Study the Effect of Co-Channel Interference in STC MIMO-OFDM System and Mitigation of CCI using Beamforming Technique

In this modern age of high speed wireless data communication, Multiple input multiple output orthogonal frequency division multiplexing (MIMO-OFDM) schemes have recently drawn wide interests due to their capability of high data rate transmission over multipath fading channels. This thesis work introduces the study of multi- user and multi-antenna MIMO-OFDM systems. In this work, the performances of two main classes of MIMO-OFM system i.e. multi-user and multi-antenna MIMO-ODM techniques have been studied. The transmitted data is sent using BPSK, QPSK modulation techniques. The performance of the system in Rayleigh and AWGN channel is studied. Space time coding technique also used in transmitting side of the multi-antenna MIMO system.Study and analysis of the effect of co-channel interference over wireless communication system is considered the main objective of this project work .Beamforming technique is one of the best techniques to mitigate co-channel interference. There are several beamforming techniques like LMS, RLS style beamforming techniques. LMS style adaptive beamforming technique is applied to the system. The performance of the LMS style beamforming technique for mitigation of co-channel interference has been analyzed for different modulation techniques.The performance comparison between the adaptive beamforming and null steering beamforming techniques is carried out for the space time coded MIMO-OFDM system. From the performance analysis, it is observed that to mitigate the co-channel interference in ST coded MIMO-OFDM system, adaptive beamforming technique outperforms the method based on the null steering beamforming

Notes on the discovery and ecology of the invasive armoured catfish Pterygoplichthys disjunctivus (Weber, 1991) and the exotic cichlid Amphilophus trimaculatus (Gunther, 1867) from Southern West Bengal, India

This paper documents the first occurrence of the exotic, highly invasive, South American armoured sucker mouth catfish Pterygoplichthys disjunctivus (Weber, 1991) from the brackish waters of the Sundarban Tiger Reserve, West Bengal, India and the Central American cichlid Amphilophus trimaculatus (Gunther, 1867) from Southern Bengal, India. Notes on the possible threats due to invasion, sources of introduction, extent of spread and management of these and other invasive species are discussed in the paper

Effect of Binding Energies on the Encounter Desorption

The abundance of interstellar ice constituents is usually expressed with respect to the water ice because, in denser regions, a significant portion of the interstellar grain surface would be covered by water ice. The binding energy (BE) or adsorption energy of the interstellar species regulates the chemical complexity of the interstellar grain mantle. Due to the high abundance of water ice, the BE of surface species with the water is usually provided and widely used in astrochemical modeling. However, the hydrogen molecules would cover some part of the grain mantle in the denser and colder part of the interstellar medium. Even at around similar to 10 K, few atoms and simple molecules with lower adsorption energies can migrate through the surface. The BE of the surface species with H-2 substrate would be very different from that of a water substrate. However, adequate information regarding these differences is lacking. Here, we employ the quantum chemical calculation to provide the BE of 95 interstellar species with H-2 substrate. These are representative of the BEs of species to a H-2 overlayer on a grain surface. On average, we notice that the BE with the H-2 monomer substrate is almost ten times lower than the BE of these species reported earlier with the H2O c-tetramer configuration. The encounter desorption of H and H-2 was introduced [with E-D (H, H-2) = 45 K and E-D (H-2, H-2) = 23 K] to have a realistic estimation of the abundances of the surface species in the colder and denser region. Our quantum chemical calculations yield higher adsorption energy of H-2 than that of H [E-D (H, H-2) = 23-25 K and E-D (H-2, H-2) = 67-79 K]. We further implement an astrochemical model to study the effect of encounter desorption with the present realistic estimation. The encounter desorption of the N atom [calculations yield E-D (N, H-2) = 83 K] is introduced to study the differences with its inclusion

Molecular association of glucose-6- phosphate isomerase and pyruvate kinase M2 with glyceraldehyde-3-phosphate dehydrogenase in cancer cells

Background: For a long time cancer cells are known for increased uptake of glucose and its metabolization through glycolysis. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a key regulatory enzyme of this pathway and can produce ATP through oxidative level of phosphorylation. Previously, we reported that GAPDH purified from a variety of malignant tissues, but not from normal tissues, was strongly inactivated by a normal metabolite, methylglyoxal (MG).Molecular mechanism behind MG mediated GAPDH inhibition in cancer cells is not well understood. Methods: GAPDH was purified from Ehrlich ascites carcinoma (EAC) cells based on its enzymatic activity. GAPDH associated proteins in EAC cells and 3-methylcholanthrene (3MC) induced mouse tumor tissue were detected by mass spectrometry analysis and immunoprecipitation (IP) experiment, respectively. Interacting domains of GAPDH and its associated proteins were assessed by in silico molecular docking analysis. Mechanism of MG mediated GAPDH inactivation in cancer cells was evaluated by measuring enzyme activity, Circular dichroism (CD) spectroscopy, IP and mass spectrometry analyses. Result: Here, we report that GAPDH is associated with glucose-6-phosphate isomerase (GPI) and pyruvate kinase M2 (PKM2) in Ehrlich ascites carcinoma (EAC) cells and also in 3-methylcholanthrene (3MC) induced mouse tumor tissue. Molecular docking analyses suggest C-terminal domain preference for the interaction between GAPDH and GPI. However, both C and N termini of PKM2 might be interacting with the C terminal domain of GAPDH. Expression of both PKM2 and GPI is increased in 3MC induced tumor compared with the normal tissue. In presence of 1 mM MG,association of GAPDH with PKM2 or GPI is not perturbed, but the enzymatic activity of GAPDH is reduced to 26.8 ± 5 % in 3MC induced tumor and 57.8 ± 2.3 % in EAC cells. Treatment of MG to purified GAPDH complex leads to glycation at R399 residue of PKM2 only, and changes the secondary structure of the protein complex. Conclusion: PKM2 may regulate the enzymatic activity of GAPDH. Increased enzymatic activity of GAPDH in tumor cells may be attributed to its association with PKM2 and GPI. Association of GAPDH with PKM2 and GPI could be a signature for cancer cells. Glycation at R399 of PKM2 and changes in the secondary structure of GAPDH complex could be one of the mechanisms by which GAPDH activity is inhibited in tumor cells by MG

Hepatoprotective Activity of Liposomal Flavonoid against Arsenite-Induced Liver Fibrosis

Arsenic, the environmental metalloid toxicant, is known to induce oxidative damage to liver and produce hepatic fibrosis. The theme of our study was to optimize and evaluate the therapeutic efficacy of galactosylated liposomal flavonoidal antioxidant, quercetin (QC), in combating arsenic-induced hepatic fibrogenesis. The rats of the hepatic damage group were injected s.c. a single dose of sodium arsenite (NaAsO2) (100.06 �M/kg b. wt. in 0.5 ml of physiological saline). Hepatocytes and stellate cells were separated. Mitochondrial membranes were isolated from all those separated cells. Oxidative damage was monitored at different isolated subcellular parts of different hepatic cells. Liver fibrosis was also induced by the injection of NaAsO2. Galactosylated liposomal QC injection before NaAsO2 treatment checked fibrogenesis completely by protecting the liver from oxidative attack in cellular and subcellular levels. The maximal protections from hepatocellular and fatty metamorphosis, necrosis, Kupffer cell hyperplasia, fibrosis, and in the deposition of collagen contents were observed and reconfirmed by our histopathological and histochemical analysis when rats were treated with galactosylated liposomal QC before NaAsO2 injection. Application of galactosylated liposomal QC may be a potent therapeutic approach for NaAsO2-induced fibrogenesis through a complete protection against oxidative attack in cellular and subcellular parts of rat liver