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Published literature is sparse on topics associated with eared seal (otariid) dentistry. The objective of this study was to establish consensus on effective management of dental disease in otariids, using a Delphi approach. A total of 25 veterinarians with experience managing dental disease in seven species of otariids participated in the Delphi process. Oral lesions and their contributing risk factors were ranked according to perceived frequency. Consensus statements for best practices were agreed upon for a variety of topics within the categories of planning and preparation, procedural details, intervention strategies, and postoperative care. Panelist comments were collated into a Supplementary File to assist clinicians in forming their own conclusions on topics for which no consensus yet exists. Opportunities for future research include factors associated with oral lesions, ideal anesthetic management, identification of ideal candidates for endodontic therapies, ideal local and regional anesthesia, ideal suture and closure techniques, particularly with the goal of reducing dehiscence as a postoperative complication, and ideal postoperative care options.

The purpose of the document was to provide guidelines for the practice of companionanimal dentistry for the veterinary profession. Since veterinary dentistry is constantly progressing, the guidelines were updated this year.

With modern veterinary medicine prolonging the lives of pets, more and more dental disease is occurring in older patients. Dental diseases have a bearing on the pet's quality of life and should be addressed. By being on the lookout for periodontal disease, fractured teeth, feline odontoclastic resorptive lesions and chronic ulcerative gingivostomatis, the practitioner can add years of quality life to the patient.

Why has the U.S. stock market performed so well over the long term? Although non-governance factors have almost certainly played a role, it is likely improved governance and incentives have contributed as well. Because chief executives have more equity ownership than they did 20 years ago, they care more about stock prices. Institutional investors have become increasingly important and are more likely to push for higher stock returns. And boards have become more independent. In other words, the U.S. corporate governance and compensation systems are far from hopeless. The scandals have merely exposed weaknesses. For example, CEO stock ownership sometimes does create an incentive to inflate accounting numbers; most boards do not sufficiently restrict executives' ability to exercise options, sell shares or hedge their positions through derivatives; and most options do not appear as expenses on company income statements, with the result that boards may undervalue the cost of issuing options. A system designed to eliminate all excessive behaviour would pose far greater risks than the behaviour itself. The Draconian regulations required would foster inordinate caution and suppress experimentation at a time when we need more organizational experimentation than ever to take advantage of new information and communication technologies. Enron was an experiment that failed. We learn from the failure not by withdrawing into a shell, but rather by improving control structures and corporate governance in a way that allows continued experimentation -- and occasional failures.

Liver X receptors (LXRα and LXRβ) are important regulators of cholesterol and lipid metabolism, and their activation has been shown to inhibit cardiovascular disease and reduce atherosclerosis in animal models. Small molecule agonists of LXR activity are therefore of great therapeutic interest. However, the finding that such agonists also promote hepatic lipogenesis has led to the idea that hepatic LXR activity is undesirable from a therapeutic perspective. To investigate whether this might be true, we performed gene targeting to selectively delete LXRα in hepatocytes. Liver-specific deletion of LXRα in mice substantially decreased reverse cholesterol transport, cholesterol catabolism, and cholesterol excretion, revealing the essential importance of hepatic LXRα for whole body cholesterol homeostasis. Additionally, in a pro-atherogenic background, liver-specific deletion of LXRα increased atherosclerosis, uncovering an important function for hepatic LXR activity in limiting cardiovascular disease. Nevertheless, synthetic LXR agonists still elicited anti-atherogenic activity in the absence of hepatic LXRα, indicating that the ability of agonists to reduce cardiovascular disease did not require an increase in cholesterol excretion. Furthermore, when non-atherogenic mice were treated with synthetic LXR agonists, liver-specific deletion of LXRα eliminated the detrimental effect of increased plasma triglycerides, while the beneficial effect of increased plasma HDL was unaltered. In sum, these observations suggest that therapeutic strategies that bypass the liver or limit the activation of hepatic LXRs should still be beneficial for the treatment of cardiovascular disease.

The cycle of gallbladder filling and emptying controls the flow of bile into the intestine for digestion. Here we show that fibroblast growth factor-15, a hormone made by the distal small intestine in response to bile acids, is required for gallbladder filling. These studies demonstrate that gallbladder filling is actively regulated by an endocrine pathway and suggest a postprandial timing mechanism that controls gallbladder motility.

This paper describes and considers explanations for changes in corporate governance and merger activity in the United States since 1980. Corporate governance in the 1980s was dominated by intense merger activity distinguished by the prevalence of leveraged buyouts (LBOs) and hostility. After a brief decline in the early 1990s, substantial merger activity resumed in the second half of the decade, while LBOs and hostility did not. Instead, internal corporate governance mechanisms appear to have played a larger role in the 1990s. We conclude by considering whether these changes and the movement toward shareholder value are likely to be permanent.

Both heliophysics and planetary physics seek to understand the complex nature of the solar wind's interaction with solar system obstacles like Earth's magnetosphere, the ionospheres of Venus and Mars, and comets. Studies with this objective are frequently conducted with the help of single or multipoint in situ electromagnetic field and particle observations, guided by the predictions of both local and global numerical simulations, and placed in context by observations from far and extreme ultraviolet (FUV, EUV), hard X-ray, and energetic neutral atom imagers (ENA). Each proposed interaction mechanism (e.g., steady or transient magnetic reconnection, local or global magnetic reconnection, ion pick-up, or the Kelvin- Helmholtz instability) generates diagnostic plasma density structures. The significance of each mechanism to the overall interaction (as measured in terms of atmospheric/ionospheric loss at comets, Venus, and Mars or global magnetospheric/ionospheric convection at Earth) remains to be determined but can be evaluated on the basis of how often the density signatures that it generates are observed as a function of solar wind conditions. This paper reviews efforts to image the diagnostic plasma density structures in the soft (low energy, 0.1-2.0 keV) X-rays produced when high charge state solar wind ions exchange electrons with the exospheric neutrals surrounding solar system obstacles.

In this paper we focus empirical and conceptual attention on the social construction of information systems (IS) requirements, and illustrate that IS developers too often choose to ignore, and thus effectively black-box, the complexities of gathering requirements in order to simplify both the difficulties of their work and their relations with customers. The empirical contribution of this paper is evidence drawn from a study of how IS developers pursue requirements engineering and how they conceive its value. The factors we found to be important in this process include: the changing needs of the organization, the ways in which structured IS methods are enacted via experience and social competency, the formation of project groups, and finally engagement in interpersonal conflict and negotiations. Our conceptual contribution is theorization on the nature of developing requirements as a process of social learning.

Crohn's disease (CD) patients exhibit an increased frequency of Foxp3-expressing regulatory T cells (CD4+CD25+Foxp3+, Tregs) in the intestinal mucosa, which show suppressive function ex vivo despite their failure to regulate chronic activation of effector T cells in situ. This suggests that factors present in the inflamed intestinal mucosa can disrupt normal Treg function in vivo. CD is disproportionate in female patients, suggesting that estrogen (E2) may contribute to worsened clinical disease. Despite this linkage, E2 has paradoxically been shown to be immunoprotective via induction of Foxp3 expression in conventional T cells (CD4+CD25−, Tconv). The goal of this study was to determine the mechanistic contribution of E2 signaling to T cells in female ileitis subjects and to test the hypothesis that enhanced E2 signaling to estrogen receptor beta (ERb) subverts normally immunoprotective functions of E2.MethodsWe utilized the SAMP1/YitFc (SAMP) mouse model, a spontaneous model of ileitis that recapitulates many features of human CD including female sex bias. ERb-knockout mice were fully back-crossed to SAMP to generate congenic SAMP-ERb-KO mice. Tconv and Treg were isolated from the mesenteric lymph node (MLN) by flow cytometric sorting and used for downstream applications including real-time quantitative PCR (qPCR); chromatin immunoprecipitation (ChIP); and Next-Generation RNA Sequencing (RNA-Seq).ResultsSAMP-ERβ-KO mice respond to E2 solely through the estrogen receptor alpha (ERα) isoform and not through ERb, making them a convenient tool to study the contribution of ERa/ERb signaling to ileitis. We observed significantly decreased ileal inflammation in 10-week-old SAMP-ERb-KO-F mice compared to native SAMP-F, resulting in a loss of female sex bias and a restoration of MLN Tregs in SAMP-ERb-KO mice. qPCR analysis revealed that Tconv from native SAMP-F express significantly lower ERα and higher ERβ mRNA levels compared to SAMP-M, leading to an overall increase in ERβ/ERα ratios in native female SAMP. Interestingly, SAMP-ERβ-KO mice displayed equivalent ERa gene expression among male and female Tconv, further implicating elevated expression of ERβ as a potential contributor to the female sex bias in SAMP. Additionally, ChIP assays revealed faulty transcription-factor binding of E2 to target gene promoters in Tconv from native SAMP-F, suggesting that nuclear factor activity of ER is compromised in SAMP-F. RNA-Seq experiments using MLN Tregs revealed distinct patterns of gene expression among native male and female SAMP, as well as among SAMP-ERb-KO mice compared to native SAMP, suggesting that perhaps as a consequence of altered ERa/ERb expression, native SAMP-F Tregs display an aberrant genetic signature.ConclusionsThe interplay between E2 and lymphocyte function is a relatively understudied area with the potential to uncover novel gene-regulatory mechanisms operating downstream of nuclear hormone receptors that may influence development of IBD and other autoinflammatory diseases. Collectively, our data suggest that E2-ERa signaling is immunoprotective in the setting of intestinal inflammation and that female sex bias persists due to elevated ratios of ERb/ERa expression in conventional T cells. Differential gene expression in male and female SAMP Tregs suggests that faulty E2 signaling in females results in aberrant Treg differentiation and/or function, contributing to worsened clinical disease.