1,833 research outputs found
A Downwind View of the Cathedral: Using Rule Four to Allocate Wind Rights
No full textThe rapid pace of U.S. wind energy development is generating a growing number of conflicts over competing wind rights. The “wake” of a commercial wind turbine creates turbulence and unsteady wind flow that can reduce the productivity of other wind turbines situated downwind. Existing law is unclear as to whether a landowner who installs a wind turbine on its property is liable for the lost productivity of a downwind neighbor’s turbine resulting from such wake effects. Legal uncertainty as to how competing wind rights are shared among neighbors can induce wind energy developers to abandon otherwise lucrative turbine sites situated near property lines, thus forfeiting valuable wind resources. This paper applies Calabresi and Melamed’s familiar “Cathedral” model to determine which rule regime would best promote the efficient allocation of competing wind rights while maintaining consistency with existing law. Surprisingly, the Cathedral model’s infamous and rarely-applied “Rule Four” seems best-suited for addressing these conflicts
Observations upon a treatise, entitled A description of the Plain of Troy, by Monsieur Le Chevalier /
No full textErrata: p. [1] at end.Signatures: [A]1 B-H⁴.Includes bibliographical references.ESTC(RLIN)Mode of access: Internet.Library copy bound with: Description of the plain of Troy : with a map of that region, delineated from an actual survey : read in French before the Royal Society of Edinburgh, Feb. 21 and 28 and March 21 1791 / by the author, M. Chevalier. Edinburgh : Printed for T. Cadell, 1791. (90-B15413
Activation of Estrogen Response Element-independent ERα signaling protects female mice from diet-induced obesity
No full text17β-estradiol (E2) regulates central and peripheral mechanisms that control energy and glucose homeostasis predominantly through estrogen receptor α (ERα) acting via receptor binding to estrogen response elements (ERE). ERα signaling is also involved in mediating the effects of E2 on diet-induced obesity (DIO), although the roles of ERE-dependent and -independent ERα signaling in ameliorating the effects of DIO remain largely unknown. We hypothesize that ERE-dependent ERα signaling is necessary to ameliorate the effects of DIO. We addressed this question using ERαKO (KO) and ERαKIKO (KIKO) female mice; the latter expressing an ERα that lacks a functional ERE binding domain. Females were ovariectomized, fed low-fat (LFD) or high-fat (HFD) diet, and orally dosed with vehicle or estradiol benzoate (EB, 300 μg/kg). After 9 weeks, body composition, glucose and insulin tolerance, peptide hormone and inflammatory cytokine levels, and hypothalamic arcuate nucleus and liver gene expression were assessed. EB reduced body weight and body fat in WT, regardless of diet, and in HFD-fed KIKO, in part by reducing energy intake and feeding efficiency. EB reduced fasting glucose levels in KIKO mice fed both diets but augmented glucose tolerance only in HFD-fed KIKO. Plasma insulin and IL-6 were elevated in KIKO and KO compared to WT on a LFD. Expression of arcuate neuropeptide and receptor genes and liver fatty acid biosynthesis genes was altered by HFD and by EB through ERE-dependent and -independent mechanisms. Therefore, ERE-independent signaling mechanisms in both the brain and peripheral organs mediate, in part, the effects of E2 during DIO.Peer reviewe
Regulation of gene expression by 17β-estradiol in the arcuate nucleus of the mouse through ERE-dependent and ERE-independent mechanisms
No full text17β-Estradiol (E2) modulates gene expression in the hypothalamic arcuate nucleus (ARC) to control homeostatic functions. In the ARC, estrogen receptor (ER) α is highly expressed and is an important contributor to E2's actions, controlling gene expression through estrogen response element (ERE)-dependent and -independent mechanisms. The objective of this study was to determine if known E2-regulated genes are regulated through these mechanisms. The selected genes have been shown to regulate homeostasis and have been separated into three subsections: channels, receptors, and neuropeptides. To determine if ERE-dependent or ERE-independent mechanisms regulate gene expression, two transgenic mouse models, an ERα knock-out (ERKO) and an ERα knock-in/knock-out (KIKO), which lacks a functional ERE binding domain, were used in addition to their wild-type littermates. Females of all genotypes were ovariectomized and injected with oil or estradiol benzoate (E2B). Our results suggest that E2B regulates multiple genes through these mechanisms. Of note, Cacna1g and Kcnmb1 channel expression was increased by E2B in WT females only, suggesting an ERE-dependent regulation. Furthermore, the NKB receptor, Tac3r, was suppressed by E2B in WT and KIKO females but not ERKO females, suggesting that ERα-dependent, ERE-independent signaling is necessary for Tac3r regulation. The adrenergic receptor Adra1b was suppressed by E2B in all genotypes indicating that ERα is not the primary receptor for E2B's actions. The neuropeptide Tac2 was suppressed by E2B through ERE-dependent mechanisms. These results indicate that E2B activates both ERα-dependent and independent signaling in the ARC through ERE-dependent and ERE-independent mechanisms to control gene expression.Peer reviewe
Estrogen response element-independent signaling partially restores post-ovariectomy body weight gain but is not sufficient for 17β-estradiol's control of energy homeostasis
No full textThe steroid 17β-estradiol (E2) modulates energy homeostasis by reducing feeding behavior and increasing energy expenditure primarily through estrogen receptor α (ERα)-mediated mechanisms. Intact ERαKO female mice develop obesity as adults exhibiting decreased energy expenditure and increased fat deposition. However, intact transgenic female mice expressing a DNA-binding-deficient ERα (KIKO) are not obese and have similar energy expenditure, activity and fat deposition as to wild type (WT) females, suggesting that non-estrogen response element (ERE)-mediated signaling is important in E2 regulation of energy homeostasis. Initial reports did not examine the effects of ovariectomy on energy homeostasis or E2's attenuation of post-ovariectomy body weight gain. Therefore, we sought to determine if low physiological doses of E2 (250 ng QOD) known to suppress post-ovariectomy body weight gain in WT females would suppress body weight gain in ovariectomized KIKO females. We observed that the post-ovariectomy increase in body weight was significantly greater in WT females than in KIKO females. Furthermore, E2 did not significantly attenuate the body weight gain in KIKO females as it did in WT females. E2 replacement suppressed food intake and fat accumulation while increasing nighttime oxygen consumption and activity only in WT females. E2 replacement also increased arcuate POMC gene expression in WT females only. These data suggest that in the intact female, ERE-independent mechanisms are sufficient to maintain normal energy homeostasis and to partially restore the normal response to ovariectomy. However, they are not sufficient for E2's suppression of post-ovariectomy body weight gain and its effects on metabolism and activity.Peer reviewe
Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse
No full textA significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.Peer reviewe
The interaction of fasting, caloric restriction, and diet-induced obesity with 17β-estradiol on the expression of KNDy neuropeptides and their receptors in the female mouse
No full textArcuate neurons that coexpress kisspeptin (Kiss1), neurokinin B (Tac2), and dynorphin (Pdyn) mediate negative feedback of 17β-estradiol (E2) on the HPG axis. Previous studies report that fasting and caloric restriction reduce arcuate Kiss1 expression. The objective of this study was to determine the interactions of E2 with fasting, caloric restriction, and diet-induced obesity on KNDy gene and receptor expression. Ovariectomized female mice were separated into control and estradiol benzoate (E2B)-treated groups. E2B decreased Kiss1 and the tachykinin 2 receptor, Tac3r, in ARC tissue and Tac2 in Tac2 neurons. Diet-induced obesity decreased Kiss1 in oil-treated animals and the kisspeptin receptor, Kiss1r and Tac3r in the ARC of E2B-treated animals. Chronic caloric (30%) restriction reduced all three neuropeptides in oil-treated females and Kiss1r by E2B in CR animals. Taken together, our experiments suggest that steroidal environment and energy state negatively regulate KNDy gene expression in both ARC and Tac2 neurons.Peer reviewe
Differential gene regulation of GHSR signaling pathway in the arcuate nucleus and NPY neurons by fasting, diet-induced obesity, and 17β-estradiol
No full textGhrelin’s receptor, growth hormone secretagogue receptor (GHSR), is highly expressed in the arcuate nucleus (ARC) and in neuropeptide Y (NPY) neurons. Fasting, diet-induced obesity (DIO), and 17β-estradiol (E2) influence ARC Ghsr expression. It is unknown if these effects occur in NPY neurons. Therefore, we examined the expression of Npy, Agrp, and GHSR signaling pathway genes after fasting, DIO, and E2 replacement in ARC and pools of NPY neurons. In males, fasting increased ARC Ghsr and NPY Foxo1 but decreased NPY Ucp2. In males, DIO decreased ARC and NPY Ghsr and Cpt1c. In fed females, E2 increased Agrp, Ghsr, Cpt1c, and Foxo1 in ARC. In NPY pools, E2 decreased Foxo1 in fed females but increased Foxo1 in fasted females. DIO in females suppressed Agrp and augmented Cpt1c in NPY neurons. In summary, genes involved in GHSR signaling are differentially regulated between the ARC and NPY neurons in a sex-dependent manner.Peer reviewe
Remarks and observations on the plain of Troy, made during an excursion in June, 1799 /
No full textSignatures: pi⁴ A-G⁴.Errata: p. [2] at end; p. [1] and [3] at end blank.ESTC(RLIN)Mode of access: Internet.Library copy bound with: Description of the plain of Troy : with a map of that region, delineated from an actual survey : read in French before the Royal Society of Edinburgh, Feb. 21 and 28 and March 21 1791 / by the author, M. Chevalier. Edinburgh : Printed for T. Cadell, 1791. (90-B15413
Toward a More Strategic National Stockpile
No full textThe COVID–19 pandemic exposed major deficiencies in the United States’ approach to stockpiling for emergencies. States, cities, and hospitals across the country had meager inventories of critical medical items on hand when the pandemic first reached U.S. soil, and the federal government’s Strategic National Stockpile proved far too small to serve the country’s needs in the first several months of the crisis. As nationwide shortages spread, many state governments were compelled to bid against each other to procure scarce medical supplies—a distribution approach that disadvantaged low-income and minority communities and left countless healthcare professionals and staff ill-equipped to protect themselves against a deadly virus. These severe supply shortages, which hindered the country’s early pandemic response, have since generated an unprecedented push to reform the nation’s stockpiling policy structure. This Article uses a simple cost-benefit model to highlight shortcomings in the existing U.S. stockpiling policy regime and to identify specific avenues for addressing them. Among other things, U.S. stockpiling policies need to better account for important differences in the rotatability of supplies and should incentivize more private stockpiling of the most rotatable emergency items. Targeted reforms of commandeering laws and price-gouging restrictions could further strengthen private incentives to stockpile and may even help to clarify how states and the federal government share responsibilities in the nation’s stockpiling effort. And much more federal support is needed to incentivize the build-out and maintenance of domestic supply chains for the least-rotatable emergency goods. Such tailoring of policies and programs to better fit the unique attributes of stockpiling activities can help ensure the nation is far better equipped to respond the next time disaster strikes
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