Universal geometric entanglement close to quantum phase transitions

Under successive Renormalization Group transformations applied to a quantum state $\ket{\Psi}$ of finite correlation length $\xi$, there is typically a loss of entanglement after each iteration. How good it is then to replace $\ket{\Psi}$ by a product state at every step of the process? In this paper we give a quantitative answer to this question by providing first analytical and general proofs that, for translationally invariant quantum systems in one spatial dimension, the global geometric entanglement per region of size $L \gg \xi$ diverges with the correlation length as $(c/12) \log{(\xi/\epsilon)}$ close to a quantum critical point with central charge $c$, where $\epsilon$ is a cut-off at short distances. Moreover, the situation at criticality is also discussed and an upper bound on the critical global geometric entanglement is provided in terms of a logarithmic function of $L$.Comment: 4 pages, 3 figure

Butyrate augments interferon-α-induced S phase accumulation and persistent tyrosine phosphorylation of cdc2 in K562 cells

Interferon-α (IFN-α) is a clinically useful cytokine for treatment of a variety of cancers, including chronic myelocytic leukaemia (CML). Most CML cells are sensitive to IFN-α; however, its biological effects on leukaemic cells are incompletely characterized. Here, we provide evidence that IFN-α induces a significant increase in the S phase population in human CML leukaemic cell line, K562, and that the S phase accumulation was augmented by sodium butyrate. In contrast, neither sodium butyrate alone, nor sodium butyrate plus IFN-γ, affected the cell cycle in K562 cells. These data suggest that the effect of sodium butyrate depended upon IFN-α-mediated signalling. The ability of leukaemic cells to exhibit the S phase accumulation after stimulation by IFN-α plus sodium butyrate correlated well with persistent tyrosine phosphorylation of cdc2, whereas treatment with IFN-γ plus sodium butyrate did not affect its phosphorylation levels. Considering that dephosphorylation of cdc2 leads to entry to the M phase, the persistent tyrosine phosphorylation of cdc2 may be associated with the S phase accumulation induced by IFN-α and sodium butyrate. In addition, another human CML leukaemic cell line, MEG-01, also showed the S phase accumulation after stimulation with IFN-α plus sodium butyrate. Taken together, our studies reveal a novel effect of sodium butyrate on the S phase accumulation and suggest its clinical application for a combination therapy with IFN-α, leading to a great improvement of clinical effects of IFN-α against CML cells. © 1999 Cancer Research Campaig

Growth hormone (GH) and triglyceride-rich lipoprotein (TRL) metabolism : effect of one month of dicontinued growth hormone treatment in growth hormone hormone deficient patients

International audienceAim: Growth hormone (GH) deficiency is associated with increased cardiovascular mortality. Insulin resistant states and lipid profile alterations with hypertriglyceridemia, decreased HDL cholesterol, increased small and dense LDL and postprandial hyperlipidemia are commonly observed in GH deficient patients but GH specific function in triglyceride-rich lipoprotein (TRL) metabolism regulation remains unclear. Methods: Lipids and apolipoproteins (apo) profiles were investigated in fasting and postprandial states in plasma and TRL fractions during a test meal before (M0) and after one month of discontinued GH treatment (M1) in GH deficient patients (n=10). Results: After one month of discontinued GH treatment, GH levels remained unchanged but IGF-1 decreased significantly (-12,12±2,36nmol/L). We observed a significant weight loss (-1,31±0,45kg) together with body composition significant changes : lean mass decrease and fat mass increase (-1,17±0,41kg and +0,36±0,16kg respectively), and insulin resistance parameters modifications with a significant HOMA-index reduction (-0,45±0,19) associated with both significant decreased fasting insulin and C-peptide (-2,04±0,78Mui/L and -0,15±0,05nmol/L respectively) but fasting plasma glucose remained unchanged. Fasting plasma triglycerides and apoC-III levels decreased significantly (-0,41±0,16mmol/L and -23,07±6,93mg/L respectively), main other fasting lipid parameters assessed in the plasma fraction (total, LDL and HDL cholesterol, but also apoA1, apoB, apoB48 and apoC-II) were unchanged. Triglycerides but also apoC-II and apoC-III levels assessed in TRL fraction decreased significantly both in fasting and postprandial states after GH discontinuation. Conclusions: Lipid profiles alterations both in fasting and postprandial states were observed in GH deficient patients after GH treatment discontinuation suggesting a specific role of GH in TRL metabolism specifically altered in this pathology

Agonist-induced up-regulation of platelet-activating factor receptor messenger RNA in human monocytes

Platelet-activating factor (PAF) is a potent inflammatory mediator and it actions are mediated via specific cell surface receptors which are coupled to G-proteins. PAF stimulates several functions in monocytes and may modulate the expression of its own receptor. To investigate the possible modulation of PAF receptor mRNA expression Northern blot analysis of total RNA from human monocytes was performed using the cDNA of human leukocyte PAF receptor as a probe. Following the addition of 100 nM PAF, there was a 2.0-fold increase in PAF receptor mRNA at 60 minutes after the stimulation, which was inhibited by pretreatment with the PAF receptor antagonist WEB 2086. This increase returned to control level at 120 and 180 min. The increase of PAF receptor mRNA was statistically significant for 10 nM to 1 μM of PAF, while 100 nM of lysoPAF did not increase PAF receptor mRNA levels. These results suggest that PAF receptor expression can be regulated by PAF itself at the transcriptional level.link_to_subscribed_fulltex