高效液相色谱法测定婴幼儿乳粉中烟酰胺的不确定度评定

建立高效液相色谱法测定婴幼儿乳粉中烟酰胺不确定度的数学模型,并根据JJF 1135—2005《化学分析测量不确定度评定》和JJF 1059—1999《测量不确定度评定与表示》中的有关规定,逐层对乳粉中烟酰胺测量不确定度来源进行评估,最后给出合成标准不确定度和扩展不确定度;婴幼儿乳粉中烟酰胺测定结果为(63.01±3.50)mg/kg,k=2,p=95%。通过评定,提出影响检测结果的主要因素为样品前处理过程、标准溶液、标准曲线拟合等。     

应用GB 5009.89-2016检测乳粉中烟酸和烟酰胺含量实例及探讨

目的探讨说明使用GB 5009.89-2016的高效液相色谱法进行实际乳粉中烟酸和烟酰胺含量检测时容易产生误解的细节,并提出适当建议。方法样品按照标准方法进行处理与检测,考察烟酸和烟酰胺的色谱峰形、分离度及响应值;以连续6次重复进样的相对标准偏差来检验方法的精密度;以加标回收法来检验方法的准确度。结果在该方法条件下,烟酸和烟酰胺的色谱峰分离完全,响应值高,峰形尖锐对称;烟酸和烟酰胺色谱峰的保留时间分别在8.438 min和10.515 min附近,相对标准偏差分别为0.085%和0.079%;烟酸的加标回收率为94.4%,烟酰胺的加标回收率为95.1%。结论为了保证实验的重复性和结果的准确性,建议样品前处理过程中的称样量和稀释倍数为确切的数值。在此前提下运用该方法检测乳粉中烟酸和烟酰胺含量精密度高,结果准确可靠。     

来那度胺-烟酰胺共晶的制备与表征

采用溶剂研磨法制备了难溶性药物来那度胺与烟酰胺的共晶,并使用差示扫描量热分析(DSC)、热重分析(TGA)、X射线粉末衍射(PXRD)和红外光谱(IR)对其进行了表征。此外,采用密度泛函理论(DFT)和B3LYP/6-31G(d)基组,通过高斯计算对来那度胺和烟酰胺之间的作用力进行了理论分析。计算和实验结果均表明了来那度胺与烟酰胺之间可形成共晶(1∶1)。     

乳饮料中烟酸和烟酰胺的液相色谱检测方法

建立一种测定乳饮料中烟酸和烟酰胺含量的高效液相色谱法。样品经乙晴萃取后进样,采用C18 100 mm×2.1 mm色谱柱分离,流动相为甲醇、异丙醇、庚烷磺酸钠。紫外检测;A-R261 nm,RSD为0.56%~0.82%(n=5),标准曲线r=0.999 8,平均回收率分别为98.2%,烟酸最低检出限为6.25μg/100 g,烟酰胺最低检出限为12.5μg/100 g。     

沉淀聚合法制备烟酰胺分子印迹聚合物微球

以烟酰胺为模板分子,甲基丙烯酸为功能单体,乙二醇二甲基丙烯酸酯为交联剂,偶氮二异丁腈为引发剂,乙腈为溶剂,采用沉淀聚合法制备了烟酰胺分子印迹聚合物,通过静态平衡吸附和色谱分析对印迹聚合物进行表征,结果表明,印迹聚合物对烟酰胺分子具有很好的吸附能力和特异识别性。     

Chemical composition,fatty acid content and antioxidant potential of meat from goats supplemented with Moringa (Moringa oleifera) leaves,sunflower cake and grass hay

The present study determined the chemical composition, fatty acid (FA) content and antioxidant capacity of meat from goats supplemented with Moringa oleifera leaves (MOL) or sunflower cake (SC) or grass hay (GH). The meat from goat supplemented with MOL had higher concentrations of total phenolic content (10.62 ± 0.27 mg tannic acid equivalent E/g). The MOL significantly scavenged 2,2′-azino-bis-3-ethylbenzothiazoline-6-sulfonic-acid (ABTS) radical to 93.51 ± 0.19% (93.51 ± 0.19%) and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical to 58.95 ± 0.3% than other supplements. The antioxidative effect of MOL supplemented meat on catalase (CAT), reduced glutathione (GSH), superoxide dismutase (SOD) and lipid oxidation (LO) was significantly (P < 0.05) higher than other meat from goat feed on grass hay or those supplemented with sunflower seed cake. The present study indicated that the anti-oxidative potential of MOL may play a role in improving meat quality (chemical composition, colour and lipid stability).     

尼克酰胺对白介素-1β损伤的离体大鼠胰岛细胞的保护作用

目的 观察尼克酰胺(NA)对白细胞介素-ip(IL-1(3)诱导的胰岛细胞损害的保护作用。方法 应用体外单层培养的大鼠胰岛细胞,分别检测IL-1(3, NA(10, 20 mmol/L)及其联合对胰岛细胞亚硝醆盐生成,肤岛素分泌以及胞内DNA,胰岛素含量和细胞活性的影响。结果 由IL-1β谓导的肤岛細胞亚硝醆盐生成量显著增加,同时胰岛素基础分泌以及葡萄糖刺激的胰岛素释放均明显减少;胰岛细胞内DNA,狹岛素含量及细胞活性（MTT值）均显著下降（P均<0.001);较高浓度及其的NA(20 mmol/1,)能阻断这些抑制作用（P均<0.001);而较低浓度的NA（10 mmol/L)虽不能阻断IL-1β诱导的NO生成对葡萄糖刺激的肤岛素释放的抑制作用,但对IL-lβ介导的其它抑制作用仍呈现保护性故应（P均<0.01)。结论 一氧化氮(NO)虽然参与IL-lβ诱导的胰岛细胞的损害过程,但可能不是唯一的故应分子。NA可能通过包括抑制NO生成等多方面机制,实现对IL-1β诱导的胰岛細胞损害的保护作用。     

米根霉生产L-乳酸过程中乳酸脱氢酶对发酵产生的影响

研究了米根霉发酵生产Ｌ－乳酸过程中培养条件对乳酸脱氢酶和Ｌ－乳酸发酵水平的影响,着重讨论了乳酸脱氢酶活力对Ｌ－乳酸发酵水平的关系。     

Fe3+对活性污泥系统的影响

通过小试研究了微量Fe3+对活性污泥系统的影响.将浓度为3 mg/L,5 mg/L,10 mg/L,20 mg/L,30 mg/L,50 mg/L和80 mg/L的Fe3+分别投加到活性污泥系统中,反应4 h后测定系统出水COD、活性污泥的SVI、脱氢酶活性及其EPS组分.结果表明,Fe3+浓度小于50 mg/L时对活性污泥的脱氢酶活性具有促进作用,浓度为10 mg/L时促进作用最强;Fe3+浓度在80 mg/L以下均具有良好的絮凝作用,浓度在30 mg/L以下时絮凝作用最强.两种作用的共同结果影响系统对COD的去除效果.对活性污泥EPS组分的测定表明,Fe3+的絮凝作用对SVI的影响是主要的.     

Dysfunction of Mitochondria in Alzheimer’s Disease: ANT and VDAC Interact with Toxic Proteins and Aid to Determine the Fate of Brain Cells

Alzheimer’s disease (AD), certainly the most widespread proteinopathy, has as classical neuropathological hallmarks, two groups of protein aggregates: senile plaques and neurofibrillary tangles. However, the research interest is rapidly gaining ground in a better understanding of other pathological features, first, of all the mitochondrial dysfunctions. Several pieces of evidence support the hypothesis that abnormal mitochondrial function may trigger aberrant processing of amyloid progenitor protein or tau and thus neurodegeneration. Here, our aim is to emphasize the role played by two ‘bioenergetic’ proteins inserted in the mitochondrial membranes, inner and outer, respectively, that is, the adenine nucleotide translocator (ANT) and the voltage-dependent anion channel (VDAC), in the progression of AD. To perform this, we will magnify the ANT and VDAC defects, which are measurable hallmarks of mitochondrial dysfunction, and collect all the existing information on their interaction with toxic Alzheimer’s proteins. The pathological convergence of tau and amyloid β-peptide (Aβ) on mitochondria may finally explain why the therapeutic strategies used against the toxic forms of Aβ or tau have not given promising results separately. Furthermore, the crucial role of ANT-1 and VDAC impairment in the onset/progression of AD opens a window for new therapeutic strategies aimed at preserving/improving mitochondrial function, which is suspected to be the driving force leading to plaque and tangle deposition in AD.