四种大宗常用中药饮片中黄曲霉毒素污染状况分布比较研究

目的 测定不同来源的4种大宗常用中药饮片中黄曲霉毒素（AFB₁、AFB₂、AFG₁和AFG₂）的含量，比较不同基质中药饮片中黄曲霉毒素的分布状况。方法 基于免疫亲和柱净化-高效液相色谱分离-荧光检测器（IAC-HPLC-FLD）方法，分析不同产地共75批中药样品。结果 柏子仁、薏苡仁、决明子及党参共计75批中药饮片中，阳性检出：26批柏子仁（AFs 1.22-46.67 μg·kg^-1，AFB₁ 1.22-31.40 μg·kg^-1）、4批薏苡仁（AFs 1.97-41.13 μg·kg^-1，AFB₁ 1.97-36.40 μg·kg^-1）、1批决明子（AFs 13.65 μg·kg^-1，AFB₁ 12.60 μg·kg^-1），阳性率41%，超标率15%。阳性样品经 LC-MS/MS确证，排除假阳性。4种大宗常用中药饮片柏子仁、薏苡仁、决明子、党参中黄曲霉毒素的污染水平依次降低，阳性检出率分别为77%、29%、7%、0%，表明中药材中黄曲霉毒素的污染状况与药材基质密切相关。结论 针对易污染AFs的中药品种，需进一步加强其污染状况的全面检测分析，为黄曲霉毒素的有效防控以及完善中药的质量标准提供科学依据，从而保障中药用药安全。     

Therapeutic effect of mesenchymal stem cell on Hashimoto’s thyroiditis in a rat model by modulating Th17/Treg cell balance

Abstract

The autoimmune condition Hashimoto’s thyroiditis (HT) is a disease wherein lymphocytes mediate the autoimmune damage and destruction of the thyroid gland. There are currently no effective means of treating HT, with the primary strategies of thyroid hormone therapy, surgery, or immunomodulatory therapy being associated with serious risks and side effects. There is thus a clear and urgent need to identify novel treatments for HT. In this study, we utilize female SD rats induced HT to evaluated the ability of transplanted MSCs to regulate Th17/Treg interactions in a rat Hashimoto’s thyroiditis (HT) model system. The results showed that Rats in the HT model group exhibited increased thyroid autoantibody levels consistent with successful model development, whereas these levels were lower in rats treated with MSCs. There were also fewer thyroid lesions and less lymphoid infiltration of the thyroid in MSC-treated rats relative to HT model rats, as well as fewer Th17 cells and more Treg cells – an observation consistent with the cytokine analyses. All of these showed that MSCs can regulate Th17/Treg interactions in a rat Hashimoto’s thyroiditis (HT) model system. It suggested that transplanted MSCs could be a potential immunotherapy strategy for the treatment of Hashimoto’s thyroiditis.     

SA脂质体介导GFP／bFGF基因在豚鼠耳蜗中的表达

目的 :观察天然碱性脂 (Stearylamine,SA)脂质体介导绿色荧光蛋白 /碱性成纤维细胞生长因子(GFP/bFGF)基因于不同时间段豚鼠耳蜗中的表达 ,为进一步研究耳聋的基因治疗提供实验基础。方法 :取豚鼠 1 6只 ,分成 4组 ,每组 4只。其中 3只右耳圆窗内注入SA -GFP/bFGF复合物 ,1只同法注入生理盐水作为对照。分别于术后第 2、7、1 4、2 1天取材。在荧光显微镜下观察GFP的表达 ,用免疫组化法检测bFGF的转导情况。结果 :荧光显微镜下见双侧耳蜗于术后第 2天开始部分细胞发出绿色荧光 ,第 7天达到高峰 ,支持细胞及内外毛细胞均显荧光 ,细胞轮廓清晰 ;第 1 4天开始减弱 ,第 2 1天消失。免疫组化染色显示 ,除血管纹外 ,耳蜗各回Corti器、螺旋韧带、螺旋缘及螺旋神经节细胞均有高浓度的表达产物 ,对照动物呈阴性表达。结论 :SA脂质体介导的GFP/bFGF基因单耳给药双侧耳蜗均有高效表达 ,为进一步研究基因治疗耳聋提供了可能。     

piRNA在生殖系统中的功能研究进展

piRNA（Piwi—interacting RNA）是2006年发现的一种新的小RNA，长度约24到30个核苷酸，其作用与Dicer酶无关．与Piwi蛋白家族成员相结合才能发挥作用。目前研究piRNA的功能都基本限定在生殖细胞中，近来研究表明piRNA对于生殖细胞功能的很多环节有巨大的影响，而且对生殖支持细胞的影响的研究也有了进展。本文就piRNA在生殖系统中的功能的研究进展作一综述。     

剖宫产孕妇硬膜外给局麻药的药代动力学

为了解孕妇硬膜外给局麻药的药代动力学，选择２０名实施剖宫产手术的健康临产妇，随机分成硬膜外腔给予了哌卡因组（Ｂ１组）和给予利多卡因组（Ｌ组）。另外， ６例非妊娠患者硬膜外腔给予了哌卡因（Ｂ２组）。Ｂ１和Ｂ２组均给予０．７５％丁哌卡因１～１．５ｍｇ·ｋｇ－１，Ｌ组给予２％利多卡因４～４．５ｍｇ·ｋｇ－１。采用高效液相色谱（ＨＰＬＣ）测定硬膜外给药后血浆药物浓度。结果表明三组病例血药浓度均在安全范围内。Ｂ１组的血药浓度达高峰时间（Ｔｐｅａｋ）和脐静脉与母体血药浓度比（ＵＶ／ＭＶ）值均小于Ｌ组，表明丁哌卡因在硬膜外腔的吸收比利多卡因快，且透过胎盘屏障的药量小于利多卡因，新生儿Ａｐｇａｒ评分在娩出后５分钟均为１０分。Ｂ１组的药代动力学参数与Ｂ２组基本相似。结论：剖宫产手术硬膜外腔给予临床剂量的局麻药是安全的。     

粉防己碱舒张离体新西兰白兔阴茎海绵体平滑肌的机制研究

目的观察粉防己碱(tetrandrine,Tet)对阴茎海绵体平滑肌胞内钙释放和胞外钙内流的影响,初步探讨其舒张作用的机制。方法采用离体阴茎海绵体平滑肌肌条张力记录法,观察Tet对去氧肾上腺素(phenylephrine,PE)和氯化钾(KCI)诱导收缩的肌条的影响；采用无Ca~(2 )-复Ca~(2 )实验法,观察Tet对PE诱导的依赖细胞内钙和细胞外钙的肌条收缩反应的影响。结果Tet对PE或kcl诱导的肌条收缩均具有浓度依赖性的抑制作用。100μmol/L Tet可抑制20μmol/L PE引起的依赖细胞内钙和细胞外钙的肌条收缩(P＜0．05)；结论Tet可通过阻滞电压依赖性钙通道、受体依赖性钙通道和抑制细胞内钙库释放,从而介导其对海绵体平滑肌的舒张作用。     

乌鲁木齐市家蝇抗药性现状及发展趋势分析

目的 分析乌鲁木齐市家蝇对化学杀虫剂的抗药性现状及发展趋势，探讨防制对策。方法 常规微量点滴法。结果 对溴氰菊酯的抗性系数在24．00-253．67；对敌敌畏的抗性系数在11.44-53.24;对二氯苯醚菊酯抗性系数在9.29-36.10，对氯氰菊酯的抗性系数在2.32-9.62。结论：8年来家蝇对4种杀虫剂的抗药性在不断上升，仍保持较高水平，但迅速上升的趋势开始减缓。     

二至丸对四氯化碳所致小鼠ALT升高的预防作用

目的研究二至丸水提物、女贞子、墨旱莲的保肝作用.方法通过检测血清酶学指标,观察二至丸对四氯化碳肝损伤模型的保护作用.结果用药各组均具有降低丙氨酸氨基转移酶(ALT)作用,以二至丸超声水提液和水煎液作用最强,女贞子皂甙和墨旱莲乙酸乙酯提取物的混合物可作为复方保肝降酶的有效部位,但两者不同混合比例的保肝降酶作用应作进一步研究,以寻找最佳配比,达到最佳保肝效果.结论用药各组均具有保肝降酶作用,女贞子皂甙和墨旱莲乙酸乙酯提取物的混合物可作为二至丸复方的保肝降酶的有效部位.     

PHAGAQUOSONOGRAM (PASG) DIAGNOSIS FOR CANCER OF GASTRIC CARDIA A PRELIMINARY STUDY OF 223 PATIENTS

Phagaquosonographies (PASG) of 100 normal subjects and 223 patients with cardiac cancer (CC) were analyzed. The apparatus was self-designed and self-manufactured. The wave patterns and the pre-ejection period and other 8 quantitative indices in PASG were compared and patients with CC were found to have abnormal levels (P less than 0.01). The phagaquosonograms in 82 patients with esophageal, gastric or cardias (non-cancer) diseases served as controls. The PASG showed positive results in 97.3%, suspicious in 2.3% and negative in 0.4% of CC cases and 100% negative in the normal subjects. It was 1.2% positive, 8.5% suspicious and 90.3% negative in the esophageal, cardiac or gastric non-cancer diseases. PASG has high sensitivity (97.3%), and typical characteristics (98.8%). It is shown that this method can be used in screening, diagnosis, differential diagnosis and prediction of prognosis of cardiac cancer.     

Outgrowth-regulating actions of glutamate in isolated hippocampal pyramidal neurons

The present study examined the effects of glutamate on the outgrowth of dendrites and axons in isolated hippocampal pyramidal-like neurons in cell culture. During the first day of culture the survival and outgrowth of these neurons was unaffected by high concentrations (up to 1 nM) of glutamate, quisqualic acid (QA), kainic acid (KA), and N-methyl-D-aspartic acid. Beginning on day 2 of culture high levels of glutamate, KA and QA were toxic to the majority of pyramidal neurons, while subtoxic levels of these agents caused a well-defined, dose-dependent, sequence of effects on dendritic outgrowth. At increasing concentrations of glutamate, QA, and KA, the following events were observed: (1) dendritic outgrowth rates were reduced, while axonal elongation rates were unaffected; (2) dendritic length was reduced, while axons continued to grow; (3) dendrites regressed dramatically, and axonal outgrowth rate was reduced. These dendrite-specific effects of glutamate were apparently mediated at the growth cones since focal application of glutamate to individual dendritic growth cones resulted in suppression of growth cone activity and a regression of the dendrite; axons were unaffected by focal glutamate application. Pharmacological tests using glutamate receptor agonists and antagonists demonstrated that receptors of the KA/QA type mediated the glutamate effects on outgrowth and survival. The calcium channel blocker Co2+ prevented both glutamate neurotoxicity and glutamate-induced dendritic regression. Ionophore A23187 and elevations in extracellular K+ levels each caused a dose-dependent series of outgrowth and survival responses similar to those caused by glutamate. Taken together, these results indicate that activation of glutamate receptors leads to the opening of voltage-dependent calcium channels; the resulting increases in calcium influx lead to the observed alterations in dendritic outgrowth and neuronal survival.