Application of a rapid exchange extension catheter technique in type B2/C nonocclusive coronary intervention via a transradial approach.

BACKGROUND: In transradial intervention procedures, poor back-up support and noncoaxial alignment of the guide catheter (GC) may result in failure of the balloon or stent to reach the targeted lesion. Methods to provide extra back-up support using the original GC and wire can improve procedural success with reduced complications. A rapid exchange guide extension catheter provides convenient and efficient back-up support while preserving the initial GC and inserted wire. AIM: To evaluate the efficacy and safety of rapid exchange extension catheter in the treatment of type B2/C nonocclusive coronary lesions via the radial access. METHODS: A total of 135 patients with type B2/C nonocclusive lesions who were treated via the transradial approach were enrolled in the study. The clinical characteristics, indications for use of the rapid exchange extension catheter, and procedural details and results were reviewed and analyzed. All procedure-related complications and major adverse cardiovascular events were recorded during the in-hospital stay and follow-up period. RESULTS: The most common indication for the use of a rapid exchange extension catheter was vascular tortuosity (37.8%), followed by heavy calcification (28.9%), long lesions (20.0%), proximal stent (6.7%), in-stent restenosis (5.2%), and coronary origin anomalies (1.5%). The following technologies failed in passing targeted lesions before delivering the rapid exchange catheter: Multiple predilatation technique (57%), buddy wire technique (33.4%), balloon anchoring technique (5.9%), and cutting balloon modification (3.7%). The mean depth of the extension catheter intubation was 20.56 ± 13.05 mm, and the mean rapid exchange catheter service time was 18.9 ± 9.7 min. The mean length and diameter of stents were 33.5 ± 14.4 mm and 2.75 ± 0.45 mm, respectively. The total rate of technique success (balloon or stent successful crossing of the target lesion with this technique) was 94.8%. CONCLUSION: The rapid exchange extension catheter technique showed acceptable safety and efficacy in the transradial coronary interventions of type B2/C nonocclusive coronary lesions. We recommend this technique to assist in complex lesion intervention via radial access.

The effect of early and late tracheotomy on outcomes in patients: a systematic review and cumulative meta-analysis.

OBJECTIVE: To compare the effect of early tracheotomy (ET) and late tracheotomy (LT) on ventilator-associated pneumonia (VAP) incidence and short-term mortality in critically ill patients who received mechanical ventilation. DATA SOURCES: We searched databases of PubMed, Embase, and others for randomized controlled trials (RCTs) that compared ET (≤ 8 days after admission to the intensive care unit, initiation of translaryngeal intubation, or initiation of mechanical ventilation) with LT (≥ 6 days) in critically ill patients. REVIEW METHODS: The overall odds ratio (OR) was estimated by traditional meta-analysis. In addition, cumulative meta-analysis was conducted by adding 1 study at a time in the order of year of publication. RESULTS: A total of 11 RCTs involving 1436 patients (708 in the ET group and 728 in the LT group) were included in this analysis. Early tracheotomy could significantly reduce the short-term mortality (OR = 0.74; 95% confidence interval [CI] [0.58, 0.95]) but did not reduce the VAP incidence (OR = 0.70; 95% CI [0.47, 1.04]). The cumulative meta-analysis showed that evidence of the benefit of ET on VAP incidence was unstable over time. In contrast, the difference in short-term mortality was stable from the first appearance during the cumulative meta-analysis. CONCLUSION: Early tracheotomy could improve short-term mortality but did not alter VAP incidence. Many factors may be responsible for the unstable results during cumulative meta-analysis, and further study is still needed to explore the optimal timing of tracheotomy.

Chronic intermittent hypoxic preconditioning suppresses pilocarpine-induced seizures and associated hippocampal neurodegeneration.

Mild brief hypoxia can protect against neuronal damage induced by epileptic seizures, at least in part by inhibiting apoptosis. Further elucidation of the antiepileptic mechanisms and optimization of the conditioning protocols are required before this strategy can be considered for clinical intervention. In this study, we compared the effects of different hypoxic preconditioning protocols on spontaneous recurrent seizures (SRS), intracellular free calcium concentration ([Ca(2+)]i), and apoptosis rate following pilocarpine-induced status epilepticus (SE). Male Sprague Dawley rats were subjected to either chronic intermittent hypobaric hypoxia (CIHH) or chronic intermittent normobaric hypoxia (CINH) (both for 6h/day × 28 consecutive days) prior to pilocarpine-induced SE. The possible anticonvulsant and neuroprotective effects of CIHH and CINH were compared by video monitoring of behavioral seizure activity (frequency, delay), Nissl staining and Fluoro-Jade B (FJB) staining to examine changes in the morphology of hippocampal pyramidal neurons, and flow cytometry to detect the quantification of [Ca(2+)]i and cell apoptosis. Both hypoxic preconditioning protocols reduced the frequency and severity of SRS, suppressed post-ictal [Ca(2+)]i elevations, and inhibited neuronal apoptosis in the rat hippocampus compared to pilocarpine alone, but CIHH was more effective than CINH. Thus, mild hypoxic pretreatment, particularly when delivered as CIHH, may be a novel strategy for the clinical prevention and treatment of epilepsy.

Temperature dependence of Raman scattering in bulk 4H-SiC with different carrier concentration.

Raman spectra of three bulk 4H-SiC wafers with different free carrier concentration were measured at temperature from 80 K to 873 K. As temperature increases, Raman peaks of most optical phonon modes show monotonous down shift. An anomalous non-monotonous variation with temperature, was observed in the A(1) longitudinal optical (LO) mode from doped samples. Two methods of theoretical fitting, one-mode (LO-plasma coupled (LOPC) mode) and two-mode (A(1)(LO) + LOPC) fitting, are employed to analyze this anomalous phenomenon. Theoretical simulations for temperature dependent Raman spectra by using two methods are critically examined. It turns out that one-mode method conforms well the experimental results, while two-mode method is untenable in physics. The non-monotonous variation of blue-red shifts with temperature for LOPC mode from doped 4H-SiC could be explained by the influence from ionization process of impurities on the process of Raman scattering. A quantitative description on temperature dependent Raman spectra for doped 4H-SiC is achieved, which matches well to experimental data.

Activation of Nrf2-ARE signal pathway in hippocampus of amygdala kindling rats.

Oxidative stress resulting from excessive free-radical release is likely implicated in the initiation and progression of epilepsy. Therefore, antioxidant therapies have received considerable attention in epilepsy treatment. It is well known that the transcription factor NF-E2-related factor (Nrf2) binds to antioxidant response element (ARE) to induce antioxidant and phase II detoxification enzymes under conditions of oxidative stress, which reduces oxidative stress and accumulation of toxic metabolites. However, whether Nrf2-ARE pathway is activated after seizure has not been studied. In the present study, Wistar rats were rapidly kindled in the amygdala. Twenty-four hours after the last seizure, the hippocampus of control, sham and kindled rats were examined for oxidative stress parameters (malondialdehyde and glutathione) by spectrophotometry, the expression of Nrf2, heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase-1 (NQO1) were determined using immunohistochemistry, Western blot and real-time fluorescence quantitative polymerase chain reaction (PCR). The results showed that the kindled seizures induced oxidative stress, the expression of Nrf2, HO-1 and NQO1 at protein or gene levels significantly increased in hippocampus after seizure. According to these results, it could be postulated that Nrf2-ARE signal pathway was activated in the hippocampus after seizure.

[Effect of amiloride on the pathology of a rat model of chronic obstructive pulmonary disease].

OBJECTIVE: To study the effects of amiloride, an inhibitor of urokinase, on pathological and pathophysiological changes of chronic obstructive pulmonary disease (COPD) model, and to investigate the role of urokinase plasminogen activator system components in the pathogenesis of COPD. METHODS: Healthy Wistar rats (n = 24) were randomly divided into a control group, a model group and an amiloride group. After 7 weeks, lung function measurements were performed. The total and different white blood cell counts of bronchoalveolar lavage fluid (BALF) were determined, and collagen deposition of lung sections was observed by picrosirius staining. The expressions of u-PA, u-PAR and PAI-1 in bronchial lung tissues were examined by immunohistochemical analysis. RESULTS: In the model group the expiratory resistance (Re) was significantly higher than that of the control group and the amiloride group, while forced expiratory volume in the 0.3 s/forced expiratory capacity (FEV(0.3)/FVC%) and peak expiratory flow (PEF) were significantly lower than those of the other two groups. Significant increase in total white blood cells and percentage of neutrophils and macrophages in BALF was found in the model group as compared to the control group and the amiloride group. The collagen deposition, mainly type I collagen, in airway walls was significantly increased in the model group. The levels of u-PA, u-PAR and PAI-1 in the model group [(0.166 +/- 0.010), (0.158 +/- 0.024), (0.171 +/- 0.012), respectively] were significantly higher than those in the control group [(0.137 +/- 0.015), (0.122 +/- 0.009), (0.144 +/- 0.005), respectively] and the amiloride group [(0.126 +/- 0.004), (0.120 +/- 0.010), (0.122 +/- 0.004), respectively]. F values were 32.463, 4.094, 79.562 respectively, and all P < 0.001. Moreover, u-PAR protein level was positively correlated with neutrophils in BALF in the model group (r = 0.754, P = 0.031). CONCLUSION: Administration of u-PA inhibitor-amiloride significantly alleviated airway inflammation and the pathological changes in COPD rats, suggesting that the u-PA system components are key mediators regulating the inflammatory reaction and tissue remodeling in the pathological process of COPD.

[Protective effect of hydrophilic Salvia monomer on liver ischemia/reperfusion injury induced by pro-inflammatory cytokines].

OBJECTIVE: To observe the changes of tumor necrosis factor alpha (TNF alpha), interleukin 8 (IL-8) in liver ischemia/reperfusion injury and the protective effect of hydrophilic Salvia monomer MP-1 on them. METHODS: Hypothermic hypoxia reoxygenation model of human liver sinusoidal endothelial cell line and ischemia/reperfusion model of isolated rat liver were used. TNF alpha and IL-8 were measured with ELISA kits. Cell injury was excluded by trypan blue stain, sinusoidal endothelial cell function was assessed by hyaluronic acid uptake rate through RIA. Liver function was assayed by alanine transaminase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) release as well as output of bile flow. RESULTS: During hypoxia reoxygenation, sinusoidal endothelial cell injury, TNF alpha and IL-8 increased significantly in time-dependent manner, while sinusoidal cell function decreased. Cell injury was positively correlated to the released amount of TNF alpha (r = 0.949, P < 0.05) and IL-8 (r = 0.892, P < 0.05), respectively, the mortality could be reduced within 6 hrs by adding anti-TNF alpha monoclonal antibody and increased by treating with recombinant human TNF alpha. Function of isolated rat liver lowered alone the increasing of low temperature ischemia/reperfusion time. MP-1 could markedly lower the mortality of endothelial cells and TNF alpha and IL-8 release, it also could alleviate ischemia/reperfusion injury to isolated rat liver. CONCLUSION: TNF alpha participated in liver ischemia/reperfusion injury directly, and MP-1 might alleviate the injury through inhibiting TNF alpha and IL-8.