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Shi-Jye Chu

Publications and source records attributed to Shi-Jye Chu.

16 recordsLinked to original sources
PubMed2006

Initial serum glucose level as a prognostic factor in the first acute myocardial infarction.

STUDY OBJECTIVE: We assess the prognostic role of initial glucose levels in patients with a first acute myocardial infarction in the emergency department (ED). METHODS: We conducted a 3-year retrospective cohort study. Patients with a first acute myocardial infarction were recruited from the ED of a tertiary hospital from January 1, 2001, to December 31, 2003. Initial glucose levels in the ED were stratified into 3 levels (normal < 140 mg/dL; intermediate 140 to 200 mg/dL; and high > or = 200 mg/dL). Logistic and Cox regression models were applied to estimate the 1-month short-term and 1-year long-term adverse prognoses, respectively. RESULTS: A total of 198 eligible subjects (159 men and 39 women; mean age 63.1+/-14.2 years) were recruited. The estimated survival curves among the 3 initial glucose levels were significantly different (P=.0002). After adjustment for sex, age, diabetic status, reperfusion therapy, and infarct subtype, the adjusted odds ratio for short-term prognosis progressed with higher levels when compared with the normal level (intermediate level: odds ratio 3.87; 95% confidence interval [CI] 1.71 to 8.78; high level: odds ratio 5.16; 95% CI 1.97 to 13.51). High initial glucose level was an important risk factor for long-term adverse prognosis (hazard ratio 3.08; 95% CI 1.59 to 5.98). CONCLUSION: A high initial glucose level in the ED is an important and independent predictor of short- and long-term adverse prognoses in patients with first acute myocardial infarction.

Blood Glucose↗
PubMed2006

Aortic dissection.

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Aortic Dissection↗
PubMed2006

Influence of hyperbaric oxygen on tumor necrosis factor-alpha and nitric oxide production in endotoxin-induced acute lung injury in rats.

We previously demonstrated that hyperbaric oxygen (HBO) treatment alleviated lipopolysaccharide (LPS)-induced acute lung injury in rats. However, the mechanisms responsible for the protective effect are still not fully understood. To obtain further information on the protective effect of HBO, in this study we investigated the role of tumor necrosis factor-alpha (TNF-alpha) and nitric oxide (NO) in intratracheal spraying LPS-induced acute lung injury in rats after HBO or hyperoxia treatment. The results showed that HBO but not hyperoxia attenuated the TNF-alpha level in plasma and bronchoalveolar lavage (BAL) fluid, NO concentration in BAL and plasma, and inducible NO synthase protein expression in lung tissue based on the Western blotting and immunohistochemical staining.

Acute Disease↗
PubMed2006

Early diagnosis of thyrotoxic periodic paralysis: spot urine calcium to phosphate ratio.

OBJECTIVES: To identify a clinically reliable index of thyrotoxic periodic paralysis (TPP), a life-threatening emergency with unique and effective therapies. DESIGN: Diagnostic study. SETTING: University teaching hospital. PATIENTS: Fifty-three consecutive patients with hypokalemic paralysis during a 3-yr period and 30 thyrotoxic patients without paralysis as the thyrotoxic control group. INTERVENTIONS: For patients with hypokalemic paralysis, blood and second-void spot urine samples were obtained and measured by routine laboratory prior to therapy. For the thyrotoxic control group, blood and spot urine were collected when they visited outpatient clinics. MEASUREMENTS AND MAIN RESULTS: Twenty-nine patients fulfilled the criteria for TPP. Compared with the thyrotoxic control group, the TPP group had significant decreases in plasma potassium (K) and phosphate concentrations associated with very low urine K and phosphate excretion. Compared with the non-TPP group, the TPP group had significantly lower plasma creatinine and phosphate levels, a significantly higher urine calcium to creatinine ratio (0.25 +/- 0.12 vs. 0.08 +/- 0.07 mg/mg, p < .001), and a significantly lower urine phosphate to creatinine ratio (0.08 +/- 0.05 vs. 0.31 +/- 0.23 mg/mg, p < .001). The urine calcium to phosphate ratio had greater discriminatory power between TPP and non-TPP hypokalemic paralysis (4.1 +/- 2.3 vs. 0.5 +/- 0.6 mg/mg, p < .001). Using a urine calcium to phosphate ratio cutoff value of 1.7 mg/mg, sensitivity and specificity for TPP were 100% and 96%, respectively. CONCLUSIONS: Hypercalciuria and hypophosphaturia are characteristic features of TPP.

Adult↗
PubMed2005

L-Arginine prevents air embolism-induced acute lung injury in rats.

OBJECTIVE: Pulmonary air embolism, causing vessel obstruction and primary or secondary reactions of blood, can lead to acute lung injury. In addition, nitric oxide has been known to play a key role in various causes of lung injury. In this study we employed the isolated rat lung model to investigate the effects of l-arginine on air embolism-induced lung injury. DESIGN: Randomized, controlled study. SETTING: Animal-care facility procedure room. SUBJECTS: Forty-two adult male Sprague-Dawley rats each weighing 250-350 g. INTERVENTIONS: Infusion of air at the rate of 0.25 mL/min for 1 min into the pulmonary artery in isolated and perfused rat lung resulted in pulmonary hypertension and lung edema. Air embolism elicited a significant increase in microvascular permeability as measured by the capillary filtration coefficient, lung weight gain, lung weight-to-body weight ratio, pulmonary arterial pressure, and protein concentration of bronchoalveolar lavage fluid. MEASUREMENTS AND MAIN RESULTS: Pretreatment with L-arginine (4 mmol/L) significantly attenuated the acute lung injury induced by air embolism as shown by a significant decrease in all of the assessed variables but did not alter the pulmonary arterial pressure (p < .05). The protective effect of l-arginine was blocked when N(G)-nitro-L-arginine methyl ester (5 mmol/L) was added. Pretreatment with N(G)-nitro-L-arginine methyl ester exacerbated air embolism-induced lung injury. CONCLUSIONS: Our findings suggest that L-arginine can prevent air embolism-induced lung injury.

Acute Disease↗
PubMed2005

Effects of various body temperatures after lipopolysaccharide-induced lung injury in rats.

STUDY OBJECTIVES: In this study, we determined the effects of various body temperatures (BTs) after initiation of lipopolysaccharide (LPS)-induced lung injury. DESIGN AND SETTING: Forty-nine, adult, male, Sprague-Dawley rats each weighing 300 to 400 g were used METHODS: The treated rats were challenged with intraperitoneal (IP) administration of 5 mg/kg LPS. Control animals received IP saline solution injections. After 16 h, treated and control animals were anesthetized. The animals received direct intratracheal (IT) injection of LPS (1 mg/0.2 mL) or saline solution (control animals). A cooling or heating blanket was then used to control BT. The rats were randomly assigned to three control groups of mild hypothermia (34 degrees C) plus saline solution, normothermia (37 degrees C) plus saline solution, and mild hyperthermia (39 degrees C) plus saline solution, and three LPS groups of mild hypothermia plus LPS, normothermia plus LPS, and mild hyperthermia plus LPS, where each condition was maintained for 5 h. The mean arterial pressure (MAP) and blood gas concentrations were measured. BAL was done in the left lung 5 h after the IT injection of LPS with temperature control. Parts of the right lung were excised for myeloperoxidase (MPO) and malondialdehyde (MDA) measurements, whereas the rest was collected for wet/dry (W/D) ratio determination. RESULTS: Normothermia plus LPS caused significantly increased W/D ratio, LDH activities, protein concentrations, and tumor necrosis factor-alpha concentrations in BAL fluid, and MPO activities and MDA levels in lung tissues when compared to saline solution control group. MAP and Pao(2) were significantly decreased. The pathologic picture also showed increased neutrophil infiltration in lung tissues. In contrast, treatment with mild hypothermia but not hyperthermia significantly attenuated these parameters when compared with the normothermia-plus-LPS group. CONCLUSIONS: These experimental data suggest that mild hypothermia applied after initiation of acute lung injury induced by LPS in rats had a protective effect by inhibiting the inflammatory reaction.

Analysis of Variance↗
PubMed2004

Effects of various antioxidants on endotoxin-induced lung injury and gene expression: mRNA expressions of MnSOD, interleukin-1beta and iNOS.

Antioxidants have been shown to be effective in attenuating acute lung injury. In this study, we determine the effects of various antioxidants by different mechanisms on the lipopolysaccharide (LPS)-induced changes. LPS was administered intravenously at a dose of 10 mg/kg to anesthetized rats. LPS induced a significant decrease in blood pressure (P < 0.01) and increased exhaled nitric oxide (NO) from 3.60+/-0.18 to 35.53+/-3.23 ppb (P < 0.01) during an observation period of 4 h. Plasma nitrate concentrations also increased from 0.61+/-0.06 to 1.54+/-0.22 micromol/l (P < 0.05). LPS-induced oxygen radical release from white blood cells isolated from rat peripheral blood also increased significantly (P < 0.001). After the experiment, the lung weight was obtained and lung tissues were taken for the determination of mRNA expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta) and manganese superoxide dismutase (MnSOD). Histological examination of the lungs was also performed. In the control group injected with saline solution, mRNA expressions of iNOS, IL-1beta, TNF-alpha and MnSOD were absent. Four hours after LPS administration, mRNA expressions of iNOS, IL-1beta, and MnSOD were significantly enhanced, but TNF-alpha was not discernibly expressed. LPS also caused a twofold increase in lung weight. Pathological examination revealed endothelial cell damage and interstitial edema. Various antioxidants were given 1 h after LPS administration. These agents include SOD, catalase (CAT), SOD + CAT or vitamin C (ascorbic acid). These antioxidants effectively reversed the systemic hypotension, reduced the quantity of exhaled NO and plasma nitrate concentration, and prevented acute lung injury. Administration of various antioxidants also significantly attenuated LPS-induced oxygen radical release by rat white blood cells. LPS induced mRNA expressions of MnSOD and iNOS were significantly depressed by these antioxidants. However, only SOD + CAT and vitamin C inhibited the mRNA expression of IL-1beta. These results suggest that oxygen radicals are responsible for LPS-induced lung injury. Antioxidants can attenuate the lung injury by inhibiting mRNA expressions of iNOS and IL-1beta.

Animals↗
PubMed2004

Effect of hyperbaric oxygen on endotoxin-induced lung injury in rats.

Oxygen therapy remains the main component of the ventilation strategy for treatment of patients with acute lung injury. Hyperbaric oxygen therapy (HBO(2)) is the intermittent administration of 100% oxygen at pressure greater than sea level and has been applied widely to alleviate a variety of hypoxia-related tissue injuries. The purpose of this study was to evaluate the effect of hyperbaric oxygen on acute lung injury induced by intratracheal spraying of lipopolysaccharide (LPS) in rats. Male Sprague-Dawley rats underwent implantation of a carotid artery catheter under general anesthesia. Aerosolized LPS was delivered twice into the lungs via intratracheal puncture. Animals were either breathing room air (n = 27) or subjected to hyperbaric oxygen (HBO(2)) exposure (n = 27) 1 h after LPS spraying. Acute lung injury was evaluated 5 h and 24 h later. Compared with the control group, intratracheal spraying of LPS caused profound hypoxemia, greater wet/dry weight ratio (W/D) of the lung (5.67 +/- 0.22 vs. 4.98 +/- 0.19), and higher protein concentration (1706 +/- 168 vs. 200 +/- 90 mg/L) and LDH activity (129 +/- 30 vs. 46 +/- 15, mAbs/min) in bronchoalveolar lavage (BAL) fluid. Intratracheal spraying of LPS also caused significant WBC sequestration in the lung tissue. HBO2 treatment significantly reverted hypoxemia, reduced lung injury measures evaluated at 5 and 24 h, and enhanced 24-h animal survival rate (chi = 5.08, P = 0.024). The malondialdehyde (MDA) concentrations in lung tissue and serum were both increased after LPS spraying. Neither single HBO(2) therapy nor five sequential daily treatments enhanced MDA production in lung tissue or serum. Our results suggested that hyperbaric oxygen might reduce acute lung injury caused by intratracheal spraying of LPS in rats. This treatment modality is not associated with enhancement of oxidative stress to the lung.

Administration, Inhalation↗
PubMed2004

Protective effect of U74500A on phorbol myristate acetate-induced acute lung injury.

1. The present study was designed to determine whether U74500A could ameliorate acute lung injury (ALI) induced by phorbol myristate acetate (PMA) in our rat isolated lung model compared with any amelioration induced by dimethylthiourea (DMTU), superoxide dismutase (SOD) and catalase. 2. Acute lung injury was induced successfully by PMA during 60 min of observation. At 2 microg/kg, PMA elicited a significant increase in microvascular permeability (measured using the capillary filtration coefficient Kfc), lung weight gain, the lung weight/bodyweight ratio, pulmonary arterial pressure and protein concentration of the bronchoalveolar lavage fluid. 3. Pretreatment with 1.5 mg/kg U74500A significantly attenuated ALI; there was no significant increase in any parameters measured, except for pulmonary arterial pressure. The protective effect of U74500A was approximately the same as that of 600 mg/kg DMTU. However, 6000 U/kg SOD, 50,000 U/kg catalase and 6000 U/kg SOD + 50,000 U/kg catalase had no protective effect. 4. These experimental data suggest that U74500A significantly ameliorates ALI induced by PMA in rats.

Animals↗
PubMed2004

Pharmacological modulation of TNF production in macrophages.

The quantity and duration of production of tumor necrosis factor (TNF) is tightly controlled due to its potential to cause serious harm. For example, TNF release in response to overwhelming bacterial infection has been implicated as the first step in potentially lethal septic shock. Prostaglandins and leukotrienes are thought to play opposing roles in regulating TNF production by monocytes and macrophages. We investigated the effects of 5 drugs on the production of TNF by cells of the murine macrophage line RAW264 after stimulation with bacterial lipopolysaccharide endotoxin (LPS). These drugs were of the following 3 classes: cyclooxygenase inhibitors indomethacin (indo) and ibuprofen (ibu); 5-lipoxygenase inhibitors VZ 65 and AA-861; and methylxanthine pentoxyfilline (PTX). While indo and ibu treatment resulted in increased TNF production, PTX, VZ 65, and AA-861 significantly inhibited TNF production, whether administered simultaneously with LPS or 30 min after LPS treatment. VZ 65 and AA-861 also inhibited prostaglandin E2 (PGE2) production, coupled with an absence of any rise in intracellular cAMP. Leukotriene B4 (LTB4) levels peaked at 15 min and approached background level at 30 min after LPS treatment. Taken together, these data suggest that VZ 65 and AA-861 may inhibit TNF production through mechanism(s) independent of LTB4 production. VZ 65, AA-861, and PTX all diminished the rate of TNF mRNA transcription, yet VZ 65 and AA-861 appeared to enhance message stability. We conclude that while PTX reduced TNF protein levels by inhibiting TNF mRNA transcription, both VZ 65 and AA-861 exerted opposing effects on TNF transcription and increased mRNA stability.

Animals↗
PubMed2003

Diagnosing thyrotoxic periodic paralysis in the ED.

Thyrotoxic periodic paralysis (TPP) and sporadic periodic paralysis (SPP) are the most common causes of hypokalemic periodic paralysis (HPP) in EDs in Asia. Their neuromuscular presentations are almost indistinguishable. We conducted this study to identify clinical clues that can help EPs distinguish between TPP and SPP. Thirty-four patients presenting to the ED with HPP were enrolled during a 3-year period. They did not have known hyperthyroidism before the attack and no family history of paralysis. They all had low K(+) excretion rates. Vital signs and blood biochemistry, including acid-base and electrolytes, were measured. TPP was subsequently established by thyroid function tests. Twenty patients had TPP and 14 patients had SPP. There was no significant difference in age and sex distribution between them. Systolic (SBP) but not diastolic blood pressure (SBP 145 +/- 4 vs 128 +/- 4 mm Hg, P < 0.001) and heart rate (106 +/- 3 vs 73 +/- 3 beats/min, P < 0.001) were significantly higher in those experiencing TPP than SPP. Among the biochemical factors, only plasma phosphate concentration (2.2 +/- 0.2 vs 3.2 +/- 0.2 mg/dL, P < 0.001) was significantly lower in those experiencing TPP than SPP. Systolic hypertension, tachycardia, and hypophosphatemia are clinical clues favoring the diagnosis of TPP.

Adult↗
PubMed2002

A role for cysteinyl leukotrienes in airway remodeling in a mouse asthma model.

Airway inflammation and remodeling in chronic asthma are characterized by airway eosinophilia, hyperplasia of goblet cells and smooth muscle, and subepithelial fibrosis. We examined the role of leukotrienes in a mouse model of allergen-induced chronic lung inflammation and fibrosis. BALB/c mice, after intraperitoneal ovalbumin (OVA) sensitization on Days 0 and 14, received intranasal OVA periodically Days 14-75. The OVA-treated mice developed an extensive eosinophil and mononuclear cell inflammatory response, goblet cell hyperplasia, and mucus occlusion of the airways. A striking feature of this inflammatory response was the widespread deposition of collagen beneath the airway epithelial cell layer and also in the lung interstitium in the sites of leukocytic infiltration that was not observed in the saline-treated controls. The cysteinyl leukotriene(1) (CysLT(1)) receptor antagonist montelukast significantly reduced the airway eosinophil infiltration, mucus plugging, smooth muscle hyperplasia, and subepithelial fibrosis in the OVA-sensitized/challenged mice. The presence of Charcot-Leyden-like crystals in airway macrophages and the increased interleukin (IL)-4 and IL-13 mRNA expression in lung tissue and protein in BAL fluid seen in OVA-treated mice were also inhibited by CysLT(1) receptor blockade. These data suggest an important role for cysteinyl leukotrienes in the pathogenesis of chronic allergic airway inflammation with fibrosis.

Acetates↗
PubMed2002

Fructose-1,6-diphosphate attenuates acute lung injury induced by ischemia-reperfusion in rats.

OBJECTIVE: To determine whether fructose-1,6-diphosphate (FDP) pretreatment can attenuate acute lung injury induced by ischemia-reperfusion in our isolated lung model in rats. DESIGN: Randomized, controlled study. SETTING: Animal care facility procedure room. SUBJECTS: Twenty-four adult male Sprague-Dawley rats each weighing 250-350 g. INTERVENTIONS: Typical acute lung injury in rats was induced successfully by 10 mins of hypoxia followed by 75 mins of ischemia and 50 mins of reperfusion. Ischemia-reperfusion significantly increased microvascular permeability as measured by the capillary filtration coefficient, lung weight gain, lung weight to body weight ratio, pulmonary arterial pressure, and protein concentration of bronchoalveolar lav-age fluid. MEASUREMENTS AND MAIN RESULTS: Pretreatment with FDP significantly attenuated the acute lung injury induced by ischemia-reperfusion as shown by a significant decrease in all of the assessed variables (p <.05 p <.001). The protective effect of FDP was nearly undetectable when promazine (an ecto-adenosine 5-triphosphatase inhibitor) was added before FDP pretreatment. CONCLUSIONS: Pretreatment with FDP significantly ameliorates acute lung injury induced by ischemia-reperfusion in rats.

Animals↗