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Summary: The channel plays a significant role as the multipath in Multiple Input Multiple Output‐Orthogonal Frequency Division Multiplexing (MIMO‐OFDM) systems. The precoding‐based channel estimation algorithms estimate the channel capacity at the receiver node and they provide efficient channel estimates under worst case channel scenarios. To estimate the channel capacity in the mobile node, semi‐blind scenario is a crucial task in Multi User (MU) MIMO systems. Therefore, a semi blind sparse channel estimation algorithm is demonstrated in the MU‐MIMO system to provide better performance. In the transmitter side, the signal modulation is performed with the help of Quadrature Phase Shift Keying (QPSK), and the modulated signal is given to Pulse Shaping Algorithm (PSA) to reduce the inter‐carrier interference as well as inter symbol interference. At each transmitter, the Inverse Fast Fourier Transforms (IFFT) technique is used for mapping the symbols and then the mapped signal is send to the receiver. In the receiver side, the FFT, pulse reshaping, and QPSK demodulation blocks are serially connected and perform inverse operations of the transmitter in the receiver. Then, the sparse channel is estimated at the receiver by using the semi blind sparse algorithm, where the parameters are optimized by using the Hybridized Drosophila with Virus Colony Search Optimization (HD‐VCSO). The objective function of the developed sparse channel estimation is the reduction of Minimum Mean Square Error (MMSE) in the channel. The performance of the developed sparse channel estimation algorithm is analyzed through different conventional algorithms to validate the effectiveness of the proposed algorithm. [ABSTRACT FROM AUTHOR]

Background: Abnormal fetal movements are implicated in joint pathologies such as arthrogryposis and developmental dysplasia of the hip (DDH). Experimentally induced paralysis disrupts joint cavitation and morphogenesis leading to postnatal abnormalities. However, the developmental window(s) most sensitive to immobility—and therefore the best time for intervention—have never been identified. Here, we systematically vary the timing and duration of paralysis during early chick hip joint development. We then test whether external manipulation of immobilized limbs can mitigate the effects of immobility. Results: Timing of paralysis affected the level of disruption to joints, with paralysis periods between embryonic days 4 and 7 most detrimental. Longer paralysis periods produced greater disruption in terms of failed cavitation and abnormal femoral and acetabular geometry. External manipulation of an immobilized limb led to more normal morphogenesis and cavitation compared to un‐manipulated limbs. Conclusions: Temporary paralysis is detrimental to joint development, particularly during days 4 to 7. Developmental processes in the very early stages of joint development may be critical to DDH, arthrogryposis, and other joint pathologies. The developing limb has the potential to recover from periods of immobility, and external manipulation provides an innovative avenue for prevention and treatment of developmental joint pathologies. Key Findings: In the hip joints of immobilised chick embryos, timing of paralysis affected the level of disruption to joints, with paralysis periods between embryonic days four and seven most detrimental.Longer paralysis periods produced greater disruption in terms of failed cavitation and abnormal femoral and acetabular geometry.External manipulation of an immobilised limb led to more normal morphogenes is and cavitation compared to unmanipulated limbs. [ABSTRACT FROM AUTHOR]

This study prospectively quantified wastage of cancer chemotherapeutic drugs in an oncology unit to find the associated cost in 3 months. Retrospective analysis of drug usage for 12 months was also conducted to determine the expected drug loss in 1 year. The effect of vial sharing was evaluated under the assumption of sharing. A significant drug wastage of 19.72% (95% confidence interval [CI], 14.52–24.93%) in 3 months and 17.14% (95% CI 14.69–19.59%) in 1 year occurred in our oncology unit. Number of vials purchased (r = 0.362, p < 0.01), weight (r = −0.146, P < .01) and body surface area (r = −0.26, P < .01) correlated with the drug wasted. Vial sharing assumption showed a 9% (95% CI, 2.5–15.5%) reduction in cost in 1 year. [ABSTRACT FROM AUTHOR]

Background and Purpose Opioid receptor function is modulated by post-activation events such as receptor endocytosis, recycling and/or degradation. While it is generally understood that the peptide ligand gets co-endocytosed with the receptor, relatively few studies have investigated the role of the endocytosed peptide and peptide processing enzymes in regulating receptor function. In this study, we focused on endothelin-converting enzyme 2 ( ECE2), a member of the neprilysin family of metallopeptidases that exhibits an acidic pH optimum, localizes to an intracellular compartment and selectively processes neuropeptides including opioid peptides in vitro, and examined its role in modulating μ receptor recycling and resensitization. Experimental Approach The effect of ECE2 inhibition on hydrolysis of the endocytosed peptide was examined using thin-layer chromatography and on μ opioid receptor trafficking using either elisa or microscopy. The effect of ECE2 inhibition on receptor signalling was measured using a c AMP assay and, in vivo, on antinociception induced by intrathecally administered opioids by the tail-flick assay. Key Results The highly selective ECE2 inhibitor, S136492, significantly impaired μ receptor recycling and signalling by only those ligands that are ECE2 substrates and this was seen both in heterologous cells and in cells endogenously co-expressing μ receptors with ECE2. We also found that ECE2 inhibition attenuated antinociception mediated only by opioid peptides that are ECE2 substrates. Conclusions and Implications These results suggest that ECE2, by selectively processing endogenous opioid peptides in the endocytic compartment, plays a role in modulating opioid receptor activity. Linked Articles This article is part of a themed section on Opioids: New Pathways to Functional Selectivity. To view the other articles in this section visit [ABSTRACT FROM AUTHOR]

The tensile and impact performance of intimately mixed (IM) hybrid composites based on glass fiber (GF) and pineapple leaf fiber (PALF) was investigated. The composite was fabricated at constant volume fraction of fiber 0.3 Vf (fiber 0.3 and matrix 0.7). Keeping the volume fraction of matrix a constant (0.7 Vf), we have varied the PALF/GF ratio from 0 to 1. Incorporation of 0.1 volume fraction of GF increases the tensile strength of the hybrid composite by about 28%. The tensile strength showed a further increase when the volume fraction is changed to 0.7 and 0.9 Vf of GF. Intimately mixed hybrid composites exhibited higher impact strength than the individual fiber composites; the composite of PALF/GF ratio 70:30 showed maximum impact strength of 1203 J/m. A positive hybrid effect is observed for impact properties. Scanning electron micrographs of the fractured surfaces were examined to understand the fiber-matrix adhesion. POLYM. COMPOS., 2012. © 2012 Society of Plastics Engineers [ABSTRACT FROM AUTHOR]

Endothelin-converting enzyme (ECE)-2 is a metalloprotease that possesses many properties consistent with it being a neuropeptide-processing enzyme. This protease is found primarily in neural tissues, with high levels of expression in midbrain, cerebellum, hypothalamus, frontal cortex and spinal cord and moderate levels in hippocampus and striatum. To evaluate its role in neural function, mice have been generated lacking this enzyme. Physical appearance, autonomic reflexes, motor co-ordination, balance, locomotor activity and spontaneous emotional responses appear normal in these knockout (KO) mice. However, these mutants display deficits in learning and memory as evidenced by marked impairment in the Morris water maze. Knockout mice are also deficient in object recognition memory where they show delays in discerning changes in object location and in recognizing the introduction of a novel object. In this study, perseveration appears to interfere with learning and memory. Finally, mutants are impaired in social transmission of food preference where they show poor short-term memory and perturbations in long-term memory; the latter can be ameliorated by reminder cues. As ECE-2 has been implicated in Alzheimer’s disease, the deficits in learning and memory in the KO mice may provide unique insights into processes that may contribute to this disease and possible other disorders of cognition. [ABSTRACT FROM AUTHOR]

Abstract: Prodynorphin, a multifunctional precursor of several important opioid peptides, is expressed widely in the CNS. It is processed at specific single and paired basic sites to generate various biologically active products. Among the prohormone convertases (PCs), PC1 and PC2 are expressed widely in neuroendocrine tissues and have been proposed to be the major convertases involved in the biosynthesis of hormonal and neural peptides. In this study we have examined the physiological involvement of PC2 in the generation of dynorphin (Dyn) peptides in mice lacking active PC2 as a result of gene disruption. Enzymological and immunological assays were used to confirm the absence of active PC2 in these mice. The processing profiles of Dyn peptides extracted from brains of these mice reveal a complete lack of Dyn A-8 and a substantial reduction in the levels of Dyn A-17 and Dyn B-13. Thus, PC2 appears to be involved in monobasic processing, leading to the generation of Dyn A-8, Dyn A-17, and Dyn B-13 from prodynorphin under physiological conditions. Brains of heterozygous mice exhibit only half the PC2 activity of wild-type mice; however, the levels of Dyn peptides in these mice are similar to those of wild-type mice, suggesting that a 50% reduction in PC2 activity is not sufficient to significantly reduce prodynorphin processing. The disruption of the PC2 gene does not lead to compensatory up-regulation in the levels of other convertases with similar substrate specificity because we find no significant changes in the levels of PC1, PC5/PC6, or furin in these mice as compared with wild-type mice. Taken together, these results support a critical role for PC2 in the generation of Dyn peptides. [ABSTRACT FROM AUTHOR]

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Although transgenic mouse models of Alzheimer's disease (AD) recapitulate amyloid-beta (Abeta)-related pathologies and cognitive impairments, previous studies have mainly evaluated their hippocampus-dependent memory dysfunctions using behavioral tasks such as the water maze and fear conditioning. However, multiple memory systems become impaired in AD as the disease progresses and it is important to test whether other forms of memory are affected in AD models. This study was designed to use conditioned taste aversion (CTA) and contextual fear conditioning paradigms to compare the phenotypes of hippocampus-independent and -dependent memory functions, respectively, in 5XFAD amyloid precursor protein/presenilin-1 transgenic mice that harbor five familial AD mutations. Although both types of memory were significantly impaired in 5XFAD mice, the onset of CTA memory deficits ( approximately 9 months of age) was delayed compared with that of contextual memory deficits ( approximately 6 months of age). Furthermore, 5XFAD mice that were genetically engineered to have reduced levels of beta-site amyloid precursor protein-cleaving enzyme 1 (BACE1) (BACE1(+/-).5XFAD) exhibited improved CTA memory, which was equivalent to the performance of wild-type controls. Importantly, elevated levels of cerebral beta-secretase-cleaved C-terminal fragment (C99) and Abeta peptides in 5XFAD mice were significantly reduced in BACE1(+/-).5XFAD mice. Furthermore, Abeta deposition in the insular cortex and basolateral amygdala, two brain regions that are critically involved in CTA performance, was also reduced in BACE1(+/-).5XFAD compared with 5XFAD mice. Our findings indicate that the CTA paradigm is useful for evaluating a hippocampus-independent form of memory defect in AD model mice, which is sensitive to rescue by partial reductions of the beta-secretase BACE1 and consequently of cerebral Abeta.