The Session Initiation Protocol (SIP) was designed for wire line networks. It was developed to initiate, modify and terminate sessions between two hosts on a network. When the Internet expanded to include wireless hosts, SIP did not scale well for these wireless hosts because of the nature of the wireless channel. Also, there were issues with mobility and real time communication. This thesis proposes improvements to some of the extensions to SIP, for better performance over wireless channels. We investigate the call setup time for various transport mechanisms viz. TCP and UDP, and study the performance of a dynamic Session Timers compared to the current standard of a periodic refresh mechanism, where the frequency of UPDATEs vary with the condition of the wireless channel. We also propose a handoff algorithm that reduces the handover time with decreased packet losses.

During stress-induced apoptosis, the initiator caspase-9 is activated by the Apaf-1 apoptosome and must remain bound in order to retain significant catalytic activity. Nevertheless, in apoptotic cells, the vast majority of processed caspase-9 is paradoxically observed outside of the complex. We demonstrate herein that apoptosome-mediated cleavage of procaspase-9 occurs exclusively through a CARD-displacement mechanism, so that unlike the effector procaspase-3, procaspase-9 cannot be processed by the apoptosome as a typical substrate. Indeed, procaspase-9 possessed higher affinity for the apoptosome and could displace processed caspase-9 from the complex, thereby facilitating a continuous cycle of procaspase-9 recruitment/activation, processing, and release from the complex. Due to its rapid autocatalytic cleavage, however, procaspase-9 per se contributed little to the activation of procaspase-3. Thus, the Apaf-1 apoptosome functions as a proteolytic-based “molecular timer”, wherein the intracellular concentration of procaspase-9 sets the overall duration of the timer, procaspase-9 autoprocessing activates the timer, and the rate at which processed caspase-9 dissociates from the complex (and thus loses its capacity to activate procaspase-3) dictates how fast the timer “ticks” over. To understand the physiological relevance of molecular timer in vivo, we are currently generating caspase-9 knock-in mouse models. These mouse models will enhance our understanding of the importance of caspase-9 processing within the apoptosome. / text

The microcontroller and the coding is the heart of making a timer. The strategic release planning is gotten from the concept of how a door machine with password access functions. In this thesis project, all that has been studied in school such as circuit theory, electronics, digital design and microprocessors basic and programming course are combined to the success of this project. Therefore the objective is producing a practical knowledge of what has been studied which is the timer with password access. The method used was an inspiration gotten after reviewing many materials in some respective topic related to designing a timer. The particular method comes from creating an SPI Interface from the Programmer to the Microcontroller to Make Transferring More Convenient. The performance of the MCU, LCD and keypad was just as was expected in the software code and hardware also. The password is inputted, timer is set appropriately and timer runs till port is opened. To conclude, the result can be achieved in different method but this method was for an easy method for beginners. / 0764353558

No description available.

A substrate was developed for measuring the milk clotting strength of rennet preparations on an automatic clot-timer . The substrate contained 8 percent pasteurized skim milk solids, 1 percent chloroform, 0.3 percent 200 bloom gelatin, 0.03 M added CaCl2 and was buffered to pH 6.6 with 0.057 M cacodylic acid and 0.042 M triethanolamine. The substrate was shelf-stable for 18 days at room temperatures. It was found that rennet preparations could be standardized to within 1 percent of each other, in terms of milk clotting strength, by use of the substrate on the automatic clot-timer. The method appears to have advantages over conventional rennet standardizing procedures. The research included studies on the effect of chloroform, nonfat dry milk and CaCl2 concentrations; heat and ionizing radiation on the substrate coagulation time.

FAculty of SCience School of Cheistry 9910913j messai@auvum.chem.wits.ac.za / The monodentate phosphine complexes bui3PMX (2a: M = Cu, X = Cl, 2b: M = Cu, X = I, 2c: M = Ag, X = Cl, 2d: M = Au, X = Cl) were synthesised in high yields from bui3P and MX. Their reaction with [Li{μ-N(R)C(but)C(H)R}]2 (R = SiMe3) gave the monomeric complexes bui3PCuN(R)C(but)=C(H)R (3a) and bui3PMC(H)RC(but)=NR (3b: M = Ag, 3c: M = Au) in moderate to high yields. The bonding mode in the 1-aza-allyl complexes 3a-c was found to depend strongly on the metal ion, with 3a being an enamide complex and 3b and 3c iminoalkyl complexes. The reaction of bidentate ligand dpmaaH2 (2,3-bis(diphenylphosphino)maleic acid) with R2Sn-precursors led to novel dialkyl tin dpmaa complexes (R2Sn)(O,O dpmaa) (6) (where 6a, R = Me; 6b, R = Bu) were synthesized. Complexation of the tin/phosphine complexes led to the heterobimetallic complexes {Au[(dpmaaO,O)(SnR2)]2}Cl (7a and 8a) {Au[(dpmaaO,O)(SnR2)][dpmaaH2]}Cl (7b and 8b) (where 7a and 8a, R = Me; 7b and 8b, R = Bu) and the mixed metal complexes {Au[(dpmaaO,O)(RuCl)]2}Cl (9a) {Au[(dpmaaO,O)(SnBu2)(dpmaaO,O)RuCl)]}Cl (9b) and {Au[(dpmaaO,O)(RuCl)][dpmaa]}Cl (9c). All compounds were fully characterised by multinuclear NMR spectroscopy and microanalysis (not 3a, 3b, 4 and 5) solid state IR spectroscopy (KBr-pellets) (4-9) and mass spectrometry (6-8). The solid state structures of complexes 2c, 2d, 3c, 6a and 6b (two polymorphs) have been determined by X-ray crystallography revealing the presence of rare trimeric macrocycles in the case of 6a and 6b. The anti-tumour activity of the metal complexes (6b and 7-9) was tested on a single cell-line (except 7a and 8a which were on eight cell-lines) and their activity was compared to cisplatin.

This thesis focuses on the circadian clock genes and their involvement in the photoperiodic time measurement in the linden bug, Pyrrhocoris apterus. Application of the molecular biology methods enabled us to propose the architecture of circadian clockwork. We also investigated the role of several previously undescribed players in the circadian clock. Furthermore, by using molecular biology methods we focused on the involvement of core circadian clock genes in the photoperiodism.

This thesis describes the design of a DSP based air detector system to prevent air embolism during Hemodialysis, which is a treatment option for kidney failure disease. Hemodialysis consists of removing blood from the body, filtering and treating the blood to remove toxic substances such as wastes and fluids, reestablishing proper chemical levels in the blood and returning the processed blood to the body. The functions of hemodialysis are performed through the use of a dialyzer, which is also known as an artificial kidney. During hemodialysis small air bubbles may infiltrate the tubing used during the therapy and combine to form larger air bubbles that are harmful to the patient. If an air bubble is large enough and enters the patient's circulatory system, the blood flow can be blocked and the patient can die by embolism. Most of the hemodialysis instruments in use today are equipped with air detection systems, which are based on analog design and digital microcontroll ers. This thesis presents a design method based strictly on DSP technology. The Motorola DSP 56824EVM was considered suitable for this biomedical application since its performance parameters include high-speed, multi-signal control capability, reliability and stability. These performance parameters are considered to be the most important when designing biomedical instruments dealing with human beings' life and safety. The objective of this research was the development and implementation of a DSP algorithm for the detection and measurement of the sizes of air bubbles in a fluid. In addition the algorithm had to possess the capability, when appropriate, to initiate protective and awareness measures such as triggering a tube clamp as well as activating visual and audio alarms. The air detection was accomplished by means of a commercial air detector module, which was based on piezo ceramic and ultrasound sensing. The function of the tubing clamp was to stop the fluid flow in the tubing and prevent an air bubble from entering the patient's circulatory system. A secondary goal of this research was to exploit the capability of the DSP 56824EVM and demonstrate its suitability for biomedical applications.

京都大学 / 0048 / 新制・課程博士 / 博士(理学) / 甲第22281号 / 理博第4595号 / 新制||理||1659(附属図書館) / 京都大学大学院理学研究科生物科学専攻 / (主査)教授 沼田 英治, 准教授 森 哲, 教授 曽田 貞滋 / 学位規則第4条第1項該当 / Doctor of Science / Kyoto University / DFAM

During the early development of Xenopus laevis embryos, cells divide without checkpoints. At the midblastula transition (MBT), the cell cycle is remodeled as the division time lengthens and checkpoints are acquired. Initiation of the MBT depends upon the degradation of maternally supplied cyclin E, which is the regulatory partner of the cyclin dependent kinase, Cdk2. To study the program that drives cyclin E degradation and cell cycle remodeling at the MBT, embryos were treated with two cell cycle inhibitors, GST-D34Xic1 and XChk1. Injection of embryos with GST-D34Xic1, a stoichiometric inhibitor of cyclin E/Cdk2, delays degradation of cyclin E and onset of the MBT. GST-D34Xic1 lowers Wee1 level, a kinase that maintains Cdks in an inactivate state. Eventual degradation of cyclin E is preceded by degradation of GST-D34Xic1. The mathematical modelers, Andrea Ciliberto and John Tyson, incorporated the data into a kinetic model and set of ordinary differential equations. The model accurately described the experimental data and made additional predictions, which were tested experimentally. Additionally, embryos were injected with mRNA encoding XChk1, a kinase that activates Wee1 and inhibits Cdc25, the phosphatase opposing Wee1. Like GST-D34Xic1, XChk1 inhibits cyclin E/Cdk2 and delays the degradation of cyclin E. In contrast to GST-D34Xic1, XChk1 elevates the level of Wee1 at a time when sibling controls begin the MBT, despite cell cycle arrest. Since XChk1 inhibits both Cdk1 and Cdk2, and GST-D34Xic1 inhibits only Cdk2, we propose Cdk1 destabilizes Wee1, whereas Cdk2 elevates Wee1 level. Prior to the MBT, when cyclin E/Cdk2 is active, Wee1 is maintained. After cyclin E/Cdk2 is destroyed at the MBT, Wee1 is degraded. / Master of Science