Auto-configuration of Physical Cell ID in LTE femtocellular systems using Self Organizing Networks

The commercial success of cellular networks, combined with advances in digital electronics, signal processing, and telecommunications research have lead to the design of next generation 4G-based long term evolution (LTE) wireless systems. The key essence of these emerging, LTE cellular systems lie in deployment of multiple femtocells for improved coverage and higher data rates. However, the arbitrary deployment of a wide number of femtocells makes the configuration, management and planning of LTE systems quite complex and challenging. In order to support dynamic and efficient network configuration, every cell needs to be assigned a particular Physical Cell ID (PCID). In this paper we show that the dynamic, optimal PCID allocation problem in LTE systems is NP-complete. Subsequently we provide a near-optimal solution using Self-Organizing Networks which models the problem using new merge operations and explores the search space using a suitable randomized algorithmic approach. We also discuss two feasible options for dynamic auto-configuration of the system and analyze the algorithm to prove its convergence. Simulation results point out that our proposed near-optimal solution dynamically achieves ～85?90 % of global optimal auto-configuration in computationally feasible time.     

The 5-HT1-like receptors mediating inhibition of sympathetic vasopressor outflow in the pithed rat: operational correlation with the 5-HT1A, 5-HT1B and 5-HT1D subtypes

1. It has been suggested that the inhibition of sympathetically-induced vasopressor responses produced by 5-hydroxytryptamine (5-HT) in pithed rats is mediated by 5-HT1-like receptors. The present study has re-analysed this suggestion with regard to the classification schemes recently proposed by the NC-IUPHAR subcommittee on 5-HT receptors. 2. Intravenous (i.v.) continuous infusions of 5-HT and the 5-HT1 receptor agonists, 8-OH-DPAT (5-HT1A), indorenate (5-HT1A), CP 93,129 (5-HT1B) and sumatriptan (5-HT(1B/1D)), resulted in a dose-dependent inhibition of sympathetically-induced vasopressor responses. 3. The sympatho-inhibitory responses induced by 5-HT, 8-OH-DPAT, indorenate, CP 93,129 or sumatriptan were analysed before and after i.v. treatment with blocking doses of the putative 5-HT receptor antagonists, WAY 100635 (5-HT1A), cyanopindolol (5-HT(1A/1B)) or GR 127935 (5-HT(1B/1D)). Thus, after WAY 100635, the responses to 5-HT and indorenate, but not to 8-OH-DPAT, CP 93,129 and sumatriptan, were blocked. After cyanopindolol, the responses to 5-HT, indorenate and CP 93,129 were abolished, whilst those to 8-OH-DPAT and sumatriptan (except at the lowest frequency of stimulation) remained unaltered. In contrast, after GR 127935, the responses to 5-HT, CP 93,129 and sumatriptan, but not to 8-OH-DPAT and indorenate, were abolished. 4. In additional experiments, the inhibition induced by 5-HT was not modified after 5-HT7 receptor blocking doses of mesulergine. 5. The above results suggest that the 5-HT1-like receptors, which inhibit the sympathetic vasopressor outflow in pithed rats, display the pharmacological profile of the 5-HT1A, 5-HT1B and 5-HT1D, but not that of 5-HT7, receptors.     

Electronic transmission across a metal /conjugated-oligomer/metal structure: role of intrinsic disorder

We have studied electronic transmission across metal/conjugated-oligomer/metal structures: (a) one oligomer chain, and (b) two oligomer chains sandwiched between metal contacts, in the presence of lattice fluctuations. The lattice fluctuations are approximated by static white noise disorder. Resonant transmission occurs when the energy of an incoming electron coincides with a discrete electronic level of the oligomer. Because of disorder there is an enhancement of electronic transmission for energies that lie within the electronic gap of the oligomer. If fluctuations are sufficiently strong, a transmission peak within the gap is found at the midgap energy E = 0 for degenerate conjugated oligomers. For the two-chain case the spatial mirror symmetry is broken and coherence between the wavefunctions of two chains is partly lost when fluctuations are introduced.     

Simultaneous measurements of thermal conductivity and diffusivity of Se80Te20-xInx (x = 2, 4, 6 and 10) chalcogenide glasses at room temperature

Measurements of thermal conductivity and thermal diffusivity of twin pellets of Se₈₀Te_20-xIn_x (x = 2, 4, 6 and 10) glasses, prepared under a load of 5 tons were carried out at room temperature using transient plane source (TPS) technique. The measured values of both thermal conductivity and diffusivity were used to determine the specific heat per unit volume of the said materials in the composition range of investigation. Results indicated that both the values of thermal conductivity and thermal diffusivity increased with the addition of indium at the cost of tellurium whereas the specific heat remained almost constant. This compositional dependence behaviour of the thermal conductivity and diffusivity has been explained in terms of the iono-covalent type of bond which In makes with Se as it is incorporated in the Se-Te glass.     

Evolution of surface deformation during fatigue of PH 13-8 Mo stainless steel using atomic force microscopy

The relationship between microstructure and nucleation of fatigue cracks in PH 13‐8 Mo stainless steel was explored with the use of atomic force microscopy (AFM) that allowed an accurate quantitative characterization of the surface features. Fully reversed strain‐ controlled fatigue tests were performed at 0.4 and 0.6% strain amplitudes, and the evolution of the surface deformation was observed at various fractions of life. At 0.4% strain amplitude, fatigue surface damage occurred first in the shape of streaks about 4 nm deep that formed at the interface between martensite laths and at prior austenite grain boundaries, and eventually coalesced to form crack nuclei. The increase in strain amplitude to 0.6% led to the formation of large extrusions, on average between 2 and 5 μm long with heights between 10 and 200 nm, which were the preferred crack nucleation sites.     

Serotonin receptors: subtypes, functional responses and therapeutic relevance

Recent, rapid progress in the molecular biology of serotonin (5-HT) receptors requires conceptual re-thinking with respect to receptor classification. Thus, based on operational criteria (agonist and antagonist rank order), as well as transduction mechanisms involved and the structure of the receptor protein, the Nomenclature Committee of the Serotonin Club has proposed the following classification and nomenclature: the main receptor types 5-HT1 to 5-HT4, recombinant receptors (e.g. 5-ht5 to 5-ht7) and 'orphan' receptors. The aim of the present review is to discuss the events leading to this classification, the criteria for and functional responses mediated by various 5-HT receptors, as well as the therapeutic possibilities with 5-HT ligands.     

Status of iodine deficiency in selected blocks of Kangra District, Himachal Pradesh

Using polymerase chain reaction single strand conformational polymorphism (PCR-SSCP) and EB staining technique, paraffin-embeded sections of 20 hydatidiform mole and 4 choriocarcinoma were detected in the exons 5 and 8 of p53 gene. The results showed that mutations of p53 gene were 0/9 in the normal chorionic villi, 6/20 (30%) in hydatidiform mole and 3/4 in choriocarcinoma. This study suggests that mutations of p53 gene may be an important event in human gestational trophoblastic neoplastigenesis and its progression.     

Insulin down-regulates the inducible nitric oxide synthase pathway: nitric oxide as cause and effect of diabetes?

Evidence in this paper indicates that insulin can down-regulate the inducible nitric oxide synthase (iNOS) pathway in vivo. The iNOS pathway is up-regulated in diabetes-prone rats and mice and is associated with an autoimmune process. However, the results presented here indicate that macrophage nitric oxide (NO) production and iNOS mRNA expression are also elevated in rats or mice made diabetic by streptozotocin injection in which there is no primary autoimmune component. Insulin administration reduces NO production in autoimmune-prone and streptozotocin-induced diabetic rodents. Finally, insulin decreases macrophage NO production in normal hosts. These results indicate that the autoimmune paradigm is inadequate to explain increased NO in diabetes. As a potential mechanism to explain insulin-mediated regulation of NO production, TGF-1 may be involved because 1) macrophages from diabetic mice produce less TGF-beta1 than macrophages from normal hosts; 2) the circulating TGF-beta1 level is lower in diabetic mice; and 3) insulin administration increases circulating TGF-beta1 in normal mice. Together, these results provide evidence that increased NO in diabetes is not only a cause but also an effect of beta-cell destruction and results in part from a heretofore unrecognized immunomodulatory activity of insulin.