Childhood overweight and obesity are major health problems with immediate and long-term consequences of staggering magnitude. Despite this, there are few preventive and therapeutic strategies of proven effectiveness available to public health and clinical practitioners. Accruing such evidence is currently and appropriately a health policy priority, but there is an urgent need to intervene even before comprehensive solutions are fully established. The aim of this Clinical Report on Overweight Children and Adolescents is to present information on current understanding of pathogenesis and treatment of overweight and obesity. We report on the epidemiology, molecular biology and medical conditions associated with overweight; on dietary, exercise, behavioral, pharmacological and surgical treatments; and on the primary prevention of overweight in children and adolescents.

In vivo isotope-fractionation factors were determined for hydrogen and oxygen between plasma water samples and samples of urine, saliva, respiratory water vapor, and carbon dioxide in 20 normal adults. The isotope-fractionation factors ranged from 0.944 to 1.039 for 2H in breath water vapor and for 18O in breath CO2, respectively. When corrected for isotope fractionation, the 2H- and 18O-dilution spaces determined from urine, saliva, respiratory water, and CO2 were within -0.10 +/- 1.09 kg (mean +/- SD, n = 60) and 0.04 +/- 0.68 kg (n = 80), respectively, of the values determined from plasma. In the absence of these corrections, we observed a 6% overestimation of 2H-dilution space and a 1% overestimation of 18O-dilution space from the use of respiratory water values. A 4% underestimation of the 18O-dilution space was observed for breath CO2 without correction for isotope fractionation.

The small intestine is a complex organ system that is vital to the life of the individual. There are a number of congenital anomalies that occur and present most commonly in infancy; however, some may not present until adulthood. Most congenital anomalies of the small intestine will present with obstructive symptoms while some may present with vomiting, abdominal pain, and/or gastrointestinal bleeding. Various radiologic procedures can aid in the diagnosis of these lesions that vary depending on the particular anomaly. Definitive therapy for these congenial anomalies is surgical, and in some cases, surgery needs to be performed urgently. The overall prognosis of congenital anomalies of the small intestine is very good and has improved with improved medical management and the advent of newer surgical modalities. The congenital anomalies of the small intestine reviewed in this article include malrotation, Meckel's diverticulum, duodenal web, duodenal atresia, jejunoileal atresia, and duplications.

SUMMARY A comprehensive GPS velocity field along the Dead Sea Fault System (DSFS) provides new constraints on along-strike variations of near-transform crustal deformation along this plate boundary, and internal deformation of the Sinai and Arabian plates. In general, geodetically derived slip rates decrease northwards along the transform (5.0 ± 0.2 to 2.2 ± 0.5 mm yr−1) and are consistent with geological slip rates averaged over longer time periods. Localized reductions in slip rate occur where the Sinai Plate is in ∼N–S extension. Extension is confined to the Sinai side of the fault and is associated with prominent changes in transform geometry, and with NW–SE striking, left-lateral splay faults, including the Carmel Fault in Israel and the Roum Fault in Lebanon. The asymmetry of the extensional velocity gradients about the transform reflects active fragmentation of the Sinai Plate along the continental margin. Additionally, elastic block modelling of GPS velocities requires an additional structure off-shore the northern DSF segment, which may correspond with a fault located along the continental margin, suggested by prior geophysical studies.

Erythropoietic protoporphyria is a disorder of heme synthesis in which deficient ferrochelatase activity leads to excess production and biliary excretion of protoporphyrin. The main clinical features, photosensitivity and hepatobiliary disease that may progress to liver failure, are caused by the toxicity of protoporphyrin. Liver transplantation has been used to treat liver failure in erythropoietic protoporphyria, but excess production of protoporphyrin by the bone marrow continues causing recurrence of liver disease in the majority of patients. This is the first report of successful sequential liver and bone marrow transplantation in a patient with liver failure as a result of erythropoietic protoporphyria. This combination corrected the severe phenotype, resolving the severe photosensitivity and halting erythropoietic protoporphyria associated liver graft injury. Splenectomy seemed to facilitate the successful bone marrow transplant.