The adverse effect of treatment prolongation in cervical cancer by high-dose-rate intracavitary brachytherapy.

BACKGROUND AND PURPOSE: The potential risk of prolongation of treatment time in cervical cancer has been reported for many low-dose rate (LDR) studies, with an estimated loss of local control ranging from 0.3 to 1.6% per day of treatment prolongation. Since the treatment schedule for fractionated high-dose rate intracavitary brachytherapy (HDRICB) is not directly comparable with that for low-dose rate studies, this report aims to evaluate the adverse effect of treatment prolongation specifically for cervical cancer treated with HDRICB. MATERIAL AND METHODS: From September 1992 to December 1997, 257 patients diagnosed with uterine cervical cancer (35 Ib, 26 IIa, 122 IIb, 10 IIIa, 57 IIIb, 7 IVa), who underwent external radiotherapy combined with between two and four courses of HDRICB and a minimum of 3 years of follow-up (median 57 months), were analyzed. Treatment consisted of irradiation of the whole pelvis with 44-45 Gy consisting of 22-25 fractions by 5 weeks, with the dose boosted to 54-58 Gy (with central shielding) for patients diagnosed as FIGO stage IIb-IVa bilateral parametrial disease. HDRICB was performed using an Ir-192 remote afterloading technique at 1-week intervals. The standard prescribed dose for each course of HDRICB was 7.2 Gy to point A for three insertions (before July 1995), or 6.0 Gy to point A for four insertions (after July 1995). Total prescribed point A doses (external beam radiotherapy+HDRICB) ranged from 58 to 71.6 Gy (median, 65.6 Gy) for stage IB-IIA, while analogous dosage for larger lesions (stage IIb-IVa) ranged from 59 to 75.6 Gy (median, 65.6 Gy). Kaplan-Meier and multivariate analyses were used to test the effect of treatment time on pelvic control rate (PCR) and cause-specific survival (CSS) at 5 years. RESULTS: Median treatment time was 63 days. For all stages of disease, the 5-year CSS and PCR were significantly different comparing treatment times of less than and greater than or equal to 63 days [83% and 65% (P=0.004], 93% and 83% (P=0.02), respectively]. These associations were also significant for stage Ib/IIa [97% and 79% (P=0.01), and 100% and 87% (P=0.02), respectively), but not for stage IIb [75% and 72% (P=0.79), and 93% and 87% (P=0.83), respectively] or stage III [66% and 49% (P=0.2), and 83% and 72% (P=0.21), respectively]. Multivariate analysis identified three prognostic factors for CSS, stage (P<0.001), tumor response to external RT (P=0.001), and overall treatment time (OTT; P=0.006). Prognostic factors for pelvic failure were stage (P<0.001), tumor response to external RT (P=0.001), and OTT (P=0.03). Prolongation of treatment time resulted in a daily decrease in pelvic control rate of 0.67% overall, and 0.43% for stage Ib-IIa, 0.57% for stage IIb, and 0.73% for stage III patients. CONCLUSION: Analysis of the data from the current study demonstrates that the adverse effect of treatment prolongation was observed later in the treatment course for the high-dose rate (HDR) series compared to the LDR analog, however, treatment-time prolongation still negatively influenced the cause-specific survival and pelvic control rate for both dosage groups.     

p21对缺血-再灌注损伤后肾小管上皮细胞演变的影响

目的 探讨p21对缺血-再灌注损伤（IRI）后肾小管上皮细胞演变的影响。方法 选择低龄（2个月龄）和高龄（12个月龄）p21（＋／＋）和p21（-／-）鼠，建立左肾IRI模型。于IRI后0、1、3、7d及1、3、6个月光镜下观察肾小管组织学变化，采用免疫组化法检测肾小管上皮细胞增殖细胞核抗原（PCNA）表达，组织化学染色观察肾小管上皮细胞衰老相关β-半乳糖苷酶（SA-β-gal）活力，末端脱氧核糖转移酶介导的生物素化脱氧尿嘧啶缺刻标记技术（TUNEL）检测肾小管上皮细胞凋亡。结果 IRI后0d，肾小管以坏死为主，高龄鼠比低龄鼠严重、p21（-／-）鼠比p21（＋／＋）鼠严重（P均〈0．05）。肾小管上皮细胞凋亡在IRI 1d后出现，7d达高峰，且高龄鼠比低龄鼠明显、p21（-／-）鼠比p21（＋／＋）鼠明显（P均d0．05）。低龄鼠IRI后1个月出现SA—β-gal染色阳性的肾小管上皮细胞，而对侧肾此时未见衰老细胞，3和6个月时衰老的肾小管上皮细胞显著增多，且p21（＋／＋）鼠比p21（-／-）鼠明显（P〈0．05）；p21（＋／＋）高龄鼠IRI后0d双肾即可见大量的SA-β-gal染色阳性肾小管上皮细胞，且较p21（-／-）鼠显著增多（P〈O．05），但1d后，p21（＋／＋）和p21（-／-）鼠IRI肾衰老细胞均明显减少（P均〈0．05），1个月后又呈进行性增加，且p21（＋／＋）鼠始终比p21（-／-）鼠严重。高龄和低龄p21（＋／＋）鼠PCNA阳性染色细胞出现的几率差异无显著性（P〉0．05），但低龄鼠细胞增殖能力要强于高龄鼠；而p21（-／-）鼠的细胞增殖能力明显强于p21（＋／＋）鼠，低龄鼠更为显著（P均〈0．05）。对高龄鼠IRI后1d细胞衰老和凋亡进行相关分析显示，二者呈显著负相关Cp21（＋／＋）鼠：r=-0．82，P〈0．001,p21（-／-）鼠：r=-0．76，P〈0．0013。结论 ①IRI可促进正常肾小管上皮细胞衰老的进程；②已经进入衰老状态的肾小管上皮细胞在遭受IRI刺激后，更易走向死亡[坏死和（或）凋亡]；③p21在IRI所致肾小管上皮细胞演变过程中发挥重要的调控作用。     

自酸蚀封闭剂与玻璃离子联合用于托槽粘结的临床观察

目的：评价自酸蚀粘结剂与树脂加强型玻璃离子联合用于正畸托槽粘结的临床使用效果。方法：随机选择50名患者，采用自身对照的方法进行为期12个月的临床观察。385个托槽用自酸蚀封闭剂（3MESEP）和光固化树脂加强型玻璃离子水门汀（FUJI ORTHO LC）粘结，390个托槽用京津釉质粘结剂粘结。观察托槽脱落的时间和脱落后粘结剂在牙面上的残留量，计算托槽脱落率和粘结材料残留指教。结果：光固化树脂加强型玻璃离子水门汀和自酸蚀封闭剂粘结的托槽脱落率为10．1％；京津釉质粘结剂粘结的托槽脱落率为9．0％，两者差异没有统计学意义（P〉0．05）。两种材料粘结的托槽脱落后，牙釉质上的粘结材料残留指教差异无显著统计学意义（P〉0．05）。结论：自酸蚀封闭剂和树脂加强型玻璃离子所构成的粘结技术粘结正畸托槽的粘结强度，可以满足正畸治疗的需要，在临床上有广阔的应用前景。     

99mTc-depreotide生长抑素受体显像的临床应用研究

生长抑素受体显像近年来研究较多，depreotide已成为其研究热点之一。Depreotide在诊断与鉴别诊断临床常见的孤立性肺结节方面有其独特优势；此外，^99mTc—depreotide生长抑素受体显像在乳腺癌、甲状腺癌、淋巴瘤等肿瘤及甲状腺相关性眼病等非肿瘤性疾病也有一定应用前景。     

老年认知功能障碍与脑结构CT测量的相关性研究

目的探讨脑萎缩与老年认知功能障碍之间的相关性。方法对开滦集团公司1063名离退休职工进行健康查体,用简易精神状态量表(MMSE)评定认知功能,按分界值将本次研究对象分为认知功能障碍组和认知功能正常组,同时用CT线性测量脑的相关部位以诊断脑萎缩情况,并对各型脑萎缩与认知功能的相关系数及提示老年认知功能障碍的敏感度、特异度、准确度进行分析。结果1063名观察对象中符合入选标准并资料完整者共计511名,其中108名有认知功能障碍,髓质脑萎缩55名、皮质萎缩5名、混合型萎缩30名;认知功能正常者403名,髓质脑萎缩214名、皮质萎缩13名、混合型萎缩62名。认知功能障碍组脑萎缩的发病率高于认知功能正常组,差异具有统计学意义(P<0.005);2组间颞叶海马钩回间距(26.86mm±3.73mmvs25.95mm±3.80mm)及海马钩回间距/大脑左右径的比值(0.21±0.02vs0.20±0.02)差异具有统计学意义(P<0.05);海马钩回间距、皮质脑萎缩、混合型脑萎缩与认知功能障碍呈负相关(分别为r=-0.094,P=0.034,r=-0.156,P≈0.000,r=-0.147,P≈0.000),以海马钩回间距20mm提示老年认知功能障碍的敏感度最高(98.14%),混合型脑萎缩的特异度(84.86%)、准确度最高(72.80%)。结论CT测量相关脑结构,判断脑萎缩类型可以为老年认知功能障碍的诊断提供有价值的信息。     

实验性肝纤维化大鼠肝组织钠-氢交换泵-1的表达

Na^＋/H^-交换泵（NHE）为参与细胞内外Na^＋/H^-交换的细胞膜大分子。已证实有6种形式的NHE，分别命名为NHE1～NHE6，其中以NHE-1组织分布最广泛。NHE-1与人类疾病的关系是近年才刚刚开始研究的领域。其与肝纤维化的关系逐渐被人们认识。近年的研究结果表明，细胞因子、生长因子及氧应激激活HSC都与NHE-1有密切的关系。我们通过观察肝纤维化大鼠肝组织中NHE-1 mRNA表达的变化，以期了解NHE-1在肝纤维化发生发展中的作用。     

保罗样激酶基因沉默体外抑制胶质瘤细胞侵袭与生长

目的观察保罗样激酶1基因(plk1)沉默对胶质瘤细胞株-H4体外生长的抑制作用,探讨plk1基因作为胶质瘤治疗靶点的可行性。方法化学合成小片断干扰RNA(siRNA)抑制plk1基因的表达,Western blot检测plk1蛋白质的表达变化,流式细胞仪检测H4细胞周期分布及凋亡程度的变化,体外侵袭实验检测H4细胞侵袭能力的变化,MTT法检测H4细胞增殖速度的变化。结果经siRNA作用48h后,plk1蛋白质水平明显降低;较多的H4细胞聚集于G2/M期附近(P<0.05);细胞凋亡明显上升(P<0.05);细胞体外侵袭能力下降(P<0.05);增殖速度明显缓于对照组(P< 0.05)。结论靶向plk1的siRNA可在体外抑制胶质瘤细胞H4的侵袭与增殖,plk1有可能成为新的潜在胶质瘤治疗靶点。     

Is chronic nitrate therapy associated with a different clinical presentation of acute coronary syndrome?

BACKGROUND: Nitrate therapy can induce ischemic preconditioning with a consequent increase in tolerance to ischemia. In the context of acute coronary syndromes (ACS), nitrates may result in a different presentation. with greater protection. OBJECTIVES: To investigate in a population of patients with ACS whether previous chronic use of nitrates results in a different presentation of ACS. METHODS: We studied 287 patients (65 +/- 13 years, 66% male) admitted to our department in the first six months of 2005 with ACS (with and without ST-segment elevation). Of these, 8% were under nitrate therapy at the time of admission. In this group, 27% presented ACS without ST-segment elevation, while in the group without nitrates this value was 58% (p = 0.005). By univariate analysis, the use of nitrates was a predictor of the preferential occurrence of non-ST-segment elevation ACS (OR 0.27, 95% CI 0.10-0.71). After correction for the potential influence of variables (age, gender, previous revascularization and smoking) by multivariate logistic regression, nitrate therapy remained a borderline predictor of clinical presentation as non-ST-segment elevation ACS (OR 0.37, 95% CI 0.13-1.04, p = 0.059). CONCLUSIONS: Previous use of nitrates was associated with a tendency to present as non-ST-segment elevation ACS. This finding may be explained by the hypothesis that nitrates induce pharmacological preconditioning, reducing the transmural extent of myocardial infarction.