Experimental determination of the Onsager coefficients of transport for Ce(0.8)Pr(0.2)O(2-delta).

For a mixed oxide-ion and electron conducting oxide, with oxygen vacancies (V(O)) and electrons (e') or holes (h ) as charge carriers, a flux of (V(O)) (J(i)) can in principle be driven, not only directly by its own electrochemical potential gradient (inverted Delta eta(i)), but also indirectly by that of electrons (inverted Delta eta(e)), and vice versa for the flux of electrons (J(e)). It is common practice to assume that electrons and mobile ions migrate independently, despite the lack of experimental evidence in support of this. Here, all the Onsager coefficients, including the cross coefficients, have been measured for Ce(0.8)Pr(0.2)O(2-delta) within the a(O(2)) range 10(-21)-1 at 800 degrees C, using local ionic and electronic probes in a four-probe configuration. The cross coefficients of transport were found to be negligible in comparison to the direct coefficients in the a(O(2)) range 10(-21)-10(-4), but of the same order of magnitude as the direct coefficients for high a(O(2)) values (10(-2)-1). This is in contrast to the commonly used assumption that the two types of carriers migrate independently, i.e. that L(ie) = 0.

Rapid progression from hypertrophic cardiomyopathy to heart failure in a patient with Becker's muscular dystrophy.

We describe the case of a 17-year-old boy with Becker's muscular dystrophy (BMD) presenting with rapid progression from hypertrophic cardiomyopathy to heart failure within 2 years. Initial echocardiogram showed severe hypertrophy of left ventricle (LV) and right ventricle (RV) with normal chamber size, and preserved LV systolic function. Microscopic study of cardiac muscle obtained by endomyocardial biopsy of the interventricular septum showed severe hypertrophy of the muscle fibers and interstitial fibrosis. Follow-up echocardiogram 2 years after the first examination exhibited marked dilated LV and RV with severe LV global hypokinesia. Follow-up endomyocardial biopsy demonstrated increased interstitial cellular matrix. Immunohistochemical staining for dystrophin revealed significant loss of dystrophin along the sarcoplasmic membrane of the right biceps brachii muscle, compatible with BMD.

A novel method of brachytherapy using local delivery of 99mTc-HMPAO for coronary stent restenosis.

BACKGROUND: Restenosis after percutaneous coronary intervention (PCI) is a matter that still remains to be resolved. Herein, the inhibitory effect of locally delivered 99mTc-HMPAO (hexamethyl propylene amine oxime) on neointimal hyperplasia after coronary stenting was examined in a pocine model, and its safety and efficacy observed in patients with coronary stent restenosis. METHODS: After a stent overdilation injury, local radioisotope delivery using 99mTc-HMPAO was applied to one coronary artery (Group I) and control therapy to another (Group II) in each of 10 pigs. Follow-up coronary angiogram (CAG) and histopathologic assessment were performed 4 weeks after stenting. Eleven patients (10 males and one female, 62.4 +/- 5.7 years of age) underwent local administration of 30 mCi/ 2 mL 99mTc-HMPAO shortly after PCI, via a Dispatch Catheter, followed by a whole body scan to evaluate the distribution of the 99mTc-HMPAO, as well as a thallium-201 (TI-201) myocardial scan to evaluate myocardial perfusion. The major adverse cardiac events (MACE) were assessed during a one-year clinical follow-up. RESULTS: On histopathological analysis, the neointimal areas were 1.2 +/- 0.6 and 2.7 +/- 0.4 mm2 (p=0.002), and the histopathological areas of stenosis were 27.16.3 and 53.4 +/- 5.2% in Groups I and II (p=0.001), respectively. In the clinical study, there was no in-hospital MACE. On a quantitative coronary angiographic analysis, the minimal luminal diameter was increased from 0.4 +/- 0.3 to 2.9 +/- 0.2 mm, and diameter stenosis decreased from 84.2 +/- 9.5 to 16.3 +/- 11.0% following PCI. Follow-up CAG was performed in 9 cases (81.8%) and restenosis occurred in 2 (22.2%). On a follow-up CAG, the minimal luminal diameter, diameter stenosis rate, lumen loss and loss index were 2.0 +/- 0.8 mm, 27.7 +/- 2.9%, 0.7 +/- 0.7 mm and 0.2 +/- 0.3, respectively. During the one-year clinical follow-up there were no cases of death or acute MI, but two cases of target vessel revascularization (18.2%). CONCLUSION: Local delivery of 99mTc-HMPAO, a novel radiotherapy, can be used safely and effectively for coronary stent restenosis.

A case of acute myocardial infarction after blunt chest trauma in a young man.

Coronary artery injury rarely occurs after blunt chest trauma, but it can lead to extensive myocardial infarction and be frequently overlooked. A 16-yr-old man was presented with comatose mental state and rapid respiration rate. He ran into guard rail while riding a motorcycle. In routine examination, his electrocardiogram showed Q wave and 2 mm ST segment elevation in all precordial leads, I and aVL. The cardiac enzymes were also elevated: creatine kinase (CK)-MB was 300 U/L, and cardiac specific troponin I was 5.7 ng/mL. Two-dimensional echocardiography showed anteroseptal akinesia with severely depressed left ventricular function, ejection fraction of 28%. He could not receive any anticoagulation or thrombolytic therapy because of his brain lesion. Three weeks later, his mental state improved. A diagnostic coronary angiogram revealed total occlusion in the proximal left anterior descending artery (LAD) with collaterals from the right coronary artery and left circumflex artery. We successfully performed a percutaneous coronary intervention for the LAD lesion, and the final angiogram showed a good coronary flow without residual stenosis.

The long-term clinical results of a platelet glycoprotein IIb/IIIa receptor blocker (Abciximab: Reopro) coated stent in patients with coronary artery disease.

BACKGROUND: Previously, the inhibition of coronary restenosis with Abciximab (ReoPro)-coated stent in a porcine model was reported. ReoPro inhibits platelet aggregation, the proliferation of vascular smooth muscle cells and the inflammatory reaction. METHODS: A prospective randomized trial was performed to compare two types of stent for revascularization in the native coronary artery. The primary effective end points were major adverse coronary events (MACE): cardiac death, acute myocardial infarction, target vessel revascularization (TVR) and restenosis at the 6-month clinical and angiographic follow-ups. RESULTS: One hundred and fifty-five patients were enrolled between August 2001 and June 2003. The mean ages (56.0 +/- 10.0 vs. 56.9 +/- 10.8 years), baseline diameter of stenosis and minimal luminal diameter were no different between the two groups. There was one myocardial infarction and revascularization during the hospital stay in control stent group. During the clinical follow-up there were two myocardial infarctions in control group. Follow-up coronary angiograms were performed in 62.3% (48/77) and 65.4% (51/78) of the coated and control groups, respectively. The diameter of stenosis and late loss were significantly less in the ReoPro-coated stent group compared with the controls (16.4 +/- 5.8% vs. 34.3 +/- 6.1%, p = 0.009; and 0.33 +/- 0.28 mm vs. 0.88 +/- 0.41 mm; p = 0.002). The restenosis and TVR rates of the ReoPro-coated stent were relatively lower compared with the control stent [14.6% (7/48) vs. 29.4% (15/51), p = 0.062; and 9.2% (7/76) vs. 14.7% (11/75); p = 0.327]. CONCLUSION: A ReoPro-coated stent is safe, and may be effective in the prevention of coronary restenosis.