Limosilactobacillus balticus sp. nov., Limosilactobacillus agrestis sp. nov., Limosilactobacillus albertensis sp. nov., Limosilactobacillus rudii sp. nov. and Limosilactobacillus fastidiosus sp. nov., five novel Limosilactobacillus species isolated from the vertebrate gastrointestinal tract, and proposal of six subspecies of Limosilactobacillus reuteri adapted to the gastrointestinal tract of specific vertebrate hosts

Ten strains, BG-AF3-A(T), pH52_RY, WF-MT5-A(T), BG-MG3-A, Lr3000(T), RRLNB_1_1, STM3_1(T), STM2_1, WF-MO7-1(T) and WF-MA3-C, were isolated from intestinal or faecal samples of rodents, pheasant and primate. 16S rRNA gene analysis identified them as Limosilactobacillus reuteri. However, average nucleotide identity and digital DNA-DNA hybridization values based on whole genomes were below 95 and 70%, respectively, and thus below the threshold levels for bacterial species delineation. Based on genomic, chemotaxonomic and morphological analyses, we propose five novel species with the names Limosilactobacillus balticus sp. nov. (type strain BG-AF3-A(T)=DSM 110574(T)=LMG 31633(T)), Limosilactobacillus agrestis sp. nov. (type strain WF-MT5-A(T)=DSM 110569(T)=LMG 31629(T)), Limosilactobacillus albertensis sp. nov. (type strain Lr3000(T)=DSM 110573(T)=LMG 31632(T)), Limosilactobacillus rudii sp. nov. (type strain STM3_1(T)=DSM 110572(T)=LMG 31631(T)) and Limosilactobacillus fastidiosus sp. nov. (type strain WF-MO7-1(T)=DSM 110576(T)=LMG 31630(T)). Core genome phylogeny and experimental evidence of host adaptation of strains of L. reuteri further provide a strong rationale to consider a number of distinct lineages within this species as subspecies. Here we propose six subspecies of L. reuteri: L. reuteri subsp. kinnaridis subsp. nov. (type strain AP3(T)=DSM 110703(T)=LMG 31724(T)), L. reuteri subsp. porcinus subsp. nov. (type strain 3c6(T)=DSM 110571(T)=LMG 31635(T)), L. reuteri subsp. murium subsp. nov. (type strain lpuph1(T)=DSM 110570(T)=LMG 31634(T)), L. reuteri subsp. reuteri subsp. nov. (type strain F 275(T)=DSM 20016(T)=ATCC 23272(T)), L. reuteri subsp. suis subsp. nov. (type strain 1063(T)=ATCC 53608(T)=LMG 31752(T)) and L. reuteri subsp. rodentium subsp. nov. (type strain 100-23(T)=DSM 17509(T)=CIP 109821(T))

Suitability of potyviral recombinant virus-like particles bearing a complete food allergen for immunotherapy vaccines

Peer reviewe

Follistatin-controlled activin-HNF4 alpha-coagulation factor axis in liver progenitor cells determines outcome of acute liver failure

Background and Aims In patients with acute liver failure (ALF) who suffer from massive hepatocyte loss, liver progenitor cells (LPCs) take over key hepatocyte functions, which ultimately determines survival. This study investigated how the expression of hepatocyte nuclear factor 4 alpha (HNF4 alpha), its regulators, and targets in LPCs determines clinical outcome of patients with ALF. Approach and Results Clinicopathological associations were scrutinized in 19 patients with ALF (9 recovered and 10 receiving liver transplantation). Regulatory mechanisms between follistatin, activin, HNF4 alpha, and coagulation factor expression in LPC were investigated in vitro and in metronidazole-treated zebrafish. A prospective clinical study followed up 186 patients with cirrhosis for 80 months to observe the relevance of follistatin levels in prevalence and mortality of acute-on-chronic liver failure. Recovered patients with ALF robustly express HNF4 alpha in either LPCs or remaining hepatocytes. As in hepatocytes, HNF4 alpha controls the expression of coagulation factors by binding to their promoters in LPC. HNF4 alpha expression in LPCs requires the forkhead box protein H1-Sma and Mad homolog 2/3/4 transcription factor complex, which is promoted by the TGF-beta superfamily member activin. Activin signaling in LPCs is negatively regulated by follistatin, a hepatocyte-derived hormone controlled by insulin and glucagon. In contrast to patients requiring liver transplantation, recovered patients demonstrate a normal activin/follistatin ratio, robust abundance of the activin effectors phosphorylated Sma and Mad homolog 2 and HNF4 alpha in LPCs, leading to significantly improved coagulation function. A follow-up study indicated that serum follistatin levels could predict the incidence and mortality of acute-on-chronic liver failure. Conclusions These results highlight a crucial role of the follistatin-controlled activin-HNF4 alpha-coagulation axis in determining the clinical outcome of massive hepatocyte loss-induced ALF. The effects of insulin and glucagon on follistatin suggest a key role of the systemic metabolic state in ALF.Cancer Signaling networks and Molecular Therapeutic

Systemic losses due to counterparty risk in a stylized banking system

We report a study of a stylized banking cascade model investigating systemic risk caused by counterparty failure using liabilities and assets to define banks' balance sheet. In our stylized system, banks can be in two states: normally operating or distressed and the state of a bank changes from normally operating to distressed whenever its liabilities are larger than the banks' assets. The banks are connected through an interbank lending network and, whenever a bank is distressed, its creditor cannot expect the loan from the distressed bank to be repaid, potentially becoming distressed themselves. We solve the problem analytically for a homogeneous system and test the robustness and generality of the results with simulations of more complex systems. We investigate the parameter space and the corresponding distribution of operating banks mapping the conditions under which the whole system is stable or unstable. This allows us to determine how financial stability of a banking system is influenced by regulatory decisions, such as leverage; we discuss the effect of central bank actions, such as quantitative easing and we determine the cost of rescuing a distressed banking system using re-capitalisation. Finally, we estimate the stability of the UK and US banking systems comparing the years 2007 and 2012 by using real data

Study of substrate orientations impact on Ultra Thin Buried Oxide (UTBOX) FDSOI High-K Metal gate technology performances

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