The effect of the nano-silica support on the catalytic reduction of water by gold, silver and platinum nanoparticles--nanocomposite reactivity.

Pt°-NPs, prepared by the reduction of Pt(IV) salts with borohydride, do not catalyse the reduction of water in the presence of the strongly-reducing ˙C(CH3)2OH radicals. However, supporting the same metal nanoparticles (M°-NPs) with SiO2 alters the catalytic properties enabling the reaction. This effect depends both on the nature of M° and concentration of the composite nanoparticles. At low nanocomposite concentration: for M = Au nearly no effect is observed; for M = Ag the support decreases the catalytic reduction of water and for M = Pt the support initiates the catalytic process. At high nanocomposite concentration: for M = Au the reactivity is considerably lower and for M = Ag or Pt no catalysis is observed. Furthermore, for M = Ag or Pt H2 reduces the ˙C(CH3)2OH radicals.

Detection of chemical threat agents in drinking water by an early warning real-time biomonitor.

Having a safe water supply for civilian organizations and military personnel is an important objective to avoid toxic contamination of civilians and soldiers. Chemical warfare (CW) agents, especially organophosphorous nerve compounds, are the most toxic of known chemical agents. The Daphnia Toximeter system is a continuously working test system that uses Daphnia magna as a sensitive organism for monitoring drinking water. Both small doses (allowable for short-term water ingestion) and graduated higher concentrations induced toxic reactions in the Daphnia Toximeter system, leading to alarms sounding. The system is sensitive to a wide range of CW agents and their hydrolysis products. Concentrations below acute human toxicity can be discovered in a very short time, with the actual time depending on the concentrations applied. In every case alarms were triggered within 2 h at concentrations in water low enough for that water to be allowed for use as drinking water in exceptional conditions.

Correlation of acute and chronic defibrillation threshold with upper limit of vulnerability determined in normal sinus rhythm.

BACKGROUND: The upper limit of vulnerability (ULV) is the stimulus strength above which ventricular fibrillation cannot be induced, even when the stimulus occurs during the vulnerable period of the cardiac cycle. Determination of ULV using T-wave shocks during ventricular pacing has been shown to closely correlate with the defibrillation threshold (DFT) at ICD implantation. However, there are no data correlating ULV determined in sinus rhythm at ICD implantation, with DFT determined at implantation or during long-term follow-up. This is of clinical importance since ULV may be used to estimate DFT during ICD implantation, both during ventricular pacing or sinus rhythm. METHODS AND RESULTS: Twenty-one patients receiving a transvenous ICD system were studied prospectively. There were 16 males and 5 females, mean age 68 +/- 15 years, with mean ejection fraction 37.4 +/- 17.4%. All had structural heart disease. The ULV was defined as the lowest energy that did not induce ventricular fibrillation with shocks at 0, 20 and 40ms before the peak of the T-wave, using a step-down protocol. The initial energy tested was 15J and the lowest energy 2J. DFT was determined following a similar step-down protocol. The DFT was defined as the lowest energy that successfully defibrillated the ventricles. The linear correlation coefficient between ULV and DFT was r = 0.73 (p < 0.001). At implant, mean ULV was 9.2 +/- 5J, not statistically different from mean DFT 9.4 +/- 4J. ULV plus 5J successfully defibrillated 19 of 21 patients. During long-term follow-up of 10.1 +/- 1.8 months in eight patients, DFT was 8.8 +/- 5.8J, not significantly different than the DFT of 7.5 +/- 4.1J or ULV of 8.0 +/- 5.3 at implant. CONCLUSION: 1) When determined during normal sinus rhythm the ULV significantly correlates with DFT. 2) ULV testing might be used in lieu of standard DFT testing to confirm adequate lead placement thus minimizing or eliminating VF inductions, particularly in hemodynamically unstable patients. 3) Since ULV + 5J has a high probability of successful defibrillation in most patients, programming ICD first shock energy for VF at ULV + 5J may result in lower first shock energies compared to the standard methods of programming first shock energy at twice DFT. CONDENSED ABSTRACT: The purpose of this study was to determine if the upper limit of vulnerability (ULV) determined during normal sinus rhythm correlates with the defibrillation threshold (DFT), as has been previously shown when determined during ventricular pacing. The linear correlation coefficient between the ULV and DFT was r = 0.73 (p < 0.001). Mean ULV at implant was 9.2 +/- 5J, not statistically different from mean DFT of 0.4 +/- 4J. During long-term follow-up of 10.1 +/- 1.8 months in 8 patients, DFT was 8.75 +/- 8J, not significantly different than the DFT of 7.5 +/- 4.1J or ULV of 8.0 +/- 5.3 at implant. Shocks energies of ULV + 5J successfully defibrillated 19 of 21 patients at implant and 8 of 8 at follow-up. This study indicates that the ULV determined in normal sinus rhythm closely correlates with the DFT, and that ULV + 5J defibrillated most patients. ULV testing could be used to predict DFT and reduce or eliminate the need for DFT testing and VF induction. Programming ICD first shock energy for VF to ULV + 5J will result in lower energy than that used with standard DFT testing.

Right atrial compartmentalization using radiofrequency catheter ablation for management of patients with refractory atrial fibrillation.

INTRODUCTION: Atrial fibrillation (AF) is often refractory to antiarrhythmic drugs, and patients who are intolerant of AF may require the maze operation for cure. As a less invasive alternative, a catheter-based, right atrial compartmentalization procedure was evaluated. METHODS AND RESULTS: Twelve patients with AF refractory to Class I and III antiarrhythmic drugs were studied. Four linear right atrial radiofrequency ablations were performed, from superior to inferior vena cava in the posterior wall and interatrial septum, anteriorly from the superior vena cava to the tricuspid annulus through the appendage, and across the tricuspid valve-inferior vena cava isthmus. The radiofrequency catheter was dragged along each line three to four times, until the atrial electrogram amplitude decreased by 75% and there was bidirectional conduction block in the tricuspid valve-inferior vena cava isthmus. One complication occurred: sinus node dysfunction requiring a pacemaker. Eight patients were discharged from the hospital on no antiarrhythmic drugs, and four were discharged on previously ineffective antiarrhythmic drugs. Total duration of follow-up was 21.3 +/- 11.2 months. Four patients discharged on previously ineffective antiarrhythmic drugs had no recurrence of AF. One patient discharged off antiarrhythmic drugs had no recurrence of AF. Seven patients discharged off antiarrhythmic drugs had recurrent AF by 12.6 +/- 13.0 months (median 6, range 1 to 39); 3 of these 7 responded to previously ineffective antiarrhythmic drugs without further AF and 4 did not. Thus, 8 of 12 patients (67%) had suppression of AF after ablation on previously ineffective medication or no medication. CONCLUSION: Right atrial compartmentalization may alter the substrate for AF, thus improving the efficacy of previously ineffective antiarrhythmic drugs. Because it is relatively safe, it may be a reasonable adjunctive intervention to maintain sinus rhythm in patients with drug-refractory AF.

Conduction velocity in the tricuspid valve-inferior vena cava isthmus is slower in patients with type I atrial flutter compared to those without a history of atrial flutter.

INTRODUCTION: In human type I atrial flutter, the electrophysiologic substrate is unclear. In order to determine if slow conduction is mechanistically important, we evaluated conduction velocity in the tricuspid valve-inferior vena cava (TV-IVC) isthmus, right atrial free wall, and interatrial septum in patients with and without a history of atrial flutter undergoing electrophysiologic study. METHODS AND RESULTS: Nine patients with (group 1) and nine without a history of type 1 atrial flutter (group 2) were studied. Conduction time (msec) in the right atrial free wall, TV-IVC isthmus (bidirectional), and interatrial septum was measured during pacing in sinus rhythm at cycle lengths of 600, 500, 400, and 300 msec from the low lateral right atrium and coronary sinus ostium. Conduction velocity (cm/sec) was calculated by dividing the distance between pacing electrodes and sensing electrodes (cm) by the conduction time (sec). Conduction velocity was slower in the TV-IVC isthmus in group 1 (range 37 +/- 8 to 42 +/- 8 cm/sec) versus group 2 (range 50 +/- 8 to 55 +/- 9 msec) at all pacing cycle lengths (P < 0.05). However, conduction velocity was not different in the right atrial free wall or interatrial septum between groups 1 and 2. Conduction velocity was also slower in the TV-IVC isthmus than in the right atrial free wall and interatrial septum in group 1 patients, at all pacing cycle lengths (P < 0.05). Atrial flutter cycle length correlated with total atrial conduction time (r > or = 0.832, P < 0.05). CONCLUSION: Slow conduction in the TV-IVC isthmus may be mechanistically important for the development of human type I atrial flutter.

The mechanism of termination of reentrant activity in ventricular fibrillation.

The reentrant wave fronts in ventricular fibrillation (VF) have only a limited life span. The mechanisms by which these reentrant wave fronts terminate are unknown. We performed computerized mapping studies in six open-chest dogs before and after right ventricular subendocardial ablation with Lugol's solution. Recordings were made with 56 bipolar electrodes separated by 3 mm. Baseline pacing was performed on the right side of the tissue to create parallel activation wave fronts. A premature 50-V shock of either anodal or cathodal polarity was given to a bar electrode on the upper edge of the tissue. Counterclockwise reentrant wave fronts and VF were induced both before (60 episodes) and after (57 episodes) subendocardial ablation with either anodal or cathodal shocks. Among these reentrant wave fronts, 8 episodes before and 10 episodes after ablation had over 10 rotations (P = NS). The reentrant wave fronts in other episodes terminated with an average of 3.2 +/- 1.9 rotations before and 3.1 +/- 1.8 rotations after the ablation (P = NS). The reentrant wave-front cycle length was 118 +/- 19 milliseconds before and 124 +/- 20 milliseconds after ablation (P = .001). Conduction block occurred when the wave front was traveling across the myocardial fibers. When conduction was blocked in these episodes, the leading edge of the reentrant wave front encountered tissue that had been excited within the past 58 +/- 12 milliseconds (range, 28 to 77 milliseconds), which corresponded to 47 +/- 12% of the preceding VF cycle length. This period was significantly shorter than the recovery period in the same region that had allowed conduction (91 +/- 19 milliseconds; range, 48 to 137 milliseconds), which corresponded to 72 +/- 18% of the preceding VF cycle length (P < .001). In nine episodes, reentrant wave-front activity terminated when wave fronts that had originated from outside the mapped tissue interfered with the reentrant pathways. Conclusions are as follows: (1) The refractory period of fibrillating ventricular muscle ranges from 48 to 77 milliseconds. Because the refractory period is much shorter than the VF cycle length, a large excitable gap is present in the reentrant circuit. The presence of a large excitable gap contributes to reentrant wave-front termination. (2) Myocardial fiber orientation is an important determinant of the site of conduction block. (3) Although subendocardial ablation slowed the wave-front propagation, it did not prevent the generation and the maintenance of reentry and VF.

A reappraisal of ventricular fibrillation threshold testing.

To test the hypothesis that ventricular fibrillation (VF) threshold testing is a probability function, 12 open-chest dogs were studied. The VF thresholds were tested by scanning the T wave with either the single premature stimulus method or with the train stimulus method. The dose-response curve method was used to determine the probability of inducing VF with different strengths of premature stimulation. Conventional methods and up-down methods were also used to test the VF threshold. The results showed that the VF threshold is a probability function. The conventional method VF threshold for the single premature stimulus and for the train stimulus methods corresponded to the current strength associated with a 23.4 +/- 13.2 and a 33.2 +/- 19.5% probability of VF (P < 0.05), respectively. In comparison, the triplicate VF threshold determined by the up-down algorithm method resulted in values that were not significantly different from a 50% probability of inducing VF, with a good correlation (r = 0.90, P < 0.001 for single and r = 0.89, P = 0.003 for the train stimulus method). We conclude that: 1) The VF threshold is a probability function, and 2) the triplicate VF threshold determined by the up-down algorithm method is the best alternative to the dose-response curve method in estimating 50% probability of inducing VF.

Holter documented sudden death in a patient with an implanted defibrillator.

A 68-year-old man with recurrent attacks of monomorphic ventricular tachycardia (VT) received a pacer cardioverter defibrillator featuring antitachycardia pacing and cardioversion/defibrillation. Over 300 episodes of VT were successfully terminated by antitachycardia pacing. During Holter monitoring the patient experienced supraventricular tachycardia with delivery of multiple antitachycardia pacing, cardioversion, and defibrillation therapies ending with the death of the patient. The following factors played a role in the unfortunate outcome of this patient: 1. triggering of VT therapy by an unexpected high sinus rate; 2. atrial fibrillation induced by cardioversion therapy; 3. a gradual and continuous increase in rate during atrial fibrillation possibly caused by repeated VT and ventricular fibrillation therapies and/or by a thrombus, found at autopsy, in a bypass graft; and 4. the limited ability of presently available defibrillators to distinguish between ventricular and supraventricular arrhythmias.

Effect of congestive heart failure treatment on incidence and prognosis of ventricular tachyarrhythmias.

The prognosis for patients with congestive heart failure (CHF) is poor, with a mortality exceeding 50% within 5 years from diagnosis. This poor prognosis remains despite improved pharmacological therapy. Because the prevalence of sudden death among these patients is high, reported to exceed 40%, the prognostic importance of ventricular tachyarrhythmias has attracted much interest. Long-term electrocardiographic monitoring of patients with CHF reveals a high prevalence of ventricular premature beats, which in many patients occur frequently or are complex according to Lown criteria. Ventricular tachycardia (three or more consecutive beats) has been recorded in 40% or more of the patient population. Whether the occurrence and/or severity of ventricular tachyarrhythmia detected on Holter electrocardiograms relates to the subsequent prognosis is, however, debated. The occurrence of ventricular tachyarrhythmia may just be an expression of severely compromised left ventricular function, which, in turn, decides the subsequent outcome of the disease. Besides myocardial injury, patients with CHF have many factors that may contribute to the high prevalence of ventricular arrhythmias. Among these are elevated levels of plasma norepinephrine. Angiotensin II may increase the sensitivity to sympathetic nervous system arousal but also promotes renal loss of potassium and magnesium. Treatment with digitalis and diuretic drugs may provoke arrhythmias as well. Heart failure therapy may, however, also improve ventricular arrhythmias. Accordingly, it has been demonstrated that captopril therapy significantly reduces ventricular prematurity, compared with digitalis. In contrast, however, enalapril improvement of mortality was due to a reduction of progressive heart failure, with no difference seen in the incidence of sudden cardiac death (the CONSENSUS study).(ABSTRACT TRUNCATED AT 250 WORDS)

[Detection of infectious hemorrhagic disease of domestic rabbits (rabbit viral hemorrhagic disease) in wild rabbits (Oryctolagus cuniculus)]. / Nachweis der infektiösen hämorrhagischen Erkrankung der Hauskaninchen (Rabbit Viral Hemorrhagic Disease) bei Wildkaninchen (Oryctolagus cuniculus).

The occurrence of Rabbit Viral Hemorrhagic Disease of domestic rabbits in the population of wild rabbits in Germany was proven through detection of antigen (hemagglutination) in spleen and liver in one animal and through detection of specific antibody in another animal. There was no epizootic connection between the two animals (different locations). The necropsy and histopathologic findings are presented from five wild rabbits which died from RVHD.

Intratracheal instillation of automobile exhaust condensate in Syrian golden hamsters.

Male Syrian golden hamsters were intratracheally instilled with automobile exhaust condensate at dose levels of 0.306, 0.613, 1.25, 2.5, and 5.0 mg/hamster once a fortnight for 78 weeks. While a total of six tumors were found in the trachea and lung, hamsters treated with the vehicle only showed no respiratory tract neoplasms. Bronchiogenic adenomatous proliferations and hyperplastic nodules in the lung occurred in all groups, with a significant difference in incidence being seen between the high-dose groups and the controls.

Effect of diazepam on microsomal diethylnitrosamine metabolism in gerbils.

Dealkylation of diethylnitrosamine (DEN) by a liver microsomal fraction was measured after treatment of the Mongolian gerbil with DEN, Valium, or DEN plus Valium. Valium-dosed male and female animals showed strongly stimulated deethylase levels compared with the controls. This was also true of the DEN-treated females. Combined treatment (DEN + Valium) resulted in a significant loss of activity compared with treatment with DEN only, but was not significantly lower than that in the controls. Significant differences were also found between the experimental groups in microsomal enzymes. Metabolism of 14C-DEN to 14CO2 by gerbil liver slices in vitro showed dose-dependent inhibition by Valium. Kinetic analysis of DEN-dealkylation by purified gerbil microsomes revealed at least two Km values. In the microsomal system, diazepam inhibited DEN-dealkylation significantly at low substrate levels.

Carcinogenicity of vinylethylnitrosamine in Syrian golden hamsters.

Syrian golden hamsters received weekly s.c. doses of 5.0, 2.5, 1.25 or 0.63 mg/kg b.w. vinylethylnitrosamine (VEN). As dose levels increased, average survival time decreased, tumor multiplicity increased as did the total tumor rate which was between 50% and 100%. The main target of VEN effect was the respiratory tract where a positive dose-response relationship was established for neoplastic growth.

Scanning electron microscopical investigations on the respiratory epithelium of the Syrian golden hamster III. Regeneration after traumatic injury.

To investigate the extent to which intratracheal intubation may alter the respiratory epithelium of the Syrian golden hamsters, single and repeated intubations were undertaken and the resulting injury and subsequent epithelial regeneration were examined by scanning electron microscopy. Generally, epithelial injury as a result of a single intubation had healed ad integrum within 20 to 40 days. On the other hand, repeated treatment often caused tracheitis and led to prolonged regeneration which sometimes persisted as papillary hyperplasia 40 days after the final intubation. The appropriateness of intratracheal instillation as a method of administering chemical carcinogens and the similarity of the epithelial regeneration processes to early neoplastic alterations of the epithelium are discussed.

Comparative study of the carcinogenic effect of BHP and BAP on NMRI mice.

The carcinogenic effects of N-bis(2-hydroxypropyl)nitrosamine (BHP) and N-bis(2-acetoxypropyl)nitrosamine (BAP) were studied in NMRI mice treated subcutaneously once weekly for life. The highest incidences of tumours were found in the lung (73-100%), in the liver (67-100%) and nasal cavity (0-33%) in both sexes of mice. Data were similar in animals treated with BHP or BAP. These tumours were adenomas, adenocarcinomas and squamous cell carcinomas (nasal cavity and lung) as well as hemangio-endotheliomas and hemangioendotheliosarcomas (liver). The lung tumours were found in the control mice (27-50%) 20 weeks later than in the experimental animals. The rate of malignant neoplasms rose with increasing survival and decreasing dose levels.

A comparative study of the chronic effects of magenta, paramagenta, and phenyl-beta-naphthylamine in Syrian golden hamsters.

Groups of Syrian golden hamsters were treated with magenta, paramagenta, or phenyl-beta-napthylamine intragastrically, twice weekly for life at maximum tolerated doses. No tumors could be found that were associated with the treatment.