RESUMO
Phased array technology features rapid and directional scanning and has become a promising approach for remote sensing and wireless communication. In addition, element-level digitization has increased the feasibility of complicated signal processing and simultaneous multi-beamforming processes. However, the high cost and bulky characteristics of beam-steering systems have prevented their extensive application. In this paper, an X-band element-level digital phased array radar utilizing fully integrated complementary metal-oxide-semiconductor (CMOS) transceivers is proposed for achieving a low-cost and compact-size digital beamforming system. An 8-10 GHz transceiver system-on-chip (SoC) fabricated in 65 nm CMOS technology offers baseband filtering, frequency translation, and global clock synchronization through the proposed periodic pulse injection technique. A 16-element subarray module with an SoC integration, antenna-in-package, and tile array configuration achieves digital beamforming, back-end computing, and dc-dc conversion with a size of 317 × 149 × 74.6 mm3. A radar demonstrator with scalable subarray modules simultaneously realizes range sensing and azimuth recognition for pulsed radar configurations. Captured by the suggested software-defined pulsed radar, a complete range-azimuth figure with a 1 km maximum observation range can be displayed within 150 ms under the current implementation.
RESUMO
The insulin-like growth factor-II/mannose 6-phosphate receptor (IGF2R) over-expression correlates with heart disease progression. The IGF2R is not only an IGF2 clearance receptor, but it also triggers signal transduction, resulting in cardiac hypertrophy, apoptosis and fibrosis. The present study investigated the nuclear factor IL-3 (NFIL3), a transcription factor of the basic leucine zipper superfamily, and its potential pro-survival effects in cardiomyocytes. NFIL3 might play a key role in heart development and act as a survival factor in the heart, but the regulatory mechanisms are still unclear. IGF2 and IGF2R protein expression were highly increased in rat hearts subjected to hemorrhagic shock. IGF2R protein expression was also up-regulated in H9c2 cells exposed to hypoxia. Over-expression of NFIL3 in H9c2 cardiomyoblast cells inhibited the induction of hypoxia-induced apoptosis and down-regulated IGF2R expression levels. Gel shift assay, double-stranded DNA pull-down assay and chromatin immune-precipitation analyses indicated that NFIL3 binds directly to the IGF2R promoter region. Using a luciferase assay, we further observed NFIL3 repress IGF2R gene promoter activity. Our results demonstrate that NFIL3 is an important negative transcription factor, which through binding to the promoter of IGF2R, suppresses the apoptosis induced by IGF2R signaling in H9c2 cardiomyoblast cells under hypoxic conditions.
Assuntos
Hipóxia/metabolismo , Miócitos Cardíacos/citologia , Miócitos Cardíacos/metabolismo , Receptor IGF Tipo 2/metabolismo , Proteínas Repressoras/metabolismo , Animais , Apoptose/genética , Apoptose/fisiologia , Linhagem Celular , Fator de Crescimento Insulin-Like II/metabolismo , Ligação Proteica , Ratos , Receptor IGF Tipo 2/genética , Proteínas Repressoras/genética , Choque Hemorrágico/metabolismo , Transdução de Sinais/genética , Transdução de Sinais/fisiologiaRESUMO
Newly recorded ticks and emerging tick-borne pathogens have recently been reported in subtropical and tropical East Asia. In this study, a total of 1,615 ticks (259 Haemaphysalis hystricis, 1334 Rhipicephalus microplus, 19 H. flava, and 3 R. haemaphysaloides) were collected by flagging from vegetation in Taiwan during 2019-2021. All 1,615 captured tick samples tested negative for SFTSV and Borrelia, but 12 of 356 tick samples tested positive for PCR amplification of a fragment of the 18S rRNA gene of Babesia spp., with an infection rate of 3.37 % (12/356) and a minimum infection rate of 0.74 % (12/1,615). Among the 12 detected Babesia spp., 11 were identified as Babesia bigemina in R. microplus, and the other one, detected in H. hystricis, was classified as an unnamed novel Babesia sp. Interestingly, the 18S rRNA sequence from the isolate detected in H. hystricis shared 98.79 % to 99.50 % identity with those of recent isolates from Japan, China and Nigeria. The exact origin of the Babesia species is not known, but the findings highlight the importance of international cooperation and the exchange of information on ticks and tick-borne pathogens. This represents a rare report of a Babesia sp. identified in H. hystricis, a tick species that has been proposed as a novel vector for some Babesia spp. This study supports H. hystricis as a possible vector of Babesia spp.
Assuntos
Babesia , Borrelia , Ixodidae , Rhipicephalus , Doenças Transmitidas por Carrapatos , Animais , Babesia/genética , Taiwan/epidemiologiaRESUMO
The gut microbiota plays a critical role in chronic kidney disease (CKD) and hypertension. Trimethylamine-N-oxide (TMAO) and trimethylamine (TMA) are gut microbiota-derived metabolites, and both are known uraemic toxins that are implicated in CKD, atherosclerosis, colorectal cancer and cardiovascular risk. Therefore, the detection and quantification of TMAO, which is a metabolite from gut microbes, are important for the diagnosis of diseases such as atherosclerosis, thrombosis and colorectal cancer. In this study, a new "colour-switch" method that is based on the combination of a plasma separation pad/absorption pad and polyallylamine hydrochloride-capped manganese dioxide (PAH@MnO2) nanozyme was developed for the direct quantitative detection of TMAO in whole blood without blood sample pretreatment. As a proof of concept, a limit of quantitation (LOQ) of less than 6.7 µM for TMAO was obtained with a wide linear quantification range from 15.6 to 500 µM through quantitative analysis, thereby suggesting potential clinical applications in blood TMAO monitoring for CKD patients.
Assuntos
Microbioma Gastrointestinal , Metilaminas/análise , Aterosclerose , Humanos , Compostos de Manganês , Óxidos/análise , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/prevenção & controleRESUMO
BACKGROUND: The peroxisome is a single membrane-bound organelle in eukaryotic cells involved in lipid metabolism, including ß-oxidation of fatty acids. The human genetic disorder X-linked adrenoleukodystrophy (X-ALD) is caused by mutations in the ABCD1 gene (encoding ALDP, a peroxisomal half ATP-binding cassette [ABC] transporter). This disease is characterized by defective peroxisomal ß-oxidation and a large accumulation of very long-chain fatty acids in brain white matter, adrenal cortex, and testis. ALDP forms a homodimer proposed to be the functional transporter, whereas the peroxisomal transporter in yeast is a heterodimer comprising two half ABC transporters, Pxa1p and Pxa2p, both orthologs of human ALDP. While the carboxyl-terminal domain of ALDP is engaged in dimerization, it remains unknown whether the same region is involved in the interaction between Pxa1p and Pxa2p. METHODS/PRINCIPAL FINDINGS: Using a yeast two-hybrid assay, we found that the carboxyl-terminal region (CT) of Pxa2p, but not of Pxa1p, is required for their interaction. Further analysis indicated that the central part of the CT (designated CT2) of Pxa2p was indispensable for its interaction with the carboxyl terminally truncated Pxa1_NBD. An interaction between the CT of Pxa2p and Pxa1_NBD was not detected, but could be identified in the presence of Pxa2_NBD-CT1. A single mutation of two conserved residues (aligned with X-ALD-associated mutations at the same positions in ALDP) in the CT2 of the Pxa2_NBD-CT protein impaired its interaction with Pxa1_NBD or Pxa1_NBD-CT, resulting in a mutant protein that exhibited a proteinase K digestion profile different from that of the wild-type protein. Functional analysis of these mutant proteins on oleate plates indicated that they were defective in transporter function. CONCLUSIONS/SIGNIFICANCE: The CT of Pxa2p is involved in its interaction with Pxa1p and in transporter function. This concept may be applied to human ALDP studies, helping to establish the pathological mechanism for CT-related X-ALD disease.