Necrotizing leukoencephalopathy associated with nonconvulsive status epilepticus and periodic short-interval diffuse discharges: a clinicopathological study.

We describe the clinical, neuroimaging and neuropathological features of an immunocompromised patient diagnosed as having refractory nonconvulsive status epilepticus (NCSE), and whose consecutive electroencephalograms (EEGs) revealed persistent periodic short-interval diffuse discharges (PSIDDs). Prominent subcortical white matter lesions in keeping with the diagnosis of multifocal necrotizing leukoencephalopathy may be neuropathological substrate of NCSE with persistent PSIDDs.     

Synergistic effect of growth hormone-releasing hormone (GHRH) and clonidine in stimulating GH release in young and old dogs

The effect of acute administration of growth hormone-releasing hormone (GHRH), clonidine (CLO), an alleged GHRH releaser, or GHRH and clonidine given simultaneously was studied in young and old dogs. Simultaneous administration of CLO induced in young dogs an additive effect on GH release and potentiated in old dogs the GHRH-induced GH release, with the GH response being clearly higher than the sum of the GH responses to GHRH or CLO alone. These data suggest that CLO promotes GH release in the dog also by inhibition of somatostatin release.     

Determination of the membrane-buffer partition coefficient of flunitrazepam, a lipophilic drug

The partition coefficient (P) of a benzodiazepine, flunitrazepam (FNTZ), was determined in a synaptosomal membrane/buffer system. A two component model was used, one of the components reflecting the drug partitioning into the membrane, and the other the amount of drug in the aqueous phase retained by the pellet after the centrifugation. The quantity of [3H]FTNZ measured as nonspecifically bound to the membrane includes both components so, the second one had to be discounted and in order to determined its magnitude a parallel experiment was performed using a non-partitioning hydrophilic drug (gamma-[3H]aminobutyric acid, [3H]GABA). The assay required previous determination of the fraction of the total volume of the incubation system that corresponded to membrane (fm). The fm value was calculated from the density value (delta) determined by a picnometer method. The results obtained were: delta = 1.66 +/- 0.02; fm = (1.6 +/- 0.2) 10(-3); P = 18.5 +/- 0.8. This P value could explain nonspecific effects of BZDs on some functions of the neuronal membrane.     

Pseudoneoplastic lesions of the testis and paratesticular structures

Pseudotumors or tumor-like proliferations (non-neoplastic masses) and benign mimickers (non-neoplastic cellular proliferations) are rare in the testis and paratesticular structures. Clinically, these lesions (cysts, ectopic tissues, and vascular, inflammatory, or hyperplastic lesions) are of great interest for the reason that, because of the topography, they may be relevant as differential diagnoses. The purpose of this paper is to present an overview of the pseudoneoplasic entities arising in the testis and paratesticular structures; emphasis is placed on how the practicing pathologist may distinguish benign mimickers and pseudotumors from true neoplasia. These lesions can be classified as macroscopic or microscopic mimickers of neoplasia.     

Analysis of Ig and T-cell receptor genes in 40 childhood acute lymphoblastic leukemias at diagnosis and subsequent relapse: implications for the detection of minimal residual disease by polymerase chain reaction analysis

The rearrangement patterns of Ig and T-cell receptor (TcR) genes were studied by Southern blot analysis in 30 precursor B-cell acute lymphoblastic leukemias (B-ALLs) and 10 T-ALLs at diagnosis and subsequent relapse. Eight precursor B-ALLs appeared to contain biclonal/oligoclonal Ig heavy-chain (IgH) gene rearrangements at diagnosis. Differences in rearrangement patterns between diagnosis and relapse were found in 67% (20 cases) of precursor B-ALLs (including all eight biclonal/oligoclonal cases) and 50% (five cases) of T-ALLs. In precursor B-ALLs, especially changes in IgH and/or TcR-delta gene rearrangements were found (17 cases), but also changes in TcR-beta, TcR- gamma, Ig kappa, and/or Ig lambda genes (11 cases) occurred. The changes in T-ALLs concerned the TcR-beta, TcR-gamma, TcR-delta, and/or IgH genes. Two precursor B-ALLs showed completely different Ig and TcR gene rearrangement patterns at relapse, suggesting the absence of a clonal relation between the leukemic cells at diagnosis and relapse and the development of a secondary leukemia. The clonal evolution in the other 23 ALL patients was based on continuing rearrangement processes and selection of subclones. The development of changes in Ig and TcR gene rearrangement patterns was related to remission duration, suggesting an increasing chance of continuing rearrangement processes with time. These immunogenotypic changes at relapse occurred in a hierarchical order, with changes in IgH and TcR-delta genes occurring after only 6 months of remission duration, whereas changes in other Ig and TcR genes were generally detectable after 1 to 2 years of remission duration. The heterogeneity reported here in Ig and/or TcR gene rearrangement patterns at diagnosis and relapse might hamper polymerase chain reaction (PCR)-mediated detection of minimal residual disease (MRD) using junctional regions of rearranged Ig or TcR genes as PCR targets. However, our data also indicate that in 75% to 90% of ALLs, at least one major rearranged IgH, TcR-gamma, or TcR-delta band (allele) remained stable at relapse. We conclude that two or more junctional regions of different genes (IgH, TcR-gamma, and/or TcR-delta) should be monitored during follow-up of ALL patients for MRD detection by use of PCR techniques. Especially in biclonal/oligoclonal precursor B-ALL cases, the monitoring should not be restricted to rearranged IgH genes, but TcR-gamma and/or TcR-delta genes should be monitored as well, because of the extensive changes in IgH gene rearrangement patterns in this ALL subgroup.     

Glucose-6-phosphate dehydrogenase variants: reexamination of G6PD Chicago and Cornell and a new variant (G6PD Pea Ridge) resembling G6PD Chicago

Two large and unrelated families were investigated for hereditary nonspherocytic hemolytic anemia associated with deficiency of erythrocyte glucose-6-phosphate dehydrogenase (G6PD). In both families, the kinetic and electrophoretic features of the G6PD variants resembled those of G6PD Chicago. Further investigation revealed that members of one of these families previously had been characterized as having the G6PD variants Chicago and Cornell. However, it is clear that each of these terms has been applied to the same variant in this single large kindred. In the second family, we describe a newly identified variant with unique characteristics, which we have designated G6PD Pea Ridge. G6PD Pea Ridge resembles G6PD Chicago but differs in electrophoretic mobility and in a few kinetic parameters. It exhibits an unusually high Ki for NADPH and thus appears to be insensitive to product inhibition. As other cases previously considered to be the Chicago variant become more fully characterized, this probably will be shown to be a heterogeneous group of variants.     

Development of radiopaque,biocompatible, antimicrobial,micro-particle fillers for micro-CT imaging of simulated periodontal pockets

Objectives

Approximately 10⁹ bacteria can be harbored within periodontal pockets (PP) along with inflammatory byproducts implicated in the pathophysiology of systemic diseases linked to periodontitis (PD). Calculation of this inflammatory burden has involved estimation of total pocket surface area using analog data from conventional periodontal probing which is unable to determine the three-dimensional (3-D) nature of PP. The goals of this study are to determine the radiopacity, biocompatibility, and antimicrobial activity of transient micro-particle fillers in vitro and demonstrate their capability for 3-D imaging of artificial PP (U.S. Patent publication number: 9814791 B2).