心脏黏液瘤48例外科治疗

 目的　探讨心脏黏液瘤的临床诊断与外科手术治疗的特点。方法　1997年1月至2007年12月收治的48例心脏黏液瘤患者在体外循环下接受手术治疗，同期施行三尖瓣成形术5例，房间隔缺损修补术6例，二尖瓣成形术2例，二尖瓣替换术1例。结果　所有患者术前均经彩色超声明确诊断。全部患者在体外循环下切除肿瘤，无死亡病例。其中左心房黏液瘤42例，右心房黏液瘤6例。经病理证实全部为黏液瘤。共获随访22例，2例黏液瘤患者术后12个月复发。结论　彩色超声心动图对心脏黏液瘤的确诊具有特殊价值，心脏黏液瘤有阻碍血流、栓塞和猝死的危险，一经确诊应尽快手术切除。     

右心房石化心脏黏液瘤1例

心脏黏液瘤是最常见的原发性心脏肿瘤,多见于左心房,右心房少见,心室罕见[1]。部分黏液瘤呈实质性,也可见大片钙化,甚至钙化扩展到肿瘤的大部分区域,整个肿瘤呈一个钙化的包块,被称为"石化心脏黏液瘤"[1]。我院2003年2月至2013年1月经外科手术切除的149例心脏黏液瘤     

心脏黏液瘤3例报告

心脏肿瘤较少见 ,我院１９９８年６月至２００２年１０月经彩超诊断 ,并经省级医院手术证实心脏黏液瘤３例 ,现报告如下 :例１ ,女性 ,４２岁 ,反复心悸、乏力１年 ,加重１个月。查体 :Ｔ３８．３℃ ,ＢＰ１４／９ｋＰａ,一般情况稍差 ,颈静脉轻度怒张 ,三尖瓣听诊区可闻及双期杂音。余无殊。彩超检查见 :右房扩大 ,４５ｍｍ×５６ｍｍ ,右房内见一强回声光团 ,大小为２８ｍｍ×２５ｍｍ ,借一蒂附着于三尖瓣隔叶根部 ,随心动周期在右房与三尖瓣口间活动 ,收缩期返回右房内 ,舒张期脱入三尖瓣口 ,造成三尖瓣口梗阻。彩色多普勒血流显像（Ｃ…     

47例心脏黏液瘤的诊治分析

目的 探讨心脏黏液瘤诊治的经验，减少误诊。方法 对47例心脏黏液瘤患者诊疗确诊后进行全麻体外循环下心内直视手术摘除，分析、总结。结果 许多心脏黏液瘤患者症状不典型，容易误诊。结论 对怀疑心脏黏液瘤的患者应及早作心脏超声确诊，尽早手术，减少栓塞，猝死等并发症。     

白细胞介素6与癌变

白细胞介素6(IL-6)是一种多生物活性的细胞因子,它涉及到机体内许多生理和病理的复杂过程。并与临床诸多重要疾病的发生和转归密切相关。由于上述原因,IL-6在被发现的早期,根据其功能和特性被冠以多种不同的名称。经分子克隆研究,现已明确它的分子结构,并对名称作了统一,但原名之一——杂交瘤/浆细胞瘤生长因子很容易使人联想到其与肿瘤细胞的生长有关。目前许多学者通过大量临床和实验研究,认为IL-6参与某些肿瘤的发生和发展过程。作者就近期有关资料作一概述。     

CNC心脏黏液瘤的研究进展

Carney综合征（carney complex,CNC）是一种因17号染色体基因突变导致的累及全身多器官系统的罕见疾病,具有家族聚集性的特点。临床表现以皮肤改变、心脏肿瘤等多见。本文围绕CNC心脏黏液瘤的发病特点,说明散发性心脏黏液瘤与CNC心脏肿瘤的不同,阐述CNC心脏黏液瘤临床表现并结合超声心动图等多种辅助检查明确心脏黏液瘤的诊断优势,说明CNC的诊断标准,为临床诊断和治疗提供方向。心脏黏液瘤治疗方法目前主要包括:胸骨正中切开术、微创等,介绍两种术式利弊,为临床治疗提供参考。本文针对CNC累及心脏的临床表现、辅助检查、治疗等进行概述,以期为临床医生提高诊断率和选择合适治疗方案提供思路。     

白细胞介素10和白细胞介素6在淋巴瘤中的表达及其意义

 【摘要】　目的　探讨白细胞介素（IL）-10和IL-6在不同类型淋巴瘤组织与血浆中的表达及其意义。方法　收集97例淋巴瘤患者石蜡组织和血浆标本,应用免疫组织化学和酶联免疫吸附试验（ELISA）的方法观察组织与血浆中IL-10和IL-6表达情况。结果　IL-10和IL-6在不同类型淋巴瘤组织中皆呈阳性表达,且各亚型之间差异无统计学意义（χ2＝0.815,χ2＝0.542,均P＞0.05）;IL-10和IL-6分别在肿瘤中的巨噬细胞和血管内皮细胞也有不同程度的阳性表达。淋巴瘤患者血浆IL-10和IL-6水平[（232.57±191.59）pg／ml、（80.70±89.68）pg／ml]高于健康对照组[（59.12±68.35）pg／ml、（45.68±33.66）pg／ml],差异有统计学意义（t＝6.968,t＝2.896,P＜0.05）;血浆IL-10和IL-6水平随肿瘤细胞表达强度增强而增强（χ2＝0.815,χ2＝0.542,P＜0.05）;IL-10和IL-6在淋巴瘤细胞表达强度两者呈正相关（rs＝0.394,P＜0.05）。结论　IL-10和IL-6在淋巴瘤患者淋巴瘤组织和血浆中都有表达,淋巴瘤患者血浆IL-10和IL-6水平高于健康对照组,二者在淋巴瘤的发生、发展中起着一定的作用,可能作为淋巴瘤诊断的辅助指标。     

47例心脏黏液瘤的诊治分析

目的　探讨心脏黏液瘤诊治的经验 ,减少误诊。方法　对 47例心脏黏液瘤患者诊疗确诊后进行全麻体外循环下心内直视手术摘除 ,分析、总结。结果　许多心脏黏液瘤患者症状不典型 ,容易误诊。结论　对怀疑心脏黏液瘤的患者应及早作心脏超声确诊 ,尽早手术 ,减少栓塞 ,猝死等并发症。     

核因子κB白细胞介素6和白细胞介素8在食管癌组织中的表达及意义

目的研究核因子(NF-κB)、白细胞介素6(IL-6)和白细胞介素8(IL-8)在食管癌组织中的表达及意义。方法收集48例食管癌组织,以癌旁正常食管黏膜组织为对照,采用免疫组化SABC法检测NF-κB、IL-6和IL-8的蛋白表达情况,并分别探讨与食管癌临床病理特征的相关关系。结果在食管癌组织、癌旁正常组织中,NF-κB的阳性表达率分别为79.2%和45.8%,IL-6为75.0%和41.7%,IL-8为83.3%和52.1%,差异均具有统计学意义(均P<0.05)。食管癌组织中NF-κB的表达与IL-6和IL-8的表达密切相关。NF-κB、IL-8的表达与淋巴结转移和分期相关,IL-6的表达与脉管受侵、淋巴结转移和分期相关。结论 NF-κB及下游的炎症因子的高表达与食管癌的临床病理特征密切相关,提示NF-κB途径在食管癌的发生发展中起着重要的作用。     

乳腺癌患者白介素6及其受体的测定和临床意义

目的研究白介素６（ＩＬ６）及其受体与乳腺癌的发生、发展关系。方法应用ＥＬＩＳＡ检测法及ＡＢＣ免疫组化法测定４５例乳腺癌、１０例良性乳腺病ＩＬ６及其受体水平,并以１７例健康妇女为对照。结果乳腺癌外周血清ＩＬ６、可溶性受体（ｓＩＬ６Ｒα、ｓｇｐ１３０）水平明显高于良性病组及正常对照组,且随病情进展而升高,与腋窝淋巴结转移呈正相关。标本中癌组织ＩＬ６及其膜性受体（ＩＬ６Ｒα、ｇｐ１３０）阳性表达率均为６８．９％,与临床特征无关,良性组织及正常组织中三者阳性率均为１００％。结论提示ＩＬ６、ｓＩＬ６Ｒα和ｓｇｐ１３０可能是反映乳腺癌生物学行为及预后的重要指标。     

肺癌患者白介素6浓度水平的变化分析

目的:探讨肺癌患者血清、痰、诱导痰中白介素6(Ⅱ-6)的水平.方法:选择有病理学依据的中心性肺癌21例及健康对照组29例,测定其血清、痰、诱导痰的白介素6浓度.结果:肺癌组与对照组血清、痰、诱导痰中白介素6浓度之间有差别(P＜0.05),其血清、痰、诱导痰有相关性,r＞0.594,P＜0.05.结论:肺癌组的血清、痰、诱导痰中白介素6浓度有较高水平,痰与诱导痰相关性最好.     

肺癌患者白介素6浓度水平的变化分析

目的 :探讨肺癌患者血清、痰、诱导痰中白介素 6 (IL 6 )的水平。方法 :选择有病理学依据的中心性肺癌 2 1例及健康对照组 2 9例 ,测定其血清、痰、诱导痰的白介素 6浓度。结果 :肺癌组与对照组血清、痰、诱导痰中白介素 6浓度之间有差别 (P <0 .0 5 ) ,其血清、痰、诱导痰有相关性 ,r >0 .5 94 ,P <0 .0 5。结论 :肺癌组的血清、痰、诱导痰中白介素 6浓度有较高水平 ,痰与诱导痰相关性最好。     

IL-6、IL-8与卵巢癌

与卵巢癌有关的细胞因子众多,其中IL-6和IL-8的异常表达在卵巢癌的发生、发展中起着十分重要的作用.对其深入探究将有助于阐明卵巢癌的发病机制,协助临床诊断和病情估计,并为卵巢癌的生物治疗提供新的线索和途径.     

心脏黏液瘤36例手术治疗的回顾性分析

目的 总结心脏黏液瘤的外科治疗经验.方法 36例心脏黏液瘤患者(左心房黏液瘤32例,右心房黏液瘤3例,左心室黏液瘤1例)均在低温体外循环下接受黏液瘤摘除术,1例同时行三尖瓣成形术,1例同时行二尖瓣成形术.结果 全组无围手术期死亡病例,随访18(2 ～36)个月,无一例术后复发和远处种植转移.结论 心脏黏液瘤手术疗效好,确诊后应立即手术.     

Interleukin-6 and Granulocyte Colony-stimulating Factor Synergistically Increase Peripheral Blood Progenitor Cells in Myelosuppressive Mice

We previously reported a successful peripheral blood stem cell harvest by co-administration of recombinant human (rh) interleukin-6 (IL-6) and rh granulocyte colony-stimulating factor (G-CSF) in normal mice. In the present study, to evaluate further the utility of this observation for autologous peripheral blood stem cell transplantation, we examined the effects of rhIL-6 and rhG-CSF on peripheral blood granulocyte-macrophage colony-forming units (CFU-GM) in carboplatin (CBDCA)-induced and irradiation-induced myelosuppressive mouse models. After CBDCA administration, blood cell counts decreased to the nadir, and then recovered to a normal level. In this recovery phase, the peripheral CFU-GM level increased to 3.8-fold higher than the pretreatment level. Administration of rhIL-6 (10 μg/day) alone induced a 40-fold increase in peripheral CFU-GM from the normal level at day 14. In combination with rhG-CSF (0.35 μg/day), which alone induced a 74-fold increase, rhIL-6 synergistically increased the CFU-GM level by 1200-fold. In irradiated mice, similar results were observed. Administration of rhIL-6 at 3 and 10 μg/day significantly increased CFU-GM. Interestingly, in combination with rhG-CSF, a lower dose of rhIL-6 (1 μg/day) could induce CFU-GM increase. We also examined CFU-GM distribution in bone marrow, spleen and peripheral blood. Cytokine administration induced not only a change of CFU-GM distribution, but also an increase in total CFU-GM counts per mouse. These results suggest that co-administration of rhIL-6 and rhG-CSF may be useful for autologous peripheral blood stem cell transplantation.     

癌症疼痛患者外周血中IL-1β、IL-6、TNF-α的检测

[目的]通过检测肿瘤患者外周血中IL-1β、IL-6、TNF-α的表达水平，探讨IL-1β、IL-6、TNF-α的表达与癌症疼痛的关系。[方法]选取38例癌症疼痛的肿瘤患者作为病例组，同时选取30例健康人群和30例无疼痛的肿瘤患者作为对照组，两组均采集空腹时静脉血5ml，采用ELISA法检测IL-1β、IL-6、TNF-α的水平。[结果]癌症疼痛患者外周血IL-1β、IL-6、TNF-α的表达水平明显高于对照组（P〈0．05），30例健康人群和30例无疼痛的肿瘤患者两组之间也具有明显差异（P〈0．05），轻度疼痛组表达水平显著低于中重度疼痛组（P〈0．05），吗啡治疗疼痛效果差的患者外周血中细胞因子IL-1β、IL_6、TNF-α的表达水平明显高于吗啡治疗疼痛效果好的患者（P〈0．05）。[结论]癌症疼痛患者IL-1β、IL-6、TNF-α的表达水平明显增高，与疼痛程度有着密切的关系，其高表达可能与吗啡止痛效果欠佳有关。     

Interleukin-6 and its receptor in cancer: implications for translational therapeutics

Interleukin-6 (IL-6) plays a major role in the response to injury or infection and is involved in the immune response, inflammation, and hematopoiesis. Its deregulation impacts numerous disease states, including many types of cancer. Consequently, modulating IL-6 may be an innovative therapeutic strategy in several diseases. A review of relevant published literature regarding IL-6 and its receptor was performed. In addition, a review of the relevance of this cytokine system to human illness, particularly in cancer, was undertaken. IL-6 is a pleiotropic cytokine that is involved in the physiology of virtually every organ system. Aberrant expression of this cytokine has been implicated in diverse human illnesses, most notably inflammatory and autoimmune disorders, coronary artery and neurologic disease, gestational problems, and neoplasms. In cancer, high levels of circulating IL-6 are observed in almost every type of tumor studied and predict a poor outcome. Furthermore, elevated IL-6 levels are associated strongly with several of the striking phenotypic features of cancer. Several molecules have been developed recently that target the biologic function of IL-6. Early results in the clinic suggest that this strategy may have a significant salutary impact on diverse tumors. The field of cytokine research has yielded a deep understanding of the fundamental role of IL-6 and its receptor in health and disease. Therapeutic targeting of IL-6 and its receptor in cancer has strong biologic rationale, and there is preliminary evidence suggesting that targeting of the IL-6 system may be beneficial in the treatment of cancer.     

Interleukin-6 and melanoma

Interleukin-6 (IL-6) is a pleiotropic immunomodulatory cytokine produced by various types of cells, including melanoma cells. IL-6 plays a major role in the pathogenesis and development of malignancies. It promotes tumour growth by inhibition of apoptosis and induces tumour angiogenesis. IL-6 is deregulated in many types of cancers, and increased serum concentration of IL-6 has been correlated with a worse prognosis in patients with different cancers, including melanoma. Several serum cytokines including IL-6 play an important role in the development and progression of melanoma; however, the specific biological functions of IL-6 in progression of melanoma are unknown. In this review, we present studies on cell cultures and mouse models and summarize published clinical studies on IL-6 and melanoma.     

Interleukin-6 and its receptor, key players in hepatobiliary inflammation and cancer

In recent years, the relationship between interleukin-6 (IL-6), hepatobiliary inflammation, and cancer has been studied. It is becoming clear that this cytokine plays an important role in the pathogenesis of both cholangiocarcinoma (CCA, cancer of the bile ducts) and hepatocellular carcinoma (HCC, cancer arising from the liver parenchyma). Inflammation due to various chronic hepatobiliary diseases including hepatitis B, hepatitis C, alcoholic liver injury, and primary sclerosing cholangitis (PSC) has been associated with increased levels of IL-6 and with increased rates of malignancy. In this review, we will summarize the current knowledge linking inflammation to hepatobiliary cancer, and discuss the key role of IL-6 and its signaling pathways in mediating this link. We will first review the major signaling pathways that are triggered when IL-6 engages its receptor. These include PI3 kinase, JAK/STAT, p38 MAP kinase and others that ultimately lead to cell proliferation, protection from apoptosis and increased metastatic potential. We will then discuss data linking IL-6 and hepatobiliary cancer, namely HCC and CCA.