FAULT-TOLERANT DISTRIBUTED CHANNEL ALLOCATION ALGORITHMS FOR CELLULAR NETWORKS

In cellular networks, channels should be allocated efficiently to support communication betweenmobile hosts. In addition, in cellular networks, base stations may fail. Therefore, designing a faulttolerantchannel allocation algorithm is important. That is, the algorithm should tolerate failuresof base stations. Many existing algorithms are neither fault-tolerant nor efficient in allocatingchannels.We propose channel allocation algorithms which are both fault-tolerant and efficient. In theproposed algorithms, to borrow a channel, a base station (or a cell) does not need to get channelusage information from all its interference neighbors. This makes the algorithms fault-tolerant,i.e., the algorithms can tolerate base station failures, and perform well in the presence of thesefailures.Channel pre-allocation has effect on the performance of a channel allocation algorithm. Thiseffect has not been studied quantitatively. We propose an adaptive channel allocation algorithmto study this effect. The algorithm allows a subset of channels to be pre-allocated to cells. Performanceevaluation indicates that a channel allocation algorithm benefits from pre-allocating allchannels to cells.Channel selection strategy also inuences the performance of a channel allocation algorithm.Given a set of channels to borrow, how a cell chooses a channel to borrow is called the channelselection problem. When choosing a channel to borrow, many algorithms proposed in the literaturedo not take into account the interference caused by borrowing the channel to the cells which havethe channel allocated to them. However, such interference should be considered; reducing suchinterference helps increase the reuse of the same channel, and hence improving channel utilization.We propose a channel selection algorithm taking such interference into account.Most channel allocation algorithms proposed in the literature are for traditional cellular networkswith static base stations and the neighborhood relationship among the base stations is fixed.Such algorithms are not applicable for cellular networks with mobile base stations. We proposea channel allocation algorithm for cellular networks with mobile base stations. The proposedalgorithm is both fault-tolerant and reuses channels efficiently.KEYWORDS: distributed channel allocation, resource planning, fault-tolerance, cellular networks,3-cell cluster model

Function of the Stem Cell Transcription Factor SALL4 in Hematopoiesis

SALL4 is a zinc finger DNA-binding protein that has been well characterized in development and in embryonic stem cell (ESC) maintenance. Notably, SALL4 may be one of the few genes that are also involved in tissue stem cells in adults, and SALL4 protein expression has been correlated with the presence of stem and progenitor cell populations in various organ systems and also in human cancers. In normal hematopoiesis, SALL4 expression is restricted to the rare hematopoietic stem/progenitor cell (HSC/HPC) fractions but is rapidly silenced following lineage differentiation. In hematopoietic malignancies, however, SALL4 is persistently expressed and its expression levels are linked with deteriorated disease status. Furthermore, SALL4 activation participates in the pathogenesis of tumor initiation and disease progression. This chapter summarizes recent advances in our knowledge of SALL4 biology with a focus on its regulatory functions in normal and leukemic hematopoiesis. A better understanding of SALL4’s biologic functions and mechanisms is needed to facilitate the development of advanced therapies in future

Isolation, characterization, and in vitro propagation of infantile hemangioma stem cells and an in vivo mouse model

<p>Abstract</p> <p>Background</p> <p>Infantile hemangiomas (IH) are the most common benign tumors of infancy. The typical clinical course consists of rapid growth during the first year of life, followed by natural and gradual involution over a multi-year time span through unknown cellular mechanisms. Some tumors respond to medical treatment with corticosteroids or beta-blockers, however, when this therapy fails or is incomplete, surgical extirpation may be necessary. Noninvasive therapies to debulk or eliminate these tumors would be an important advance. The development of an <it>in vitro </it>cell culture system and an animal model would allow new insights into the biological processes involved in the development and pathogenesis of IH.</p> <p>Results</p> <p>We observed that proliferative stage IH specimens contain significantly more SALL4+ and CD133+ cells than involuting tumors, suggesting a possible stem cell origin. A tumor sphere formation assay was adapted to culture IH cells <it>in vitro</it>. Cells in IH tumor spheres express GLUT1, indicative of an IH cell of origin, elevated levels of VEGF, and various stem/progenitor cell markers such as SALL4, KDR, Oct4, Nanog and CD133. These cells were able to self-renew and differentiate to endothelial lineages, both hallmarks of tumor stem cells. Treatment with Rapamycin, a potent mTOR/VEGF inhibitor, dramatically suppressed IH cell growth <it>in vitro</it>. Subcutaneous injection of cells from IH tumor spheres into immunodeficient NOD-SCID mice produced GLUT1 and CD31 positive tumors with the same cellular proliferation, differentiation and involution patterns as human hemangiomas.</p> <p>Conclusions</p> <p>The ability to propagate large numbers of IH stem cells <it>in vitro </it>and the generation of an <it>in vivo </it>mouse model provides novel avenues for testing IH therapeutic agents in the future.</p

Tunable van Hove singularity without structural instability in Kagome metal CsTi3_3Bi5_5

In Kagome metal CsV$_3$Sb$_5$, multiple intertwined orders are accompanied by both electronic and structural instabilities. These exotic orders have attracted much recent attention, but their origins remain elusive. The newly discovered CsTi$_3$Bi$_5$ is a Ti-based Kagome metal to parallel CsV$_3$Sb$_5$. Here, we report angle-resolved photoemission experiments and first-principles calculations on pristine and Cs-doped CsTi$_3$Bi$_5$ samples. Our results reveal that the van Hove singularity (vHS) in CsTi$_3$Bi$_5$ can be tuned in a large energy range without structural instability, different from that in CsV$_3$Sb$_5$. As such, CsTi$_3$Bi$_5$ provides a complementary platform to disentangle and investigate the electronic instability with a tunable vHS in Kagome metals

Regulation of expression of starch synthesis genes by ethylene and ABA in relation to the development of rice inferior and superior spikelets

Later-flowering spikelets in a rice panicle, referred to as the inferior spikelets, are usually poorly filled and often limit the yield potential of some rice cultivars. The physiological and molecular mechanism for such poor grain filling remains unclear. In this study the differentially expressed genes in starch synthesis and hormone signalling between inferior and superior spikelets were comprehensively analysed and their relationships with grain filling was investigated. DNA microarray and real-time PCR analysis revealed that a group of starch metabolism-related genes showed enhanced expression profiles and had higher transcript levels in superior spikelets than in inferior ones at the early and middle grain-filling stages. Expression of the abscisic acid (ABA) synthesis genes, 9-cis-epoxycarotenoid dioxygenase 1 (NCED1) and NCED5, and the ethylene synthesis genes, 1-aminocyclopropane-1-carboxylate oxidase 1 (ACO1) and ACO3, declined with development of the caryopses. Meanwhile, if compared with inferior spikelets, expression of these genes in superior spikelets decreased faster and had lower transcript profiles, especially for ethylene. ABA concentration and ethylene evolution rate showed similar trends to their gene expression. Exogenous supply of ABA reduced the sucrose synthase (SUS) mRNA level and its enzyme activity in detached rice grains, while exogenously supplied ethephon (an ethylene-releasing reagent) suppressed the expression of most starch synthesis genes; that is, SUS, ADP-glucose pyrophosphorylase (AGPase), and soluble starch synthase (SSS), and down-regulated their enzyme activities. In summary, it is concluded that the relatively high concentrations of ethylene and ABA in inferior spikelets suppress the expression of starch synthesis genes and their enzyme activities and consequently lead to a low grain-filling rate

A Novel SALL4/OCT4 Transcriptional Feedback Network for Pluripotency of Embryonic Stem Cells

Background: SALL4 is a member of the SALL gene family that encodes a group of putative developmental transcription factors. Murine Sall4 plays a critical role in maintaining embryonic stem cell (ES cell) pluripotency and self-renewal. We have shown that Sall4 activates Oct4 and is a master regulator in murine ES cells. Other SALL gene members, especially Sall1 and Sall3 are expressed in both murine and human ES cells, and deletions of these two genes in mice lead to perinatal death due to developmental defects. To date, little is known about the molecular mechanisms controlling the regulation of expressions of SALL4 or other SALL gene family members. Methodology/Principal Findings: This report describes a novel SALL4/OCT4 regulator feedback loop in ES cells in balancing the proper expression dosage of SALL4 and OCT4 for the maintenance of ESC stem cell properties. While we have observed that a positive feedback relationship is present between SALL4 and OCT4, the strong self-repression of SALL4 seems to be the “break” for this loop. In addition, we have shown that SALL4 can repress the promoters of other SALL family members, such as SALL1 and SALL3, which competes with the activation of these two genes by OCT4. Conclusions/Significance: Our findings, when taken together, indicate that SALL4 is a master regulator that controls its own expression and the expression of OCT4. SALL4 and OCT4 work antagonistically to balance the expressions of other SALL gene family members. This novel SALL4/OCT4 transcription regulation feedback loop should provide more insight into the mechanism of governing the “stemness” of ES cells