Computations on Sofic S-gap Shifts

Let $S=\{s_{n}\}$ be an increasing finite or infinite subset of $\mathbb N \bigcup \{0\}$ and $X(S)$ the $S$-gap shift associated to $S$. Let $f_{S}(x)=1-\sum\frac{1}{x^{s_{n}+1}}$ be the entropy function which will be vanished at $2^{h(X(S))}$ where $h(X(S))$ is the entropy of the system. Suppose $X(S)$ is sofic with adjacency matrix $A$ and the characteristic polynomial $\chi_{A}$. Then for some rational function $Q_{S}$, $\chi_{A}(x)=Q_{S}(x)f_{S}(x)$. This $Q_{S}$ will be explicitly determined. We will show that $\zeta(t)=\frac{1}{f_{S}(t^{-1})}$ or $\zeta(t)=\frac{1}{(1-t)f_{S}(t^{-1})}$ when $|S|<\infty$ or $|S|=\infty$ respectively. Here $\zeta$ is the zeta function of $X(S)$. We will also compute the Bowen-Franks groups of a sofic $S$-gap shift.Comment: This paper has been withdrawn due to extending results about SFT shifts to sofic shifts (Theorem 2.3). This forces to apply some minor changes in the organization of the paper. This paper has been withdrawn due to a flaw in the description of the adjacency matrix (2.3

Computability and dynamical systems

In this paper we explore results that establish a link between dynamical systems and computability theory (not numerical analysis). In the last few decades, computers have increasingly been used as simulation tools for gaining insight into dynamical behavior. However, due to the presence of errors inherent in such numerical simulations, with few exceptions, computers have not been used for the nobler task of proving mathematical results. Nevertheless, there have been some recent developments in the latter direction. Here we introduce some of the ideas and techniques used so far, and suggest some lines of research for further work on this fascinating topic

Loss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins on lysosomes, damaging lysosomal function and predicting the dramatic susceptibility of Irgm1-deficient mice to infection

The interferon-γ (IFN-γ)-inducible immunity-related GTPase (IRG), Irgm1, plays an essential role in restraining activation of the IRG pathogen resistance system. However, the loss of Irgm1 in mice also causes a dramatic but unexplained susceptibility phenotype upon infection with a variety of pathogens, including many not normally controlled by the IRG system. This phenotype is associated with lymphopenia, hemopoietic collapse, and death of the mouse.Deutscher Akademischer Austausch Dienst (DAAD); International Graduate School in Development Health and Disease (IGS-DHD); Deutsche For-schungsgemeinschaft (SFBs 635, 670, 680); Max-Planck-Gesellschaft (Max Planck Fellowship)

Exogenous Ether Lipids Predominantly Target Mitochondria

Ether lipids are ubiquitous constituents of cellular membranes with no discrete cell biological function assigned yet. Using fluorescent polyene-ether lipids we analyzed their intracellular distribution in living cells by microscopy. Mitochondria and the endoplasmic reticulum accumulated high amounts of ether-phosphatidylcholine and ether-phosphatidylethanolamine. Both lipids were specifically labeled using the corresponding lyso-ether lipids, which we established as supreme precursors for lipid tagging. Polyfosine, a fluorescent analogue of the anti-neoplastic ether lipid edelfosine, accumulated to mitochondria and induced morphological changes and cellular apoptosis. These data indicate that edelfosine could exert its pro-apoptotic power by targeting and damaging mitochondria and thereby inducing cellular apoptosis. In general, this study implies an important role of mitochondria in ether lipid metabolism and intracellular ether lipid trafficking

Cox proportional hazards deep neural network identifies peripheral blood complete remission to be at least equivalent to morphologic complete remission in predicting outcomes of patients treated with azacitidine - a prospective cohort study by the AGMT

The current gold standard of response assessment in patients with myelodysplastic syndromes (MDS), chronic myelomonocytic leukemia (CMML), and acute myeloid leukemia (AML) is morphologic complete remission (CR) and CR with incomplete count recovery (CRi), both of which require an invasive BM evaluation. Outside of clinical trials, BM evaluations are only performed in ~50% of patients during follow-up, pinpointing a clinical need for response endpoints that do not necessitate BM assessments. We define and validate a new response type termed "peripheral blood complete remission" (PB-CR) that can be determined from the differential blood count and clinical parameters without necessitating a BM assessment. We compared the predictive value of PB-CR with morphologic CR/CRi in 1441 non-selected, consecutive patients diagnosed with MDS (n = 522; 36.2%), CMML (n = 132; 9.2%), or AML (n = 787; 54.6%), included within the Austrian Myeloid Registry (aMYELOIDr; NCT04438889). Time-to-event analyses were adjusted for 17 covariates remaining in the final Cox proportional hazards (CPH) model. DeepSurv, a CPH neural network model, and permutation-based feature importance were used to validate results. 1441 patients were included. Adjusted median overall survival for patients achieving PB-CR was 22.8 months (95%CI 18.9-26.2) versus 10.4 months (95%CI 9.7-11.2) for those who did not; HR = 0.366 (95%CI 0.303-0.441; p < .0001). Among patients achieving CR, those additionally achieving PB-CR had a median adjusted OS of 32.6 months (95%CI 26.2-49.2) versus 21.7 months (95%CI 16.9-27.7; HR = 0.400 [95%CI 0.190-0.844; p = .0161]) for those who did not. Our deep neural network analysis-based findings from a large, prospective cohort study indicate that BM evaluations solely for the purpose of identifying CR/CRi can be omitted

Heat stress causes spatially-distinct membrane re-modelling in K562 leukemia cells

Cellular membranes respond rapidly to various environmental perturbations. Previously we showed that modulations in membrane fluidity achieved by heat stress (HS) resulted in pronounced membrane organization alterations which could be intimately linked to the expression and cellular distribution of heat shock proteins. Here we examine heat-induced membrane changes using several visualisation methods. With Laurdan two-photon microscopy we demonstrate that, in contrast to the enhanced formation of ordered domains in surface membranes, the molecular disorder is significantly elevated within the internal membranes of cells preexposed to mild HS. These results were compared with those obtained by anisotropy, fluorescence lifetime and electron paramagnetic resonance measurements. All probes detected membrane changes upon HS. However, the structurally different probes revealed substantially distinct alterations in membrane heterogeneity. These data call attention to the careful interpretation of results obtained with only a single label. Subtle changes in membrane microstructure in the decision-making of thermal cell killing could have potential application in cancer therapy

Consequences of late-stage non-small cell lung cancer cachexia on muscle metabolic processes

Introduction: Loss of muscle is common in patients with advanced non-small cell lung cancer (NSCLC), and contributes to the high morbidity and mortality of this group. The exact mechanisms behind the loss of muscle are unclear. Patients and methods: To investigate this, 4 patients with stage IV NSCLC meeting the clinical definitions for sarcopenia and cachexia were recruited, along with 4 age-matched healthy volunteers. Following an overnight fast, biopsies were obtained from the vastus lateralis and key components associated with inflammation and the control of muscle protein, carbohydrate and fat metabolism assessed. Results: Compared to healthy volunteers, significant increases in mRNA levels for interleukin-6 and NFκB signalling were observed in NSCLC patients along with lower intramyocellular lipid content in slow-twitch fibres. While a significant decrease in phosphorylation of mTOR signalling protein 4E-BP1 (Ser65) was observed along with a trend towards reduced p70 S6K (Thr389) phosphorylation (P=0.06), there was no difference between groups for mRNA levels of MAFbx and MuRF1, chymotrypsin-like activity of the proteasome, or protein levels of multiple proteasome subunits. Moreover, despite decreases in intramyocellular lipid content, no robust changes in mRNA levels for key proteins involved in insulin signalling, glycolysis, oxidative metabolism or fat metabolism were observed. Conclusions: These findings suggest that an examination of the contribution of suppressed mTOR signalling in the loss of muscle mass in late-stage NSCLC patients is warranted and reinforces our need to understand the potential contribution of impaired fat metabolism and muscle protein synthesis in the aetiology of cancer cachexia