个体化假体复合组织工程技术修复兔下颌骨缺损

目的研究快速成型（RP）技术辅助下制作的个体化假体复合珊瑚羟基磷灰石（CHA）、重组人骨形成蛋白2（rhBMP-2）修复兔下颌骨缺损的成骨效果。 方法以27只新西兰大白兔为实验对象，随机数字表法平均分成3组（每组9只），全部建立下颌骨连续性缺损模型，并在兔下颌骨缺损区分别植入个体化假体+自体骨（A组）、个体化假体+CHA（B组）、个体化假体+CHA+rhBMP-2（C组）。分别于术后4、12、24周3个时间点处死动物取材，进行大体标本观察，以及骨钙素（OC）、Ⅰ型胶原（COL-1）的免疫组化观察，分别比较各组修复骨缺损的能力，并对实验数据进行重复测量设计资料的单因素方差分析。 结果术后24周各组实验兔外形均对称，通过OC及COL-1的吸光度检测，骨缺损区均有大量新骨形成，A组（0.537 ± 0.010）、C组（0.530 ± 0.010）可见大量骨小梁及编织骨结构，缺损区的新骨OC、COL-1的免疫组化观察基本一致，差异无统计学意义（t = 0.007，P>0.05）；但A组强于B组（0.415 ± 0.009，t = 0.122，P<0.001）；C组也强于B组（t = 0.121，P<0.001），差异均有统计学意义。 结论在兔下颌骨缺损修复中，通过RP技术和组织工程技术相结合，CHA复合rhBMP-2后成骨能力明显增强，成骨效能肯定，为后期的临床应用提供可靠的实验基础。     

高校附属医院文化建设和党建工作的关系研究

文化建设与党建工作之间存在着一定的关联,随着经济的不断发展,我国卫生管理体制改革也不断深入,在此过程中,对于高校附属医院文化建设和党建工作提出更高水平的要求。从医院层面来看,通过加强文化建设以及发展党建工作,能够有效提高医院的凝聚力,促进医院树立良好的形象、培养优秀的医护人员等。文化建设和党建工作息息相关,在医院管理与发展的过程中,两者之间相辅相成。文章在研究的过程中,采用访谈法、问卷调查法等方法,通过访谈法、问卷调查法对医院各个方面人员进行调查,根据调查结果总结高校附属医院文化建设和党建工作的关系。     

妊娠梅毒36例临床分析

目的回顾性分析妊娠梅毒36例,研究妊娠梅毒临床及辅助检查特点,寻求早期有效处置措施,改善妊娠结局,将梅毒对妊娠的危害降至最低。方法回顾性分析2016年6月至2020年10月于东台市中医院皮肤科性病中心门诊就诊的36例妊娠梅毒患者的资料,依次接受快速血浆反应素环状卡片试验(RPR)和梅毒螺旋体抗体明胶颗粒凝集试验(TPPA),并根据检查结果为患者实施有效治疗。结果36例妊娠梅毒患者RPR检查结果显示,滴度1∶2~1∶8之间18例,1∶16~1∶32之间12例,1∶32以上6例;TPPA检查显示患者均呈阳性。36例患者中1例临近分娩未接受治疗,1例青霉素过敏给予红霉素治疗,其余予以芐星青霉素治疗,患者中死胎1例,人工流产2例,自然流产2例。产后新生儿7例RPR阳性,TPPA检查显示均呈阳性;跟踪随访得知多数患者在1年内RPR结果转为阴性,仅有3例1年后转阴。结论妊娠梅毒患者早期运用RPR、TPPA检查方法进行诊断,并及时采取有效治疗方案进行处理,可有效预防不良妊娠结局,并改善新生儿预后情况。     

声门型喉癌T_3病变喉部分切除术后疗效评价

目的　探讨喉部分切除术对声门型喉癌T3 病变的可行性及修复材料的选择。方法　对 1986年 1月～ 1994年 1月 78例行喉部分切除术的声门型喉癌T3 病变患者的术式及修复方法进行了回顾性分析。结果　患者 3年、5年生存率分别为 88 5 %、75 6 % ,局部复发率 15 4%。应用了梨状窝粘膜 甲状软骨板外侧软骨膜、会厌软骨瓣及带状肌双肌双蒂瓣 3种方法修复创面 ,均获得了较好的喉功能恢复。结论　喉部分切除术是根治声门型喉癌T3 病变合理、有效的方式 ,但不能完全替代全喉切除术 ,应根据切除范围选择合理的修复方式。     

18例原发性结外型非何杰金淋巴瘤临床分析

恶性淋巴瘤有少部分患者可首发于淋巴结外，本文报告18例原发于结外的非何杰金淋巴瘤，其中发生于胃肠道的9例，头颈部6例，其他部位少见。病理学特点多为弥漫型。手术在结外非何杰金淋巴瘤的诊断和治疗中占首要地位。本组结外非何杰金淋巴瘤首选手术16例，首选化疗2例，总的完全缓解（CR）为13例，占72％。     

Cholangiocyte endothelin 1 and transforming growth factor beta1 production in rat experimental hepatopulmonary syndrome

BACKGROUND & AIMS: Hepatic production and release of endothelin 1 plays a central role in experimental hepatopulmonary syndrome after common bile duct ligation by stimulating pulmonary endothelial nitric oxide production. In thioacetamide-induced nonbiliary cirrhosis, hepatic endothelin 1 production and release do not occur, and hepatopulmonary syndrome does not develop. However, the source and regulation of hepatic endothelin 1 after common bile duct ligation are not fully characterized. We evaluated the sources of hepatic endothelin 1 production after common bile duct ligation in relation to thioacetamide cirrhosis and assessed whether transforming growth factor beta1 regulates endothelin 1 production. METHODS: Hepatopulmonary syndrome and hepatic and plasma endothelin 1 levels were evaluated after common bile duct ligation or thioacetamide administration. Cellular sources of endothelin 1 were assessed by immunohistochemistry and laser capture microdissection of cholangiocytes. Transforming growth factor beta1 expression and signaling were assessed by using immunohistochemistry and Western blotting and by evaluating normal rat cholangiocytes. RESULTS: Hepatic and plasma endothelin 1 levels increased and hepatopulmonary syndrome developed only after common bile duct ligation. Hepatic endothelin 1 and transforming growth factor beta1 levels increased over a similar time frame, and cholangiocytes were a major source of each peptide. Transforming growth factor beta1 signaling in cholangiocytes in vivo was evident by increased phosphorylation and nuclear localization of Smad2, and hepatic endothelin 1 levels correlated directly with liver transforming growth factor beta1 and phosphorylated Smad2 levels. Transforming growth factor beta1 also stimulated endothelin 1 promoter activity, expression, and production in normal rat cholangiocytes. CONCLUSIONS: Cholangiocytes are a major source of hepatic endothelin 1 production during the development of hepatopulmonary syndrome after common bile duct ligation, but not in thioacetamide-induced cirrhosis. Transforming growth factor beta1 stimulates cholangiocyte endothelin 1 expression and production. Cholangiocyte-derived endothelin 1 may be an important endocrine mediator of experimental hepatopulmonary syndrome.     

Endothelin-1 Activation of the Endothelin B Receptor Modulates Pulmonary Endothelial CX3CL1 and Contributes to Pulmonary Angiogenesis in Experimental Hepatopulmonary Syndrome

Hepatic production and release of endothelin-1 (ET-1) binding to endothelin B (ET_B) receptors, overexpressed in the lung microvasculature, is associated with accumulation of pro-angiogenic monocytes and vascular remodeling in experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL). We have recently found that lung vascular monocyte adhesion and angiogenesis in HPS involve interaction of endothelial C-X3-C motif ligand 1 (CX3CL1) with monocyte CX3C chemokine receptor 1 (CX3CR1), although whether ET-1/ET_B receptor activation influences these events is unknown. Our aim was to define if ET-1/ET_B receptor activation modulates CX3CL1/CX3CR1 signaling and lung angiogenesis in experimental HPS. A selective ET_B receptor antagonist, BQ788, was given for 2 weeks to 1-week CBDL rats. ET-1 (±BQ788) was given to cultured rat pulmonary microvascular endothelial cells overexpressing ET_B receptors. BQ788 treatment significantly decreased lung angiogenesis, monocyte accumulation, and CX3CL1 levels after CBDL. ET-1 treatment significantly induced CX3CL1 production in lung microvascular endothelial cells, which was blocked by inhibitors of Ca²⁺ and mitogen-activated protein kinase (MEK)/ERK pathways. ET-1–induced ERK activation was Ca²⁺ independent. ET-1 administration also increased endothelial tube formation in vitro, which was inhibited by BQ788 or by blocking Ca²⁺ and MEK/ERK activation. CX3CR1 neutralizing antibody partially inhibited ET-1 effects on tube formation. These findings identify a novel mechanistic interaction between the ET-1/ET_B receptor axis and CX3CL1/CX3CR1 in mediating pulmonary angiogenesis and vascular monocyte accumulation in experimental HPS.Cirrhosis and portal hypertension result in vascular alterations in several organ systems, which impair the function of these organs.^1,2 The hepatopulmonary syndrome (HPS) is one such complication, in which intrapulmonary vascular abnormalities cause abnormal arterial gas exchange in 5% to 30% of cirrhotic patients.^3–5 The presence of HPS significantly decreases quality of life and increases mortality in those affected.⁶ Currently, the pathogenesis of vascular alterations in HPS is incompletely understood, limiting the development of effective medical therapies.Chronic common bile duct ligation (CBDL) in the rat is an established experimental model of HPS that reproduces the physiological abnormalities of human disease.^7–16 These animals develop pulmonary microvascular dilations and also develop vascular remodeling, which is linked to the accumulation of intravascular monocytes and vascular endothelial growth factor-A (VEGF-A) production.^11,12,17,18 Pulmonary vasodilation results, in large part, from Ca²⁺-dependent and protein kinase B/Akt–independent activation of pulmonary vascular endothelial nitric oxide synthase (eNOS)/NO, by hepatic production and release of endothelin-1 (ET-1) and stimulation of lung vascular endothelin B (ET_B) receptors.^9,19 ET-1/ET_B receptor activation also enhances pulmonary vascular monocyte accumulation,¹⁴ thereby promoting angiogenesis through monocyte VEGF-A production and activation of Akt and ERK. However, how ET-1/ET_B receptor activation modulates monocyte accumulation and whether ET_B receptor activation has direct effects on angiogenesis are unknown.We have recently found that the chemokine ligand/receptor pair C-X3-C motif ligand 1 (CX3CL1)/CX3C chemokine receptor 1 (CX3CR1) is up-regulated in the pulmonary microvasculature after CBDL and contributes to monocyte accumulation and to angiogenesis after CBDL.²⁰ Interaction between the membrane-bound form of CX3CL1 with CX3CR1 is unique in the ability to cause firm adhesion between cell types (monocyte-endothelium).^21–24 In addition, the secreted soluble form of CX3CL1, through interaction with the CX3CR1 on endothelial cells, can drive angiogenesis through Akt and ERK activation.²⁵ However, whether ET-1/ET_B receptor activation after CBDL influences monocyte accumulation or angiogenesis by affecting lung CX3CL1/CX3CR1 expression has not been tested. Therefore, the aims of the present study were to define if the ET-1/ET_B receptor activation modulates the pulmonary CX3CL1/CX3CR1 axis and to determine how it contributes to vascular remodeling in experimental HPS. To do this, we assessed the effects of selective ET receptor inhibition on pulmonary angiogenesis and CX3CL1/CX3CR1 expression in vivo and evaluated the effects of exogenous ET-1 on pulmonary microvascular endothelial cell CX3CL1 expression and angiogenesis in vitro.     

甘氨酸龈下喷砂联合引导组织再生术治疗种植体周围炎

目的探讨甘氨酸龈下喷砂联合引导组织再生术（GTR）治疗种植体周围炎的有效性。 方法28例伴有牙槽骨吸收的种植体周围炎患者,按照随机、双盲、对照原则将种植体（共34枚）分成2组,分别行GTR,其中试验组（n= 18）在术中使用甘氨酸龈下喷砂系统对种植体表面进行清创;对照组（n= 16）采用塑料刮治器对种植体表面进行清创。在治疗前（基线）、治疗后3个月、治疗后6个月和治疗后12个月进行临床指标的检测,包括菌斑指数（PLI）、出血指数（BI）、探诊深度（PD）、临床附着水平（CAL）及影像学垂直骨增量。数据采用重复测量资料的方差分析,每个时间点采用独立样本t检验进行分析,试验组和对照组分别进行治疗前与治疗后的自身对比,并在基线、治疗后3个月、治疗后6个月和治疗后12个月进行临床指标的组间对比,以P<0.05为差异有统计学意义。 结果在基线,试验组和对照组各临床指标差异无统计学意义（P>0.05）。各组术后PLI、BI、PD、CAL及影像学垂直骨增量均较治疗前（基线）有明显改善,差异有统计学意义（P<0.05）。患者治疗后3个月,试验组与对照组BI、PLI、PD、CAL差异均有统计学意义（t_BI= 5.103,P_BI= 0.031;t_PLI= 5.556,P_PLI= 0.025;t_PD= 4.440,P_PD= 0.043;t_CAL= 4.879,P_CAL= 0.034）。患者治疗后6个月,试验组和对照组的PD、CAL差异均有统计学意义（t_PD= 4.994,P_PD= 0.033;t_CAL= 4.831,P_CAL= 0.035）。患者治疗后12个月,试验组和对照组的PD、CAL差异均有统计学意义（t_PD= 4.302,P_PD= 0.046;t_CAL= 4.325,P_CAL= 0.048）。患者治疗后6及12个月,试验组与对照组种植体的PLI和BI均有改善,但差异无统计学意义（P>0.05）。患者影像学垂直骨增量在治疗后3、6、12个月试验组较对照组增加更明显,差异均有统计学意义（t₃=4.831,P₃= 0.035;t₆= 4.412,P₆= 0.044;t₁₂= 5.087,P₁₂= 0.031）。 结论在改善种植体周围炎炎症水平及促进牙槽骨再生方面,甘氨酸龈下喷砂联合GTR较机械刮治联合GTR更具优势,可考虑在GTR中使用甘氨酸龈下喷砂来提高种植体周围炎的治疗效果。     

超声引导下椎旁神经阻滞治疗带状疱疹相关疼痛的Meta分析

文题释义： 椎旁神经阻滞：是通过将局麻药物注射到椎旁间隙内而实现,阻滞包括椎旁脊神经和其分支以及交感干,具有简单、易行、有效及低廉等特点。 带状疱疹相关疼痛：是由于潜伏在感觉神经节的水痘带状疱疹病毒被重新激活引起的近期或远期疼痛。主要包括带状疱疹急性期疼痛(即带状疱疹痛)和带状疱疹后神经痛。疼痛常表现为典型的病理性神经痛特点,主要特征是自发痛、痛觉过敏、感觉异常等,呈电击样、烧灼样、针刺样等疼痛。 背景：目前临床研究显示超声引导下椎旁神经阻滞治疗胸腰段带状疱疹相关疼痛有显著效果,并在临床上得到了广泛使用。 目的：系统评价超声引导下椎旁神经阻滞治疗胸腰段带状疱疹相关疼痛的有效性及安全性,为临床治疗提供参考依据。 方法：检索PubMed、The Cochrane Library、EMBASE、CNKI、WanFang Data、VIP以及CBM等数据库,检索时限为建库至2019-01-01。根据制定的纳入和排除标准,收集有关超声引导下椎旁神经阻滞治疗及药物治疗胸腰段带状疱疹急性期疼痛或带状疱疹后神经痛的随机对照试验,以超声引导下胸椎旁神经阻滞组作为实验组,药物治疗组或传统椎旁神经阻滞组作为对照组。依据Cochrane Handbook 5.1.0偏倚风险评估工具评价纳入文献质量。通过Revman 5.3软件对文献数据进行Meta分析。 结果与结论：①最终纳入11项随机对照试验研究文献,共916例受试者;②Meta分析结果显示：与对照组相比,超声引导下椎旁神经阻滞组的镇痛效果更好,在1-4周内临床镇痛效果最佳,采用随机效应模型下分析,1周：MD=-0.91,95%CI(-1.22,-0.61),P < 0.000 01;2周：MD=-1.11,95%CI(-1.52,-0.70),P < 0.000 01;3周：MD= -1.26,95%CI(-1.79,-0.74),P < 0.000 01;4周：MD= -0.90,95%CI(-1.57,-0.24),P=0.007;同时睡眠质量及治疗有效率均有提高[固定效应模型下分析,OR=3.63,95%CI(2.38,5.53),P < 0.000 01],统计结果差异有显著性意义,并且具有未增加整个治疗过程的不良反应等优点;③结果说明,超声引导下椎旁神经阻滞治疗胸腰段带状疱疹相关疼痛是安全和有效的。 ORCID: 0000-0001-7945-6411(宋旭东) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程