Isolated peritoneal donor-related plasmacytoma 3 years after liver transplantation: a case report.

Organ transplantation carries a risk of disease transmission from donor to recipient, primarily infection or malignancy. Although donors are thoroughly screened, donor-related malignancies are reported to occur in 0.01% of solid organ transplants. Plasma cell neoplasm, to the best of our knowledge, has not been reported as a donor-transmitted malignancy in liver transplantation. We describe a liver transplant from a donor with unrecognized plasmacytoma requiring retransplantation. Three years after the first transplant a single peritoneal mass was detected on surveillance imaging and radically excised; HLA phenotyping confirmed the mass to be an isolated extra-medullary plasmacytoma of chimeric donor and recipient origin.

Clinicopathologic features of post-transplant lymphoproliferative disorders arising after pediatric small bowel transplant.

Few studies examined the clinicopathologic features of PTLD arising in pediatric SBT patients. Particularly, the association between ATG and PTLD in this population has not been described. Retrospective review of 81 pediatric patient charts with SBT--isolated or in combination with other organs--showed a PTLD incidence of 11%, occurring more frequently in females (median age of four yr) and with clinically advanced disease. Monomorphic PTLD was the most common histological subtype. There was a significant difference in the use of ATG between patients who developed PTLD and those who did not (p < 0.01); a similar difference was seen with the use of sirolimus (p < 0.001). These results suggested a link between the combination of ATG and sirolimus and development of more clinically and histologically advanced PTLD; however, the risk of ATG by itself was not clear. EBV viral loads were higher in patients with PTLD, and median time between detection of EBV to PTLD diagnosis was three months. However, viral loads at the time of PTLD diagnosis were most often lower than at EBV detection, thereby raising questions on the correlation between decreasing viral genomes and risk of PTLD.

Pathogenicity of two Egyptian H5N1 highly pathogenic avian influenza viruses in domestic ducks.

Domestic ducks have been implicated in the dissemination and evolution of H5N1 highly pathogenic avian influenza (HPAI) viruses. In this study, two H5N1 HPAI viruses belonging to clade 2.2.1 isolated in Egypt in 2007 and 2008 were analyzed for their pathogenicity in domestic Pekin ducks. Both viruses produced clinical signs and mortality, but the 2008 virus was more virulent, inducing early onset of neurological signs and killing all ducks with a mean death time (MDT) of 4.1 days. The 2007 virus killed 3/8 ducks with a MDT of 7 days. Full-genome sequencing and phylogenetic analysis were used to examine differences in the virus genes that might explain the differences observed in pathogenicity. The genomes differed in 49 amino acids, with most of the differences found in the hemagglutinin protein. This increase in pathogenicity in ducks observed with certain H5N1 HPAI viruses has implications for the control of the disease, since vaccinated ducks infected with highly virulent strains shed viruses for longer periods of time, perpetuating the virus in the environment and increasing the possibility of transmission to susceptible birds.

Additive noise properties of active matrix flat-panel imagers.

A detailed theoretical and empirical investigation of additive noise for indirect detection, active matrix flat-panel imagers (AMFPIs) has been performed. Such imagers comprise a pixelated array, incorporating photodiodes and thin-film transistors (TFTs), and an associated electronic acquisition system. A theoretical model of additive noise, defined as the noise of an imaging system in the absence of radiation, has been developed. This model is based upon an equivalent-noise-circuit representation of an AMFPI. The model contains a number of uncorrelated noise components which have been designated as pixel noise, data line thermal noise, externally coupled noise, preamplifier noise and digitization noise. Pixel noise is further divided into the following components: TFT thermal noise, shot and 1/f noise associated with the TFT and photodiode leakage currents, and TFT transient noise. Measurements of various additive noise components were carried out on a prototype imaging system based on a 508 microm pitch, 26 x 26 cm2 array. Other measurements were performed in the absence of the array, involving discrete components connected to the preamplifier input. Overall, model predictions of total additive noise as well as of pixel, preamplifier, and data line thermal noise components were in agreement with results of their measured counterparts. For the imaging system examined, the model predicts that pixel noise is dominated by shot and 1/f noise components of the photodiode and TFT at frame times above approximately 1 s. As frame time decreases, pixel noise is increasingly dominated by TFT thermal noise. Under these conditions, the reasonable degree of agreement observed between measurements and model predictions provides strong evidence that the role of TFT thermal noise has been properly incorporated into the model. Finally, the role of the resistance and capacitance of array data lines in the model was investigated using discrete component circuits at the preamplifier input. Measurements of preamplifier noise and data line thermal noise components as a function of input capacitance and resistance were found to be in reasonable agreement with model predictions.

A quantitative investigation of additive noise reduction for active matrix flat-panel imagers using compensation lines.

A quantitative investigation of a technique for reducing correlated noise in indirect detection active matrix flat-panel imagers has been reported. Correlated noise in such systems arises from the coupling of electronic noise, originating from fluctuations in external sources such as power supplies and ambient electromagnetic sources, to the imaging array via its address lines. The noise reduction technique involves the use of signals from columns of compensation line pixels located in relatively close proximity to the columns of normal imaging pixels on the array. Compensation line pixels are designed to be as sensitive to externally-coupled noise as columns of normal imaging pixels but are insensitive to incident radiation. For each imaging pixel, correlated noise is removed by subtracting from the imaging pixel signal a signal derived from compensation line pixels located on the same row. The effectiveness of various implementations of this correction has been examined through measurements of signal and noise from individual pixels as well as of noise power spectra. These measurements were performed both in the absence of radiation as well as with x rays. The effectiveness of the correction was also demonstrated qualitatively by means of an image of a hand phantom. It was found that the use of a single compensation line dramatically reduces external noise through removal of the correlated noise component. While this form of the correction increases non-radiation-related uncorrelated noise, the effect can be largely reduced through the introduction of multiple compensation lines. Finally, a position-dependent correction based on compensation lines on both sides of the array was found to be effective when the magnitude of the correlated noise varied linearly across the array.

Strategies to improve the signal and noise performance of active matrix, flat-panel imagers for diagnostic x-ray applications.

A theoretical investigation of factors limiting the detective quantum efficiency (DQE) of active matrix flat-panel imagers (AMFPIs), and of methods to overcome these limitations, is reported. At the higher exposure levels associated with radiography, the present generation of AMFPIs is capable of exhibiting DQE performance equivalent, or superior, to that of existing film-screen and computed radiography systems. However, at exposure levels commonly encountered in fluoroscopy, AMFPIs exhibit significantly reduced DQE and this problem is accentuated at higher spatial frequencies. The problem applies both to AMFPIs that rely on indirect detection as well as direct detection of the incident radiation. This reduced performance derives from the relatively large magnitude of the square of the total additive noise compared to the system gain for existing AMFPIs. In order to circumvent these restrictions, a variety of strategies to decrease additive noise and enhance system gain are proposed. Additive noise could be reduced through improved preamplifier, pixel and array design, including the incorporation of compensation lines to sample external line noise. System gain could be enhanced through the use of continuous photodiodes, pixel amplifiers, or higher gain x-ray converters such as lead iodide. The feasibility of these and other strategies is discussed and potential improvements to DQE performance are quantified through a theoretical investigation of a variety of hypothetical 200 microm pitch designs. At low exposures, such improvements could greatly increase the magnitude of the low spatial frequency component of the DQE, rendering it practically independent of exposure while simultaneously reducing the falloff in DQE at higher spatial frequencies. Furthermore, such noise reduction and gain enhancement could lead to the development of AMFPIs with high DQE performance which are capable of providing both high resolution radiographic images, at approximately 100 microm pixel resolution, as well as variable resolution fluoroscopic images at 30 fps.

A review of achievements of the national schistosomiasis control program in middle and upper Egypt areas.

In Egypt the "national schistosomiasis control program" was formulated to control transmission by reduction of prevalence and intensity of current infections, and thereby achieve an acceptable level of schistosomiasis disease control. The program was implemented foremost in Middle Egypt (1977) and Upper Egypt (1980), collectively extending 800 km alongside of the River Nile and accommodate about 10.5 million people. Schistosoma haematobium has been essentially the prevailing species infection in both areas. The strategy of control entailed both area-wide mollusciciding with niclosamide, and selective population chemotherapy with metrifonate. Evaluation in 1986 showed that prevalence dropped from pre-control 29.4% in Middle Egypt and 26.3% in Upper Egypt to 6% and 7.8% respectively, together with a remarkable drop of infections among children. Also mean intensity attained low levels consistent of low grade infections. It is evident therefore that in these areas where an enhancement of schistosomiasis infections had been anticipated the employment of the twofold strategy effected a state of low-prevalence/low-intensity signifying a lowered reservoir of infection and a substantial interference with the potentials of transmission.

Comparison of deficits in electrical self-stimulation after ibotenic acid lesion of the lateral hypothalamus and the medial prefrontal cortex.

The aim of the present study was to compare the self-stimulation deficit produced by a unilateral injection of the neurotoxin, ibotenic acid, in the lateral hypothalamus (LH) to the deficit produced by the same unilateral injection in the medial prefrontal cortex (MPC). Four groups of adult male Sprague-Dawley rats were used: in two control groups, electrodes were bilaterally implanted in the LH (5 rats) or in the MPC (6 rats) and self-stimulation (ICSS) was obtained separately with the right and left electrodes. In the two experimental groups the intrinsic neurons of the LH (8 rats) or of the MPC (10 rats) were destroyed unilaterally by local injection of ibotenic acid (4 micrograms in 0.5 microliter); the other side served as the sham-lesioned control. Ten days later ICSS electrodes were implanted bilaterally, one in the lesioned area, the other in the contralateral region. As in the case of the control rats, ICSS was determined separately for each electrode, first by a rate dependent test (nose-poke) then by a 'rate-free' test (shuttle-box). In the LH and MPC control rats, ICSS responses were the same with stimulation on either side. In the LH-lesioned rats, the ICSS rates measured with the nose-poke test were significantly decreased with stimulation on the lesioned side, whereas rates with stimulation of the non-lesioned LH were normal. Likewise, while shuttle responses with stimulation of the non-lesioned LH were normal, the OFF-time was increased and the ON-time was decreased with stimulation of the lesioned LH. In the MPC-lesioned rats, ICSS (nose-poke) was totally suppressed and the shuttle responses were disorganized since neither the ON- nor the OFF-times changed in response to increasing current intensities. Nose-poke responses with stimulation of the non-lesioned MPC were just about normal. These results show that in the two brain regions studied local neurons are involved in ICSS. The difference in the magnitude of the deficit observed suggests, that the neuronal circuits involved in MPC self-stimulation are poorly represented whereas in the LH many neuronal circuits involved in these mechanisms overlap.

Alterations of noradrenaline and serotonin uptake and metabolism in chronic cobalt-induced epilepsy in the rat.

The high affinity uptake of noradrenaline and serotonin, and the concentrations of these monoamines and their metabolites, have been measured in the perifocal cortical area at various stages of the evolution of cobalt-induced epilepsy in the rat. Noradrenaline uptake was maximally reduced at days 8-10 after cortical cobalt application, a time corresponding to the onset of epileptic discharges; it remained diminished during the spiking activity period of the focus (days 14-20) and was back to normal values at day 40, at which time the epileptic syndrome had disappeared. Serotonin uptake was also diminished at days 8-10 but to a lesser extent than was noradrenaline uptake. In the homotopic cerebral cortex contralateral to cobalt application, noradrenaline uptake was reduced at day 10 only and to a lesser extent than in the perifocal area, whereas serotonin uptake was unaffected. Kinetic analysis of the cobalt-induced monoamine uptake alterations at day 10 revealed a diminution of the maximal velocity with no change in the Km. Noradrenaline and dihydroxyphenylethyleneglycol concentrations in the perifocal area were also maximally reduced at days 8-10 but were unaffected at day 2 and day 40 post cobalt application. A reduction of serotonin levels in the perifocal area was observed only at days 8-10 while 5-hydroxyindoleacetic acid remained unaffected throughout the time period studied. The levels of these monoamines and their metabolites were unchanged in the homotopic contralateral cortex 2-40 days after cobalt application. These results indicate that cortical cobalt application induces alterations of the biochemical indices of the density of noradrenaline-containing terminals that closely parallel the evolution of the epileptic syndrome. These data further emphasize the important role of the cortical noradrenergic system in cobalt-induced epilepsy.

Neurochemical lesion of the locus coeruleus of the rat does not suppress the sedative effect of clonidine.

The locus coeruleus of male rats was destroyed bilaterally by injection of 6-hydroxydopamine. Rats injected with the vehicle and normal rats served as controls. Starting 20 days after the lesion, the locomotor activity of all rats was measured for 5 min every day. For the first 6 days, the lesioned rats were significantly less active than control rats; from the 7th to the 15th day, on the other hand, the locomotor activity of the two groups of rats was the same. From the 16th day onwards, the sedative effect of small doses of clonidine (2.5-100 micrograms/kg) was measured in lesioned and control animals. In spite of an almost total loss of noradrenaline in the cerebral cortex and hippocampus and a 33% loss of noradrenaline in the brain-stem of the lesioned rats, the sedative effect of clonidine was the same as in the control rats. This result suggests that the sedation produced by clonidine is not dependent on presynaptically located alpha 2-adrenoceptors.

Enhancement of learning four weeks after stimulation of the nucleus locus coeruleus in the rat: differential effects of dorsal noradrenergic bundle lesion and lesion of the locus coeruleus proper.

In previous studies we showed that electrical stimulation of the nucleus locus coeruleus produced, four weeks later, a significant improvement in performance in acquisition of food-reinforced operant conditioning. In the two experiments reported here, we tested the role of the dorsal noradrenergic bundle and of the locus coeruleus proper in this long-term effect. Lesioning the dorsal noradrenergic bundle did not have a clear and consistent effect, whereas lesion of the nucleus coeruleus proper suppressed almost totally the beneficial effect of the stimulation. In the first experiment, the dorsal noradrenergic bundle was lesioned by local bilateral injection of 6-hydroxydopamine, 8 days before stimulation of the locus coeruleus. Four weeks after the stimulation, the rats were tested for acquisition of the operant task. Three control groups were used: not lesioned but stimulated, lesioned but not stimulated, and not lesioned/not stimulated. The locus coeruleus stimulation produced the same improvement of performance at the beginning of the acquisition, whether or not the dorsal noradrenergic bundle had been lesioned. However, a significant decrement of performance was observed in lesioned and stimulated rats during the last 40 min of the acquisition. In the second experiment, the locus coeruleus proper was destroyed by bilateral local injection of 6-hydroxydopamine and the locus coeruleus region was stimulated 15 days later. Three control groups were used, as in the first experiment. All the rats were tested 4 weeks later for acquisition of the operant task. The locus coeruleus lesion significantly attenuated the beneficial effect of the stimulation; however, the performance of the lesioned and stimulated rats was still significantly superior to that of the lesioned but not stimulated rats. These results suggest that the noradrenergic locus coeruleus system is involved in the long-term effect, but that the rostral projections passing through the dorsal bundle, in front of the lesion, are not critically involved in the observed effect.

[Is an alteration of noradrenergic afferents involved in focal epilepsies? (author's transl)]. / Une altération des afférences noradrénergiques est-elle en cause dans les épilepsies focales?

Previous studies have indicated that noradrenergic system could be involved in various models of chemically, electrically or genetically induced epilepsy. The relationship between the development of a chronic cobalt focus in the rat and the alterations of the cortical noradrenergic system has been studied by means of biochemical analysis of the NA cortical content combined with the glyoxylic acid-induced fluorescence method and the micro-iontophoretic technique. It can be suggested that the noradrenergic system may influence the initiation, spread and disappearance of the epileptic syndrome: (1) The beginning of epileptic discharges coincides with a drop in the NA cortical content, with decrease in number of the NA-containing terminals and with a hypersensitivity of the cortical neurons to iontophoretically applied NA. (2) The termination of the epileptic syndrome coincides with an increase in density of the cortical noradrenergic innervation (sprouting) and consequently with an increase in NA cortical concentrations and a return to normal values of the NA threshold of the cortical neurons.