颈动脉海绵窦瘘的血管内治疗

目的：探讨有关颈动脉海绵窦瘘经血管内治疗的研究进展.方法：广泛查阅国内外相关颈动脉海绵窦瘘血管内治疗的资料,并进行分析和总结.结果：多种血管内技术可以安全、有效地治疗颈动脉海绵窦瘘.结论：随着神经介入放射学的发展,血管内栓塞治疗法以其创伤小、方法简便、疗效可靠的优点成为治疗颈动脉海绵窦瘘的首选方法.     

大鼠脾气虚胃溃疡证病结合模型胃肠粘膜局部免疫-神经-内分泌网络的变化

目的 探讨脾气虚胃溃疡证病结合模型中胃肠粘膜局部神经内分泌免疫(INE)网络的变化及其作用。方法 免疫组织化学染色和图像分析技术。结果 脾气虚合并胃溃疡模型中胃粘膜D细胞分泌SST的活性显著增强；空、回肠分泌SP、VIP神经元的活性增强；胃粘膜免疫细胞分泌IL-2的活性增强。结论 大鼠脾气虚胃溃疡模型的SST、SP、VIP、IL-2的合成及分泌水平发生了改变，表明胃肠粘膜局部免疫、神经、内分泌网络均发生了一定程度的变化，是脾虚胃溃疡发生的重要因素。     

Correlated expression of inducible nitric oxide synthase and P53, bax in benign and malignant diseased gallbladder

Our goal has been to investigate the expression and correlated significance of inducible nitric oxide synthase (iNOS) and P53, Bax in benign and malignant gallbladder diseases. We detected the expression of iNOS, P53 and Bax in the gallbladder wall by SP immunohistochemistry in 16 cases of chronic cholecystitis, 11 cases of chronic cholecystitis with adenomyoma and 24 cases of gallbladder adenocarcinoma. The percentage of positively marked tumor cells was counted under microscope and the intensity of immunoreactivity was graded. SPSS10.0 statistical software was applied for statistical analysis. In this study, we found that: (1) Both benign and malignant diseased gallbladder wall expressed iNOS and Bax. Compared to benign diseased gallbladders, their expression in adenocarcinoma was decreased (p < 0.05), P53 was expressed strongly only in nuclei of adenocarcinoma cells of some cases. (2) In benign and malignant diseased gall-bladders, iNOS expression was related positively to Bax (p < 0.01), the expression of P53 and Bax had a negative relationship (p < 0.01). The results suggested that both chronic cholecystitis and chronic cholecystitis with adenomyoma carry the risk of becoming malignant, especially the latter. NO is an important mediated molecule in cancer, there are intimate relationships between gallbladder cancer and apoptosis.     

乳管瘘的诊断和治疗

目的 探讨乳管瘘的诊断和治疗方法。方法 分析总结乳管瘘46例，诊断主要依据病史、体征和病理检查，治疗是用美兰注入瘘管作标记，彻底切除瘘管，术后给予对需氧菌和厌氧菌有效的抗生素。结果 46例均经手术治愈，术后随访6个月-5年无复发。结论 结合病史，体征易于诊断。对疑为恶性病变或结核病人行细胞学检查或病理切片检查。为了防止乳瘘管复发，应彻底切除瘘管。     

Epidermal growth factor and insulin short‐term increase hPepT1‐mediated glycylsarcosine uptake in Caco‐2 cells

Aims: Little is known about the physiological regulation of the human intestinal di/tri‐peptide transporter, hPepT1. In the present study we evaluated the effects of epidermal growth factor (EGF) and insulin on hPepT1‐mediated dipeptide uptake in the intestinal cell line Caco‐2. Methods: Caco‐2 cells were grown on filters for 23–27 days. Apical dipeptide uptake was measured using [¹⁴C]glycylsarcosine([¹⁴C]Gly‐Sar). HPepT1 mRNA levels were investigated using RT‐PCR, cytosolic pH was determined using the pH‐sensitive fluorescent probe BCECF. Results: Basolateral application of EGF increased [¹⁴C]Gly‐Sar uptake with an ED₅₀ value of 0.77 ± 0.25 ng mL^?1 (n = 3?6) and a maximal stimulation of 33 ± 2% (n = 3?6). Insulin stimulated [¹⁴C]Gly‐Sar uptake with an ED₅₀ value of 3.5 ± 2.0 ng mL^?1 (n = 3?6) and a maximal stimulation of approximately 18% (n = 3?6). Gly‐Sar uptake followed simple Michaelis‐Menten kinetics. K_m in control cells was 0.98 ± 0.11 mM (n = 8) and V_max was 1.86 ± 0.07 nmol cm^?2 min^?1 (n = 8). In monolayers treated with 200 ng mL^?1 of EGF, K_m was 1.11 ± 0.05 mM (n = 5) and V_max was 2.79 ± 0.05 nmol cm^?2 min^?1 (n = 5). In monolayers treated with 50 ng mL^?1 insulin, K_m was 1.03 ± 0.08 mM and V_max was 2.19 ± 0.06 nmol cm^?2 min^?1 (n = 5). Kinetic data thus indicates an increase in the number of active transporters, following stimulation. The incrased Gly‐Sar uptake was not accompanied by changes in hPepT1 mRNA, nor by measurable changes in cytosolic pH. Conclusions: Short‐term stimulation with EGF and insulin caused an increase in hPepT1‐mediated uptake of Gly‐Sar in Caco‐2 cell monolayers, which could not be accounted for by changes in hPepT1 mRNA or proton‐motive driving force.     

Monocyte chemoattractant protein-1 (MCP-1) inhibits the intestinal-like differentiation of monocytes

Monocytes (MO) migrating into normal, non-inflamed intestinal mucosa undergo a specific differentiation resulting in a non-reactive, tolerogenic intestinal macrophage (IMAC). Recently we demonstrated the differentiation of MO into an intestinal-like macrophage (MAC) phenotype in vitro in a three-dimensional cell culture model (multi-cellular spheroid or MCS model). In the mucosa of patients with inflammatory bowel disease (IBD) in addition to normal IMAC, a reactive MAC population as well as increased levels of monocyte chemoattractant protein 1 (MCP-1) is found. The aim of this study was to investigate the influence of MCP-1 on the differentiation of MO into IMAC. MCS were generated from adenovirally transfected HT-29 cells overexpressing MCP-1, macrophage inflammatory protein 3 alpha (MIP-3alpha) or non-transfected controls and co-cultured with freshly elutriated blood MO. After 7 days of co-culture MCS were harvested, and expression of the surface antigens CD33 and CD14 as well as the intracellular MAC marker CD68 was determined by flow-cytometry or immunohistochemistry. MCP-1 and MIP-3alpha expression by HT-29 cells in the MCS was increased by transfection at the time of MCS formation. In contrast to MIP-3alpha, MCP-1 overexpression induced a massive migration of MO into the three-dimensional aggregates. Differentiation of IMAC was disturbed in MCP-1-transfected MCS compared to experiments with non-transfected control aggregates, or the MIP-3alpha-transfected MCS, as indicated by high CD14 expression of MO/IMAC cultured inside the MCP-1-transfected MCS, as shown by immunohistochemistry and FACS analysis. Neutralization of MCP-1 was followed by an almost complete absence of monocyte migration into the MCS. MCP-1 induced migration of MO into three-dimensional spheroids generated from HT-29 cells and inhibited intestinal-like differentiation of blood MO into IMAC. It may be speculated that MCP-1 could play a role in the disturbed IMAC differentiation in IBD mucosa.     

先天性冠状动脉瘘的临床解剖及外科治疗

目的:总结先天性冠状动脉瘘(CAF)的临床解剖特征及外科治疗效果。方法:本组26例,男16例,女10例,年龄7个月～58岁,平均(17.6±13.2)岁。右冠状动脉心腔瘘65.4%(17例),其中瘘口位于右心室6例,左心室2例,右心房5例,左心房4例;左冠状动脉心腔瘘26.9%(7例),其中瘘口位于右心室5例,左心室2例;左冠状动脉肺动脉瘘7.7%(2例)。单个瘘口23例,多个3例。根据其临床解剖特征,CAF在体外循环下闭合18例,非体外循环下直接结扎或缝扎8例,合并畸形同期处理。结果:本组患者无死亡。23例随访1个月～8年,平均2.8年,均无心肌梗死及残余瘘。22例心功能恢复至Ⅰ级,1例Ⅱ级。结论:外科治疗先天性冠状动脉瘘是安全和有效的方法,根据CAF的临床解剖特征,选用合适的手术方式是成功手术的关键。     

兔小肠黏膜下层与软骨细胞体外培养

目的观察软骨细胞在兔小肠黏膜下层(SIS)上的生长特性,为使SIS作为软骨组织工程化的载体打下基础。方法用物理和化学方法处理兔小肠黏膜下层,将不同浓度的兔软骨细胞与SIS进行体外共培养,分别进行组织学、相差显微镜和扫描电镜观察。结果经物理和化学处理的SIS纯度高、孔隙多,胶原纤维未受损;软骨细胞在SIS材料上生长、黏附、增殖,并能长入材料的孔隙内,分泌大量的细胞外基质成分。结论SIS细胞相容性良好,不影响软骨细胞的形态,对细胞生长和功能表达无抑制作用,是一种较理想的软骨细胞载体。     

新型射频组织焊接电极的设计、仿真与实验研究

目的 设计一种新型射频组织焊接电极,提高吻合口生物力学强度的同时减少组织热损伤。 方法 设计表面存在镂空结构的新型电极(梅花形电极),以环形电极作为对照组,在射频能量作用下完成肠道组织焊接,通过撕脱力和爆破压测试研究焊接吻合口的生物力学特性,采用有限元电-热-力多场耦合仿真分析和热电偶探针研究焊 接过程中的组织热损伤,并对微观组织结构进行检查。 结果 当焊接功率 120 W、焊接时间 8 s、压合压强 20 kPa时,肠道吻合口呈现最优的生物力学特性。 与环形电极对照组相比,梅花形电极组吻合口生物力学强度更高,撕脱力和爆破压分别从(8. 62±1. 22) N、(81. 7±3. 36) mmHg 增加到 (9. 54±1. 24) N、(89. 4±4. 15) mmHg,且组织热损伤显著减少,组织微观结构连接更为紧密。 结论 该新型电极在提高吻合口生物力学强度的同时可减少组织热损伤,进而实现更好的吻合效果。 研究结果可为实现人体管腔组织的无缝连接提供参考。     

Acute cytomegalovirus infection modulates the intestinal microbiota and targets intestinal epithelial cells

Primary and recurrent cytomegalovirus (CMV) infections frequently cause CMV colitis in immunocompromised as well as inflammatory bowel disease (IBD) patients. Additionally, colitis occasionally occurs upon primary CMV infection in patients who are apparently immunocompetent. In both cases, the underlying pathophysiologic mechanisms are largely elusive - in part due to the lack of adequate access to specimens. We employed the mouse cytomegalovirus (MCMV) model to assess the association between CMV and colitis. During acute primary MCMV infection of immunocompetent mice, the gut microbial composition was affected as manifested by an altered ratio of the Firmicutes to Bacteroidetes phyla. Interestingly, these microbial changes coincided with high-titer MCMV replication in the colon, crypt hyperplasia, increased colonic pro-inflammatory cytokine levels, and a transient increase in the expression of the antimicrobial protein Regenerating islet-derived protein 3 gamma (Reg3γ). Further analyses revealed that murine and human intestinal epithelial cell lines, as well as primary intestinal crypt cells and organoids represent direct targets of CMV infection causing increased cell death. Accordingly, in vivo MCMV infection disrupted the intestinal epithelial barrier and increased apoptosis of intestinal epithelial cells. In summary, our data show that CMV transiently induces colitis in immunocompetent hosts by altering the intestinal homeostasis.