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Cardiac magnetic resonance imaging (CMR) has emerged as a valuable diagnostic tool for cardiac diseases. However, a significant drawback of CMR is its slow imaging speed, resulting in low patient throughput and compromised clinical diagnostic quality. The limited temporal resolution also causes patient discomfort and introduces artifacts in the images, further diminishing their overall quality and diagnostic value. There has been growing interest in deep learning-based CMR imaging algorithms that can reconstruct high-quality images from highly under-sampled k-space data. However, the development of deep learning methods requires large training datasets, which have so far not been made publicly available for CMR. To address this gap, we released a dataset that includes multi-contrast, multi-view, multi-slice and multi-coil CMR imaging data from 300 subjects. Imaging studies include cardiac cine and mapping sequences. The 'CMRxRecon' dataset contains raw k-space data and auto-calibration lines. Our aim is to facilitate the advancement of state-of-the-art CMR image reconstruction by introducing standardized evaluation criteria and making the dataset freely accessible to the research community. [ABSTRACT FROM AUTHOR]

Diabetic kidney disease (DKD), a chronic kidney disease, is characterized by progressive fibrosis caused due to persistent hyperglycemia. The development of fibrosis in DKD determines the patient prognosis, but no particularly effective treatment. Here, small extracellular vesicles derived from mesenchymal stem cells (MSC-sEV) have been used to treat DKD fibrosis. Single-cell RNA sequencing was used to analyze 27,424 cells of the kidney, we have found that a novel fibrosis-associated TGF-β1+Arg1+ macrophage subpopulation, which expanded and polarized in DKD and was noted to be profibrogenic. Additionally, Actin+Col4a5+ mesangial cells in DKD differentiated into myofibroblasts. Multilineage ligand-receptor and cell-communication analysis showed that fibrosis-associated macrophages activated the TGF-β1/Smad2/3/YAP signal axis, which promotes mesangial fibrosis-like change and accelerates renal fibrosis niche. Subsequently, the transcriptome sequencing and LC-MS/MS analysis indicated that MSC-sEV intervention could restore the levels of the kinase ubiquitin system in DKD and attenuate renal interstitial fibrosis via delivering CK1δ/β-TRCP to mediate YAP ubiquitination degradation in mesangial cells. Our findings demonstrate the unique cellular and molecular mechanisms of MSC-sEV in treating the DKD fibrosis niche at a single-cell level and provide a novel therapeutic strategy for renal fibrosis. [ABSTRACT FROM AUTHOR]

Objective To express two scFv-Fc fusion proteins of anti-CEA scFv-Fc and anti-CA19-9 scFv-Fc in HEK293 cells efficiently, and to determinate the affinity of two single chain antibodies. Methods Two scFv gene sequences obtained from GenBank were optimized and synthesized. They and pET32a(+) formed double prokaryotic expression vectors, anti-CEA scFv/pET32a(+) and anti-CA19-9 scFv/pET32a(+), respectively, which were translated into E.coli BL21 (DE3) and induced expression with IPTG. Two scFv genes (deleted terminators) were amplified by PCR; in addition, through overlapping region amplification method, we added IL-2 signal peptide into the upstream of anti-CEA scFv gene, getting three scFv genes, and connected these genes respectively with pTT5 containing human IgG1 Fc gene (Fc/pTT5) to constitute three eukaryotic expression vectors (anti-CEA scFv(-t)-Fc/pTT5, IL2-anti-CEA scFv(-t)-Fc/pTT5 and anti-CA19-9 scFv(-t)-Fc/pTT5). Three recombinant plasmids of scFv were transferred into HEK293 cells by Lipofectamine. We purified and identified expressing products by rProtein-A FF affinity chromatography, competitive cellular Elisa and Western blot. Results Western blot analysis showed that three scFv-Fc fusion proteins were expressed in HEK293 cells. Competitive binding test showed that antibody concentrations of anti-CEA scFv-Fc and anti-CA19-9 scFv-Fc were 8.2 nmol/L and 6.0 nmol/L, respectively. Conclusion anti-CEA scFv and anti-CA19-9 scFv could express in HEK293 cells, and their purified products could recognize tumor cell surface antigens CEA and CA19-9, although their expression efficiency is relatively low.

Renal interstitial fibrosis (RIF) is a fundamental pathological feature of chronic kidney disease (CKD). However, toxicity and poor renal enrichment of fibrosis inhibitors limit their further applications. In this study, a platform for CKD therapy is developed using superparamagnetic iron oxide nanoparticles (SPION) decorated mesenchymal stem cells derived extracellular vesicles with carboxyl terminus of Hsc70-interacting protein (CHIP) high expression (SPION-EVs) to achieve higher renal-targeting antifibrotic therapeutic effect. SPION-EVs selectively accumulate at the injury renal sites under an external magnetic field. Moreover, SPION-EVs deliver CHIP to induce Smad2/3 degradation in renal tubular cells which alleviates Smad2/3 activation-mediated fibrosis-like changes and collagen deposition. The extracellular vesicle engineering technology provides a potential nanoplatform for RIF therapy through CHIP-mediated Smad2/3 degradation. [ABSTRACT FROM AUTHOR]

Recently, magnetoelectric (ME) antennas have become a hot topic in the field of antenna miniaturization in the very-low-frequency (VLF) band because their size can be reduced to one-ten-thousandth of the size of conventional electric antennas. However, they still suffer from narrow transmission/reception bandwidth and weak radiation intensity. To address these issues, VLF thin-film ME antennas with a microbridge structure are designed, and the method of array connection is used. Test results show that the detection limit of the ME antenna unit is 636 pT/√Hz at 23 kHz and the radiant magnetic field intensity at 0.12 m is 0.87 nT (input power of 10 mW). By series-connecting three ME antenna units with the same resonance frequency, the output response has been increased to 1.72 times and the EM wave radiation intensity is increased to 1.9 times compared to a single unit. By parallel-connecting two ME antenna units with different resonance frequencies, the output response bandwidth has been expanded to 1.56 times compared to a single unit, and the signal radiation bandwidth has been expanded to 1.47 times. This work provides a valuable reference for the future larger-scale arraying of ME antennas. [ABSTRACT FROM AUTHOR]

Esophageal carcinoma is one of the important lethal tumors in the world, but the mechanism of esophageal cancer progression is still unclear. The long non-coding RNAs are known to regulate tumor progression. Here we report that BRAF-activated nonprotein coding RNA (BANCR) is associated with the development of esophageal squamous cell carcinoma (ESCC). The expression levels of BANCR in 132 ESCC tumor tissues detected by quantitative real-time PCR were significantly higher than that in the adjacent normal tissues. The expression level of BANCR was down-regulated by transfecting small interrupting RNA against BANCR (BANCR siRNA) in Eca109 cells. Eca109 and TE-1 cells transfected with BANCR siRNA led to the delayed cell cycles compared to the cells transfected with negative control siRNA. Moreover, MTT assays demonstrated that Eca109 cells transfected with BANCR siRNA resulted in the inhibition of cell proliferation. These results suggested that BANCR advances the development and progression of ESCC cells through regulating their cell cycles.