Amplatzer封堵器的生物学性能及经导管介入治疗房间隔缺损

目的:评价经导管置入Amplatzer封堵器治疗继发孔房间隔缺损的治疗效果。方法:①选择2002-08/2006-04在兰州市第一人民医院心外科住院的继发孔型房间隔缺损65例,男26例,女39例;平均年龄(18±8)岁;平均房间隔缺损直径(19.3±7.2)mm。纳入患者对手术方案知情同意。②手术所用封堵器为美国公司的Amplatzer房间隔缺损封堵器,是一种新型的适于关闭二孔型房间隔缺损的装置,它由具有自膨胀性的双盘及连接双盘的腰部三部分组成。双盘状结构恢复记忆形状后可以稳定封堵房间隔缺损的边缘部分,降低残余分流的发生率。③根据选择封堵器大小的方式(即球囊测量或经胸超声心动图直接观察)将患者分为球囊测量组38例和经胸超声心动图测量组27例。均在透视及经胸超声心动图监视下经导管置入Amplatzer封堵器封堵房间隔缺损。同时测量患者缺损扩张直径、封堵器大小,记录X射线透视时间和手术时间。④术后即刻、24h、3个月及1年分别行经胸超声心动图、心电图及X射线检查评价治疗效果。⑤超声心动图显示完全无分流为无分流;残余分流血流宽度≤1mm为微量分流;血流宽度1.0～2.0mm为少量残余分流;血流宽度2～4mm为中量残余分流;血流宽度>4mm为大量残余分流。⑥组间计量资料差异比较采用两个独立样本t检验,组间手术效果比较采用两个独立样本的等级资料秩和检验。结果:①技术成功率:65例房间隔缺损患者,64例封堵器置入成功,技术成功率为98%。②选择封堵器直径:球囊测量组缺损扩张直径为(20.4±6.1)mm,选择的封堵器直径为(21.6±5.7)mm,与经胸超声心动图测量组相近[(22.5±4.3),(25.1±4.9)mm,P>0.05]。③术后残余分流情况:术后即刻经胸超声心动图显示,球囊测量组35例完全无分流,经胸超声心动图组有23例,差异不明显(P>0.05);术后24h,球囊测量组36例完全无分流,经胸超声心动图组有24例,差异不明显(P>0.05);术后3个月,球囊测量组37例完全无分流,经胸超声心动图组有25例,差异不明显(P>0.05);术后1年完成随访的52例患者均未见封堵器移位及房间隔缺损再通。④X射线平片检查:全部显示肺血减少,右心房、室缩小。结论:封堵器直径比球囊测量的房间隔缺损扩张直径大1.0～2.0mm,比超声心动图测量的大2～6mm封堵效果好,成功率高。     

Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid

Elevated plasma homocysteine, an independent risk factor for cardiovascular disease (CVD) can be lowered by administration of pharmacological doses of folic acid. The effect of lower doses in apparently normal subjects is currently unknown but is highly relevant to the question of food fortification. Healthy male volunteers (n = 30) participated in a chronic intervention study (26 weeks). Folic acid supplements were administered daily at doses increasing from 100 micrograms (6 weeks), to 200 micrograms (6 weeks), to 400 micrograms (14 weeks). Fasting blood samples collected before, during and 10 weeks post intervention were analysed for plasma homocysteine, serum and red- cell folate levels. Results, expressed as tertiles of baseline plasma homocysteine concentration, showed significant (p < or = 0.001) homocysteine lowering in the top (10.90 +/- 0.83 mumol/l) and middle (9.11 +/- 0.49 mumol/l) tertiles only. In the low tertile, where the mean baseline homocysteine level was 7.07 +/- 0.84 mumol/l, no significant response was observed. Of the three folic acid doses, 200 micrograms appeared to be as effective as 400 micrograms, while 100 micrograms was clearly not optimal. There is thus a minimal level of plasma homocysteine below which folic acid has no further lowering effect, probably because an optimal folate status has been reached. A dose as low as 200 micrograms/day of folic acid is effective in lowering plasma homocysteine concentrations in apparently normal subjects. Any public health programme for lowering homocysteine levels, with the goal of diminishing CVD risk, should not be based on unnecessarily high doses of folic acid.      

End‐of‐life care in the head and neck cancer patient

Past the point of no longer being able to control malignancies of the oral cavity and head and neck, the decision‐making process must shift to one that essentially concerns itself with creating comfort for the patient. The role of family, physicians, and other caregivers becomes, in many ways, more directed as active neoplasia‐related concerns become less relevant. Challenges remain significant in terms of continuing management of prior treatment‐related side effects and functional impairments to providers concerning themselves with maintenance of dignity, honoring the wishes of the family, and creating full understanding of on the part of all parties concerned what the goals of treatment cessation and palliation are key as death approaches.     

Prevalence of GB virus type C/hepatitis G virus RNA and of anti-E2 in individuals at high or low risk for blood-borne or sexually transmitted viruses: evidence of sexual and parenteral transmission

BACKGROUND: The first epidemiologic evidence of GB virus type C (GBV- C)/hepatitis G virus (HGV) infection showed a high prevalence of asymptomatic carriers in blood donors and in populations at risk for blood-borne viruses. However, by using only viral RNA polymerase chain reaction, those studies underestimated the true spread of GBV-C/HGV infection. The combined detection of GBV-C/HGV RNA and of anti-E2 (which reflects recovery from infection) is necessary to define accurately the prevalence of GBV-C/HGV. STUDY DESIGN AND METHODS: The presence of both anti-E2 and GBV-C/HGV RNA was searched for in 1438 serum samples collected from various groups of individuals at low or high risk for blood-borne or sexually transmitted viruses (blood donors, organ donors, unselected pregnant women, immunocompetent or immunodepressed multiply transfused patients, HIV-positive or HIV- negative homosexual men, intravenous drug addicts). RESULTS: The presence of GBV-C/HGV RNA and/or anti-E2 (exposure to GBV-C/HGV) was frequent in populations at risk for blood-borne or sexually transmitted viruses. GBV-C/HGV appeared also to be sexually transmitted, with transmission from male to female more efficient than vice versa. A particularly elevated level of exposure to GBV-C/HGV was observed in homosexual men. In immunocompetent individuals, the prevalence of anti- E2 was about twice that of GBV-C/HGV RNA, which suggests the frequency of recovery from GBV-C/HGV infection. Most of the GBV-C/HGV RNA- positive individuals had no biochemical evidence of liver damage. CONCLUSIONS: GBV-C/HGV is frequent in populations at risk for blood- borne or sexually transmitted viruses. GBV-C/HGV is not a hepatitis virus, and it seems appropriate to rename it.     

Platelet adhesion to collagen types I through VIII under conditions of stasis and flow is mediated by GPIa/IIa (alpha 2 beta 1-integrin)

Platelet adhesion to fibrillar collagens (types I, II, III, and V) and nonfibrillar collagens (types IV, VI, VII, and VIII) was investigated in the presence of physiologic concentrations of divalent cations under conditions of stasis and flow. Under static conditions, platelet adhesion was observed to collagen types I through VII but not to type VIII. Under flow conditions, platelet adhesion to collagen types I, II, III, and IV was almost independent of shear rates above 300/s. Collagen type V was nonadhesive. Platelet adhesion to collagen type VI was shear rate-dependent and optimal at a rate of 300/s. Collagen types VII and VIII showed minor reactivity and supported platelet adhesion only between shear rates 100 to 1,000/s. Monoclonal antibody (MoAb) 176D7, directed against platelet membrane glycoprotein Ia (GPIa; very late antigen [VLA]-alpha 2 subunit), completely inhibited platelet adhesion to all collagens tested, under conditions of both stasis and flow. Platelet adhesion to collagen type III at shear rate 1,600/s was only inhibited for 85%. The concentration of antibody required for complete inhibition of platelet adhesion was dependent on the shear rate and the reactivity of the collagen. An MoAb directed against GPIIa (VLA-beta subunit) partially inhibited platelet adhesion to collagen. These results show that GPIa-IIa is a major and universal platelet receptor for eight unique types of collagen.     

Analysis of Ig and T-cell receptor genes in 40 childhood acute lymphoblastic leukemias at diagnosis and subsequent relapse: implications for the detection of minimal residual disease by polymerase chain reaction analysis

The rearrangement patterns of Ig and T-cell receptor (TcR) genes were studied by Southern blot analysis in 30 precursor B-cell acute lymphoblastic leukemias (B-ALLs) and 10 T-ALLs at diagnosis and subsequent relapse. Eight precursor B-ALLs appeared to contain biclonal/oligoclonal Ig heavy-chain (IgH) gene rearrangements at diagnosis. Differences in rearrangement patterns between diagnosis and relapse were found in 67% (20 cases) of precursor B-ALLs (including all eight biclonal/oligoclonal cases) and 50% (five cases) of T-ALLs. In precursor B-ALLs, especially changes in IgH and/or TcR-delta gene rearrangements were found (17 cases), but also changes in TcR-beta, TcR- gamma, Ig kappa, and/or Ig lambda genes (11 cases) occurred. The changes in T-ALLs concerned the TcR-beta, TcR-gamma, TcR-delta, and/or IgH genes. Two precursor B-ALLs showed completely different Ig and TcR gene rearrangement patterns at relapse, suggesting the absence of a clonal relation between the leukemic cells at diagnosis and relapse and the development of a secondary leukemia. The clonal evolution in the other 23 ALL patients was based on continuing rearrangement processes and selection of subclones. The development of changes in Ig and TcR gene rearrangement patterns was related to remission duration, suggesting an increasing chance of continuing rearrangement processes with time. These immunogenotypic changes at relapse occurred in a hierarchical order, with changes in IgH and TcR-delta genes occurring after only 6 months of remission duration, whereas changes in other Ig and TcR genes were generally detectable after 1 to 2 years of remission duration. The heterogeneity reported here in Ig and/or TcR gene rearrangement patterns at diagnosis and relapse might hamper polymerase chain reaction (PCR)-mediated detection of minimal residual disease (MRD) using junctional regions of rearranged Ig or TcR genes as PCR targets. However, our data also indicate that in 75% to 90% of ALLs, at least one major rearranged IgH, TcR-gamma, or TcR-delta band (allele) remained stable at relapse. We conclude that two or more junctional regions of different genes (IgH, TcR-gamma, and/or TcR-delta) should be monitored during follow-up of ALL patients for MRD detection by use of PCR techniques. Especially in biclonal/oligoclonal precursor B-ALL cases, the monitoring should not be restricted to rearranged IgH genes, but TcR-gamma and/or TcR-delta genes should be monitored as well, because of the extensive changes in IgH gene rearrangement patterns in this ALL subgroup.