Persistent reduced ecosystem respiration after insect disturbance in high elevation forests

Amid a worldwide increase in tree mortality, mountain pine beetles (Dendroctonus ponderosae Hopkins) have led to the death of billions of trees from Mexico to Alaska since 2000. This is predicted to have important carbon, water and energy balance feedbacks on the Earth system. Counter to current projections, we show that on a decadal scale, tree mortality causes no increase in ecosystem respiration from scales of several square metres up to an 84 km2 valley. Rather, we found comparable declines in both gross primary productivity and respiration suggesting little change in net flux, with a transitory recovery of respiration 6–7 years after mortality associated with increased incorporation of leaf litter C into soil organic matter, followed by further decline in years 8–10. The mechanism of the impact of tree mortality caused by these biotic disturbances is consistent with reduced input rather than increased output of carbon

Young and Intermediate-age Distance Indicators

Distance measurements beyond geometrical and semi-geometrical methods, rely mainly on standard candles. As the name suggests, these objects have known luminosities by virtue of their intrinsic proprieties and play a major role in our understanding of modern cosmology. The main caveats associated with standard candles are their absolute calibration, contamination of the sample from other sources and systematic uncertainties. The absolute calibration mainly depends on their chemical composition and age. To understand the impact of these effects on the distance scale, it is essential to develop methods based on different sample of standard candles. Here we review the fundamental properties of young and intermediate-age distance indicators such as Cepheids, Mira variables and Red Clump stars and the recent developments in their application as distance indicators.Comment: Review article, 63 pages (28 figures), Accepted for publication in Space Science Reviews (Chapter 3 of a special collection resulting from the May 2016 ISSI-BJ workshop on Astronomical Distance Determination in the Space Age

A Neptune-mass exoplanet in close orbit around a very low-mass star challenges formation models

Stars and planetary system

Astronomical Distance Determination in the Space Age: Secondary Distance Indicators

The formal division of the distance indicators into primary and secondary leads to difficulties in description of methods which can actually be used in two ways: with, and without the support of the other methods for scaling. Thus instead of concentrating on the scaling requirement we concentrate on all methods of distance determination to extragalactic sources which are designated, at least formally, to use for individual sources. Among those, the Supernovae Ia is clearly the leader due to its enormous success in determination of the expansion rate of the Universe. However, new methods are rapidly developing, and there is also a progress in more traditional methods. We give a general overview of the methods but we mostly concentrate on the most recent developments in each field, and future expectations. © 2018, The Author(s)

Cardiovascular risk in patients with growth hormone deficiency: effects of growth hormone substitution

OBJECTIVE: To review the literature on the increased cardiovascular risk in patients with growth hormone (GH) deficiency and the positive effects of GH replacement. METHODS: We analyze the factors that contribute to cardiovascular risk in GH deficiency, including body composition and lipid profile, and summarize GH treatment strategies and results described in the literature. RESULTS: The prominent clinical finding in patients with GH deficiency is the increased abdominal fat, even in patients with normal weight. Cardiac ejection volume tends to be decreased, and arterial distensibility is diminished. The lipid status is also worsened, accompanied by increased inflammatory markers, such as highly sensitive C-reactive protein. Typically, GH treatment reduces visceral fat and increases muscle mass, changes that diminish cardiovascular risk. Because of direct effects as well as increased hemodynamic performance and increased blood volume, cardiac performance is improved. With GH therapy, total cholesterol and low-density lipoprotein levels decrease by 10% to 20%, and inflammatory markers such as C-reactive protein decline. Carbohydrate metabolism during moderate to long-term treatment is minimally affected, although obese patients with GH deficiency on rare occasion may have hyperglycemia or even diabetes. CONCLUSION: The relevance of the beneficial effects of GH on the cardiovascular system is strongly suggested but not fully proved. The results in a large cohort of GH-treated patients (the KIMS or Pharmacia and Upjohn International Metabolic Surveillance database) demonstrated no difference in cardiovascular risk in comparison with that in a control population after a mean of 3 years of treatment

The effects of growth hormone deficiency and replacement on glucocorticoid exposure in hypopituitary patients on cortisone acetate and hydrocortisone replacement

Objective 11?-hydroxysteroid dehydrogenase type 1 (11?HSD1) converts inactive cortisone to active cortisol. 11?HSD1 activity is increased in GH deficiency and inhibited by GH and IGF-I in acromegaly. However it is not known whether these changes in cortisol metabolism exert significant effects during hydrocortisone therapy, and the effect has not been studied in patients taking cortisone acetate. We have studied the effect of GH induced 11?HSD1 inhibition in hypopituitary adults with severe GH deficiency to determine whether this inhibition has a different magnitude of effect when patients are taking different forms of glucocorticoid replacement therapy.Design, patients and measurements We have taken the ratio of 11-hydroxy/11-oxo cortisol metabolites (Fm/Em), an established measure of net 11?HSD activity to reflect the likely balance of cortisol to cortisone exposure in tissues expressing 11?HSD1, principally the liver and adipose tissue. We recruited 10 hypopituitary adults all on established glucocorticoid replacement therapy, but who were not receiving GH. Patients were treated with their standard hydrocortisone therapy for one week and an equivalent dose of cortisone acetate in its place for one week in random order. Serial serum cortisol assessments and urine steroid profiles were performed on each treatment. All patients were then established on GH therapy for at least three months before the two-week cycle was repeated. Fm/Em was also measured in a control population (20F, 20M).Results Prior to GH, the ratio Fm/Em was greater with hydrocortisone compared with cortisone acetate replacement (1·17 ± 0·28 and 0·52 ± 0·09 respectively, P < 0·001) or with normal subjects (normal males: 0·81 ± 0·24, females 0·66 ± 0·14). Following GH replacement Fm/Em fell in patients on hydrocortisone and cortisone acetate (Pre-GH: 0·84 ± 0·40, Post-GH: 0·70 ± 0·34, P < 0·05) confirming the inhibition of 11?HSD1 by GH/IGF-I. Conversely, the ratio of urinary free cortisol/cortisone did not change indicating unchanged 11?HSD2 activity. Mean circulating cortisol also fell in all subjects after GH. This effect was greater during cortisone acetate treatment (?18·7%, P < 0·0001), than during hydrocortisone replacement (?10·9%, P < 0·05).Conclusions Our data suggest that tissue exposure to glucocorticoid is supra-physiological in hypopituitary patients with untreated GH deficiency taking hydrocortisone replacement therapy. This situation is ameliorated by GH replacement therapy. However, local and circulating cortisol concentrations are more vulnerable to the inhibitory effect of GH on 11?HSD1 in patients taking cortisone acetate, such that serum cortisol assessments should be made in patients taking cortisone acetate after GH therapy to ensure that glucocorticoid replacement remains adequate

The effect of growth hormone replacement therapy on adrenal androgen secretion in adult onset hypopituitarism

OBJECTIVE: Growth hormone replacement therapy in GH-deficient children is associated with enhanced adrenal androgen production, raising the possibility that GH might stimulate adrenocortical hormone secretion. This has not been extensively investigated in adults to date. GH is a potent modulator of the activity of the 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) enzyme and by altering cortisol metabolism can affect the function of the hypothalamo-pituitary-adrenal (HPA) axis and therefore potentially of adrenal androgen secretion. This study examined the effects of GH replacement in GH-deficient adults on adrenal androgen secretion. DESIGN: Prospective study of the effect of GH replacement therapy on adrenal androgen production in patients with adult onset hypopituitarism over a 12-month period. PATIENTS AND METHODS: Thirty adult GH-deficient patients were classified into two groups according to their cortisol responses to an insulin-induced hypoglycaemia or a glucagon stimulation test: 13 patients were adrenocorticotropic hormone (ACTH)-sufficient (nine females, age 45.1 +/- 3 years), whereas 17 patients were ACTH-deficient (11 females, age 45.5 +/- 3 years). Serum samples were collected before patients were initiated on GH replacement therapy using a dose titration regimen, and after 6 and 12 months on GH therapy for measurement of serum IGF-I, dehydroepiand-rosterone sulphate (DHEAS), Delta4-Androstenedione (A4), testosterone, cortisol, sex hormone binding globulin (SHBG) and cortisol binding globulin (CBG). RESULTS: Six months after the initiation of GH replacement therapy, serum IGF-I levels were within the normal age-related reference range in both groups of patients and this was maintained at 12 months [in all patients 0 vs. 6 months: median (interquartile range): 92.5 ng/ml (73-116 ng/ml) vs. 191 ng/ml (159-224 ng/ml), P < 0.01]. In both ACTH-sufficient and -deficient groups of GH-deficient patients, pretreatment serum DHEAS levels were lower than the normal age-related reference range (P < 0.01); the ACTH-deficient patients had significantly lower DHEAS levels than the ACTH-sufficient patients [median (interquartile range): 0.5 micro mol/l (0.4-1.2 micro mol/l) vs. 1.5 micro mol/l (0.6-2.7 micro mol/l), P < 0.05]. Following GH replacement therapy, median levels of serum DHEAS levels rose from 1.5 micro mol/l (0.6-2.7 micro mol/l) to 1.9 micro mol/l (1.9-3.9 micro mol/l) in ACTH-sufficient patients, increasing in 11 of the 13 patients (P < 0.02). In this group, the median percentage increase from baseline was 32% at 6 months (P < 0.05). In contrast, baseline serum DHEAS levels [0.5 micro mol/l (0.4-1.2 micro mol/l)] declined in or from the measurable range in 47% of ACTH-deficient patients [median -16%; range -36-0] and only in one patient a + 0.2 micro mol/l increase was observed. GH dose requirements tended to be lower in ACTH-sufficient patients [1.2 U/day (0.8-1.4 U/day) vs. 1.6 U/day (1.0-2.0 U/day); P = 0.062]. There were no significant changes in serum testosterone, A4, SHBG and/or CBG levels, compared to the pretreatment levels, in either group of patients over the 12 months of GH replacement. CONCLUSIONS: This study shows that median serum DHEAS levels are significantly lower in GH-deficient patients, even those with intact ACTH reserve, than in aged-matched controls. GH replacement therapy is associated with a significant increase in mean serum DHEAS only in ACTH-sufficient patients. These findings are consistent with either (i) GH stimulation of adrenal androgen production in the permissive presence of ACTH or (ii) an inhibitory effect of GH on 11beta-HSD type 1 activity leading to enhanced cortisol clearance, subsequent activation of the HPA axis and ACTH-mediated androgen secretion