玻璃体切除术治疗外伤性眼内炎62例

0　引言　外伤性眼内炎是眼外伤的常见并发症 ,对视力及眼球威协极大 .由于病原体随致伤物直接进入眼内 ,在眼内和玻璃体繁殖 ,产生剧烈炎症反应 ,对眼内组织造成严重破坏 .如不及时而有效的控制 ,终使视力丧失 ,眼球萎缩 .近年随着现代玻璃体手术的发展 ,外伤性眼内炎的治愈率明显提高 .现将我科收治的 6 2例报告如下 .1　对象和方法1 .1　对象 1 996 - 0 6 / 1 998- 0 6我院连续收治 6 2例外伤性眼内炎 ,其中男 5 0例 ,女 1 2例 ,年龄 2～ 45岁 ,平均 1 6 .5岁 .1 4岁以下儿童 38例 ,占 6 1 .3% .以致伤原因分类 :角膜穿通伤30例 ,巩膜穿…     

亮氨酸脑啡肽的电子结构及构效关系研究

对亮氨酸脑啡肽进行了量子化学(INDO)计算,研究其电子结构特征,讨论其活性部位、作用机理及构效关系。同吗啡和R31833进行了活性部位的电子结构与空间结构比较,推断它们的活性药效结构具有共同特点,与阿片受体相互作用时作用方式相同,作用部位有对应关系,因而具有相同的药理性质。     

The management of stage I--II Hodgkin's disease with irradiation alone or combined modality therapy: the Stanford experience

At Stanford University, between 1968 and 1978, 230 patients with pathologic stage I--II Hodgkin's disease were treated on prospective clinical trials with either irradiation alone or irradiation followed by 6 cycles of adjuvant combination chemotherapy. The actuarial survival at 10 yr was 84% for patients in either treatment group. Freedom from relapse at 10 yr was 77% among patients treated with irradiation alone and 84% after treatment with combined modality therapy [p(Gehan) = 0.09]. Freedom from second relapse at 10 yr was 89% and 94%, respectively [p(Gehan) = 0.56]. Several prognostic factors were evaluated in order to identify patients at high risk for relapse or with poor ultimate survival after initial treatment with irradiation alone. Systemic symptoms, histologic subtype, age, and limited extranodal involvement (E-lesions) did not affect the prognosis of patients and failed to identify patients whose survival could be improved by the routine use of combined modality therapy. Patients with large mediastinal masses (mediastinal mass ratio greater than or equal to 1/3) had a significantly poorer freedom from relapse when treated with irradiation alone than when treated initially with combined modality therapy [45% versus 81% at 10 yr, p(Gehan) = 0.03). The 10-yr survival of these patients, however, was not significantly different (84% versus 74%). The implications of these observations on the management of patient with early stage Hodgkin's disease are discussed.     

Testicular endocrine function in GH receptor gene disrupted mice.

The consequences of disruption of GH receptor gene in GH receptor knockout mice on testicular function were evaluated. Adult male GH receptor knockout mice and their normal siblings were divided in to two subgroups and treated with either saline or ovine LH (0.3 microg/g BW) in saline. One hour after saline or LH administration, blood was obtained via heart puncture. Plasma IGF-I, LH, FSH, PRL, androstenedione, and testosterone levels were measured by RIAs. Testicular LH and PRL receptor numbers as well as pituitary LHbeta-subunit and testicular sulfated glycoprotein-2 mRNA levels were measured. Also, testicular morphometric analysis was performed. Unlike in normal, wild-type mice, the circulating IGF-I was undetectable in GH receptor knockout mice. The plasma PRL levels were (P<0.01) higher in GH receptor knockout mice than in their normal siblings. The basal LH secretion was similar in normal and GH receptor knockout mice. However, the circulating FSH levels were lower (P<0.001) in GH receptor gene disrupted mice. Administration of LH resulted in a significant (P<0.001) increase in plasma testosterone levels in both GH receptor knockout and normal mice. However, this testosterone response was attenuated (P < 0.01) in GH receptor knockout mice. Plasma androstenedione responses were similar in both GH receptor knockout and normal mice. Testicular LH and PRL receptor numbers were significantly decreased in GH receptor knockout mice. The results of the morphometric analysis of the testis revealed that the Leydig cell volume per testis was reduced in mice with GH receptor gene disruption. The steady-state of LHbeta-subunit and testicular sulfated glycoprotein-2 mRNA levels were not different in GH receptor knockout mice relative to their normal siblings. The present in vivo study demonstrates that in GH receptor knockout mice, LH action on the testis in terms of testosterone secretion is significantly attenuated and suggests that this is due to a decrease in the number of testicular LH receptors. The reduced number of PRL receptors may contribute to the diminished responsiveness of testicular steroidogenesis to LH by decreased ability to convert androstenedione to testosterone. These changes are most likely due to the absence of circulating IGF-I. These findings provide evidence that systemic IGF-I plays a major modulatory role in testicular endocrine function.     

7β-(6-取代-2-喹诺酮-3-乙酰氨基)头孢菌素的合成

以6-取代-2-喹诺酮-3-乙酸为侧链,用CDI法和潘化酯法与7-ADCA,7-ACA,7-ACT,和7-ACD缩合,合成了16个新的7β-(6-取代-2-喹诺酮-3-乙酰氨基)头孢菌素类化合物,通过溶媒转提,葡聚糖凝胶(Sephadex LH-20)柱层析及离心薄层层析分离精制,得到纯品。初步体外抑菌试验表明:新化合物对革兰氏阳性及某些阴性菌具有高度敏感性。大多数化合物对所试试验菌的抗菌活性与头孢唑啉和青霉素G钠相当,有些比它们还强。     

Cloning and expression of the gene involved in Sanfilippo B syndrome (mucopolysaccharidosis III B)

Sanfilippo B syndrome is caused by a deficiency of alpha-N- acetylglucosaminidase, a lysosomal enzyme involved in the degradation of heparan sulphate. Accumulation of the substrate in lysosomes results in degeneration of the central nervous system with progressive dementia often combined with hyperactivity and aggressive behaviour. In order to clone the deficient gene, we purified the enzyme from human placenta and obtained amino acid sequence information. Alignment of one of the CNBr generated internal peptides to sequence from the database revealed the chromosomal location of the gene in the 5' upstream flanking region of the gene for 17-beta-hydroxysteroid-dehydrogenase at 17q21.1. The available DNA sequence was used to clone the cDNA coding for alpha-N- acetylglucosaminidase and analyse its gene structure. The gene is fully contained in the 5' upstream flanking region of the gene for 17-beta- hydroxysteroid-dehydrogenase and interrupted by five introns. The cDNA clone has a length of 2575 bp and encodes a protein of 743 amino acids. Chinese hamster ovary cells transfected with the cDNA construct show alpha-N-acetylglucosaminidase activity about 17-fold over background. This will allow correction studies with NAG deficient Sanfilippo B cell lines and facilitate the development of enzyme replacement therapy for these patients.      

A new and weakly antispasmodic protoberberine alkaloid from Rhizoma Coptidis

A new protoberberine alkaloid, 3‐hydroxy‐2‐methoxy‐9,10‐methylenedioxy‐8‐oxo‐protoberberine, along with three known compounds, was isolated from Rhizoma Coptidis. The new compound displayed weak antispasmodic activity against acetylcholine‐induced contraction in isolated guinea‐pig ileum with an IC₅₀ of 83.7 μm . Copyright © 2010 John Wiley & Sons, Ltd.     

颈动脉血管重构特征在自发性高血压大鼠体内的表现

目的:血管重构是高血压的重要病理变化,是高血压导致器官损害的结构基础。实验观察自发性高血压大鼠颈动脉中层组织学的相关变化,以验证血管重构的特点。方法:实验于2006-06/2007-03在福建医科大学附属协和医院心血管内科实验室完成。①实验材料及分组:12周龄雄性自发性高血压大鼠10只,同性别周龄的WKY大鼠10只为对照,喂养18周后终止实验。②实验过程及评估:开始及每2周测鼠尾收缩压。实验结束后,麻醉后取颈动脉,行苏木精-伊红、苦味酸-天狼星红、弹力纤维和胶原纤维的双重染色(P/VB法),利用计算机辅助成像系统测算颈动脉中膜厚度、腔径、血管中膜厚/腔径、中膜横截面积、中膜细胞平均核面积及中膜的胶原面积百分比、弹性纤维面积百分比、弹性纤维面积与胶原面积的比值。SP免疫组织化学染色检测α-平滑肌肌动蛋白、增殖细胞核抗原、纤维粘连蛋白、层粘连蛋白等抗原在颈动脉壁的表达,并计算颈动脉中膜细胞增殖指数;以原位末端标记法标记血管壁的凋亡细胞,计算颈动脉中膜细胞凋亡指数。结果:20只大鼠全部进入结果分析。①自发性高血压大鼠实验开始和结束前的收缩压均>150mmHg,高于WKY大鼠(P<0.01)。②自发性高血压大鼠颈动脉中膜厚度、腔径、中膜厚度/腔径、中膜横截面积、中膜胶原面积百分比均高于WKY大鼠(P<0.01),而中膜弹性纤维面积百分比、弹性纤维面积与胶原面积比值均低于WKY大鼠(P<0.01)。③α-平滑肌肌动蛋白在两组大鼠颈动脉中膜均可表达,提示中膜细胞为血管平滑肌细胞。④自发性高血压大鼠中膜血管平滑肌细胞平均核面积大于WKY大鼠(P<0.01),中膜细胞增殖指数与WKY大鼠差异无显著性(P>0.05),中膜细胞凋亡指数显著低于WKY大鼠(P<0.01)。⑤自发性高血压大鼠颈动脉中膜纤维粘连蛋白、层粘连蛋白的光密度值(IA值)及染色阳性面积百分比高于WKY大鼠(P<0.01)。⑥颈动脉中膜血管平滑肌细胞凋亡指数与中膜横截面积呈显著负相关(r=-0.872,P<0.01);纤维连接蛋白表达的吸光度值与中膜横截面积呈显著正相关(r=0.954,P<0.01)。结论:自发性高血压大鼠颈动脉存在明显的重构,其特点为中膜肥厚、平滑肌细胞肥大、凋亡减少及胶原、纤维粘连蛋白、层粘连蛋白的过度沉积。     

Uterine Vascular Lesions

Vascular lesions of the uterus are rare; most reported in the literature are arteriovenous malformations (AVMs). Uterine AVMs can be congenital or acquired. In recent years, there has been an increasing number of reports of acquired vascular lesions of the uterus following pregnancy, abortion, cesarean delivery, and curettage. It can be seen from these reports that there is confusion concerning the terminology of uterine vascular lesions. There is also a lack of diagnostic criteria and management guidelines, which has led to an increased number of unnecessary invasive procedures (eg, angiography, uterine artery embolization, hysterectomy for abnormal vaginal bleeding). This article familiarizes readers with various vascular lesions of the uterus and their management.Key words: Uterine arteriovenous malformations, Uterine hemangioma, Placental chorioangioma, Uterine arteriovenous fistula, Uterine pseudoaneurysm, Acquired AVMVascular lesions of the uterus are very rare; most reported in the literature are arteriovenous malformations (AVMs). Uterine vascular malformations can be congenital or acquired. Recently, there has been a rise in the number of reported cases following pregnancy, abortion, and curettage. Many of these studies report spontaneous resolution of vascular lesions during follow-up; in addition, there is an increasing trend toward use of uterine artery embolization (UAE) to treat these lesions. In many of the reported studies, the diagnosis of uterine vascular malformation was made as early as the second day after a delivery or an abortion. In a study by Timmerman and colleagues,¹ out of 30 cases reported as uterine AVM based on Doppler study, only 3 were true AVMs. Rufener and associates² conducted a sonologic evaluation of postpartum and postabortion uterine vascular lesions that were reported as AVMs; the study revealed that, on pathologic examination, none turned out to be AVMs. Thus, we observe that there is confusion with regard to the terminology of vascular lesions such as uterine AVM, vascular malformation, arteriovenous fistula (AVF), and non-AVM vascular abnormalities of the uterus. The term malformation, however, is generally used to describe defects in the structure of an organ or region of the body resulting from an intrinsically abnormal process of development. Therefore, spontaneous resolution of a malformation in a short period of time is unlikely. An investigation by Mulliken and Glowacki,³ published in 1982, provided the groundwork for a proper identification of vascular lesions. Vascular tumors grow by cellular (mainly endothelial) hyperplasia: the very common hemangioma is, in reality, a benign vascular tumor. In contrast, vascular malformations have a quiescent endothelium and are considered to be localized defects of vascular morphogenesis, likely caused by dysfunction in pathways regulating embryogenesis and vasculogenesis. Therefore, the terms vascular abnormality or vascular lesion seem to best describe hypervascular areas within the uterus seen on color Doppler ultrasound, unless they are proven to be an AVM by angiography or pathologic examination. Many of these vascular lesions are increasingly being managed by UAE. Although there have been various reports of successful pregnancy following UAE, there have also been reports of ectopic pregnancy following UAE.⁴It is important to correctly identify various vascular lesions in the uterus to avoid unnecessary invasive intervention. This article aims to familiarize the reader with various vascular lesions of the uterus and their management.Uterine AVM is a rare condition, and the true incidence is not yet known. A study by O’Brien and associates⁵ showed an incidence of AVM of 4.5% in 464 pelvic sonographic examinations performed for pelvic bleeding. AVM has been described in patients between 18 and 72 years of age, and may be congenital or acquired pathologic conditions.⁶ The congenital form is very rare and is the result of a defect in embryonic vascular differentiation or a premature arrest in the development of the capillary plexus leading to multiple abnormal connections between arteries and veins.⁷ These congenital AVMs often penetrate the surrounding tissue and can cause an elaborate collateral vascular network. Furthermore, these congenital lesions can grow as pregnancy progresses.⁸The International Society for the Study of Vascular Anomalies classification system divides vascular anomalies into two primary biologic categories: (1) vasoproliferative or vascular neoplasms and (2) vascular malformations. The major distinction between the two categories is whether there is increased endothelial cell turnover, which is ultimately determined by the identification of mitoses seen on histopathology. Vasoproliferative neoplasms have increased endothelial cell turnover (ie, they proliferate and undergo mitosis) because they are neoplasms. Vascular malformations do not have increased endothelial cell turnover; rather, they are structural abnormalities of the capillary, venous, lymphatic, and arterial system, and can be congenital or acquired.