Background: Paid maternity leave benefits all of society, reducing infant mortality and providing economic gains. It is endorsed by international treaties. Paid maternity leave is important for breastfeeding, bonding, and recovery from childbirth. Not all mothers have access to adequate paid maternity leave. Key Information: Paid leave helps meet several of the 17 United Nations' Sustainable Development Goals (2, 3, 4, 5, 8, and 10), including fostering economic growth. A family's expenses will rise with the arrival of an infant. Paid leave is often granted with partial pay. Many low-wage workers earn barely enough to meet their needs and are unable to take advantage of paid leave. Undocumented immigrants and self-employed persons, including those engaging in informal work, are often omitted from maternity leave programs. Recommendations: Six months of paid leave at 100% pay, or cash equivalent, should be available to mothers regardless of income, employment, or immigration status. At the very minimum, 18 weeks of fully paid leave should be granted. Partial pay for low-wage workers is insufficient. Leave and work arrangements should be flexible whenever possible. Longer flexible leave for parents of sick and preterm infants is essential. Providing adequate paid leave for partners has multiple benefits. Increasing minimum wages can help more families utilize paid leave. Cash benefits per birth can help informal workers and undocumented mothers afford to take leave. Equitable paid maternity leave must be primarily provided by governments and cannot be accomplished by employers alone.
We describe three mutations of the red-cell anion exchangerband 3 (AE1, SLC4A1) gene associated with distalrenal tubular acidosis (dRTA) in families from Malaysia and Papua NewGuinea: Gly(701)-->Asp (G701D), Ala(858)-->Asp(A858D) and deletion of Val(850) (DeltaV850). The mutationsA858D and DeltaV850 are novel; all three mutations seem to berestricted to South-East Asian populations. South-East Asianovalocytosis (SAO), resulting from the band 3 deletion of residues400-408, occurred in many of the families but did not itselfresult in dRTA. Compound heterozygotes of each of the dRTA mutationswith SAO all had dRTA, evidence of haemolytic anaemia and abnormal red-cell properties. The A858D mutation showed dominant inheritance and therecessive DeltaV850 and G701D mutations showed a pseudo-dominantphenotype when the transport-inactive SAO allele was also present. Red-cell and Xenopus oocyte expression studies showed that theDeltaV850 and A858D mutant proteins have greatly decreased aniontransport when present as compound heterozygotes (DeltaV850/A858D,DeltaV850/SAO or A858D/SAO). Red cells with A858D/SAO had only 3% ofthe SO(4)(2-) efflux of normal cells, thelowest anion transport activity so far reported for human red cells. The results suggest dRTA might arise by a different mechanism for eachmutation. We confirm that the G701D mutant protein has an absoluterequirement for glycophorin A for movement to the cell surface. Wesuggest that the dominant A858D mutant protein is possibly mis-targetedto an inappropriate plasma membrane domain in the renal tubular cell,and that the recessive DeltaV850 mutation might give dRTA because ofits decreased anion transport activity.