基于小波模极大原理的脉象特征提取研究

目的 根据小波分析原理，研究脉象特征提取方法，以有效解决基于时域或频域的传统方法所无法准确提取脉象特征的问题。方法 运用小波模极大方法进行脉象信号周期分割和基本分解，沿时间排列并符号化脉象波上升沿与下降沿的模极大特征点、脉象波谷底和波峰的模极大特征点。结果 确定了不明显的重搏前波、重搏波，以及在主波上升沿和下降沿上出现的不规则脉波，并进一步准确提取了脉象信号的多尺度特征和各种时域特征。结论 采用此方法进行脉象信号的特征点定位并进一步完成特征提取，具有简单、快速、准确等特点，为进一步进行脉象分类识别研究奠定了基础。     

Biexponential diffusion tensor analysis of human brain diffusion data.

Several studies have shown that in tissues over an extended range of b-factors, the signal decay deviates significantly from the basic monoexponential model. The true nature of this departure has to date not been identified. For the current study, line scan diffusion images of brain suitable for biexponential diffusion tensor analysis were acquired in normal subjects on a clinical MR system. For each of six noncollinear directions, 32 images with b-factors ranging from 5 to 5000 s/mm2 were collected. Biexponential fits yielded parameter maps for a fast and a slow diffusion component. A subset of the diffusion data, consisting of the images obtained at the conventional range of b-factors between 5 and 972 s/mm2, was used for monoexponential diffusion tensor analysis. Fractional anisotropy (FA) of the fast-diffusion component and the monoexponential fit exhibited no significant difference. FA of the slow-diffusion biexponential component was significantly higher, particularly in areas of lower fiber density. The principal diffusion directions for the two biexponential components and the monoexponential solution were largely the same and in agreement with known fiber tracts. The second and third diffusion eigenvector directions also appeared to be aligned, but they exhibited significant deviations in localized areas.     

Radiofrequency Ablation of Concealed Left Free-Wall Accessory Pathways Without Coronary Sinus Catheterization:

Ablation of Concealed Accessory Pathways. Introduction: Feasibility of radiofrequency (RF) ablation using a two-catheter technique without coronary sinus catheterization was studied in 100 consecutive patients with a single concealed left free-wall accessory path-way.
Methods and Results: Tachycardia was induced by electrical stimulation in the right atrium/right ventricle, and the presence of a concealed left free-wall accessory pathway was suggested electrocardiographically (negative P wave in leads I and/or a VL during orthodromic tachycardia) or by earlier atrial activation in the pulmonary artery compared to the high right atrium. Mapping of the mitral annulus was performed during right ventricular pacing or orthodromic tachycardia, and RF energy was applied at the site with the earliest retrograde atrial activation. Ablation was considered effective if tachycardia could not be induced, and if VA dissociation or exclusive retrograde nodal conduction was observed. Ablation was initially successful in 98 of 100 patients. Mean number of radiofrequency pulses were 3.2 ± 2. Mean fluoroscopy time and total procedure time was 14 ± 9 and 107 ± 32 minutes, respectively. There were no complications related to the procedure. At a mean follow-up of 22 ± 13 months, two patients experienced tachycardia recurrence and required a second procedure, which was successful.
Conclusions: Our results suggest that RF catheter ablation of concealed left free-wall accessory pathways can be safely, effectively, and rapidly performed using a simplified two-catheter technique with no need for coronary sinus catheterization.     

Partial k-space reconstruction in single-shot diffusion-weighted echo-planar imaging.

Partial k-space sampling is frequently used in single-shot diffusion-weighted echo-planar imaging (DW-EPI) to reduce the TE and thereby improve the SNR. However, it increases the sensitivity of the technique to bulk rotational motion, which introduces a phase gradient across the tissue that shifts the echo in k-space. If the echo is displaced into the high spatial frequencies, conventional homodyne reconstruction fails, causing intensity oscillations across the image. Zero-padding, on the other hand, compromises the image resolution and may cause truncation artifacts. We present an adaptive version of the homodyne algorithm that detects the location of the echo in k-space and adjusts the center and width of the homodyne filters accordingly. The adaptive algorithm produces artifact-free images when the echo is shifted into the high positive k-space range, and reduces to the standard homodyne algorithm in the absence of bulk motion.     

内毒素休克大鼠核因子κB活化规律及其在生物蝶呤诱生中的作用

目的观察内毒素休克大鼠血浆及主要脏器核因子(NF)κB活化规律及其对生物蝶呤(BH4)和一氧化氮(NO)表达水平的影响,探讨内毒素休克时NF-κB信号通路对BH4诱生NO的分子调控机制及其与多器官功能损害的关系。方法将47只大鼠按表格随机法分为正常组(8只)、内毒素／脂多糖(LPS)组(24只,每观察时相点8只,均同时注射LPS制成休克模型)和拮抗组[15只,每观察时相点5只,均同时注射LPS并以吡咯烷二硫代氨基甲酸盐(PDTC)拮抗]。休克及拮抗组于注射LPS后2、6、12 h观察,并与正常组同法处死,无菌留取大鼠血标本及肝、肺、肾组织,测定组织中NF-κB活性和三磷酸鸟苷环水解酶Ⅰ(GTP-CHⅠ)和诱导型一氧化氮合酶(iNOS)mRNA表达水平、血浆和组织中的BH4含量及NO水平、肝脏和肾脏功能指标、肺组织髓过氧化物酶活性。结果与正常组(例如肺组织中NF-κB活性为26±6)比较,LPS组大鼠组织中NF-κB迅速活化(P<0．01),并于注射后2 h达峰值(肺组织中为291±44);LPS组各组织中GTP-CHⅠ和iNOS mRNA表达、BH4和NO水平也较正常组明显升高(P<0．05或0．01),至伤后12 h仍持续较高水平。此外,该组相应器官功能均受到不同程度的损害。应用PDTC的拮抗组大鼠各组织中NF-κB活性均较LPS组有所降低,GTP-CHⅠ、iNOS mRNA表达及BH4、NO水平显著受抑,肝、肺、肾功能明显改善。结论内毒素休克时机体内NF-κB通路高度活化,并对BH4／NO系统具有明显调节效应;可通过下调BH4介导的iNOS的过度活化抑制NF-κB信号途径,从而减轻组织炎性反应,对机体脏器功能起到保护作用。     

Orthograde transport and release of insulin-like growth factor I from the inferior olive to the cerebellum

Insulin-like growth factor I (IGF-I) and its receptor are expressed in functionally related areas of the rat brain such as the inferior olive and the cerebellar cortex. A marked decrease of IGF-I levels in cerebellum is found when inferior olive neurons are lesioned. In addition, Purkinje cells in the cerebellar cortex depend on this growth factor to survive and differentiate in vitro. Thus, we consider it possible that IGF-I forms part of a putative trophic circuitry encompassing the inferior olive and the cerebellar cortex and possibly other functionally connected areas. To test this hypothesis we have studied whether IGF-I may be taken up, transported, and released from the inferior olive to the cerebellum. We have found that ¹²⁵I-IGF-I is taken up by inferior olive neurons in a receptor-mediated process and orthogradely transported to the cerebellum. Thus, radioactivity found in the cerebellar lobe contralateral to the injection site in the inferior olive was immunoprecipitated by an anti-IGF-I antibody, co-eluted with ¹²⁵I-IGF-I in an HPLC column, and co-migrated with ¹²⁵I-IGF-I in an SDS-urea polyacrylamide gel electrophoresis. Time-course studies indicated that orthograde axonal transport is relatively rapid since 30 min after the injection, radiolabeled IGF-I was already detected in the contralateral cerebellum. Furthermore, transport of IGF-i from the inferior olive is specific since when ¹²⁵I-neurotensin was injected in the inferior olive or when ¹²⁵I-IGF-I was injected in the pontine nucleus, no radiactivity was found in the contralateral cerebellum. In addition, no specific transport of ¹²⁵I-IGF-I was found in climbing fiber-deafferented rats or when excess unlabeled IGF-I was co-injected with ¹²⁵I-IGF-I. We next studied whether IGF-I is released by inferior olive neurons. We found that the release of IGF-I from cerebellar slices of normal rats was significantly greater in response to depolarizing stimuli than that from slices obtained of climbing fiber-deafferented animals. Indeed, in vitro release of IGF-I in response to KCI or veratridine was almost completely abolished in the latter. These data suggest that IGF-I is taken up by inferior olive neurons through IGF-I receptors and transported to the cerebellum through their axons without any major modification. Moreover, the release of IGF-I from the cerebellum after depolarization depends on the presence of climbing fiber afferents. Altogether these results indicate that the olivo-cerebellar pathway is able to take up, orthogradely transport, and release IGF-I. Since a similar process has been described in the visual system for basic fibroblast growth factor (bFGF), we propose that IGF-I, bFGF, and possibly other growth factors may constitute afferent trophic signals involved in plastic mechanisms within specific neural circuitries. © 1993 Wiley-Liss, Inc.     

导管射频消融术治疗持续性交界区反复性心动过速2例报告

本文报告两例持续性交界区反复性心动过速(PJRT)患者,应用导管射频消融术治疗,成功地阻断了位于后间隔具有递减传导特性的稳若旁路.随访7～10个月.病人无心动过速发作,提示导管射频消融术是治疗PJRT的有效方法.     

急性冠脉综合征患者强化抗栓治疗研究进展

急性冠脉综合征（ACS）是冠心病的严重类型,ACS患者不仅病死率较高,还存在缺血事件（如缺血性卒中、心肌梗死）复发风险。血小板聚集及血栓形成是导致ACS的重要原因。为降低缺血事件的发生风险,临床推荐ACS患者接受阿司匹林联合强效P2Y12抑制剂的双联抗血小板治疗12个月。然而在标准双联抗血小板治疗下,ACS患者残余缺血风险（经抗栓治疗后仍残留的缺血事件发生风险）仍旧较高。因此为进一步降低缺血事件发生风险,临床对强化抗栓方案的研究也逐渐增多。本文通过总结强化抗栓治疗方案的作用机制及其最新研究进展,发现延长双联抗血小板治疗时间、三联抗血小板治疗、双通道抑制（抗血小板联合抗凝治疗）等强化抗栓治疗方案可降低缺血事件发生风险,为进一步指导临床个体化抗栓治疗及明确最佳抗栓策略提供了参考。     

ACE2基因通过调控Nrf2/HO-1通路改善肾缺血再灌注损伤

目的 探讨血管紧张素转化酶2(ACE2)对缺氧复氧诱导的肾小管上皮细胞HK-2氧化应激、炎症、凋亡及核因子E2相关因子2(Nrf2)/血红素加氧酶1(HO-1)信号通路的影响。 方法 将ACE2慢病毒转染HK-2细胞,按照实验需要分为常氧组(Control组)、缺氧复氧模型组(H/R组)、缺氧复氧转染阴性对照慢病毒组(H/R-NC组)和缺氧复氧转染ACE2慢病毒组(H/R-ACE2组)。细胞经H/R处理后,通过CCK-8法检测细胞活力;RT-PCR及ELISA法检测炎症因子白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)水平;比色法检测超氧化物歧化酶(SOD)、丙二醛(MDA)表达水平;Western blotting法检测胱天蛋白酶3(Caspase-3)、B淋巴细胞瘤-2基因(Bcl-2)、Bcl-2关联X蛋白(Bax)、Nrf2、HO-1的蛋白水平。采用Nrf2抑制剂ML385以及HO-1抑制剂SnPPIX抑制Nrf2/HO-1通路,Western blotting法检测Caspase-3、Bcl-2、Bax、Nrf2、HO-1的蛋白表达水平变化,比色法检测SOD和MDA表达变化。 结果 与Control组相比,H/R组细胞活力降低(t=7.58,P<0.001),MDA含量和炎症因子IL-6、TNF-α和IL-1β表达水平以及细胞凋亡相关蛋白Caspase-3、Bax蛋白水平均增加(t_MDA=11.08,P_MDA<0.001;t_PCR-IL-6=5.82,P_PCR-IL6<0.001;t_PCR-TNF-α=7.69,P_PCR-TNF-α<0.001;t_PCR-IL-1β=4.80,P_PCR-IL-1β=0.001;t_ELISA-IL-6=34.11,P_ELISA-IL-6<0.001;t_ELISA-TNF-α=14.12,P_ELISA-TNF-α<0.001;t_ELISA-IL-1β=9.63,P_ELISA-IL-1β<0.001;t_Caspase-3=2.73,P_Caspase-3=0.026;t_Bax=27.75,P_Bax<0.001),SOD活性、Bcl-2和ACE2蛋白水平下降(t_SOD=7.74,P_SOD<0.001;t_Bcl-2=75.49,P_Bcl-2<0.001;t_ACE2=11.41,P_ACE2<0.001)。与H/R组相比,H/R-ACE2组细胞活力增加(t=3.61,P=0.002),MDA含量和炎症因子IL-6、TNF-α和IL-1β表达水平以及细胞凋亡相关蛋白Caspase-3、Bax蛋白水平均下降(t_MDA=6.15,P_MDA<0.001;t_PCR-IL-6=3.34,P_PCR-IL-6=0.006;t_PCR-TNF-α=3.65,P_PCR-TNF-α=0.007;t_PCR-IL-1β=4.06,P_PCR-IL-1β=0.004;t_ELISA-IL-6=14.62,P_ELISA-IL-6<0.001;t_ELISA-TNF-α=10.42,P_ELISA-TNF-α<0.001;t_ELISA-IL-1β=8.65,P_ELISA-IL-1β<0.001;t_Caspase-3=3.74,P_Caspase-3=0.006;t_Bax=30.52,P_Bax<0.001),SOD活性、Bcl-2和ACE2蛋白水平增加(t_SOD=3.58,P_SOD=0.007;t_Bcl-2=63.86,P_Bcl-2<0.001;t_ACE2=58.72,P_ACE2<0.001),Nrf2/HO-1信号通路被激活蛋白水平增加(t_Nrf2=44.55,P_Nrf2<0.001;t_HO-1=14.19,P_HO-1<0.001)。然而ML385和SnPPIX处理会抑制ACE2基因过表达在H/R中HK-2细胞的保护作用(F_Bax=11.02,P_Bax=0.003;F_Bcl-2=21.48,P_Bcl-2<0.001;F_Caspase-3=20.80,P_Caspase-3<0.001;F_SOD=133.49,P_SOD<0.001;F_MDA=14.06,P_MDA=0.001)。 结论 ACE2在HK-2细胞缺氧复氧损伤中具有抑制氧化应激、调节炎症、改善凋亡的作用,Nrf2/HO-1信号通路发挥重要作用。     

基于FAERS的地舒单抗安全警戒信号挖掘与评价

基于FAERS数据库挖掘安全警戒信号,分析评估地舒单抗潜在不良反应信号,为其临床使用提供一定参考依据。方法 通过Openvigil 2.1访问 FAERS 数据库,将地舒单抗作为主要药物,检索自该药首次上市时间（2010年5月—2021年9月）的数据,获得与地舒单抗相关的不良事件报告记录。使用报告比值比法（ROR）和贝叶斯置信度递进神经网络法（BCPNN）筛选地舒单抗安全警戒信号,挖掘潜在的不良反应,并通过工具BioPortal对不良事件信号挖掘结果进行系统分类,通过判断信号间置信区间的变化,发现与药物不良事件关联性较大的信号。结果 从FAERS数据库中收集到270503份不良反应事件（ADE）报告,根据ROR法和BCPNN法共得到343个不良事件信号,通过信号间同义合并、剔除与药物无关的信号后,得到316个不良事件信号。地舒单抗的不良事件系统分类主要为肌肉骨骼和结缔组织疾病、医学检查、胃肠道疾病。FAERS数据库的信号挖掘结果发现,高风险且说明书中未收录的安全警戒信号包括颞下颌关节综合征、下颌脓肿、雌激素缺乏症、血液甲状旁腺激素增加,计算高风险信号的置信区间显示颞下关节综合征较有可能发展成为新的不良反应;另外,也发现种植体周围炎为具有临床意义的可疑警戒信号,但有待进一步观察研究。结论 基于FAERS数据库的信号挖掘结果提示临床应规范使用地舒单抗,治疗期间需警惕患者是否出现颞下颌关节综合征、下颌脓肿、雌激素缺乏症、血液甲状旁腺激素增加等不良反应事件,以便尽早发现尽早处理,从而有效降低临床用药风险