Impact of optical coherence tomography- and coronary angioscopy-assessed neointimal tissue characteristics on occurrence of periprocedural myonecrosis in patients with in-stent restenosis

Several characteristics of neointimal tissues, including neoatherosclerotic progression, have been reported in lesions with in-stent restenosis (ISR). However, the effects of these characteristics on outcomes after percutaneous coronary intervention (PCI) for ISR lesions remain unclear. We assessed the relationships between neointimal tissue characteristics and the occurrence of periprocedural myonecrosis (PMN) after PCI in ISR lesions. We investigated 72 ISR lesions in 72 patients with stable angina pectoris (SAP) who underwent pre- and post-revascularization optical coherence tomography (OCT) and coronary angioscopy (CAS). All lesions were classified as with PMN, defined by an elevated peak high-sensitivity cardiac troponin-T level during the 24-h post-PCI period, and without PMN. PMN was observed in 23 (31.9?%) lesions. PMN lesions had higher frequencies of OCT-derived thin-cap fibroatheroma (26.1 vs. 6.1?%, P?=?0.03), CAS-derived intensive yellow neointima (30.4 vs. 10.2?%, P?=?0.04), neointima with complex surface (60.9 vs. 28.6?%, P?=?0.01), and CAS-derived atheromatous appearance (CAS-AAP), defined as yellow plaque including complex thrombi underneath disrupted neointimal coverage after ballooning (47.8 vs. 16.3?%, P?=?0.008) at the most stenotic sites inside stents, compared to lesions without PMN. Multivariate logistic regression analysis identified CAS-AAP (odds ratio: 3.568, 95?% confidence interval: 1.109–11.475, P?=?0.033) as an independent predictor of PMN. For ISR lesions in SAP patients, an OCT- and CAS-based assessment of neointimal tissue characteristics might help to predict the occurrence of PMN.     

Deficiency of electroneutral K+–Cl− cotransporter 3 causes a disruption in impulse propagation along peripheral nerves

Nerve conduction requires the fine tuning of ionic currents through delicate interactions between axons and Schwann cells. The K⁺–Cl⁻ cotransporter (KCC) family includes four isoforms (KCC1–4) that play an important role in the maintenance of cellular osmotic homeostasis via the coupled electroneutral movement of K⁺ and Cl⁻ with concurrent water flux. Mutation in SLC12A6 gene encoding KCC3 results in an autosomal recessive disease, known as agenesis of the corpus callosum associated with peripheral neuropathy. Nevertheless, the role of KCC3 in nerve function remains a puzzle. In this study, the microscopic examination of KCC isoforms expressed in peripheral nerves showed high expression of KCC2–4 in nodal segments of the axons and in the perinucleus and microvilli of Schwann cells. The KCC inhibitor [[(dihydroindenyl)oxy]alkanoic acid] but not the Na⁺–K⁺–2Cl⁻‐cotransport inhibitor (bumetanide) dose‐dependently suppressed the amplitude and area of compound muscle action potential, indicating the involvement of KCC activity in peripheral nerve conduction. Furthermore, the amplitude and area under the curve were smaller, and the nerve conduction velocity was slower in nerves from KCC3^−/− mice than in nerves from wild‐type mice, while the expression pattern of KCC2 and KCC4 was similar in KCC3 kockout and wild‐type strains. KCC3^−/− mice also manifested a prominent motor deficit in the beam‐walking test. This is the first study to demonstrate that the K⁺–Cl⁻ cotransporter activity of KCC3 contributes to the propagation of action potentials along peripheral nerves. © 2010 Wiley‐Liss, Inc.     

A case of afebrile miliary tuberculosis that progressed from tuberculous spondylitis with iliopsoas abscess

We present a case of a 78-year-old woman who visited our hospital for chronic atrial fibrillation. She consulted an orthopedic surgeon for lumbar pain in August 2009 and has been followed up for osteoporosis. However, her lumbar pain became exacerbated. In December 2009, clinical examination revealed that the pain was caused by tuberculous spondylitis and iliopsoas abscess. Diffuse miliary shadow, which was undetected earlier, was noted on chest roentgenogram; she was diagnosed with miliary tuberculosis. Lumbar pain is common in elderly individuals and should be regarded as one of the tuberculosis symptoms, considering its atypical course in elderly patients.     

胸段硬膜外镇痛对腹腔镜结直肠手术后疼痛和肠功能的影响

目的加速康复外科（fast track surgery,FTS）理念重点强调术后应用胸段硬膜外镇痛。文中探讨胸段硬膜外镇痛对腹腔镜结直肠手术后疼痛和肠道功能恢复的影响。方法采用相同围手术期处理的腹腔镜结直肠手术患者50例,随机分为静脉镇痛组（静脉组）和胸段硬膜外镇痛组（硬膜外组）,每组25例。静脉组采用静脉注射曲马朵自控镇痛,硬膜外组采用胸段硬膜外注射罗派卡因和芬太尼自控镇痛,测定2组患者的视觉模拟评分（visual analogue scale,VAS）,记录术后排气时间、口服半流饮食时间和术后住院天数,观察记录不良反应及并发症。结果硬膜外组在术后第1天、第2天休息、咳嗽以及行走时的VAS明显低于静脉组（P〈0.05,P〈0.01）,术后排气时间、口服半流饮食时间及术后住院天数明显短于静脉组（P〈0.05）,2组术后并发症及再住院率差异无统计学意义（P〉0.05）。结论胸段硬膜外镇痛应用于腹腔镜结直肠手术患者,可提供术后有效的镇痛,并能促进术后肠功能恢复,达到快速康复的目的。     

阿糖胞苷＋阿克拉霉素＋粒系集落刺激因子方案治疗急性髓系白血病疗效与染色体核型关系

目的探讨阿糖胞苷＋阿克拉霉素＋粒系集落刺激因子（CAG）方案治疗急性髓系白血病（AML）的临床疗效及与染色体核型的关系。方法31例AML患者采用CAG方案化疗,并用G显带常规技术对患者的核型进行分析。结果按医学研究委员会标准分成预后良好、中等和差3组,预后中等组完全缓解率高,良好组与差组完全缓解率接近。结论CAG方案治疗AML疗效肯定,染色体核型分析对CAG方案化疗疗效及预后判断有指导意义。     

神经外科呼吸道病原菌的分布及其耐药性的临床分析

目的:了解神经外科危重病人呼吸道感染病原菌的分布及耐药性,为临床医师用药提供参考。方法:回顾性分析2008年11月至2010年11月神经外科痰标本细菌培养及药敏的结果,细菌鉴定参照《全国临床检验操作规程》严格执行。结果:痰培养阳性率达到98.6%,以铜绿假单胞菌和肺炎克雷伯菌为主,多为混合感染,且耐药率高。结论:神经外科呼吸道感染严重,临床医师应该足够重视,合理应用抗生素。     

眶颅骨纤维异常增殖症病灶手术切除与缺损区钛金属修复

目的:研究眶颅骨纤维异常增殖症手术切除病灶的时机和方法,总结病灶切除后钛金属修复骨缺损的经验,对手术的疗效进行评估。方法:对21 例出现视功能障碍或明显外观影响的患者进行术前常规冠状位、水平位、矢状位及三维CT 扫描。对眶颅骨病变范围大的患者,将CT 扫描图像数据输入计算机,经过处理后制作钛金属三维实体修复体;对于累及眶颅骨病变范围较小的患者,则用手工的方法在手术中制作近似于正常眼眶和颅骨部的修复体。全部病例均采用经颅手术切除病变骨组织,并用钛板和钛网修复缺损区。结果:21 例患者中18 例一次性切除干净,3 例累及海绵窦区域者进行姑息性切除。13 例伴有不同程度的视力下降,11 例术后视力明显上升,视力恢复在3~5 行。外观畸形的11 例患者术后得到明显改善。结论:眶颅骨纤维异常增殖症患者只要影响到视功能或造成眶颅外观畸形,应该尽早进行手术切除。钛金属修复手术后遗留的骨缺损具有牢固、可塑性强、固定简易等优点。     

A cascade targeting strategy for brain neuroglial cells employing nanoparticles modified with angiopep-2 peptide and EGFP-EGF1 protein

Targeted drug delivery to selected brain cell types is a crucial step in enhancing therapeutic effects while limiting side effects in non-target cells. Here we report on the development and evaluation of a new cascade targeting delivery system that employs PEG-PCL nanoparticles modified with both an angiopep-2 peptide and a EGFP-EGF1 protein for precise targeting of brain neuroglial cells. Angiopep-2 penetrates the blood-brain barrier and EGFP-EGF1 binds neuroglial cells, providing the system with two stages of targeting. In vitro studies demonstrated that both bEnd.3 cells and neuroglial cells had a higher uptake of angiopep-2 and EGFP-EGF1 conjugated nanoparticles (AENP) as compared to unmodified nanoparticles. Ex vivo imaging showed that AENP had higher accumulation in the brain over unmodified nanoparticles and EGFP-EGF1 modified nanoparticles. Fluorescent in situ hybridization of brain slides demonstrated that AENP co-localized with neuroglial cells. Transmission electron microscopy further showed that AENP could target and enter neuroglial cells. This newly developed cascade targeting delivery system that precisely targets neuroglial cells has great potential in the diagnosis and treatment of neuroglial related diseases. Replacing EGFP-EGF1 and angiopep-2 with other ligands may extend the utility of the system to diagnose and treat organ diseases beyond brain.     

Altered glucose metabolism and preserved energy charge and neuronal structures in the brain of mouse intermittently exposed to hypoxia

The key for an animal to survive prolonged hypoxia is to avoid rapid decline in ATP levels in vital organs such as the brain. This can be well achieved by a very few of hypoxia-tolerant animals such as freshwater turtles and newborn animals, since these animals can substantially suppress their metabolic levels by coordinated regulation of ATP-producing and ATP-demanding pathways. However, most animals, especially adult mammals, can only tolerate a short period of hypoxia since they are unable to maintain constant ATP levels and energy charge in vital organs during prolonged hypoxic exposure. Here, we described a special mouse model, in which a hypoxia intolerant adult mouse gradually built up an ability to survive prolonged hypoxia after intermittent hypoxic exposures. This increased ability was accompanied by reductions in body temperature and O₂ consumption as well as transient variations in blood pCO₂, pO₂ and pH. The glucose and energy metabolism in the brain of the mouse altered similarly to those reported in the brain of hypoxic turtles. Activities of phosphofructokinase and pyruvate kinase, the two rate-limiting enzymes controlling the rate of glycolysis decreased to baseline levels after a short period of increase. In contrast, the activity of complex I, the major enzyme complex controlling oxidative phosphorylation, was kept inhibited. These alterations in the ATP-producing pathway suggest the occurrence of reverse Pasteur effect, indicating that the animal had entered a hypometabolic state favoring maintenance of ATP level and energy charge in hypoxic conditions. In supporting this idea, the ATP levels and energy charge as well as neuronal structures in the brain were well preserved. This study provides evidence for a possibility that a hypoxic intolerant animal can build up an ability to survive prolonged hypoxia through regulation of its glucose and energy metabolism after an appropriate hypoxic training, which deserves further investigation.