黄原胶/溶菌酶体系相转变及其DSC分析

为探索黄原胶(XG)/溶菌酶(Ly)复合体系在自动酸化条件下相行为及在制备纳米凝胶过程中分子结构变化,采用透光率及热力学分别分析XG/Ly复合体系连续相转变规律及模拟碱和碱热偶合处理过程中XG和Ly的热力学特性。实验表明在连续酸化过程中,XG/Ly复合体系发生共溶体系、可溶性复合物、三维网络结构连续相转变过程,不同XG/Ly质量条件(3∶1、1∶1和1∶3)下发生相互作用的pH点分别为10.46、10.85和10.64,说明Ly可加快XG/Ly体系相转变进程;热力学分析表明制备纳米凝胶过程中XG及Ly原有结构均发生改变。      

香蕉低聚糖的通便功能评价

为比较不同品种香蕉低聚糖的通便功能,选取皇帝蕉(Musa AA Pisang Mas)和粉蕉(Musa ABB Pisang Awak),提取低聚糖后分别设置两种浓度(高剂量组2.5 g/(kg·BW·d)和低剂量组1.25 g/(kg·BW·d)),参考《保健食品检验与评价技术规范(2003版)》中\     

不同富硒方法对茶油品质特性及功能性成分的影响

以施肥富硒与生物化学富硒两种方法制得的富硒茶油为样本,测定硒含量、感官品质、理化指标、脂肪酸组成及功能性成分,探讨两种富硒方法对茶油的品质特性及功能性成分的影响。实验结果表明:施肥富硒法、生物化学富硒法茶油的硒含量分别提高至0.11 mg/kg及0.49 mg/kg,达到了我国相关富硒标准,生物化学方法的富硒效果比施肥富硒更显著;施肥富硒方法所得茶油具有更好的感官品质;两种富硒方法均降低了茶油的酸值、过氧化值,对茶油的碘值、皂化值、脂肪酸组成无明显影响;两种富硒方法对茶油中豆甾醇含量、谷甾醇含量及茶多酚含量整体上无明显影响,但生物化学富硒方法制得的茶油中α-生育酚及角鲨烯含量明显降低。总的来讲,两种富硒方法均显著提高了茶油硒含量,达到了富硒水准,其中施肥富硒方法富硒周期长,所得茶油具有更好的感官品质;生物化学富硒方法更快捷、效果更显著,但对茶油中的部分功能性成分造成了破坏。      

油溶性胭脂红酸衍生物的制备及性质评价

胭脂虫红色素是一种水溶性极好却不溶于大多数有机溶剂及油脂类的天然红色素,为了改善其油溶性从而拓展其运用领域,可对胭脂红色素的有效染色成分胭脂红酸进行结构修饰。本文通过对胭脂红酸进行甲酯化、酰化两步化学反应制备了5种胭脂红酸衍生物,应用傅里叶变换红外光谱（FTIR）对5种产物进行了结构的初步表征,借助紫外-可见（UV-Vis）光谱等方法考察了产物的溶解性及酸、碱、光、热、金属离子对产物稳定性的影响。结果表明5种产物的主要成分中增加了酯基和烷基;产物可溶于有机溶剂和油类物质,在玉米油中的溶解度从高至低的顺序为CE5>CE2>CE4>CE1>CE3,其中产物CE5在玉米油中可溶解12.8 g/L;产物在中性溶液中较稳定,光及热稳定性良好,金属离子Cu²⁺、Fe³⁺和Al³⁺可使色素产物褪色,而Na+和Mg²⁺却能增色。5种胭脂红酸衍生物油溶性及稳定性良好,且保留了胭脂虫红色素的优良染色能力,具有潜在的应用价值和前景。      

中国沙棘乙醇提取物的体外及对HepG2细胞的抗氧化活性

本文从生化角度全面分析了中国沙棘乙醇提取物的体外抗氧化活性,并在评价细胞毒性的基础上,以Hep G2细胞为模型,利用流式细胞仪评估了提取物的细胞抗氧化能力。结果表明,中国沙棘乙醇提取物对ABTS自由基具有良好的清除效果,当浓度为5 mg/m L时,其清除能力与阳性对照BHT相当;中国沙棘乙醇提取物对NO自由基也有良好的清除效果,但其整体清除能力不及BHT;当浓度为5 mg/m L时,中国沙棘乙醇提取物对亚油酸脂质过氧化表现抑制,但其抑制效果低于BHT;中国沙棘乙醇提取物的总抗氧化能力随浓度的增大而增强,当浓度为5 mg/m L时,其总抗氧化能力与同浓度下的BHT接近。在浓度为0.05~5 mg/m L范围内,中国沙棘乙醇提取物对Hep G2细胞不显示毒性;当处理浓度为0.5、1、5 mg/m L时,中国沙棘乙醇提取物的阳性细胞率与阳性对照相比分别降低了75.22%、72.36%和78.2%。中国沙棘乙醇提取物不仅在体外条件下具有良好的抗氧化活性,而且在Hep G2细胞内表现出良好的抗氧化能力。      

Effect of Glucocorticosteroids in Diamond-Blackfan Anaemia: Maybe Not as Elusive as It Seems

Diamond-Blackfan anaemia (DBA) is a red blood cell aplasia that in the majority of cases is associated with ribosomal protein (RP) aberrations. However, the mechanism by which this disorder leads to such a specific phenotype remains unclear. Even more elusive is the reason why non-specific agents such as glucocorticosteroids (GCs), also known as glucocorticoids, are an effective therapy for DBA. In this review, we (1) explore why GCs are successful in DBA treatment, (2) discuss the effect of GCs on erythropoiesis, and (3) summarise the GC impact on crucial pathways deregulated in DBA. Furthermore, we show that GCs do not regulate DBA erythropoiesis via a single mechanism but more likely via several interdependent pathways.     

Gal3 Plays a Deleterious Role in a Mouse Model of Endotoxemia

Lipopolysaccharide (LPS)-induced endotoxemia induces an acute systemic inflammatory response that mimics some important features of sepsis, the disease with the highest mortality rate worldwide. In this work, we have analyzed a murine model of endotoxemia based on a single intraperitoneal injection of 5 mg/kg of LPS. We took advantage of galectin-3 (Gal3) knockout mice and found that the absence of Gal3 decreased the mortality rate oflethal endotoxemia in the first 80 h after the administration of LPS, along with a reduction in the tissular damage in several organs measured by electron microscopy. Using flow cytometry, we demonstrated that, in control conditions, peripheral immune cells, especially monocytes, exhibited high levels of Gal3, which were early depleted in response to LPS injection, thus suggesting Gal3 release under endotoxemia conditions. However, serum levels of Gal3 early decreased in response to LPS challenge (1 h), an indication that Gal3 may be extravasated to peripheral organs. Indeed, analysis of Gal3 in peripheral organs revealed a robust up-regulation of Gal3 36 h after LPS injection. Taken together, these results demonstrate the important role that Gal3 could play in the development of systemic inflammation, a well-established feature of sepsis, thus opening new and promising therapeutic options for these harmful conditions.     

3′5-Dimaleamylbenzoic Acid Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by parenchymal scarring, leading progressively to alveolar architecture distortion, respiratory failure, and eventually death. Currently, there is no effective treatment for IPF. Previously, 3′5-dimaleamylbenzoic acid (3′5-DMBA), a maleimide, demonstrated pro-apoptotic, anti-inflammatory, and anti-cancer properties; however, its potential therapeutic effects on IPF have not been addressed. Bleomycin (BLM) 100 U/kg was administered to CD1 mice through an osmotic minipump. After fourteen days of BLM administration, 3′5-DMBA (6 mg/kg or 10 mg/kg) and its vehicle carboxymethylcellulose (CMC) were administered intragastrically every two days until day 26. On day 28, all mice were euthanized. The 3′5-DMBA effect was assessed by histological and immunohistochemical staining, as well as by RT-qPCR. The redox status on lung tissue was evaluated by determining the glutathione content and the GSH/GSSG ratio. 3′5-DMBA treatment re-established typical lung histological features and decreased the expression of BLM-induced fibrotic markers: collagen, α-SMA, and TGF-β1. Furthermore, 3′5-DMBA significantly reduced the expression of genes involved in fibrogenesis. In addition, it decreased reduced glutathione and increased oxidized glutathione content without promoting oxidative damage to lipids, as evidenced by the decrease in the lipid peroxidation marker 4-HNE. Therefore, 3′5-DMBA may be a promising candidate for IPF treatment.     

Establishing In-House Cutoffs of CSF Alzheimer’s Disease Biomarkers for the AT(N) Stratification of the Alzheimer Center Barcelona Cohort

Background: Clinical diagnosis of Alzheimer’s disease (AD) increasingly incorporates CSF biomarkers. However, due to the intrinsic variability of the immunodetection techniques used to measure these biomarkers, establishing in-house cutoffs defining the positivity/negativity of CSF biomarkers is recommended. However, the cutoffs currently published are usually reported by using cross-sectional datasets, not providing evidence about its intrinsic prognostic value when applied to real-world memory clinic cases. Methods: We quantified CSF Aβ1-42, Aβ1-40, t-Tau, and p181Tau with standard INNOTEST^® ELISA and Lumipulse G^® chemiluminescence enzyme immunoassay (CLEIA) performed on the automated Lumipulse G600II. Determination of cutoffs included patients clinically diagnosed with probable Alzheimer’s disease (AD, n = 37) and subjective cognitive decline subjects (SCD, n = 45), cognitively stable for 3 years and with no evidence of brain amyloidosis in 18F-Florbetaben-labeled positron emission tomography (FBB-PET). To compare both methods, a subset of samples for Aβ1-42 (n = 519), t-Tau (n = 399), p181Tau (n = 77), and Aβ1-40 (n = 44) was analyzed. Kappa agreement of single biomarkers and Aβ1-42/Aβ1-40 was evaluated in an independent group of mild cognitive impairment (MCI) and dementia patients (n = 68). Next, established cutoffs were applied to a large real-world cohort of MCI subjects with follow-up data available (n = 647). Results: Cutoff values of Aβ1-42 and t-Tau were higher for CLEIA than for ELISA and similar for p181Tau. Spearman coefficients ranged between 0.81 for Aβ1-40 and 0.96 for p181TAU. Passing–Bablok analysis showed a systematic and proportional difference for all biomarkers but only systematic for Aβ1-40. Bland–Altman analysis showed an average difference between methods in favor of CLEIA. Kappa agreement for single biomarkers was good but lower for the Aβ1-42/Aβ1-40 ratio. Using the calculated cutoffs, we were able to stratify MCI subjects into four AT(N) categories. Kaplan–Meier analyses of AT(N) categories demonstrated gradual and differential dementia conversion rates (p = 9.815⁻²⁷). Multivariate Cox proportional hazard models corroborated these findings, demonstrating that the proposed AT(N) classifier has prognostic value. AT(N) categories are only modestly influenced by other known factors associated with disease progression. Conclusions: We established CLEIA and ELISA internal cutoffs to discriminate AD patients from amyloid-negative SCD individuals. The results obtained by both methods are not interchangeable but show good agreement. CLEIA is a good and faster alternative to manual ELISA for providing AT(N) classification of our patients. AT(N) categories have an impact on disease progression. AT(N) classifiers increase the certainty of the MCI prognosis, which can be instrumental in managing real-world MCI subjects.