Development of XLPE insulated DC cable

This paper describes the development of dc XLPE cable. Through a series of material investigations, an XLPE compound containing highly purified special filler was developed. To check the dc insulation performance of the cable insulated with this new material, a prototype cable with 9 mm insulation thickness was manufactured. It was confirmed that the performance of the prototype cable was excellent. Based on the study of the prototype cable, a 250-kV dc cable with 20 mm insulation thickness was designed and manufactured. Through a series of voltage tests, excellent dc insulation performance of the developed cable was verified.     

Palmitoyl-L-carnitine modifies the myocardial levels of high-energy phosphates and free fatty acids

Long-chain acylcarnitines, such as palmitoyl-L-carnitine (PALCAR), are known to accumulate in the myocardium during ischemia. We examined whether exogenous PALCAR modifies the myocardial levels of high-energy phosphates (HEP) and free fatty acids (FFA) in the heart, and whether d-cis-diltiazem and l-cis-diltiazem, an optical isomer having less potent Ca2+ channel blocking action than d-cis-diltiazem, attenuate the PALCAR-induced myocardial changes. Rat hearts were perfused aerobically at a constant flow according to the Langendorff's technique, while being paced electrically. PALCAR (5 microM) decreased the tissue levels of adenosine triphosphate and creatine phosphate and increased the tissue level of adenosine monophosphate, and produced mechanical dysfunction. In addition, PALCAR (5 microM) increased markedly the tissue levels of FFA, especially those of arachidonic and palmitoleic acids, and the release of creatine kinase (CK) from the myocardium. These alterations in the myocardial levels of HEP and FFA induced by PALCAR were significantly attenuated by d-cis-diltiazem (15 microM) or l-cis-diltiazem (15 microM). Both drugs also attenuated the PALCAR-induced CK release. The present study demonstrates that PALCAR modifies the tissue levels of HEP and FFA in the heart and that both d-cis- and l-cis-diltiazem protect the myocardium against the PALCAR-induced changes through mechanisms other than Ca2+ channel blocking action.     

A case of huge abscess extended from anterior neck to left lung and lateral chest wall

62-year-old woman admitted our hospital with pain of left upper extremity from the left chest and dysphasia. Chest X-ray showed the huge mass shadow in the left lung field. Diabetes mellitus and inflammatory reaction such as high fervor, leukocytosis, CRP and ESR accentuation were recognized. Conservative therapy was done at first, but mass shadow on X-ray increased, and swelling appeared from the neck to the left lateral chest wall. And the same site appeared like subcutaneous emphysema. Computed Tomography showed mass shadow which was enlarged and spread in lung parenchyma and left chest wall with bubble image. Incision and open drainage was performed for the left chest wall but origin bacteria was detected in neither anaerobic nor aerobic culture of pus. Inflammation and mass shadow of left upper lung field have decreased gradually. The patient discharged without bronchoalveolar fistula. Abscess extending from the neck or chest wall with diabetes mellitus is very rare.     

Evolution and resolution of long-term cardiac memory

BACKGROUND: Cardiac memory (CM) refers to T-wave changes induced by ventricular pacing or arrhythmia that accumulate in magnitude and duration with repeated episodes of abnormal activation. We report herein the kinetics of long-term CM and its association with the ventricular action potential. METHODS AND RESULTS: Dogs were paced from the ventricles at rates of 110 to 120 bpm for approximately 3 weeks. CM characterized by gradual sinus rhythm T vector rotation toward the paced QRS vector evolved in all dogs regardless of pacing site (left ventricular [LV] anterior apex or base, posterior LV, or right ventricular free wall). Cardiac hemodynamics and myocardial flow (microsphere studies) were unaltered by the pacing. Recovery time for the memory T wave to return to control increased with duration of the previous pacing. The protein synthesis inhibitor cycloheximide markedly (P<.05) and reproducibly attenuated evolution of CM. When pacing was performed from the atrium, CM did not occur. Standard microelectrode techniques were used to study action potential from the LV free wall of control and CM dogs. CM was associated with increased action potential duration in epicardial and endocardial but not midmyocardial cells, significantly altering the transmyocardial gradient for repolarization. CONCLUSIONS: CM is a dynamic process for which the final T vector is predicted by the paced QRS vector and which is associated with significant changes in epicardial and endocardial but not midmyocardial cell action potential duration, such that the transmural gradient of repolarization is altered. It is unaccompanied by evidence of altered hemodynamics or flow, requires a change in pathway of activation, and appears to require new protein synthesis.     

Covariance miss-specification and the local influence approach in sensitivity analyses of longitudinal data with drop-outs

Our work examines the performance of proposed local influence diagnostics applied to multivariate normal longitudinal data with drop-outs: these diagnostics prove to be ambiguous as they are sensitive not only to the presence of anomalous records, as intended, but also, unfortunately, to the misspecification of the longitudinal covariance structure of the response. We suggest an unambiguous index for detecting covariance misspecification, and recommend that an analyst use this index first to confirm that the covariance structure is well specified before attempting to interpret the influence diagnostics.     

Enhancement of peroxynitrite-evoked acetylcholine release by hydroxyl radical scavengers from mouse cerebral cortical neurons

We investigated the effects of hydroxyl radical scavengers on peroxynitrite (OONO-)-evoked acetylcholine (ACh) release from mouse cerebral cortical neurons. N,N'-dimethylthiourea, a hydroxyl radical scavenger, dose-dependently increased OONO(-)-evoked ACh release. Other hydroxyl radical scavengers such as uric acid and mannitol, also enhanced OONO(-)-evoked ACh release, although these enhancing effects were not found in the absence of OONO-. In addition, OONO(-)-induced [45Ca2+]influx was significantly facilitated by the scavengers, whereas no effects of the scavengers on [45Ca2+]influx was observed in the absence of OONO-. These results indicate that hydroxyl radical scavengers enhance OONO(-)-evoked ACh release via the facilitation of OONO(-)-induced [45Ca2+]influx.     

Comparison of susceptibility to apoptosis induced by rhTNF-alpha and cycloheximide between human circulating and exudated neutrophils

OBJECTIVE: Peroxynitrite and hydroxyl radical, reactive oxidants produced during reperfusion, are potent triggers of DNA single strand breakage. DNA injury triggers the activation of the nuclear enzyme poly (ADP-ribose) synthetase (PARS), which contributes to cellular energetic depletion. Using 3-aminobenzamide, an inhibitor of PARS, we investigated the role of PARS in the pathogenesis of myocardial reperfusion injury in a rat model. METHODS AND RESULTS: Occlusion of the left main coronary artery (one hour) followed by reperfusion (one hour) in the anesthetized rat caused severe cardiac necrosis, neutrophil infiltration, and increased plasma creatine phosphokinase activity. There was significant peroxynitrite production during reperfusion, as indicated by a massive increase in nitrotyrosine in the necrotic myocardium. Reperfusion was also associated with a significant loss of myocardial ATP. In vivo administration of the PARS inhibitor 3-aminobenzamide (10 mg/kg i.v.) to rats subjected to myocardial ischemia and reperfusion, reduced myocardial infarct size and blunted the increase in plasma creatine phosphokinase activity and myeloperoxidase activity in infarcted hearts. In addition, 3-aminobenzamide partially preserved the myocardial ATP levels. In vitro, pharmacological inhibition of PARS also ameliorated peroxynitrite-induced cytotoxicity in rat cardiac myocytes and human endothelial cells. CONCLUSION: 3-aminobenzamide has significant protective effects in myocardial reperfusion injury. We hypothesize that activation of PARS activation plays a role in the pathophysiology of acute myocardial infarction.     

Dynamic dialysis method. III. Effect of sulfonamides on the binding of warfarin with bovine serum albumin

Enflurane, a fluorinated methylethyl ether, is metabolized, in part, to inorganic fluoride. Methoxyflurane has similar metabolism, and cases of fluoride ion-induced renal failure have been reported after its use. This prospective study was initiated to determine fluoride ion kinetics after enflurance anesthesia in 16 healthy patients, 18 anephric patients, and 6 patients each having a creatinine clearance of less than 5 ml/min (on dialysis). Serum and urine inorganic fluoride levels were determined. There was no clinical or statistical significance difference among the 3 groups with respect to maximum inorganic fluoride ion concentration or the time to reach it. The fluoride ion values were never above the 50 muM level that has been reported to cause subclinical renal toxicity. The fluoride ion concentration in serum fell rapidly after termination of anesthesia even in the anephric patients. This is presumed to be due to uptake of the ion by bone. Patients with low creatinine clearance also have low fluoride ion clearance. Statistical but not clinical significance was found in the comparison between pre-enflurane and the 24-hr fluoride ion values in the anephric and low creatine clearance patients, but this did not persist after one dialysis.     

The evolution of neurophysiological features in holoprosencephaly

The evolution of EEG, visual and auditory evoked responses (VER and AER) and sleep is described in three cases of semilobar holoprosencephaly. During the neonatal period, the waking EEG was characterized by almost continuous high amplitude rhythmic alpha-theta activity in case 1 and 2, which became discontinuous during quiet sleep. Moderate amplitude rhythmic alpha-theta waves were seen in case 3. This rhythmic alpha-theta activity gradually disappeared with increasing age, being replaced by non-specific slow dysrhythmia. In case 3, the subsequent EEGs were characterized by focal spikes at 4 months, multifocal spikes at 5 and 6 months, hypsarrhythmia at 8 months and bisynchronous diffuse sharp and slow wave discharges at 2 years and 7 months. Ictal EEGs were characterized by desynchronization and/or rapid synchronization, epileptic recruiting rhythm and postical high amplitude slow waves. Definite but mostly abnormal VERs or AERs were obtained in all three cases. In two cases, the evoked responses showed a progressive decrease in amplitude and VERs were abolished finally. No sleep cycle could be identified during the neonatal period probably because of frequent seizures. In two cases no circadian rhythm of sleep developed, although almost normal REM-NREM sleep cycle was present.