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The digital correlator is one of the most crucial data processing components of a radio telescope array. With the scale of radio interferometeric array growing, many efforts have been devoted to developing a cost-effective and scalable correlator in the field of radio astronomy. In this paper, a 192-input digital correlator with six CASPER ROACH2 boards and seven GPU servers has been deployed as the digital signal processing system for Tianlai cylinder pathfinder located in Hongliuxia observatory. The correlator consists of 192 input signals (96 dual-polarization), 125-MHz bandwidth, and full-Stokes output. The correlator inherits the advantages of the CASPER system, for example, low cost, high performance, modular scalability, and a heterogeneous computing architecture. With a rapidly deployable ROACH2 digital sampling system, a commercially expandable 10 Gigabit switching network system, and a flexible upgradable GPU computing system, the correlator forms a low-cost and easilyupgradable system, poised to support scalable large-scale interferometeric array in the future. [ABSTRACT FROM AUTHOR]

The fragile X premutation (PM) allele contains a CGG expansion of 55-200 repeats in the FMR1 gene's promoter. Male PM carriers have an elevated risk of developing neurological and psychiatric changes, including an approximately 50% risk of the fragile X-associated tremor/ataxia syndrome (FXTAS). The aim of this study was to assess the relationships of regional white matter hyperintensities (wmhs) semi-quantitative scores, clinical status, motor (UPDRS, ICARS, Tremor) scales, and cognitive impairments, with FMR1-specific genetic changes, in a sample of 32 unselected male PM carriers aged 39-81 years. Half of these individuals were affected with FXTAS, while the non-FXTAS group comprised subcategories of non-affected individuals and individuals affected with non-syndromic changes. The dynamics of pathological processes at the cellular level relevant to the clinical status of PM carriers was investigated using the enzyme AMP-activated protein kinase (AMPK), which is a highly sensitive cellular stress-sensing alarm protein. This enzyme, as well as genetic markers - CGG repeat number and the levels of the FMR1 mRNA - were assessed in blood lymphoblasts. The results showed that the repeat distribution for FXTAS individuals peaked at 85-90 CGGs; non-FXTAS carriers were distributed within the lowest end of the PM repeat range, and non-syndromic carriers assumed an intermediate position. The size of the CGG expansion was significantly correlated, across all three categories, with infratentorial and total wmhs and with all motor scores, and the FMR1 mRNA levels with all the wmh scores, whilst AMPK activity showed considerable elevation in the non-FXTAS combined group, decreasing in the FXTAS group, proportionally to increasing severity of the wmhs and tremor/ataxia. We conclude that the size of the CGG expansion relates to the risk for FXTAS, to severity of infratentorial wmhs lesions, and to all three motor scale scores. FMR1 mRNA shows a strong association with the extent of wmhs, which is the most sensitive marker of the pathological process. However, the AMPK activity findings - suggestive of a role of this enzyme in the risk of FXTAS - need to be verified and expanded in future studies using larger samples and longitudinal assessment.

Security schemes of pair wise key establishment ensure communication security in wireless sensor networks. Dynamic key-path in pair wise key establishment farther increases communication security in the networks. Establishing scheme and algorithm for dynamic key-path in pair wise key for wireless sensor networks were presented based on the encoding peculiarity and high fault-tolerant ability of named H（k,u,m,v,n） （hierarchical hypercube） of cluster distributed sensor networks. Theoretic studies and figures of computer simulation show that the algorithm has good reliability per- formance and high efficiency, which is suitable for cluster distributed sensor networks.

The obesity epidemic has led to an increased incidence of nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes. AMP-activated protein kinase (Ampk) regulates energy homeostasis and is activated by [...]

Individuals who are obese are frequently insulin resistant, putting them at increased risk of developing type 2 diabetes and its associated adverse health conditions. The accumulation in adipose tissue of macrophages in an inflammatory state is a hallmark of obesity-induced insulin resistance. Here, we reveal a role for AMPK β1 in protecting macrophages from inflammation under high lipid exposure. Genetic deletion of the AMPK β1 subunit in mice (referred to herein as β[1.sup.-/-] mice) reduced macrophage AMPK activity, acetyl-CoA carboxylase phosphorylation, and mitochondrial content, resulting in reduced rates of fatty acid oxidation. β[1.sup.-/-] macrophages displayed increased levels of diacylglycerol and markers of inflammation, effects that were reproduced in WT macrophages by inhibiting fatty acid oxidation and, conversely, prevented by pharmacological activation of AMPK β1-containing complexes. The effect of AMPK β1 loss in macrophages was tested in vivo by transplantation of bone marrow from WT or β[1.sup.-/-] mice into WT recipients. When challenged with a high-fat diet, mice that received β[1.sup.-/-] bone marrow displayed enhanced adipose tissue macrophage inflammation and liver insulin resistance compared with animals that received WT bone marrow. Thus, activation of AMPK β1 and increasing fatty acid oxidation in macrophages may represent a new therapeutic approach for the treatment of insulin resistance., Introduction Obesity is associated with increased production of inflammatory cytokines, which are important contributing factors to the development of insulin resistance (1) and defects in fatty acid metabolism (2). In [...]

The AMP-activated protein kinase (AMPK) is an [alpha][beta][gamma] heterotrimer that acts as a master metabolic regulator to maintain cellular energy balance following increased energy demand and increases in the AMP/ATP ratio. This regulation provides dynamic control of energy metabolism, matching energy supply with demand that is essential for the function and survival of organisms. AMPK is inactive unless phosphorylated on Thr172 in the [alpha]-catalytic subunit activation loop by upstream kinases (LKB1 or calcium-calmodulin-dependent protein kinase kinase [beta]). How a rise in AMP levels triggers AMPK [alpha]-Thr172 phosphorylation and activation is incompletely understood. Here we demonstrate unequivocally that AMP directly stimulates [alpha]-Thr172 phosphorylation provided the AMPK [beta]-subunit is myristoylated. Loss of the myristoyl group abolishes AMP activation and reduces the extent of [alpha]-Thr172 phosphorylation. Once AMPK is phosphorylated, AMP further activates allosterically but this activation does not require [beta]-subunit myristoylation. AMP and glucose deprivation also promote membrane association of myristoylated AMPK, indicative of a myristoyl-switch mechanism. Our results show that AMP regulates AMPK activation at the initial phosphorylation step, and that [beta]-subunit myristoylation is important for transducing the metabolic stress signal. myristome | signal transduction | adenylate charge | [gamma]-subunit doi/ 10.1073/pnas.1009705107