Wireless Multichannel Multipoint Broadcast Service for Mobile Stations

In wireless Multicast Broadcast Service (MBS), the common channel is used to multicast the MBS content to the Mobile Stations (MSs) on the MBS calls within the coverage area of a Base Station (BS), which causes interference to the dedicated channels serving the traditional calls, and degrades the system capacity. The MBS zone technology is proposed in Mobile Communications Network (MCN) standards to improve system capacity and reduce the handoff delay for the wireless MBS calls. In the MBS zone technology, a group of BSs form an MBS zone, where the macro diversity is applied in the MS, the BSs synchronize to transmit the MBS content on the same common channel, interference caused by the common channel is reduced, and the MBS MSs need not perform handoff while moving between the BSs in the same MBS zone. However, when there is no MBS MS in a BS with the MBS zone technology, the transmission on the common channel wastes the bandwidth of the BS. It is an important issue to determine the condition for the MBS Controller (MBSC) to enable the MBS zone technology by considering the Quality of Services (QoS) for traditional calls and MBS calls are used to reduce the dependency over the common channel and also it is going to reduce the delay over the network. By enabling Dynamic Channel Allocation (DCA) and Enhance Dynamic Channel Allocation (EDCA) we are going to overcome these problems

The C-Terminal Domain of the MutL Homolog from Neisseria gonorrhoeae Forms an Inverted Homodimer

The mismatch repair (MMR) pathway serves to maintain the integrity of the genome by removing mispaired bases from the newly synthesized strand. In E. coli, MutS, MutL and MutH coordinate to discriminate the daughter strand through a mechanism involving lack of methylation on the new strand. This facilitates the creation of a nick by MutH in the daughter strand to initiate mismatch repair. Many bacteria and eukaryotes, including humans, do not possess a homolog of MutH. Although the exact strategy for strand discrimination in these organisms is yet to be ascertained, the required nicking endonuclease activity is resident in the C-terminal domain of MutL. This activity is dependent on the integrity of a conserved metal binding motif. Unlike their eukaryotic counterparts, MutL in bacteria like Neisseria exist in the form of a homodimer. Even though this homodimer would possess two active sites, it still acts a nicking endonuclease. Here, we present the crystal structure of the C-terminal domain (CTD) of the MutL homolog of Neisseria gonorrhoeae (NgoL) determined to a resolution of 2.4 Å. The structure shows that the metal binding motif exists in a helical configuration and that four of the six conserved motifs in the MutL family, including the metal binding site, localize together to form a composite active site. NgoL-CTD exists in the form of an elongated inverted homodimer stabilized by a hydrophobic interface rich in leucines. The inverted arrangement places the two composite active sites in each subunit on opposite lateral sides of the homodimer. Such an arrangement raises the possibility that one of the active sites is occluded due to interaction of NgoL with other protein factors involved in MMR. The presentation of only one active site to substrate DNA will ensure that nicking of only one strand occurs to prevent inadvertent and deleterious double stranded cleavage

Immature Platelet Fraction: Its Clinical Utility in Thrombocytopenia Patients

Objectives Etiology of thrombocytopenia is multifactorial and its pathogenesis should be distinguished for appropriate management. Newly formed immature platelets are called reticulated platelets (RPs) and can be estimated in peripheral blood using automated hematology analyzers, which express them as immature platelet fraction (IPF). In the present study we intend to assess and establish the clinical utility of IPF in differentiating the two major causes of thrombocytopenia—decreased production and increased destruction of platelets—along with determining its significance in monitoring patients with thrombocytopenia. Materials and Methods Sixty-one cases of thrombocytopenia and 101 healthy controls with normal platelet count were included in the study. IPF and all the other usual blood cell parameters were measured using a fully automated hematology analyzer. Based on the pathogenesis of thrombocytopenia, the cases were divided into groups and the difference in IPF value between the groups was evaluated. Results The reference range of IPF among healthy controls was estimated to be 0.7 to 5.7%. The mean IPF was significantly higher in patients with increased peripheral destruction of platelets (13.4%) as compared to patients with decreased production of platelets (4.6%). The optimal cutoff value of IPF for differentiating patients with increased peripheral destruction of platelets from patients with decreased production of platelets was 5.95% with a sensitivity of 88% and specificity of 75.9%. Conclusion Measurement of IPF is useful for detecting evidence of increased platelet production and helps in the initial evaluation of thrombocytopenia patients. It is a novel diagnostic method which can be used to differentiate patients with thrombocytopenia due to increased destruction of platelets from patients with thrombocytopenia due to bone marrow failure/suppression