\u3ci\u3eFaits Accomplis\u3c/i\u3e in the Shadow of Shifting Power

The military fait accompli is so understudied a phenomenon in the international relations literature that even its definition is not widely known. A fait accompli is a unilateral revision to the status quo in an ongoing dispute over some distribution of benefits. Though recent work has demonstrated that faits accomplis are relatively common events in international history and current international relations, the subject remains undertheorized and empirically underexplored. This dissertation seeks to open up the conversation about faits accomplis in two complementary ways. First, it advances an original formal model of faits accomplis in the shadow of power shifts, interacting the effects of dynamic power on a rising state’s decision to use faits accomplis to revise the status quo in an ongoing territorial dispute. Second, it tests the predictions of the theoretical model against the evidence amassed in two cases of territorial disputes, China’s maritime territorial disputes with its Southeast Asian neighbors in the South China Sea, and those with Japan in the East China Sea. The dissertation aims contribute to the international relations literature at three levels of generality: China’s security strategies, the security dynamics of East and Southeast Asia, and the growing body of work on faits accomplis in security studies. I offer and apply a coherent structural explanation of China’s behavior in the South China Sea while also providing insight into when and where we might expect faits accomplis in other contexts, and under what conditions such faits accomplis may give rise to war

Fish larval nutrition and feed formulation: knowledge gaps and bottlenecks for advances in larval rearing

Despite considerable progress in recent years, many questions regarding fish larval nutrition remain largely unanswered, and several research avenues remain open. A holistic understanding of the supply line of nutrients is important for developing diets for use in larval culture and for the adaptation of rearing conditions that meet the larval requirements for the optimal presentation of food organisms and/or microdiets. The aim of the present review is to revise the state of the art and to pinpoint the gaps in knowledge regarding larval nutritional requirements, the nutritional value of live feeds and challenges and opportunities in the development of formulated larval diets.Norwegian Ministry of Fisheries; Research Council of Norway [CODE-199482, GutFeeling-190019]; Spanish Ministry of Science and Innovation MICINN + FEDER/ERDF [AGL2007-64450-C02-01, CSD2007-0002]; project HYDRAA [PTDC/MAR/71685/2006]; Fundacao para a Ciencia e a Tecnologia (FCT), Portugal; FEDER; EC [LIFECYCLE- 222719]; EU RTD [FA0801]info:eu-repo/semantics/publishedVersio

MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node structure was a distinct process that preceded the strong increases in B cells at the site. The selective increases in B cell frequencies were due not to proliferation but rather to cytokine-mediated repositioning of B cells to the lymph nodes, as shown with various gene-targeted and bone marrow irradiation chimeras. These studies demonstrated that B. burgdorferi infection induced type I interferon receptor (IFNR) signaling in lymph nodes in a MyD88- and TRIF-independent manner and that type I IFNR indirect signaling was required for the excessive increases of naive B cells at those sites. It did not, however, drive the observed histopathological changes, which occurred independently also from major shifts in the lymphocyte-homing chemokines, CXCL12, CXCL13, and CCL19/21, as shown by quantitative reverse transcription-PCR (qRT-PCR), flow cytometry, and transwell migration experiments. Thus, B. burgdorferi infection drives the production of type I IFN in lymph nodes and in so doing strongly alters the cellular composition of the lymph nodes, with potential detrimental effects for the development of robust Borrelia-specific immunity

Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation

Lymphadenopathy is a hallmark of acute infection with Borrelia burgdorferi, a tick-borne spirochete and causative agent of Lyme borreliosis, but the underlying causes and the functional consequences of this lymph node enlargement have not been revealed. The present study demonstrates that extracellular, live spirochetes accumulate in the cortical areas of lymph nodes following infection of mice with either host-adapted, or tick-borne B. burgdorferi and that they, but not inactivated spirochetes, drive the lymphadenopathy. The ensuing lymph node response is characterized by strong, rapid extrafollicular B cell proliferation and differentiation to plasma cells, as assessed by immunohistochemistry, flow cytometry and ELISPOT analysis, while germinal center reactions were not consistently observed. The extrafollicular nature of this B cell response and its strongly IgM-skewed isotype profile bear the hallmarks of a T-independent response. The induced B cell response does appear, however, to be largely antigen-specific. Use of a cocktail of recombinant, in vivo-expressed B. burgdorferi-antigens revealed the robust induction of borrelia-specific antibody-secreting cells by ELISPOT. Furthermore, nearly a quarter of hybridomas generated from regional lymph nodes during acute infection showed reactivity against a small number of recombinant Borrelia-antigens. Finally, neither the quality nor the magnitude of the B cell responses was altered in mice lacking the Toll-like receptor adaptor molecule MyD88. Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi's accumulation in lymph nodes

Borrelia burgdorferi BBK32 Inhibits the Classical Pathway by Blocking Activation of the C1 Complement Complex

Citation: Garcia, B. L., Zhi, H., Wager, B., Hook, M., & Skare, J. T. (2016). Borrelia burgdorferi BBK32 Inhibits the Classical Pathway by Blocking Activation of the C1 Complement Complex. Plos Pathogens, 12(1), 28. doi:10.1371/journal.ppat.1005404Pathogens that traffic in blood, lymphatics, or interstitial fluids must adopt strategies to evade innate immune defenses, notably the complement system. Through recruitment of host regulators of complement to their surface, many pathogens are able to escape complement-mediated attack. The Lyme disease spirochete, Borrelia burgdorferi, produces a number of surface proteins that bind to factor H related molecules, which function as the dominant negative regulator of the alternative pathway of complement. Relatively less is known about how B. burgdorferi evades the classical pathway of complement despite the observation that some sensu lato strains are sensitive to classical pathway activation. Here we report that the borrelial lipoprotein BBK32 potently and specifically inhibits the classical pathway by binding with high affinity to the initiating C1 complex of complement. In addition, B. burgdorferi cells that produce BBK32 on their surface bind to both C1 and C1r and a serum sensitive derivative of B. burgdorferi is protected from killing via the classical pathway in a BBK32-dependent manner. Subsequent biochemical and biophysical approaches localized the anti-complement activity of BBK32 to its globular C-terminal domain. Mechanistic studies reveal that BBK32 acts by entrapping C1 in its zymogen form by binding and inhibiting the C1 subcomponent, C1r, which serves as the initiating serine protease of the classical pathway. To our knowledge this is the first report of a spirochetal protein acting as a direct inhibitor of the classical pathway and is the only example of a biomolecule capable of specifically and noncovalently inhibiting C1/C1r. By identifying a unique mode of complement evasion this study greatly enhances our understanding of how pathogens subvert and potentially manipulate host innate immune systems

A review on broodstock nutrition of marine pelagic spawners: the curious case of the freshwater eels (Anguilla spp.)

To sustain eel aquaculture, development of reproduction in captivity is vital. The aim of this review is to assess our current knowledge on the nutrition of broodstock eels in order to improve the quality of broodstock under farming conditions, drawing information from wild adult eels and other marine pelagic spawners. Freshwater eels spawn marine pelagic eggs with an oil droplet (type II), and with a large perivitelline space. Compared with other marine fish eggs, eel eggs are at the extreme end of the spectrum in terms of egg composition, even within this type II group. Eel eggs contain a large amount of total lipids, and a shortage of neutral lipids has been implied a cause for reduced survival of larvae. Eel eggs have higher ARA but lower EPA and DHA levels than in other fish. Too high levels of ARA negatively affected reproduction in the Japanese eel, although high levels of 18:2n-6 in the eggs of farmed eels were not detrimental. The total free amino acid amount and profile of eel eggs appears much different from other marine pelagic spawners. Nutritional intervention to influence egg composition seems feasible, but responsiveness of farmed eels to induced maturation might also require environmental manipulation. The challenge remains to succeed in raising European eel broodstock with formulated feeds and to enable the procurement of viable eggs and larvae, once adequate protocols for induced maturation have been developed

Borrelia burgdorferi Infection-Induced Persistent IgM Secretion Controls Bacteremia, but Not Bacterial Dissemination or Tissue Burden.

Infection with Borrelia burgdorferi causes Lyme disease in humans. In small rodents, the natural reservoir species of this spirochete, infections lead to only modest disease manifestations, despite causing persistence infection. Although B cell responses are central for controlling bacterial tissue burden and disease manifestations, they lack classical aspects of T-dependent responses, such as sustained IgG affinity maturation and longevity, corresponding with a rapid collapse of germinal centers. Instead, the Ab response is characterized by strong and ongoing secretion of IgM, whose origins and impact on protective immunity to B. burgdorferi remain unknown. In this article, we demonstrate that B. burgdorferi infection-induced IgM in mice was produced continuously, mainly by conventional B, not B-1 cells, in a T-independent manner. Although IgM was passively protective and restricted early bacteremia, its production had no effects on bacterial dissemination into solid tissues, nor did it affect Borrelia tissue burden. The latter was controlled by the induction of bactericidal IgG, as shown comparing infections in wild type mice with those of mice lacking exclusively secreted IgM-/-, all class-switched Abs via deletion of aicda (AID-/-), and all secreted Abs (secreted IgM-/- × AID-/-). Consistent with the notion that B. burgdorferi infection drives production of IgM over more tissue-penetrable IgG, we demonstrated increased short- and long-term IgM Ab responses also to a coadministered, unrelated Ag. Thus, the continued production of IgM may explain the absence of B. burgdorferi in the blood

Alien Registration- Hastey, Walter (Bangor, Penobscot County)

https://digitalmaine.com/alien_docs/15793/thumbnail.jp