Association between cord blood IgE and genetic polymorphisms of interleukin-4, the β-subunit of the high-affinity receptor for IgE, lymphotoxin-α, and tumor Necrosis factor-α

High cord blood immunoglobulin E (cbIgE) is known to be associated with increased risks of atopic diseases in childhood. The relationship between genetic polymorphisms and high cbIgE has not been well documented. A cross-sectional study was conducted to assess the association between cbIgE and genetic polymorphisms of interleukin (IL)-4 -590C/T, the beta-subunit of the high-affinity receptor for IgE (FcepsilonRI-beta) E237G, lymphotoxin (LT)-alphaNcoI alleles, and tumor necrosis factor (TNF)-alpha -308G/A. A total of 320 mother-neonate pairs were recruited from four maternity hospitals from different locations of Taiwan. Cord blood was obtained and assayed for cbIgE. Polymerase chain reaction followed by restriction fragment length polymorphism was used to assess the genotypes. Three hundred pairs of mothers and neonates were included in the final analysis. Infants with IL-4 -590 C allele were found to have higher risk of elevated cbIgE (> or =0.35 IU/ml, 24.3%) (p = 0.004). After adjusting for gender, birth order, maternal age, and history of allergic disease in maternal and paternal families, odds ratios for CC and CT genotypes were 4.41 and 3.16 (95% confidence interval 0.78-22.67, and 1.66-6.13), respectively, using TT genotype as reference. The genotypes of FcepsilonRI-beta, LT-alpha, and TNF-alpha were not associated with cbIgE before or after the adjustment. Our finding suggested a significant association of cbIgE with genetic polymorphism of IL-4 -590C/T, but not with the genotypes of FcepsilonRI-beta, LT-alpha, and TNF-alpha.     

股前外侧区穿支动脉的形态学研究及皮瓣设计

目的探讨以旋股外侧动脉降支为蒂的皮瓣设计方法，以便增加术前多普勒定位的准确性。方法6具动脉灌注明胶-氧化铅混悬液的新鲜成人整尸标本，解剖观测股前外侧区穿支，通过血管造影术和拍摄X线片测量其直径、行程、分支和定位。用3D—doctor和Scion Image软件分别测量穿支供血的趋向性、三维重建和单穿支供血面积。结果股前外侧区共有外径大于0．5mm穿支16支，平均外径0．8mm，平均供血面积45．61cm^2，其中20％为肌间隙穿支，80％为肌皮穿支。平均蒂长为（3．15±1．43）cm。自旋股外侧动脉降支发出的穿支在浅筋膜中的平均长度为2．63cm。结论改良的氧化铅-明胶灌注技术可以为皮动脉和穿支皮瓣的研究提供高质量的血管造影图像。本研究发现股前外侧单穿支皮瓣的最大供血面积是30cm×20cm。以股前外侧区穿支设计的穿支皮瓣可以移植到下肢或身体其他部位。     

子宫内膜异位症患者血清TNF-α和TNF-β的测定

目的:了解子宫内膜异位症（简称内异症）患者血清中肿瘤坏死因子-α(TNF-α)和肿瘤坏死因子-β（TNF-β）的水平以及在腹腔镜保守性手术治疗前后的变化。方法:采用酶联免疫吸附法检测82例内异症患者（内异症组）和68例非内异症妇女（对照组）血清中TNF-α和TNF-β的含量及49例手术前后两者水平的变化。结果：内异症组血清TNF-α和TNF-β含量均显著高于对照组（Ｐ<0.01），且二者表达量随病情加重有上升趋势（Ｐ<0.05）。手术后Ⅲ～Ⅳ期患者血清中的TNF-α和Ⅰ～Ⅳ期患者血清TNF-β的含量随着内异灶的清除逐渐下降。结论:检测患者血清中TNF-α和TNF-β的含量，对术后随访、监测及手术效果的评价具有重要意义。     

EPO预处理对培养心肌细胞缺氧/复氧损伤TNF-α表达的影响及机制

目的 观察促红细胞生成素（erythropoietin，EPO）预处理对培养心肌细胞缺氧复氧前后TNF-α表达的影响，并进一步研究其可能的NF-kB信号机制。方法采用培养乳鼠心肌细胞建立缺氧复氧损伤模型，分为对照组、EPO组[缺氧复氧前24h，培养液中加入终浓度10U/ml的重组人促红素（recombinant human erythropoietin，RHuEPO）]、EPO＋吡咯烷二硫氨基甲酸盐（PDTC）组（缺氧复氧前24h，加入终浓度10U／ml的RHuEPO和5μg/ml的PDTC）和PDTC组（缺氧复氧前24h，加入终浓度5μg/ml的PDTC）。分别于缺氧复氧损伤前后，以RT-PCR和western blot检测各组心肌细胞TNF-α基因表达变化，同时以EMSA检测各组心肌细胞NF-kB活性变化。结果缺氧复氧损伤前，各组心肌细胞TNF-α基因表达水平差异无统计学意义，均较弱。损伤后各组心肌细胞TNF-α基因表达水平较损伤前对照组显著升高（P〈0．01），而EPO组TNF-α基因表达水平低于其他各组（P〈0．01）。缺氧复氧损伤前EPO组NF-kB活性高于其他各组（P〈0．01），损伤后各组NF-kB活性显著高于损伤前对照组（P〈0．01），EPO组NF-kB活性低于其他各组（P〈0．01）。结论EPO预处理抑制缺氧复氧后心肌细胞TNF-α基因表达升高，可能与缺氧复氧后NF-kB活性升高被抑制有关。EPO预处理可能通过NF-kB活化的负反馈机制抑制缺氧复氧后心肌细胞NF-kB活性的升高。     

MRI对累及头颈部淋巴组织病变的鉴别意义

目的:基于累及头颈部淋巴组织病变的临床不典型性,旨在探讨MRI对其进行鉴别诊断的客观依据。方法:对本组22例可疑累及头颈部淋巴组织的各类病变进行MRI检查并与病理学结果进行对照。结果:MRI对本组22例累及淋巴组织病变的诊断与病理学诊断的符合率(21/22)约为95%。结论:MRI是对累及头颈部淋巴组织病变的重要检查手段,并能为明确其诊断提供客观依据。     

TNF-α和低氧对胰腺癌细胞表达VEGF-A、C的调节

目的:探讨细胞活素肿瘤坏死因子-α(TNF-α)、SNAP(S-Nitroso-Nacetyl-penicillamine)对胰腺癌细胞产生血管内皮生长因子A、C(VEGF-A、C)的调节.方法:用Northern杂交和Western杂交法分析6种人胰腺癌细胞株中VEGF-A、C基因和蛋白的表达;以TNF-α或SNAP刺激其中两个细胞株后用逆转录-聚合酶链式反应技术(RT-PCR)分析其VEGF-A、C基因的表达.结果:Northern杂交法显示这6种胰腺癌细胞株均有4.1kb VEGF-A基因和2.4kb VEGF-C基因的表达;Western杂交法显示它们均有分子量为43kD的VEGF-A蛋白质和分子量为55kD的VEGF-C蛋白质的表达.RT-PCR分析法显示:TNF-α使细胞株COLO-357产生VEGF-A、VEGF-C mRNA分别减少约1～2.5倍、1～2倍,使细胞株CAPAN-1产生VEGF-A、VEGF-C mRNA分别减少约1倍、1.6～2.5倍;而SNAP刺激细胞株COLO-357产生VEGF-A mRNA增加约5倍,刺激细胞株CAPAN-1产生VEGF-A mRNA增加约4倍,但对这两种细胞株产生VEGF-C mRNA均无明显刺激作用.结论:细胞活素TNF-α和低氧通过调节血管内皮生长因子A、C的表达而影响胰腺癌细胞的生物学特性,抑制癌细胞的增殖,促进其凋亡、死亡或进展、恶化.     

Human Tumor–infiltrating Lymphocytes Transfected with Tumor Necrosis Factor Gene Could Augment Cytotoxicity to Autologous Tumor Cells

Human tumor–infiltrating lymphocytes (TILs) derived from pleural or ascitic fluid were incubated with recombinant interleukin 2 and transfected with human tumor necrosis factor (TNF) a gene by the lipofection procedure. The resulting TILs secreted significant amounts of TNF in the culture supernatant and exhibited cytotoxicity against established cell lines, such as K562 and Daudi, and autologous tumor cells. The TNF gene–transfected TILs exhibited an augmented killing of autologous tumor cells.     

Effects of tumor necrosis factor alpha on parathyroid hormone-induced increases in osteoblastic cell cyclic AMP

Summary Tumor necrosis factor α (10⁻¹⁰–10⁻⁸M) had no effects on cyclic AMP production by the osteoblastic osteosarcomal cells, Saos-2 and G292, or normal rat calvarial cells. The cytokine did, however, inhibit the parathyroid hormone (PTH)-induced effect on cyclic AMP in the Saos-2 and normal rat osteoblastic cells. This inhibitory effect did not occur on prostaglandin E₂-induced cyclic AMP increases in the osteoblastic cells. Interleukin-1 (10 U/ml −100 U/ml) did not produce any effect on basal levels or PTH-induced cyclic AMP increases in these cells.     

Arsenical necrosis of the jaws

After a brief historical review of the use of arsenic in dental practice two cases of arsenical necrosis of the jaws, affecting the maxilla and mandible respectively, are reported. Both patients were treated conservatively over an extended period with excellent results. It is concluded that there is no justification, whatsoever, for the use of arsenic in modern dental practice and that, although prolonged, conservative treatment of chemical necrosis of the jaws is preferable to more radical treatment.