A Call-Admission Control (CAC) Algorithm for Providing Guaranteed QoS in Cellular Networks

Future broadband wireless access systems are expected to integrate various classes of mobile terminals (MTs), each class with a different type of quality of service (QoS) requirement. When the load on a wireless network is high, the guarantee of QoS for each class of MTs is a challenging task. This study considers two classes of MTs—profiled MTs and nonprofiled or regular MTs. It is assumed that profiled users require a guaranteed QoS. The measure of QoS is the probability of forced termination of a call that was allowed to access the network. Two previous handoff prioritization schemes—(i) prerequest scheme and (ii) guard channel scheme—decrease handoff failure (and hence forced termination). In this work, we compare and contrast both the schemes through extensive simulation and we find that neither guard channel nor channel prerequest scheme can guarantee a desired level of QoS for the profiled MTs. We then propose a novel call-admission control (CAC) algorithm that can maintain any desired level of QoS, while the successful call completion rate is very high. In the proposed algorithm, the new call arrival rate is estimated continuously, and when the estimated arrival rate is higher than a predetermined level, some new calls are blocked irrespective of the availability of channels. The objective of this new call preblocking is to maintain a cell's observed new call arrival rate at no more than the predetermined rate. We show that the proposed method can guarantee any desired level of QoS for profiled users.     

Synthesis and Biological Evaluation of Imidazo[2,1‐b][1,3,4]thiadiazole‐Linked Oxindoles as Potent Tubulin Polymerization Inhibitors

A series of imidazo[2,1‐b][1,3,4]thiadiazole‐linked oxindoles composed of an A, B, C and D ring system were synthesized and investigated for anti‐proliferative activity in various human cancer cell lines; test compounds were variously substituted at rings C and D. Among them, compounds 7 ((E)‐5‐fluoro‐3‐((6‐p‐tolyl‐2‐(3,4,5‐trimethoxyphenyl)‐imidazo[2,1‐b][1,3,4]thiadiazol‐5‐yl)methylene)indolin‐2‐one), 11 ((E)‐3‐((6‐p‐tolyl‐2‐(3,4,5‐trimethoxyphenyl)imidazo[2,1‐b][1,3,4]thiadiazol‐5‐yl)methylene)indolin‐2‐one), and 15 ((E)‐6‐chloro‐3‐((6‐phenyl‐2‐(3,4,5‐trimethoxyphenyl)imidazo[2,1‐b][1,3,4]thiadiazol‐5‐yl)methylene)indolin‐2‐one) exhibited potent anti‐proliferative activity. Treatment with these three compounds resulted in accumulation of cells in G₂/M phase, inhibition of tubulin assembly, and increased cyclin‐B1 protein levels. Compound 7 displayed potent cytotoxicity, with an IC₅₀ range of 1.1–1.6 μM , and inhibited tubulin polymerization with an IC₅₀ value (0.15 μM ) lower than that of combretastatin A‐4 (1.16 μM ). Docking studies reveal that compounds 7 and 11 bind with αAsn101, βThr179, and βCys241 in the colchicine binding site of tubulin.