Toxicity associated with iron overload found in hemochromatosis: possible mechanism in a rat model.

Hemochromatosis is characterized by pathologic iron overload which often leads to various pathological conditions. The mechanism by which excess iron induces these conditions is not clearly understood. Using rats as the model, this investigation was conducted to explore the mechanism of toxicity associated with iron overload. Sprague-Dawley male rats were fed a 3% carbonyl iron-supplemented diet for eight weeks to achieve iron accumulation. Liver iron reached approximately 2 mg/g which is more than 16 times the control values (mean +/- SD, 0.12 +/- 0.02 mg/g, p < 0.001). Serum iron was consistently higher in the experimental rats (mg/L): 3.41 +/- 0.58 versus 1.89 +/- 0.18, p < 0.001. The high levels of iron accompanied enhanced oxidative damage in the hepatic nuclear DNA when 8-hydroxy-2'-deoxyguanosine (8-OHdG) was measured as a product of DNA oxidation. The levels of 8-OHdG in the experimental samples were significantly higher than the controls (8-OHdG X 10(-5)/dG): 4.22 +/- 1.82 versus 1.84 +/- 0.33, p < 0.05. The results of serum enzyme assays suggest that iron overload caused mild hepatocellular damage: alanine transaminase significantly increased; lactate dehydrogenase did not change; alkaline phosphatase decreased. Since the accumulation of 8-OHdG in the nuclear DNA is highly deleterious to cells, these data suggest oxidative damage in the nuclear DNA may be a critical factor in inducing diseases associated with iron overload.     

肠外营养对呼吸功能不全患者的影响

从加强医疗病房的重危患餐巾选取因呼吸衰竭而给予呼吸机支持的患者40例,随机分为A组20例进行肠外营养(parenteral nutrition,PN)治疗,B组20例未行PN治疗。对通气/换气功能各指标进行分析,结果两组患者的呼吸频率、pH、PaO_2、PaCO_2及HCO_3~-无明显差异;A组氧分压与吸入气氧浓度比值轻度降低,而肺泡-动脉氧压差及肺内分流明显升高。提示PN中的脂肪乳和高糖可能是导致呼吸功能改变的重要因素。     

Ⅰ期非小细胞肺癌淋巴结微转移规律的研究

目的探讨几个问题：（1）Ⅰ期非小细胞肺癌淋巴结微转移比率；（2）淋巴结微转移与肿瘤大小、病理类型、细胞分化程度、部位、分型、分期进行Logstic回归分析，确定影响微转移的主要因素；（3）探讨微转移的方式、顺序。方法对91例非小细胞肺癌清扫的肺门和隆突下淋巴结进行MCK（AEI／AE3）免疫组化标志检测微转移的存在。另外收集45例肺部良性病变手术时切除的肺门淋巴结45枚和Ⅱ期、Ⅲ期肺癌常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化（SP法）标志，分别作为阴性和阳性对照。结果45例肺部良性病变手术时切除的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阴性；Ⅱ期和Ⅲ期常规病理检查阳性的肺门淋巴结45枚进行MCK（AEI／AE3）免疫组化标志均为阳性。91例Ⅰ期非小细胞肺癌总的微转移率为49％（45／91）。结论Ⅰ期非小细胞肺癌淋巴结中存在微转移；Ⅰb期非小细胞肺癌微转移率明显高于Ⅰa期；有必要对Ⅰb期非小细胞肺癌进行术后化疗；肿瘤分期和分化程度是影响淋巴结微转移的主要因素；淋巴结微转移遵循肺门到纵隔的途径；腺癌存在跳跃式微转移。     

Poxvirus-based vaccine therapy for patients with advanced pancreatic cancer

Purpose  

An open-label Phase 1 study of recombinant prime-boost poxviruses targeting CEA and MUC-1 in patients with advanced pancreatic cancer was conducted to determine safety, tolerability and obtain preliminary data on immune response and survival.     

脑脓肿的诊断及治疗

目的：进一步探讨脑脓肿发病情况，影像学表现，选择最佳治疗方法，提高治疗效果。方法：回顾分析１４７裂离脓肿的发病，病因，影像学表现，治疗方法及死亡率下降因素，结果：脑脓肿发病年龄较年青，血源性及隐源性脑脓肿发病率升高，ＣＴ结合ＭＲＩ可明确诊断，选择最佳手术方法。ＣＴ应用后死亡率由２３．８％下降到７．５％，结论：ＣＴ为脑脓肿最主要的诊断方法，ＣＴ定位下穿刺排脓可治愈大部分脑脓肿。     

年轻人冠状动脉壁平滑肌细胞的表型变化及其与巨噬细胞的关系——免疫组织化学研究

选用年轻人冠状动脉材料，免疫组织化学方法，观察了弥漫性内膜增厚、脂纹、动脉粥样硬化斑块中平滑肌细胞的免疫表型变化，并将这些变化同巨噬细胞进行了联系。结果表明，凡是有巨噬细胞浸润之处，不管何种病变，该处的平滑肌细胞便失去了相应抗体的反应性，但仍能被抗间叶细胞抗体所标记，提示平滑肌细胞已经发生表型转变。这一现象说明巨噬细胞在平滑肌细胞表型转变过程中起重要作用，有助于人们对动脉粥样硬化病变、冠脉成形术后再狭窄病变发生过程的认识。     

荆芥连翘汤对促进皮肤溃疡愈合的影响

目的 观察荆芥连翘汤对小鼠皮肤溃疡的治疗作用。方法 建立小鼠皮肤创伤和烫伤两种皮肤溃疡模型．比较荆芥连翘汤以及rhEGF的用药组和自身对照组小鼠皮肤溃疡面积，用昆微镜观察溃疡面炎症细胞浸润情况。结果 和自身对照组相比，荆芥连翘汤可明显缩小小鼠皮肤溃疡面积（P〈0．001），同时炎症细胞浸润显著减少（P〈0．001）；荆芥连翘汤用药组疗效显著优于rhEGF用药组。结论 荆芥连翘汤可明显促进小鼠皮肤溃疡的愈合。     

The effects of plantago-mucilage A from the seeds ofPlantago asiatica on the immune responses in ICR mice

Effects of plantago-mucilage A (P-MA) on the immune responses were studied in ICR mice. Mice were divided into 4 groups (10 mice/group), and P-MA at doses of 7, 21 and 63 mg/kg were orally administered to mice once a day for 21 consecutive days. Mice were immunized and challenged with sheep red blood cells (SRBC). P-MA at 63 mg/kg/day significantly increased the body weight gain and the relative weights of spleen and thymus, as compared with those in controls. However, there were no significant effects on liver weight due to P-MA treatment. Plaque forming cells (PFC) and hemagglutination (HA) titers to SRBC were significantly enhanced in mice dosed at 21 and 63 mg/kg/day P-MA, as compared with those in controls. Delayed-type hypersensitivity (DTH) reaction to SRBC, phagocyte activity and circulating leukocyte were also significantly increased in mice dosed at 63 mg/kg/day P-MA. These results demonstrate that P-MA markedly enhances both humoral immune and allergic reaction to SRBC at concentrations which don’t act on the relative weight of liver.     

Blocking effects of polyunsaturated fatty acids on Na+ channels of neonatal rat ventricular myocytes.

Recent evidence indicates that polyunsaturated long-chain fatty acids (PUFAs) prevent lethal ischemia-induced cardiac arrhythmias in animals and probably in humans. To increase understanding of the mechanism(s) of this phenomenon, the effects of PUFAs on Na+ currents were assessed by the whole-cell patch-clamp technique in cultured neonatal rat ventricular myocytes. Extracellular application of the free 5,8,11,14,17-eicosapentaenoic acid (EPA) produced a concentration-dependent suppression of ventricular, voltage-activated Na+ currents (INa). After cardiac myocytes were treated with 5 or 10 microM EPA, the peak INa (elicited by a single-step voltage change with pulses from -80 to -30 mV) was decreased by 51% +/- 8% (P < 0.01; n = 10) and 64% +/- 5% (P < 0.001; n = 21), respectively, within 2 min. Likewise, the same concentrations of 4,7,10,16,19-docosahexaenoic acid produced the same inhibition of INa. By contrast, 5 and 10 microM arachidonic acid (AA) caused less inhibition of INa, but both n - 6 and n - 3 PUFAs inhibited INa significantly. A monounsaturated fatty acid and a saturated fatty acid did not. After washing out EPA, INa returned to the control level. Raising the concentration of EPA to 40 microM completely blocked INa. The IC50 of EPA was 4.8 microM. The inhibition of this Na+ channel was found to be dose and time, but not use dependent. Also, the EPA-induced inhibition of INa was voltage dependent, since 10 microM EPA produced 83% +/- 7% and 29% +/- 5% inhibition of INa elicited by pulses from -80 to -30 mV and from -150 to -30 mV, respectively, in single-step voltage changes. A concentration of 10 microM EPA shifted the steady-state inactivation curve of INa by -19 +/- 3 mV (n = 7; P < 0.01). These effects of PUFAs on INa may be important for their antiarrhythmic effect in vivo.