A record of seafloor methane seepage across the last 150 million years.

Seafloor methane seepage is a significant source of carbon in the marine environment. The processes and temporal patterns of seafloor methane seepage over multi-million-year time scales are still poorly understood. The microbial oxidation of methane can store carbon in sediments through precipitation of carbonate minerals, thus providing a record of past methane emission. In this study, we compiled data on methane-derived carbonates to build a proxy time series of methane emission over the last 150 My and statistically compared it with the main hypothesised geological controllers of methane emission. We quantitatively demonstrate that variations in sea level and organic carbon burial are the dominant controls on methane leakage since the Early Cretaceous. Sea level controls methane seepage variations by imposing smooth trends on timescales in the order of tens of My. Organic carbon burial is affected by the same cyclicities, and instantaneously controls methane release because of the geologically rapid generation of biogenic methane. Both the identified fundamental (26-27 My) and higher (12 My) cyclicities relate to global phenomena. Temporal correlation analysis supports the evidence that modern expansion of hypoxic areas and its effect on organic carbon burial may lead to higher seawater methane concentrations over the coming centuries.

Cerebrospinal fluid levels of magnesium in patients with preeclampsia after treatment with intravenous magnesium sulfate: a preliminary report.

The purpose of this study is twofold: (1) to correlate magnesium levels of serum with those of cerebrospinal fluid in patients with preeclampsia receiving intravenous magnesium sulfate, and (2) to determine whether the magnesium ion crosses the blood-brain barrier in significant amounts after intravenous magnesium sulfate therapy. Of the 21 patients in whom spinal anesthesia was used for delivery, ten patients with preeclampsia with therapeutic serum magnesium levels made up the study group and 11 term nontreated normotensive gravid women served as controls. At the time of spinal anesthesia, a 1 ml aliquot of cerebrospinal fluid was obtained from each patient. The mean cerebrospinal fluid magnesium level for the control group was 2.56 +/- 0.19 mg/dl (range 2.2 to 2.8 mg/dl). For the preeclamptic group who received intravenous magnesium sulfate, the mean cerebrospinal fluid magnesium level was 3.04 +/- 0.12 mg/dl (range 2.9 to 3.2 mg/dl). Although only a small amount of magnesium crosses the blood-brain barrier after intravenous magnesium sulfate treatment, this increment is highly significant (p less than 0.001).

Properties of adenylate cyclase in the cardiovascular tissues of renal hypertensive rats.

Adenylate cyclase activity in the myocardium and aorta of Grollman one-kidney renal hypertensive rats (RHR) and sham-operated control rats was compared. The experimental rats revealed significantly higher blood pressure and cardiac hypertrophy 6-8 weeks postoperation as compared to controls. Basal, guanine nucleotide-, fluoride-, and isoproterenol-stimulated adenylate cyclase activities were consistently decreased in the myocardium of RHR as compared to control rats. Similar changes were observed in aorta of RHR; however, the magnitude of difference was greater in aorta as compared to myocardium. The kinetic properties of enzyme with regard to the Ka (quantity of agonist required for half-maximal stimulation of adenylate cyclase) values for GTP, Gpp (NH)p, and GTP-gamma-S in the absence and presence of isoproterenol and the Ka values for isoproterenol in the presence of GTP, Gpp(NH)p, or GTP-gamma-S were comparable in RHR and control rats. However, Vmax of adenylate cyclase stimulation by guanine nucleotides, isoproterenol, and fluoride was reduced in RHR as compared to control rats. No differences between RHR and control rat myocardial membranes were observed in the affinity of [3H]DHA binding. However, the number of binding sites was reduced 20-25% in RHR as compared to control rats. These data would suggest that the number of receptor--cyclase complexes may be reduced in the RHR.