Hot super-Earths stripped by their host stars.

Simulations predict that hot super-Earth sized exoplanets can have their envelopes stripped by photoevaporation, which would present itself as a lack of these exoplanets. However, this absence in the exoplanet population has escaped a firm detection. Here we demonstrate, using asteroseismology on a sample of exoplanets and exoplanet candidates observed during the Kepler mission that, while there is an abundance of super-Earth sized exoplanets with low incident fluxes, none are found with high incident fluxes. We do not find any exoplanets with radii between 2.2 and 3.8 Earth radii with incident flux above 650 times the incident flux on Earth. This gap in the population of exoplanets is explained by evaporation of volatile elements and thus supports the predictions. The confirmation of a hot-super-Earth desert caused by evaporation will add an important constraint on simulations of planetary systems, since they must be able to reproduce the dearth of close-in super-Earths.

Ensemble asteroseismology of solar-type stars with the NASA Kepler mission.

In addition to its search for extrasolar planets, the NASA Kepler mission provides exquisite data on stellar oscillations. We report the detections of oscillations in 500 solar-type stars in the Kepler field of view, an ensemble that is large enough to allow statistical studies of intrinsic stellar properties (such as mass, radius, and age) and to test theories of stellar evolution. We find that the distribution of observed masses of these stars shows intriguing differences to predictions from models of synthetic stellar populations in the Galaxy.

Oral L-ornithine-L-aspartate therapy of chronic hepatic encephalopathy: results of a placebo-controlled double-blind study.

BACKGROUND/AIMS: In the current state of knowledge of the pathophysiology of hepatic encephalopathy, a reduction in hyperammonemia is the most important evidence of effective treatment. Therefore, the therapeutic efficacy of oral L-ornithine-L-aspartate, which improves impaired ammonia detoxification, was investigated in patients with cirrhosis, hyperammonemia and stable, overt, chronic hepatic encephalopathy, and in subclinical hepatic encephalopathy in a randomized, double-blind, placebo-controlled clinical trial. METHODS: Oral L-ornithine-L-aspartate was administered three times daily at fixed times for 14 consecutive days in a total dose of 18 g per day. The design was chosen to prevent an increase in ammonia induced by a protein meal of 0.25 g/kg body weight, given at the start of the daily treatment period. Efficacy variables were: fasting and postprandial ammonia concentration, Number-Connection-Test time, mental state grades, and a Portosystemic Encephalopathy Index. Analyses were based on the total study sample of 32 placebo- and 34 L-ornithine-L-aspartate-treated patients as well as on the subgroup samples in the overt (20 placebo- and 23 L-ornithine-L-aspartate-treated) and subclinical hepatic encephalopathy (12 placebo- and 11 L-ornithine-L-aspartate-treated) patients. RESULTS: Number Connection Test performance times (p<0.01) as well as fasting (p<0.01) and postprandial (p<0.05) venous blood ammonia concentrations in the L-ornithine-L-aspartate-treated group showed improvement in comparison to placebo. Also, the mental state grade (p<0.05) and the Portosystemic Encephalopathy Index (p<0.01), improved to a much greater degree in the L-ornithine-L-aspartate group than in the placebo group. Adverse events were observed in neither the placebo nor the L-ornithine-L-aspartate-treated patients. CONCLUSION: Oral L-ornithine-L-aspartate is a safe, well-tolerated treatment with a good compliance rate and a beneficial therapeutic effect in patients with cirrhosis and stable, overt, chronic hepatic encephalopathy.

Weight reduction and salt restriction in hypertension: effects on blood pressure and intracellular electrolytes.

In 16 essential hypertensives on a program of energy restriction (800 kcal/day) with and without simultaneous salt restriction, the effects on blood pressure and intracellular Na+ and Ca2+ in red blood cells were studied. A decrease in blood pressure and intracellular free Na+ and Ca2+ was only observed in the cases of simultaneous energy and salt restriction. The beneficial effect of weight reduction in hypertension thus depends on a diminished salt intake and is probably mediated by changes in intracellular free Ca2+.

Treatment of resistant hypertension by phlebotomy.

In 15 essential hypertensives resistant against a standard triple combination of antihypertensive drugs phlebotomy was performed. Mean arterial pressure was lowered from 140.1 +/- 12.2 mm Hg to 123.8 +/- 14.9 mm Hg after 14 days. No serious side effects were observed. The duration of the hypotensive effect of phlebotomy was about 4 weeks. Phlebotomy can be used in addition to drug treatment in resistant essential hypertension.

Characterization of very low density lipoproteins and intermediate density lipoproteins of normo- and hyperlipidemic apolipoprotein E-2 homozygotes.

Triglyceride-rich lipoproteins derived from ten normo- and hyperlipidemic apoE-2 homozygotes were analyzed for their composition, beta-VLDL content, and their ability to induce cholesteryl ester storage in macrophages. In six of these probands apoE sequence analysis revealed that the cysteine residues were at positions 112 and 158 of the amino acid sequence (Rall et al. 1983. J. Clin. Invest. 71: 1023-1031). ApoE-2 of these six and the other four patients was further analyzed by SDS electrophoresis to exclude the presence of apoE-2* (Rall et al. 1982. Proc. Natl. Acad. Sci. USA. 79: 4696-4700). The relative serum concentrations of free and esterified cholesterol transported in the d less than 1.006 g/ml and d 1.006-1.019 g/ml lipoproteins of the apoE-2 homozygotes was significantly higher as compared to controls. Compositional analysis of these lipoproteins revealed a relative reduction of triglycerides and a relative increase of cholesteryl esters as compared to controls. In most patients, with increasing serum triglyceride levels the cholesteryl ester concentration increased in d less than 1.006 g/ml and d 1.006-1.019 g/ml lipoproteins. However, in three patients with a low content of beta-VLDL, the increase in the d less than 1.006 g/ml fraction cholesterol was mostly due to free cholesterol and not due to cholesteryl esters. The degree of the macrophage cholesteryl ester accumulation induced by d less than 1.006 g/ml lipoproteins was mostly dependent on the concentration of the beta-migrating fraction (beta-VLDL). The amount of beta-VLDL and pre-beta-VLDL contained in the d less than 1.006 g/ml fraction was determined densitometrically after electrophoretic separation. It could be demonstrated that the beta-VLDL content in the d less than 1.006 g/ml fraction of the apoE-2 homozygous patients was largely independent of serum triglyceride and serum cholesterol levels. When macrophages were incubated with the IDL fraction (d 1.006-1.019 g/ml) from the apoE-2 patients, no significant increase in cellular cholesteryl esters above control levels was observed. Studies with purified lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) clearly revealed that both enzymes interacted with apoE-2 VLDL (binding, hydrolysis) to a lesser degree compared to control preparations. However, the apoE-2 VLDL preparations containing a low content of beta-VLDL were better substrates for LPL and HTGL than those containing a high beta-VLDL content. It is concluded from our studies that the plasma beta-VLDL content in apoE-2 homozygotes is a major determinant for cholesteryl ester accumulation in macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)

Intracellular sodium and calcium during antihypertensive treatment.

In 49 untreated essential hypertensives the effects of the loop diuretic, piretanide, in a dose of 12 mg daily (n = 14) and of 6 mg daily (n = 18) as well as of beta blockers (pindolol, metipranolol, atenolol, n = 17) on blood pressure, intracellular Ca++ and Na+ activity in red blood cells were examined. Intracellular ion activities were measured by ion-selective electrodes. The higher dose of piretanide caused a decrease of intracellular Ca++ activity and an increase of intracellular Na+ activity. Under the lower dose of piretanide there was a comparable decrease of intracellular Ca++ activity but no significant change of intracellular Na+ activity. Beta blockers decreased intracellular Ca++ activity but left intracellular Na+ activity unchanged. It is concluded that intracellular free Ca++ plays an important role in the regulation of vascular tone in essential hypertension. There seems to be no direct relation between intracellular free Na+ and blood pressure under antihypertensive therapy.

Intracellular calcium in essential hypertension. A parameter for assessing effective antihypertensive treatment.

The effects of the loop diuretic piretanide on blood pressure and intra-erythrocytic free Na+ and Ca2+ were examined in 14 essential hypertensives. Intra-erythrocytic Ca2+ activity was found to decrease (P less than 0.01) and Na+ activity to increase (P less than 0.05). In spontaneously hypertensive rats (SHRs) hypovolaemia abolished the humoral transmission of hypertension to normotensive rats. Therefore the decrease in intracellular Ca2+, which may be responsible for the diminished vascular tone under diuretic treatment, could be mediated by a suppression of humoral factors due to diuretic-induced hypovolaemia.

Intracellular electrolytes and hormonal parameters during weight reduction.

The mechanisms of the blood pressure lowering effect of weight reduction have not yet been fully elucidated. In this study the intracellular electrolyte composition and hormonal parameters were monitored in 12 obese subjects during a 10-day diet with 800 kcal/day. A decrease in intracellular free Na+ (p less than 0.05) and Mg2+ (p less than 0.01) and in total intracellular K+ (p less than 0.05) was observed. Furthermore, plasma aldosterone and renin activity (p less than 0.05) increased, probably due to a moderate simultaneous salt restriction. There was also an increase in plasma PGI2 concentration (p less than 0.05). The observed decrease in intracellular free Na+ may be caused by salt restriction. The decrease in intracellular K+ and free Mg2+ may be induced by hormonal factors, e.g. an altered insulin secretion. Possible causes for the known hemodynamic effects of weight reduction are the diminution of intracellular Na+ and the increase in plasma PGI2.

Obesity, hypertension and intracellular electrolytes.

Intracellular activities of sodium and calcium were determined in red cells of patients with obesity. Compared to normal people mean intracellular sodium and calcium were higher in obese patients. However, increased intracellular sodium and calcium could only be observed in those patients with obesity suffering from hypertension or showing a familial disposition to hypertension. In contrast there was no difference in intracellular sodium and calcium between obese normotensives lacking a familial disposition to hypertension and normal people. Thus, our results suggest, that the observed variations in intracellular sodium and calcium in obesity are due to an enhanced blood pressure or a familial disposition to hypertension and not specific for obesity.

[Intracellular electrolytes and serum lipids in relation to dietary fatty acid intake]. / Intrazelluläre Elektrolyte und Serumlipide in Abhängigkeit von der diätetischen Fettsäurezufuhr.

In 12 moderately obese female probands without metabolic abnormalities, intracellular Mg++ activity, Na+ activity and Na+ concentration, and serum triglycerides, total cholesterol and HDL cholesterol were measured under a diet with fatty acids varying in the degree of saturation. During the diet with mainly saturated fatty acids the intracellular Na+ activity and concentration fell from 7.34 +/- 2.02 to 6.37 +/- 1.43 (p less than 0.05) and from 5.28 +/- 0.57 to 4.98 +/- 0.80 mmol/l respectively (mean values +/- SD). Intracellular Mg++ activity fell from 1.36 +/- 0.23 to 1.20 +/- 0.17 mmol/l (p less than 0.05). During the subsequent diet consisting of mainly polyunsaturated fatty acids, intracellular Na+ activity and concentration rose to 7.95 +/- 2.81 and 5.17 +/- 0.91 mmol/l respectively (p less than 0.05). The intracellular Mg++ activity showed a further decrease to 1.04 +/- 0.14 mmol/l (p less than 0.01). During the diet consisting of mainly saturated fatty acids there was a significant correlation between the changes in HDL cholesterol and intracellular Na+ activity (r = -0,78; p less than 0.01). The initial values of intracellular Mg++ correlated with HDL cholesterol (r = 0.53; p less than 0.05). Thus, moderate obesity at any rate was not associated with intracellular electrolyte disturbances. The composition of dietary fatty acids affects intracellular electrolyte composition. This may be caused on the one hand by modified membrane function due to the uptake of the various fatty acids into the membrane, and on the other hand by changes in the synthesis of prostaglandins depending on the intake of precursors.

Radioimmunoassay for vasoactive intestinal polypeptide (VIP) in plasma before and during endoscopic examinations.

A specific and sensitive radioimmunoassay of human vasoactive intestinal polypeptide using synthetic VIP as standard preparation and antiserum to synthetic VIP R 502 (Yanaihara et al. 15) is described. No crossreactions with a number of other gastrointestinal hormones such as glucagon, secretin, GIP, HPP or substance P was detected. Aprotinin (Trasylol, Bayer) or heparin had no influence on the antigen--antibody reaction. High concentrations of sodium or potassium chloride in plasma, or hyperlipoproteinemia, did not interfere with the antiserum in the described system. Basal plasma concentration of VIP in 18 females (means +/- sem = 24.05 +/- 1.79 VIP/l) and 20 males (means +/- sem = 24.11 +/- 1.91 pmol/l VIP) showed no sex specific variations. During gastroscopy plasma VIP levels were significantly higher than basal values, showing a peak secretion when the gastric antrum was inspected. During the entire colonoscopic examination, VIP levels were significantly higher than basal values. Endoscopic examination may possibly liberate VIP from the VIP containing cells which can be found throughout the gastrointestinal tract.