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Dual open‐slot antennas were integrated in the metal back case and metal frame of a tablet computer for long‐term evolution applications. The single feed dual excitation source antennas were sufficiently narrow (2 mm) for installation between the metal frame and metal back case of the tablet computer. Each antenna had two open‐slot radiators (slot 1 and slot 2) with embedded filter circuits to enable wideband (699‐906 and 1710‐2690 MHz) operation required for LTE applications. The filter circuit values were adjusted to make the impedance more smooth and excite the desired modes. The proposed multiple‐input‐multiple‐output antennas were installed lengthwise on the long sides of the tablet and facing in operate directions. In this configuration, the user hand grip did not interfere with antenna performance, and isolation was improved (> 20 dB). The operating mechanism of the proposed antenna with matching circuits is described in detail. The effects of the user hand grip and the embedded display panel are also discussed. [ABSTRACT FROM AUTHOR]

A novel dual-feeding technique for a broadband circularly polarized aperture-coupled microstrip antenna operating in a 2.45 GHz system is presented. The dual feeds are placed in orthogonal directions, and are connected to a Wilkinson power divider with a 90° phase shift between its two output feedlines. Proper positioning of the coupling slots results in high port solution (>40 dB), and a purity of circular polarization is obtained. A broad impedance bandwidth (VSWR≤2) of about 54.7% and a 1 dB axial-ratio bandwidth of about 9.8% were achieved. © 2001 John Wiley & Sons, Inc. Microwave Opt Technol Lett 28: 100–101, 2001. [ABSTRACT FROM AUTHOR]

Abstract: Lead-free (Na0.5K0.5)NbO3 ceramics doped with CaTiO3 (0–3mol%) have been prepared by the conventional mixed oxide method in this paper. All of the CaTiO3 doped (Na0.5K0.5)NbO3 specimens do not deliquesce as exposed to water for a long time. The samples are characterized by X-ray diffraction analysis, Raman scattering spectra, scanning electron microscopy, and atomic force microscopy. The dielectric, piezoelectric and ferroelectric properties are also investigated. The results show that the addition of CaTiO3 is very effective in preventing the deliquescence and in improving the electric properties of (Na0.5K0.5)NbO3 ceramics. Finally, surface acoustic wave devices based on lead-free ceramics have been successfully fabricated and their characterization is presented. [Copyright &y& Elsevier]

Abstract: Lead-free (Na0.5K0.5)NbO3 ceramics doped with 0.5mol% CaTiO3 have been prepared by the conventional mixed-oxide method with sintering temperature at 1040–1120°C in this paper. The samples are characterized by X-ray diffraction analysis and scanning electron microscopy. The dielectric, piezoelectric and ferroelectric properties are also investigated. The results present that the increase of the sintering temperature is very effective in improving the density and electric properties. However, the properties of the samples would be deteriorated as they are sintered over the optimum temperature. The NKN-0.5%CT ceramics show excellent properties with sintering temperature at 1100°C. [Copyright &y& Elsevier]

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive and behavioral decline. Acrolein, an environmental pollutant and endogenous compound, is implicated in AD development. This research employs bibliometric analysis to assess current trends and key areas concerning acrolein-AD interaction., Methods: The Web of Science was used to extensively review literature on acrolein and AD. Relevant data were systematically gathered and analyzed using VOSviewer, CiteSpace, and an online bibliometric tool., Results: We identified 120 English publications in this specialized field across 19 journals. The Journal of Alzheimer's Disease was the most prominent. The primary contributors, both in terms of scientific output and influence, were the USA, the University of Kentucky, and Ramassamy C, representing countries/regions, institutions, and authors, respectively. In this field, the primary focus was on thoroughly studying acrolein, its roles, and its mechanisms in AD utilizing both in vivo and in vitro approaches. A significant portion of the research was based on proteomics, revealing complex molecular processes. The main focuses in the field were "oxidative stress," "lipid peroxidation," "amyloid-beta," and "cognitive impairment." Anticipated future research trajectories focus on the involvement of the internalization pathway, covering key areas such as synaptic dysfunction, metabolism, mechanisms, associations, neuroinflammation, inhibitors, tau phosphorylation, acrolein toxicity, brain infarction, antioxidants, chemistry, drug delivery, and dementia. Our analysis also supported our previous hypothesis that acrolein can interact with amyloid-beta to form a protein adduct leading to AD-like pathology and altering natural immune responses., Conclusion: This study provides a broad and all-encompassing view of the topic, offering valuable insights and guidance to fellow researchers. These emerging directions underscore the continuous exploration of the complexities associated with AD. The analyses and findings aim to enhance our understanding of the intricate relationship between acrolein and AD for future research., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Jallow, Nguyen, Sanotra, Hsu, Lin and Lin.)

Background: Sjogren's syndrome (SS) is a systemic autoimmune disease featured with a dry mouth and dry eyes. Several autoantibodies, including anti-SSA, anti-SSB, antinuclear antibodies can be detected in patients with SS. Oxidation-specific epitopes (OSEs) can be formed from malondialdehyde (MDA)-modified protein adducts and trigger chronic inflammation. In this study, our purposes were used serum levels of anti-MDA-modified peptide adducts autoantibodies to evaluate predictive performance by machine learning algorithms in primary Sjögren's syndrome (pSS) and assess the association between pSS and healthy controls., Methods: Three novel MDA-modified peptide adducts, including immunoglobulin (Ig) gamma heavy chain 1 (IGHG1) 102-131 , complement factor H (CFAH) 1045-1062 , and Ig heavy constant alpha 1 (IGHA1) 307-327 were identified and validated. Serum levels of protein, MDA-modified protein adducts, MDA, and autoantibodies recognizing unmodified peptides and MDA-modified peptide adducts were measured. Statistically significance in correlations and odds ratios (ORs) were estimated., Results: The random forest classifier utilized autoantibodies combination composed of IgM anti-IGHG1 102-131 , IgM anti-IGHG1 102-131 MDA and IgM anti-IGHA1 307-327 achieved predictive performance as an accuracy of 88.0%, a sensitivity of 93.7%, and a specificity of 84.4% which may be as potential diagnostic biomarkers to differentiate patients with pSS from rheumatoid arthritis (RA), and secondary SS in RA and HCs., Conclusions: Our findings imply that low levels of IgA anti-IGHG1 102-131 MDA (OR = 2.646), IgA anti-IGHG1 102-131 (OR = 2.408), IgA anti-CFAH 1045-1062 (OR = 2.571), and IgA anti-IGHA1 307-327 (OR = 2.905) may denote developing risks of pSS, respectively., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

We and others have shown that MPM (micropeptide in mitochondria) regulates myogenic differentiation and muscle development. However, the roles of MPM in cancer development remain unknown. Here we revealed that MPM was downregulated significantly in human hepatocellular carcinoma (HCC) tissues and its decrease was associated with increased metastasis potential and HCC recurrence. Gain- and loss-of-function investigations disclosed that in vitro migration/invasion and in vivo liver/lung metastasis of hepatoma cells were repressed by restoring MPM expression and increased by silencing MPM. Mechanism investigations revealed that MPM interacted with NDUFA7. Mitochondrial complex I activity was inhibited by overexpressing MPM and enhanced by siMPM, and this effect of siMPM was attenuated by knocking down NDUFA7. The NAD + /NADH ratio, which was regulated by complex I, was reduced by MPM but increased by siMPM. Treatment with the NAD + precursor nicotinamide abrogated the inhibitory effect of MPM on hepatoma cell migration. Further investigations showed that miR-17-5p bound to MPM and inhibited MPM expression. miR-17-5p upregulation was associated with MPM downregulation in HCC tissues. These findings indicate that a decrease in MPM expression may promote hepatoma metastasis by increasing mitochondrial complex I activity and the NAD + /NADH ratio., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 The American Society of Gene and Cell Therapy. Published by Elsevier Inc. All rights reserved.)

Background: Rheumatoid arthritis (RA) is an autoimmune disorder with systemic inflammation and may be induced by oxidative stress that affects an inflamed joint. Our objectives were to examine isotypes of autoantibodies against 4-hydroxy-2-nonenal (HNE) modifications in RA and associate them with increased levels of autoantibodies in RA patients., Methods: Serum samples from 155 female patients [60 with RA, 35 with osteoarthritis (OA), and 60 healthy controls (HCs)] were obtained. Four novel differential HNE-modified peptide adducts, complement factor H (CFAH) 1211-1230 , haptoglobin (HPT) 78-108 , immunoglobulin (Ig) kappa chain C region (IGKC) 2-19 , and prothrombin (THRB) 328-345 , were re-analyzed using tandem mass spectrometric (MS/MS) spectra (ProteomeXchange: PXD004546) from RA patients vs. HCs. Further, we determined serum protein levels of CFAH, HPT, IGKC and THRB, HNE-protein adducts, and autoantibodies against unmodified and HNE-modified peptides. Significant correlations and odds ratios (ORs) were calculated., Results: Levels of HPT in RA patients were greatly higher than the levels in HCs. Levels of HNE-protein adducts and autoantibodies in RA patients were significantly greater than those of HCs. IgM anti-HPT 78-108 HNE, IgM anti-IGKC 2-19 , and IgM anti-IGKC 2-19 HNE may be considered as diagnostic biomarkers for RA. Importantly, elevated levels of IgM anti-HPT 78-108 HNE, IgM anti-IGKC 2-19 , and IgG anti-THRB 328-345 were positively correlated with the disease activity score in 28 joints for C-reactive protein (DAS28-CRP). Further, the ORs of RA development through IgM anti-HPT 78-108 HNE (OR 5.235, p < 0.001), IgM anti-IGKC 2-19 (OR 12.655, p < 0.001), and IgG anti-THRB 328-345 (OR 5.761, p < 0.001) showed an increased risk. Lastly, we incorporated three machine learning models to differentiate RA from HC and OA, and performed feature selection to determine discriminative features. Experimental results showed that our proposed method achieved an area under the receiver operating characteristic curve of 0.92, which demonstrated that our selected autoantibodies combined with machine learning can efficiently detect RA., Conclusions: This study discovered that some IgG- and IgM-NAAs and anti-HNE M-NAAs may be correlated with inflammation and disease activity in RA. Moreover, our findings suggested that IgM anti-HPT 78-108 HNE, IgM anti-IGKC 2-19 , and IgG anti-THRB 328-345 may play heavy roles in RA development.

An efficient method for the diversity-oriented synthesis of spiropentadiene pyrazolones and 1 H -oxepino[2,3- c ]pyrazoles is reported. The methodology attributes O -acylation of phosphorus zwitterions which were formed by a tandem phospha-1,6-addition of PBu 3 to α,β,γ,δ -unsaturated pyrazolones, further generating betaine intermediates that preferentially resulted in the aforementioned cyclic products in a diversity-oriented manner. The mechanistic investigations revealed that formation of the betaines is the key step to provide the products via an intramolecular Wittig reaction or an unprecedented δ- C -acylation/cyclization/Wittig reaction.

Micropeptides belong to a class of newly identified small molecules with <100 amino acids in length, and their functions remain largely unknown. Here, we identified a novel muscle-enriched micropeptide that was localized to mitochondria (named MPM, micropeptide in mitochondria) and upregulated during in vitro differentiation of C2C12 myoblasts and in vivo early postnatal skeletal muscle development, and muscle regeneration after cardiotoxin (CTX) damage. Downregulation of MPM was observed in the muscular tissues of tibial muscular dystrophy and Duchenne muscular dystrophy patients. Furthermore, MPM silencing inhibited the differentiation of C2C12 myoblasts into myotubes, whereas MPM overexpression stimulated it. MPM -/- mice exhibited smaller skeletal muscle fibers and worse muscle performance, such as decrease in the maximum grip force of limbs, the latency to fall off rotarod, and the exhausting swimming time. Muscle regeneration was also impaired in MPM -/- mice, as evidenced by lower expression of Pax7, MyoD, and MyoG after CTX injection and smaller regenerated myofibers, compared with wild-type mice. Mechanistical investigations based on both gain- and loss-of function studies revealed that MPM increased oxygen consumption and ATP production of mitochondria. Moreover, ectopic expression of PGC-1α, which can enhance mitochondrial respiration, attenuated the inhibitory effect of siMPM on myogenic differentiation. These results imply that MPM may promote myogenic differentiation and muscle fiber growth by enhancing mitochondrial respiratory activity, which highlights the importance of micropeptides in the elaborate regulatory network of both myogenesis and mitochondrial activity and implicates MPM as a potential target for muscular dystrophy therapy.

This study identified and validated four differentially expressed novel malondialdehyde (MDA)-modified peptide adducts and evaluated autoantibodies against native and MDA-modified peptides among Taiwanese women patients with rheumatoid arthritis (RA), osteoarthritis (OA) and healthy controls (HCs). Ig kappa chain C region 76-99 , alpha-1-antitrypsin 284-298 , alpha-2-macroglobulin 824-841 , and apolipoprotein B-100 4022-4040 exhibiting 2-fold differences in relative modification ratios were identified by concanavalin A (Con A) affinity chromatography, 1D SDS-PAGE, in-gel digestion, nano-LC/MS/MS and nano-LC/MS using pooled serum-derived Con A-captured proteins from 9 RA and 9 age-matched HCs. Furthermore, the levels of proteins, serum MDA, and MDA-modified protein adducts were further validated against individual serum from 20 RA and 20 HCs, and autoantibodies against native and their MDA-modified peptides used 45 RA, 30 OA and 45 HCs. Levels of serum MDA and MDA-modified protein adducts were significantly higher in RA than HCs but protein levels were not significantly different. Serum Igs G and M against MDA-modified peptides showed better diagnostic performance in differentiating among patients with RA, OA and HCs, with an area under the receiver operating characteristic curve of 0.96-0.98, sensitivity of 88.9%-97.8%, and specificity of 88.9%-100%. Autoantibodies against MDA-modified epitopes become useful clinical biomarkers for RA., Biological Significance: By using a label-free relative quantitative proteomic analysis of concanavalin A (Con A)-bound serum samples, the current study discovered and validated malondialdehyde (MDA)-modified peptide adducts as novel biomarkers for differentiating between rheumatoid arthritis (RA) patients and healthy controls (HCs). In addition, the serum levels of MDA, proteins, and MDA-modified protein adducts as well as the MDA modification of proteins were determined. Isotypes of autoantibodies against MDA-modified peptide adducts can be used as serological biomarkers for further discriminating among RA patients, osteoarthritis patients and HCs. This strategy can become the basis for identifying potential diagnostic and pathological biomarkers for RA., (Copyright © 2017 Elsevier B.V. All rights reserved.)