Absence of slow particle transport in the many-body localized phase

We analyze the saturation value of the bipartite entanglement and number entropy starting from a random product state deep in the many-body localized (MBL) phase. By studying the probability distributions of these entropies we find that the growth of the saturation value of the entanglement entropy stems from a significant reshuffling of the weight in the probability distributions from the bulk to the exponential tails. In contrast, the probability distributions of the saturation value of the number entropy are converged with system size, and exhibit a sharp cutoff for values of the number entropy which correspond to one particle fluctuating across the boundary between the two halves of the system. Our results therefore rule out slow particle transport deep in the MBL phase and confirm that the slow entanglement entropy production stems uniquely from configurational entanglement

Continuous Statistical Models: With or Without Truncation Parameters?

Lifetime data are usually assumed to stem from a continuous distribution supported on [0, b) for some b ≤ ∞. The continuity assumption implies that the support of the distribution does not have atom points, particularly not at 0. Accordingly, it seems reasonable that with an accurate measurement tool all data observations will be positive. This suggests that the true support may be truncated from the left. In this work we investigate the effects of adding a left truncation parameter to a continuous lifetime data statistical model. We consider two main settings: right truncation parametric models with possible left truncation, and exponential family models with possible left truncation. We analyze the performance of some optimal estimators constructed under the assumption of no left truncation when left truncation is present, and vice versa. We investigate both asymptotic and finite-sample behavior of the estimators. We show that when left truncation is not assumed but is, in fact present, the estimators have a constant bias term, and therefore will result in inaccurate and inefficient estimation. We also show that assuming left truncation where actually there is none, typically does not result in substantial inefficiency, and some estimators in this case are asymptotically unbiased and efficient

Exponential families of mixed Poisson distributions

If I=(I1,…,Id) is a random variable on [0,∞)d with distribution μ(dλ1,…,dλd), the mixed Poisson distribution MP(μ) on View the MathML source is the distribution of (N1(I1),…,Nd(Id)) where N1,…,Nd are ordinary independent Poisson processes which are also independent of I. The paper proves that if F is a natural exponential family on [0,∞)d then MP(F) is also a natural exponential family if and only if a generating probability of F is the distribution of v0+v1Y1+cdots, three dots, centered+vqYq for some qless-than-or-equals, slantd, for some vectors v0,…,vq of [0,∞)d with disjoint supports and for independent standard real gamma random variables Y1,…,Yq

Electronic structure of and Quantum size effect in III-V and II-VI semiconducting nanocrystals using a realistic tight binding approach

We analyze the electronic structure of group III-V semiconductors obtained within full potential linearized augmented plane wave (FP-LAPW) method and arrive at a realistic and minimal tight-binding model, parameterized to provide an accurate description of both valence and conduction bands. It is shown that cation sp3 - anion sp3d5 basis along with the next nearest neighbor model for hopping interactions is sufficient to describe the electronic structure of these systems over a wide energy range, obviating the use of any fictitious s* orbital, employed previously. Similar analyses were also performed for the II-VI semiconductors, using the more accurate FP-LAPW method compared to previous approaches, in order to enhance reliability of the parameter values. Using these parameters, we calculate the electronic structure of III-V and II-VI nanocrystals in real space with sizes ranging upto about 7 nm in diameter, establishing a quantitatively accurate description of the band-gap variation with sizes for the various nanocrystals by comparing with available experimental results from the literature.Comment: 28 pages, 8 figures, Accepted for publication in Phys. Rev.

Distribution and Extinction of Ungulates during the Holocene of the Southern Levant

BACKGROUND: The southern Levant (Israel, Palestinian Authority and Jordan) has been continuously and extensively populated by succeeding phases of human cultures for the past 15,000 years. The long human impact on the ancient landscape has had great ecological consequences, and has caused continuous and accelerating damage to the natural environment. The rich zooarchaeological data gathered at the area provide a unique opportunity to reconstruct spatial and temporal changes in wild species distribution, and correlate them with human demographic changes. METHODOLOGY: Zoo-archaeological data (382 animal bone assemblages from 190 archaeological sites) from various time periods, habitats and landscapes were compared. The bone assemblages were sorted into 12 major cultural periods. Distribution maps showing the presence of each ungulate species were established for each period. CONCLUSIONS: The first major ungulate extinction occurred during the local Iron Age (1,200-586 BCE), a period characterized by significant human population growth. During that time the last of the largest wild ungulates, the hartebeest (Alcelaphus buselaphus), aurochs (Bos primigenius) and the hippopotamus (Hippopotamus amphibius) became extinct, followed by a shrinking distribution of forest-dwelling cervids. A second major wave of extinction occurred only in the 19th and 20th centuries CE. Furthermore, a negative relationship was found between the average body mass of ungulate species that became extinct during the Holocene and their extinction date. It is thus very likely that the intensified human activity through habitat destruction and uncontrolled hunting were responsible for the two major waves of ungulate extinction in the southern Levant during the late Holocene

Sophisticated Framework between Cell Cycle Arrest and Apoptosis Induction Based on p53 Dynamics

The tumor suppressor, p53, regulates several gene expressions that are related to the DNA repair protein, cell cycle arrest and apoptosis induction, which activates the implementation of both cell cycle arrest and induction of apoptosis. However, it is not clear how p53 specifically regulates the implementation of these functions. By applying several well-known kinetic mathematical models, we constructed a novel model that described the influence that DNA damage has on the implementation of both the G2/M phase cell cycle arrest and the intrinsic apoptosis induction via its activation of the p53 synthesis process. The model, which consisted of 32 dependent variables and 115 kinetic parameters, was used to examine interference by DNA damage in the implementation of both G2/M phase cell cycle arrest and intrinsic apoptosis induction. A low DNA damage promoted slightly the synthesis of p53, which showed a sigmoidal behavior with time. In contrast, in the case of a high DNA damage, the p53 showed an oscillation behavior with time. Regardless of the DNA damage level, there were delays in the G2/M progression. The intrinsic apoptosis was only induced in situations where grave DNA damage produced an oscillation of p53. In addition, to wreck the equilibrium between Bcl-2 and Bax the induction of apoptosis required an extreme activation of p53 produced by the oscillation dynamics, and was only implemented after the release of the G2/M phase arrest. When the p53 oscillation is observed, there is possibility that the cell implements the apoptosis induction. Moreover, in contrast to the cell cycle arrest system, the apoptosis induction system is responsible for safeguarding the system that suppresses malignant transformations. The results of these experiments will be useful in the future for elucidating of the dominant factors that determine the cell fate such as normal cell cycles, cell cycle arrest and apoptosis

Frequency Domain Analysis Reveals External Periodic Fluctuations Can Generate Sustained p53 Oscillation

p53 is a well-known tumor suppressor protein that regulates many pathways, such as ones involved in cell cycle and apoptosis. The p53 levels are known to oscillate without damping after DNA damage, which has been a focus of many recent studies. A negative feedback loop involving p53 and MDM2 has been reported to be responsible for this oscillatory behavior, but questions remain as how the dynamics of this loop alter in order to initiate and maintain the sustained or undamped p53 oscillation. Our frequency domain analysis suggests that the sustained p53 oscillation is not completely dictated by the negative feedback loop; instead, it is likely to be also modulated by periodic DNA repair-related fluctuations that are triggered by DNA damage. According to our analysis, the p53-MDM2 feedback mechanism exhibits adaptability in different cellular contexts. It normally filters noise and fluctuations exerted on p53, but upon DNA damage, it stops performing the filtering function so that DNA repair-related oscillatory signals can modulate the p53 oscillation. Furthermore, it is shown that the p53-MDM2 feedback loop increases its damping ratio allowing p53 to oscillate at a frequency more synchronized with the other cellular efforts to repair the damaged DNA, while suppressing its inherent oscillation-generating capability. Our analysis suggests that the overexpression of MDM2, observed in many types of cancer, can disrupt the operation of this adaptive mechanism by making it less responsive to the modulating signals after DNA damage occurs

Explaining oscillations and variability in the p53-Mdm2 system

<p>Abstract</p> <p>Background</p> <p>In individual living cells p53 has been found to be expressed in a series of discrete pulses after DNA damage. Its negative regulator Mdm2 also demonstrates oscillatory behaviour. Attempts have been made recently to explain this behaviour by mathematical models but these have not addressed explicit molecular mechanisms. We describe two stochastic mechanistic models of the p53/Mdm2 circuit and show that sustained oscillations result directly from the key biological features, without assuming complicated mathematical functions or requiring more than one feedback loop. Each model examines a different mechanism for providing a negative feedback loop which results in p53 activation after DNA damage. The first model (ARF model) looks at the mechanism of p14^ARFwhich sequesters Mdm2 and leads to stabilisation of p53. The second model (ATM model) examines the mechanism of ATM activation which leads to phosphorylation of both p53 and Mdm2 and increased degradation of Mdm2, which again results in p53 stabilisation. The models can readily be modified as further information becomes available, and linked to other models of cellular ageing.</p> <p>Results</p> <p>The ARF model is robust to changes in its parameters and predicts undamped oscillations after DNA damage so long as the signal persists. It also predicts that if there is a gradual accumulation of DNA damage, such as may occur in ageing, oscillations break out once a threshold level of damage is acquired. The ATM model requires an additional step for p53 synthesis for sustained oscillations to develop. The ATM model shows much more variability in the oscillatory behaviour and this variability is observed over a wide range of parameter values. This may account for the large variability seen in the experimental data which so far has examined ARF negative cells.</p> <p>Conclusion</p> <p>The models predict more regular oscillations if ARF is present and suggest the need for further experiments in ARF positive cells to test these predictions. Our work illustrates the importance of systems biology approaches to understanding the complex role of p53 in both ageing and cancer.</p