Milk sharing: from private practice to public pursuit

After only six months, a commerce-free internet-based milk-sharing model is operating in nearly 50 countries, connecting mothers who are able to donate breast milk with the caregivers of babies who need breast milk. Some public health authorities have condemned this initiative out of hand. Although women have always shared their milk, in many settings infant formula has become the "obvious" alternative to a mother's own milk. Yet an internationally endorsed recommendation supports mother-to-mother milk sharing as the best option in place of a birth mother's milk. Why then this rejection? Several possibilities come to mind: 1) ignorance and prejudice surrounding shared breast milk; 2) a perceived challenge to the medical establishment of a system where mothers exercise independent control; and 3) concern that mother-to-mother milk sharing threatens donor milk banks. We are not saying that milk sharing is risk-free or that the internet is an ideal platform for promoting it. Rather, we are encouraging health authorities to examine this initiative closely, determine what is happening, and provide resources to make mother-to-mother milk sharing as safe as possible. Health authorities readily concede that life is fraught with risk; accordingly, they promote risk-reduction and harm-minimisation strategies. Why should it be any different for babies lacking their own mothers' milk? The more that is known about the risks of substituting for breast milk, the more reasonable parental choice to use donor milk becomes. We believe that the level of intrinsic risk is manageable through informed sharing. If undertaken, managed and evaluated appropriately, this made-by-mothers model shows considerable potential for expanding the world's supply of human milk and improving the health of children

Classification of non-indigenous species based on their impacts: Considerations for application in marine management

Assessment of the ecological and economic/societal impacts of the introduction of non-indigenous species (NIS) is one of the primary focus areas of bioinvasion science in terrestrial and aquatic environments, and is considered essential to management. A classification system of NIS, based on the magnitude of their environmental impacts, was recently proposed to assist management. Here, we consider the potential application of this classification scheme to the marine environment, and offer a complementary framework focussing on value sets in order to explicitly address marine management concerns. Since existing data on marine NIS impacts are scarce and successful marine removals are rare, we propose that management of marine NIS adopt a precautionary approach, which not only would emphasise preventing new incursions through pre-border and at-border controls but also should influence the categorisation of impacts. The study of marine invasion impacts requires urgent attention and significant investment, since we lack the luxury of waiting for the knowledge base to be acquired before the window of opportunity closes for feasible management

The enlargement of the Suez Canal and introduction of non-indigenous species to the Mediterranean Sea

The Suez Canal is one of the most important waterways in the world – during the last year 17,148 ships passed through the Canal – reducing emissions, saving time, and operating costs to shippers. The rapid increase in ship size from the “Post-Suezmax” (> 12,000 TEU) to the latest container vessels (> 19,000 TEU) now requires enlargements of port facilities and canals. A project of this magnitude, and with potentially negative environmental outcomes, requires a transparent and scientifically sound “Environmental Impact Assessment” (EIA). An explicit obligation on Parties to the Convention on Biological Diversity (https://www.cbd.int/doc/ legal/cbd-en.pdf) was made to consider transboundary impacts on biodiversity, particularly those associated with invasive non-indigenous species

Plexin D1 determines body fat distribution by regulating the type V collagen microenvironment in visceral adipose tissue

Proceedings of the National Academy of Sciences of the United States of America112144363-436

'Double trouble': the expansion of the Suez Canal and marine bioinvasions in the Mediterranean Sea

4 páginasPeer reviewe

Oesophageal and sternohyal muscle fibres are novel Pax3-dependent migratory somite derivatives essential for ingestion

Striated muscles that enable mouth opening and swallowing during feeding are essential for efficient energy acquisition, and are likely to have played a fundamental role in the success of early jawed vertebrates. The developmental origins and genetic requirements of these muscles are uncertain. Here, we determine by indelible lineage tracing in mouse that fibres of sternohyoid muscle (SHM), which is essential for mouth opening during feeding, and oesophageal striated muscle (OSM), which is crucial for voluntary swallowing, arise from Pax3-expressing somite cells. In vivo Kaede lineage tracing in zebrafish reveals the migratory route of cells from the anteriormost somites to OSM and SHM destinations. Expression of pax3b, a zebrafish duplicate of Pax3, is restricted to the hypaxial region of anterior somites that generate migratory muscle precursors (MMPs), suggesting that Pax3b plays a role in generating OSM and SHM. Indeed, loss of pax3b function led to defective MMP migration and OSM formation, disorganised SHM differentiation, and inefficient ingestion and swallowing of microspheres. Together, our data demonstrate Pax3-expressing somite cells as a source of OSM and SHM fibres, and highlight a conserved role of Pax3 genes in the genesis of these feeding muscles of vertebrates

Plexin D1 determines body fat distribution by regulating the type V collagen microenvironment in visceral adipose tissue

PLEXIN D1 (PLXND1) has been implicated in body fat distribution and type 2 diabetes by genome-wide association studies, but the mechanism is unknown. We show here that Plxnd1 regulates body fat distribution in zebrafish by controlling the visceral adipose tissue (VAT) growth mechanism. Plxnd1 deficiency in zebrafish resulted in induction of a hyperplastic state and reduced lipid deposition in VAT. Regulation of VAT was dependent on the induction of the type V collagen, col5a1, suggesting that Plxnd1 controls body fat distribution by determining the status of VAT extracellular matrix. Plxnd1-deficient zebrafish were protected from high-fat-induced insulin resistance, and human PLXND1 mRNA was positively associated with type 2 diabetes. These results suggest that the role of Plxnd1 in body fat distribution and insulin signaling is conserved from zebrafish to humans