内镜下粘膜切除术治疗早期胃癌36例护理

早期胃癌（early gastric cancer,EGC）是指胃癌病变位于粘膜或粘膜下层,而无论病灶大小和是否有淋巴结转移。内镜下粘膜切除术（endoscopic mucosal resection,EMR）是应用辅助技术在内镜下对消化道较小的无蒂浅表性恶性病变行病灶切除的方法。随着内镜技术和器械的改进与发明,EMR技术得到不断改进与创新,已成为治疗早期胃癌的重要手段     

378例早期胃癌病理特征分析

目的：研究378例早期胃癌(early gastric cancer,EGC)的病理特征及临床意义。方法：回顾分析2012年8月至2014年8月河北医科大学第四医院378例EGC标本的肿瘤直径、浸润深度、肉眼分型、组织学分型、淋巴结转移进行检查。结果：全组病例男性312例,女性66例;182例肿瘤局限在粘膜层,196例侵及粘膜下层;发生部位主要位于贲门222例(58.73%);肉眼分型以Ⅱ型为主(53.44%);组织学类型以管状腺癌为主(77.25%);出现淋巴结转移20例(5.29%)。结论：浸润深度、组织学类型、淋巴结转移等是EGC组织病理学诊断的重要指标。     

128例内镜黏膜下剥离术治疗早期胃癌的护理

<正>胃癌是常见的恶性肿瘤之一,早期胃癌是指病灶不超过黏膜下层而无论有无转移的胃癌。早期胃癌的早期诊断和治疗大大提高了胃癌患者的预后[1]。随着消化内镜诊断和治疗技术的不断发展,内镜黏膜下剥离术(endoscopic submucosal dissection,ESD)使早期胃癌病灶切除范围更加扩大,并且安全可靠,是内镜下黏膜切除术(EMR)的补充和演进,目前已成为消化道早癌及其它肿瘤的内镜下切除的新技术[2]。为了探讨ESD治疗早期胃癌的最佳护理措施,现将我院128例经ESD治疗的早     

早期胃癌淋巴结转移与病理特征相关性分析及手术方式选择

目的探讨影响早期胃癌（EGC）淋巴结转移的相关病理学因素,为EGC的手术方式选择提供参考。方法回顾性分析228例早期胃癌患者的临床病理特征及淋巴结转移情况,分析早期胃癌的大小、原发部位、大体分型、组织学分型、侵润深度及分化程度等与淋巴结转移的相关性以及手术方式的选择。结果 228例EGC患者中出现淋巴结转移31例（13.6%）,其中粘膜内癌10例（7.9%）,粘膜下癌21例（20.6%）。单因素分析发现EGC淋巴结转移与肿瘤大小、肿瘤侵润深度及分化程度相关（P〈0.01）,而与肿瘤的大体分型、组织学类型、肿瘤部位无关（P〉0.05）。多因素分析发现肿瘤直径大于2 cm、粘膜下癌及分化程度低是EGC淋巴结转移的独立危险因素。对于肿瘤直径小于2 cm、分化程度较高的粘膜内癌并无淋巴结转移的EGC,建议行内镜下粘膜切除术（EMR）或内镜粘膜下剥离术（ESD）治疗。结论肿瘤直径大于2 cm、粘膜下癌及分化程度低是EGC淋巴结转移的独立危险因素,淋巴结转移影响了早期胃癌手术方式。     

经鼻内窥镜选择性鼻中隔粘膜下切除术

目的：探讨经鼻内窥镜选择性鼻中隔粘膜下切除术的意义及手术方法。方法：根据不同的手术目的对204例需要行鼻中隔手术的病人，经鼻内窥镜实施选择性鼻中隔粘膜下切除术。结果：采用该技术对单纯性鼻中隔偏曲患者手术临床治愈率100％，其手术有效治愈头痛、鼻阻及鼻出血等鼻中隔偏曲临床症状，达到临床治疗目的。未出现鼻腔粘连、鼻中隔穿孔等并发症。有2例形成鼻中隔血肿，经放置引流管处理后治愈。对于解除高位鼻中隔偏曲解剖异常引发的鼻窦炎，手术后效果良好。取鼻中隔软骨做为修补材料手术效果满意。结论：经鼻内镜选择性鼻中隔粘膜下切除术目的性强、方法灵活、创伤小、并发症少、手术效果确切。     

内镜联合选择性环氧合酶2抑制剂治疗食管粘膜不典型性增生的临床研究

目的探究内镜联合选择性环氧合酶2抑制剂治疗食管粘膜不典型性增生的安全性与有效性。方法收集临床食管粘膜不典型性增生患者63例，随机分成2组，对照组30例单纯采用内镜治疗，研究组33例在内镜治疗的基础上加用选择性环氧合酶2抑制剂；比较2组患者治疗前后的病灶情况、临床症状改善程度以及血管内皮生长因子（VEGF）的表达情况。结果经过12个月的随访，研究组治疗好转率达到75．76％，血清中的VEGF含量也得到了明显抑制，与对照组相比均具有显著的统计学差异（P〈0．05）。结论内镜联合选择性环氧合酶2抑制剂治疗食管粘膜不典型性增生不仅有效而且安全。     

内镜下微创治疗结肠巨大息肉35例的护理分析

探讨内镜下微创治疗结肠巨大息肉护理体会。方法35例巨大结肠息肉患者内镜下行高频电凝电切术。35例结肠巨大息肉患者内镜下微创治疗成功。其中有1例并发出血,经金属夹闭后,止血成功。有1例术后迟发出血,经止血剂应用止血成功,无穿孔病例。结果依据巨大息肉蒂的粗细、长短等情况,选择含有粘膜下注射的高频电凝电切联合治疗息肉更安全。护士根据内镜下微创治疗的特点,通过健康宣教,术前准备、术中配合、术后观察进行针对性的护理,是手术成功的关键。     

胃癌中TGF-β1、HIF-1α、VEGF的表达及临床意义

目的观察转化生长因子-β1(transforming growth factor-β1,TGF-β1)、低氧诱导因子-1α(hypoxia inducible factor-1α,HIF-1α)及血管内皮生长因子(vascular endothelial growth factor,VEGF)在胃癌组织及癌旁组织中的表达,探讨其与胃癌恶性生物学行为间的相关性。方法采用免疫组化SABC法检测手术切除胃癌组织中的TGF-β1、HIF-1α及VEGF的表达,分析其与胃癌患者的病理分级、组织学类型、淋巴结转移及TNM分期等临床病理参数的关系,探讨其作为判断胃癌患者预后指标的可能性。结果 TGF-β1、HIF-1α、VEGF在150例胃癌组织中,阳性率分别为62.7%、59.3%和63.3%;在癌旁组织中阳性率分别为10.7%、22%和13.3%,三者在胃癌组织中的表达明显高于癌旁组织(P<0.05)。TGF-β1的表达与肿瘤的浸润深度、淋巴结转移及TNM分期密切相关(P<0.05);TGF-β1阳性的患者比其阴性的患者更易发生淋巴结和远处转移;HIF-1α、VEGF的表达与肿瘤的组织学类型、淋巴结转移及TNM分期有相关性(P<0.05)。结论胃癌组织中TGF-β1、HIF-1α、VEGF表达与肿瘤的生物学特征密切相关,可能是肿瘤侵袭转移的机制之一;检测TGF-β1、HIF-1α、VEGF对预测肿瘤侵袭转移及判断预后具有一定价值。     

应用内镜黏膜下剥离术处理食管黏膜病变疗效评价

目的应用内镜黏膜下剥离术(ESD)处理食管早癌及癌前病变,评价其疗效和安全性。方法回顾性分析2008年10月至2009年10月分别于复旦大学附属中山医院和新疆医科大学第六附属医院内镜检查及病理诊断为早期食管癌及癌前病变35例患者,其中男性24例,女性11例;年龄38～78岁,平均年龄60岁。对患者行内镜下治疗,观察术中出血、穿孔及术后食管狭窄的发生情况,统计病灶完整大块切除率与组织学完全切除率,通过随访评价复发或转移情况,对内镜治疗短期效果进行初步评价。结果完成ESD操作28例,7例(20.0%)改为内镜下黏膜切除术(EMR)切除,手术耗时20～125min,平均耗时65 min。颈部气肿1例,术中穿孔2例(5.7%),术中少量出血8例(22.9%),术后延迟性出血1例。组织学治愈26例(74.3%)。除2例手术治疗外,32例完成随访,1例(3.3%)失访。随访4～26个月,中位随访时间10个月。随访中,3例复发,复发率9.4%(3/32),3例发生术后食管狭窄包括1例复发病例。结论 ESD治疗早期食管癌及癌前病变具有较好的疗效和安全性。     

食管贲门粘膜撕裂症的内镜下诊断与治疗

目的探讨食管贲门粘膜撕裂症(MWS)的内镜下诊断及治疗。方法回顾性分析14例经内镜诊治的MWS的临床资料。结果MWS病变以右侧壁的贲门粘膜多见。7例患者内镜下止血效果显著。结论内镜是确诊MWS的首选方法。内镜止血效果肯定,方法简便。     

E-cadherin, N-cadherin, and calretinin in pleural effusions: the good, the bad, the worthless

The distinction between reactive mesothelial cells (RMC), malignant mesothelioma (MM), and metastatic adenocarcinoma (ACA) in pleural effusions may be impossible based on morphology alone. E-cadherin, N-cadherin, and calretinin are newly described immunocytochemical markers which can potentially be utilized for facilitating this distinction. E-cadherin and N-cadherin are calcium-dependent intercellular adhesion molecules expressed in epithelial cells and mesenchymal/mesothelial cells, respectively. The differential expression of E-cadherins in epithelial cells and N-cadherins in mesothelial cells has been utilized to differentiate reactive mesothelial cells, MMs and ACAs. Calretinin is a calcium-binding protein within the family of EF-hand proteins. It is abundantly expressed in peripheral and central nervous tissues, and has been shown to consistently immunoreact with mesothelial cells. We studied cell block sections from 77 pleural effusions (22 RMC, 26 MM, and 29 ACA) to investigate the potential immunocytochemical use of anti-E-cadherin, anti-N-cadherin, and anti-calretinin antibodies for differentiating between RMC, MM, and ACA in pleural effusions. A modified avidin-biotin peroxidase complex (ABC) method was used. E-cadherin immunostaining was observed in 14% of RMC, 46% of MMs, and 97% of ACAs. A distinct membrane staining pattern was seen in ACAs. The pattern of staining was cytoplasmic in all reactive RMC and varied from membrane to cytoplasmic in MMs. Anti-N-cadherin immunoreacted with 77% of RMC, 35% of MMs, and 48% of ACAs. Twenty-seven percent of RMC, 58% of MMs, and 31% of ACAs immunoreacted with anti-calretinin. Based on these results, we conclude that anti-E-cadherin is a potentially useful marker in the distinction of ACA cells from RMC. However, it is not as useful for the distinction of ACA and MM. Anti-N-cadherin and anti-calretinin did not reliably distinguish between reactive mesothelial, MM, and ACA cells in pleural effusions.     

Nasal obstruction, the airway, and the athlete

Rhinitis is a common condition that affects a significant proportion of the general population, as well as a high proportion of athletes. Nasal congestion is a predominate symptom of the late-phase reaction in allergic rhinitis and can have far-reaching effects that extend through the airway and beyond the nose. Rhinitis is often found in conjunction with asthma and is a risk factor for asthma. Nasal obstruction, which does not permit conditioning of inspired air by the nasal turbinates, may contribute to asthma symptoms and the development of asthma. These adverse conditions may be especially troublesome for the high-performance athlete who has increased nasal airflow turbulence and who competes under extreme conditions that may worsen rhinitis and asthma. Under the theory of the unified airway, an immune response induced in the nose may extend into the lungs via cytokines and other inflammatory mediators. Nasal congestion can significantly contribute to sleep dysfunction, leading to daytime fatigue and decreased performance. Treatment of allergic rhinitis can improve sleep and foster productivity. Control of rhinitis and nasal congestion, which is obtained by various therapies, may reverse lower airway tendency to bronchoconstriction.     

Multiple sclerosis,the microbiome,TLR2, and the hygiene hypothesis

The pathophysiology of autoimmune diseases such as Multiple Sclerosis (MS) involves a complex interaction between genetic and environmental factors. Studies of monozygotic twins suggest a significant role for environmental factors in susceptibility to MS. Numerous studies, driven by the “Hygiene Hypothesis,” have focused on the role of environmental factors in allergic and autoimmune diseases. The hygiene hypothesis postulates that individuals living in environments that are too “clean” lack the requisite exposure to “immune-tolerizing” microbial products, resulting in poorly regulated immune systems and increased immune-mediated diseases. Interestingly, few studies have linked MS with the hygiene hypothesis. Similarly, although numerous studies have examined the role of the microbiome in autoimmune diseases, there has been no consistent documentation of disease-specific alterations in the MS microbiome. In this review, we present evidence that integrating the hygiene hypothesis and the microbiome allows for the identification of novel pathophysiologic mechanisms in MS.Our central hypothesis is that the microbiome in MS represents a “defective environment” that fails to provide normal levels of “TLR2-tolerizing” bacterial products to the systemic immune system. Consistent with the hygiene hypothesis, we posit that this defective microbiome function results in abnormally regulated systemic innate immune TLR2 responses that play a critical role in both the inflammatory and defective remyelinative aspects of MS. We have completed proof of concept studies that support the inflammatory, remyelinating, and human immune response components of this paradigm. Our studies suggest that induction of TLR2 tolerance may represent a novel approach to treating MS, inhibiting autoimmune inflammation while simultaneously facilitating remyelination.