MIMO Evolution toward 6G: End-User-Centric Collaborative MIMO

In 6G, the trend of transitioning from massive antenna elements to even more massive ones is continued. However, installing additional antennas in the limited space of user equipment (UE) is challenging, resulting in limited capacity scaling gain for end users, despite network side support for increasing numbers of antennas. To address this issue, we propose an end-user-centric collaborative MIMO (UE-CoMIMO) framework that groups several fixed or portable devices to provide a virtual abundance of antennas. This article outlines how advanced L1 relays and conventional relays enable device collaboration to offer diversity, rank, and localization enhancements. We demonstrate through system-level simulations how the UE-CoMIMO approaches lead to significant performance gains. Lastly, we discuss necessary research efforts to make UE-CoMIMO available for 6G and future research directions.Comment: 7 pages, 5 figures, 1 table. This work has been accepted in IEEE Communications Magazin

Targeted profiling of chlorinated transformation products and the parent micropollutants in the aquatic environment: A comparison between two coastal cities

This study investigated chlorinated transformation products (TPs) and their parent micropollutants, aromatic pharmaceuticals and personal care products (PPCPs) in the urban water bodies of two metropolitan cities. Nine PPCPs and 16 TPs were quantitatively or semi-quantitatively determined using isotope dilution techniques and liquid chromatography-tandem mass spectrometry. TPs and most PPCPs were effectively removed by conventional wastewater treatments in a wastewater treatment plant (WWTP). Chlorinated parabens and all PPCPs (at concentrations below 1000 ng/L) were present in the waters receiving treated wastewater. By contrast, the waters receiving untreated wastewater contained higher levels of PPCPs (up to 9400 ng/L) and more species of chlorinated TPs including chlorinated parabens, triclosan, diclofenac, and bisphenol A. The very different chemical profiles between the water bodies of the two cities of similar geographical and climatic properties may be attributed to their respective uses of chemicals and policies of wastewater management. No apparent increase in the number of species or abundances of TPs was observed in either the chlorinated wastewater or the seawater rich in halogens. This is the first study to elucidate and compare the profiles of multiple TPs and their parent PPCPs in the water bodies of coastal cities from tropical islands. Our findings suggest that chlorinated derivatives of bisphenol A, diclofenac, triclosan, and parabens in the surface water originate from sources other than wastewater disinfection or marine chlorination. Although further studies are needed to identify the origins, conventional wastewater treatments may protect natural water bodies against contamination by those chlorinated substances

Astrocyte elevated gene-1 (AEG-1) is a marker for aggressive salivary gland carcinoma

<p>Abstract</p> <p>Background</p> <p>Astrocyte elevated gene-1 (AEG-1) is associated with tumorigenesis and progression in diverse human cancers. The present study was aimed to investigate the clinical and prognostic significance of AEG-1 in salivary gland carcinomas (SGC).</p> <p>Methods</p> <p>Real-time PCR and western blot analyses were employed to examine AEG-1 expression in two normal salivary gland tissues, eight SGC tissues of various clinical stages, and five pairs of primary SGC and adjacent salivary gland tissues from the same patient. Immunohistochemistry (IHC) was performed to examine AEG-1 protein expression in paraffin-embedded tissues from 141 SGC patients. Statistical analyses was applies to evaluate the diagnostic value and associations of AEG-1 expression with clinical parameters.</p> <p>Results</p> <p>AEG-1 expression was evidently up-regulated in SGC tissues compared with that in the normal salivary gland tissues and in matched adjacent salivary gland tissues. AEG-1 protein level was positively correlated with clinical stage (<it>P </it>< 0.001), T classification (<it>P </it>= 0.008), N classification (<it>P </it>= 0.008) and M classifications (<it>P </it>= 0.006). Patients with higher AEG-1 expression had shorter overall survival time, whereas those with lower tumor AEG-1 expression had longer survival time.</p> <p>Conclusions</p> <p>Our results suggest that AEG-1 expression is associated with SGC progression and may represent a novel and valuable predictor for prognostic evaluation of SGC patients.</p

Association between copy number variation of complement component C4 and Graves' disease

<p>Abstract</p> <p>Background</p> <p>Gene copy number of complement component <it>C4</it>, which varies among individuals, may determine the intrinsic strength of the classical complement pathway. Presuming a major role of complement as an effecter in peptide-mediated inflammation and phagocytosis, we hypothesized that <it>C4 </it>genetic diversity may partially explain the development of Graves' disease (GD) and the variation in its outcomes.</p> <p>Methods</p> <p>A case-control study including 624 patients with GD and 160 healthy individuals were enrolled. CNV of <it>C4 </it>isotypes (<it>C4A </it>and <it>C4B</it>) genes were performed by quantitative real-time polymerase chain reaction analysis. Statistical comparison and identification of CNV of total <it>C4, C4 </it>isotypes (<it>C4A </it>and <it>C4B</it>) and <it>C4 </it>polymorphisms were estimated according to the occurrence of GD and its associated clinical features.</p> <p>Results</p> <p>Individuals with 4, 2, and 2 copies of <it>C4</it>, <it>C4A </it>and <it>C4B </it>genes, especially those with A2B2 polymorphism may associate with the development of GD (p = 0.001, OR = 10.994, 95% CI: 6.277-19.255; p = 0.008, OR = 1.732, 95% CI: 1.190-2.520; p = 2.420 × 10-5, OR = 2.621, 95% CI: 1.791-3.835; and <it>p </it>= 1.395 × 10^-4, OR = 2.671, 95% CI: 1.761-4.052, respectively). Although the distribution of copy number for total <it>C4</it>, <it>C4 </it>isotypes as well as <it>C4 </it>polymorphisms did not associate with the occurrence of goiter, nodular hyperplasia, GO and myxedema, <2 copies of <it>C4A </it>may associate with high risk toward vitiligo in patients with GD (<it>p </it>= 0.001, OR = 5.579, 95% CI: 1.659-18.763).</p> <p>Conclusions</p> <p>These results may be further estimated for its clinical application on GD and the vitiligo in patients with GD.</p

Analgesic and Anti-Inflammatory Activities of Methanol Extract of Ficus pumila L. in Mice

This study investigated possible analgesic and anti-inflammatory mechanisms of the methanol extract of Ficus pumila (FPMeOH). Analgesic effects were evaluated in two models including acetic acid-induced writhing response and formalin-induced paw licking. The results showed FPMeOH decreased writhing response in the acetic acid assay and licking time in the formalin test. The anti-inflammatory effect was evaluated by λ-carrageenan-induced mouse paw edema and histopathological analyses. FPMeOH significantly decreased the volume of paw edema induced by λ-carrageenan. Histopathologically, FPMeOH abated the level of tissue destruction and swelling of the edema paws. This study indicated anti-inflammatory mechanism of FPMeOH may be due to declined levels of NO and MDA in the edema paw through increasing the activities of SOD, GPx, and GRd in the liver. Additionally, FPMeOH also decreased the level of inflammatory mediators such as IL-1β, TNF-α, and COX-2. HPLC fingerprint was established and the contents of three active ingredients, rutin, luteolin, and apigenin, were quantitatively determined. This study provided evidence for the classical treatment of Ficus pumila in inflammatory diseases

Apoptosis induction in BEFV-infected Vero and MDBK cells through Src-dependent JNK activation regulates caspase-3 and mitochondria pathways

Our previous report demonstrated that bovine ephemeral fever virus (BEFV)-infected cultured cells could induce caspase-dependent apoptosis. This study aims to further elucidate how BEFV activates the caspase cascade in bovine cells. BEFV replicated and induced apoptosis in Vero and Madin-Darby bovine kidney (MDBK) cells, and a kinetic study showed a higher efficiency of replication and a greater apoptosis induction ability of BEFV in Vero cells. Src and c-Jun N-terminal kinase (JNK) inhibitor, but not extracellular signal-regulated kinase (ERK) or p38 inhibitor, alleviated BEFV-mediated cytopathic effect and apoptosis. In BEFV-infected Vero and MDBK cells, BEFV directly induced Src tyrosine-418 phosphorylation and JNK phosphorylation and kinase activity, which was inhibited specifically by SU6656 and SP600125, respectively. The caspase cascade and its downstream effectors, Poly (ADP-ribose) polymerase (PARP) and DFF45, were also activated simultaneously upon BEFV infection. In addition, cytochrome c, but not Smac/DIABLO, was released gradually from mitochondria after BEFV infection. SU6656 suppressed Src, JNK, and caspase-3 and -9 activation, as well as PARP and DFF45 cleavage; SP600125 reduced JNK and caspase-3 and -9 activation, as well as PARP and DFF45 cleavage. Taken together, these results strongly support the hypothesis that a Src-dependent JNK signaling pathway plays a key role in BEFV-induced apoptosis. The molecular mechanism identified in our study may provide useful information for the treatment of BEFV

Sialylation of vasorin by ST3Gal1 facilitates TGF-β1-mediated tumor angiogenesis and progression.

ST3Gal1 is a key sialyltransferase which adds α2,3-linked sialic acid to substrates and generates core 1 O-glycan structure. Upregulation of ST3Gal1 has been associated with worse prognosis of breast cancer patients. However, the protein substrates of ST3Gal1 implicated in tumor progression remain elusive. In our study, we demonstrated that ST3GAL1-silencing significantly reduced tumor growth along with a notable decrease in vascularity of MCF7 xenograft tumors. We identified vasorin (VASN) which was shown to bind TGF-β1, as a potential candidate that links ST3Gal1 to angiogenesis. LC-MS/MS analysis of VASN secreted from MCF7, revealed that more than 80% of its O-glycans are sialyl-3T and disialyl-T. ST3GAL1-silencing or desialylation of VASN by neuraminidase enhanced its binding to TGF-β1 by 2- to 3-fold and thereby dampening TGF-β1 signaling and angiogenesis, as indicated by impaired tube formation of HUVECs, suppressed angiogenesis gene expression and reduced activation of Smad2 and Smad3 in HUVEC cells. Examination of 114 fresh primary breast cancer and their adjacent normal tissues showed that the expression levels of ST3Gal1 and TGFB1 were high in tumor part and the expression of two genes was positively correlated. Kaplan Meier survival analysis showed a significantly shorter relapse-free survival for those with lower expression VASN, notably, the combination of low VASN with high ST3GAL1 yielded even higher risk of recurrence (p = 0.025, HR = 2.967, 95% CI = 1.14-7.67). Since TGF-β1 is known to transcriptionally activate ST3Gal1, our findings illustrated a feedback regulatory loop in which TGF-β1 upregulates ST3Gal1 to circumvent the negative impact of VASN