Effects of Tiaomaiyin and Its Disassembled Prescription on Expression of L-type Calcium Channel β2 Subunit in Rat Model of Tachyarrhythmia

[Objectives] To study the effects of Tiaomaiyin and its disassembled prescription on expression of L-type calcium channel β2 subunit in rat model of tachyarrhythmia. [Methods] Sixty Wistar rats were randomly divided into model group,Tiaomaiyin prescription group( whole prescription group),main efficacy group of removing heat to cool blood( blood cooling group),and auxiliary drug efficacy group of benefiting qi and nourishing heart( qi benefiting group),auxiliary efficacy group of promoting flow of qi and blood circulation( qi flow promoting group),and amiodarone group( western medicine group). Aconitine was given 7 d after the intragastric administration of the corresponding drugs,and the time of occurrence of arrhythmia in each group was observed. The left ventricular myocardium was subjected to reverse transcription-polymerase chain reaction and Western blotting. [Results] The ventricular premature beats( VPB) time in the whole prescription group and western medicine group was significantly longer than that in the model group. Ventricular tachycardia( VT),ventricular fibrillation( VF),and cardiac arrest( CA) were longer in the whole prescription group,blood cooling group,and western medicine group. The mRNA and protein expression of L-type calcium channel β2 subunit in the whole prescription group,blood cooling group and western medicine group were significantly decreased. [Conclusions] Tiaomaiyin whole prescription group and blood cooling group can reduce the occurrence time of tachyarrhythmia and reduce the expression of LTCC β2 in myocardium.

Antiepileptic Drug-Induced Apoptosis Was Prevented by L-Type Calcium Channel Activator in Cultured Rat Cortical Cells

Experimental data have shown that antiepileptic drugs cause neurodegeneration in developing rats. Valproate (VPA) is the drug of choice in primary generalized epilepsies, and carbamazepine (CBZ) is one of the most prescribed drugs in partial seizures. These drugs block sodium channels, thereby reducing sustained repetitive neuronal firing. The intracellular mechanisms whereby AEDs induce neuronal cell death are unclear. We examined whether AEDs induce apoptotic cell death in cultured cortical cells and whether calcium ions are involved in the AED-induced cell death. VPA and CBZ increased apoptotic cell death and induced morphological changes that were characterized by cell shrinkage and nuclear condensation or fragmentation. Incubation of cortical cultures with VPA or CBZ decreased phospho-Akt levels. CBZ decreased the intracellular calcium levels. On the other hand, FPL64176, an L-type calcium channel activator, increased the intracellular calcium levels and prevented the AED-induced apoptosis. Glycogen synthase kinase-3 inhibitors, such as alsterpaullone and azakenpaullone, prevented the AED-induced apoptosis. These results suggest that intracellular calcium level changes are associated with AEDs and apoptosis and that the activation of glycogen synthase kinase-3 is involved in the death of rat cortical neurons.

The Effect of Extrogenous Phosphocreatine on L-type Calcium Current in Ischemic Guinea Pig Ventricular Myocytes

Objectives Heart failure （HF） is one of the most common outcome for all kinds of heart diseases, the effects of energetic therapy on HF remains controversial, especially to ischemic HF. The aim of this study was to explore the effect of exogenous phosphocreatine with different concentration on L-type calcium（I Cc-L） current in ischemic ventricular myocytes of guinea pig and to investigate its underlying electrophysiological mechanism for the treatment of ischemic HF. Methods Single ventricular myocytes were isolated enzymatically from left ventricle of guinea pig. Peak I Ca-L current were recorded using patch clamp techniques in the whole-cell configuration when myocytes had been superfused with normal Tyrode solution, simple ischemic solution, ischemic solution containing phosphocreatine with different concentration for 10 minutes respectively. Results Peak I Ca-L current density of myocytes superfused with simple simulated ischemic solution was remarkably inhibited by 80.6 ± 5.2% compared with myocytes superfused with normal Tyrode solution（P〈0.05）. Ischemic solution containing phosphocreatine of 5, 10, 20, 30mmol/L inhibited Peak I Ca-L current density by （53.8±6.7）%, （41.8 ± 8.2）%, （38.1±7.4）%, （36.6±9.7）% respectively. There was no statistical significance among phosphocreation of 10, 20, 30 mmol / L. Conclusions Extrogenous phosphocreatine could reverse the inhibition of I Ca-L current under ischemic condition, which could be the ionic basis for the treatment of ischemic heart failure. 0-10 mmol/L phosphocreatine exerted significant dose-effect relationship which no longer existed as concentration more than 10 mmol/L. It is supposed that phosphocreatine increased I Ca-L current by many pathways rather than simple substrate for ATP synthesis.

Experimental Study on Hydrodynamics of L-type Podded Propulsor in Straight-ahead Motion and Off-Design Conditions

试验性的测试被进行评估 L 类型 podded propulsor 的水动力学性能在直向前，用一台开水的测量仪器的运动和离开设计条件为 podded propulsors 由作者发展了，拖引坦克的一个轮船模型，并且在水粒子图象 velocimetry (PIV ) 下面测量系统。在条件的三种类型下面， L 类型 podded propulsor 的主要参数被测量，包括推进器戳和转矩，以及整个豆荚单位的戳，方面力量，和时刻。另外，在推进器和神气之间的节上的流动领域被分析。试验性的结果证明动态 azimuthing 率和方向和转弯的方向在推进器和整个豆荚单位上影响力量。因为推进器旋转的效果，力量不均匀地在左、正确的 azimuthing 方向之间被散布。这研究的调查结果为关于 L 类型 podded propulsors 的进一步的研究提供一个基础。

Ferulic acid enhances insulin secretion by potentiating L-type Ca^(2+)channel activation

Objective To investigate the effect of ferulic acid,a natural compound,on pancreatic beta cell viability,Ca^(2+)channels,and insulin secretion.Methods We studied the effects of ferulic acid on rat insulinoma cell line viability using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide viability assay.The whole-cell patch-clamp technique and enzyme-linked immunosorbent assay were also used to examine the action of ferulic acid on Ca^(2+)channels and insulin secretion,respectively.Results Ferulic acid did not affect cell viability during exposures up to 72 h.The electrophysiological study demonstrated that ferulic acid rapidly and concentration-dependently increased L-type Ca^(2+)channel current,shifting its activation curve in the hyperpolarizing direction with a decreased slope factor,while the voltage dependence of inactivation was not affected.On the other hand,ferulic acid have no effect on T-type Ca^(2+)channels.Furthermore,ferulic acid significantly increased insulin secretion,an effect inhibited by nifedipine and Ca^(2+)-free extracellular fluid,confirming that ferulic acid-induced insulin secretion in these cells was mediated by augmenting Ca^(2+)influx through L-type Ca^(2+)channel.Our data also suggest that this may be a direct,nongenomic action.Conclusion This is the first electrophysiological demonstration that acute ferulic acid treatment could increase L-type Ca^(2+)channel current in pancreaticβcells by enhancing its voltage dependence of activation,leading to insulin secretion.

Amlodipine inhibits the proliferation and migration of esophageal carcinoma cells through the induction of endoplasmic reticulum stress

BACKGROUND L-type calcium channels are the only protein channels sensitive to calcium channel blockers,and are expressed in various cancer types.The Cancer Genome Atlas database shows that the mRNA levels of multiple L-type calcium channel subunits in esophageal squamous cell carcinoma tumor tissue are significantly higher than those in normal esophageal epithelial tissue.Therefore,we hypothesized that amlodipine,a long-acting dihydropyridine L-type calcium channel blocker,may inhibit the occurrence and development of esophageal cancer(EC).AIM To investigate the inhibitory effects of amlodipine on EC through endoplasmic reticulum(ER)stress.METHODS Cav1.3 protein expression levels in 50 pairs of EC tissues and corresponding paracancerous tissues were examined.Subsequently,the inhibitory effects of amlodipine on proliferation and migration of EC cells in vitro were detected using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide and Transwell assays.In vivo experiments were performed using murine xenograft model.To elucidate the underlying mechanisms,in vitro cell studies were performed to confirm that ER stress plays a role in inhibition proliferation and migration of EC cells treated with amlodipine.RESULTS The expression level of Cav1.3 in esophageal carcinoma was 1.6 times higher than that in paracancerous tissues.Amlodipine treatment decreased the viability of esophageal carcinoma cells in a dose-and time-dependent manner.In vivo animal experiments also clearly indicated that amlodipine inhibited the growth of EC tumors in mice.Additionally,amlodipine reduces the migration of tumor cells by inhibiting epithelial-mesenchymal transition(EMT).Mechanistic studies have demonstrated that amlodipine induces ER stress-mediated apoptosis and suppresses EMT.Moreover,amlodipine-induced autophagy was characterized by an increase in autophagy lysosomes and the accumulation of light chain 3B protein.The combination of amlodipine with the ER stress inhibitor 4-phenylbutyric acid further confirmed the role of the ER stress response in amlodipine-induced apoptosis,EMT,and autophagy.Furthermore,blocking autophagy increases the ratio of apoptosis and migration.CONCLUSION Collectively,we demonstrate for the first time that amlodipine promotes apoptosis,induces autophagy,and inhibits migration through ER stress,thereby exerting anti-tumor effects in EC.

Sevoflurane postconditioning alleviates action potential duration shortening and L-type calcium current suppression induced by ischemia/reperfusion injury in rat epicardial myocytes

Background It has been proved that sevoflurane postconditioning （SpostC） could protect the heart against myocardial ischemia/reperfusion injury, however, there has been few research focused on the electrophysiological effects of SpostC. The objective of the study was to investigate the effects of SpostC on action potential duration （APD） and L-type calcium current （Ica, L） in isolated cardiomyocytes. Methods Langendorff perfused SD rat hearts were randomly assigned to one of the time control （TC）, ischemia/reperfusion （I/R, 25 minutes of ischemia followed by 30 minutes of reperfusion）, and SpostC （postconditioned with 3% sevoflurane） groups. At the end of reperfusion, epicardial myocytes were dissociated enzymatically for patch clamp studies. Results Sevoflurane directly prolonged APD and decreased peak Ica, L densities in epicardial myocytes of the TC group （P〈0.05）. I/R injury shortened APD and decreased peak Ica, L densities in epicardial myocytes of the I/R group （P〈0.05）. SpostC prolonged APD and increased peak Ica, L densities in epicardial myocytes exposed to I/R injury （P〈0.05）. SpostC decreased intracellular reactive oxygen species （ROS） levels, reduced the incidence of ventricular tachycardia and ventricular fibrillation, and decreased reperfusion arrhythmia scores compared with the I/R group （all P〈0.05）. Conclusions SpostC attenuates APD shortening and Ica, L suppression induced by I/R injury. The regulation of APD and lea, L by SpostC might be related with intracellular ROS modulation, which contributes to the alleviation of reperfusion ventricular arrhvthmia.

48份水稻骨干材料香味及Badh2变异类型的鉴定

为促进香稻育种,明确水稻重要种质资源中香味基因的存在情况,本研究将传统香味鉴定方法(KOH浸泡法)与分子标记技术相结合,对48份水稻骨干材料的香味及香味基因Badh2变异类型进行鉴定。结果表明,在48份供试材料中,利用KOH浸泡法检测到具有香味的材料有44份;利用香味基因Badh2的7种等位基因变异类型功能标记检测到含有香味的材料有43份,其中,有41份为纯合香型,2份为杂合型,等位基因Badh2-E2的变异类型有37份,等位基因Badh2-E7的变异类型有6份,未检测到等位基因Badh2-E4-5、Badh2-E12、Badh2-E13、Badh2-UTR和Badh2-Pro的变异类型。通过比较KOH浸泡法与分子标记技术,发现仅有1份材料检测结果不同,明水香稻(X23)用KOH浸泡法检测出具有香味,但本研究所用的Badh2的7种等位基因变异类型功能标记却未检测出含有香味,说明该材料可能属于Badh2其他已报道的或新的等位基因变异类型,也可能是含有新的香味基因。

PA1b, a plant peptide, induces intracellular [Ca^(2+)] in- crease via Ca^(2+) influx through the L-type Ca^(2+) channel and triggers secretion in pancreatic β cells

Using alginic acid to adsorb polypeptides at pH 2.7, we isolated a peptide pea albumin 1b (PA1b) from pea seeds. The PA1b is a single chain peptide consisting of 37 amino acid residues with 6 cysteines which constitutes the cystine-knot structure. Using microfluorometry and patch clamp techniques, we found that PA1b significantly elevated the intracellular calcium level ([Ca2+ ]i) and elicited membrane capacitance increase in the primary rat pancreatic β cells. The PA1b effect on [Ca2+]i elevation was abolished in the absence of extracellular Ca2+ or in the presence of L-type Ca2+ channel blocker, ni- modipine. Interestingly, we found that PA1b significantly depolarized membrane potential, which could lead to the opening of voltage-dependent L-type Ca2+ channels and influx of extracellular Ca2+, and then evoke robust secretion. In this study we identified the plant peptide PA1b which is capable of affecting the excitability and function of mammalian pancreatic β cell.

L-type Calcium Channels are Involved in Iron-induced Neurotoxicity in Primary Cultured Ventral Mesencephalon Neurons of Rats

In the present study,we investigated the mechanisms underlying the mediation of iron transport by Ltype Ca^2+ channels(LTCCs)in primary cultured ventral mesencephalon(VM)neurons from rats.We found that cotreatment with 100 lmol/L FeSO4 and MPP^+(1-methyl-4-phenylpyridinium)significantly increased the production of intracellular reactive oxygen species,decreased the mitochondrial transmembrane potential and increased the caspase-3 activation compared to MPP^+ treatment alone.Co-treatment with 500 lmol/L CaCl2 further aggravated the FeSO4-induced neurotoxicity in MPP^+-treated VM neurons.Co-treatment with 10 lmol/L isradipine,an LTCC blocker,alleviated the neurotoxicity induced by co-application of FeSO4 and FeSO4/CaCl2.Further studies indicated that MPP^+treatment accelerated the iron influx into VM neurons.In addition,FeSO4 treatment significantly increased the intracellular Ca^2+ concentration.These effects were blocked by isradipine.These results suggest that elevated extracellular Ca^2+ aggravates ironinduced neurotoxicity.LTCCs mediate iron transport in dopaminergic neurons and this,in turn,results in elevated intracellular Ca^2+ and further aggravates iron-induced neurotoxicity.

Endothelin-1 induces intracellular [Ca^(2+)] increase via Ca^(2+) influx through the L-type Ca^(2+) channel, Ca^(2+)-induced Ca^(2+) release and a pathway involving ET_A receptors, PKC, PKA and AT1 receptors in cardiomyocytes

Using fura-2-acetoxymethyl ester (AM) fluorescence imaging and patch clamp techniques, we found that endothelin-1 (ET-1) significantly elevated the intracellular calcium level ([Ca2+]i) in a dose-dependent manner and activated the L-type Ca2+ channel in cardiomyocytes isolated from rats. The effect of ET-1 on [Ca2+]i elevation was abolished in the presence of the ETA receptor blocker BQ123, but was not affected by the ETB receptor blocker BQ788. ET-1-induced an increase in [Ca2+]i, which was inhibited 46.7% by pretreatment with a high concentration of ryanodine (10 μmol/L), a blocker of the ryanodine receptor. The ET-1-induced [Ca2+]i increase was also inhibited by the inhibitors of protein kinase A (PKA), protein kinase C (PKC) and angiotensin type 1 receptor (AT1 receptor). We found that ET-1 induced an enhancement of the amplitude of the whole cell L-type Ca2+ channel current and an increase of open-state probability (NPo) of an L-type single Ca2+ channel. BQ123 completely blocked the ET-1-induced increase in calcium channel open-state probability. In this study we demonstrated that ET-1 regulates calcium overload through a series of mechanisms that include L-type Ca2+ channel activation and Ca2+-induced Ca2+ release (CICR). ETA receptors, PKC, PKA and AT1 receptors may also contribute to this pathway.

煤层气L型水平井防窜气排采控制方法研究

煤层气采用L型水平井开发,可使单井稳产气量达到8000m^(3)/d以上,但由于L型水平井无沉砂口袋,无法靠重力实现气、水自然分离,易发生油管窜气,导致泵效大幅下降,制约进一步排水降压。前期通过优化排采举升工艺,油管窜气现象得到了一定缓解,但对低流压产气井和高流压产气井的治理效果仍然不理想。以沁水盆地樊庄-郑庄区块L型水平井为例,通过研究分析56口发生油管窜气井的气、水变化规律,建立了窜气严重程度评价指标,利用灰色关联度法找出影响油管窜气的主控因素,明确产生油管窜气的原因,并在优化排采制度方面提出了2种防治油管窜气的方法。结果表明:井筒环空的液柱高度是引发油管窜气的先决条件,油管窜气随液柱高度降低突然发生,当液柱高度大于75m时,出水口不窜气或以轻、中度窜气为主;当液柱高度小于75m时,以重度窜气为主,且发生窜气后其窜气程度随液柱高度的降低呈指数增大。气液比是影响窜气程度大小的关键因素,且窜气程度随气液比的增大呈对数增大,当气液比小于30时,以轻度和中度窜气为主,当气液比大于30时,以重度窜气为主。通过控制恒定高套压,采取“控压排水”法,可有效提高泵吸入口附近两相流的持液率;通过控制日产气量,采取“控产排水”法,将泵吸入口附近的气液比降低至30以下,可有效降低油管窜气程度。在此基础上,结合防窜气排采举升工艺,最终实现油管窜气的标本兼治。

L型氨基酸转运蛋白1的表达对非霍奇金淋巴瘤临床病理特征和预后的影响

目的:检测非霍奇金淋巴瘤(NHL)组织中L型氨基酸转运蛋白1(LAT1)的表达,分析LAT1对患者临床病理特征和预后的影响。方法:收集2017年1月至2019年4月在本院接受治疗的NHL患者92例,免疫组织化学检测NHL组织中LAT1的表达,比较不同病理特征(包括性别、Ann Arbor分期、结外浸润、Ki-67)患者组间LAT1的表达差异,单因素和多因素Cox回归分析影响患者死亡的危险因素,受试者工作曲线(ROC)检测NHL组织中LAT1阳性细胞百分比对患者死亡的预测价值,分析LAT1阳性细胞百分比对患者生存率的影响。结果:LAT1在NHL组织中呈阳性表达,Ann Arbor分期III期和IV期组LAT1高表达率高于I期组,结外浸润组LAT1高表达率高于无结外浸润组,Ki-67阳性表达组LAT1高表达率高于阴性表达组,比较差异均有统计学意义(均P<0.05)。LAT1高表达组治疗3个疗程后的缓解率为70.7%,低于低表达组的91.2%,比较差异有统计学意义(P<0.05)。Ann Arbor分期III期、IV期、结外浸润、Ki-67阳性表达和LAT1表达增加(即LAT1阳性细胞比例评分≥2)为患者死亡的危险因素。LAT1阳性细胞百分比预测NHL死亡的截断值为45.6%,曲线下面积为0.905(95%CI:0.897-0.924)。LAT1高水平组(LAT1阳性细胞百分比≥45.6%)3年生存率为50.00%,低于LAT1低水平组的78.26%(P<0.05)。结论:LAT1在NHL组织中表达水平增加,影响患者的肿瘤分期和结外浸润,是患者死亡的危险因素。

大果木姜子油调控miR-328基因抗心律失常H9c2细胞的机制研究

目的:探讨大果木姜子油通过调控miR-328基因抗心律失常H9c2细胞的可能机制。方法:慢病毒转染构建miR-328过表达H9c2细胞株,再运用生物机能实验系统构建H9c2细胞和miR-328过表达H9c2细胞心律失常模型。将H9c2细胞分为正常对照组、模型组、大果木姜子油组、miR-328过表达组和miR-328过表达+大果木姜子油组。根据分组条件培养结束后,qPCR检测H9c2细胞中miR-328相对表达量;ELISA检测炎性因子IL-1β、IL-6、TGF-β含量;比色法检测SOD活性和MDA浓度;DCFH荧光探针检测ROS水平;流式细胞术检测细胞凋亡率;Western Blot检测H9c2细胞L型钙通道相关蛋白表达。结果:成功构建H9c2细胞和miR-328过表达H9c2细胞心律失常模型。与正常对照组比较,模型组和miR-328过表达组细胞TGF-β、SOD活性及CaM、CaMKⅡ、p-CaMKⅡ蛋白表达显著降低,细胞凋亡率、miR-328及CaV1.2蛋白表达和IL-1β、IL-6、MDA、ROS水平显著升高(P<0.01)。经大果木姜子油干预后,心律失常模型细胞形态改善,上述指标均被显著逆转(P<0.01)。结论:大果木姜子油可改善心律失常H9c2细胞,其作用机制可能与调控miR-328基因降低炎症因子水平、调节氧化应激、抑制细胞凋亡及调节L型钙通道相关蛋白表达有关。

Contribution of spontaneous L-type Ca^(2+) channel activation to the genesis of Ca^(2+) sparks in resting cardiac myocytes

Ca2+ sparks are the elementary events of intracellular Ca2+ release from the sarcoplasmic reticulum in cardiac myocytes. In order to investigate whether spontaneous L-type Ca2+ channel activation contributes to the genesis of spontaneous Ca2+ sparks, we used confocal laser scanning microscopy and fluo-4 to visualize local Ca2+ sparks in intact rat ventricular myocytes. In the presence of 0.2 mmol/L CdCl2 which inhibits spontaneous L-type Ca2+ channel activation, the rate of occurrence of spontaneous Ca2+ sparks was halved from 4.20 to 2.04 events/(100 μm·s), with temporal and spatial properties of individual Ca2+ sparks unchanged. Analysis of the Cd2+-sensitive spark production revealed an open probability of ～10-5 for L-type channels at the rest membrane potentials (-80 mV). Thus, infrequent and stochastic openings of sarcolemmal L-type Ca2+ channels in resting heart cells contribute significantly to the production of spontaneous Ca2+ sparks.

鼻中隔延长移植矫正L型硅胶假体隆鼻术后的短鼻畸形

目的探讨鼻中隔延长移植矫正L型硅胶假体隆鼻术后的短鼻畸形。方法使用鼻中隔尾侧延长移植、鼻中隔帽榫延长移植、鼻中隔延伸移植等3种不同的移植方法,对既往使用L型硅胶假体隆鼻患者的短鼻畸形进行手术修复。结果本组21例患者术后鼻整体形态良好,鼻尖突出度及旋转度满意,术后随访临床效果满意,鼻尖形态稳定,无鼻尖下垂、塌陷等并发症出现。结论鼻中隔延长移植是矫正L型硅胶隆鼻患者短鼻畸形的有效方法,个体化设计移植物才能获得满意的手术效果。

基于GYT双标图对北部冬麦区国审小麦品种的回溯分析

北部冬麦区是我国重要的小麦主产区之一,对该麦区历年国审小麦品种进行回溯分析有助于小麦品种资源的合理利用。本研究基于产量与熟期、穗数、穗粒数、千粒重、容重、品质指数、抗病指数和抗寒指数等性状的组合,采用品种-产量×性状组合(GYT,genotype by yield×trait)双标图方法对2003-2023年期间北部冬麦区47个国审小麦品种进行了综合分析和分类评价。结果表明,47个国审小麦品种可划分为4个特征显著的品种类型。其中,Ⅰ型品种综合表现优秀,在产量与早熟性、抗病性、抗寒性、千粒重和容重等性状组合上表现突出,在产量与穗数、穗粒数和品质指数组合上表现优良,在生产上推广应用价值最高,主要包括京麦179、京农16和津麦3118等8个品种。Ⅱ型品种综合表现优良,在产量与品质指数、穗数组合上表现突出,在产量与抗病指数、抗寒指数组合上表现稍差,在生产上推广应用价值较高,但应注意生产安全,主要包括京麦202、京农19和轮选158等13个品种。Ⅲ型品种的产量与抗病和抗寒指数组合最好,但在其余性状组合上表现差,综合生产应用价值有限,可作为抗性亲本。Ⅳ型品种综合表现较差,可选择单性状表现优良的品种作为育种亲本应用。根据各品种在GYT双标图ATA轴上的投影位置,筛选出综合表现优良的京麦179、京农16、津麦3118、京麦189、京麦202、京花12号、京农19、轮选158和中麦623等品种。本研究采用GYT双标图分析方法基于“产量-性状”组合水平对北部冬麦区小麦品种进行综合评价和分类研究,为其他作物和地区的类似研究提供了参考。

Activation of sigma-1 receptor enhances synaptosomal Ca^(2+) via L-type C^(2+) channel in cortical neuron

Sigma-1 receptors are unique receptors that are postulated to act as intracellular amplifiers for signal transduction within cells of the nervous system. The present paper studied the

Contribution of L-type Ca^(2+) channel to the regulation of coronary arterial smooth muscle contraction is different in rats and mice

Background L-type calcium channel participates in the regulation of a variety of physical and pathological process. In vasculature, it mainly mediated agonist-induced vascular smooth muscle contraction. However, it is not clear whether there are differences in L-type calcium channel mediated vessel responses to certain vasoconstrictors among different species. Methods The coronary arteries were dissected from the heart of rats and mice respectively. The coronary arterial ring contraction was measured by Multi Myograph System. Results Endothelin-1, U46619 and 5-HT could produce concentration-dependent vasoconstriction of coronary arterial rings from rats and mice. Compared with rats, the vessel rings of mice were more sensitive to ET-1 and U46619, and less sensitive to 5-HT. The L-type Ca2~ channel blocker nifedipine could significantly inhibit the coronary artery contractions induced by ET-1, U46619 and 5-HT. The inhibitory effect of i ixM nifedipine on ET-1 and 5-HT-induced coronary artery contractions were stronger in mice than in rats, but its effect on U46619 induced-vessel contractions was much weaker in mice than in rats. Conclusions L-type Ca2＋ channel plays an important role in the coronary arterial contraction, but the responses to vasoconstrictor and L-type Ca2＋ channel blocker are different between rats and mice, thus suggesting that the coronary arteries of rats and mice have different biological characteristics.

SRP72基因突变致骨髓衰竭综合征1型1例

骨髓衰竭综合征1型(BMFS1)是一种罕见的骨髓衰竭性疾病,由SRP72(NM_006947.4)基因突变所致,需要进行造血干细胞移植(HSCT)治疗。基因检测对该病的诊断和治疗方法选择至关重要。本文报道1例由SRP72基因c.1502+1G>A自发突变致BMFS1的患儿,并顺利实施HSCT治疗,患儿最终痊愈。本研究发现的c.1502+1G>A变异,未检索到与BMFS1相关的文献报道。本例患儿的发现扩展了SRP72基因致病性变异谱和表型谱,为BMSF1的早期诊断和正确治疗的选择提供了典型案例。