An evidence-based specialist breast nurse role in practice: a multicentre implementation study

The objective of this study was to examine the feasibility, implementation, acceptability and impact of an evidence-based specialist breast care nurse (SBN) model of care in Australia. Primary data were collected from four diverse Australian breast cancer treatment centres over a 12-month period. The design was a multicentre demonstration project. Information about the provision of care and patient needs was collected through prospective logs. Structured interviews were conducted with women who received the SBN intervention ( N  = 167) and with a control group of women treated prior to the intervention period ( N  = 133). Health professionals ( N  = 47) were interviewed about their experience of the SBN. Almost all women had contact with an SBN at five scheduled consultations and 67% of women in the intervention group requested at least one additional consultation with the SBN. Women in the intervention group were more likely to receive hospital fact sheets and to be told about and participate in clinical trials. Ninety-eight per cent of women reported that the availability of an SBN would affect their choice of hospital, with 48% indicating that they would recommend only a hospital with a SBN available. Health professionals reported that SBNs improved continuity of care, information and support for the women, and resulted in more appropriate referrals and use of the time of other members of the team. In conclusion, the SBN model is feasible and acceptable within diverse Australian treatment centres; there is evidence that some aspects of care were improved by the SBN.     

抗重组EB病毒抗原双重抗体检测血清学诊断鼻咽癌的研究

背景与目的：在评估4种EB病毒抗原酶联免疫吸附法的基础上,探讨优化抗重组：EB病毒抗原双重抗体检测应用于血清学诊断鼻咽癌。方法：收集广州地区57例治疗前鼻咽癌患者和58例健康成人的血清。应用：EB病毒特异抗原(谷胱甘肽转移酶重组融合蛋白)为基础的4种免疫酶联吸附法,即：EBNA1-IgA,EBNA1-Igg,Zta-IgA和Zta-IgG检测血清中抗EB病毒的抗体水平。结果：EBNA1-IgA的灵敏度(O．9123)和阴性预测值(0．9074)是单独使用4种ELISA实验中最高的。Zta-IgA具有最高的正确率(π,0．8870)和Youden指数(J,0．7738)。当评估配对的ELISA时,EBNA1-IgA和Zta-IgA双重阳性的所有指标是4种双重阳性实验中最高的。5例：EBNA1-IgA阴性的鼻咽癌患者呈Zta-IgA阳性,而7例Zta-IgA阴性的鼻咽癌患者呈EBNA1-IgA阳性。结论：EBNA1-IgA酶联免疫吸附的单独检测在血清学诊断鼻咽癌时优于其他3项(EBNA1-IgG、Zta-IgA和Zta-IgG)单独酶联免疫吸附检测。EBNA1-IgA和Zta-IgA两项的组合应用在血清学诊断鼻咽癌时有互补作用,是血清学检测的合适组合。     

Cyclooxygenase-2 upregulates vascular endothelial growth factor expression and angiogenesis in human gastric carcinoma

Although gastric cancer with cyclooxygenase (COX)-2 overexpression is associated with poor prognosis, the mechanistic pathway remains unknown. We examined the associations between expressions of COX-2 and vascular endothelial growth factor (VEGF) in both gastric cancer cells and in human gastric cancer. The gastric cell line, Kato III, was transiently transfected with cox-2 expressing vector. The levels of COX-2, prostaglandin (PG) E2 and VEGF expression were measured post-transfection. Additionally, expressions of COX-2 and VEGF in human gastric cancer were determined by immunohistochemistry in archive gastrectomy specimens. Tumor angiogenesis was assessed by the microvessel density (MVD), which was determined by anti-CD34 immunostaining. Transient transfection of Kato III with cox-2 was associated with increased COX-2 expression, higher PGE2 production and upregulated VEGF expressions. Treatment with NS398, a specific COX-2 inhibitor, reduced VEGF expression in COX-2 expressing Kato III cells by 25%. Among the 67 gastric cancers examined, COX-2 overexpression was found in 45 (67%) cases whereas increased VEGF expression was detected in 46 (69%) cases. There was a significant association between COX-2 and VEGF expressions in gastric cancer (r=0.25, p=0.041). Additionally, tumor MVD was associated with both COX-2 (r=0.32, p=0.008) and VEGF (r=0.39, p=0.001) expressions. Our results showed that overexpression of COX-2 in both gastric cells and primary gastric cancer is associated with upregulation of VEGF and angiogenesis. Future studies should evaluate the potential anti-angiogenic effect of COX-2 inhibitors on human gastric cancer.     

Characterisation of somatostatin actions on knee joint blood vessels of the rat

The effects of somatostatin on blood flow, plasma extravasation and knee joint sizes in the rat were investigated. Topical bolus administrations of somatostatin (10 pmol-100 nmol) onto the exposed rat knee joint capsules produced dose-dependent increases in knee joint blood flow with an ED(50) value of 1.7 nmol, and a maximum increase of 109.7%. The peak vasodilator response was observed at 1 min following drug administration, and it subsided at 5 min. Treatment of the rat knee with a somatostatin receptor antagonist cyclo(7-aminoheptanoul-Phe-D-Trp-Lys-Thr[Bzl] (cyclo-somatostatin; 2 x 20 nmol) significantly suppressed the somatostatin-induced vasodilator response, but treatment with the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 2 x 50 nmol) or the cyclo-oxygenase inhibitor flurbiprofen (2 x 10 nmol) had no effect. Unilateral intraarticular injections of somatostatin (10 nmol) produced no change on blood flow and sizes of the rat knee joints, but elicited marked ipsilateral Evans blue extravasation. Cyclo-somatostatin at doses of 2 x 20 and 2 x 50 nmol did not affect the plasma extravasation response to somatostatin. The present findings indicate the vasodilator effect of somatostatin is mediated by receptors sensitive to cyclo-somatostatin inhibition, but its plasma extravasation effect might be mediated by somatostatin receptor types that are resistant to inhibition by cyclo-somatostatin. There is no evidence that nitric oxide and prostaglandins are involved in the somatostatin-induced vasodilator response. It is suspected that the vascular effects of somatostatin demonstrated in this study would play a part in the innate response of an inflammatory reaction.     

Refractory hypotension in preterm infants with adrenocortical insufficiency

Five preterm, very low birthweight infants with severe hypotension and adrenocortical insufficiency are described. The profound hypotension was resistant to volume expansion and inotrope treatment, but responded promptly to corticosteroid treatment. A human corticotrophin releasing hormone (hCRH) test performed before corticosteroid treatment showed adequate pituitary response, and the endocrine dysfunction was identified at the adrenal level. Corticosteroid treatment should be considered and could be life saving in severely hypotensive preterm infants who do not respond to conventional treatment with volume expanders and inotropes.     

Postoperative vaginal vault brachytherapy for node-negative Stage II (occult) endometrial carcinoma

OBJECTIVE: The aim of this study is to look at the efficacy of extended surgical staging and postoperative vaginal vault brachytherapy in patients with Stage II (occult) endometrial carcinoma. METHODS: Between January 1989 and December 1997, there were 30 patients with Stage II (occult) endometrial carcinoma who received postoperative vaginal vault brachytherapy as the only adjuvant treatment. The study group consisted of 15 of these patients who had extended surgical staging (including lymphadenectomy). RESULTS: At a median follow-up of 36 months (range 17 to 113 months), there has been no recurrence. There were no major complications from surgery. Only 1 patient had mild rectal bleeding following vaginal vault brachytherapy and there were no grade 3 or 4 bowel toxicities. CONCLUSIONS: Extended surgical staging and postoperative vaginal vault brachytherapy for Stage II (occult) endometrial carcinoma is associated with minimal morbidity and excellent survival.     

Epidemiology and infection control implications of Acinetobacter spp. in Hong Kong

In a previous study, we showed that Acinetobacter genomic DNA group 3 was the most common species among blood culture isolates and was commonly found on superficial carriage sites of the healthy and the sick, which are different findings from those reported in Europe and North America. We used amplified ribosomal DNA restriction analysis and pulsed-field gel electrophoresis to study further the molecular epidemiology of acinetobacters in our region. Over a study period of 6 weeks with 136 consecutive routine clinical isolates (1.33% of all specimens), genomic DNA groups 2 (Acinetobacter baumannii), 3, and 13TU were obtained from 59 of 69 positive patients. There is a significant difference in the specimen sources of the three genomic DNA groups, with group 13TU being significantly associated with the respiratory tract (chi-square exact test, P = 0.0064). Settle plates showed a significantly heavier environmental load from the intensive care unit (ICU) than from the four surgical wards examined (22 of 70 versus 76 of 120 plates with <5 colonies; chi-square test, P < 0. 0001). Genomic group 3 accounted for 6 of 12 clusters of possibly related strains among patients, between patients and the ICU environment, and in the ICU environment. Genomic groups 2 and 3 accounted for 21% of the 132 genomically identified isolates recovered from 21 of 41 local vegetables, 53 of 74 fish and meat samples, and 22 of 60 soil samples. Group 13TU was present only in patients' immediate surroundings. The role played by the environment and by human carriage should be evaluated in order to devise a cost-effective infection control program pertinent to our situation of acinetobacter endemicity.     

Nitric oxide induces extensive apoptosis in endometrial epithelial cells in the presence of progesterone: involvement of mitogen-activated protein kinase pathways

During trophoblast invasion, luminal and glandular endometrial epithelial cells (EEC) have been found to undergo apoptosis through undetermined mechanisms. We postulate that nitric oxide (NO) and progesterone may mediate apoptosis in EEC because they are produced by trophoblasts at concentrations that can cause apoptosis in non-uterine cells. Using a cultured EEC line, RL95-2, we found that sodium nitroprusside (SNP) or S-nitroso-N-acetylpenicillamine (SNAP), two commonly used NO-releasing agents, caused the death of EEC in a dose-dependent manner and progesterone markedly enhanced NO-induced cytotoxicity. Cells treated with NO/progesterone showed a significant increase in the percentage of condensed nuclei, as detected by DAPI staining, and in caspase-3 activity, indicating that these cells underwent apoptosis. Immunoblot analysis revealed that SNP/NO could activate extracellular signal-regulated kinase (ERK) and, to a lesser extent, p38 mitogen-activated protein kinase (MAPK). While pretreatment with PD98059 (an ERK inhibitor) did not prevent cell death, the addition of SB203580 (a p38 MAPK inhibitor) effectively rescued the cells from NO/progesterone treatment. Moreover, SNP/NO-induced p38 MAPK activation was significantly up-regulated by progesterone. Our results demonstrate that NO and progesterone may synergistically activate p38 MAPK to induce apoptosis in EEC, a process that may facilitate implantation.