Impacts of Mauritia flexuosa degradation on the carbon stocks of freshwater peatlands in the Pastaza-Marañón river basin of the Peruvian Amazon

Tropical peat swamp forests (PSF) are characterized by high quantities of carbon (C) stored as organic soil deposits due to waterlogged conditions which slows down decomposition. Globally, Peru has one of the largest expanse of tropical peatlands, located primarily within the Pastaza-Marañón river basin in the Northwestern Peru. Peatland forests in Peru are dominated by a palm species—Mauritia flexuosa, and M. flexuosa-dominated forests cover ~?80% of total peatland area and store ~?2.3 Pg C. However, hydrologic alterations, land cover change, and anthropogenic disturbances could lead to PSF’s degradation and loss of valuable ecosystem services. Therefore, evaluation of degradation impacts on PSF’s structure, biomass, and overall C stocks could provide an estimate of potential C losses into the atmosphere as greenhouse gases (GHG) emissions. This study was carried out in three regions within Pastaza-Marañón river basin to quantify PSF’s floristic composition and degradation status and total ecosystem C stocks. There was a tremendous range in C stocks (Mg C ha^?1) in various ecosystem pools—vegetation (45.6–122.5), down woody debris (2.1–23.1), litter (2.3–7.8), and soil (top 1 m; 109–594). Mean ecosystem C stocks accounting for the top 1 m soil were 400, 570, and 330 Mg C ha^?1 in Itaya, Tigre, and Samiria river basins, respectively. Considering the entire soil depth, mean ecosystem C stocks were 670, 1160, and 330 Mg C ha^?1 in Itaya, Tigre, and Samiria river basins, respectively. Floristic composition and calcium to Magnesium (Ca/Mg) ratio of soil profile offered evidence of a site undergoing vegetational succession and transitioning from minerotrophic to ombrotrophic system. Degradation ranged from low to high levels of disturbance with no significant difference between regions. Increased degradation tended to decrease vegetation and forest floor C stocks and was significantly correlated to reduced M. flexuosa biomass C stocks. Long-term studies are needed to understand the linkages between M. flexuosa harvest and palm swamp forest C stocks; however, river dynamics are important natural drivers influencing forest succession and transition in this landscape.

     

Prenatal diagnosis of congenital cytomegalovirus infection in 189 pregnancies with known outcome

An Erratum has been published for this article in Prenatal Diagnosis 21(7) 2001, 605. Prenatal diagnosis (PD) of fetal cytomegalovirus (CMV) infection was performed in 242 pregnancies, with known outcome in 189 cases. In 141/189 pregnancies, PD was carried out on account of suspicious maternal CMV serology up to gestational week (WG) 23, and in 48 cases on account of abnormal ultrasonic findings detected between WG 18 and 39. Chorionic villus samples (n=6), amniotic fluid (AF, n=176) and/or fetal blood specimens (n=80) were investigated for detection of virus by cell culture, shell vial assay, PCR and/or CMV-specific IgM antibodies. Of 189 fetuses correctly evaluated by CMV detection either in fetal tissue following therapeutic abortion/stillbirth (n=24) or in urine of neonates within the first 2 weeks of life (n=33), 57 were congenitally infected. In women with proven or suspected primary infection, the intrauterine transmission rates were 20.6% (7/34) and 24.4% (10/41), respectively. Of the congenitally infected live-born infants, 57.6% (19/33) had symptoms of varying degree. The overall sensitivity of PD in the serologic and ultrasound risk groups was 89.5% (51/57). A sensitivity of 100% was achieved by combining detection of CMV-DNA and CMV-specific IgM in fetal blood or by combined testing of AF and fetal blood for CMV-DNA or IgM antibodies. There was no instance of intrauterine death following the invasive procedure. The predictive value of PD for fetal infection was 95.7% (132/138) for negative results and 100% (51/51) for positive results. Correct results for congenital CMV infection by testing AF samples can be expected with samples obtained after WG 21 and after a time interval of at least 6 weeks between first diagnosis of maternal infection and PD. In case of negative findings in AF or fetal blood and the absence of ultrasound abnormalities at WG 22–23, fetal infection and neonatal disease could be excluded with high confidence. Positive findings for CMV infection in AF and/or fetal blood in combination with CMV suspicious ultrasound abnormalities predicted a high risk of cytomegalic inclusion disease (CID). Furthermore, detection of specific IgM antibodies in fetal blood was significantly correlated with severe outcome for the fetus or the newborn (p=0.0224). However, normal ultrasound of infected fetuses at WG 22–23 can neither completely exclude an abnormal ultrasound at a later WG and the birth of a severely damaged child nor the birth of neonates which are afflicted by single manifestations at birth or later and of the kind which are not detectable by currently available ultrasonographic techniques. Copyright © 2001 John Wiley & Sons, Ltd.     

Prenatal diagnosis of NADH:ubiquinone oxidoreductase deficiency

NADH:ubiquinone oxidoreductase (complex I of the mitochondrial respiratory chain) deficiency is a severe disorder with an often early fatal outcome. Prenatal diagnosis for complex I defects currently relies mainly on biochemical assays of complex I in fetal tissues such as chorionic villi (CV), and is only in a minority of cases possible by means of mutational analysis of nuclear-encoded genes of complex I. We report on our experience to date with prenatal diagnosis in pregnancies at risk for complex I deficiency. We measured complex I activity in native CV and/or cultured CV in 23 pregnancies in 15 families. In accordance with the results of the investigations in CV, 15 children were born clinically unaffected. Two prenatally diagnosed unaffected fetuses and two prenatally diagnosed affected fetuses were lost prematurely with spontaneous or provoked abortions, respectively. Two affected children were born (prenatally found to be affected). In two pregnancies a discrepancy between native and cultured cells was found. We conclude that prenatal diagnosis for complex I deficiency can be reliably performed. Pitfalls were encountered in using cultured CV as a result of maternal cell contamination (MCC). Future research on pathogenic nuclear mutations underlying complex I deficiency will extend the possibilities for prenatal diagnosis at the molecular level. Copyright © 2001 John Wiley & Sons, Ltd.