Finite Element Analysis of Strain Effects on Electronic and Transport Properties in Quantum Dots and Wires

Lattice mismatch in layered semiconductor structures with submicron length scales leads to extremely high nonuniform strains. This paper presents a finite element technique for incorporating the effects of the nonuniform strain into an analysis of the electronic properties of SiGe quantum structures. Strain fields are calculated using a standard structural mechanics finite element package and the effects are included as a nonuniform potential directly in the time independent Schrodinger equation; a k-p Hamiltonian is used to model the effects of multiple valence subband coupling. A variational statement of the equation is formulated and solved using the finite element method. This technique is applied to resonant tunneling diode quantum dots and wires; the resulting densities of states confined to the quantum well layers of the devices are compared to experimental current-voltage I(V) curves.Comment: 17 pages (LaTex), 18 figures (JPEG), submitted to Journal of Applied Physic

New optimization methods in Data Mining

Data mining is a modern area of science dealing with the learning from given data in order to make predictions and estimations. Applications of Data mining can be found in various areas of academical and non academical life. This paper introduces new contributions by continuous optimization as a key technology in data mining. The methods suggested for solution of such important problems as clustering and classification, were recently obtained by the authors in collaboration with members of EURO working group EUROPT

Interleukin 8 in postoperative delirium - preliminary findings from two studies

OBJECTIVE: Studies have suggested that inflammation contributes to the pathogenesis of postoperative delirium, but previous results on the proinflammatory cytokine IL-8 in plasma are contradictory. Additionally, a significant fraction of IL-8 is bound to erythrocytes, but the relevance of whole blood IL-8 in delirium has not been studied. In this work, we analyzed the association of postoperative delirium with levels of unbound IL-8 in plasma and levels of IL-8 in whole blood in patients from two studies which were conducted in our department and have not been presented previously. We assessed the prognostic value of whole blood IL-8. METHODS: Plasma/whole blood IL-8 was measured at least once in N ​= ​504 patients preoperatively, on day one (d1) and/or three months after surgery in the BioCog observational study. Whole blood IL-8 was measured in N ​= ​64 patients from the PHYDELIO trial preoperatively, on d1 and d7 after surgery. For the determination of whole blood IL-8, EDTA-preserved blood samples underwent lysis by adding Triton-X100 surfactant. Plasma and whole blood IL-8 levels were assessed with two different immunoassay kits. Delirium was appraised systematically for seven postoperative days according to DSM criteria using two comparable protocols consisting of validated screening tools. RESULTS: Delirium occurred in 25% of BioCog and 14% of PHYDELIO patients. In BioCog, IL-8 was elevated on d1 and in delirious patients. A steeper postoperative increase in delirium was confounded by surgery-related factors. A crescendo-decrescendo pattern of whole blood IL-8 levels was observed in non-delirious patients with a peak on d1. This pattern was more distinct in delirious BioCog patients, but inverted in delirious PHYDELIO patients. Preoperative whole blood IL-8>318.4 ​pg/mL (reference <150 ​pg/mL) had adequate sensitivity (0.79/0.78) and specificity (0.53/0.67) for delirium in both samples. CONCLUSION: Our results contribute to an inflammatory hypothesis of postoperative delirium

Import Substitution Industrialization [ISI]: An approach to Global Economic Sustainability

Globalisation has over the years brought about openness, thus creating an inextricable link among countries through various channels, including trade and investment. Consequently, there has been a substantial expansion in trade in goods and services and the flow of foreign direct investment between developed and developing countries. Even though, both have benefitted from this global openness, the balance of benefits is mainly tilted to developed countries, reinforced by the fact that developing countries have been importing more and exporting less to these countries – a reflection of the under-developed state of their industrial sector, which is evident in their export of mainly unrefined or primary products, with little or no value addition taking place. This gives attestation to the presence of an insignificant import substitution-oriented manufacturing activity in such countries, which have rendered them heavily reliant on imports for their survival – by extension making them highly susceptible to external risks and shocks. This brought about the inception of ISI, which originated from as early as in the 1930s through into the 1960s in Latin America and some parts of Asia and Africa – a notion that was meant to incorporate three stages, namely ‘domestic production of previously imported non-durable consumer goods, extension of production to a wide-range of consumer durables and complex manufactured items and finally, exporting of manufactured goods, with the vision of diversifying to multiple range of items’ (Bussell,, n/d)

Modeling the Basal Dynamics of P53 System

The tumor suppressor p53 has become one of most investigated genes. Once activated by stress, p53 leads to cellular responses such as cell cycle arrest and apoptosis.Most previous models have ignored the basal dynamics of p53 under nonstressed conditions. To explore the basal dynamics of p53, we constructed a stochastic delay model by incorporating two negative feedback loops. We found that protein distribution of p53 under nonstressed condition is highly skewed with a fraction of cells showing high p53 levels comparable to those observed under stressed conditions. Under nonstressed conditions, asynchronous and spontaneous p53 pulses are triggered by basal DNA double strand breaks produced during normal cell cycle progression. The first peaking times show a predominant G1 distribution while the second ones are more widely distributed. The spontaneous pulses are triggered by an excitable mechanism. Once initiated, the amplitude and duration of pulses remain unchanged. Furthermore, the spontaneous pulses are filtered by ataxia telangiectasia mutated protein mediated posttranslational modifications and do not result in substantial p21 transcription. If challenged by externally severe DNA damage, cells generate synchronous p53 pulses and induce significantly high levels of p21. The high expression of p21 can also be partially induced by lowering the deacetylation rate.Our results demonstrated that the dynamics of p53 under nonstressed conditions is initiated by an excitable mechanism and cells become fully responsive only when cells are confronted with severe damage. These findings advance our understanding of the mechanism of p53 pulses and unlock many opportunities to p53-based therapy

EMSY overexpression disrupts the BRCA2/RAD51 pathway in the DNA-damage response: implications for chromosomal instability/recombination syndromes as checkpoint diseases

EMSY links the BRCA2 pathway to sporadic breast/ovarian cancer. It encodes a nuclear protein that binds to the BRCA2 N-terminal domain implicated in chromatin/transcription regulation, but when sporadically amplified/overexpressed, increased EMSY level represses BRCA2 transactivation potential and induces chromosomal instability, mimicking the activity of BRCA2 mutations in the development of hereditary breast/ovarian cancer. In addition to chromatin/transcription regulation, EMSY may also play a role in the DNA-damage response, suggested by its ability to localize at chromatin sites of DNA damage/repair. This implies that EMSY overexpression may also repress BRCA2 in DNA-damage replication/checkpoint and recombination/repair, coordinated processes that also require its interacting proteins: PALB2, the partner and localizer of BRCA2; RPA, replication/checkpoint protein A; and RAD51, the inseparable recombination/repair enzyme. Here, using a well-characterized recombination/repair assay system, we demonstrate that a slight increase in EMSY level can indeed repress these two processes independently of transcriptional interference/repression. Since EMSY, RPA and PALB2 all bind to the same BRCA2 region, these findings further support a scenario wherein: (a) EMSY amplification may mimic BRCA2 deficiency, at least by overriding RPA and PALB2, crippling the BRCA2/RAD51 complex at DNA-damage and replication/transcription sites; and (b) BRCA2/RAD51 may coordinate these processes by employing at least EMSY, PALB2 and RPA. We extensively discuss the molecular details of how this can happen to ascertain its implications for a novel recombination mechanism apparently conceived as checkpoint rather than a DNA repair system for cell division, survival, death, and human diseases, including the tissue specificity of cancer predisposition, which may renew our thinking about targeted therapy and prevention