Telemetry of Programmed and Measured Data in Pacing System Evaluation and Follow-up

Telemetry of programmed and measured data is an important feature of many pacemakers currently used in clinical practice. The ability to receive non-invasive data from the implanted device constitutes a major advantage for the long-term follow-up of the patients and of device performance. There are numerous types of data retrievable via telemetry: parameters of device characteristics (output, battery longevity, impedance, etc), event recorders or counters, event markers, and endocardial electrograms. Ideally, this information should be beneficial in the longitudinal surveilance of modern pacemakers.     

Design and Performance of Blanket Heat Shields for Neonates

ABSTRACT. Background: Several designs of plastic blanket heat shields are in use. This study was done to compare different designs for their efficiency in reducing heat loss. Methods: Four heat shield designs were tested by sequentially covering each of 14 infants (wt. 640–2030 g) cared for under radiant warmers. The power consumption of the radiant warmers was measured as a surrogate for. heat loss. All designs were tested for a total of 20 min on all infants. Results were calculated as percent change in power consumption from shield to shield. The most efficient design was further modified and evaluated in another group of 14 infants (wt. 700–1180 g). Results: The relative reductions in power consumption were: no shield (control) –0%, a plastic foil over the side rails: –17%, a single layer close to the infant but excluding the head: –34%, the same as double layer –37% and the most efficient one, a single layer covering the whole infant –42%. A modification of this design, tested in the second group of infants, reduced power consumption by 13% (95% CI –5.9/–19.7), ( p < 0.004) when compared to the single layer covering the whole infant. It was tucked under the connecting tubes to the ventilator. It also reduced the risk for displacement and allowed for the endotracheal tube to be suctioned without removing the blanket. Conclusion: Modifications of the design of heat shield blankets for infants resulted in significant increases in efficiency.     

Quantification of the Modifications in the Dominant Frequency of Ventricular Fibrillation under Conditions of Ischemia and Reperfusion: An Experimental Study

The characteristics of ventricular fibrillatory signals vary as a function of the time elapsed from the onset of arrhythmia and the maneuvers used to maintain coronary perfusion. The dominant frequency (FrD) of the power spectrum of ventricular fibrillation (VF) is known to decrease after interrupting coronary perfusion, though the corresponding recovery process upon reestablishing coronary flow has not been quantified to date. With the aim of investigating the recovery of the FrD during reperfusion after a brief ischemic, period, 11 isolated and perfused rabbit heart preparations were used to analyze the signals obtained with three unipolar epicardial electrodes (E1-E3) and a bipolar electrode immersed in the thermostatizfid organ bath (E4), following the electrical induction of VF. Recordings were made under conditions of maintained coronary perfusion (5 min), upon interrupting perfusion (15 mini, and after reperfusion (5 min), FrD was determined using Welch's method. The variations in FrD were quantified during both ischemia and reperfusion, based on an exponential model AFrD = A exp (-t/C). During ischemia ΔFrD is the difference between FrD and the minimum value, while t is the time elapsed from the interruption of coronary perfusion. During reperfusion ΔFrD is the difference between the maximum value and FrD, while t is the time elapsed from the restoration of perfusion, A is one of the constants of the model, and C is the time constant. FrD exhibited respective initial values of 16.20 ± 1.67, 16.03 ± 1.38, and 16.03 ± 1.80 Hz in the epicardial leads, and 15.09 ±1.07 Hz in the bipolar lead within the bath. No significant variations were observed during maintained coronary perfusion. The fit of the FrD variations to the model during ischemia and reperfusion proved significant in nine experiments. The mean time constants C obtained on fitting to the model during ischemia were as follows: El =294.4 ± 75.6, E2 = 225.7 ± 48.5, E3 = 327.4 ± 79.7, and E4 = 298.7 ± 43.9 seconds. The mean values of C obtained during reperfusion, and the significance of the differences with respect to the ischemic period were: El = 57.5 ± 8.4 (P ± 0.01), E2 = 64.5 ± 11.2 (P0.01), E3 = 80.7 ± 13.3 (P < 0.01), and E4 = 74.9 ± 13.6 (P < 0.0001). The time course variations of the FrD of the VF power spectrum fit an exponential model during ischemia and reperfusion. The time constants of the model during reperfusion after a brief ischemic period are significantly shorter than those obtained during ischemia.     

CYP1A2 activity, gender and smoking, as variables influencing the toxicity of caffeine

We have investigated several factors that might be related to the occurrence of toxic effects during the performance of a urinary test with caffeine (300  mg p.o), in 120 healthy volunteers. A total of 218 toxic effects were self-reported by eighty-two (68%) subjects. Females and nonsmokers were at the highest risk (chi-square test, P =0.01). Furthermore, two nonsmoking females experienced a symptomatology with delirium, restlessness, muscle tremor, vomiting and wakefulness. Among females and nonsmokers, those subjects who experienced toxic effects had lower caffeine N3-demethylation index (CYP1A2 activity) compared with unaffected females (1.87±0.51 vs 1.47±0.27, P <0.0005) and nonsmokers (1.69±0.23 vs 1.49±0.31, P <0.02). Caffeine N1- and N7-demethylations indices were also lower among females ( P <0.0005) and nonsmokers ( P <0.02) who reported toxic symptoms. We conclude that CYP1A2 activity, gender and smoking are variables to be considered as influencing the toxicity of caffeine.     

Viral Persistence in Neurons Alters Synaptic Plasticity and Cognitive Functions without Destruction of Brain Cells

Neurons have a restricted expression of MHC heavy chain molecules which prevents presentation of antigens of infecting viruses. As a result, such infected cells escape immune surveillance and allow the establishment of noncytolytic persistent infection. Here we show that a chronic noncytolytic viral infection bothin vitroandin vivoselectively perturbed the expression of GAP-43, a protein that plays a central role in neuronal plasticity processes accompanying learning and memory. GAP-43 expression was greatly decreased in the hippocampus, an area of heightened viral replication, while synaptic density was preserved. Concurrently, the ability to learn tasks was significantly impaired in these persistently infected mice. Yet, infected neurons remained free from structural injury.     

Acute Spermatogenic Effects of Bromoacetic Acids

Chlorine and bromine can react with natural organic substancesin source waters to form haloacetic acids, major disinfectionby-products of water chlorination. Several toxic effects includingtesticular damage have been attributed to the chloroacetic acidsbut little information is available on the bromine analogues.In this report we present the results of acute toxicity andacute spermatotoxicity studies of monobromoacetic acid (MBAA)and dibromoacetic acid (DBAA). In adult male rats the acuteoral toxicity of MBAA was 10-fold that of DBAA (LD50 177 vs1737 mg/kg). No reproductive-related endpoints were affectedin rats given a single dose of 100 mg MBAA/kg or 14 daily dosesof 25 mg MBAA/kg/day. In rats dosed with DBAA, serum testosteronefell to 17% of control 2 days after a single dose of 1250 mg/kgbut returned to control levels by Day 14. Marked effects onsperm motion were seen on post-treatment Days 14 and 28. Degenerativeflagellar changes in cauda sperm were present on Day 14 whileabnormal sperm head shapes and flagellar degeneration were observedin both caput and cauda sperm on Day 28. Histopathology indicatedaltered spermiation at all timepoints as evidenced by retentionof Step 19 spermatids beyond Stage VIII of the cycle of theseminiferous epithelium. Disorganization, distortion, and degenerationof late spermatids were also observed. On Day 14 structuresresembling residual bodies were rarely seen in the testis butwere numerous in the epididymis. Caput sperm counts were decreased on Day 2 and cauda sperm counts were decreased on Days14 and 28. The data indicate that DBAA is a testicular toxicantin the rat with late and elongating spermatids being particularlysusceptible germinal cells.     

Effects of Dihydrotestosterone and Estradiol on Experimental IgA Nephropathy Induced by Vomitoxin

Ingestion of the trichothecene vomitoxin (VT) by mice induceseffects that mimic the common human glomerulonephritis, IgAnephropathy (IgAN). These include elevation of serum IgA, IgAimmune complexes, and mesangial IgA deposition. Based on previousobservations that male mice are more prone to VT-induced IgAN,the effects of castration of male and female B6C3F1 mice andsex hormone supplementation on several immunopathologic indicatorsof the disease were compared. In the first study, castratedand intact male and female mice were fed control AIN-76A dietor the same diet containing 10 ppm VT for 12 weeks. At Week12, all but the intact female group fed VT exhibited increasedserum IgA, with castrated female mice having greater levelsthan intact females. When microscopic hematuria was used asan indicator of disease severity in intact VT-fed mice, erythrocytecounts for males exceeded those for females at weeks 4 and 12.VT-fed, castrated females exhibited greater hematuria than intactcounterparts, whereas VT-fed, castrated males had lower urinaryerythrocyte counts than intact counterparts. In a second study,castrated male and female mice were implanted with controlledrelease pellets of placebo, 5-dihydrotestosterone (DHT), or17ß-estradiol (E₂) and then were fed either controldiet or a 10 ppm VT diet for 8 weeks. Castrated male and femalemice treated with VT and DHT pellet exhibited more severe hematuria,higher IgA levels, and greater mesangial IgA deposition thanmice exposed to the same diet with placebo or E₂ pellet at Week8. While VT-fed animals with an E₂ pellet exhibited greaterhematuria and mesangial IgA deposition at Week 8 than the placebogroups, their IgA levels were not significantly elevated overthose for VT-fed mice with a placebo pellet. Relative to twoother pathologic markers for IgAN, the aforementioned effectsin both studies were generally consistent with mesangial depositionof complement component C₃ but not IgG. The results suggestthat (1) enhanced male susceptibility to VT-induced IgAN maybe related to modulation by the biologically active androgenDHT and (2) while castration of females increased severity ofVT-induced IgAN, supplementation of castrated male or femalemice with E₂ did not reverse this effect but rather increaseddisease severity.