss of XPF-1/ERCC-1, a protein involved in nucleotide excision repair (NER), homologous recombination (HR) and interstrand crosslink (ICL) repair, showed the highest impairment of functional and stress resilience measures along with a shortened lifespan. brc-1 mutants, with a well-defined role in HR and ICL are short-lived and highly sensitive to acute stressors, specifically oxidative stress. In contrast, ICL mutant, fcd-2 did not impact lifespan or most healthspan measures. Our efforts also uncover that DNA repair mutants show high sensitivity to oxidative stress with age, suggesting that this measure could act as a primary proxy for healthspan. Together, these data suggest that impairment of multiple DNA repair genes can drive functional/physiological aging. Further studies to examine specific DNA repair genes in a tissue specific manner will help dissect the importance and mechanistic role of these repair systems in biological aging.

Clinical perspective and practices on pleural effusions in chronic systemic inflammatory diseases.

Systemic inflammatory diseases are a heterogeneous family of autoimmune chronic inflammatory disorders that affect multiple systems within the human body. Connective tissue disease (CTD) is a large group within this family characterised by immune-mediated inflammation of the connective tissue. This group of disorders are often associated with pleural manifestations. CTD-induced pleuritis exhibits a wide variety of symptoms and signs including exudative pleural effusions and chest pain. Accurate estimation of prevalence for CTD-related pleuritis is challenging as small effusions are asymptomatic and remain undetected. Rheumatoid arthritis and systemic lupus erythematosus are frequent CTDs and present with pleural pathology in approximately 5-20% and 17-60% of cases, respectively. By contrast, pleural involvement in systemic sclerosis, eosinophilia-myalgia syndrome, mixed connective tissue disease, ankylosing spondylitis, polymyositis and dermatomyositis syndrome is rare. Clinical management depends on the severity of symptoms; however, most effusions resolve spontaneously. In this review we discuss the pathophysiological mechanisms and the clinical considerations of CTD-induced pleuritis.