Sea level rise and the drivers of daily water levels in the Sacramento-San Joaquin Delta.

Water levels in deltas and estuaries vary on multiple timescales due to coastal, hydrologic, meteorologic, geologic, and anthropogenic factors. These diverse factors increase the uncertainty of, and may bias, relative sea level rise (RSLR) estimates. Here, we evaluate RSLR in San Francisco Bay and the Sacramento-San Joaquin Delta, USA by applying a physics-based, nonlinear regression to 50 tide gauges that determines the spatially varying controls on daily mean water level for water years 2004-2022. Results show that elevated river flow and pumping (99th percentile) raise water level up to 6 m and lower it up to 0.35 m, respectively, and coastal water level variations are attenuated by 30-60% within the Delta. Strong westerly winds raise water level up to 0.17 m, and tidal-fluvial interaction during spring tides and low discharge raises water level up to 0.15 m. Removal of these interfering factors greatly improves RSLR estimates, narrowing 95% confidence intervals by 89-99% and removing bias due to recent drought. Results show that RSLR is spatially heterogeneous, with rates ranging from - 2.8 to 12.9 mm y-1 (95% uncertainties < 1 mm y-1). RSLR also exceeds coastal SLR of 3.3 mm y-1 in San Francisco at 85% of stations. Thus, RSLR in the Delta is strongly influenced by local vertical land motion and will likely produce significantly different, location-dependent future flood risk trajectories.

The Role of Intensifying Precipitation on Coastal River Flooding and Compound River-Storm Surge Events, Northeast Gulf of Mexico.

Destructive coastal floods are commonly increasing in frequency and may be caused by global precipitation intensification. Such connections through climate, watershed, and river processes are poorly understood because of complex interactions in transitional fluvial-marine environments where flooding is caused by rivers, marine storm surge, or both in compound events. To better understand river floods along the fluvial-marine transition, we study watersheds of the northeastern Gulf of Mexico using long-term observations. Results show intensifying precipitation decreased precipitation-discharge lag times, increasing river-flood frequency and the likelihood of compound events in fluvial-marine transitions. This reduction in lag time occurred when the Atlantic Multidecadal Oscillation and El Niño Southern Oscillation began strongly affecting river discharge through the advection of moist air, intensifying precipitation. Along the fluvial-marine transition, compound events were largest in inland reaches. However, for inland reaches, compound event water levels did not exceed the floods caused solely by river flooding, the largest flood hazard in these systems. Our results demonstrate precipitation and river discharge play critical roles in coastal flooding and will likely escalate flooding as the climate continues to warm and intensify precipitation.

Oculocerebrocutaneous syndrome: a case report, a follow-up, and differential diagnostic considerations.

Oculocerebrocutaneous syndrome consists essentially of orbital cysts and microphthalmia/anophthalmia, focal dermal defects, skin appendages and malformations of the central nervous system. Up to now, about 20 sporadic cases have been reported. Limited information is available on the clinical spectrum and on the natural history. We present the long-term follow-up of a 19 year-old patient who was one of the first two patients described by Delleman and Oorthuys in 1981. Furthermore, we report on a new case presenting with bilateral anophthalmia and orbital cysts, typical skin lesions, a complex brain malformation and cleft lip palate. This infant died due to the severe cerebral malformations at the age of 10 months. Encephalocraniocutaneous lipomatosis, focal dermal hypoplasia and microphthalmia with linear skin defects (MLS) syndrome are discussed as the most important differential diagnostic entities.

Stability of esmolol hydrochloride in intravenous solutions.

The stability of esmolol hydrochloride in a variety of i.v. solutions was studied. Solutions of esmolol hydrochloride 10 mg/mL were prepared separately in 0.45% sodium chloride injection, 0.9% sodium chloride injection, 5% dextrose injection, 5% dextrose and 0.45% sodium chloride injection, 5% dextrose and 0.9% sodium chloride injection, 5% dextrose with lactated Ringer's injection, lactated Ringer's injection, 5% sodium bicarbonate injection, and 5% dextrose injection with potassium chloride 40 meq/L. One glass and one polyvinyl chloride container of each solution (except glass only in the case of the solution in 5% sodium bicarbonate injection) were stored in the dark at 5 degrees C, under ambient room light at 23-27 degrees C, in the dark at 40 degrees C, and under intense light at 25-30 degrees C. At storage intervals up to 168 hours, samples were tested for esmolol hydrochloride concentration by high-performance liquid chromatography. Optical density and pH were also measured. Esmolol hydrochloride was stable in the various i.v. fluids for at least 168 hours when stored at 5 degrees C or 23-27 degrees C, for at least 24 hours when stored under intense light, and, with one exception, for at least 48 hours when stored at 40 degrees C. When mixed with 5% sodium bicarbonate injection, the drug was stable for only about 24 hours at 40 degrees C. There were no substantial changes in optical density or pH. The type of container had no effect on stability. With one exception, esmolol hydrochloride was stable in all the i.v. solutions under all the conditions tested.

Clinical signs and lesions in gnotobiotic pigs inoculated with Shiga-like toxin I from Escherichia coli.

Gnotobiotic pigs were used as a model to study the contribution of Shiga-like toxin I to natural disease caused by enterohemorrhagic Escherichia coli in calves and human beings. Eleven 2- to 7-day-old gnotobiotic pigs of either sex, obtained by closed hysterotomy, were injected intramuscularly with graded doses of partially purified Shiga-like toxin I derived from a lysogenized Escherichia coli strain. Four other gnotobiotic pigs were injected with a mock toxin preparation obtained from a nonlysogenized culture of the same E. coli strain. All toxin-injected pigs developed diarrhea, and three displayed signs of neurologic disease. Pigs either died or were euthanatized 2 to 4 days post-inoculation. Necrosis of muscle was grossly evident at the site of injection in all toxin-inoculated pigs. Hemorrhage in the lumen of the small and large intestines and blood in the feces were also evident in two toxin-inoculated pigs. Microscopically, severe necrotizing myositis at the injection site, multifocal encephalomalacia, and mucosal infarcts and hemorrhage in the small and large intestines were seen. In small vessels at lesion sites, endothelial cells were frequently swollen or necrotic. Pigs inoculated with mock toxin did not develop diarrhea or exhibit signs of neurologic disease, and the only apparent lesion was mild microscopic myositis at the injection site in 1/4 pigs. The results of this study indicate that Shiga-like toxin I causes vascular damage and ischemic necrosis in the intestines and brains of gnotobiotic pigs. These lesions are similar to those seen in the intestines of calves and human beings with hemorrhagic colitis and in the brains of human beings with thrombotic thrombocytopenic purpura.