The CDO market Functioning and implications in terms of financial stability.

The result of relatively recent financial innovations, collateralised debt obligations (CDOs) are securities that represent a portfolio of bank loans and/or different financial instruments. Part securitisation instrument part credit derivative, these increasingly-popular structured finance products are used by financial institutions for various purposes, ranging from reducing their cost of financing to exploiting arbitrage opportunities or transferring credit risk. Irrespective of their form, CDOs are issued in different tranches that are tailored using securitisation techniques. The process of tranching allows credit risk and returns on their underlying portfolio to be redistributed to investors in an ad hoc fashion. CDOs are part of an ongoing trend of converting credit risk into a marketable commodity. This process started with securitisation, and was then sustained by the development of credit ratings and corporate bond markets and, more recently, by that of credit derivatives. While CDO issuance represents at most the equivalent of a sixth of that of corporate bonds, the influence of these products has a far greater significance because of the amount of credit risk they allow to be transferred. The sharp growth in synthetic structures backed by credit derivatives, especially in Europe, has heightened this trend. The rapid development of CDOs has improved non-bank investors’ access to credit markets and has enabled them to overcome the obstacles posed by the size and limited diversification of the corporate bond market, notably in Europe where bank intermediation remains predominant. Investors can now choose portfolios with specific risk-return profiles and take exposures to credit risk previously confined to banks’ balance sheets, such as SME loans. Given that CDOs are credit risk transfer instruments, they facilitate the redistribution of this risk within the financial and banking sector and even beyond, while increasing the degree of completeness of the credit market. They should therefore have a positive impact on financial stability. However, as is often the case with financial innovations, evaluating CDOs and the risks they entail, particularly in the case of Synthetic CDOs, requires the use of complex techniques that are not always sufficiently tried and tested. Both investors and market participants may thus be exposed to relatively high potential losses. At present, this risk does not appear to be of a systemic nature given the size and relative newness of the market. Nonetheless, if this market continues to grow at its current pace, attracting increasing numbers of investors, in particular in Europe where CDOs are predominantly synthetic, systemic risk may emerge. Moreover, growth in CDO issuance seems to have contributed to the marked narrowing of spreads over the past two years on all credit markets. This trend raises questions as to the links between the CDO market and the corporate bond and credit derivatives markets, and deserves particular attention with regard to the risk of the propagation and amplification of strains that may arise on the CDO market due to its still limited liquidity and transparency.

Productivity, heritability and stability analysis of a Moroccan sugar beet germplasm

Received: January 19th, 2021 ; Accepted: March 27th, 2021 ; Published: April 6th 2021 ; Correspondence: [email protected] testing is the second part of maternal recurrent selection scheme adopted by INRA-Morocco for the national sugar beet breeding programme. The objective of this study is sugar beet germplasm productivity, heritability and stability analysis. The studied material concern 18 half-sib families (HSF) preselected initially for their seed production potential. Trials were conducted using randomised complete blocks designs during, 2013/14, 2014/15, 2015/16, 2017/18 campaigns in two experimental fields of INRA-Morocco; Sidi Allal Tazi (34° 30' N, 6° 19' W) and Larache (35° 11’ N, 6° 09’ W). Evaluated parameters concern the vigour, root weight (RW), leaf biomass yield (LBY), and sugar content (Sc). Data analysis by comparative procedures explores different accordance degrees of HSF versus controls. Good vegetative growth was observed, 85.6% closer to the maximal indicated scale level. The RW was significantly influenced by the genotype and reached a maximum of 1.06 kg versus 1.08 kg average recorded by controls. Sugar content recorded mean was 20.97% in HSF versus 21.39% in the controls. Most of HSF revealed mean values close to Z-type variety. Estimated heritability was 0.5 for RW, 0.2 for the LBY, and 0.02 for Sc. Sugar content was influenced by the environment and explained by the AMMI model (73.6%) versus 53.9% and 44.4% for root weight and leaf biomass yield respectively. The AMMI stability values showed F11, F12, F16, and F17 families as the most performing and stable HSF. Results demonstrate the relevance of the maternal recurrent selection scheme of the on-going national breeding programme

Validation of the LUMIPULSE automated immunoassay for the measurement of core AD biomarkers in cerebrospinal fluid

OBJECTIVES: The core cerebrospinal fluid (CSF) biomarkers; total tau (tTau), phospho-tau (pTau), amyloid β 1-42 (Aβ 1-42), and the Aβ 1-42/Aβ 1-40 ratio have transformed Alzheimer's disease (AD) research and are today increasingly used in clinical routine laboratories as diagnostic tools. Fully automated immunoassay instruments with ready-to-use assay kits and calibrators has simplified their analysis and improved reproducibility of measurements. We evaluated the analytical performance of the fully automated immunoassay instrument LUMIPULSE G (Fujirebio) for measurement of the four core AD CSF biomarkers and determined cutpoints for AD diagnosis. METHODS: Comparison of the LUMIPULSE G assays was performed with the established INNOTEST ELISAs (Fujirebio) for hTau Ag, pTau 181, β-amyloid 1-42, and with V-PLEX Plus Aβ Peptide Panel 1 (6E10) (Meso Scale Discovery) for Aβ 1-42/Aβ 1-40, as well as with a LC-MS reference method for Aβ 1-42. Intra- and inter-laboratory reproducibility was evaluated for all assays. Clinical cutpoints for Aβ 1-42, tTau, and pTau was determined by analysis of three cohorts of clinically diagnosed patients, comprising 651 CSF samples. For the Aβ 1-42/Aβ 1-40 ratio, the cutpoint was determined by mixture model analysis of 2,782 CSF samples. RESULTS: The LUMIPULSE G assays showed strong correlation to all other immunoassays (r>0.93 for all assays). The repeatability (intra-laboratory) CVs ranged between 2.0 and 5.6%, with the highest variation observed for β-amyloid 1-40. The reproducibility (inter-laboratory) CVs ranged between 2.1 and 6.5%, with the highest variation observed for β-amyloid 1-42. The clinical cutpoints for AD were determined to be 409 ng/L for total tau, 50.2 ng/L for pTau 181, 526 ng/L for β-amyloid 1-42, and 0.072 for the Aβ 1-42/Aβ 1-40 ratio. CONCLUSIONS: Our results suggest that the LUMIPULSE G assays for the CSF AD biomarkers are fit for purpose in clinical laboratory practice. Further, they corroborate earlier presented reference limits for the biomarkers

Astrocyte biomarker signatures of amyloid-β and tau pathologies in Alzheimer’s disease

Astrocytes can adopt multiple molecular phenotypes in the brain of Alzheimer's disease (AD) patients. Here, we studied the associations of cerebrospinal fluid (CSF) glial fibrillary acidic protein (GFAP) and chitinase-3-like protein 1 (YKL-40) levels with brain amyloid-β (Aβ) and tau pathologies. We assessed 121 individuals across the aging and AD clinical spectrum with positron emission tomography (PET) brain imaging for Aβ ([18F]AZD4694) and tau ([18F]MK-6240), as well as CSF GFAP and YKL-40 measures. We observed that higher CSF GFAP levels were associated with elevated Aβ-PET but not tau-PET load. By contrast, higher CSF YKL-40 levels were associated with elevated tau-PET but not Aβ-PET burden. Structural equation modeling revealed that CSF GFAP and YKL-40 mediate the effects of Aβ and tau, respectively, on hippocampal atrophy, which was further associated with cognitive impairment. Our results suggest the existence of distinct astrocyte biomarker signatures in response to brain Aβ and tau accumulation, which may contribute to our understanding of the complex link between reactive astrogliosis heterogeneity and AD progression

The Alpha Linolenic Acid Content of Flaxseed is Associated with an Induction of Adipose Leptin Expression

Dietary flaxseed has cardioprotective effects that may be achieved through its rich content of the omega-3 fatty acid, alpha linolenic acid (ALA). Because ALA can be stored in adipose tissue, it is possible that some of its beneficial actions may be due to effects it has on the adipose tissue. We investigated the effects of dietary flaxseed both with and without an atherogenic cholesterol-enriched diet to determine the effects of dietary flaxseed on the expression of the adipose cytokines leptin and adiponectin. Rabbits were fed one of four diets: a regular (RG) diet, or a regular diet with added 0.5% cholesterol (CH), or 10% ground flaxseed (FX), or both (CF) for 8 weeks. Levels of leptin and adiponectin expression were assessed by RT-PCR in visceral adipose tissue. Consumption of flaxseed significantly increased plasma and adipose levels of ALA. Leptin protein and mRNA expression were lower in CH animals and were elevated in CF animals. Changes in leptin expression were strongly and positively correlated with adipose ALA levels and inversely correlated with levels of en face atherosclerosis. Adiponectin expression was not significantly affected by any of the dietary interventions. Our data demonstrate that the type of fat in the diet as well as its caloric content can specifically influence leptin expression. The findings support the hypothesis that the beneficial cardiovascular effects associated with flaxseed consumption may be related to a change in leptin expression

Hyperactive Neuroendocrine Secretion Causes Size, Feeding, and Metabolic Defects of C. elegans Bardet-Biedl Syndrome Mutants

Bardet-Biedl syndrome, BBS, is a rare autosomal recessive disorder with clinical presentations including polydactyly, retinopathy, hyperphagia, obesity, short stature, cognitive impairment, and developmental delays. Disruptions of BBS proteins in a variety of organisms impair cilia formation and function and the multi-organ defects of BBS have been attributed to deficiencies in various cilia-associated signaling pathways. In C. elegans, bbs genes are expressed exclusively in the sixty ciliated sensory neurons of these animals and bbs mutants exhibit sensory defects as well as body size, feeding, and metabolic abnormalities. Here we show that in contrast to many other cilia-defective mutants, C. elegans bbs mutants exhibit increased release of dense-core vesicles and organism-wide phenotypes associated with enhanced activities of insulin, neuropeptide, and biogenic amine signaling pathways. We show that the altered body size, feeding, and metabolic abnormalities of bbs mutants can be corrected to wild-type levels by abrogating the enhanced secretion of dense-core vesicles without concomitant correction of ciliary defects. These findings expand the role of BBS proteins to the regulation of dense-core-vesicle exocytosis and suggest that some features of Bardet-Biedl Syndrome may be caused by excessive neuroendocrine secretion

Adult Type 3 Adenylyl Cyclase–Deficient Mice Are Obese

Background: A recent study of obesity in Swedish men found that polymorphisms in the type 3 adenylyl cyclase (AC3) are associated with obesity, suggesting the interesting possibility that AC3 may play a role in weight control. Therefore, we examined the weight of AC3 mice over an extended period of time. Methodology/Principal Findings: We discovered that AC3 2/2 mice become obese as they age. Adult male AC3 2/2 mice are about 40 % heavier than wild type male mice while female AC3 2/2 are 70 % heavier. The additional weight of AC3 2/2 mice is due to increased fat mass and larger adipocytes. Before the onset of obesity, young AC3 2/2 mice exhibit reduced physical activity, increased food consumption, and leptin insensitivity. Surprisingly, the obesity of AC3 2/2 mice is not due to a loss of AC3 from white adipose and a decrease in lipolysis. Conclusions/Significance: We conclude that mice lacking AC3 exhibit obesity that is apparently caused by low locomotor activity, hyperphagia, and leptin insensitivity. The presence of AC3 in primary cilia of neurons of the hypothalamus suggests that cAMP signals generated by AC3 in the hypothalamus may play a critical role in regulation of body weight