A Multi-hop Topology Control Based on Inter-node Range Measurement for Wireless Sensor Networks Node Localization

In centralized range-based localization techniques, sufficiency of inter-node range information received by the base station strongly affects node position estimation results. Successful data aggregation is influenced by link stability of each connection of routes, especially in a multi-hop topology model. In general, measuring the inter-node range is only performed for position determination purposes. This research introduces the use of inter-node range measurement information for link selection in a multi-hop route composition in order to increase the rate of data aggregation. Due to irregularity problems of wireless media, two areas of node communication have been considered. The regular communication area is the area in which other nodes are able to perform symmetrical communication to the node without failure. The irregular area is the area in which other nodes are seldom able to communicate. Due to its instability, some existing methods tried to avoid the irregular area completely. The proposed method, named Virtual Boundaries (VBs) prioritizes these areas. The regular communication area’s nodes have high priority to be selected as link vertices; however, when there is no link candidate inside this area, nodes within the irregular area will be selected with respect to their range to the parent node. This technique resulted in a more robust multi-hop topology that can reduce isolated node numbers and increase the percentage of data collected by the base station accordingly

Range-based Localization implanting Packet Reception Derived Ranges for Sparse Distributed Wireless Sensor Networks

In centralized range-based localization techniques, sufficiency of inter-node range information received by the base station is strongly affects nodes position estimation accuracy. In real flooded wireless sensor networks (WSNs), the density of network will be varying from part to part. Nodes spared in low density part will potentially have insufficient or even none range information. This research proposed a range-based localization method for sparse distributed WSNs which combined measured range and non-confidential range derived from the packet reception rate (PRR) for cases of insufficiency range information

Role of Nitrogen on Growth and Seed Yield of Soybean and a New Fertilization Technique to Promote Nitrogen Fixation and Seed Yield

Soybean is an important crop for human food and feed for livestock. World soybean production is increasing especially in North and South America. Soybean seeds contain a high percentage of protein about 35–40%, and they require a large amount of nitrogen compared with other crops. Soybean plants make root nodules with rhizobia, and rhizobia can fix atmospheric N2 and give the fixed N to the host soybean plants. Also, soybean can absorb nitrogen usually nitrate from soil or fertilizers. The amount of total assimilated nitrogen in shoot is proportional to the soybean seed yield either from nitrogen fixation or from nitrogen absorption, and the nitrogen availability is very important for soybean cultivation. Maintenance of a high and long-term nitrogen fixation activity is very important for a high production of soybean. However, application of chemical nitrogen fertilizers usually depresses nodule formation and nitrogen fixation. Nitrate in direct contact with a nodulated part of roots causes severe inhibition of nodule growth and nitrogen fixation, although a distant part of nodules from nitrate application gives no or little effect. Deep placement of slow-release nitrogen fertilizers, coated urea, or lime nitrogen promoted the growth and seed yield and quality of soybean without depressing nitrogen fixation

UV エンドヌクレアーゼ オ ケッソン シタ ブンレツ コウボ ニオケル シガイセン ソンショウ ミトコンドリア DNA ノ シュウフク

P(論文)departmental bulletin pape

The Shortest Isoform of Dystrophin (Dp40) Interacts with a Group of Presynaptic Proteins to Form a Presumptive Novel Complex in the Mouse Brain

Duchenne muscular dystrophy (DMD) causes cognitive impairment in one third of the patients, although the underlying mechanisms remain to be elucidated. Recent studies showed that mutations in the distal part of the dystrophin gene correlate well with the cognitive impairment in DMD patients, which is attributed to Dp71. The study on the expression of the shortest isoform, Dp40, has not been possible due to the lack of an isoform specific antibody. Dp40 has the same promoter as that found in Dp71 and lacks the normal C-terminal end of Dp427. In the present study, we have raised polyclonal antibody against the N-terminal sequence common to short isoforms of dystrophin, including Dp40, and investigated the expression pattern of Dp40 in the mouse brain. Affinity chromatography with this antibody and the consecutive LC-MS/MS analysis on the interacting proteins revealed that Dp40 was abundantly expressed in synaptic vesicles and interacted with a group of presynaptic proteins, including syntaxin1A and SNAP25, which are involved in exocytosis of synaptic vesicles in neurons. We thus suggest that Dp40 may form a novel protein complex and play a crucial role in presynaptic function. Further studies on these aspects of Dp40 function might provide more insight into the molecular mechanisms of cognitive impairment found in patients with DMD

Mutations in UVSSA cause UV-sensitive syndrome and impair RNA polymerase IIo processing in transcription-coupled nucleotide-excision repair

UV-sensitive syndrome (UVSS) is a genodermatosis characterized by cutaneous photosensitivity without skin carcinoma1, 2, 3, 4. Despite mild clinical features, cells from individuals with UVSS, like Cockayne syndrome cells, are very UV sensitive and are deficient in transcription-coupled nucleotide-excision repair (TC-NER)2, 4, 5, which removes DNA damage in actively transcribed genes6. Three of the seven known UVSS cases carry mutations in the Cockayne syndrome genes ERCC8 or ERCC6 (also known as CSA and CSB, respectively)7, 8. The remaining four individuals with UVSS, one of whom is described for the first time here, formed a separate UVSS-A complementation group1, 9, 10; however, the responsible gene was unknown. Using exome sequencing11, we determine that mutations in the UVSSA gene (formerly known as KIAA1530) cause UVSS-A. The UVSSA protein interacts with TC-NER machinery and stabilizes the ERCC6 complex; it also facilitates ubiquitination of RNA polymerase IIo stalled at DNA damage sites. Our findings provide mechanistic insights into the processing of stalled RNA polymerase and explain the different clinical features across these TC-NER–deficient disorders