1,347 research outputs found

    Titration procedures for nasal CPAP: Automatic CPAP or prediction formula?

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    Background: The best method for titration Of continuous positive airway pressure (CPAP) therapy in obstructive sleep apnea (OSA) syndrome has not yet been established. The 90th or 95th percentiles of the pressure titrated over time by automatic CPAP (A-CPAP) have been recommended as reference for prescribing therapeutic fixed CPAP (F-CPAP). We compared A-CPAP to F-CPAP. which was determined by a common prediction formula. Methods: Forty-five patients who were habituated to F-CPAP underwent titration polysomnography. In a double-blind randomized order, each patient used an A-CPAP device in the autotitration and in the fixed pressure mode during one half of the night. Apnea-hypopnea index (AHI) and pressure profiles were primary outcomes. Bias and precision were additionally assessed for both CPAP modes. Results: No significant differences in various sleep parameters or in subjective sleep quality evaluation were found. The AHI was effectively lowered in both CPAP modes (A-CPAP 7.7 [10.8] events/h versus F-CPAP 5.4 (9.0] events/h, p = 0.061). Comparison of group means showed that F-CPAP closely paralleled mean (Pmean) and median (P50). but not the 95th percentile (P95) pressure. of A-CPAP. While bias was lowest for Pmean and P50. there was a lack of precision in all A-CPAP pressure categories. Conclusions: We confirm that F-CPAP set by prediction formula is not worse in terms of AHI control than A-CPAP. On average. F-CPAP parallels Pmean and P50 but not P95. However. due to imprecise matching. individual F-CPAP values cannot be derived front Pmean or P50

    Preinfarction angina protects against out-of-hospital ventricular fibrillation in patients with acute occlusion of the left coronary artery

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    AbstractOBJECTIVESThe goal of this study was to evaluate the effect of preconditioning on out-of-hospital ventricular fibrillation (VF) in patients with acute myocardial infarction (AMI).BACKGROUNDMore than half of the deaths associated with AMI occur out of the hospital and within 1 h of symptom onset. In humans, preinfarction angina (PA), which can serve as a surrogate marker for preconditioning, reduces infarct size, but the protective effect against out-of-hospital VF has not been investigated.METHODSPreinfarction angina status and acute coronary angiographic findings of 72 consecutive patients with AMI complicated by out-of-hospital VF were compared with 144 matched controls without this complication.RESULTSPreinfarction angina is associated with a lower risk for VF (odds ratio [OR]: 0.40, 95% confidence interval [CI]: 0.18 to 0.88). In patients with acute occlusion of the left coronary artery (LCA) (n = 136), the risk reduction is pronounced (OR: 0.25, 95% CI: 0.10 to 0.66), whereas, in patients with acute occlusion of the right coronary artery (RCA) (n = 67), the protective effect of PA on VF was not observed (OR: 2.25, 95% CI: 0.45 to 11.22). Subgroup and multivariate analyses show that the protective effect is independent of cardiovascular risk factors, preinfarction treatment with beta-adrenergic blocking agents or aspirin, the presence of collaterals or residual antegrade flow or the extent of coronary artery disease.CONCLUSIONSPreinfarction angina protects against out-of-hospital VF in patients with acute occlusion of the LCA. This protection is independent of risk factors or coronary anatomy. A larger study is needed to examine the apparently different effect in patients with acute occlusion of the RCA

    Enhancement of tumorigenicity of human breast adenocarcinoma cells in nude mice by matrigel and fibroblasts.

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    The failure of MCF7 cells to induce the formation of tumours after sub-cutaneous inoculation into athymic nude mice can be obviated by the simultaneous injection of an extract of basement membrane proteins (matrigel). Tumour growth is promoted and the latency period is low (2 to 4 weeks). In the absence of matrigel, the simultaneous inoculation of fibroblasts and MCF7 cells also resulted in the development of tumours, but with a longer latency period (about 2 months). The tumorigenic synergy between matrigel and fibroblasts was evidenced by co-inoculating MCF7 cells MDA-MB 231 cells with fibroblasts and matrigel. This co-inoculation decreased the delay of appearance of the tumours and/or accelerated the tumour growth, depending upon the number of fibroblasts injected. Repeated injections of fibroblasts conditioned medium, at the site of inoculum of tumour cells also enhanced tumour growth, suggesting the involvement of soluble factors secreted by fibroblasts. Histologically, tumours induced by co-inoculation of tumour cells and fibroblasts contained more stromal structures including vimentin-positive cells, fibronectin and interstitial collagens. These data suggest that human tumours may be reconstituted and grown in athymic nude mice using basement membrane components and fibroblasts as inductors

    APETx4, a novel sea anemone toxin and a modulator of the cancer-relevant potassium channel K<sub>V</sub>10.1

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    The human ether-à-go-go channel (hEag1 or KV10.1) is a cancer-relevant voltage-gated potassium channel that is overexpressed in a majority of human tumors. Peptides that are able to selectively inhibit this channel can be lead compounds in the search for new anticancer drugs. Here, we report the activity-guided purification and electrophysiological characterization of a novel KV10.1 inhibitor from the sea anemone Anthopleura elegantissima. Purified sea anemone fractions were screened for inhibitory activity on KV10.1 by measuring whole-cell currents as expressed in Xenopus laevis oocytes using the two-microelectrode voltage clamp technique. Fractions that showed activity on Kv10.1 were further purified by RP-HPLC. The amino acid sequence of the peptide was determined by a combination of MALDI- LIFT-TOF/TOF MS/MS and CID-ESI-FT-ICR MS/MS and showed a high similarity with APETx1 and APETx3 and was therefore named APETx4. Subsequently, the peptide was electrophysiologically characterized on KV10.1. The selectivity of the toxin was investigated on an array of voltage-gated ion channels, including the cardiac human ether-à-go-go-related gene potassium channel (hERG or Kv11.1). The toxin inhibits KV10.1 with an IC50 value of 1.1 μM. In the presence of a similar toxin concentration, a shift of the activation curve towards more positive potentials was observed. Similar to the effect of the gating modifier toxin APETx1 on hERG, the inhibition of Kv10.1 by the isolated toxin is reduced at more positive voltages and the peptide seems to keep the channel in a closed state. Although the peptide also induces inhibitory effects on other KV and NaV channels, it exhibits no significant effect on hERG. Moreover, APETx4 induces a concentration-dependent cytotoxic and proapoptotic effect in various cancerous and noncancerous cell lines. This newly identified KV10.1 inhibitor can be used as a tool to further characterize the oncogenic channel KV10.1 or as a scaffold for the design and synthesis of more potent and safer anticancer drugs

    Influence of simulated spring frost on growth and yield of three barley cultivars

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    Spring barley was sown on 4 dates between 28 April and 21 May to evaluate the effect of a simulated frost at the 2-leaf stage on growth and yield. A portable field freezing chamber was used to subject the plants to a -5.6 deg C stress. The frost caused 49, 64 and 68% injury to the leaves and delayed heading by 2.4, 1.4 and 2.4 days in cv. Galt, Atlas and Olli, resp. Frost also reduced the number of tillers/plant, ripe ears/plant and plants/plot in all cv. Although the late-maturing cv. Galt had the most leaf frost resistance, the av. yield reduction (13.8%) was similar in all 3 cv. Complete defoliation by clipping resulted in no further reduction in yield than that which occurred from partial defoliation by freezing. Delayed sowing reduced yield by 8.6%. Frost reduced yield by 9.8% at the 2 early sowing dates and by 17.1% at the 2 later sowing date
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