Evaluation and effects of the Omron 725 CIC device for measuring blood pressure in a hypertension clinic.

BACKGROUND: We compared the Omron 725 CIC device (Omron Healthcare Inc., Vernon Hills, Illinois, USA), which is designed to register the blood pressure on the arm, with a mercury sphygmomanometer. In addition, we evaluated the possible impact that this device might have on the decisions made in a hypertension clinic. METHODS: Patients (n=183) older than 18 years (range 18-84 years) with a wide range of systolic (87-197 mmHg) and diastolic (48-108 mmHg) blood pressures were included. Some of the standards of the Association for the Advancement of Medical Instrumentation and of the British Hypertension Society were used to evaluate the results of the automated device in clinical practice. RESULTS: Using Bland-Altman analysis, an underestimation of both measures was observed with the automated Omron 725 CIC device; the systolic pressure was 3.6+/-8.8 mmHg too low with a very wide range of -13.7 to 20.9 and the diastolic pressure was also 4.4+/-6.3 mmHg too low with a range of -8.1 to 16.9. Clinical decisions could have been changed in 24 of the 116 hypertensive patients (20.6%) if the readings of the automated device had been used instead of using the readings of a mercury sphygmomanometer. These could have included modifying the dosage or changing the medicine used. CONCLUSION: The blood pressure measurements by Omron 725 CIC are different from those of blood pressure readings taken with a mercury sphygmomanometer and this could affect clinical decisions in the diagnosis and follow-up of a hypertensive patient in an office environment.

In vivo and in vitro sensitization of leukemic cells to adriamycin-induced apoptosis by pentoxifylline. Involvement of caspase cascades and IkappaBalpha phosphorylation.

UNLABELLED: The aim of this work was to investigate whether in vivo and in vitro pentoxifylline (PTX) sensitizes hematological tumor cells to adriamycin (ADM)-induced apoptosis, and to investigate the involvement of caspase cascades and phosphorylated forms of IkappaBalpha. Balb/c mice inoculated intraperitoneally with L5178-Y murine lymphoma cells were used for in vivo experiments and for survival studies. The U937 human monocytic cell line was used for in vitro experiments. Both cell lines were treated under similar experimental conditions with PTX and/or ADM to assess their effects on apoptosis. Apoptosis was evaluated by fluorescence microscopy with ethidium bromide and acridine orange staining and confirmed by electrophoretic DNA analysis. Caspase inhibitors Z-VAD-fmk, Z-DEVD-fmk, and Z-LEHD-fmk were used to investigate the involvement of caspase cascades. C-terminally and Ser32 phosphorylated forms of IkappaBalpha were evaluated in cytoplasmic extracts in the absence or presence of TNFalpha. RESULTS: In vivo, PTX (50 mg/kg) with ADM (5 mg/kg) increased the apoptotic index relative to PTX or ADM administered alone, time- and dose-dependently. DNA laddering appeared in lymphoma cells treated with PTX+ADM at 24 h, whereas neither untreated control, PTX-, nor ADM-treated cells showed DNA fragmentation. All (100%) tumor-bearing mice treated with PTX (25 mg/kg)+ADM (2.5 mg/kg) survived for 1 year, whereas the mortality rates of mice treated with either PTX or ADM alone at the same doses were similar to that of untreated tumor-bearing mice (28+/-3 days). Caspase inhibitors inhibited apoptosis more efficiently in PTX- or ADM-treated cultures than in PTX+ADM-treated cultures. Pretreatment with TNFalpha (10 ng/mL) increased apoptosis in PTX- or ADM-treated U937 cells. However, the apoptotic index of PTX+ADM-treated cultures was significantly reduced and the expression of C-terminally and Ser32 phosphorylated IkappaBalpha was reduced. PTX sensitizes hematological malignancies to ADR-induced apoptosis. An independent caspase pathway is involved in PTX+ADM-induced apoptosis. The phosphorylation status of IkappaBalpha is closely related via TNFalpha to the possible mechanisms of drug resistance.

Gamma-irradiation induced apoptosis in peritoneal macrophages by oxidative stress. Implications of antioxidants in caspase mitochondrial pathway.

The in vivo and in vitro development of apoptosis induced by gamma-irradiation was studied in mouse peritoneal macrophages. The apoptosis index was measured by fluorescence microscopy and DNA electrophoresis. In vivo apoptosis was greatest eight days after 8 Gy total body gamma-irradiation. A DNA ladder electrophoretic pattern was only observed in the gamma-irradiated group. The participation of reactive oxygen species in apoptosis induction was investigated by pretreating mice with the antioxidants superoxide dismutase, catalase, vitamin E or lipopolysaccharide before gamma-irradiation. Measurement of serum lipoperoxides showed oxidative stress in the gamma-irradiated mice and the protection given by the antioxidants. These results were confirmed using in vitro cultures of peritoneal macrophages: gamma-irradiated groups and antioxidant-pretreated gamma-irradiation groups showed results similar to those observed with in vivo irradiation. A loss of mitochondrial membrane potential (delta psi(m)) was also observed by microscopy in the gamma-irradiated cell cultures. Experiments with caspase inhibitors confirmed the participation of caspase 3 and caspase 9.

In vivo adriamycin-induced apoptosis in peritoneal murine macrophages: partial participation of a caspase cascade.

BACKGROUND: Adriamycin (ADM) is a potent antitumor drug that induces apoptosis (AP) in tumor cells. AP is modulated by caspases and by mitogen-activated protein kinases (MAPK) as well as by the mitochondrial membrane potential (deltapsim). We studied the participation of these systems in peritoneal macrophages from ADM-treated mice. MATERIALS AND METHODS: Balb/c mice were either treated with ADM (5 mg/kg, i.p.) or with 0.85% NaCl solution (controls). One hour later, peritoneal cells were harvested and cultured for 28 h. AP was evaluated by ethidium bromide and acridine orange staining; deltapsim was monitored using a MitoCapture stain Kit; DNA integrity was assessed by electrophoretic analysis. Animals were treated (i.p.) 1 h before ADM administration with Z-LEHD-FMK, Z-DEVD-FMK, or Z-VAD-FMK (caspase-9, caspases-3, 7,10 and general caspase inhibitors, respectively) or with PD169316 (a MAPKp38 inhibitor). RESULTS: ADM induced a higher rate of AP and the characteristic electrophoretic DNA ladder pattern. Mice treated with caspases inhibitors plus ADM showed significant reductions in AP and DNA laddering; in contrast, no differences were observed in mice treated with PD169316 plus ADM in comparison with ADM alone. ADM also induced early loss of the deltapsim. CONCLUSION: In these experimental conditions, ADM induced AP in a mainly caspase-9-dependent manner and this was related to a reduction in the deltapsim.

Hemosiderosis pulmonar idiopática / Idiopathic pulmonary hemosiderosis

Introducción. La hemosiderosis pulmonar idiopática (HPI) es un padecimiento poco frecuente, se presenta más en el niño que en el adulto. Se ha reportado que la combinación de prednisona y un inmunosupresor modifican la evolución clínica. En este trabajo se presenta una serie de 10 pacientes con HPI que fueron tratados con prednisona y azatioprina.Material y métodos. Se describe la evolución clínica de 10 casos con HPI con edades comprendidas entre 1 y 9 años. Después de controlar clínicamente el sangrado pulmonar en su fase aguda se les administró prednisona y azatioprina de forma continua por un período mínimo de 3 años.Resultados. Con el tratamiento, 3 pacientes desde el inicio no volvieron a presentar sangrado pulmonar, sólo 1 paciente requirió de transfusión sanguínea y ningún paciente se hospitalizó. Una paciente falleció 1 año después de terminar con su tratamiento. En mayo de 1999 se evaluaron 8 pacientes que terminaron el tratamiento, se encontró la función respiratoria anormal en todos; en 2 había secuelas clínicas y ninguno presentaba alteraciones radiológicas.Conclusiones. La prednisona y la azatioprina provieron de una mejoría clínica inmediata. Después de suspender el tratamiento todos presentaron función respiratoria alterada en un grado no significativo.