Laparoscopic Management of Adnexal Masses

Retrospective study of 121 cases of adnexal masses which were managed laparoscopically was carried out. The aim of study was to evaluate the safety and effectiveness of laparoscopic management of adnexal masses. In 120 cases, procedure was completed safely with minimum morbidity. In one case laparotomy had to be done to complete the procedure. In 76 cases cystectomy was done, 26 required salpingo-oophorectomy and 19 required only salpingectomy. Histologic evaluation revealed 30 functional cysts, 36 endometriotic cysts, 11 dermoids, 9 serous cystadenomas, 3 mucinous cystadenomas, 11 parovarian cysts, 19 cases of hydrosalpinx and 2 cases of tuberculosis.Key Words: Adnexal mass, Laparoscopy, Ovarian cyst     

Lipid rafts mediate the interaction between myelin-associated glycoprotein (MAG) on myelin and MAG-receptors on neurons

The interaction between myelin-associated glycoprotein (MAG), expressed at the periaxonal membrane of myelin, and receptors on neurons initiates a bidirectional signalling system that results in inhibition of neurite outgrowth and maintenance of myelin integrity. We show that this involves a lipid-raft to lipid-raft interaction on opposing cell membranes. MAG is exclusively located in low buoyancy Lubrol WX-insoluble membrane fractions isolated from whole brain, primary oligodendrocytes, or MAG-expressing CHO cells. Localisation within these domains is dependent on cellular cholesterol and occurs following terminal glycosylation in the trans-Golgi network, characteristics of association with lipid rafts. Furthermore, a recombinant form of MAG interacts specifically with lipid-raft fractions from whole brain and cultured cerebellar granule cells, containing functional MAG receptors GT1b and Nogo-66 receptor and molecules required for transduction of signal from MAG into neurons. The localisation of both MAG and MAG receptors within lipid rafts on the surface of opposing cells may create discrete areas of high avidity multivalent interaction, known to be critical for signalling into both cell types. Localisation within lipid rafts may provide a molecular environment that facilitates the interaction between MAG and multiple receptors and also between MAG ligands and molecules involved in signal transduction.     

跟骨定量超声骨质测量参数与骨密度及骨组织形态计量学指标的关系

目的:分析跟骨定量超声骨质测量中各参数与骨密度及形态计量学指标的相关性。方法:选择2004-01/2005-12广州市第六人民医院和中山大学三院骨科小腿以上截肢患者38例,将其跟骨定量超声测定的超声振幅衰减平均值与健康青年人骨峰值进行比较,>-2.5 SD者为骨量正常组(12例),<-2.5 SD者为骨质疏松组(26例)。分别进行跟骨定量超声、双能X线骨密度测量仪及骨形态计量学测量,应用直线相关分析法分析跟骨定量超声测定中各参数与骨密度及骨组织形态计量学各指标的相关性。结果:38例全部进入结果分析。①骨质疏松组跟骨超声振幅衰减平均值和骨硬度指数值均小于骨量正常组(P<0.01)。②骨量正常组跟骨骨密度值显著高于骨质疏松组[(352±16),(233±14)mg/cm2,P<0.01]。③骨量正常组跟骨平均骨小梁间距或弥散度低于骨质疏松组而松质骨体积高于骨质疏松组(P<0.05)。④超声振幅衰减平均值和骨硬度指数与骨密度呈直线正相关(r=0.814,0.326,P<0.01,0.05)。⑤超声传播速度与骨小梁游离末端、平均骨小梁间距呈直线负相关(r=-0.688,-0.712,P<0.01),与小梁间连点数、松质骨体积呈直线正相关(r=0.672,0.794,P<0.01);骨硬度指数与平均骨小梁间距呈直线负相关(r=-0.358,P<0.05),与松质骨体积呈直线正相关(r=0.513,P<0.01)。结论:跟骨定量超声测量中,超声振幅衰减平均值能较好地反映骨的密度,超声传播速度能较好地反映骨的质量,而骨硬度指数能较综合地反映骨强度的改变。     

Continuous infusion cisplatin and etoposide chemotherapy for cancer of unknown primary site (CUPS) in Taiwan, a region with a high prevalence of endemic viral infections

BACKGROUND: To evaluate the efficacy and toxicity of cisplatin/etoposide continuous infusion chemotherapy for cancer of unknown primary site in Taiwan, a region with a high prevalence of endemic viral infections. METHOD: Between April 1994 and February 1996, 20 patients with a diagnosis of CUPS were treated, including 15 males and five females, of average age 63.3 years (range 41-83 years). Continuous intravenous infusion of etoposide 80 mg/m2 and cisplatin 25 mg/m2 was given for 3 days every 3 weeks. Pretreatment tumor marker and viral serology studies were performed for baseline evaluation. Nearly two-thirds of the patients had poorly differentiated carcinoma. The average number of metastatic sites was 2.65 (range 1-4), with liver and lymph node involvement predominating. RESULTS: The overall response rate was 25% (95% CI 17.7-32.3%); 30.7% for poorly differentiated cancers and 25% for well differentiated cancers. Median survival was 4 months (range 1-12 months), 4.8 months for patients attaining partial response. Toxicity was moderate, grade 3 and 4 neutropenia occurred in 55% and grade 3 and 4 thrombocytopenia in 40%; other toxicities were mild. CA125 and CA199 were elevated in more than 50% of patients. Viral serology studies were not significantly different from those of the indigenous population. CONCLUSION: Etoposide and cisplatin combination chemotherapy has modest activity in patients with extensive CUPS and, at the schedule and dosage given, it is associated with moderate toxicity.      

World Workshop on Oral Medicine VI: a systematic review of medication‐induced salivary gland dysfunction

The aim of this paper was to perform a systematic review of the pathogenesis of medication‐induced salivary gland dysfunction (MISGD). Review of the identified papers was based on the standards regarding the methodology for systematic reviews set forth by the World Workshop on Oral Medicine IV and the PRISMA statement. Eligible papers were assessed for both the degree and strength of relevance to the pathogenesis of MISGD as well as on the appropriateness of the study design and sample size. A total of 99 papers were retained for the final analysis. MISGD in human studies was generally reported as xerostomia (the sensation of oral dryness) without measurements of salivary secretion rate. Medications may act on the central nervous system (CNS) and/or at the neuroglandular junction on muscarinic, α‐and β‐adrenergic receptors and certain peptidergic receptors. The types of medications that were most commonly implicated for inducing salivary gland dysfunction were those acting on the nervous, cardiovascular, genitourinary, musculoskeletal, respiratory, and alimentary systems. Although many medications may affect the salivary flow rate and composition, most of the studies considered only xerostomia. Thus, further human studies are necessary to improve our understanding of the association between MISGD and the underlying pathophysiology.