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Chu H.,Institute of Aerospace and Undersea Medicine | Ma H.-I.,Triservice General Hospital | Hueng D.-Y.,Triservice General Hospital | Hueng D.-Y.,National Defense Medical Center
Neurology India | Year: 2012

Objective: Decompressive hemicraniectomy is accepted as the most effective life-saving treatment for malignant middle cerebral artery (MCA) infarction. However, the outcome remains hard to predict. This study examined the efficacy of using the Glasgow Coma Scale (GCS) and Acute Physiology and Chronic Health Evaluation (APACHE) II scores before emergency craniectomy for predicting clinical outcome in malignant MCA infarction. Materials and Methods: Seventy-nine consecutive patients with malignant MCA infarction treated from January 2006 to October 2010 were retrospectively analyzed. The GCS and APACHE II scores within the first 24 h of neurological deterioration or before decompressive hemicraniectomy, were used to predict short-term functional outcome rated by the modified Rankin Scale (mRS). The receiver operating characteristic (ROC) curve was obtained to determine the accuracy and best cut-off value for each scoring system. Results: At 6 months, there was dramatic life-saving effect of surgery, with a significant reduction in mortality rate (from 71% to 19%, P < 0.001). After the ROC analysis, cut-off values of pre-operative GCS > 8 (P = 0.003) and APACHE II <13 (P = 0.006) were sufficiently sensitive and specific to predict favorable outcome (mRS 0-3). Conclusions: Pre-operative GCS and APACHE II scores are useful tools in predicting outcomes for patients with malignant MCA infarction who underwent decompressive hemicraniectomy. Copyright © Wolters Kluwer 2012. Source

Chiang K.-T.,Aerospace Physiology Research Laboratory | Yang C.-S.,Aerospace Physiology Research Laboratory | Chiou W.-Y.,Gangshan Armed Forces Hospital | Chu H.,Institute of Aerospace and Undersea Medicine
Aviation Space and Environmental Medicine | Year: 2012

Background: Military aircrew members undergo regular aviation physiology training, including hypobaric chamber fl ight to demonstrate the effects of hypoxia at altitude on human physiology and to strengthen hypoxia awareness. Premature near syncope under hypoxia will jeopardize fl ight safety. However, the causes of such abnormality may not be apparent. Case Report: We present a case of a healthy army helicopter pilot who suffered repeated premature near syncope and bradycardia during chamber fl ight at 18,000 ft (5486 m). He had no previous record of fainting. A passive head-up tilt table study under normoxia revealed cardiovascular responses compatible with vasovagal syncope. After considering the nature of the abnormality, mission characteristics, and the operating altitude for the helicopter, the pilot was granted a restricted waiver, with missions limited to below 10,000 ft (3048 m) in multicrew helicopters. Discussion: Evaluation of hypoxic syncope focuses on cardiovascular, neurologic, and psychiatric systems. The possibility of newly acquired dysautonomia as the cause of hypoxia syncope was supported by normal hypoxia tolerance in previous chamber fl ights and the results of the head-up tilt table study. The possible pathophysiology of hypoxic syncope and its association with a vasovagal constitution is presented. For a previously healthy helicopter pilot, impaired hypoxia tolerance may cause in-fl ight incapacitation. The cause should be investigated and the possibility of recurrence in fl ight should be evaluated before an adequate aeromedical decision can be made. © by the Aerospace Medical Association, Alexandria, VA. Source

Tang S.-E.,Graduate Institute of Medical science | Tang S.-E.,National Defense Medical Center | Wu C.-P.,Landseed Hospital | Wu S.-Y.,Institute of Aerospace and Undersea Medicine | And 6 more authors.
Free Radical Biology and Medicine | Year: 2014

Stanniocalcin-1 (STC1) is an endogenous glycoprotein whose anti-inflammatory effects occur through induction of uncoupling proteins to reduce oxidative stress. In this study, we tested the hypothesis that exogenous recombinant human STC1 (rhSTC1) protects against lipopolysaccharide (LPS)-induced acute lung injury in mice. Anesthetized C57BL/6 mice underwent intratracheal spraying of LPS (20 μg/10 g body wt), and lung injury was assessed 24 h later by analyzing pulmonary edema, bronchoalveolar lavage fluid, and lung histopathology. Lung inflammation, oxidative stress, and expression of STC1 and its downstream uncoupling protein 2 (UCP2) were analyzed at specific time points. Expression of UCP2 was suppressed initially but was subsequently upregulated after STC1 elevation in response to intratracheal administration of LPS. Intratracheal rhSTC1 treatment 1 h before or after LPS spraying significantly attenuated pulmonary inflammation, oxidative stress, cell apoptosis, and acute lung injury. Pretreatment with STC1 short interfering RNA 48 h before LPS spraying inhibited the expression of STC1 and UCP2 and significantly increased the extent of lung injury. These findings suggest that STC1 is an endogenous stress protein that may counteract LPS-induced lung injury by inhibiting the inflammatory cascade and inducing antioxidant and antiapoptotic mechanisms. However, the potential clinical application of STC1 and the direct linkage between UCP2 and LPS-induced lung injury remain to be further investigated. © 2014 Elsevier Inc. Source

Chu H.,Institute of Aerospace and Undersea Medicine | Chu H.,National Defense Medical Center | Li M.-H.,Institute of Aerospace and Undersea Medicine | Huang Y.-C.,Institute of Aerospace and Undersea Medicine | Lee S.-Y.,Institute of Aerospace and Undersea Medicine
BMC Complementary and Alternative Medicine | Year: 2013

Background: Flight simulators have been used to train pilots to experience and recognize spatial disorientation, a condition in which pilots incorrectly perceive the position, location, and movement of their aircrafts. However, during or after simulator training, simulator sickness (SS) may develop. Spatial disorientation and SS share common symptoms and signs and may involve a similar mechanism of dys-synchronization of neural inputs from the vestibular, visual, and proprioceptive systems. Transcutaneous electrical nerve stimulation (TENS), a maneuver used for pain control, was found to influence autonomic cardiovascular responses and enhance visuospatial abilities, postural control, and cognitive function. The purpose of present study was to investigate the protective effects of TENS on SS.Methods: Fifteen healthy young men (age: 28.6 ± 0.9 years, height: 172.5 ± 1.4 cm, body weight: 69.3 ± 1.3 kg, body mass index: 23.4 ± 1.8 kg/m2) participated in this within-subject crossover study. SS was induced by a flight simulator. TENS treatment involved 30 minutes simultaneous electrical stimulation of the posterior neck and the right Zusanli acupoint. Each subject completed 4 sessions (control, SS, TENS, and TENS + SS) in a randomized order. Outcome indicators included SS symptom severity and cognitive function, evaluated with the Simulator Sickness Questionnaire (SSQ) and d2 test of attention, respectively. Sleepiness was rated using the Visual Analogue Scales for Sleepiness Symptoms (VAS-SS). Autonomic and stress responses were evaluated by heart rate, heart rate variability (HRV) and salivary stress biomarkers (salivary alpha-amylase activity and salivary cortisol concentration).Results: Simulator exposure increased SS symptoms (SSQ and VAS-SS scores) and decreased the task response speed and concentration. The heart rate, salivary stress biomarker levels, and the sympathetic parameter of HRV increased with simulator exposure, but parasympathetic parameters decreased (p < 0.05). After TENS treatment, SS symptom severity significantly decreased and the subjects were more able to concentrate and made fewer cognitive test errors (p < 0.05).Conclusions: Sympathetic activity increased and parasympathetic activity decreased after simulator exposure. TENS was effective in reducing SS symptoms and alleviating cognitive impairment.Trial registration number: Australia and New Zealand Clinical Trials Register: http://ACTRN12612001172897. © 2013 Chu et al.; licensee BioMed Central Ltd. Source

Wu S.-Y.,Institute of Aerospace and Undersea Medicine | Li M.-H.,Institute of Aerospace and Undersea Medicine | Ko F.-C.,Taoyuan Armed Forces General Hospital | Wu G.-C.,Taoyuan Armed Forces General Hospital | And 3 more authors.
PLoS ONE | Year: 2013

Hypercapnic acidosis (HCA) has protective effects in animal models of acute lung injury, but the mechanism underlying the effect of HCA is unclear. Heme oxygenase-1 (HO-1) is an antioxidant enzyme that protects tissue from inflammation injury. We investigated whether HO-1 contributes to the protective effects of HCA in ischemia-reperfusion (IR)-induced lung injury. Typical acute lung injury in rats was successfully induced by 40 min of ischemia and 90 min of reperfusion in an isolated perfused lung model. The rat lungs were randomly assigned to the control group, IR group or IR + HCA group with or without zinc protoporphyrin IX (ZnPP), an HO-1 activity inhibitor. At the end of the experiment, bronchoalveolar lavage fluid (BALF) and lung tissues were collected to evaluate the degree of lung injury. In in vitro experiments, HO-1 siRNA transfected A549 cells were exposed to a normoxic or hypoxia-reoxygenation (H/R) environment in the presence or absence of HCA. IR caused significant increases in the pulmonary arterial pressure, lung weight to body weight and wet/dry ratios, lung weight gain, capillary filtration coefficient, lung injury scores, neutrophil infiltration, and concentrations of protein and TNF-α in the BALF. IR also induced degradation of inhibitor of nuclear factor (NF)-κB-α, increased IκB kinase (IKK)-β phosphorylation and nuclear translocation of NF-κB, and up-regulated HO-1 expression and activity. Furthermore, IR decreased Bcl-2 protein expression and increased the number of active caspase-3 stained cells. HCA treatment enhanced HO-1 expression and activity, and accordingly reduced IKK-NF-κB signaling, inhibited apoptosis, and significantly attenuated IR-induced changes. Treatment with ZnPP partially blocked the protective effect of HCA. In addition, HO-1 siRNA significantly reversed HCA-mediated inhibition of NF-κB signaling in A549 cells subjected to H/R. In conclusion, the protective effect of HCA in IR lung injury in rats was mediated in part by the anti-inflammatory and anti-apoptotic action of HO-1. © 2013 Wu et al. Source

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