Cost-Effective Engineered Cementitious Composites with Hybrid PVA and Basalt/PP Fiber: A Study on Compressive, Tensile and Impact Performance.

Currently, oil-coated PVA fibers are the most commonly used material in ECC research. However, the high price limits the application of PVA-ECC in practical engineering. In order to reduce the cost, one of the methods is to partially replace the PVA fibers in ECC. In order to demonstrate the feasibility of PVA/BF-ECC and PVA/PP-ECC, polyvinyl alcohol fibers (PVA), basalt fibers (BFs) and polypropylene fibers (PP) were added at 0.5%, 1.0% and 1.5% by volume of PVA in addition to 1% by volume of PVA. Subsequently, tensile, compression and drop-weight impact tests were conducted on single or hybrid fiber concrete. The results showed that the post-peak compression toughness, tensile strength, and initial cracking impact strength of PVA/BF-ECC and PVA/PP-ECC increased significantly with the increase in the volume ratio of BF and PP fibers, while the performance of PVA-ECC materials with the same fiber volume ratio decreased slightly. Therefore, the cost can be reduced by designing hybrid PVA/BF-ECC materials that meet the performance requirements. The experimental evidence presented in this study demonstrates the feasibility and reasonable prospect of the new hybrid PVA/BF-ECC.

Nomogram constructed by immunological and inflammatory indicators for predicting prognosis of patients with esophageal squamous cell carcinoma treated with neoadjuvant chemoradiotherapy plus surgery.

Objectives: At present, esophageal squamous cell carcinoma (ESCC) patients accepting neoadjuvant chemoradiotherapy (nCRT) plus surgery lack corresponding prognostic indicators. This study aimed to construct a prognostic prediction model for ESCC patients undergoing nCRT and surgery based on immune and inflammation-related indicators. Methods: We retrospectively analyzed the levels of serum immune- and inflammation-related indicators of ESCC patients before receiving nCRT plus surgery in the training cohort (99 patients) and validation cohort (67 patients), which were collected from 2007 to 2020. Univariate and multivariate Cox survival analyses were conducted to evaluate the indicators to set up a nomogram associated with the patients' overall survival (OS). The prediction accuracy and discriminative ability of the nomogram were measured by the concordance index (C-index), decision curve, calibration curve, integrated discrimination improvement (IDI), and net reclassification improvement (NRI). Results: Univariate and multivariate Cox analyses demonstrated that immune globin A (IgA) and C-reactive protein (CRP) were independent risk factors. A nomogram based on IgA, CRP, and cTNM stage was established for predicted OS in the training cohort and validated in the validation cohort. The C-index of the nomogram was 0.820 (95% CI: 0.705-0.934), which was higher than that of the cTNM stage (0.655 (95% CI: 0.546-0.764), p < 0.05) in the training cohort, and similar results were observed in the validation cohort (0.832 (95% CI: 0.760-0.903 vs 0.635 (95% CI: 0.509-0.757), p < 0.001). Furthermore, the prediction accuracy and net benefit of the nomogram verified by the calibration curve, decision curve, NRI, and IDI were satisfactory in the training and validation cohorts. Conclusion: The newly constructed nomogram concluding serum IgA, CRP, and cTNM stage might be helpful in the prognosis prediction for ESCC patients receiving nCRT plus surgery.

Enhanced ROS production leads to excessive fat accumulation through DAF-16 in Caenorhabditis elegans.

Growing evidence shows that enhanced reactive oxygen species (ROS) production is an important contributor to obesity and its co-morbidities, but the functional link between ROS and obesity remains elusive. In this study we used the model animal Caenorhabditis elegans to explore the role of ROS in obesity. Initially, when ROS production was enhanced by treatment with low concentration of paraquat or juglone, both abnormal high fat accumulation and fatty acid composition were observed in wild type worms. We found that the abnormal fat accumulation was associated with increased expression of fat-5, which encodes an isoform of stearoyl-CoA synthetase, and which is regulated by daf-16 encoding the forkhead transcription factor and being activated by downregulation daf-2. When mutant daf-16 worms were used, the abnormal fat accumulation induced by ROS was suppressed. Collectively, we demonstrate that enhanced ROS production can lead to excessive fat accumulation and the change of fatty acid composition. This abnormal phenomenon at least in part depends on the daf-16 pathway by which fat-5 was regulated. The results point towards a role of ROS in obesity in the context of important conserved signaling pathway, thereby guide further studies and future therapeutic interventions.

Mitoferrin-1 is Involved in the Progression of Alzheimer's Disease Through Targeting Mitochondrial Iron Metabolism in a Caenorhabditis elegans Model of Alzheimer's Disease.

In mammals, mitoferrin-1 and mitoferrin-2, two homologous proteins of the mitochondrial solute carrier family are required for iron delivery into mitochondria. However, there is only one kind, called W02B12 (mitoferrin-1 or mfn-1), in Caenorhabditis elegans and its regulatory mechanism is unknown. In this study, we used C. elegans strains CL2006 and GMC101 as models to investigate what role mitoferrin-1 played in Alzheimer's disease (AD). We found that knockdown of mitoferrin-1 by feeding-RNAi treatment extended lifespans of both strains of C. elegans. In addition, it reduced the paralysis rate in the GMC101 strain. These results suggest that mitoferrin-1 may be involved in the progression of Alzheimer's disease. Knockdown of mitoferrin-1 was seen to disturb mitochondrial morphology in the CB5600 strain. We tested whether knockdown of mitoferrin-1 could influence mitochondrial metabolism. Analysis of mitochondrial iron metabolism and mitochondrial ROS showed that knockdown of mitoferrin-1 could reduce mitochondrial iron content and reduce the level of mitochondrial ROS in the CL2006 and GMC101 strains. These results confirm that knockdown of mitoferrin-1 can slow the progress of disease in Alzheimer model of C. elegans and suggest that mitoferrin-1 plays a major role in mediating mitochondrial iron metabolism in this process.