Inter-subnet localized mobility support for host identity protocol

Host identity protocol (HIP) has security support to enable secured mobility and multihoming, both of which are essential for future Internet applications. Compared to end host mobility and multihoming with HIP, existing HIP-based micro-mobility solutions have optimized handover performance by reducing location update delay. However, all these mobility solutions are client-based mobility solutions. We observe that another fundamental issue with end host mobility and multihoming extension for HIP and HIP-based micro-mobility solutions is that handover delay can be excessive unless the support for network-based micro-mobility is strengthened. In this study, we co-locate a new functional entity, subnet-rendezvous server, at the access routers to provide mobility to HIP host. We present the architectural elements of the framework and show through discussion and simulation results that our proposed scheme has achieved negligible handover latency and little packet loss

Distributed mobility management with mobile Host Identity Protocol proxy

The architectural evolution from hierarchical to flatter networks creates new challenges such as single points of failure and bottlenecks, non-optimal routing paths, scalability problems, and long handover delays. The cellular networks have been hierarchical so that they are largely built on centralized functions based on which their handover mechanisms have been built. They need to be redesigned and/or carefully optimized. The mobility extension to Host Identity Protocol (HIP) proxy, mobile HIP Proxy (MHP), provides a seamless and secure handover for the Mobile Host in the hierarchical network. However, the MHP cannot ensure the same handover performance in flatter network because the MHP has also utilized the features offered by the hierarchical architecture. This paper extends the MHP to distributed mobile HIP proxy (DMHP). The performance evaluation of the DMHP in comparison to MHP and other similar mobility solutions demonstrates that DMHP does indeed perform well in the flatter networks. Moreover, the DMHP supports both efficient multi-homing and handover management for many mobile hosts at the same time to the same new point of attachment

On the habitat use of the Neotropical whip spider Charinus asturius (Arachnida: Amblypygi)

The non-random occupation of habitats is termed habitat selection. Some species of whip spiders select trees with burrows at their base, while others use substrates such as rocks. Here, we investigated the habitat use by Charinus asturius Pinto-da-Rocha, Machado & Weygoldt, 2002, an endemic species of Ilhabela Island in Brazil. We found that C. asturius is more likely to be found under rocks that cover larger areas of substrate. Our results also suggest the existence of territorialism in C. asturius and show that C. asturius adults may be found again on the same rock a week later. Additionally, our data show that C. asturius is present in a greater area of Ilhabela than previously documented.Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2014/19191-3, 2015/01518-9]Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [133214/2015-0]Univ Sao Paulo, Escola Artes Ciencias & Humanidades, Lab Ecol Sensorial & Comportamento Artropodes, Rua Arlindo Bettio 1000, BR-03828000 Sao Paulo, SP, BrazilUniv Sao Paulo, Inst Biociencias, Programa Pos Grad Zool, Rua Matao 321,Travessa 14, BR-05508900 Sao Paulo, BrazilUniv Sao Paulo, Inst Psicol, Dept Psicol Expt, Ave Prof Mello de Morais,1721 Butanta, BR-05508030 Sao Paulo, SP, BrazilUniv Fed Sao Paulo, Programa Pos Grad Ecol & Evolucao, Rua Prof Artur Riedel 275, BR-09972270 Diadema, BrazilUniv Fed Sao Paulo, Programa Pos Grad Ecol & Evolucao, Rua Prof Artur Riedel 275, BR-09972270 Diadema, BrazilFAPESP: [2014/19191-3, 2015/01518-9]CNPq: [133214/2015-0]Web of Scienc

Avaliação de famílias e progênies de arroz de terras altas, em Vilhena, RO, em 2012/13.

O objetivo desse trabalho foi avaliar e selecionar famílias e progênies de arroz de terras altas

Avaliação de famílias e progênies de arroz de terras altas, em Vilhena, RO, em 2011/12.

O objetivo desse trabalho foi avaliar famílias e progênies de arroz de terras altas, em Rondônia

Subcellular heterogeneity of ryanodine receptor properties in ventricular myocytes with low T-tubule density

Rationale: In ventricular myocytes of large mammals, not all ryanodine receptor (RyR) clusters are associated with T-tubules (TTs); this fraction increases with cellular remodeling after myocardial infarction (MI). Objective: To characterize RyR functional properties in relation to TT proximity, at baseline and after MI. Methods: Myocytes were isolated from left ventricle of healthy pigs (CTRL) or from the area adjacent to a myocardial infarction (MI). Ca2+ transients were measured under whole-cell voltage clamp during confocal linescan imaging (fluo-3) and segmented according to proximity of TTs (sites of early Ca2+ release, F>F50 within 20 ms) or their absence (delayed areas). Spontaneous Ca2+ release events during diastole, Ca2+ sparks, reflecting RyR activity and properties, were subsequently assigned to either category. Results: In CTRL, spark frequency was higher in proximity of TTs, but spark duration was significantly shorter. Block of Na+/Ca2+ exchanger (NCX) prolonged spark duration selectively near TTs, while block of Ca2+ influx via Ca2+ channels did not affect sparks properties. In MI, total spark mass was increased in line with higher SR Ca2+ content. Extremely long sparks (>47.6 ms) occurred more frequently. The fraction of near-TT sparks was reduced; frequency increased mainly in delayed sites. Increased duration was seen in near-TT sparks only; Ca2+ removal by NCX at the membrane was significantly lower in MI. Conclusion: TT proximity modulates RyR cluster properties resulting in intracellular heterogeneity of diastolic spark activity. Remodeling in the area adjacent to MI differentially affects these RyR subpopulations. Reduction of the number of sparks near TTs and reduced local NCX removal limit cellular Ca2+ loss and raise SR Ca2+ content, but may promote Ca2+ waves

Myosin VI in PC12 cells plays important roles in cell migration and proliferation but not in catecholamine secretion

Myosin VI (MVI) is the only known myosin walking towards minus end of actin filaments and is believed to play distinct role(s) than other myosins. We addressed a role of this unique motor in secretory PC12 cells, derived from rat adrenal medulla pheochromocytoma using cell lines with reduced MVI synthesis (produced by means of siRNA). Decrease of MVI expression caused severe changes in cell size and morphology, and profound defects in actin cytoskeleton organization and Golgi structure. Also, significant inhibition of cell migration as well as cell proliferation was observed. Flow cytometric analysis revealed that MVI-deficient cells were arrested in G0/G1 phase of the cell cycle but did not undergo increased senescence as compared with control cells. Also, neither polyploidy nor aneuploidy were detected. Surprisingly, no significant effect on noradrenaline secretion was observed. These data indicate that in PC12 cells MVI is involved in cell migration and proliferation but is not crucial for stimulation-dependent catecholamine release

The Role for HNF-1β-Targeted Collectrin in Maintenance of Primary Cilia and Cell Polarity in Collecting Duct Cells

Collectrin, a homologue of angiotensin converting enzyme 2 (ACE2), is a type I transmembrane protein, and we originally reported its localization to the cytoplasm and apical membrane of collecting duct cells. Recently, two independent studies of targeted disruption of collectrin in mice resulted in severe and general defects in renal amino acid uptake. Collectrin has been reported to be under the transcriptional regulation by HNF-1α, which is exclusively expressed in proximal tubules and localized at the luminal side of brush border membranes. The deficiency of collectrin was associated with reduction of multiple amino acid transporters on luminal membranes. In the current study, we describe that collectrin is a target of HNF-1β and heavily expressed in the primary cilium of renal collecting duct cells. Collectrin is also localized in the vesicles near the peri-basal body region and binds to γ-actin-myosin II-A, SNARE, and polycystin-2-polaris complexes, and all of these are involved in intracellular and ciliary movement of vesicles and membrane proteins. Treatment of mIMCD3 cells with collectrin siRNA resulted in defective cilium formation, increased cell proliferation and apoptosis, and disappearance of polycystin-2 in the primary cilium. Suppression of collectrin mRNA in metanephric culture resulted in the formation of multiple longitudinal cysts in ureteric bud branches. Taken together, the cystic change and formation of defective cilium with the interference in the collectrin functions would suggest that it is necessary for recycling of the primary cilia-specific membrane proteins, the maintenance of the primary cilia and cell polarity of collecting duct cells. The transcriptional hierarchy between HNF-1β and PKD (polycystic kidney disease) genes expressed in the primary cilia of collecting duct cells has been suggested, and collectrin is one of such HNF-1β regulated genes

RyRCa2+ Leak Limits Cardiac Ca2+ Window Current Overcoming the Tonic Effect of Calmodulin in Mice

Ca2+ mediates the functional coupling between L-type Ca2+ channel (LTCC) and sarcoplasmic reticulum (SR) Ca2+ release channel (ryanodine receptor, RyR), participating in key pathophysiological processes. This crosstalk manifests as the orthograde Ca2+-induced Ca2+-release (CICR) mechanism triggered by Ca2+ influx, but also as the retrograde Ca2+-dependent inactivation (CDI) of LTCC, which depends on both Ca2+ permeating through the LTCC itself and on SR Ca2+ release through the RyR. This latter effect has been suggested to rely on local rather than global Ca2+ signaling, which might parallel the nanodomain control of CDI carried out through calmodulin (CaM). Analyzing the CICR in catecholaminergic polymorphic ventricular tachycardia (CPVT) mice as a model of RyR-generated Ca2+ leak, we evidence here that increased occurrence of the discrete local SR Ca2+ releases through the RyRs (Ca2+ sparks) causea depolarizing shift in activation and a hyperpolarizing shift inisochronic inactivation of cardiac LTCC current resulting in the reduction of window current. Both increasing fast [Ca2+]i buffer capacity or depleting SR Ca2+ store blunted these changes, which could be reproduced in WT cells by RyRCa2+ leak induced with Ryanodol and CaM inhibition.Our results unveiled a new paradigm for CaM-dependent effect on LTCC gating and further the nanodomain Ca2+ control of LTCC, emphasizing the importance of spatio-temporal relationships between Ca2+ signals and CaM function