Changes in the content and antioxidative activity of β-carotene and its metabolite vitamin A during gastrointestinal digestion and absorption and optimisation of HPLC-based detection

The β-Carotene (BC), an important precursor of vitamin A (VA), possesses antioxidant activity but is fat-soluble and has low bioavailability. In previous in-vitro assays evaluating antioxidant and 2,2′-azobis(2-amidinopropane) dihydrochloride (AAPH) free radical scavenging, both BC and VA showed a strong ability to scavenge radicals and protected cells from oxidative stress. Here, we used artificially simulated gastrointestinal digestion and Caco-2 cell absorption models to evaluate the bioavailability of the BC during gastrointestinal digestion and absorption using high-performance liquid chromatography (HPLC) analysis. We observed high absorptive and transfer rates of BC and detected retinol metabolites (Vitamin A). Therefore, BC can be detected in the acidic gastrointestinal environment using HPLC. Optimised method provided better separation of BC and VA in the column, improving the accuracy of the test results.     

Improving gelling properties of myofibrillar proteins incorporating with cellulose micro/nanofibres

The effects of cellulose microfibres (CMFs, Average size: 100 ± 5 μm) and cellulose nanofibres (CNFs, Average size: 60 ± 3 nm) on the properties of myofibrillar protein (MP) gels from duck breast meat were studied. The results demonstrated that CMFs and CNFs were mostly connected to MP by non-covalent bonds, the diffusion and cross-linking of MP molecules was promoted, and a denser and more complete gel network was formed. With the increases of CMFs and CNFs concentration (0–10%), the hardness was increased by 13.15% and 19.78% for CMFs10% and CNFs10% gels, respectively, and the elasticity was increased by 40% and 80%, respectively. At the same concentration (0–10%), the increase in gel hardness, viscoelasticity and immobilised water content was greater in the CNFs-MP group than in the CMFs-MP group. The CNFs-MP group had a tighter gel network, and CNFs had a better potential to improve the gelation performance of MP.     

用于电弧检测的电力专用SoC设计

针对传统的电弧电路故障检测结果不准确的问题,设计用于电弧检测的SoC系统,并且在55nm工艺下进行流片验证。采用包含两种结构的模数转换器的片上电压源,设计了锁相环以及复位电路,精度最高可达8.67 bit。验证结果表明,本设计可提高电弧检测的准确性。     

Facial-sketch Synthesis: A New Challenge

Machine Intelligence Research - This paper aims to conduct a comprehensive study on facial-sketch synthesis (FSS). However, due to the high cost of obtaining hand-drawn sketch datasets, there is a...     

Automated segmentation of brain tumor based on improved U-Net with residual units

Multimedia Tools and Applications - The study presents a new approach to automate segmentation of clinically significant brain tumor and, to a certain extent, addresses two major issues associated...     

Three dimensional reconstruction of brain tumor along with space occupying in lesions

Multimedia Tools and Applications - The three-dimensional models of brain tumors serve as diagnostic assistance for physicians, surgeons, and radiologists. The proposed system establishes an...     

Designing optical glasses by machine learning coupled with a genetic algorithm

Engineering new glass compositions have experienced a sturdy tendency to move forward from (educated) trial-and-error to data- and simulation-driven strategies. In this work, we developed a computer program that combines data-driven predictive models (in this case, neural networks) with a genetic algorithm to design glass compositions with desired combinations of properties. First, we induced predictive models for the glass transition temperature (T_g) using a dataset of 45,302 compositions with 39 different chemical elements, and for the refractive index (n_d) using a dataset of 41,225 compositions with 38 different chemical elements. Then, we searched for relevant glass compositions using a genetic algorithm informed by a design trend of glasses having high n_d (1.7 or more) and low T_g (500 °C or less). Two candidate compositions suggested by the combined algorithms were selected and produced in the laboratory. These compositions are significantly different from those in the datasets used to induce the predictive models, showing that the used method is indeed capable of exploration. Both glasses met the constraints of the work, which supports the proposed framework. Therefore, this new tool can be immediately used for accelerating the design of new glasses. These results are a stepping stone in the pathway of machine learning-guided design of novel glasses.     

Transgenerational Effects of Di(2-Ethylhexyl) Phthalate on Anogenital Distance,Sperm Functions and DNA Methylation in Rat Offspring

Di(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in the manufacture of polyvinylchloride plastics and has been associated with concerns regarding male reproductive toxicity. In this study, we hypothesized that maternal exposure to DEHP induces transgenerational inheritance of adult-onset adverse reproductive outcomes through the male germline in the F1, F2, and F3 generations of male offspring. Pregnant rats were treated with 5 or 500 mg of DEHP/kg/day through gavage from gestation day 0 to birth. The offspring body weight, anogenital distance (AGD), anogenital index (AGI), sperm count, motility, and DNA fragmentation index (DFI) were measured for all generations. Methyl-CpG binding domain sequencing was performed to analyze sperm DNA methylation status in the F3. DEHP exposure at 500 mg/kg affected AGD, AGI, sperm count, mean DFI, and %DFI in the F1; AGD, sperm count, and mean DFI in the F2; and AGD, AGI, mean DFI, and %DFI in the F3. DEHP exposure at 5 mg/kg affected AGD, AGI, sperm count, and %DFI in the F1; sperm count in the F2; and AGD and AGI in F3. Compared with the control group, 15 and 45 differentially hypermethylated genes were identified in the groups administered 5 mg/kg and 500 mg/kg DEHP, respectively. Moreover, 130 and 6 differentially hypomethylated genes were observed in the groups administered 5 mg/kg and 500 mg/kg DEHP. Overall, these results demonstrated that prenatal exposure to DEHP caused transgenerational epigenetic effects, which may explain the observed phenotypic changes in the male reproductive system.     

Syndecan-1 (CD138), Carcinomas and EMT

Cell surface proteoglycans are known to be important regulators of many aspects of cell behavior. The principal family of transmembrane proteoglycans is the syndecans, of which there are four in mammals. Syndecan-1 is mostly restricted to epithelia, and bears heparan sulfate chains that are capable of interacting with a large array of polypeptides, including extracellular matrix components and potent mediators of proliferation, adhesion and migration. For this reason, it has been studied extensively with respect to carcinomas and tumor progression. Frequently, but not always, syndecan-1 levels decrease as tumor grade, stage and invasiveness and dedifferentiation increase. This parallels experiments that show depletion of syndecan-1 can be accompanied by loss of cadherin-mediated adhesion. However, in some tumors, levels of syndecan-1 increase, but the characterization of its distribution is relevant. There can be loss of membrane staining, but acquisition of cytoplasmic and/or nuclear staining that is abnormal. Moreover, the appearance of syndecan-1 in the tumor stroma, either associated with its cellular component or the collagenous matrix, is nearly always a sign of poor prognosis. Given its relevance to myeloma progression, syndecan-1-directed antibody—toxin conjugates are being tested in clinical and preclinical trials, and may have future relevance to some carcinomas.     

Inhibition of Autophagy Does Not Re-Sensitize Acute Myeloid Leukemia Cells Resistant to Cytarabine

Elevated activation of the autophagy pathway is currently thought to be one of the survival mechanisms allowing therapy-resistant cancer cells to escape elimination, including for cytarabine (AraC)-resistant acute myeloid leukemia (AML) patients. Consequently, the use of autophagy inhibitors such as chloroquine (CQ) is being explored for the re-sensitization of AraC-resistant cells. In our study, no difference in the activity of the autophagy pathway was detected when comparing AraC-Res AML cell lines to parental AraC-sensitive AML cell lines. Furthermore, treatment with autophagy inhibitors CQ, 3-Methyladenine (3-MA), and bafilomycin A1 (BafA1) did not re-sensitize AraC-Res AML cell lines to AraC treatment. However, in parental AraC-sensitive AML cells, treatment with AraC did activate autophagy and, correspondingly, combination of AraC with autophagy inhibitors strongly reduced cell viability. Notably, the combination of these drugs also yielded the highest level of cell death in a panel of patient-derived AML samples even though not being additive. Furthermore, there was no difference in the cytotoxic effect of autophagy inhibition during AraC treatment in matched de novo and relapse samples with differential sensitivity to AraC. Thus, inhibition of autophagy may improve AraC efficacy in AML patients, but does not seem warranted for the treatment of AML patients that have relapsed with AraC-resistant disease.