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As key performance indicators, the water absorption and mechanical strength of ceramics are highly associated with sintering temperature. Lower sintering temperatures, although favorable for energy saving in ceramics production, normally render the densification degree and water absorption of as-prepared ceramics to largely decline and increase, respectively. In the present work, 0.5 wt.% MnO2, serving as an additive, was mixed with aluminosilicate ceramics using mechanical stirring at room temperature, achieving a flexural strength of 58.36 MPa and water absorption of 0.05% and lowering the sintering temperature by 50 °C concurrently. On the basis of the results of TG-DSC, XRD, MIP, and XPS, etc., we speculate that the MnO2 additive promoted the elimination of water vapor in the ceramic bodies, effectively suppressing the generation of pores in the sintering process and facilitating the densification of ceramics at a lower temperature. This is probably because the MnO2 transformed into a liquid phase in the sintering process flows into the gap between grains, which removed the gas inside pores and filled the pores, suppressing the generation of pores and the abnormal growth of grains. This study demonstrated a facile and economical method to reduce the porosity and enhance the densification degree in the practical production of aluminosilicate ceramics. [ABSTRACT FROM AUTHOR]

Here, we report a previously unrecognized syndromic neurodevelopmental disorder associated with biallelic loss-of-function variants in the RBM42 gene. The patient is a 2-year-old female with severe central nervous system (CNS) abnormalities, hypotonia, hearing loss, congenital heart defects, and dysmorphic facial features. Familial whole-exome sequencing (WES) reveals that the patient has two compound heterozygous variants, c.304C>T (p.R102*) and c.1312G>A (p.A438T), in the RBM42 gene which encodes an integral component of splicing complex in the RNA-binding motif protein family. The p.A438T variant is in the RRM domain which impairs RBM42 protein stability in vivo. Additionally, p.A438T disrupts the interaction of RBM42 with hnRNP K, which is the causative gene for Au-Kline syndrome with overlapping disease characteristics seen in the index patient. The human R102* or A438T mutant protein failed to fully rescue the growth defects of RBM42 ortholog knockout ΔFgRbp1 in Fusarium while it was rescued by the wild-type (WT) human RBM42. A mouse model carrying Rbm42 compound heterozygous variants, c.280C>T (p.Q94*) and c.1306_1308delinsACA (p.A436T), demonstrated gross fetal developmental defects and most of the double mutant animals died by E13.5. RNA-seq data confirmed that Rbm42 was involved in neurological and myocardial functions with an essential role in alternative splicing (AS). Overall, we present clinical, genetic, and functional data to demonstrate that defects in RBM42 constitute the underlying etiology of a new neurodevelopmental disease which links the dysregulation of global AS to abnormal embryonic development. [ABSTRACT FROM AUTHOR]

Objective: The relationship between the levels of the first 24-h PaCO2 and the prognosis of sepsis-associated encephalopathy (SAE) remains unclear, and the first 24-h optimal target for PaCO2 is currently inconclusive. This study was performed to investigate the correlation between PaCO2 and all-cause mortality for SAE patients, establish a reference range of the initial 24-hour PaCO2 for clinicians in critical care, and explain the possible pathophysiological mechanisms of abnormal PaCO2 levels as a higher mortality risk factor for SAE. Methods: The baseline information and clinical data of patients were extracted from the fourth edition Medical Information Mart for Intensive Care database (MIMIC-IV 2.0). Multivariate logistic regressions were performed to assess the relationship between PaCO2 and all-cause mortality of SAE. Additionally, restricted cubic splines, Kaplan-Meier Survival analyses, propensity score matching (PSM) analyses, and subgroup analyses were conducted. Results: A total of 5471 patients were included in our cohort. In the original and matched cohort, multivariate logistic regression analysis showed that normocapnia and mild hypercapnia may be associated with a more favorable prognosis of SAE patients, and survival analysis supported the findings. In addition, a U-shaped association emerged when examining the initial 24-hour PaCO2 levels in relation to 30-day, 60-day, and 90-day mortality using restricted cubic splines, with an average cut-off value of 36.3mmHg (P for nonlinearity<0.05). Below the cut-off value, higher PaCO2 was associated with lower all-cause mortality, while above the cut-off value, higher PaCO2 was associated with higher all-cause mortality. Subsequent subgroup analyses revealed similar results for the subcohort of GCS≤8 compared to the original cohort. Additionally, when examining the subcohort of GCS>8, a L-shaped relationship between PaCO2 and the three clinical endpoints emerged, in contrast to the previously observed U-shaped pattern. The findings from the subcohort of GCS>8 suggested that patients experiencing hypocapnia had a more unfavorable prognosis, which aligns with the results obtained from corresponding multivariate logistic regression analyses. Conclusion: The retrospective study revealed the association between the first 24-h PaCO2 and all-cause mortality risk (30-day, 60-day, and 90-day) for patients with SAE in ICU. The range (35mmHg-50mmHg) of PaCO2 may be the optimal target for patients with SAE in clinical practice. [ABSTRACT FROM AUTHOR]

Compressed sensing has shown great potential in speeding up MR imaging by undersampling k-space data. Generally sparsity is used as a priori knowledge to improve the quality of reconstructed image. Compressed sensing MR image (CS-MRI) reconstruction methods have employed widely used sparsifying transforms such as wavelet or total variation, which are not preeminent in dealing with MR images containing distributed discontinuities and cannot provide a sufficient sparse representation and the decomposition at any direction. In this paper, we propose a novel CS-MRI reconstruction method from highly undersampled k-space data using nonsubsampled shearlet transform (NSST) sparsity prior. In particular, we have implemented a flexible decomposition with an arbitrary even number of directional subbands at each level using NSST for MR images. The highly directional sensitivity of NSST and its optimal approximation properties lead to improvement in CS-MRI reconstruction applications. The experimental results demonstrate that the proposed method results in the high quality reconstruction, which is highly effective at preserving the intrinsic anisotropic features of MRI meanwhile suppressing the artifacts and added noise. The objective evaluation indices outperform all compared CS-MRI methods. In summary, NSST with even number directional decomposition is very competitive in CS-MRI applications as sparsity prior in terms of performance and computational efficiency. [ABSTRACT FROM AUTHOR]

Background: RHD is an autoimmune disease that arises following infection by S. pyogenes and imposes a heavy burden on public health., Material and Methods: We detected 11 selected miRNAs expressed in the cardiac tissues of 11 RHD patients and 11 controls. By employing dual-luciferase assay and Western blot, we identified the relationship between TLR2 and miR-101 and miR-101. We used ELISA to test the concentration of TNF-α, IL-1β, and IL-6., Results: In cardiac tissue of RHD patients, miR-101 was significantly down-regulated (p=0.011). Ectopically expressed miR-101 repressed the luciferase activity by 27% through targeting TLR2 3'UTR. Combined with the results of Western blot, we confirmed that TLR2 is a direct target gene of miR-101. miR-101 knock-down is related to over-stimulated immune response in PGN-activated THP-1 cells. We detected a significantly higher concentration of TNF-α (p=0.0017), IL-1β (p=0.015), and IL-6 (p=0.014) in serum samples. TLR2 had a higher expression in patients in the protein level rather than the mRNA level, indicating that post-transcriptional regulation factors play a crucial role in regulating TLR2 expression., Conclusions: The present study confirmed that miR-101 targets TLR2 3'UTR and represses TLR2 expression. This work also found an association between down-regulated miR-101 and rheumatic heart disease.