α—肾上腺素能受体阻滞剂在前列腺增生症中的应用

前列腺增生症(BPH)是老年男性常见疾病,治疗BPH的目的是解除增生前列腺组织所致的膀胱颈口梗阻症状及其所诱发的膀胱不稳定性.目前认为BPH导致膀胱颈口梗阻的因素有机械性和动力性两种.虽然外科手术能解除膀胱出口梗阻,但部分病人不适应手术治疗且手术有一定的并发症和死亡率,此外约有20%接受经尿道前列腺切除术治疗的病人,术后症状仍不能得到缓解.因此,BPH的药物治疗受到人们的重视.近年来,通过一系列的实验研究与临床实践,发现a-肾上腺素能受体(简称.a-受体)阻滞剂治疗BPH效果明显.本文拟就此类药物的临床应用作一简要介绍.     

雌激素及雌激素受体与良性前列腺增生症

<正>良性前列腺增生症(benign prostatic hyperplasia,BPH)是中老年男性排尿障碍原因中最常见的良性疾病~([1,2])。近年来越来越多的研究表明,雌激素可能参与了前列腺腺体的自稳调节和间质增生的形成,由于雌激素主要通过雌激素受体(ER)发挥生物学功能,因此,雌激素及其受体在其发病中的作用机制越来越受到重视。本文对雌激素及ER与BPH的相关性研究做一综述。     

雌激素及其受体在良性前列腺增生症与前列腺癌中的作用

雌激素及其受体与多种细胞信号发生相互作用参与BPH于Pca的形成。两种雌激素受体亚型对配体的亲和力及其在不同分化的前列腺组织中分布与表达的差异可指导新型抗雌激素药物的研究与开发。个性化的治疗方案、新一代雌激素替代药物及雌激素受体拮抗剂将具有较高的效能、较小的不良反应 ,可大大提高雌激素的治疗效果。     

雌激素及其受体在良性前列腺增生症与前列腺癌中的作用

雌激素及其受体与多种细胞信号发生相互作用参与BPH于Pca的形成。两种雌激素受体亚型对配体的亲和力及其在不同分化的前列腺组织中分布与表达的差异可指导新型抗雌激素药物的研究与开发。个性化的治疗方案、新一代雌激素替代药物及雌激素受体拮抗剂将具有较高的效能、较小的不良反应，可大大提高雌激素的治疗效果。     

前列腺增生症的药物和物理治疗

前列腺增生症(BPH)是老年男性的常见病,目前以手术治疗为主。虽然腔内泌尿外科进展迅速,但由于不少病人具有不同程度的麻醉、手术禁忌证,人们研究能否用药物及物理治疗部分代替手术治疗很有必要。现将BPH药物及物理治疗研究的进展综述如下。药物治疗一、α受体阻滞剂前列腺受植物神经系统的交感、副交感神经双重支配。在增生的前列腺组织和前列腺外科包囊内均富含α肾上腺素能受体,而β受体含量甚微。据Cainc等报道,前列腺内的α受体主要是α_1受体,     

前列腺增生症的治疗对性功能影响

前列腺增生症和性功能下降是影响老年男性生活质量的重要因素 ,临床资料表明在治疗前列腺增生的同时往往对性功能带来一定程度的影响 ,本文就前列腺增生症的药物治疗、微创治疗、手术治疗对性功能的影响作一院述     

前列腺增生症的治疗对性功能影响

前列腺增生症和性功能下降是影响老年男性生活质量的重要因素，临床资料表明在治疗前列腺增生的同时往往对性功能带来一定程度的影响，本文就前列腺增生症的药物治疗，微创治疗，手术治疗对性功能的影响作一综述。     

需外科干预的前列腺增生症术后病理标本临床分析回顾

目的探讨前列腺增生症合并前列腺炎（CP）的发病率及其治疗方式的选择。方法通过分析2000年1月至2004年12月254例前列腺增生症手术患者术后前列腺病理学结果及患者年龄分布特点做临床分析回顾。结果254例前列腺增生症手术患者术后病理证实合并前列腺炎共53例,占20．87％,其中70—80岁年龄段发病率最高达26．21％。53例中经尿道前列腺电切（TURP）46例,耻骨上经膀胱前列腺摘除术7例。结论需外科干预的前列腺增生症合并前列腺炎发病率,临床诊断时预先考虑合并前列腺炎对选择合适的治疗方法有临床意义。手术治疗以经尿道前列腺电切为首选。     

选择性α-受体阻滞剂治疗良性前列腺增生的进展

良性前列腺增生症主要通过由前列腺增大产生机械性压迫的静态因素和前列腺平滑肌神经调控的变化产生的动态因素这两个机制导致膀胱流出道梗阻。本文复习了α１－肾上腺素能受体阻滞剂治疗症状性良性前列腺增生的基础理论和临床资料及最新进展，特别提到了前列腺特异性药物的治疗作用。     

选择性α—受体阻滞剂治疗良性前列腺增生的进展

良性前列腺增生症主要通过由前列腺增大产生机械性压迫的静态因素和前列腺平滑肌神经调控的变化产生的动态因素这两个机制导致膀胱流出道梗阻。本文复习了α１－肾上腺素能受体阻滞剂治疗症状性良性前列腺增生的基础理论和临床资料及最新进展，特别提到了前列腺特异性药物的治疗作用。     

Analyses regarding estrogen and estrogen receptors in an experimental osteosarcoma

Further therapeutical investigations are necessary to obtain a satisfactory survival rate of patients by improving the conventional methods of the treatment of osteosarcoma. Our working hypothesis is that an estrogenic hormonal influence is available for the effective treatment of osteosarcoma. An attempt was made to clarify this idea using experimentally induced hamster osteosarcoma. Male and female Syrian golden hamsters were used. Small amounts of minced tumor pieces were transplanted into hamsters subcutaneously. The levels of the circulating estradiol (E2) and alkaline phosphatase (ALPase) in blood were determined after the transplantation. An estrogen receptor (ER) on tumor cells was also demonstrated. Hamsters with an increased level of serum E2 were likely to have a smaller size of primary tumors and a smaller number of nodes in the lung metastasis. These tumor cells were successfully shown to be positive for ER stain. This suggests that E2 treatment may possibly control the osteosarcoma-condition.     

New embolization method using estrogen: Effect of estrogen on microcirculation

To ascertain the mechanism of action of estrogen administered by a new embolization method, developed by the authors as a treatment method for dural arteriovenous malformations, conjugated estrogens were injected into the mesenteric artery of rabbits, and microcirculatory changes in the dominant areas were studied biomicroscopically. Conjugated estrogen induced sludging and stasis in the microcirculation, approximately in proportion to the concentration and dose.     

Mechanical strain and estrogen activate estrogen receptor alpha in bone cells.

Bone cells' early responses to estrogen and mechanical strain were investigated in the ROS 17/2.8 cell line. Immunoblotting with antiphosphorylated estrogen receptor a (ER-alpha) antibody showed that when these cells were exposed for 10 minutes to estrogen (10(-8) M) or a single period of cyclic dynamic strain (peak 3400 microepsilon, 1 Hz, 600 cycles), there was an increase in the intensity of a 66-kDa band, indicating phosphorylation of ser122 in the amino terminus of ER-alpha. Increased phosphorylation was detected within 5 minutes of exposure to estrogen and 5 minutes after the end of the period of strain. Estrogen and strain also activated the mitogen-activated protein kinase (MAPK) family member extracellular regulated kinase-1 (ERK-1). Increases in ERK activation coincided with increased ER-alpha phosphorylation. Activation of ERK-1 and the phosphorylation of ER-alpha, by both estrogen and strain, were prevented by the MAP kinase kinase (MEK) inhibitor U0126 and the protein kinase A (PKA) inhibitor (PKI). These data support previous suggestions that resident bone cells' early responses to strain and estrogen share a common pathway, which involves ER-alpha. This pathway also appears to involve PKA and ERK-mediated phosphorylation of ser122 within the amino terminus of ER-alpha. Reduced availability of this pathway when estrogen levels are reduced could explain diminished effectiveness of mechanically related control of bone architecture after the menopause.     

人前列腺癌组织雌激素受体α、β亚单位基因mRNA的表达

目的　了解雌激素受体α(ERα)、β(ERβ)mRNA在人前列腺癌 (PCa)组织中的表达状况。方法　采用半定量逆转录 聚合酶链反应 (RT PCR)技术检测 32例PCa、32例良性前列腺增生患者、12例正常前列腺组织者中ERα、ERβmRNA的表达并进行基因测序。 结果　与良性前列腺增生组织相比 ,PCa组织ERαmRNA表达明显增强 ,而ERβmRNA表达明显减弱 (均P <0 0 1)。中晚期、低分化PCa组织ERαmRNA表达明显高于早期、中高分化PCa,而ERβmRNA则相反 (均P <0 0 1)。激素抵抗型PCaERαmRNA表达增强 ,而ERβmRNA表达明显降低 (均P <0 0 5 )。 结论　ERα、ERβ在PCa组织中的不同表达状况可能与PCa组织病理生物学特性有关。对ER特别是ERβ的研究 ,有助于对PCa特别是激素抵抗型PCa的生物学特性判断和治疗。     

Urethral leiomyoma expressing estrogen receptors

A case of urethral leiomyoma is presented. The patient was a 48-year-old female who was hospitalized with a 4-year history of a progressively enlarging urethral mass. Based on clinical diagnosis of benign urethral tumor, local excision was performed. Histological diagnosis was urethral leiomyoma and the tumor cells demonstrated immunoreactivity for estrogen receptors. We report our experience of a leiomyoma of the urethra expressing estrogen receptors.     

The effects of estrogen on osteoprotegerin,RANKL, and estrogen receptor expression in human osteoblasts

Estrogen is essential for bone growth and development and for the maintenance of bone health in adulthood. The cellular responses of osteoblasts and osteoclasts to estrogen are initiated via two high-affinity receptors (ERs). Osteoblasts synthesize RANKL (receptor activator of NF-kappaB ligand), necessary for osteoclast formation and function, and osteoprotegerin (OPG), its decoy receptor. To investigate the effects of estrogen on the expression of OPG, RANKL, and ERs in human osteoblasts, cells were cultured with physiological (10(-10) M) and high-dose (10(-7) M) 17beta-estradiol for 24 and 48 h. Proteins and corresponding mRNA levels were quantitatively determined by immunocytochemistry and RT-PCR. OPG expression was significantly increased three- and sevenfold at 24 h with 10(-10) M (P < 0.05) and 10(-7) M (P < 0.01) estradiol, respectively, compared to untreated cells. Similar but smaller increases were seen at 48 h (P < 0.05). Osteoblasts treated with estradiol demonstrated increased RANKL protein expression at 24 h (P < 0.05), but this was not maintained at 48 h. ERalpha expression was significantly increased by high-dose estradiol (P < 0.01) at 24 h and dose-dependently increased at 48 h (P < 0.01), while ERbeta was only increased at 24 h (P < 0.01). The estrogen-induced protein expression of ER, OPG, and RANKL was abrogated when cells were cultured in the presence of the estrogen antagonist ICI 182780. mRNA levels at 24 h demonstrated a significant suppression of RANKL with the low-dose but not the high dose. ERalpha mRNA but not ERbeta expression was up-regulated by estrogen. Our results suggest that estrogen may exert its anti-resorptive effects on bone, at least in part, by stimulating ER and OPG expression in osteoblasts.     

Estrophilin immunoreactivity versus estrogen receptor binding activity in meningiomas: evidence for multiple estrogen binding sites

The existence of estrogen receptors in human meningiomas has long been a controversial issue. This may be explained, in part, by apparent heterogeneity of estrogen binding sites in meningioma tissue. In this study, estrogen receptors were determined in 58 meningiomas with an enzyme immunoassay using monoclonal antibodies against human estrogen receptor protein (estrophilin) and with a sensitive radioligand binding assay using 125I-labeled estradiol (125I-estradiol) as radioligand. Low levels of estrophilin immunoreactivity were found in tumors from 62% of patients, whereas radioligand binding activity was demonstrated in about 46% of the meningiomas examined. In eight (14%) tissue samples multiple binding sites for estradiol were observed. The immunoreactive binding sites correspond to the classical, high affinity estrogen receptors: the Kd for 125I-estradiol binding to the receptor was approximately 0.2 nM and the binding was specific for estrogens. The second, low affinity class of binding sites considerably influenced measurement of the classical receptor even at low ligand concentrations. The epidemiological and clinical data from patients with meningiomas, and the existence of specific estrogen receptors confirmed by immunochemical detection, may be important factors in a theory of oncogenesis.