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A result in a recent paper reported by Zhang et al. (Int J Adv Manuf Technol 57:1175–1181) is incorrect because job processing times are variable due to both deteriorating jobs and learning effects, which is not taken into account by the authors. In this note, we show by a counter-example that the published result is incorrect and provide the corrected result.

Measurement results of some properties of the Miyun 50m radio telescope (MRT50) of the National Astronomical Observatories, such as pointing calibration, antenna beams, system noise temperature, gain and gain variations with elevation are introduced. By using a new de-convolution technique developed by our group, the broadening effect on measured beams caused by the width of an extended radio source has been removed so that we obtained higher accuracy on the measurements of MRT50 beams.

Splicing the shredded paper means the technology that, according the paper, which has been shredded to design a particular algorithm to splice and recover the original paper. This paper introduced the algorithm of splicing the shredded paper based on the matching to texture feature. By means of this algorithm, we modeled for the problem of splicing the shredded paper and solved it. And, we used the algorithm to splice both pieces of English shredded paper and Chinese shredded paper. The recovered paper had proved the accuracy of the algorithm.

Background: Alcadein proteins (Alcs; Alc alpha, Alc beta and Alc gamma) are predominantly expressed in neurons, as is Alzheimer's beta-amyloid (A beta) precursor protein (APP). Both Alcs and APP are cleaved by primary alpha-or beta-secretase to generate membrane-associated C-terminal fragments (CTFs). Alc CTFs are further cleaved by gamma-secretase to secrete p3-Alc peptide along with the release of intracellular domain fragment (Alc ICD) from the membrane. In the case of APP, APP CTF beta is initially cleaved at the epsilon-site to release the intracellular domain fragment (AICD) and consequently the gamma-site is determined, by which A beta generates. The initial epsilon-site is thought to define the final gamma-site position, which determines whether A beta 40/43 or A beta 42 is generated. However, initial intracellular e-cleavage sites of Alc CTF to generate Alc ICD and the molecular mechanism that final gamma-site position is determined remains unclear in Alcs. Methodology: Using HEK293 cells expressing Alcs plus presenilin 1 (PS1, a catalytic unit of gamma-secretase) and the membrane fractions of these cells, the generation of p3-Alc possessing C-terminal gamma-cleavage site and Alc ICD possessing N-terminal epsilon-cleavage site were analysed with MALDI-TOF/MS. We determined the initial epsilon-site position of all Alc alpha, Alc beta and Alc gamma, and analyzed the relationship between the initially determined epsilon-site position and the final gamma-cleavage position. Conclusions: The initial epsilon-site position does not always determine the final gamma-cleavage position in Alcs, which differed from APP. No additional gamma-cleavage sites are generated from artificial/non-physiological positions of epsilon-cleavage for Alcs, while the artificial epsilon-cleavage positions can influence in selection of physiological gamma-site positions. Because alteration of gamma-secretase activity is thought to be a pathogenesis of sporadic Alzheimer's disease, Alcs are useful and sensitive substrate to detect the altered cleavage of substrates by gamma-secretase, which may be induced by malfunction of gamma-secretase itself or changes of membrane environment for enzymatic reaction.

Background Alcadeinα (Alcα) is a neuronal membrane protein that colocalizes with the Alzheimer's amyloid-β precursor protein (APP). Successive cleavage of APP by β- and γ-secretases generates the aggregatable amyloid-β peptide (Aβ), while cleavage of APP or Alcα by α- and γ-secretases generates non-aggregatable p3 or p3-Alcα peptides. Aβ and p3-Alcα can be recovered from human cerebrospinal fluid (CSF). We have previously reported alternative processing of APP and Alcα in the CSF of some patients with sporadic mild cognitive impairment (MCI) and AD (SAD). Results Using the sandwich enzyme-linked immunosorbent assay (ELISA) system that detects total p3-Alcα, we determined levels of total p3-Alcα in CSF from subjects in one of four diagnostic categories (elderly controls, MCI, SAD, or other neurological disease) derived from three independent cohorts. Levels of Aβ40 correlated with levels of total p3-Alcα in all cohorts. Conclusions We confirm that Aβ40 is the most abundant Aβ species, and we propose a model in which CSF p3-Alcα can serve as a either (1) a nonaggregatable surrogate marker for γ-secretase activity; (2) as a marker for clearance of transmembrane domain peptides derived from integral protein catabolism; or (3) both. We propose the specification of an MCI/SAD endophenotype characterized by co-elevation of levels of both CSF p3-Alcα and Aβ40, and we propose that subjects in this category might be especially responsive to therapeutics aimed at modulation of γ-secretase function and/or transmembrane domain peptide clearance. These peptides may also be used to monitor the efficacy of therapeutics that target these steps in Aβ metabolis