• International Journal of Computer Science & Network Security
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• v.23 no.4
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• pp.172-178
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• 2023

When the mobile device moves from the coverage of one access point to the radio coverage of another access point it needs to maintain its connection with the current access point before it successfully discovers the new access point, this process is known as handoff. During handoff the acceptable delay a voice over IP application can bear is of 50ms whereas the delay on medium access control layer is high enough that goes up to 350-500ms. This research provides a suitable methodology on medium access control layer of the IEEE 802.11 network. The medium access control layer comprises of three phases, namely discovery, reauthentication and re-association. The discovery phase on medium access control layer takes up to 90% of the total handoff latency. The objective is to effectively reduce the delay for discovery phase to ensure a seamless handoff. The research proposes a scheme that reduces the handoff latency effectively by scanning channels prior to the actual handoff process starts and scans only the neighboring access points. Further, the proposed scheme enables the mobile device to scan first the channel on which it is currently operating so that the mobile device has to perform minimum number of channel switches. The results show that the mobile device finds out the new potential access point prior to the handoff execution hence the delay during discovery of a new access point is minimized effectively.

• Journal of KIISE:Information Networking
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• v.33 no.1
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• pp.38-48
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• 2006

For extending of hot-spot of WLAN, (2) proposes internetworking scheme between wireless LAN (WLAN) and mobile ad-hoc network (MANET), which employ the same layer-2 protocol with different mode. Compared to internetworking schemes between UMTS (Universal Mobile Telecommunications Systems) and WLAN (3-4), the scheme from (2) has relatively low overhead and latencies because WLAN and MANET are physically and logically similar to each other. However, the mode switching algorithm proposed in r2] for internetworking between WLAN and MANET only considers signal strength and determines handoff, and mobile nodes following a zigzag course in pollution area may perform handoff at short intervals. Furthermore, (2) employs mobile IPv6 (MIPv6) at base, which brings still high delay on handoff and overhead due to signal message exchange. In this paper, we present optimized internetworking scheme between WLAN and MANET, modified from (2). To settle ping-pong handoff from (2), we propose adaptive mode switching algorithm. HMIPv6 is employed for IP connectivity and mobility service in WLAN, which solves some shortcomings, such as high handoff overhead and vulnerable security. For routing in MANET, OLSR is employed, which is a proactive Protocol and has optimally reduced signal broadcasting overhead. OLSR operates with current P protocol compatibly with no change or modification. The proposed internetworking scheme based on adaptive mode switching algorithm shows better performance than scheme from (2).

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.347-355
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• 1999

Background: Phospholipase C(PLC) plays a central role in cellular signal transduction and is important in cellular growth, differentiation and transformation. There are currently ten known mammalian isozymes of PLC reported to this date. Hydrolysis of phosphatidylinositol 4,5-bisphosphate($PIP_2$) by PLC produces two important second messengers, inositol 1,4,5-trisphosphate($IP_3$) and diacylglycerol. PLC-${\gamma}1$, previously, was known to be activated mainly through growth factor receptor tyrosine kinase. Other mechanisms of activating PLC-yl have been reported such as activation through tau protein in the presence of arachidonic acid in bovine brain and activation by $IP_3$, phosphatidic acid, etc. Very recently, another PLC-${\gamma}1$ activator protein such as tau has been found in bovine lung tissue, which now is considered to be AHNAK protein. But there has been no report concerning AHNAK and its associated disease to this date. In this study, we examined the expression of the PLC-${\gamma}1$ activator, AHNAK, in lung cancer specimens and their paired normal. Methods: From surgically resected human lung cancer tissues taken from twenty-eight patients and their paired normal counterparts, we evaluated expression level of AHNAK protein using immunoblot analysis of total tissue extract Immunohistochemical stain was performed with primary antibody against AHNAK protein. Results: Twenty-two among twenty-eight lung cancer tissues showed overexpression of AHNAK protein (eight of fourteen squamous cell lung cancers, all of fourteen adenocarcinomas). The resulting bands were multiple ranging from 70 to 200 kDa in molecular weight and each band was indistinct and formed a smear, reflecting mobility shift mainly due to proteolysis during extraction process. On immunohistochemistry, lung cancer tissues showed a very heavy, dense staining with anti-AHNAK protein antibody as compared to the surrounding normal lung tissue, coresponding well with the results of the western blot Conclusion: The overexpression of PLC-${\gamma}1$ activator protein, AHNAK in lung cancer may provide evidence that the AHNAK protein and PLC-${\gamma}1$ act in concerted manner in carcinogenesis.