Restoring Coal Mining-Affected Areas: The Missing Ecosystem Services.

Multi-criteria decision analysis and cost-benefit analysis, either individually or in combination, have been used as the preferred tools to develop ecosystem services valuation, presenting significant discrepancies and variations between the calculated values. To counteract this problem, a new framework was developed based on a hierarchical weighting of the non-provisioning ecosystem services, using biodiversity as the reference ecosystem service since it is the easiest to apprehend. Their monetisation was made using the average price of EU carbon dioxide emission allowances during 2019 and 2020, obtaining reasonable and comparable results in line with what was expected for the study region. However, the revised EU Emissions Trading System Directive, which will apply from 2021-2030, generated a price escalation of carbon allowances, making it necessary to adjust or rethink the proposed framework. To achieve this goal, the paper proposes the introduction of new vectors or "missing ecosystem services" to counterbalance efforts to eliminate carbon dioxide emissions without necessarily removing humans from the equation: welfare and human health. As the linkages regarding ecosystem health, ecological restoration and human health are not well known, only welfare was incorporated into the framework. The results were highly satisfactory, in line with what was expected for the study region and the ones obtained before the price escalation of carbon allowances that started in 2021.

Valuation of Ecosystem Services Based on EU Carbon Allowances-Optimal Recovery for a Coal Mining Area.

This paper presents a new way of valuing ecosystem services based on the price of EU carbon dioxide emission allowances. Its main advantage is that it facilitates the monetisation of non-provisioning ecosystem services, which is the Achilles heel of current frameworks. The research approach is built on the notion that land rehabilitation and ecological restoration involve trade-offs between ecosystem services. A quantitative assessment (valuation) of these trade-offs is necessary to make sound decisions. However, using different valuation methods to estimate monetary values creates a non-comparability in the valuation process that is difficult to correct. To address this problem, in the first place, the propagation of imprecise preference statements in hierarchical weighting is proposed, avoiding the non-comparability caused by the different current approaches while reducing the effort of preference elicitation. In the second place, to achieve consistency, monetisation of all non-provisioning ecosystem services was carried on the above comparison and the monetary valuation of the attribute with the most direct and market-related valuation possible: carbon sequestration, using the EU Emissions Trading System. A former coal mining area exemplifies the valuation of ecosystem services provided by alternative ecological restoration scenarios. The aim is to estimate their contribution to human well-being, understand the incentives faced by decision makers to manage ecosystems in different ways and assess the values of alternative solutions. An exercise is then carried out to show that the price of EU carbon permits (as of December 2021) after the price escalation that coincides with phase 4 of the allocation of allowances under the EU Emissions Trading System can be estimated by prioritising biodiversity over other ecosystem services.

Glucose-induced inhibition of the appetitive brain response to visual food cues in polycystic ovary syndrome patients.

We postulate that insulin regulation of food intake is compromised when insulin resistance is present. In order to investigate the effect of insulin sensitivity on appetitive brain responses, we conducted functional magnetic resonance imaging studies in a group of women diagnosed with polycystic ovary syndrome (PCOS) in which insulin sensitivity ranged from normal to resistant. Subjects (n=19) were imaged while viewing pictures of high calorie (HC) foods and low calorie (LC) foods after ingesting either 75 g glucose or an equivalent volume of water. The insulin sensitive group showed reduced blood oxygen level dependent (BOLD) signal in response to food pictures following glucose ingestion in numerous corticolimbic brain regions, whereas the insulin resistant group did not. There was a significant interaction between insulin sensitivity (sensitive vs resistant) and condition (water vs glucose). The largest clusters identified included the left insula, bilateral limbic/parahippocampal gyrus/culmen/midbrain, bilateral limbic lobe/precuneus, and left superior/mid temporal gyrus/parietal for HC and LC stimuli combined, the left parahippocampal gyrus/fusiform/pulvinar/midbrain for HC pictures, and the left superior/mid temporal gyrus/parietal and middle/inferior frontal gyrus/orbitofrontal cortex for LC pictures. Furthermore, BOLD signal in the anterior cingulate, medial frontal gyrus, posterior cingulate/precuneus, and parietal cortex during a glucose challenge correlated negatively with insulin sensitivity. We conclude the PCOS women with insulin resistance have an impaired brain response to a glucose challenge. The inability of postprandial hyperinsulinemia to inhibit brain responsiveness to food cues in insulin resistant subjects may lead to greater non-homeostatic eating.

Effect of insulin sensitivity on corticolimbic responses to food picture in women with polycystic ovary syndrome.

OBJECTIVE: Insulin is one of several molecules that transmit information about energy balance to the brain. It has been hypothesized that insulin resistance fosters non-homeostatic eating. The objective of the current study was to characterize corticolimbic brain responses to appetitive stimuli in subjects with insulin sensitivities ranging from resistant to normal. DESIGN AND METHODS: Sixteen women diagnosed with polycystic ovary syndrome (PCOS) underwent functional magnetic resonance imaging (fMRI) while viewing pictures of high calorie (HC) foods, low calorie (LC) foods, and control (C) pictures. RESULTS: A region of interest analysis of the blood oxygen level dependent (BOLD) signal revealed widespread activation within corticolimbic regions in response to food pictures. Activated regions included the dorsolateral prefrontal cortex (DLPFC), medial prefrontal cortex (mPFC) , insula, nucleus accumbens (NAc), pallidum, ventral tegmental area (VTA), putamen, amygdala, caudate, substantia nigra, hippocampus, pulvinar, and midbrain. Activation of the anterior cingulate, dorsolateral prefrontal cortex (DLPFC), and midbrain by HC food pictures (HC - C) and activation of the lateral orbitofrontal cortex (OFC), pallidum, substantia nigra, ventral tegmental area (VTA), pulvinar, and midbrain by LC food pictures (LC - C) was negatively correlated with insulin sensitivity. In contrast, activation of the OFC, DLPFC, insula, hypothalamus, pallidum, substantia nigra, VTA, pulvinar, and midbrain by the HC - LC contrast was positively correlated with insulin sensitivity, whereas activation of the caudate was negatively correlated. CONCLUSIONS: The association between insulin sensitivity and corticolimbic responses to food pictures may reflect abnormal brain responses to insulin feedback that contribute to the development and or perpetuation of obesity in PCOS.

Effect of menstrual cycle phase on corticolimbic brain activation by visual food cues.

Food intake is decreased during the late follicular phase and increased in the luteal phase of the menstrual cycle. While a changing ovarian steroid milieu is believed to be responsible for this behavior, the specific mechanisms involved are poorly understood. Brain activity in response to visual food stimuli was compared during the estrogen dominant peri-ovulatory phase and the progesterone dominant luteal phase of the menstrual cycle. Twelve women underwent functional magnetic resonance imaging during the peri-ovulatory and luteal phases of the menstrual cycle in a counterbalanced fashion. Whole brain T2* images were collected while subjects viewed pictures of high calorie (HC) foods, low calorie (LC) foods, and control (C) pictures presented in a block design. Blood oxygen level dependent (BOLD) signal in the late follicular phase and luteal phase was determined for the contrasts HC-C, LC-C, HC-LC, and LC-HC. Both HC and LC stimuli activated numerous corticolimbic brain regions in the follicular phase, whereas only HC stimuli were effective in the luteal phase. Activation of the nucleus accumbens (NAc), amygdala, and hippocampus in response to the HC-C contrast and the hippocampus in response to the LC-C contrast was significantly increased in the late follicular phase compared to the luteal phase. Activation of the orbitofrontal cortex and mid cingulum in response to the HC-LC contrast was greater during the luteal phase. These results demonstrate for the first time that brain responses to visual food cues are influenced by menstrual cycle phase. We postulate that ovarian steroid modulation of the corticolimbic brain contributes to changes in ingestive behavior during the menstrual cycle.

Peptide YY(3-36)-induced inhibition of food intake in female monkeys.

Peptide YY (PYY) is produced in L cells of the intestine and is released after eating. PYY circulates in a truncated form designated PYY(3-36). PYY(3-36) is thought to be a physiologic anorexigenic peptide. The objective of the current study was to test the effect of exogenous PYY(3-36) on food intake in non-human primates exposed to different ovarian steroid milieus. The study was conducted in four ovariectomized cynomolgus monkeys replaced with estrogen alone for 2 weeks followed by estrogen in combination with progesterone for 2 weeks to mimic the menstrual cycle. The effect of PYY(3-36) on food intake was tested during each week of the simulated menstrual cycle by comparing the 2 h food intake following intracerebroventricular (icv) injection of artificial cerebrospinal fluid (aCSF) or PYY(3-36). Despite considerable variation in food intake following aCSF, PYY(3-36) consistently inhibited food consumption, except during week 2 of estrogen plus progesterone replacement. PYY(3-36) reduced food consumption by 16.2 g (95% confidence interval (CI)=4.5-27.9 g) and 26.6 g (95% CI=7.3-45.9 g) in weeks 1 and 2 respectively of estrogen only treatment and by 38.2 g (95% CI=26.1-50.2 g) in week 1 of estrogen plus progesterone treatment. In contrast, PYY(3-36) injected in week 2 of estrogen plus progesterone did not consistently inhibit food intake (13.1 g; CI=-49.5-75.7). This is the first study to report the effect of PYY(3-36) on food consumption in female monkeys. We conclude that icv administration of PYY(3-36) has a strong anorexic effect in female cynomolgus monkeys and that sensitivity to PYY(3-36) may be influenced by the ovarian steroid milieu.

Effect of leptin administration on ovulation in food-restricted rhesus monkeys.

A chronic negative energy balance due to low nutritional intake or increased energy expenditure alters several neuroendocrine axes. The reproductive and thyroid axes are inhibited while the adrenal axis is stimulated. In primates, anovulation resulting from a chronic negative energy balance is a condition often referred to as nutritional amenorrhea. The objective of the current study was to determine if hypoleptinemia induced by dietary restriction is responsible for these neuroendocrine changes, particularly anovulation. Five rhesus monkeys had their dietary intake gradually reduced to inhibit ovulation. Dietary restriction inhibited follicle-stimulating hormone (FSH) and triiodothyronine (T(3)) secretion and stimulated cortisol release. Recombinant human leptin (rhleptin) administered by continuous infusion into the lateral ventricle for 16 weeks inhibited cortisol secretion but failed to stimulate FSH, T(3) or ovulation. An immune response to rhleptin was noted after 3 weeks of leptin administration. Realimentation resulted in weight gain and reversed all endocrine responses to dietary restriction, including ovulation. These results do not support a role for reduced leptin secretion in anovulation induced by dietary restriction. The inability of rhleptin to reverse anovulation induced by a negative energy balance in monkeys is in contrast to its stimulatory effect on ovulation in women with functional hypothalamic amenorrhea. Different outcomes may be attributed to the degree of negative energy balance, the immune response generated by interspecies leptin administration, and/or other experimental variables such as dose or route of administration. Attributing opposing outcomes to species differences is unwarranted until these variables can be further examined.

Effect of fasting on cocaine-amphetamine-regulated transcript, neuropeptide Y, and leptin receptor expression in the non-human primate hypothalamus.

Leptin is a cytokine produced by white adipose tissue that circulates in direct proportion to adiposity and is an important signal of energy balance. Leptin inhibits food intake in rodents by inhibiting the orexigenic neuropetides neuropeptide Y (NPY) and agouti regulated peptide (AgRP) and stimulating the anorexigenic neuropeptides alpha-melanocyte-stimulating hormone (alpha-MSH) and cocaine-amphetamine-regulated transcript (CART). In order to extend our understanding of neuroendocrine regulation of appetite in the primate, we determined the effect of a metabolic challenge on CART, NPY, and leptin receptor (Ob-R) messenger ribonucleic acid (mRNA) in the nonhuman primate (NHP) hypothalamus. Ten adult female rhesus monkeys were either maintained on a regular diet or fasted for two days before euthanasia. CART, NPY, and Ob-R mRNA were measured by in situ hybridization histochemistry (ISHH). A 2-day fast decreased CART expression in the ARC, increased NPY gene expression in the supraoptic nucleus (SON) and paraventricular nucleus (PVN), and increased Ob-R expression in the ventromedial nucleus (VMN). This is the first report that fasting inhibits CART expression and stimulates Ob-R expression in monkeys. Increased NPY expression in the SON and PVN, but not the ARC of fasted monkeys also is novel. With some exceptions, our observations are confirmatory of findings in rodent studies. Similarities in the neuroendocrine responses to a metabolic challenge in monkeys and rodents support extending existing hypotheses of neuroendocrine control of energy homeostasis to primates.

Developing a model of nutritional amenorrhea in rhesus monkeys.

Nutritional amenorrhea is defined as cessation of menstrual cycles resulting from a chronic negative energy balance. Although it is agreed that nutritional amenorrhea results from reduced secretion of GnRH, the neuroendocrine mechanisms leading to GnRH inhibition are poorly defined. Because the invasiveness of many neuroendocrine experimental approaches precludes its use in the clinical setting, we set out to establish a model of nutritional amenorrhea in rhesus monkeys. Studies were conducted in four normal-weight and one obese female rhesus monkey. Dietary intake was gradually reduced with the goal of achieving a 15-20% weight reduction. Dietary restriction inhibited ovulation in all animals. The weight loss required to inhibit ovulation ranged from 2-11% in the four normal-weight animals and was achieved with a 23% reduction in dietary intake. The time of initiating reduced food intake to first missed ovulation was 62 +/- 13 d. Greater weight loss (46% reduction) over a longer period (10 months) was required to inhibit ovulation in the obese monkey. The onset of anovulation was not preceded by changes in menstrual cycle length or progesterone secretion. Realimentation initiated ovulation at a weight that approximated the animal's weight at the time of the last ovulatory cycle during dietary restriction. By contrast, caloric intake at the return of ovulation during realimentation was 28% greater. This is the first demonstration that chronic dietary restriction can inhibit ovulation in rhesus monkeys. This model will be useful for studying the neuroendocrine mechanisms involved in diet-induced anovulation in primates.

Caloric restriction inhibits steroid-induced gonadotropin surges in ovariectomized rhesus monkeys.

We recently reported that caloric restriction inhibited ovulation in rhesus monkeys. The objective of the current study was to determine if caloric restriction affected the positive feedback response to ovarian steroids in non-human primates. Studies were conducted in four long-term ovariectomized rhesus monkeys. Animals were given an estrogen/progesterone challenge while maintained on a normal diet and on a diet that reduced body weight by approx 20%. In all cases, animals were maintained at the desired weight [based on a calculation of body mass index (BMI)] for a minimum of 4 wk before initiating the steroid challenge. Caloric restriction reduced BMI from 23.3 +/- 0.3 to 18.9 +/- 0.2 kg/m2. The estrogen/progesterone challenge elicited an LH and FSH surge in each animal maintained at a normal BMI. By contrast, gonadotropin surges were significantly compromised when monkeys were challenged at a low BMI. In addition to affecting the reproductive axis, caloric restriction stimulated cortisol release and suppressed T3 secretion. These endocrine effects of caloric restriction are consistent with our findings in ovary-intact monkeys. In summary, our previous reports in ovary-intact animals confirmed an effect of caloric restriction on tonic gonadotropin secretion leading to anovulation. Our current results suggest the effects of caloric restriction on the reproductive axis extend beyond inhibition of tonic gonadotropin secretion to include a disturbance of phasic gonadotropin secretion.

Hypoglycemia does not affect gonadotroph responsiveness to gonadotropin-releasing hormone in rhesus monkeys.

Hypoglycemia inhibits gonadotropin secretion in primates by an undefined mechanism. Some evidence suggests that hypoglycemia inhibits gonadotropin secretion independent of gonadotropin-releasing hormone (GnRH) inhibition. To this end, the effect of insulininduced hypoglycemia on the luteinizing hormone (LH) and follicle-stimulating hormone (FSH) response to graded doses of GnRH (25, 75, and 250 ng/kg) administered at 120-min intervals was determined in rhesus monkeys. A crossover design was employed such that each animal received GnRH under both hypoglycemic and euglycemic conditions. Experiments were performed in the follicular phase. Gonadotroph responsiveness to GnRH was quantified by determining the change in area under the LH (DeltaAULHC) and FSH (DeltaAUFSHC) curves that occurred in the first 60 min following each GnRH pulse. There was no statistical difference in DeltaAULHC between euglycemic and hypoglycemic animals at any GnRH dose (25 ng/kg: p = 0.19; 75 ng/kg: p = 0.41; 250 ng/kg: p = 0.46). Similarly, changes in AUFSHC following GnRH administration were comparable in euglycemic and hypoglycemic animals (25 ng/kg: p = 0.59; 75 ng/kg: p = 0.90; 250 ng/kg: p = 0.33). We conclude that hypoglycemia had no effect on gonadotroph responsiveness to GnRH. These results are consistent with the conclusion that hypoglycemia inhibits gonadotropin secretion by acting primarily at the level of the hypothalamus to reduce GnRH secretion rather than affecting pituitary responsiveness to GnRH.

Effectiveness of photodynamic ablation for destruction of endometrial explants in a rat endometriosis model.

OBJECTIVE: To evaluate the potential of photodynamic therapy with aminolevulinic acid (ALA-PDT) for ablation of endometrial explants in a rat endometriosis model and to compare the effect of ALA-PDT, electrosurgery, and surgical resection on normal peritoneum. DESIGN: Prospective controlled experimental trial. SETTING: University medical center. ANIMAL(S): Mature Sprague-Dawley female rats. INTERVENTION(S): Induction of endometriosis and subsequent treatment with ALA-PDT; electrosurgery, and simple resection, and ALA-PDT of normal peritoneum. MAIN OUTCOME MEASURE(S): Histopathological assessment. RESULT(S): Systemic ALA followed by exposure to photoactivating light for 10 or 15 minutes resulted in ablation of all explants harvested 3-4 days after treatment. Permanent destruction was confirmed by absence of regrowth by week 3. Exposure of normal peritoneum to ALA-PDT resulted in initial necrosis, with complete recovery by day 16. Adhesions were present on day 16 in 50% of cases after electrosurgery and in 100% of cases after resection. No adhesions were present in ALA-PDT-treated animals. CONCLUSION(S): Systemic ALA followed by exposure to photoactivating light at relatively low power densities for periods as brief as 10 minutes resulted in ablation of endometriotic explants. Exposure of normal peritoneum to ALA-PDT resulted in complete resurfacing. Both electrosurgery and surgical resection resulted in a greater incidence of surface adhesions.

Estrogen-induced gonadotropin surge in rhesus monkeys is not inhibited by cortisol synthesis inhibition or hypoglycemia.

Acute administration of corticotrophin-releasing hormone (CRH) has been shown to inhibit gonadotropin secretion in several species including rodents, sheep, humans, and nonhuman primates. Similarly, a variety of acute stressors have been shown to inhibit tonic gonadotropin secretion and may do so through a CRH mechanism. Stress-induced inhibition of tonic gonadotropin secretion below levels required for follicular maturation would be expected to inhibit ovulation. An additional mechanism whereby acute stressors could interfere with ovulation is through inhibition of the preovulatory gonadotropin surge. In the present study, we determined the effect of acute activation of the hypothalamic-pituitary-adrenal (HPA) axis on phasic gonadotropin secretion in female rhesus monkeys. Activation of the HPA axis was achieved by either a hypoglycemic challenge or blockage of cortisol synthesis with metyrapone, 24 h after an estradiol benzoate challenge. Neither metyrapone nor insulin-induced hypoglycemia inhibited gonadotropin secretion. In fact, the initiation of the luteinizing hormone and follicle-stimulating hormone surge was advanced by 7.4 +/- 0.4 h (p < 0.001) and 4.8 +/- 1.4 h (p = 0.04) respectively, in metyrapone-treated monkeys compared with saline controls. By contrast, hypoglycemia did not affect the gonadotropin surge. The gonadotropin surge was preceded by increased progesterone secretion in metyrapone-treated but not insulin-treated monkeys. This difference in progesterone secretion likely explains the advancement of the gonadotropin surge in the metyrapone-treated animals.