This paper investigates an iterative multiuser detection for nonbinary low density parity check (LDPC) coded multicarrier multiple level frequency shift keying system to increase system performance ...under specific signal-to-noise ratio and data rate. We propose three-level hard-limited detection probabilities over both additive white Gaussian noise (AWGN) channels and Rayleigh fading channels. During multiuser detection (MUD) process, the hard-limited detection probabilities are computed in advanced and stored in tables. By using table looking up, the MUD soft outputs can be computed efficiently. We test the reliability of soft outputs from nonbinary LDPC channel decoder for all users. If the soft output exceeds a reliability threshold, the user is declared as a reliable user. For each symbol, we count the number of reliable users on it, and, use this information to update the soft output of MUD during the iterative multiuser detection and decoding process, which cancel multiple access interference iteratively. Numerical results show that the performances of three-level hard-limited systems outperform two-level hard-limited systems over AWGN channels and Rayleigh fading channels.
Carbon fiber-reinforced polymer (CFRP) has been widely implemented in electric vehicle bodies and aircraft fuselage structures. The purpose of CFRP is to reduce the weight and impart rigidity in the ...final product. A beam structure is typically used to bear the structural load, and the rigidity of the beam can be changed by arranging the laminated fibers at different angles. In this study, a composite I-beam is used as an example in engineering components. Because the theoretical model of the superimposed composite I-beam is established, the theoretical formula is based on the theoretical assumptions of the two-dimensional composite beam, and is combined with the traditional composite plate theory to analyze the maximum bending stress, strain, and deflection. During the theoretical derivation, it is assumed that the flanges of the I-beams are divided into narrow and wide flanges. The beams are considered as structures of beams and flatbeds. When a narrow flange is loaded in the side, the wide flange has no lateral deformation, and the lateral moments are neglected. Therefore, the accuracy of this formula needs to be verified. The purpose of this study is to verify the accuracy of theoretical solutions for the deflection and stress analysis of composite beams. A finite element analysis model is used as the basis for comparing the theoretical solutions. The results indicate that when the aspect ratio of the beam is >15, the theoretical solution will have better accuracy. Without the addition of the material, when 0° ply is placed on the outermost layer of the flange of the nonsymmetric beam, the effective rigidity of the beam is increased by 4−5% compared with the symmetrical beam. The accuracy range of the theoretical solution for the composite beams can be accurately defined based on the results of this study.
OBJECTIVE:To analyze the results of acute myocardial infarction (AMI) complicated with refractory shock necessitating extracorporeal life support (ECLS) rescue and to search for associated risk ...factors.
DESIGN:Retrospective review of our 9-yr experience with patients initially presenting with AMI with shock necessitating ECLS rescue; analysis of patient outcomes.
SETTING:A university-affiliated tertiary referral medical center.
PATIENTS:Between 1994 and 2003 inclusively, 36 consecutive patients (age mean ± sd, 57 ± 10 yrs) with AMI complicated by refractory shock and undergoing cardiopulmonary resuscitation (CPR) necessitating emergent ECLS rescue were enrolled in this study.
INTERVENTION:All patients underwent CPR before ECLS, although 30 patients (83.3%) received ECLS during CPR because spontaneous circulation failed to return. All patients underwent intraaortic counterpulsation either before or following rescue. Seven patients underwent angioplasty only, and one underwent heart transplantation without any intervention. Twenty-eight patients underwent coronary artery bypass grafting (CABG), in which the beating-heart technique was used for 20 patients.
MEASUREMENTS AND MAIN RESULTS:The pre-ECLS blood lactate level was high (13.4 ± 8.5 mmol/L), as was the inotropic score (121.4 ± 117.3 μg/kg/min). Twenty-five patients (69.4%) were successfully weaned off ECLS, and 12 (48%) survived to discharge (one had a neurologic deficit). The overall mortality rate was 66.7%. A lower inotropic score, reduced blood lactate level, shorter CPR duration, surgical revascularization, and a reduced total maximal Sepsis-related Organ Failure Assessment (SOFA) score were noted among survivors. Liver failure, central nervous system failure, and renal failure mainly occurred in nonsurvivors after ECLS. The technique used for surgical revascularization (beating heart or arrested heart) did not influence the outcome. ECLS is associated with a lower mortality rate than that expected (>90%) from the resultant total maximal SOFA score (16.6 ± 3.0).
CONCLUSIONS:AMI complicated with refractory shock remains associated with a high mortality rate, even following ECLS rescue, although ECLS might afford a better chance of survival. The SOFA score can be applied to ECLS condition as a reference point for predicting outcome.
Proteinuria is an important risk factor for cardiovascular and renal morbidity and mortality. The effects of 3-hydroxy-3-methyglutaryl coenzyme A reductase inhibitor (statin) therapy on proteinuria ...in normolipidemic patients with well-controlled hypertension have not been studied. A total of 63 normolipidemic (total cholesterol <240 mg/dL) and proteinuric (300 to 3000 mg/d) patients with well-controlled blood pressure (<140/90 mm Hg) were randomized to receive either placebo (n=32) or pravastatin (10 mg/d; n=31) after a 3-month placebo period. Pravastatin lowered proteinuria after 6 months by 54% (P <0.0001). Creatinine clearance was stable throughout the study in the 2 groups. Despite unchanged plasma endothelin-1 levels throughout the study, urinary excretion of the peptide was decreased and significantly correlated with improvement in urinary protein excretion in pravastatin-treated patients (r =0.64, P =0.001). The urinary excretion of retinol-binding protein decreased after pravastatin administration, probably reflecting an improvement in tubular function. In contrast, the urinary excretion of IgG did not change significantly throughout the study in either group. Multivariate analysis revealed that proteinuria was only significantly correlated with statin use (P <0.0001, R= 0.66). Linear regression analysis in the statin-treated group did not show any correlation between changes in lipid profiles and proteinuria regression. Thus, in addition to their primary function of antilipidemia, the addition of pravastatin to treatment for well-controlled hypertension may have an additive effect on reducing proteinuria independent of hemodynamics and lipid-lowering effects, possibly through inhibiting renal endothelin-1 synthesis and improving tubular function.
Add-on and withdrawal effect of pravastatin on proteinuria in hypertensive patients treated with AT1 receptor blockers.
Although angiotensin receptor antagonists and 3-hydroxy-3-methylgultaryl ...coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to attenuate proteinuria individually, it remains unclear whether proteinuria may be additionally improved by statin therapy in well-controlled hypertensive patients treated with angiotensin receptor antagonists-based regimen and whether withdrawal of chronic statin treatment may abrogate this beneficial effect in normolipidemic patients.
A total of consecutive 82 proteinuric patients treated with antihypertensive agents, including losartan, were randomized 10mg of pravastatin or placebo with a 6-month treatment. After completing 6 months of drug treatment, the pravastatin-treated patients were randomly assigned to continue (N = 19) or withdraw (N = 17) pravastatin for a further 6 months.
Subjects treated with pravastatin had significant further improvement of proteinuria at 6 months compared with placebo group (559 ± 251mg/24 hours vs. 1262 ± 557mg/24 hours) (P < 0.0001). Of 17 patients assigned to withdraw pravastatin, proteinuria returned to the pretreatment levels and was significantly higher than those who continued treatment. Multivariate analysis revealed that proteinuric improvement was significantly correlated with the continuous statin use. Urinary excretion of endothelin-1 (ET-1) is decreased in pravastatin-treated patients, but withdrawal of statin resulted in 27% up-regulation. The linear regression models in the initial statin-treated group showed that changes in urinary ET-1 correlated with urinary protein excretion (r = 0.83,P < 0.0001).
We conclude that pravastatin administration is associated with improved proteinuria probably by inhibiting urine ET-1 levels in patients with losartan-based treatment. However, statin withdrawal abrogates this beneficial effect in patients initially responsive to this therapy.
Abstract
Background: Traffic of potentially harmful cytosolic messengers through gap junctions might cause increased injury during ischemia. The present study was to determine whether the infarct ...size-reducing effect of adjunctive estradiol administration prior to reperfusion is associated with an attenuated expression of connexin43 at the border of infarction in a canine model. Methods: Experiments were performed in 48 dogs (n=16 each group), assigned to receive either vehicle (control group), 17β-estradiol administered before coronary occlusion (early group), or 3 min before coronary reperfusion following 60-min ischemia (late group). Changes in the amount of phosphorylated connexin43 were measured by Western blot. Results: Infarct size was significantly larger in the control (38±7% of area at risk) than in the supplemented groups (16±6% in the early group; 16±8% in the late group, P<0.0001, both). Reperfusion caused a significant elevation in free radicals as measured by lucigenin-derived chemiluminescence. The rise of free radicals was significantly inhibited in animals treated with estrogen, either early or late. The amount of phosphorylated connexin43 was reduced, as assessed by Western blot in control hearts at the border zone. These changes were significantly enhanced by estrogen administration. The magnitude of infarct size positively correlated with the magnitude of phosphorylated connexin43 expression assessed by Western blot (r=0.83, P<0.0001). Confocal microscopy confirmed the changes of junctional complexes. Conclusions: This result demonstrated that the cardioprotective effect of estrogen as an antioxidant may be associated with the reduced amount of phosphorylated myocardial connexin43 protein.
1 Cardiology Section, Department of Medicine, Taipei Medical University and Chi-Mei Medical Center, Tainan; 2 National Taiwan University and Department of Pharmacy, National Taiwan University ...Hospital, Taipei; 3 Department of Surgery, Municipal Jen-Ai Hospital, Taipei; 4 Cardiology Section, Department of Surgery, National Taiwan University Hospital, Taipei; and 5 Cardiology Section, Department of Medicine, Taipei Medical University and Hospital, Taipei, Taiwan
Submitted 4 May 2004
; accepted in final form 19 January 2005
Endothelin (ET)-1 has been implicated in the development of cardiac hypertrophy. We investigated the effect of pravastatin on development of ventricular hypertrophy in spontaneously hypertensive rats (SHR) and whether the attenuated hypertrophic effect was via reduced ET-1 expression. Normolipidemic SHR were treated with one of the following therapies for 8 wk: vehicle, the nonselective ET receptor antagonists bosentan, pravastatin, mevalonate, hydralazine, or combination of pravastatin + mevalonate from the age of 8 wk at the very early stage of cardiac hypertrophy. Treatment with bosentan and pravastatin significantly decreased left ventricular mass index for body weight and cardiomyocyte sizes isolated by enzymatic dissociation. The myocardial ET-1 levels and preproET-1 mRNA assessed using real-time quantitative RT-PCR were significantly higher (both P < 0.001) in the SHR compared with Wistar-Kyoto rats. The increased tissue ET-1 levels can be inhibited after pravastatin administration. Immunohistochemical analysis confirmed the changes of ET-1. Left ventricular mass index for body weight correlated positively with tissue ET-1 levels ( P = 0.0004). A dissociation between the effects of blood pressure and cardiac structure was noted, because pravastatin and hydralazine reduced arterial pressure similarly. Pravastatin-induced effects were reversed by the addition of mevalonate. In conclusion, these results suggest a crucial role of cardiac endothelin system in the early development of ventricular hypertrophy in the SHR. Pravastatin is endowed with cardiac antihypertropic properties that are independent of its hemodynamic and hypolipidemic effects and appear to be related to their capacity to decrease cardiac ET-1 levels, which is linked to mevalonate metabolism.
cardiomyocytes; endothelin-1; immunohistochemistry
Address for reprint requests and other correspondence: N.-C. Chang, Cardiology section, Dept. of Medicine, Taipei Medical Univ. and Hospital, 252 Wu-Hsing St., Taipei, Taiwan (E-mail: ncchang{at}tmu.edu.tw )
Epidemiologic studies have shown that hypercholesterolemia is associated with increased left ventricular (LV) mass. Free radicals have been shown to be increased in hyperlipidemic patients. This ...study sought to determine whether pravastatin administration can affect LV mass in patients with untreated total cholesterol ≥240 mg/dl by reducing 8-iso-prostaglandin F2α concentrations, a reliable marker of oxidant injury. Fifty patients were randomly assigned to one of two groups, one with (n = 25) and one without (n = 25) treatment with pravastatin (10 or 20 mg/d). A group of normolipidemic control subjects was used for comparison. Echocardiograms were performed at baseline and after 6 months of therapy. Hyperlipidemic patients showed significant increases in LV mass index at baseline compared with the normolipidemic control group (125 ± 8 vs. 107 ± 5 g/m, p < 0.0001). Pravastatin treatment significantly reduced plasma total and low-density lipoprotein cholesterol levels, as well as increased high-density lipoprotein cholesterol. After 6 months of therapy with pravastatin, the magnitude of LV mass regression correlated with the magnitude of inhibition of free radical formation assessed by 8-iso-prostaglandin F2α formation (r = 0.67, p = 0.002). Multivariate analysis revealed that regression of LV mass was significantly correlated only with the changes in 8-iso-prostaglandin F2α (p < 0.0001, adjusted R = 0.83). These findings demonstrated for the first time that in addition to its primary anti-lipidemia, pravastatin may have an additional effect of reducing LV mass–independent lipid-lowering effects, possibly through attenuation of free radical formation.
Reactive cardiomyocyte hypertrophy after myocardial infarction (MI) is an important risk factor for arrhythmias. Endothelin (ET)-1 has been implicated in the development of cardiac hypertrophy. We ...investigated the effect of pravastatin on ventricular hypertrophy during remodeling after MI and whether the attenuated hypertrophic effect was via reduced regional ET-1 expression. After ligation of the anterior descending artery, male Wistar rats were randomized to either vehicle, pravastatin, mevalonate, or a combination of the two drugs for 4 weeks. Sham operation served as controls. Pravastatin decreased cardiomyocyte sizes isolated by enzymatic dissociation at the border zone. The myocardial ET-1 levels at the border zone were 6.3-fold higher (
P < 0.0001) in the vehicle group compared with sham group. The increased regional ET-1 levels can be inhibited after pravastatin administration. Immunohistochemical analysis confirmed the localization of ET-1 mainly in the cardiomyocytes. This was paralleled by a 9.8 ± 2.3-fold upregulation of preproET-1 mRNA assessed by real-time quantitative reverse transcription-polymerase chain reaction in the vehicle-treated rats, which reduced after administering pravastatin. Cardiomyocyte sizes at the border zone correlated positively with regional ET-1 levels (
P = 0.001). Arrhythmic scores during programmed stimulation were significantly higher in the vehicle group than in the pravastatin-treated group (3.0 ± 1.3 vs. 1.3 ± 1.0,
P < 0.0001). In contrast, pravastatin-induced effects were reversed by the addition of mevalonate, implicating 3-hydroxy-3-methyglutaryl-CoA reductase as the relevant target. The results of the present study suggest that the pravastatin administration after infarction can reduce the inducibility of ventricular arrhythmias as a result of attenuated cardiomyocyte hypertrophy probably through decreased tissue ET-1 level, which is linked to mevalonate metabolism.
We have previously demonstrated the effects of estrogen on modulation of myocardial ATP-sensitive K+(KATP) channel. Previous studies have demonstrated that activation of mitochondrial KATPchannel is ...a major contributor of ischemic cardioprotection. The purpose of the present study was to investigate the role of KATPchannel in estrogen-induced myocardial protection after ischemia/reperfusion in dogs. Anaesthetized dogs were subjected to 60 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. In a first study to characterize effects of sex and the dose-response profile of estrogen on infarct size, the drug was intravenously administered at 10 or 20 μ g/kg. In a second study to investigate the cardioprotective mechanisms of estrogen, vehicle, preconditioning or 17 β -estradiol (10 μ g/kg) was given, beginning 15 min prior to the 60 min occlusion period in the presence or absence of 5-hydroxydecanoate (5-HD). In the first study, administration of 17 β -estradiol resulted in a significant, dose-dependent limitation of infarct size. Estrogen administration provided myocardial protection of similar magnitude in both males and females. In the second study, infarct size in control animals averaged 39±5% of the risk region, compared with 14±5% of the risk region in estrogen-treated dogs and 6±5% of the risk region in preconditioning dogs (both P<0.0001 v controls). Pretreatment with 5-HD completely abolished preconditioning- and estrogen-induced cardioprotection. Estrogen limits myocardial infarction size resulting from coronary artery occlusion and reperfusion in a dose-dependent fashion, irrespective of gender difference. The infarct size-limiting effect of estroge was abolished by 5-HD, suggesting that the cardioprotective effect of estrogen may result from activation of myocardial mitochondrial KATPchannels.
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