d-尼古丁对血管平滑肌细胞迁移的影响

为了在分子水平上揭示吸烟导致动脉粥样硬化的机制,探讨了烟草致病的主要成分d-尼古丁对豚鼠大脑基底动脉血管平滑肌细胞GbaSM-4迁移作用的影响。应用Boyden小室实验发现,d-尼古丁具有促进GbaSM-4细胞迁移的作用。免疫荧光染色显示,在d-尼古丁作用下有GbaSM-4细胞伪足内肌动蛋白表达和分布增加的现象。为了进一步阐明d-尼古丁促进平滑肌细胞迁移作用的分子机制,应用RT-PCR方法检测到在GbaSM-4细胞内有α7型烟碱乙酰胆碱受体的表达。应用烟碱乙酰胆碱受体的特异性抑制剂甲基牛扁碱和肌肉收缩的关键酶——肌球蛋白轻链激酶（myosin light chain kinase,MLCK）抑制剂ML-9作用GbaSM-4细胞后,发现d-尼古丁对GbaSM-4细胞的诱导迁移作用被明显的抑制。采用RNA干扰技术,成功地使GbaSM-4细胞内MLCK的表达水平下调,观察到d-尼古丁对GbaSM-4细胞的诱导迁移作用也被明显的抑制。上述研究结果表明,d-尼古丁以趋化因子的作用促进血管平滑肌细胞迁移,其分子机制可能与α7型烟碱乙酰胆碱受体和MLCK等因素有关,这一发现为揭示吸烟导致动脉粥样硬化提供了实验依据。     

乳腺癌组织表皮生长因子受体、细胞角蛋白5/6、上皮钙黏蛋白表达与预后的关系研究

摘要 目的：探讨乳腺癌组织表皮生长因子受体(EGFR)、细胞角蛋白5/6(CK5/6)、上皮钙黏蛋白(E-Cad)表达与预后的关系。方法：选取我院(2015年1月～2017年12月)收治的100例接受乳腺外科手术治疗的乳腺癌患者,免疫组织化学检测乳腺癌组织和癌旁组织中EGFR、CK5/6、E-Cad表达。比较乳腺癌组织与癌旁组织中EGFR、CK5/6、E-Cad的阳性表达率,分析乳腺癌组织中EGFR、CK5/6、E-Cad表达与临床病理特征的关系,Kaplan-Meier曲线分析EGFR、CK5/6、E-Cad不同表达患者的无病生存期(DFS)和总生存期(OS)曲线,多因素Cox回归分析乳腺癌预后的影响因素。结果：乳腺癌组织中EGFR、CK5/6的阳性表达率明显高于癌旁组织,E-Cad的阳性表达率明显低于癌旁组织(P＜0.05)。乳腺癌组织中EGFR、E-Cad阳性表达率与分化程度、TNM分期相关(P＜0.05),与年龄、肿瘤直径、病理类型无关(P＞0.05);CK5/6阳性表达率与年龄、肿瘤直径、分化程度、TNM分期无关(P＞0.05),与病理类型相关(P＜0.05)。Kaplan-Meier生存曲线显示,EGFR、CK5/6阳性表达患者3年DFS和OS明显低于阴性表达患者,E-Cad阳性表达患者3年DFS和OS明显高于阴性表达患者(P＜0.05)。多因素Cox回归分析显示,TNM分期Ⅲ期(HR=5.756,95%CI：1.535～21.591)、EGFR阳性(HR=8.090,95%CI：0.954～68.616)、CK5/6阳性(HR=4.507,95%CI：0.466～43.593)为乳腺癌预后独立危险因素,E-Cad阳性(HR=0.221,95%CI：0.048～1.020)为乳腺癌预后独立保护因素(P＜0.05)。结论：乳腺癌组织中EGFR、CK5/6表达明显升高,E-Cad表达明显降低,三者为乳腺癌患者预后独立影响因素。     

nAChRα1调控尼古丁促进巨噬细胞RAW264.7增殖迁移的作用研究

目的:探讨nAChRα1是否参与调节尼古丁促进巨噬细胞RAW264.7增殖迁移的作用。方法:将体外培养的RAW264.7细胞分4组为:(1)正常对照组;(2)尼古丁组;(3)对照干扰+尼古丁组;(4)nAChRα1干扰+尼古丁组。用尼古丁(5 ng/mL)刺激巨噬细胞RAW264.7,特异性nAChRα1 si RNA用脂质体3000转染细胞,CCK-8法检测尼古丁处理3 h、24 h和48 h后细胞的增殖情况,细胞划痕实验检测细胞迁移情况,Western blot和RT-PCR检测细胞内nAChRα1、MMP-2、MMP-9的蛋白和mRNA的表达情况。结果:与空白对照组相比,尼古丁可显著促进RAW264.7细胞的增殖和迁移,增加nAChRα1、MMP-2、MMP-9的蛋白和mRNA表达;而在干扰nAChRα1表达后,尼古丁诱导的RAW264.7细胞的增殖和迁移明显被抑制,且细胞nAChRα1、MMP-2、MMP-9的蛋白和mRNA表达均显著的降低。结论:nAChRα1可介导尼古丁促进RAW264.7细胞的增殖和迁移,这可能与其参与调控尼古丁增加RAW264.7细胞分泌MMP-2、MMP-9有关。     

氟对小鼠胰岛β细胞增殖和胰岛素分泌的影响

目的:观察不同剂量氟化钠(NaF)对体外培养的小鼠胰岛β细胞增殖活力和胰岛素分泌的影响。方法:选用小鼠胰岛β细胞株Beta-TC-6作为实验对象,分别以0、0.1、0.5、1.0、2.0、4.0、8.0、16.0 mg/LNa F干预24 h、48 h、72 h、96 h观察对β细胞形态学的影响,采用四唑蓝[3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide,MTT]比色法,检测不同剂量NaF对β细胞增殖活力的影响;用酶联免疫吸附(enzyme linked immunosorbent assay,ELISA)法测定不同剂量NaF对β细胞胰岛素分泌的影响。结果:0.5 mg/L、1.0 mg/L的NaF作用72 h时,可使胰岛β细胞增殖活力和胰岛素分泌较对照组明显增强(P0.05);≥8.0 mg/L时随着NaF剂量的增加和作用时间的延长,胰岛β细胞的增殖活力和胰岛素分泌明显减弱(P0.05)且随着NaF剂量的增加和时间的延长,细胞生长缓慢,数量减少,不易贴壁或融合成片,多边形细胞减少,可见较多椭圆或圆形细胞。结论:NaF对胰岛β细胞的增殖和胰岛素分泌呈剂量效应关系,随着剂量的增大和时间的延长对细胞增殖活力和胰岛素分泌能力的抑制逐渐增强。     

缓激肽受体B1R对SD大鼠阴茎勃起功能影响的实验研究

摘要 目的：研究缓激肽受体B1R对大鼠阴茎勃起功能的影响。方法：通过腹腔注射B1受体激动剂[Des-Arg⁹]-Bradykinin与B1受体抑制剂Lys-(des-Arg⁹, Leu⁸)-Bradykinin,观察各组大鼠阴茎勃起功能,通过HE染色和Masson染色观察大鼠阴茎组织形态变化及纤维化水平的变化,通过Western-blot 检测大鼠阴茎组织TGF-β1、TNF-α与IL-6等炎症因子的表达情况。结果：（1）B1受体激动剂显著抑制大鼠阴茎勃起功能,并升高阴茎胶原纤维/肌原纤维比值;而B1受体抑制剂显著提升大鼠阴茎勃起功能,并降低阴茎胶原纤维/肌原纤维比值;（2）B1受体激动剂显著升高大鼠阴茎TGF-β1、TNF-α与IL-6蛋白表达水平,而B1受体抑制剂降低大鼠阴茎TGF-β1、TNF-α与IL-6蛋白表达水平。结论：B1受体可能通过炎症因子、阴茎组织纤维化影响阴茎勃起功能。     

下丘脑腹内侧核Orexin-1及其受体对大鼠胃酸分泌的影响及其机制

目的:探讨下丘脑腹内侧核Orexin-1及其受体对大鼠胃酸分泌的影响及其机制。方法:大鼠麻醉后侧脑室及VMH置管,大鼠分组后分别VMH注射orexin-A、[Pro~(34)]-酪酪肽、[c PP1-7、NPY~(19-23)、Ala~(31)、Aib~(32)、Gln~(34)]胰多肽;腹腔注射SB-334867;皮下注射阿托品;侧脑室微量注射GR-231118、CGP-71683。给药结束后使用幽门结扎模型检测大鼠的胃酸分泌。结果:OXA能够促进胃酸分泌,且呈量效依赖关系。腹腔注射SB-334867能够抑制胃酸分泌,且呈量效依赖关系;SB-334867能够抑制orexin-A对胃酸分泌的促进作用;阿托品不但能够抑制胃酸分泌并且还能够完全阻断OXA的促胃酸分泌作用。侧脑室微量注射GR-231118或CGP-71683胃酸及胃液量减少,呈量效依赖关系,并且能够完全阻断OXA的促胃酸分泌作用。VMH内微量注射[cPP~(1-7),NPY~(19-23),Ala~(31),Aib~(32),Gln~(34)]胰多肽胃酸分泌增多,且呈量效依赖关系。结论:Orexin-A能够作用于下丘脑VMH促进胃酸分泌,orexin受体、Y1和Y5受体以及迷走神经系统均参与该过程。     

甲状腺激素受体β与肿瘤关系研究进展

甲状腺激素受体(thyroid hormone receptors,TRs)是一种配体依赖性转录因子,由TRα和TRβ基因编码。在哺乳动物中已发现多个不同的TR亚型,分别由TRα和TRβ基因由于转录起始位点的不同或选择性剪接而产生的若干同工体。近年来被越来越多的研究证实TRs除参与调控机体正常的发育和代谢平衡外,还具有对肿瘤发生的调节作用,尤其是TRβ亚型在肿瘤的发生、发展及转移等过程中发挥重要的生物学作用,表现出了明显的肿瘤抑制功能。在多种肿瘤组织中可检测到TRβ表达的降低甚至缺失。TRβ参与调控细胞内多个信号转导通路,与肿瘤的发生发展密切相关。对TRβ参与的细胞内调控机制的研究有助于在分子水平上对肿瘤的发生发展作更深入的了解,以发掘新的肿瘤治疗靶点。本文主要对TRβ与肿瘤关系的研究进展进行综述。     

死亡受体5介导细胞凋亡的研究及应用

死亡受体DR5(death receptor 5)属于肿瘤坏死因子受体(tumor necrosis factor receptor,TNFR)超家族的成员,其胞质区部分含有死亡结构域(death domain,DD),广泛分布于各种肿瘤细胞和正常组织细胞的膜上.配体TRAIL与肿瘤细胞表面的DR5结合,可诱导大多数肿瘤凋亡,而对正常的组织几乎没有作用.近年来死亡受体DR5与细胞凋亡的关系已成为研究热点之一,对DR5介导细胞凋亡的机制和应用进展作一综述.     

慢性阻塞性肺病患者巨噬细胞功能与受体表达的关系研究

目的:研究慢性阻塞性肺病(COPD)患者气道巨噬细胞功能变化及其与受体表达的相关性。方法:将COPD患者84例按病情分为轻中度组44例,重度组40例,选取同期健康体检者40例作为对照组,获取3组诱导痰,分离痰巨噬细胞,检测3组吞噬荧光标记曲霉孢子的吞噬指数(PI),采用实时定量反转录PCR法检测3组吞噬相关受体的表达。结果:轻中度组与重度组细胞总数均多于对照组,而巨噬细胞比例却显著下降(P0.05);轻中度组与重度组巨噬细胞吞噬功能均受到抑制,3组PI比较差异有统计学意义(P0.05);3组巨噬细胞胶原结构清道夫系统(MARCO)、清道夫受体A1(SR-A1)表达量比较差异不明显(P0.05);轻中度组与对照组Toll样受体4(TLR4)表达量比较差异不明显,但重度组TLR4表达上调,与轻中度组、对照组比较差异有统计学意义(P0.05);3组MUC5A、AQP5表达量比较差异显著(P0.05);巨噬细胞PI与TLR4、黏蛋白5AC(MUC5A)表达量呈负相关(P0.05),与水通道蛋白5(AQP5)表达量呈正相关(P0.05)。结论:COPD患者巨噬细胞占细胞总数的比例下降,其吞噬功能也受到抑制,其机制可能与TLR4、MUC5A表达上调及AQP5表达下调等有关。     

Micro-CT监测尼古丁对大鼠正畸牙移动过程中牙周改建的影响

目的:探讨不同摄取量的尼古丁对大鼠正畸过程牙周改建的影响。方法:选择120只雄性Wistar大鼠并将其随机分为四组:A组-空白对照,B组-正畸模型,C组-正畸并0.01 mg/m L尼古丁给药,D组-正畸并1 mg/m L尼古丁给药。分别于实验开始后第1、3、7、14、21天通过Micro-CT和HE染色观察模型牙齿移动距离和牙周组织改变并通过ELISA实验检测IL-17的表达。结果:Micro-CT扫描显示:正畸建模组相对于空白对照组在牙移动距离、骨体积分数、骨密度等指标均有明显变化,变化最大幅度发生在D组,B、C两组之间的差异没有统计学意义(P0.05)。21天,D组移动距离达到0.80±0.06 mm,明显高于B、C组(P0.05)。相较于空白对照组(A组),B、C、D三组Micro-CT测量的骨体积分数、骨密度、骨小梁厚度均降低,D组骨密度值降至1108.36±8.86mg/cm3。HE染色结果显示:D组在21天时破骨细胞增多并出现牙根吸收陷窝伴牙周膜纤维排列混乱;ELISA检测显示B、C组IL-17的含量在第7天时达到峰值,D组则在14天含量最高。结论:高浓度的尼古丁可加速正畸牙齿的移动速度及牙槽骨吸收,增加牙周组织中的破骨细胞及IL-17表达水平。     

CHRNA5 variants moderate the effect of nicotine deprivation on a neural index of cognitive control

Individuals with reduced attention and memory cognitive control‐related processes may be motivated to smoke as a result of the cognitive enhancing effects of nicotine. Further, nicotine deprivation‐induced reductions in cognitive control may negatively reinforce smoking. Minor allele carriers at rs16969968 in the nicotinic acetylcholine receptor α5 subunit gene (CHRNA5) have been shown to exhibit both reduced cognitive control and greater nicotine dependence. It is therefore of interest to see if variants in this gene moderate the influence of nicotine deprivation on cognitive control. P3b and P3a components of the event‐related brain potential waveform evoked by a three‐stimulus visual oddball task are widely viewed as positive indices of cognitive control‐related processes. We tested the hypothesis that individuals possessing at least one minor allele at rs16969968 in CHRNA5 would show greater nicotine deprivation‐induced reductions in P3b and P3a amplitude. The sample included 72 non‐Hispanic, Caucasian heavy smokers (54 men and 18 women) with a mean age of 36.11 years (SD = 11.57). Participants completed the visual oddball task during counterbalanced nicotine and placebo smoking sessions. Findings indicated that rs16969968 status did not moderate nicotine effects on P3b or P3a, whereas variation in other CHRNA5 polymorphisms, which are not as well characterized and are not in linkage disequilibrium with rs16969968, predicted nicotine deprivation‐induced reduction of P3a amplitude: rs588765 (F_1,68 = 7.74, P = 0.007) and rs17408276 (F_1,67 = 7.34, P = 0.009). Findings are interpreted in the context of vulnerability alleles that may predict nicotine effects on cognitive control.     

急性胰腺炎伴脾脏密度减低的研究现状

急性胰腺炎是临床上较常见的急腹症,以急性上腹痛和血尿淀粉酶或脂肪酶升高为其主要的临床特点,急性胰腺炎除了对胰腺自身组织的产生损伤外,对胰腺外器官也会产生不同的损伤,并引起一系列的并发症。在急性胰腺炎的脾脏并发症中,脾梗死在CT图像中表现为脾脏密度不均匀性减低,除此之外脾脏实质的密度在CT图像中是相对比较固定的,但是在有些急性胰腺炎患者的CT图像中会出现脾脏密度一过性弥漫性减低的影像表现,治疗后复查CT显示脾脏密度恢复正常,该现象的形成原因尚不清楚,国内外有关该现象的文献报道及研究十分的有限,本文通过分析急性胰腺炎的病因及发病机制,回顾相关的文献病例,探讨急性胰腺炎伴脾脏密度一过性弥漫性减低产生的可能性原因。     

线粒体DNA4977bp大片缺失突变与喉癌的相关性研究

目的:探讨线粒体DNA4977bp大片缺失突变与喉癌的相关性。方法:选择2016年1月～2017年6月我院收治的喉乳头状瘤、喉癌患者,分别纳入良性肿瘤组、恶性肿瘤组,每组各150例。取两组患者的病变组织标本,分离癌及癌旁组织,提取总DNA,采用PCR扩增测序技术检测两组标本中线粒体DNA4977bp大片缺失突变情况。结果:基因测序结果显示恶性肿瘤组患者的线粒体DNA4977bp缺失突变率为39.33%,高于良性肿瘤组患者的1.33%,差异具有统计学意义(P0.05)。不同肿瘤分期患者的线粒体DNA4977bp缺失突变率比较,差异具有统计学意义(P0.05),且III期患者的突变率II期 I期 IV期;淋巴结转移患者的线粒体DNA4977bp缺失突变率高于淋巴结未转移患者差异具有统计学意义(P0.05)。结论:线粒体DNA4977bp大片缺失突变与喉癌的发生有关,可能促进的发生和进展。     

Effects of a neonicotinoid pesticide on thermoregulation of African honey bees (Apis mellifera scutellata)

Thiamethoxam is a widely used neonicotinoid pesticide that, as agonist of the nicotinic acetylcholine receptors, has been shown to elicit a variety of sublethal effects in honey bees. However, information concerning neonicotinoid effects on honey bee thermoregulation is lacking. Thermoregulation is an essential ability for the honey bee that guarantees the success of foraging and many in-hive tasks, especially brood rearing. We tested the effects of acute exposure to thiamethoxam (0.2, 1, 2 ng/bee) on the thorax temperatures of foragers exposed to low (22 °C) and high (33 °C) temperature environments. Thiamethoxam significantly altered honey bee thorax temperature at all doses tested; the effects elicited varied depending on the environmental temperature and pesticide dose to which individuals were exposed. When bees were exposed to the high temperature environment, the high dose of thiamethoxam increased their thorax temperature 1–2 h after exposure. When bees were exposed to the low temperature, the higher doses of the neonicotinoid reduced bee thorax temperatures 60–90 min after treatment. In both experiments, the neonicotinoid decreased the temperature of bees the day following the exposure. After a cold shock (5 min at 4 °C), the two higher doses elicited a decrease of the thorax temperature, while the lower dose caused an increase, compared to the control. These alterations in thermoregulation caused by thiamethoxam may affect bee foraging activity and a variety of in-hive tasks, likely leading to negative consequences at the colony level. Our results shed light on sublethal effect of pesticides which our bees have to deal with.     

Characterization of the human nicotinic acetylcholine receptor subunit alpha (alpha) 9 (CHRNA9) and alpha (alpha) 10 (CHRNA10) in lymphocytes

Though the nicotinic acetylcholine receptor (nAChR) subunits alpha9 and alpha 10 have been thoroughly characterized within hair cells of the organ of Corti in the inner ear, prior studies have shown that they are also expressed in lymphocytes. In this report, we sought to more definitively characterize the nAChR subunits alpha9 and alpha10 within various populations of human lymphocytes. Using a combination of techniques, including RT-PCR, single-cell RT-PCR, Northern and western blot analysis, and immunofluorescence, expression of both alpha9 and alpha 10 was demonstrated in purified populations of T-cells (CD3+, CD4+, CD8+ and the Jurkat, MT2 and CEM T-cell lines) and B-cells (CD19+, CD80+ and EBV-immortalized B-cells). Single-lymphocyte recording techniques failed to identify an ionic current in response to applied acetylcholine in either T-cells or B-cells. These results clearly demonstrate the presence of these nicotinic receptor subunits within several populations of human lymphocytes, implicating their role in the immune response. However, a lack of demonstrated response to applied acetylcholine using standard single-cell recording techniques suggests a physiology different than that seen in hair cells of the inner ear.     

IPPA08 allosterically enhances the action of imidacloprid on nicotinic acetylcholine receptors

Our previous study showed that IPPA08, a cis-configuration neonicotinoid compound with unique oxabridged substructure, acted as a specific synergist to neonicotinoid insecticides targeting nicotinic acetylcholine receptors (nAChRs). Heteropentamer nAChRs have diverse characteristics and can form canonical and noncanonical subunit interfaces. While canonical interfaces have been exploited as targets of many drugs, noncanonical interfaces have received less attention. In this study, the mechanism of IPPA08 synergism was evaluated on hybrid nAChRs consisting of three α1 subunits from the brown planthopper and two rat β1 subunits (Nlα1/rβ2) expressed in Xenopus oocytes. IPPA08 alone evoked inward currents, but only at very high concentrations, greater than 1 mM. However, at concentrations below 200 μM, IPPA08 slowed the decay of inward currents evoked by imidacloprid, but not by acetylcholine, and also increased the sensitivity of Nlα1/rβ2 to imidacloprid. Both modulations by IPPA08 were concentration-dependent in the same concentration range of 10–150 μM. Experimentally induced mutations in canonical (α+/β−) and noncanonical (β+/α−) interfaces of Nlα1/rβ2 receptors were also examined to evaluate the presence of possible binding sites for IPPA08 on the receptors. Our results showed that mutations in the canonical interfaces affected only the potency of IPPA08 as an agonist, while mutations in the noncanonical interfaces affected only the synergistic action of IPPA08. Based on these results, we propose that at low concentrations IPPA08 can act as a positive allosteric modulator of noncanonical interfaces, and likely slow the decay of currents through stabilizing the open-channel state caused by the action of imidacloprid on canonical interfaces.     

Actions of snake neurotoxins on an insect nicotinic cholinergic synapse

Here we examine the actions of six snake neurotoxins (α-cobratoxin from Naja naja siamensis, erabutoxin-a and b from Laticauda semifasciata; CM12 from N. haje annulifera, toxin III 4 from Notechis scutatus and a long toxin from N. haje) on nicotinic acetylcholine receptors in the cercal afferent, giant interneurone 2 synapse of the cockroach, Periplaneta americana. All toxins tested reduced responses to directly-applied ACh as well as EPSPs evoked by electrical stimulation of nerve XI with similar time courses, suggesting that their action is postsynaptic. Thus, these nicotinic receptors in a well-characterized insect synapse are senstive to both long and short chain neurotoxins. This considerably expands the range of snake toxins that block insect nicotinic acetylcholine receptors and may enable further pharmacological distinctions between nAChR subtypes.     

5-Aza-C 对鼻咽癌细胞端粒长度及细胞增殖的影响

目的：研究去甲基化药物5-氮杂胞嘧啶核苷（5-Azacytidine,5-Aza-C）对鼻咽癌细胞端粒长度及细胞生长增殖的影响。方法： 常规培养鼻咽癌CNE,CNE1,CNE2 及5-8F细胞系,5-Aza-C 处理鼻咽癌细胞后,甲基化测序聚合酶链反应(MSP)法检测亚端粒 区D4Z4 甲基化,端粒限制性片断检测端粒长度,CCK-8 检测细胞增殖。结果：2.5 uM浓度的5-Aza-C处理后,亚端粒区D4Z4 序 列的甲基化水平明显下降,约在15-20%之间,与处理前的甲基化水平（35-48%）有明显差异,差异均有统计学意义（P < 0.05)。在1 uM和2.5 uM浓度的5-Aza-C 处理后,四种细胞的端粒长度明显缩短,长度在2-4.5kb 之间,差异具有统计学意义(P < 0.05)。5uM 的5-Aza-C处理72 h 后,CNE,CNE1,CNE2 和5-8F 的生存率分别为51.27%,50.46%,48.85%,48.83%,10 uM 的5-azaC 处理72 h 后,CNE,CNE1,CNE2 和5-8F的生存率分别为31.64%,32.34%,30.01%,32.10%,与对照组比较差异有统计学意义（P<0.01）。结 论：5-Aza-C 能缩短端粒长度,抑制鼻咽癌细胞生长增殖活性。     

Effects of Nucleus Basalis Lesions on the Muscarinic and Nicotinic Modulation of [3H] Acetylcholine Release in the Rat Cerebral Cortex

Presynaptic muscarinic and nicotinic receptors in the cerebral cortex reportedly inhibit and increase acetylcholine (ACh) release, respectively. In this study, we investigated whether these receptors reside on cholinergic nerve terminals projecting to the cerebral cortex from the nucleus basalis magnocellularis (nbm). Adult male rats received unilateral infusions of ibotenic acid (5 micrograms/1 microliter) in the nbm. Two weeks later, cerebral cortical cholinergic markers (choline acetyltransferase activity, high-affinity choline uptake, and coupled ACh synthesis) were significantly reduced in synaptosomes prepared from the lesioned hemispheres compared to contralateral controls. The depolarization-induced release of [3H]ACh from these synaptosomes was also reduced in the lesioned hemispheres, reflecting the reduced synthesis of transmitter. However, the nbm lesions had no effect on the inhibition of release induced by 100 microM oxotremorine. Synaptosomal [3H]ACh release was not altered by nicotine or the nicotinic agonists anabaseine and 2-(3-pyridyl)-1,4,5,6-tetrahydropyrimidine. Nicotine (10-100 microM) did increase [3H]ACh release in control and lesioned hemispheres in cortical minces, but to a similar extent. These results suggest that neither muscarinic nor nicotinic receptors modulating ACh release reside on nbm-cholinergic terminals.     

雌激素和孕激素受体在粉刺性乳痈的表达及意义

目的:探讨粉刺性乳痈患者雌激素受体(ER)、孕激素受体(PR)的表达及临床意义。方法:选择我院2017年1月～2018年12月收治的80例粉刺性乳痈患者,采用免疫组化法检测其乳腺病变组织ER、PR的表达,酶联免疫吸附法(ELISA)检测血清白介素-1β(interleukin-1β, IL-1β)、IL-6及肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)水平,分析乳腺病变组织ER、PR的表达与血清IL-1β、IL-6、TNF-α水平的相关性。结果:与普通乳腺炎组、乳腺导管扩张组比较,肉芽肿组、脓肿组血清IL-1β、IL-6、TNF-α水平明显升高,与肉芽肿组比较,脓肿组血清IL-1β、IL-6、TNF-α水平亦明显升高(P0.05)。普通乳腺炎组、乳腺导管扩张组血清IL-1β、IL-6、TNF-α水平比较差异无统计学意义(P0.05)。普通乳腺炎组、乳腺导管扩张组、肉芽肿组、脓肿组ER、PR的表达水平依次降低(P0.05)。普通乳腺炎组、乳腺导管扩张组ER、PR的表达与血清IL-1β、IL-6水平均呈显著负相关,而与血清TNF-α水平无显著相关性(P0.05);肉芽肿组、脓肿组ER、PR表达与血清IL-1β、IL-6、TNF-α水平均呈显著负相关(P0.05)。结论:粉刺性乳痈患者ER、PR呈低表达或失表达,且与炎症因子及病情严重程度具有良好相关性。