351 research outputs found

    New Preamble Design for Reduced-Complexity Timing Acquisition in UWB Systems

    Get PDF
    Abstract-Low-complexity rapid timing acquisition is one of the most pivotal challenges in ultra-wideband (UWB) wireless technology whose short duration pulse results in high resolution in time. In this paper, we propose a new preamble which can reduce the performance degradation caused by diminishing the operational complexity of the coarse timing acquisition. In the reduced-complexity acquisition algorithm, the received preamble is shortened by summing its elements group-by-group and correlated with the known PN sequence having reduced length to find the maximum output value of the correlators. This acquisition algorithm introduces performance deterioration since it loses the impulsive autocorrelation property of the PN sequence after summation. Therefore, we judiciously design a new preamble sequence whose slide correlator output function shows a distinct peak at zero delay and the symmetry even after summation. Simulation results demonstrate that the reducedcomplexity acquisition algorithm exploiting the proposed preamble outperforms the algorithm using the PN sequence as the preamble, while the amount of computational reduction remains the same

    Pyruvate Dehydrogenase Kinase-mediated Glycolytic Metabolic Shift in the Dorsal Root Ganglion Drives Painful Diabetic Neuropathy

    Get PDF
    The dorsal root ganglion (DRG) is a highly vulnerable site in diabetic neuropathy. Under diabetic conditions, the DRG is subjected to tissue ischemia or lower ambient oxygen tension that leads to aberrant metabolic functions. Metabolic dysfunctions have been documented to play a crucial role in the pathogenesis of diverse pain hypersensitivities. However, the contribution of diabetes-induced metabolic dysfunctions in the DRG to the pathogenesis of painful diabetic neuropathy remains ill-explored. In this study, we report that pyruvate dehydrogenase kinases (PDK2 and PDK4), key regulatory enzymes in glucose metabolism, mediate glycolytic metabolic shift in the DRG leading to painful diabetic neuropathy. Streptozotocin-induced diabetes substantially enhanced the expression and activity of the PDKs in the DRG, and the genetic ablation of Pdk2 and Pdk4 attenuated the hyperglycemia-induced pain hypersensitivity. Mechanistically, Pdk2/4 deficiency inhibited the diabetes-induced lactate surge, expression of pain-related ion channels, activation of satellite glial cells, and infiltration of macrophages in the DRG, in addition to reducing central sensitization and neuroinflammation hallmarks in the spinal cord, which probably accounts for the attenuated pain hypersensitivity. Pdk2/4-deficient mice were partly resistant to the diabetes-induced loss of peripheral nerve structure and function. Furthermore, in the experiments using DRG neuron cultures, lactic acid treatment enhanced the expression of the ion channels and compromised cell viability. Finally, the pharmacological inhibition of DRG PDKs or lactic acid production substantially attenuated diabetes-induced pain hypersensitivity. Taken together, PDK2/4 induction and the subsequent lactate surge induce the metabolic shift in the diabetic DRG, thereby contributing to the pathogenesis of painful diabetic neuropathy

    Incidentally Detected Situs Ambiguous in Adults

    Get PDF
    Situs ambiguous is rare congenital anomaly in adults. In 2 adult patients who admitted for different cardiac problems, situs ambiguous with polysplenia was detected. A 42-year-old male admitted for radio frequent catheter ablation of atrial fibrillation, and he had left-sided inferior vena cava (IVC), hepatic segment of IVC interruption with hemiazygos continuation, multiple spleens and intestinal malrotation. And in a 52-year-old female case who was hospitalized due to infective endocarditis after implanting pacemaker for sick sinus syndrome, multiple spleens, left-sided stomach, bilateral liver with midline gallbladder, and left-sided IVC were found. Those findings were consistent with situs ambiguous with polysplenia, but their features were distinctive

    Lung function, coronary artery calcification, and metabolic syndrome in 4905 Korean males

    Get PDF
    SummaryBackgroundImpaired lung function is an independent predictor of cardiovascular mortality. We assessed the relationships of lung function with insulin resistance (IR), metabolic syndrome (MetS), systemic inflammation and coronary artery calcification score (CACS) measured by computed tomography (CT) scan an indicator of coronary atherosclerosis.MethodsWe identified 4905 adult male patients of the Health Promotion Center in Samsung Medical Center between March 2005 and February 2008 and retrospectively reviewed the following data for these patients: pulmonary function, CT-measured CACS, anthropometric measurement, fasting glucose, insulin, lipid profiles, serum C-reactive protein (CRP) and homeostatic model assessment (HOMA-IR). MetS was defined according to the AHA/NHLBI criteria.ResultsWhen the subjects were divided into four groups according to quartiles of FVC or FEV1 (% pred), serum CRP level, HOMA-IR, prevalence of MetS and CACS significantly increased as the FVC or FEV1 (% pred) decreased. The odds ratios (ORs) for MetS in the lowest quartiles of FVC and FEV1 (% pred) were 1.85 (95% CI, 1.49–2.30; p<0.001) and 1.47 (95% CI, 1.20–1.81; p<0.001) respectively. The ORs for the presence of coronary artery calcification in the lowest quartiles of FVC and FEV1 (% pred) were 1.31 (95% CI, 1.09–1.58; p=0.004) and 1.22 (95% CI, 1.02–1.46; p=0.029) respectively. Obesity, CRP, HOMA-IR, and the presence of coronary artery calcium were independent risk predictors for impaired lung function.ConclusionMetabolic syndrome, insulin resistance, coronary atherosclerosis, and systemic inflammation are closely related to the impaired lung function

    A comprehensive manually curated protein–protein interaction database for the Death Domain superfamily

    Get PDF
    The Death Domain (DD) superfamily, which is one of the largest classes of protein interaction modules, plays a pivotal role in apoptosis, inflammation, necrosis and immune cell signaling pathways. Because aberrant or inappropriate DD superfamily-mediated signaling events are associated with various human diseases, such as cancers, neurodegenerative diseases and immunological disorders, the studies in these fields are of great biological and clinical importance. To facilitate the understanding of the molecular mechanisms by which the DD superfamily is associated with biological and disease processes, we have developed the DD database (http://www.deathdomain.org), a manually curated database that aims to offer comprehensive information on protein–protein interactions (PPIs) of the DD superfamily. The DD database was created by manually curating 295 peer-reviewed studies that were published in the literature; the current version documents 175 PPI pairs among the 99 DD superfamily proteins. The DD database provides a detailed summary of the DD superfamily proteins and their PPI data. Users can find in-depth information that is specified in the literature on relevant analytical methods, experimental resources and domain structures. Our database provides a definitive and valuable tool that assists researchers in understanding the signaling network that is mediated by the DD superfamily

    The L441P Mutation of Cystic Fibrosis Transmembrane conductance Regulator and its Molecular Pathogenic Mechanisms in a Korean Patient with Cystic Fibrosis

    Get PDF
    Cystic fibrosis (CF) is an autosomal recessive disorder usually found in populations of white Caucasian descent. CF is caused by mutations in the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) gene. A 5-yr-old Korean girl was admitted complaining of coughing and greenish sputum. Chest radiographs and computed tomographic (CT) scan revealed diffuse bronchiectasis in both lungs. The patient had chronic diarrhea and poor weight gain, and the abdominal pancreaticobiliary CT scan revealed atrophy of the pancreas. Finally, CF was confirmed by the repeated analysis of the quantitative pilocarpine iontophoresis test. The chloride concentration of sweat samples taken from both forearms of the pateint was an average of 88.7 mM/L (normal value <40 mM/L). After a comprehensive search for mutations in the CFTR gene, the patient was found to carry the non-synonymous L441P mutation in one allele. Molecular physiologic analysis of the L441P mutation of CFTR revealed that the L441P mutation completely abolished the CFTR Cl- channel activity by disrupting proper protein folding and membrane trafficking of CFTR protein. These results confirmed the pathogenicity of the L441P mutation of CFTR circulating in the Korean population. The possibility of CF should be suspected in patients with chronic bronchiectasis, although the frequency of CF is relatively rare in East Asia
    corecore