Plasmoid Formation and Strong Radiative Cooling in a Driven Magnetic Reconnection Experiment.

We present the first experimental study of plasmoid formation in a magnetic reconnection layer undergoing rapid radiative cooling, a regime relevant to extreme astrophysical plasmas. Two exploding aluminum wire arrays, driven by the Z machine, generate a reconnection layer (S_{L}≈120) in which the cooling rate far exceeds the hydrodynamic transit rate (τ_{hydro}/τ_{cool}>100). The reconnection layer generates a transient burst of >1 keV x-ray emission, consistent with the formation and subsequent rapid cooling of the layer. Time-gated x-ray images show fast-moving (up to 50 km s^{-1}) hotspots in the layer, consistent with the presence of plasmoids in 3D resistive magnetohydrodynamic simulations. X-ray spectroscopy shows that these hotspots generate the majority of Al K-shell emission (around 1.6 keV) prior to the onset of cooling, and exhibit temperatures (170 eV) much greater than that of the plasma inflows and the rest of the reconnection layer, thus providing insight into the generation of high-energy radiation in radiatively cooled reconnection events.

In vitro studies on the deacetylation-reacetylation of arylamides and the transacetylation of arylamines by human and rat whole blood.

Human and rat whole blood were shown to metabolize the aromatic amides acetanilide and phenacetin by deacetylation followed by reacetylation in vitro. Derivatives of the parent compounds labelled with deuterium in the N-acetyl group produced non-labelled material after incubation. The reaction was monitored by capillary gas chromatographic-mass spectrometric (GC-MS) analysis. There was no significant difference in the acetyl group exchange of these substrates using blood samples donated by non-diabetic volunteers or Type 2 diabetic patients (respective mean +/- SEM values = 4.0 +/- 0.2% and 4.2 +/- 0.3% for trideuteroacetanilide, 6.2 +/- 0.6% and 6.1 +/- 0.3% for trideuterophenacetin). Increasing the glucose concentration in the incubation medium by 50 mmol/L significantly (P less than 0.01) increased deacetylation-reacetylation of trideuteroacetanilide in each group (4.6 +/- 0.2% and 4.7 +/- 0.2% for non-diabetic and diabetic subjects, respectively). In rat blood the amount of deacetylation-reacetylation was much higher: 7.2 +/- 0.6% and 8.3 +/- 0.7% for trideuteroacetanilide and trideuterophenacetin, respectively. Induction of experimental diabetes using streptozotocin did not significantly change the extent of deacetylation-reacetylation of either deuterated substrate (10.1 +/- 2.1% and 9.5 +/- 1.1%). Elevation of the incubation glucose concentration by 50 mmol/L produced an increase in acetyl group exchange (for trideuteroacetanilide) in diabetic (14.3 +/- 2.2%) and non-diabetic (10.6 +/- 1.0%) rats. The donation of acetyl groups (transacetylation) was observed after incubation of blood samples from both diabetic and non-diabetic human subjects and rats with trideuterophenacetin and a molar excess of aniline. This reaction significantly (P less than 0.001) decreased the acetyl group exchange of trideuterophenacetin (these values were 4.5 +/- 0.4% and 3.4 +/- 0.6% using samples from non-diabetic human subjects and rats, respectively) and demonstrated the ability of whole blood to catalyse transacetylation (acetyl-CoA-independent acetylation). There was correlation between the amount of (unlabelled) acetanilide produced by acetylation with acetyl-CoA and the percentage present as trideuteroacetanilide. The proportion of trideuteroacetanilide was higher using rat blood (e.g. the values for non-diabetic subjects were 25.5 +/- 1.7% vs 8.5 +/- 0.3%; P less than 0.001) although the total amount of acetanilide produced was lower (0.54 +/- 0.14 nmol vs 1.82 +/- 0.23 nmol; P less than 0.05) than that observed using human blood.

Combined Kirschner-Ehmer device and dorsal spinal plate fixation technique for caudal lumbar vertebral fractures in dogs.

A new surgical technique was developed for the fixation of caudal lumbar vertebral fractures in dogs. The technique provides optimal stabilization, can be used in combination with dorsal decompression, and does not require an intact spinous process on the fractured vertebra or attachment of the fixation devices to the fractured vertebra. The fixation consists of a Kirschner-Ehmer device and dorsal spinal plates. After fracture healing, only mild sedation of the dog is needed to allow removal of the external hardware used in the fixation. The technique, its indications, and its use in 5 cases are described.

Combined Kirschner-Ehmer apparatus and dorsal spinal plate fixation of caudal lumbar fractures in dogs: biomechanical properties.

The strength and rigidity of a new surgical technique for the stabilization of caudal lumbar fractures in dogs, using a Kirschner-Ehmer apparatus and a dorsal spinal plate (KE/DSP), were compared with 2 other methods of internal spinal fixation and with intact (control) spines, using a spinal test system that subjected the spines to 4-point bending. The fixation devices were applied to isolated canine lumbosacral spines (L1 to S3) from cadavers. A complete spinal separation was made in the spine implant specimens at L5-L6 by sharp dissection of all ligamentous structures connecting the two vertebrae. Bending moment vs L5-L6 angular deformation curves, and rigidity and load sustained at 10 degrees angular deformation (failure) were recorded for each fixation method and for the control spines. Values were compared by statistical analysis. The combined KE/DSP fixation and a combined vertebral body plate/dorsal spinal plate (VBP/DSP) fixation were stronger and more rigid than were the control spines and those fixed with a modified segmental-fixation method (P less than 0.05). There were no statistical differences in strength and rigidity between the 2 combined-fixation techniques. Although the VBP/DSP technique is not applicable to clinical caudal lumbar (L5-L6) fractures, it was compared in this study to the KE/DSP technique because a similar VBP/DSP technique was reported strongest in a similar study of L3-L4 simulated fractures, compared with 3 other spinal-fixation techniques that have been used in repair of caudal lumbar fractures. The technique has been used successfully in 6 dogs with caudal lumbar fractures.

Stable isotopes as probes for the metabolism of acetanilide in man and the rat.

Acetanilide with the three hydrogens of the acetyl group replaced by deuterium was administered to 9 human volunteers (50 mg p.o.) and 5 male Sprague-Dawley rats (10 mg kg-1 p.o. and 100 mg kg-1 p.o.) and urine samples collected for 8 and 48 h, respectively. Capillary gas chromatography/mass spectrometry (GC/MS) was used to determine if the major metabolite was deuterated paracetamol or a mixture of this compound with paracetamol produced by deacetylation followed by reacetylation. Acetyl group exchange of the parent compound was also studied. Conjugates of the metabolite were hydrolysed and the free compound derivatized to an O-propionyl ester before GC/MS analysis. Paracetamol containing no deuterated acetyl group was detected in all studies, together with the labelled metabolite. The mean ratio of deuterated to unlabelled paracetamol in man was approximately 8:1 and was independent of acetylator status. The acetyl group exchange measured in the rat was time-dependent but was always significantly higher than in man. The mean ratios of deuterated to unlabelled paracetamol in urine samples collected 0-4 h and 24-48 h after administration of the higher trideuteroacetanilide dose to the rats were approximately 2:1 and 4:1, respectively.

Interaction studies with bumetanide and furosemide. Effects of probenecid and of indomethacin on response to bumetanide in man.

Bumetanide was administered intravenously in doses of 0.5 and 1.0 mg to eight normal subjects with and without pretreatment with probenecid or indomethacin. Probenecid did not affect either the cumulative response or the time course of response to bumetanide. This may mean that probenecid and potentially other exogenous or endogenous organic acids do not affect the renal handling of bumetanide in normal man. Indomethacin pretreatment decreased the cumulative 4-hour excretion of sodium caused by 1.0 mg bumetanide from 276 +/- 22.9 to 202 +/- 20.9 mEq (P less than 0.003). Effects on volume and chloride paralleled those of sodium, while potassium excretion was not affected. When the response was analyzed as increment in fractional excretion over basal solute excretion, determined from separate control studies, indomethacin still decreased the response, possibly indicating that endogenous prostaglandins may play a role in determining the overall response to bumetanide.

Electrolyte excretion patterns. Intravenous and oral doses of bumetanide compared to furosemide.

The response to bumetanide and furosemide administered orally and intravenously was compared in normal subjects. Doses of bumetanide were 0.5 and 1 mg intravenously and 0.5, 1 and 2 mg orally. Doses of furosemide were 20 and 40 mg intravenously and 20, 40, and 80 mg orally. After intravenous doses of both drugs, peak natriuresis occurred during the first collection period of 30 minutes and the response returned to baseline by 3.5 hours. After oral dosing, peak effect occurred at 75 minutes and returned to baseline within 4 hours. Cumulative response was assessed for volume, sodium, potassium, and chloride excretion. The response did not differ substantially between drugs. On a milligram basis, bumetanide was approximately 50 times as potent as furosemide. For both drugs, the intravenous dose was approximately three times as potent as the oral preparation. The time course of response shows that the curves are virtually superimposable. The diuretic effect was short-lived for both diuretics. The urine volume and sodium and chloride excretion were parallel. The sodium/potassium ratio was calculated as follows: for every 200 mEq sodium excreted in 4 hours, bumetanide caused about 35 mEq and furosemide caused about 50 mEq potassium to be eliminated. Even if statistically significant, this difference does not appear to be clinically remarkable. If bumetanide offers therapeutic advantages in this regard, studies in patients with various disease states would have to be performed.