Determination of Volatile and Semivolatile Contaminants in Meat by Supercritical Fluid Extraction/Gas Chromatography/Mass Spectrometry

Meat products that were exposed to a warehouse fire were collected and examined to identify contaminants present in the samples. An extraction method using supercritical carbon dioxide at 100 atm and 60°C was developed to analyse and characterise volatile and semi-volatile compounds from the samples. The major volatile compounds were lipid oxidation products, such as hexanal and nonanal. Volatiles concentrations from fire-exposed meat products were compared to control samples to determine compositional differences. Aromatic and polycyclic aromatic hydrocarbons were identified, and naphthalene was measured in suspected fire-damaged meat products. Direct supercritical extraction from the meat samples proved to be a rapid and reproducible method to assess contamination in commercial meat products.     

基于16S rDNA测序研究白酒对大鼠肠道菌群的影响

为探究浓香型白酒对SD大鼠肠道微生态的影响,通过连续8周灌胃适当剂量乙醇,建立SD大鼠慢性酒精性肝损伤模型,同时,灌胃相同剂量的白酒,考察白酒和乙醇对SD大鼠血脂、肝脏指标的影响及造成的肠道菌群变化。结果显示,连续8周灌胃乙醇造成SD大鼠一定程度的酒精性肝损伤,而白酒组的肝损伤程度显著低于乙醇组。多样性分析表明乙醇组SD大鼠肠道菌群丰富度和多样性降低,而白酒的摄入可以回调这种现象。菌群结构分析表明乙醇干预和白酒干预之间存在显著差异,其中白酒干预组物种组成与对照组更加接近。差异性分析筛选出白酒组和乙醇组的3个潜在差异微生物标志物,分别为g＿Eubacterium＿rumminantium＿group、g＿U29-B03和g＿unclassified＿f＿Oscillospiraceae。该研究结果表明白酒可能通过调节肠道微生态来减轻乙醇诱导的轻度肝损伤。     

基于GRA-ISM-HMM的广州市肉及肉制品安全风险评估

该研究旨在利用广州食品安全风险监测2015年至2020年针对肉及肉制品样本的检测数据,构建肉及肉制品的安全风险评估模型,从而了解广州市该段时间内肉及肉制品的食品安全风险及其时变特点。该研究采取灰色关联分析方法和解释结构模型建立风险指数,并基于该指标值作为隐马尔可夫模型的观测值探讨观测背后的隐含风险状态。分析结果显示,2015~2020年所有样本综合风险指数结果都在[0,0.45]之间,总体风险都较小,其中2019年风险最高;将风险指数进行等级划分,显示2015~2020年风险等级为[1, 2, 2, 2, 3, 1];通过HMM分析得到这六年的隐藏风险等级为[0, 1, 1, 1, 2, 0],与观测风险结果一致,且HMM预测2021年风险等级为1,即表明广州肉及肉制品风险往良好态势发展。最后,进行风险差异原因分析,发现各肉制品分类之间有差异,其中腊肠、鸡肉和腊肉的风险指数较高于其他种类,而2019年增加腊肠和腊肉的检测是风险增加的一个原因。总体来说,广州肉及肉制品风险较小,但依旧需要监督改善。     

The Effect of Age and Intrinsic Aerobic Exercise Capacity on the Expression of Inflammation and Remodeling Markers in Rat Achilles Tendons

Old age, adiposity, and metabolic disorders are known as risk factors for chronic tendinopathy, which is a common problem in both athletes and the general population. However, the importance of these influencing factors has not yet been well understood. This study investigated alterations in gene expression and histology of Achilles tendons of young (10 weeks) and old (100 weeks) rats bred for low (low capacity runners, LCR) and high (high capacity runners, HCR) intrinsic aerobic exercise capacity. In this rat model, LCR displayed a phenotype of reduced exercise capacity, higher body weight, and metabolic dysfunctions compared to HCR. We hypothesized that the risk factors for tendinopathy in old LCR could lead to more pronounced impairments in Achilles tendon tissue. In quantitative real-time PCR (qPCR), age-related downregulation of tenocyte markers e.g., tenomodulin, genes related to matrix modeling and remodeling (e.g., collagens, elastin, biglycan, fibronectin, tenascin C) as well as transforming growth factor beta 3 (Tgfb3) have been detected. Inflammation marker cyclooxygenase 2 (Cox2) was downregulated in old rats, while microsomal prostaglandin E synthase 2 (Ptges2) was upregulated in old HCR and old LCR. In all groups, interleukin 6 (Il6), interleukin 1 beta (Il1b), and tumor necrosis factor alpha (Tnfa) showed no significant alteration. In histological evaluation, tendons of old rats had fewer and more elongated tenocyte nuclei than young rats. Even though a higher content of glycosaminoglycans, a sign of degeneration, was found in old HCR and LCR, no further signs of tendinopathy were detectable in tendons of old rats by histological evaluation. Low intrinsic aerobic exercise capacity and the associated phenotype did not show significant effects on gene expression and tendon histology. These findings indicate that aging seems to play a prominent role in molecular and structural alterations of Achilles tendon tissue and suggests that other risk factors associated with intrinsic aerobic exercise capacity are less influential in this rat model.     

地皮菜添加量对鸡胸肉糜凝胶特性的影响

以新鲜鸡胸肉为实验对象,探究地皮菜添加量对鸡胸肉糜蒸煮得率、保水性、色泽、质构、凝胶强度、流变特性和微观结构等的影响.结果表明:随着地皮菜添加量的增加,鸡胸肉糜的蒸煮得率和保水性呈先上升后下降的趋势,添加量在1.2％时最大,分别为95.71％和95.33％;鸡胸肉糜的L*值、a*值、b*值均显著降低(P＜0.05);硬...     

肉及肉制品碘含量检测新方法的验证

对即将实施的碘含量检测新方法进行验证分析,通过选取具有代表性的样本进行实验,研究了新方法对肉及肉制品检测结果准确性和精密度的影响.结果表明,与现有检测方法相比,新检测方法的准确性更好、精密度更高,更加适用于肉及肉制品中碘含量的测定.     

同位素稀释-气相色谱-串联质谱法同时测定肉制品中16种欧盟优控多环芳烃

目的 基于分子印迹特异性净化及同位素稀释-气相色谱-串联质谱法建立同时检测肉制品中16种欧盟优控多环芳烃的分析方法。方法 样品中加入氘代同位素内标,经正己烷-二氯甲烷(7:3, V:V)混合溶液提取,特异性分子印迹柱净化,采用DB-EUPAH色谱柱分离,在多反应监测(multiple reaction monitoring, MRM)模式下采集,内标法定量。结果 为降低基质效应,采用基质匹配标准曲线的定量方法。在0.2～200.0 ng/mL范围内,16种欧盟优控多环芳烃均有良好的线性关系,线性相关系数(r²)均大于0.9990,在1.0、5.0、10.0μg/kg3个浓度水平下进行加标回收实验, 16种欧盟优控多环芳烃的回收率在85.9%～118.3%之间,相对标准偏差(n=6)在0.4%～6.6%之间,方法的检出限为0.03～0.10μg/kg,定量限为0.10～0.30μg/kg。结论 该方法前处理简便高效、灵敏度高、准确度高、抗干扰能力强,可同时实现肉制品中16种欧盟优控多环芳烃的测定。     

拉曼光谱法快速检测猪肉脯中的掺伪鸡肉

目的 建立拉曼光谱法快速、准确、无损地检测猪肉脯样品中掺假鸡肉的方法。方法 制备33份猪肉中掺入不同比例鸡肉的肉脯样品,采集拉曼光谱数据,分别采用标准正态变换、多元散射校正、卷积平滑、归一化、一阶导数等5种不同预处理方法,对原始光谱数据进行预处理,采用连续投影算法、竞争性自适应重加权算法及随机蛙跳算法对光谱数据进行特征波长筛选,建立偏最小二乘法(partial least squares,PLS)模型对猪肉脯进行定性定量判别。结果 拉曼光谱数据经过多元散射校正处理的效果最佳,竞争性自适应重加权算法竞筛选效果更佳,构建猪肉脯中猪肉含量的PLS定量模型,其预测集决定系数和预测均方根误差分别为0.9762、7.2998。建立的PLS判别模型的校正集和预测集总判别正确率分别为100.00%和98.33%。结论 拉曼光谱分析技术可有效用于定性鉴别猪肉脯是否掺伪及定量分析猪肉肉脯中掺入鸡肉的比例,为肉脯掺假的快速无破坏性检测的应用提供支持。     

微流控芯片联用高效液相色谱-荧光检测器同时测定肉类食品中4种磺胺类药物残留

目的 建立一种使用微流控芯片进行肉类食品前处理,并结合高效液相色谱-荧光检测器(high performance liquid chromatography-fluorescence detector, HPLC-FLD)同时测定肉类食品中4种磺胺残留的方法。方法 样品先用乙酸乙酯提取后,在微流控芯片中用2 mol/L盐酸溶液反萃取和正己烷脱脂,收集盐酸流出液100μL,与0.5 g/mL醋酸钠溶液按照1:1(V:V)混合,加入0.2 g/L荧光胺50μL进行衍生化反应,采用岛津ODS-3色谱柱进行分离,流动相为乙腈-2%乙酸水溶液。结果 4种磺胺完全分离且在0.01～1.00mg/L呈良好的线性关系,在50、100、200μg/kg3个添加水平下,平均回收率为72.1%～91.6%,相对标准偏差为4.7%～13.6%,方法检出限为1～5μg/kg。结论 该方法具有快速、方便、经济、除脂效果好、环保等优点,适合肉类食品中4种磺胺类药物残留分析,并且提供了一个新的样品前处理思路。     

High,in Contrast to Low Levels of Acute Stress Induce Depressive-like Behavior by Involving Astrocytic,in Addition to Microglial P2X7 Receptors in the Rodent Hippocampus

Extracellular adenosine 5′-triphosphate (ATP) in the brain is suggested to be an etiological factor of major depressive disorder (MDD). It has been assumed that stress-released ATP stimulates P2X7 receptors (Rs) at the microglia, thereby causing neuroinflammation; however, other central nervous system (CNS) cell types such as astrocytes also possess P2X7Rs. In order to elucidate the possible involvement of the MDD-relevant hippocampal astrocytes in the development of a depressive-like state, we used various behavioral tests (tail suspension test [TST], forced swim test [FST], restraint stress, inescapable foot shock, unpredictable chronic mild stress [UCMS]), as well as fluorescence immunohistochemistry, and patch-clamp electrophysiology in wild-type (WT) and genetically manipulated rodents. The TST and FST resulted in learned helplessness manifested as a prolongation of the immobility time, while inescapable foot shock caused lower sucrose consumption as a sign of anhedonia. We confirmed the participation of P2X7Rs in the development of the depressive-like behaviors in all forms of acute (TST, FST, foot shock) and chronic stress (UCMS) in the rodent models used. Further, pharmacological agonists and antagonists acted in a different manner in rats and mice due to their diverse potencies at the respective receptor orthologs. In hippocampal slices of mice and rats, only foot shock increased the current responses to locally applied dibenzoyl-ATP (Bz-ATP) in CA1 astrocytes; in contrast, TST and restraint depressed these responses. Following stressful stimuli, immunohistochemistry demonstrated an increased co-localization of P2X7Rs with a microglial marker, but no change in co-localization with an astroglial marker. Pharmacological damage to the microglia and astroglia has proven the significance of the microglia for mediating all types of depression-like behavioral reactions, while the astroglia participated only in reactions induced by strong stressors, such as foot shock. Because, in addition to acute stressors, their chronic counterparts induce a depressive-like state in rodents via P2X7R activation, we suggest that our data may have relevance for the etiology of MDD in humans.