Current Status of Marine Protected Areas in Latin America and the Caribbean

Abstract: Marine protected areas (MPAs), including no‐take marine reserves (MRs), play an important role in the conservation of marine biodiversity. We document the status of MPAs and MRs in Latin America and the Caribbean, where little has been reported on the scope of such protection. Our survey of protected area databases, published and unpublished literature, and Internet searches yielded information from 30 countries and 12 overseas territories. At present more than 700 MPAs have been established, covering more than 300,000 km² or 1.5% of the coastal and shelf waters. We report on the status of 3 categories of protection: MPAs (limited take throughout the area), MRs (no‐take throughout the area), and mixed‐use (a limited‐take MPA that contains an MR). The majority of protected areas in Latin America and the Caribbean are MPAs, which allow some or extensive extractive activities throughout the designated area. These 571 sites cover 51,505 km² or 0.3% of coastal and shelf waters. There are 98 MRs covering 16,862 km² or 0.1% of the coastal and shelf waters. Mixed‐use MPAs are the fewest in number (87), but cover the largest area (236,853 km², 1.2%). Across Latin America and the Caribbean, many biogeographic provinces are underrepresented in these protected areas. Large coastal regions remain unprotected, in particular, the southern Pacific and southern Atlantic coasts of South America. Our analysis reveals multiple opportunities to strengthen marine conservation in Latin America and the Caribbean by improving implementation, management, and enforcement of existing MPAs; adding new MPAs and MRs strategically to enhance connectivity and sustainability of existing protection; and establishing new networks of MPAs and MRs or combinations thereof to enhance protection where little currently exists.     

H2O2 treatment boosts activity of NiFe layered double hydroxide for electro-catalytic oxidation of urea

Urea oxidation reaction (UOR) provides a method for hydrogen production besides wastewater treatment, but the current limited catalytic activity has prevented the application. Herein, we develop a novel H₂O₂ treatment strategy for tailoring the surface oxygen ligand of NiFe-layered double hydroxides (NiFe-LDH). The sample after H₂O₂ treatment (NiFeO-LDH) shows significant enhancement on UOR efficiency, with the potential of 1.37 V (RHE) to reach a current density of 10 mA/cm². The boost is attributed to the richness adsorption O ligand on NiFeO-LDH as revealed by XPS and Raman analysis. DFT calculation indicates formation of two possible types of oxygen ligands: adsorbed oxygen on the surface and exposed from hydroxyl group, lowered the desorption energy of CO₂ product, which lead to the lowered onset potential. This strategy is further extended to NiFe-LDH nano sheet on Ni foam to reach a higher current density of 440 mA/cm² of UOR at 1.8 V (RHE). The facile surface O ligand manipulation is also expected to give chance to many other electro-catalytic oxidations.     

Pilot study for the neonatal screening of fragile X syndrome

An Erratum has been published for this article in Prenatal Diagnosis 23 (9), 2003, 771. Fragile X syndrome (SFX) is the commonest form of inherited mental retardation. Due to the highly variable phenotype clinical diagnosis is complicated. In nearly all cases, the disorder is caused by expansion of a CGG-repeat in the 5′-untranslated region of the FMR1 (fragile X mental retardation-1) gene. We have evaluated the feasibility, efficiency and costs of two methodologies in order to develop a simple test to screen large populations: PCR and fragile X mental retardation-1 protein (FMRP) immunodetection. We studied 100 newborn males using PCR and immunodetection (26.91 Euro). All but one amplified the CGG repeat of the FMR1 gene within the normal size range. The sample that failed to amplify showed only 28% of FMRP expression by immunodetection study; both results indicated an affected male. A further 100 males were studied only by polymerase chain reaction (PCR) (7.8 Euro); all of them amplified within the normal size range. Both methodologies, PCR and immunodetection, are feasible for screening large populations, PCR being the most suitable, economical and less time-consuming. However, it is advisable to keep slides for immunodetection when PCR fails or the external control shows no amplification. Early detection of SFX-affected individuals would represent a great benefit for their maximum social integration, due to appropriate treatment and early stimulation and would permit a cascade screening in their pedigree. Copyright © 2002 John Wiley & Sons, Ltd.     

Prenatal diagnosis of primary anophthalmia with a 3q27 interstitial deletion involving SOX2

We report an interstitial deletion of chromosome 3q26-q28 in a fetus in which anophthalmia had been detected prenatally. FISH analysis, using BAC clones encompassing the SOX2 locus, showed that SOX2 gene was involved in the chromosomal breakpoint of the deletion. This case confirms that haploinsufficiency for SOX2 plays a crucial role in human eye development and emphasizes the necessity of careful chromosomal analysis, including FISH analysis of the 3q region, in case of prenatal discovery of anophthalmia. Copyright © 2004 John Wiley & Sons, Ltd.     

Prenatal diagnosis of complete sole trisomy 1q

The prenatal diagnosis of a complete trisomy of the long arm of chromosome 1 is reported. Major ultrasound findings included: nuchal thickening, bi-temporal narrowing, a single choroid plexus cyst, andmild ventriculomegaly. There was a mass in the chest and abdomen, pleural effusion, ascites and a hyperechoic bowel. Skin edema was present. The fetus died at 26 weeks' gestation. A literature review is presented of 17 de novo and two inherited cases with only trisomy 1q. Of note is the fact that 3/5 prenatally detected 1q trisomies have teratomas. A review of the literature reveals a dismal outcome fortrisomy 1q cases if the duplication involves bands 1q25→q32. Copyright © 2001 John Wiley & Sons, Ltd.