Protective effects of green tea extracts (polyphenon E and EGCG) on human cervical lesions

We investigated clinical efficacy of green tea extracts (polyphenon E; poly E and (-)-epigallocatechin-3-gallate [EGCG]) delivered in a form of ointment or capsule in patients with human papilloma virus (HPV) infected cervical lesions. Fifty-one patients with cervical lesions (chronic cervicitis, mild dysplasia, moderate dysplasia and severe dysplasia) were divided into four groups, as compared with 39 untreated patients as a control. Poly E ointment was applied locally to 27 patients twice a week. For oral delivery, a 200 mg of poly E or EGCG capsule was taken orally every day for eight to 12 weeks. In the study, 20 out of 27 patients (74%) under poly E ointment therapy showed a response. Six out of eight patients under poly E ointment plus poly E capsule therapy (75%) showed a response, and three out of six patients (50%) under poly E capsule therapy showed a response. Six out of 10 patients (60%) under EGCG capsule therapy showed a response. Overall, a 69% response rate (35/51) was noted for treatment with green tea extracts, as compared with a 10% response rate (4/39) in untreated controls (P<0.05). Thus, the data collected here demonstrated that green tea extracts in a form of ointment and capsule are effective for treating cervical lesions, suggesting that green tea extracts can be a potential therapy regimen for patients with HPV infected cervical lesions.     

Recording of the saphenous vein compliance by an ultrasonic echo-tracking device in the dog: effects of S 18149

BACKGROUND AND PURPOSE: Studies on risk factors for stroke have been less intensive than those for coronary disease. Only a few studies have addressed the question of the role of heredity in the occurrence of stroke. We analyzed whether a positive parental history of cardiovascular disease predicts the risk of stroke independently from other risk factors and whether the role of parental history varies by age and stroke subtypes. METHODS: This study was a prospective follow-up of 14371 middle-aged men and women. A positive parental history of cardiovascular disease was defined as either stroke or coronary disease before the age of 60 years. The end point of the follow-up was an incident case of stroke. Multivariate analyses were performed with the Cox proportional hazards model. RESULTS: The risk ratio of stroke after multifactorial adjustment (age, smoking, blood pressure, cholesterol, diabetes, and education) associated with a positive parental history of stroke was 1.89 (P = .004) in men and 1.80 (P = .007) in women. The association between parental history of stroke and the risk of stroke was stronger among subjects aged 25 to 49 years than among older subjects. Parental history of coronary disease was not associated with the risk of stroke in men, but in women it had a borderline significant association with the risk of ischemic stroke. CONCLUSIONS: A positive parental history of stroke predicted the risk of stroke independently from the other risk factors.     

Paget''s disease of bone

The protein encoded by ras and src protooncogenes are frequently activated in a constitutive state in human colorectal cancer. In this study, we investigated the effect of oncogenic p21ras and Py-MT/pp60c-src on the synthesis of syndecan-1, a membrane anchored proteoglycan playing a role in cell-matrix interaction and neoplastic growth control. To this end, we used Caco-2 cells transfected with an activated (Val-12) human Ha-ras gene or the polyoma middle T (Py-MT) oncogene, a constitutive activator of pp60c-src tyrosine kinase activity. As compared to control vector-transfected Caco-2 cells, both oncogene-transfected cells exhibited: (1) a decrease in syndecan-1 specific activity; (2) a decrease in size and sulfation of syndecan-1 ectodomain glycosaminoglycan side chains; and (3) an active heparanase specifically degrading the heparan sulfate chains. In conclusion, the tumorigenic progression induced by oncogenic p21ras or Py-MT/pp60c-src is associated with marked alterations of syndecan-1 at the post-translational level.     

Automating and improving the data quality of a nursing department quality management program at a university hospital

BACKGROUND: The development and implementation of a relational database program for nursing quality management at a university hospital was stimulated by a lack of consistent data management and analysis tools in the existing noncomputerized program. PROGRAM DEVELOPMENT AND IMPLEMENTATION: An initial software prototype implemented in the critical care service included data collection instruments for five areas: medication errors, patient falls, returns to an intensive care unit within 48 hours, hospital-acquired skin breakdown, and unplanned extubations. Access to the database was limited and paper reports only were disseminated on a scheduled basis. In a second phase, the database is being deployed throughout the nursing department using a local area network. Nurse managers will enter and interact with the quality database online and have access to graphics, reports, and action plan development. POSSIBLE ERRORS: A wide range of potential errors influences decisions on how to collect, store, retrieve, and process quality management data. Each type of error affects the nurse manager's ability to identify significant patterns or trends that are amenable to intervention. There is no right way of constructing and implementing a quality improvement database; only an optimum balance between cost, complexity, and efficacy. SUMMARY AND CONCLUSIONS: Initial feedback from end uses has been positive. A three-year experience with a personal computer database suggests that the personal computer-based information technology is appropriate for small to medium applications and can support departmentwide CQI efforts. A case scenario using simulated data is included to illustrate the use of computerized reports in assessing and taking action on an increase in falls.     

Chronic effects of glucose on insulin signaling in A-10 vascular smooth muscle cells

To examine the effects of hyperglycemia on insulin signaling in A-10 vascular smooth muscle cells, cells were treated with extracellular D-glucose and effects of insulin were studied on the diacylglycerol-protein kinase C signaling system. A-10 cells specifically bound 125I-insulin, and insulin-like growth factor-I did not displace the label. 125I-insulin binding was unaltered under hyperglycemic conditions. To determine if insulin receptors were coupled to other insulin-regulated processes, diacylglycerol, protein kinase C, and glucose transport were evaluated. Insulin increased cellular diacylglycerol (DAG) levels which were also increased following glucose treatment and not further stimulated by insulin. The uptake of 2-[3H]deoxy-D-glucose (2-DOG) was stimulated by insulin and 12-O-tetradecanoyl phorbol 13-acetate (TPA). Insulin- and TPA-stimulated 2-[3H]DOG uptake was inhibited by a protein kinase inhibitor, staurosporine. Preincubation of cells with 500 nM TPA overnight resulted in the inhibition of insulin- and TPA-stimulated 2-[3H]DOG uptake. Protein kinase C activity was translocated from cytosolic to membrane fractions following insulin treatment. Overnight glucose (25 mM) treatment resulted in a 50% decrease in protein kinase C enzyme activity and > 90% decrease in protein kinase C beta immunoreactive levels. Protein kinase C activity and levels were not affected by osmotic control media containing mannitol. A-10 cells express GLUT4-type glucose transporters. Neither insulin-regulatable glucose transporter (GLUT4) mRNA nor GLUT4 protein levels were diminished by glucose. Significant decreases in insulin- and TPA-stimulated 2-[3H]DOG uptake occurred, however, with glucose. The down-regulation of protein kinase C beta and resultant inhibition of 2-[3H]DOG uptake by chronic glucose suggests a biochemical link between hyperglycemia and DAG-protein kinase C signaling in vascular smooth muscle cells.