Plasma levels of antioxidant vitamins, selenium, total sulfhydryl groups and oxidative products in ischemic-stroke patients as compared to matched controls in Taiwan.

The possible involvement of oxidative damage and antioxidant protection has been suggested in the pathogenesis of stroke which is the second-leading cause of death in Taiwan. In this study we investigated the relationship between ischemic stroke and plasma status of antioxidants and oxidative products. Plasma levels of vitamin A, alpha-tocopherol, carotenoids, selenium (Se), total SH groups (T-SH), thiobarbituric acid-reactive substances (TBARS) and protein carbonyl, a marker of protein damage, were determined in ischemic-stroke patients (n = 36, blood sampled within 24 hrs after the clinical event) in comparison with 21 matched controls. The cholesterol-adjusted carotenoids and vitamin E were significantly lower (P < 0.05) in the plasma of ischemic-stroke patients than those of the controls. TBARS were higher (P < 0.05) in the patients than in the controls but Se, T-SH and protein carbonyls were not significantly different between the two groups. Separation of the patients into small-artery ischemic stroke (SAIS, n = 17) and large-artery ischemic stroke (LAIS, n = 19) groups revealed that both carotenoids/cholesterol and vitamin E/cholesterol ratios were significantly lower in both LAIS and SAIS groups than the controls (n = 21) while vitamin A/cholesterol was not different among the three groups. TBARS were only significantly higher in the LAIS group. The results demonstrated that, within 24 hrs after the clinical event, the acute-ischemic stroke patients had lowered levels of cholesterol-adjusted carotenoids and alpha-tocopherol but elevated levels of TBARS in the plasma as compared to the matched controls. It remains to be resolved as to whether enhanced lipid peroxidation is a cause or a result of lowered antioxidants in ischemic stroke.

Care of central venous catheters for total parenteral nutrition.

This report summarizes data obtained via a mailed questionnaire from 129 Department of Veterans Affairs (VA) hospitals regarding current practices in the care of central venous catheters (CVCs) used for total parenteral nutrition (TPN). The size of VA hospitals' acute medical-surgical beds ranged from 14 to 1320 (median 168) beds. Over 6000 patients annually received CVCs for TPN. Hospitals reported using triple-lumen catheters most frequently as their CVC for TPN (80.3%). A povidone-iodine scrub was used to prepare the skin for CVC insertion by 72.6% of reporting hospitals. Sixty percent of hospitals used transparent polyurethane dressings. Care of CVCs varied among hospitals. Catheter-related infection and sepsis rates were within the national average, although < 50% of responding hospitals provided data on these outcomes. The results of this survey point to the need for a national standardized database relative to patients receiving TPN via a CVC.

E-cadherin inhibits tumor cell growth by suppressing PI3K/Akt signaling via ß-catenin-Egr1-mediated PTEN expression.

E-cadherin is a cell-cell adhesion protein and tumor suppressor that is silenced in many malignancies. E-cadherin is thought to suppress tumor cell growth by antagonizing ß-catenin signaling. However, the role of E-cadherin in ovarian cancer progression is still controversial. In this study, we showed that loss of E-cadherin induced ovarian cancer cell growth and constitutive activation of phosphoinositide 3-kinase (PI3K)/Akt signaling by the inhibition of phosphatase and tensin homolog (PTEN) transcription through the downregulation of early growth response gene 1 (Egr1). In addition, immunofluorescence microscopy and T-cell factor promoter/luciferase reporter assays showed that E-cadherin loss was associated with enhanced nuclear ß-catenin signaling. Constitutive activation of PI3K/Akt signaling reinforced nuclear ß-catenin signaling by inactivating glycogen synthase kinase-3ß indicating cross-talk between the PI3K/Akt and ß-catenin signaling pathways. Finally, we found that E-cadherin negatively regulates tumor cell growth, in part, by positively regulating PTEN expression via ß-catenin-mediated Egr1 regulation, thus influencing PI3K/Akt signaling. In summary, endogenous E-cadherin inhibits PI3K/Akt signaling by antagonizing ß-catenin-Egr1-mediated repression of PTEN expression. Thus, the loss of E-cadherin itself may contribute to dysregulated PI3K/Akt signaling through its effects on PTEN, or it may exacerbate the frequent activation of PI3K/Akt signaling that occurs as a result of overexpression, mutation and/or amplification.

The treatment of unstable intertrochanteric fractures of the hip: a prospective trial of 150 cases.

We report a prospective clinical trial of 150 cases for the treatment of unstable intertrochanteric fracture of the neck of the femur. Three methods were tested in our series--skeletal traction with a tibial pin, medial displacement osteotomy and valgus osteotomy--with 50 patients in each group. Our results showed no significant difference between those treated with the Dimon and Hughston osteotomy and those treated by the Sarmiento osteotomy. Conservative treatment of skeletal traction for unstable fracture was found to be well tolerated by the Chinese patient. A low mortality and morbidity rate was found in this series with an overall infection rate of 4 per cent.