Transmembrane potential properties at the core of functional reentrant wave fronts in isolated canine right atria

BACKGROUND: The characteristics of transmembrane potential (TMP) at the core of functional reentry in the atrium are not well understood. METHODS and RESULTS: In protocol 1 (11 dogs), isolated perfused canine right atria were mapped from the endocardial surface while simultaneous TMPs were recorded from the epicardial surface. Episodes of reentry (n=64) were induced in the presence of 1 to 5 micromol/L acetylcholine. Successful simultaneous TMP recordings and activation maps were made in 8 episodes. The TMP was "near the core" if it was within 3.2 mm of the core; otherwise, it was considered to be "in the periphery." The mean cycle length of reentry was 110+/-35 ms. The TMP amplitude, duration (90% repolarization), and (dV/dt)max near the core (n=106) were 58+/-22 mV, 46+/-14 ms, and 33+/-20 V/s, respectively, significantly less than those in the periphery (n=241): 70+/-8 mV, 94+/-32 ms, and 55+/-10 V/s (P<0.001 for all). In 2 episodes of reentry, the cell at the core remained unexcited at its resting membrane potential. In protocol 2 (2 dogs), we performed simultaneous high-density mapping in 4 episodes of reentry and showed synchronous activation patterns on both surfaces with similar locations of the core. CONCLUSIONS: During meandering functional reentry in isolated canine right atria, (1) TMPs of cells near the core have a reduced amplitude, duration, and (dV/dt)max, and (2) cells at the core may remain unexcited at their resting membrane potential. These findings are compatible with the spiral wave concept of functional reentry in the atrium.     

Expressed sequence tags of radish flower buds and characterization of a CONSTANS LIKE 1 gene

Glutaric acidemia type I (GAI) (McKusick 231670) is an autosomal recessive disease affecting the catabolism of the amino acids lysine, hydroxylysine and tryptophan, caused by a defect in the gene encoding glutaryl-coenzyme A dehydrogenase (GCDH) and associated with severe neurological symptoms. Several pathogenic mutations in GCDH have been reported to cause GAI. One mutation, R402W, is more common than the others, which seem to be private" mutations. Here we report the entire sequences of introns 1, 2, 3, 6, 7, 8 and 9, and part of those of introns 4, 5 and 10 as well as 21 different mutations in 20 patients with GAI, corresponding to 38 out of 40 alleles.     

Role of pectinate muscle bundles in the generation and maintenance of intra-atrial reentry: potential implications for the mechanism of conversion between atrial fibrillation and atrial flutter

To determine the role of pectinate muscle (PM) bundles in the formation of intra-atrial reentry, 10 isolated canine right atrial tissues were perfused with Tyrode's solution containing 1 to 2.5 micromol/L acetylcholine (ACh). The endocardium was mapped using 477 bipolar electrodes with 1.6-mm resolution. Reentry was induced by a premature stimulus (S2). Computer simulation studies were used to investigate the importance of regional myocardial thickness in reentry formation. A total of 40 episodes of reentry were induced; 28 episodes were stationary, and the remaining 12 were nonstationary. The stationary reentry was induced either immediately after the S2 stimuli (n=9) or after an initial period of irregular activations that lasted 1460+/-1077 ms (n= 19). Of 28 episodes, 20 were initiated by conduction block along large PM ridges, leading to wave break and the initiation of reentry. The reentrant wave fronts remained stationary and rotated around these ridges as anchoring sites. During the transition from the initial irregular activations to stationary reentry, the electrogram morphology converted from "fibrillation-like" to "flutter-like" activity. In 8 episodes, initially stationary reentry converted to irregular activations because of interference with outside wave fronts (n=5) or spontaneous separation of waves from the ridges (n=3). Compared with stationary reentry, nonstationary reentry always occurred over an area without large PMs, and the mean life span was much shorter (102+/-151 versus 3.8+/-1.1 rotations, P<0.001). Computer simulation studies showed that a critical ridge thickness is needed for reentry to anchor, thereby converting fibrillation to flutter. We conclude that PM ridge forms an area where wave break occurs, allowing the initiation of reentry. It also provides a natural anchor to the reentrant wave front, lengthening the life span of reentry. The attachment and detachment of the reentrant wave front to and from the ridge determine "flutter-like" or "fibrillation-like" activity.     

Steady flow around and through a permeable circular cylinder

The steady flow around and through a porous circular cylinder was studied numerically. The effects of the two important parameters, the Reynolds and Darcy numbers, on the flow were investigated in details. The recirculating wake existing downstream of the cylinder is found to either penetrate into or be completely detached from the cylinder. It is also found that, contrary to that of the solid cylinder, the recirculating wake develops downstream of or within the porous cylinder, but not from the surface of it. These new findings provide additional evidence to Leal’s conclusion (Leal LG. Vorticity transport and wake structure for bluff bodies at finite Reynolds number. Phys Fluids A 1989;1:124) that the appearance of recirculating wakes at finite Reynolds number is due to vorticity accumulation, but not a result of the same physical phenomena associated with separation in boundary layers in adverse pressure gradients. Also presented in the current study are the variation of the critical Reynolds number for the onset of a recirculating wake as a function of Darcy number and the variation of a newly defined parameter, the penetration depth, as a function of the Reynolds number and Darcy number.     

Pediatric case of the day. Ewing sarcoma of the rib with intraspinal extension

Nitric oxide (NO) synthase (NOS)-containing cerebrocortical neurons degenerate in patients with amyotrophic lateral sclerosis (ALS) and dementia, and in transgenic mice expressing a mutated superoxide dismutase gene (G93A) associated with familial ALS. The cerebral cortex of transgenic mice displayed decreased NOS activity (p<0.001) and cGMP levels (p<0.01), but no changes in NOS content indicating that less NO is produced. Therefore, NOSN degeneration is not caused by elevated NO.     

Computational analysis of reduced-mixing personal ventilation jets

In this paper we develop a detailed computational fluid dynamics (CFD) model of a personal ventilation (PV) setup comprising a PV nozzle, seated thermal manikin and floor diffuser, then use experimental velocity and tracer gas concentration data for the same setup to validate the CFD model. Specifically, we compare CFD results with the experimental results obtained with both a conventional round nozzle and a novel low-mixing co-flow nozzle directing a PV fresh air jet toward the breathing zone (BZ) of a seated thermal manikin in a thermally controlled chamber ventilated also by a floor diffuser behind the manikin. The CFD model shows excellent agreement with the experimental data. We then exercise the CFD model to study the effect of nozzle exit boundary conditions such as turbulence intensity and length scale, flow rate and temperature, and manikin temperature on the air quality in the BZ of the heated manikin. It is shown that the air quality of the novel PV system is sensitive to the nozzle exit turbulence intensity and flow rate, and insensitive to jet temperature within the 20–26 °C range, and to body temperature within a clo range of 0–1. A companion paper presents in detail the experimental set up and results used to validate the CFD model discussed in this paper.     

Adenovirus type 2 coded single-stranded DNA binding protein: in vivo phosphorylation and modification

The adenovirus type 2-coded single-stranded DNA binding protein (DBP) was shown to be a phosphoprotein and to exist in at least two forms that differ in mobility by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. After a 30-min pulse with [35S]methionine or 32PO4, 35S- or 32P-labeled DBP had a nominal molecular weight of 74,000 whereas after a 30-min label followed by a 20-h chase, 35S- and 32P-labeled DBP had a nominal molecular weight of 77,000. Both large and small forms of 35S- and 32P-labeled DBP bound to single-stranded DNA-cellulose columns and were eluted by 0.4 to 0.6 M NaCl; both forms also were immunoprecipitated by antiserum against adenovirus type 1-simian virus 40-induced tumor cells (this antiserum contains antibodies against DBP) and by monospecific antiserum against 95 to 99% purified DBP. With highly purified 32P-DBP labeled 7 to 10 h postinfection, it was shown that the 32P radioactivity was firmly associated with protein material (i.e., not contaminating nucleic acids or phospholipids) and had properties expected of a phosphoester of an amino acid; paper electrophoresis of acid hydrolysates of this preparation identified phosphoserine but not phosphothreonine. Phosphoserine but not phosphothreonine was also identified in acid hydrolysates of another preparation of 32P-DBP labeled for 30 min, chased for 20 h, and then immunoprecipitated by adenovirus type 1-simian virus 40 antiserum.     

Identification of α-Al2O3 Precipitates in Rutile Single Crystals

After high-temperature reaction between Al₂O₃ and TiO₂ crystals, precipitates found in rutile were characterized by electron microprobe and X-ray diffraction methods and by optical and electron microscopy. The precipitates were identified as α-Al₂O₄. Geometric and crystallographic orientation relations with the TiO₂ matrix constitute a reverse case of rutile precipitation in star sapphire .