放射线联合p53基因及内皮抑素治疗小鼠前列腺癌皮下移植瘤

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.     

经尿道等离子双极汽化电切(TUPKVP)治疗前列腺增生症580例

目的:探讨经尿道等离子前列腺双极汽化电切术(TUPKVP)治疗前列腺增生的效果。方法:回顾性分析580例良性前列腺增生(BPH)患者行TUPKVP的临床资料。结果:中转开放手术2例,切除前列腺组织10~80 g,平均32.5 g。手术时间25~150 min,平均60 min,术中输血10例,无电切综合征(TURS)发生。术后随访2~36个月,患者最大尿流率升高,IPSS症状评分值降低,排尿通畅,疗效好,并发症少。结论:TUPKVP出血少,手术安全,疗效确切,是治疗前列腺增生的有效方法。     

人肝癌及癌周组织中γ-谷氨酰转肽酶、甲胎蛋白癌胚抗原的表达

用丫-谷氨酞转肽酶-甲胎蛋白(GGT-AFP)双染色法研究了人肝癌及癌周组织中GGT,AFP的表达,同时观察了癌胚抗原(CEA)的分布.20例肝癌组织中,11例GGT阳性,10例AFP阳性.13例CEA阳性.在癌周组织中,6例GGT阳性,2例AFP阳性,20例CEA阳性.证实肝细胞癌可表达GGT,AFP,增生结节属癌前期病变,与肝癌的发生有关,GGT,AFP的增高与肝癌密切相关,CEA无特异性.     

Relationship with God and the Quality of Life of Prostate Cancer Survivors

This study explored the role of relationship with God with respect to the quality of life of men with prostate cancer. Thirty-four men with prostate cancer completed questionnaires on demographic and illness factors, aspects of relationship with God (e.g., God image), nonreligious resources (e.g., optimism) and physical, social and emotion functioning. Results showed that relationship with God was a significant factor in the prediction of role, emotional and social functioning for these men after controlling for age, reported severity of treatment reactions and nonreligious resources. Notably, different aspects of relationship with God (e.g., causal attribution) evidenced different associations with functioning and the nonreligious resource of perceived health control. Such results suggest that relationship with God may function in a complex manner as a resource in coping with prostate cancer. Longitudinal research is needed to clarify the role of religious/spiritual resources in the short- and long-term quality of life of men with prostate cancer.     

抗人甲状腺球蛋白单克隆抗体的制备及其对抗原决定簇特异性的研究

用杂交瘤技术建立三株分泌抗甲状腺球蛋白(TG)单克隆抗体的杂交瘤细胞株。所获三种单克隆抗体经兔抗小鼠IgG亚类、IgM及IgA血清鉴定表明,两种为IgG_1,一种为IgA;三种含单克隆抗体小鼠腹水的滴度(ELISA法)均为51200以上;以竞争性固相抗体结合试验测定它们对抗原决定簇的特异性差异,结果发现三种单克隆抗体的抗原结合部位是不同的,但对抗原的结合有一定的相互竞争抑制现象。     

声触诊组织成像量化技术联合C-TIRADS与K-TIRADS对甲状腺结节的诊断效能比较

目的探讨声触诊组织成像量化(VTIQ)技术联合中国超声甲状腺影像报告系统(C-TIRADS)和韩国甲状腺影像分级系统(K-TIRADS)对甲状腺结节良恶性的诊断效能。 方法回顾性选择160例甲状腺结节患者,按病理结果分为良性组和恶性组。所有患者均经常规超声检查、VTIQ检查,根据C-TIRADS、K-TIRADS分级标准进行分级。ROC曲线分析C-TIRADS、K-TIRADS单独诊断或联合VTIQ对甲状腺结节良恶性的诊断效能。 结果两种系统单独应用时,K-TIRADS灵敏度低于C-TIRADS,但K-TIRADS特异性更高。与C-TIRADS、K-TIRADS比较,K-TIRADS和C-TIRADS联合VTIQ对甲状腺结节的诊断效能均有所增加,C-TIRADS联合VTIQ后特异度和灵敏度高于K-TIRADS联合VTIQ(P＜0.05)。 结论C-TIRADS或K-TIRADS联合VTIQ对甲状腺结节良恶性的诊断效能高于单独诊断,C-TIRADS联合VTIQ更有利于甲状腺良恶性判断。     

C-TIRADS及BRAFV600E基因检测对细针穿刺细胞学难以定性的甲状腺结节的诊断价值

目的 探讨中国版甲状腺影像数据与报告系统（C-TIRADS）、BRAFV600E 基因检测及二者联合对细针穿刺细胞学难以定性的甲状腺结节的诊断价值。方法 纳入我院2020年1月—2021年4月的甲状腺手术患者53例行回顾性分析,术前完成超声、细针穿刺抽吸及BRAFV600E基因检测,选取细针穿刺细胞学难以定性的患者作为研究对象,53例患者共62个结节。以手术病理结果作为金标准,比较C-TIRADS、BRAFV600E基因检测及二者联合诊断对甲状腺结节的诊断效能。结果 C-TIRADS诊断甲状腺癌的敏感性、特异性、阳性预测值、阴性预测值及准确性分别为92.50%、50.00%、77.08%、78.57%、77.42%。BRAFV600E基因诊断甲状腺癌的敏感性、特异性、阳性预测值、阴性预测值及准确性分别为55.00%、100.00%、100.00%、55.00%、70.97%。C-TIRADS联合BRAFV600E基因诊断甲状腺癌的敏感性、特异性、阳性预测值、阴性预测值及准确性分别为95.00%、50.00%、77.55%、84.62%、79.03%。C-TIRADS及联合诊断对甲状腺癌诊断的敏感性高于BRAFV600E基因检测（P<0.001）,BRAFV600E基因检测特异性及阳性预测值高于C-TIRADS及联合诊断（P<0.05）。C-TIRADS、BRAFV600E基因检测及联合诊断对甲状腺癌诊断的阴性预测值和准确性差异无统计学意义（P>0.05）。结论 C-TIRADS及BRAFV600E基因检测对于细胞学难以定性的甲状腺结节均有良好的诊断效能,术前联合应用可以更好地评估甲状腺结节     

Autonomic control of acid phosphatase exocrine secretion by the rat prostate

Summary In vivo prostatic secretion was collected from retired breeder Sprague Dawley rats using a method for isolated perfusion of the rat prostatic urethra. Enzymatic acid phosphatase determination was performed on the collected effluent. Control acid phosphatase secretion was 24.2±2.7 nm over 30 minutes. Intravenous phenylephrine 5 mg/kg stimulated a 10 fold increase in acid phosphatase secretion. The secretion seen with phenylephrine was dose dependent and could be blocked with prazosin, but not yohimbine, atropine, or propranolol. Intravenous -adrenergic agonist isoproterenol caused no increase in the secretion of rat prostatic acid phosphatese. Intravenous administration of the cholinergic agonist pilocarpine also resulted in a dose dependent rise in acid phosphatase secretion. The stimulation seen could be blocked by atropine but not phentolamine or propranolol. The stimulation of acid phosphatase secretion seen with ₁ adrenergic or cholinergic agonists was not additive. Intravenous vasoactive intestinal peptide did not stimulate acid phosphatase secretion nor did it augment the secretion induced by ₁ adrenergic or cholinergic agonists. Release of acid phosphatase into rat prostatic exocrine secretion is under both ₁ adrenergic and cholinergic control.Supported by the US Veterans Administration     

Association of common missense changes in ELAC2 (HPC2) with prostate cancer in a Japanese case–control series

 The recently identified prostate cancer susceptibility gene ELAC2 (HPC2) harbors two common missense variants, a serine to leucine substitution at residue 217 (Leu217) and an alanine to threonine substitution at residue 541 (Thr541). We genotyped the two variants in a Japanese cohort consisting of 350 prostate cancer patients 242 male population controls, and 114 male low-risk controls. Both missense alleles, Leu217 and Thr541, were carried at higher frequency in Japanese patients than in the controls (Leu217, P = 0.0012; Thr541, P = 0.0145), and the odds ratios associated with carrying these sequence variants were higher in Japanese than in Caucasians. Although the Leu217 and Thr541 variants of ELAC2 are less common in Japanese than in Caucasians, both variants confer significantly increased risk of prostate cancer in Japanese. Carriage of these variants was not associated with age at diagnosis, tumor stage, or tumor grade in these Japanese prostate cancer patients. The allele-specific pattern of risk observed in Japanese and familial Caucasian patients was qualitatively similar; however, the magnitude of that risk was considerably greater in Japanese than in Caucasians. Received: September 3, 2002 / Accepted: October 2, 2002