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This paper presents a new equalizer structure named Delay-Matched Decision-Feedback Equalizer (DMDFE) which is an effective solution to the hardware implementation of time domain adaptive Decision-Feedback Equalizer (DFE) in single carrier modulated DTV system. The transposed structure combined with the conventional transversal filter is employed in DMDFE to reduce the ghost estimation delay of feedback filter in DFE. And the DMDFE provides a one-symbol period feedback ghost estimation which enables the new structure to have the same performance with ideal Least Mean Square (LMS) DFE. The DMDFE can cope with faster fading channel and longer post-echo than transposed DFE. Meanwhile the DMDFE saves more hardware resources than the transposed DFE. Index Terms--Delay-Matched DFE, DTTB, FBF, FFF, LMS, summation delay.

Background and Purpose: Ageing is an important risk factor of non-alcoholic fatty liver disease (NAFLD). Here, we investigated whether the deficiency of nicotinamide adenine dinucleotide (NAD(+) ), a ubiquitous coenzyme, links ageing with NAFLD.Experimental Approach: Hepatic concentrations of NAD(+) , protein levels of nicotinamide phosphoribosyltransferase (NAMPT) and several other critical enzymes regulating NAD(+) biosynthesis, were compared in middle-aged and aged mice or patients. The influences of NAD(+) decline on the steatosis and steatohepatitis were evaluated in wild-type and H247A dominant-negative, enzymically-inactive NAMPT transgenic mice (DN-NAMPT) given normal or high-fat diet (HFD).Key Results: Hepatic NAD(+) level decreased in aged mice and humans. NAMPT-controlled NAD(+) salvage, but not de novo biosynthesis pathway, was compromised in liver of elderly mice and humans. Given normal chow, middle-age DN-NAMPT mice displayed systemic NAD(+) reduction and had moderate NAFLD phenotypes, including lipid accumulation, enhanced oxidative stress, triggered inflammation and impaired insulin sensitivity in liver. All these NAFLD phenotypes, especially release of pro-inflammatory factors, Kupffer cell accumulation, monocytes infiltration, NLRP3 inflammasome pathway and hepatic fibrosis (Masson's staining and α-SMA staining), deteriorated further under HFD challenge. Oral administration of nicotinamide riboside, a natural NAD(+) precursor, completely corrected these NAFLD phenotypes induced by NAD(+) deficiency alone or HFD, whereas adenovirus-mediated SIRT1 overexpression only partially rescued these phenotypes.Conclusions and Implications: These results provide the first evidence that ageing-associated NAD(+) deficiency is a critical risk factor for NAFLD, and suggest that supplementation with NAD(+) substrates may be a promising therapeutic strategy to prevent and treat NAFLD. [ABSTRACT FROM AUTHOR]

Adipokines play important roles in metabolic homeostasis and disease. We have recently identified a novel adipokine Metrnl, also known as Subfatin, for its high expression in subcutaneous fat. Here, we demonstrate a prodifferentiation action of Metrnl in white adipocytes. Adipocyte-specific knockout of Metrnl exacerbates insulin resistance induced by high-fat diet (HFD), whereas adipocyte-specific transgenic overexpression of Metrnl prevents insulin resistance induced by HFD or leptin deletion. Body weight and adipose content are not changed by adipocyte Metrnl. Consistently, no correlation is found between serum Metrnl level and BMI in humans. Metrnl promotes white adipocyte differentiation, expandability, and lipid metabolism and inhibits adipose inflammation to form functional fat, which contributes to its activity against insulin resistance. The insulin sensitization of Metrnl is blocked by PPARγ inhibitors or knockdown. However, Metrnl does not drive white adipose browning. Acute intravenous injection of recombinant Metrnl has no hypoglycemic effect, and 1-week intravenous administration of Metrnl is unable to rescue insulin resistance exacerbated by adipocyte Metrnl deficiency. Our results suggest adipocyte Metrnl controls insulin sensitivity at least via its local autocrine/paracrine action through the PPARγ pathway. Adipocyte Metrnl is an inherent insulin sensitizer and may become a therapeutic target for insulin resistance. [ABSTRACT FROM AUTHOR]

SUMMARY Aims: The purpose of this study is to investigate whether the NG2+ cells, a class of oligodendrocyte progenitor cells, is involved in the pathophysiology of stroke in stroke-prone spontaneously hypertensive rat (SHR-SP). Methods: SHR-SP, SHR, Wistar-Kyoto rats (WKY), and C57BJ/6 mice were used. Immunohistochemistry was conducted to evaluate the number of NG2+ cells in frozen brain sections. Demyelination was evaluated by Sudan black staining and serum level of myelin basic protein. Middle cerebral artery occlusion (MCAO) was performed to prepare experimental stroke model. Results: The number of NG2+ cells was significantly decreased in infarct core and increased in penumbra in WKY rats after MCAO. In brain sections of 6-month-old SHR-SP, the number of NG2+ cells was significantly ( P < 0.01) less than that in age-matched SHR and WKY rats. However, this phenomenon was not observed in 3-month-old rats. Demyelination was found in 6-month-old SHR-SP but not in 3-month-old SHR-SP. Pharmacological treatment of cuprizone in mice induced demyelination and enlargement of cerebral infarction after MCAO. Conclusion: The decline of NG2+ cells may cause demyelination and contribute to the susceptibility of SHR-SP to ischemic brain injury. [ABSTRACT FROM AUTHOR]

This paper presents the architectures, algorithms, and implementation considerations of the digital phase locked loop (DPLL) used for burst-mode packet DS-CDMA receivers. As we know, carrier offset is a rather challenging problem in CDMA system. According to different applications, different DPLL forms should be adopted to correct different maximum carrier offset in CDMA systems. One classical DPLL and two novel DPLL forms are discussed in the paper. The acquisition range of carrier offset can be widened by using the two novel DPLL forms without any performance degradation such as longer acquisition time or larger variance of the phase error. The maximum acquisition range is 1/(4T), where T is the symbol period. The design can be implemented by FPGA directly.