Estimation of average flow in ungated 3D phase contrast angiograms

Three dimensional (3D) phase contrast angiograms contain velocity data, which is discarded after the reconstruction of the projections. In extension to earlier work on velocity quantification with ungated 2D phase data, this paper shows that a useful estimate of the average velocity and flow rate can be extracted from ungated 3D phase contrast angiograms. Simulations and experiments in a phantom and in vivo were performed. For pulsatile flow and strong spin saturation, an over-estimation of the flow rate at the net in-flow end of the imaging volume and underestimation at the net out-flow end was observed. Imaging at lower RF tip angles yielded flow rates close to the correct value within the entire imaging volume. In contrast to ungated 2D experiments, the flow rates determined by repeated 3D experiments showed no variation.     

Invited. Brain edema development after MRI-guided focused ultrasound treatment

The aim of this study was to investigate a potential technique for image-guided minimally invasive neurosurgical interventions. Focused ultrasound (FUS) delivers thermal energy without an invasive probe, penetrating the dura mater, entering through the cerebrospinal fluid (CSF) space, or harming intervening brain tissue. We applied continuous on-line monitoring by MRI to demonstrate the effect of the thermal intervention on the brain tissue. For this, seven rabbits had a part of their skull removed to create access for the FUS beam into the brain through an acoustic window of 11 mm in diameter. Dura was left intact and skin was sutured. One week later, the rabbits were sonicated for 3 seconds with 21 W acoustic power, and the FUS focus was visualized with a temperature-sensitive T1-weighted MRI pulse sequence. The tissue reaction was documented over 7 days with T2-weighted images of the brain. The initial area of the central low signal intensity in the axial plane was .4 ± .3 mm², and for the bright hyperintensity surrounding the lesion, it was 2.3 ± .6 mm² (n = 7). In the coronal plane, the corresponding values were .4 ± .1 mm² and 3.4 ± .9 mm² (n = 5). The developing brain edema culminated 48 hours later and thereafter diminished during the next 5 days. Histology revealed a central necrosis in the white matter surrounded by edematous tissue with inflammatory cells. In summary, the image-guided thermal ablation technique described here produced a relatively small lesion in the white matter at the targeted location. This was accomplished without opening the dura or the need for a stereotactical device. MRI allowed on-line monitoring of the lesion setting and the deposition of thermal energy and demonstrated the tissue damage after the thermal injury.     

Standard sera in solid-phase immunoassays

Solid-phase immunoassay-derived antibody titers are often converted to weight unit concentrations with the aid of standard sera containing known antibody concentrations. Systematic studies justifying this procedure have not yet been published. We therefore investigated the magnitude of errors associated with this conversion. Antibody concentrations of thirteen sera or ascites fluids were determined by quantitative precipitation or equlibrium dialysis, and one was then used as a “standard antibody” for the others in solid-phase radioimmunoassay (SP-RIA) or enzyme-linked immunosorbent (ELISA) assays. Antibody concentrations determined by the conventional solid-phase assay (the “standard serum” has the same specificity as the “sample”) had up to fourfold errors. These errors could be reduced by basing the conversion on the combination of two standard sera instead of one. The possibility was studied of whether the conversion to weight units could be done with the aid of a standard serum directed to a different antigen than the sample antibody. Errors associated with the use of such a heterologous standard were not significantly greater than those found using the conventional conversion. A combination of two reference sera again reduced the errors. The use of such heterologous standard(s), however, requires checking the binding capacity of the antigen coats.     

Syntheses and ESR spectra of radicals produced in the thermal decomposition of tetraarylsuccinonitriles

Tetraarylsuccinonitriles 2a – e were synthesized via oxidative dimerization of diarylacetonitriles 1a – e in basic media. The thermal decomposition of 2 results in two identical cyanodiarylmethyl radicals 3 . Both ¹H and ¹³C NMR analyses of 1a – e and 2a – e and ESR spectra of 3a – e are presented and discussed. The results of ESR measurements provide a plausible explanation for the different reactivity of cyanodiarylmethyl radicals 3a – e in free radical polymerization.     

“Dark” (compacted) neurons may not die through the necrotic pathway

Dark neurons were produced in the cortex of the rat brain by hypoglycemic convulsions. In the somatodendritic domain of each affected neuron, the ultrastructural elements, except for disturbed mitochondria, were remarkably preserved during the acute stage, but the distances between them were reduced dramatically (ultrastructural compaction). Following a 1-min convulsion period, only a few neurons were involved and their environment appeared undamaged. In contrast, 1-h convulsions affected many neurons and caused swelling of astrocytic processes and neuronal dendrites (excitotoxic neuropil). A proportion of dark neurons recovered the normal structure in 2 days. The non-recovering dark neurons were removed from the brain cortex through two entirely different pathways. In the case of 1-h convulsions, their organelles swelled, then disintegrated and finally dispersed into the neuropil through large gaps in the plasma membrane (necrotic-like removal). Following a 1-min convulsion period, the non-recovering dark neurons fell apart into membrane-bound fragments that retained the compacted interior even after being engulfed by astrocytes or microglial cells (apoptotic-like removal). Consequently, in contrast to what is generally accepted, the dark neurons produced by 1-min hypoglycemic convulsions do not die as a consequence of necrosis. As regards the case of 1-h convulsions, it is assumed that a necrotic-like removal process is imposed, by an excitotoxic environment, on dark neurons that previously died through a non-necrotic pathway. Apoptotic neurons were produced in the hippocampal dentate gyrus by intraventricularly administered colchicine. After the biochemical processes had been completed and the chromatin condensation in the nucleus had reached an advanced phase, the ultrastructural elements in the somatodendritic cytoplasm of the affected cells became compacted. If present in an apparently undamaged environment such apoptotic neurons were removed from the dentate gyrus through the apoptotic sequence of morphological changes, whereas those present in an impaired environment were removed through a necrotic-like sequence of morphological changes. This suggests that the removal pathway may depend on the environment and not on the death pathway, as also assumed in the case of the dark neurons produced by hypoglycemic convulsions.     

Detection of drug-induced apoptosis by flow cytometry after alkaline extraction of ethanol fixed cells

A new flow cytometric method was developed to detect apoptotic cells with fragmented DNA and to determine cell cycle distribution of viable cells, in the same sample, by propidium iodide staining. Apoptosis, in HT58 human B lymphoma cells, was induced by etoposide and/or by staurosporine. Using appropriate alkaline solutions (between 1-10 mN NaOH in 150 mM saline) followed by neutralization with buffer solution, the fragmented DNA can be extracted quantitatively from ethanol fixed cells. Further, good resolution of the cell cycle distribution can be obtained in unimpaired cells without RNase treatment. Furthermore, unlike the widely used hypotonic-detergent extraction of unfixed cells, the suggested extraction method can prevent drug-induced disintegration of dead cells when karyorrhexis occurs. This work was supported by Hungarian National Research Foundation (OTKA I/352 and OTKA II/2622).     

Possible association between maternal recurrent orofacial herpes in pregnancy and a lower rate of preterm birth.

OBJECTIVE: To study the possible association between orofacial herpes during pregnancy and pregnancy complications including preterm birth and low birth weight, since the results of previous studies are inconsistent. METHOD: The population-based large data set of the Hungarian Case-Control Surveillance System of Congenital Abnormalities was used; pregnancies in mothers with and without recurrent orofacial herpes were compared. RESULTS. Of 38,151 newborn infants, 572 (1.5%) had mothers with recurrent orofacial herpes during pregnancy, while 37 577 had mothers with no orofacial herpes. Pregnant women with recurrent orofacial herpes had a higher prevalence of severe nausea and vomiting, threatened preterm delivery, and placental disorders but a lower prevalence of preeclampsia. Mothers with recurrent orofacial herpes during pregnancy also had a somewhat longer (0.4 weeks) gestation (adjusted t = 2.7; p = 0.006) and an obviously lower proportion of preterm births (3.5% vs. 9.3%; adjusted POR with 95% CI = 0.42, 0.27-0.65). However, there was no significant difference in the mean birth weight and rate of low birth weight infants between the two study groups. CONCLUSION: Recurrent orofacial herpes during pregnancy is associated with a smaller proportion of preterm births.