Therapeutic alternatives in the treatment of intrahepatic biliary obstruction

Intrahepatic biliary obstruction was treated in 60 patients (49 with cholangiocarcinoma and 11 with sclerosing cholangitis) who were classified according to the upper limit of their obstruction (Group I, proximal common hepatic duct; Group 2, right and left main hepatic ducts; Group 3, intrahepatic bile ducts). Thirty-six patients underwent percutaneous transhepatic biliary drainage, and 14 underwent catheterization through a T-tube track, Five of this latter group had the T-tube placed to establish a route of access for later interventional radiologic manipulations. Since most diseases that produce intrahepatic biliary obstruction are progressive, the use of any single approach is limited. The advantages of a surgically created route of access combined with the flexibility of interventional radiologic techniques help to maximize the therapy and extend the palliation that many of these patients receive.     

Specific Interferon-Gamma Producing CD4+ and CD8+ T Cells After Autologous EBV-B Stimulation: The Necessity of Restimulation

The response of T cells to produce interferon-γ, to proliferate and to become cytotoxic after specific stimulation with low dose (2%) autologous EBV-B cells was investigated in 15 EBV seropositive and five seronegative patients. A significantly higher number of interferon-γ producing cells (56 ± 24 per 10⁵ T cells) were found in a spot ELISA in EBV positive than in EBV negative patients (7 ± 2 spots, P<0.01) and it was only found with restimulation after 5–12 days of primary culture. No correlation was found between the extent of interferon-γ production, cytotoxicity or profileration. Specificity of EBV-induced interferon-γ production was demonstrated by comparison of the response to allogeneic EBV-B cells or IL-2 in the reslimulation phase. The response was stronger in CDS⁺ T cells than in CD4⁺ T cells and could be blocked in the restimulation phase with HLA class I and class II antiserum, respectively.     

Inhibition of cell movement and associated changes by hexachlorocyclohexanes due to unregulated intracellular calcium increases

Hexachlorocyclohexanes (HCCHs) are potent stimulators of polymorphonuclear leukocyte (PMN) oxidative metabolism and of mobilization of calcium from intracellular stores. It was of interest, therefore, to evaluate the effect of HCCHs on PMN orientation and chemotaxis and to determine their effectiveness as chemotaxins. Chemotaxis was evaluated using micro-Boyden chambers, f-actin was quantitated by nitrobenzoxadiazole (NBD)-phallacidin fluorescence, and microtubules were quantitated by observing the concanavalin A (Con A) capping phenomenon. We also evaluated changes in intracellular calcium [Ca2+]i using quin 2 fluorescence. We found that the HCCH isomers were not chemotaxins and that the HCCH isomers that stimulated O2- formation (delta and gamma HCCH) inhibited chemotaxis. This effect was associated with inhibition of orientation. In addition, we found extensive inhibition of both f-actin and Con A cap formation. These effects of HCCH on cell function were associated with marked increases of [Ca2+]i. This work suggests that non-receptor-mediated increases of [Ca2+]i associated with HCCH have divergent effects on cell function and suggests that physiologic responses of PMNs requiring cytoskeletal alterations, such as chemotaxis, depend on the controlled responses of receptor-mediated stimulation.     

Anti-Ata causing mild hemolytic disease of the newborn

We report here a case of moderately severe hemolytic disease of the newborn (HDN) due to anti-Ata. The gravida 5 proposita was group A rr and previously was found to have anti-Ata and -D. At the 35-week mark of this pregnancy, her anti-Ata demonstrated a titer of 256, score 79. Fluid obtained by amniocentesis at 36 weeks showed an optical density at 450 nm of 0.08 (midzone). The baby was delivered at 38 weeks by cesarean section. The cord cells were group A rr with a 3+ direct antiglobulin test. The dichloromethane eluate of the infant's cells demonstrated anti-Ata specificity only. At birth, the infant's total bilirubin (TB) was 2.1 mg per dl and the hematocrit level (Hct) was 33.8 percent. Within 8 hours, the TB had risen to 3.8 mg per dl. Phototherapy was initiated at 7-1/2 hours and maintained for 40 hours. The infant's TB rose to a maximum level of 10.5 mg per dl 24 hours after phototherapy was discontinued. At discharge 4 days postpartum, the infant's TB had dropped to 9.2 mg per dl, and the Hct value was 38 percent. On a visit 7 days postpartum, the infant's TB level had fallen to 6.5 mg per dl and the hct value was 38 percent. Transfusions were not necessary.     

人工髓核假体置入治疗腰椎间盘突出症的疗效分析

目的：观察已在临床初步开展起来的人工髓核置换术治疗腰椎间盘突出症的中、远期临床疗效及并发症,分析其对策。 方法：纳入2002-02/2004-08南方医科大学附属南方医院脊柱骨病外科采用单枚人工髓核假体置换术治疗单节段腰椎间盘突出症患者98例,获得24～48个月随访患者75例,按平均随访时间达24,36,48个月,分为24个月组（n=30）,36个月组（n=23）,48个月组（n=22）。选同期采用单纯椎间盘髓核摘除术患者30例作为对照组,评估各组术后临床疗效,主观症状采用Oswestry功能障碍指数问卷表（0%表示正常,越接近100%则功能障碍越严重）和Prolo功能评分表（小于或等于5分为差,6～7分为中等,8～10为优）评价,分析术后影像学检查并测量手术节段活动度和椎间隙高度变化情况,同时观察假体位置情况,腰椎MRI观察假体位置和软骨终板的信号变化情况。腰椎活动度=（腰椎中立角度-前屈角度）＋（后伸角度-腰椎中立角度）=后伸角度-前屈角度;为消除X射线放大率的影响,椎间隙高度变化情况采用病变椎间隙后缘高度与上位椎体中部矢状径的比值表示。 结果：75例获得24～48个月随访者,全部进入结果分析。①48个月组2例、36个月组1例发生假体脱出,二次手术取出。其余患者术后临床症状均明显缓解,疼痛消失。②24,36,48个月组及对照组术后末次Oswestry功能障碍指数均较术前降低,差异有显著性意义（14.2%,52.1%;15.5%,55.2%;15.1%,53.6%;15.5%,51.5%;P〈0.05）。③24,36,48个月组及对照组术后末次Prolo能评分均较术前升高,差异有显著性意义（8.5,4.6分;8.6,4.5分;8.7,4.3分;8.4,4.2分;P〈0.05）。④24,36,48个月组同期手术节段腰椎活动度均高于对照组,差异有显著意义（P〈0.05）。⑤24个月组手术节段椎间高度较术前降低约4%、36个月组降低约12%、48个月组降低约18%、对照组较术前降低约25%,各组术前和术后椎间隙高度比值比较,差异具有显著性意义（P〈0.05）。⑥主要并发症：早期出现术后一过性腰痛24例,假体脱出3例。中、远期发现假体下沉32例,软骨终板损伤39例。 结论：单枚人工髓核假体置换治疗腰椎间盘突出症中、远期随访临床疗效肯定,但存在较严重并发症,应慎重开展此项手术。     

T lymphocytes specific for immunoglobulin allotype. I. Igh- 1(b)-specific T cells demonstrated by suppression in vivo and cytotoxicity in vitro

We show that determinants of IgG(2a) of C57BL/6 mice (Igh-1(b)) stimulate allotypespecific T cells in BALB/c mice. Such cells are detected in two different functional assays; chronic allotype suppression and T cell-mediated cytotoxicity. A population of suppressor T cells capable of inducing chronic Igh-1(b) suppression was demonstrated by rosetting procedures to possess Igh-1(b)-specific receptors, a result interpreted as indicating that suppressor T cells may act directly upon allotype-bearing B cells. From similar populations we were also able to demonstrate Igh-1(b)-specific cytotoxic T cells. Such cells were lytic for target myeloma cells expressing the Igh-1(b) allotype of IgG28, and were ineffective against a variant cell line failing to express Igh-1(b), and other target cell lines expressing different allotypes or isotypes. The similar specificity of suppressor T cells and cytotoxic T lymphocytes for Igh-1(b) allotype raises the possibility that the target in allotype suppression is a B cell, and that allotype-specific cytotoxic T cells may play some role in regulation of allotype expression in the suppressed state.     

Low risk of viral infection after administration of vapor-heated factor VIII concentrate. International Investigator Group

A multicenter prospective study was carried out to evaluate whether a vapor-heated factor VIII concentrate transmitted blood-borne viral infections over a surveillance period of 15 months. Thirty-five patients with hemophilia and von Willebrand disease who had never received any blood components were treated. Twenty-eight were analyzed and found not to have non-A, non-B hepatitis. Sera from 20 of these 28 patients were also tested for the antibody to the hepatitis C virus. None had sero-converted during the follow-up period. None of the patients analyzed developed markers of the hepatitis B virus (n = 17) or the human immunodeficiency virus (n = 31). This vapor-heated factor VIII concentrate carries a low risk of transmitting hepatitis and human immunodeficiency virus infection.     

灯盏花素对糖尿病大鼠早期肾皮质一氧化氮和血管紧张素Ⅱ水平的影响

目的:以肾脏肥大指数、肾小球形态结构、一氧化氮和血管紧张素Ⅱ水平为指标,观察灯盏花素对糖尿病大鼠早期肾脏的保护作用。方法:实验于2006-03/06在遵义医学院珠海校区中心实验室完成。实验分组:雄性Wistar大鼠34只,腹腔单次注射链脲佐菌素65mg/kg制备糖尿病大鼠模型,将造模成功(血糖≥16.65mmol/L)30只大鼠随机分为糖尿病组和灯盏花素治疗组,每组10只;另设正常对照组10只。实验过程:灯盏花素治疗组给予20mg/(kg·d)腹腔注射灯盏花素注射液持续4周,糖尿病组及正常对照组给予同体积的生理盐水。实验评估:①4周后计算肾脏肥大指数(肾脏肥大指数=双侧肾质量/体质量׉)。②苏木精-伊红染色观察肾小球病理形态变化。③硝酸还原酶法测定血清及肾皮质组织一氧化氮水平。④放免法测血浆及肾皮质组织血管紧张素Ⅱ水平。结果:参加实验34只大鼠,有4只未达糖尿病成模标准,最终30只大鼠进入结果分析。①肾脏肥大指数:糖尿病模型组、灯盏花素治疗组显著高于正常对照组[(13.29±4.73)/1000,(11.07±2.19)/1000,(4.78±0.06)/1000,P<0.01],灯盏花素治疗组低于糖尿病模型组(P<0.05)。②肾小球病理形态:正常对照组大鼠肾小球血管袢薄而清晰,内皮细胞和系膜细胞数目正常;糖尿病大鼠肾小球血管壁可见玻璃样变性,基底膜增厚,系膜基质增生;灯盏花素治疗后肾小球血管壁未见明显变性,基底膜未见明显增厚,其病理变化明显改善。③血清及肾皮质组织一氧化氮水平:糖尿病模型组、灯盏花素治疗组显著高于正常对照组[血清一氧化氮水平:(31.36±4.21),(27.03±3.54),(25.21±3.39)μmol/L,P<0.05;肾皮质组织一氧化氮水平:(1.95±0.25),(1.27±0.32),(0.73±0.12)μmol/g,P<0.01]。灯盏花素治疗组低于糖尿病模型组(P<0.05,P<0.01)。④血浆和肾皮质组织血管紧张素Ⅱ水平:糖尿病模型组显著高于正常对照组[血浆血管紧张素Ⅱ水平:(693.98±297.22),(356.48±85.21)ng/L,P<0.05;肾皮质组织血管紧张素Ⅱ水平:(6964.56±2128.48),(3127.07±1519.98)pg/g,P<0.01]。灯盏花素治疗组低于糖尿病模型组(P<0.05)。结论:灯盏花素在降低糖尿病大鼠肾脏肥大和改善肾脏形态结构的同时还可降低外周血及肾皮质组织一氧化氮与血管紧张素Ⅱ水平,在一定程度上可改善糖尿病早期的肾损害。