The Inductive Heating of Packed Beds and its Applications to Compact Fluid Heaters and to the Regeneration of Spent Activated Carbon

In this paper, a method is presented in order to predict the behaviour of a granular medium submitted to an inductive electromagnetic field. The resulting model is intented to give an easy and reliable characterization of energy transferred to the bed. A series of experiments was carried out and permitted a validation of the hypothesis formulated over a wide domain. A first application was studied aiming at the sizing of heaters using a stainless-steel balls bed percolated by a cold fluid. Experimental investigation of temperature profiles in both solid and fluid phases and of heat transfer coefficients between them lead to the realization of a compact fluid heater working with small difference of temperature and good efficiencies. This technique was then applied to the heating of activated carbon beds so as to allow a fast and performing regeneration

Exploring concurrency and reachability in the presence of high temporal resolution

Network properties govern the rate and extent of spreading processes on networks, from simple contagions to complex cascades. Recent advances have extended the study of spreading processes from static networks to temporal networks, where nodes and links appear and disappear. We review previous studies on the effects of temporal connectivity for understanding the spreading rate and outbreak size of model infection processes. We focus on the effects of "accessibility", whether there is a temporally consistent path from one node to another, and "reachability", the density of the corresponding "accessibility graph" representation of the temporal network. We study reachability in terms of the overall level of temporal concurrency between edges, quantifying the overlap of edges in time. We explore the role of temporal resolution of contacts by calculating reachability with the full temporal information as well as with a simplified interval representation approximation that demands less computation. We demonstrate the extent to which the computed reachability changes due to this simplified interval representation.Comment: To appear in Holme and Saramaki (Editors). "Temporal Network Theory". Springer- Nature, New York. 201

Gene Expression Profile of Neuronal Progenitor Cells Derived from hESCs: Activation of Chromosome 11p15.5 and Comparison to Human Dopaminergic Neurons

BACKGROUND: We initiated differentiation of human embryonic stem cells (hESCs) into dopamine neurons, obtained a purified population of neuronal precursor cells by cell sorting, and determined patterns of gene transcription. METHODOLOGY: Dopaminergic differentiation of hESCs was initiated by culturing hESCs with a feeder layer of PA6 cells. Differentiating cells were then sorted to obtain a pure population of PSA-NCAM-expressing neuronal precursors, which were then analyzed for gene expression using Massive Parallel Signature Sequencing (MPSS). Individual genes as well as regions of the genome which were activated were determined. PRINCIPAL FINDINGS: A number of genes known to be involved in the specification of dopaminergic neurons, including MSX1, CDKN1C, Pitx1 and Pitx2, as well as several novel genes not previously associated with dopaminergic differentiation, were expressed. Notably, we found that a specific region of the genome located on chromosome 11p15.5 was highly activated. This region contains several genes which have previously been associated with the function of dopaminergic neurons, including the gene for tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, IGF2, and CDKN1C, which cooperates with Nurr1 in directing the differentiation of dopaminergic neurons. Other genes in this region not previously recognized as being involved in the functions of dopaminergic neurons were also activated, including H19, TSSC4, and HBG2. IGF2 and CDKN1C were also found to be highly expressed in mature human TH-positive dopamine neurons isolated from human brain samples by laser capture. CONCLUSIONS: The present data suggest that the H19-IGF2 imprinting region on chromosome 11p15.5 is involved in the process through which undifferentiated cells are specified to become neuronal precursors and/or dopaminergic neurons

ABCC8 (SUR1) and KCNJ11 (KIR6.2) mutations in persistent hyperinsulinemic hypoglycemia of infancy and evaluation of different therapeutic measures

Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) can occur as a result of mutations in the subunits that form the ATP-sensitive potassium. channel (K-ATP(+)) in pancreatic beta-cells which play a major role in modulating insulin secretion from the beta-cells. Mutations have been shown in the genes for these subunits, namely for the plasma membrane sulfonylurea receptor (SUR1), ABCC8, and its associated inwardly rectifying potassium channel (KIR6.2) KCNJ11 Drugs which act on K-ATP(+) channels, such as diazoxide, seem to need intact ABCC8 to be able to show their effects. Thus, it would be desirable to know the exact locus of the abnormality in the beta-cell to be able to choose the right therapeutic agent or to perform early pancreatectomy. The aim of this study was to search for the correlation between the mutations of the K-ATP(+) channel and the outcome of therapeutic measures in patients with PHHI followed for a duration of 4 months to 7.3 years. Thirteen patients (5 F, 8 M) with PHHI with a median age of 2.5 months (8 days-12.1 years) were included in the study. Therapy for PHHI was initiated either with diazoxide (n = 9) or with calcium channel blocker (n = 4) as the agent of first choice. Three patients unresponsive to drugs underwent 95% pancreatectomy. Mutation analysis Was performed by polymerase chain reaction (PCR) and single strand conformation polymorphism (SSCP) in DNA samples extracted from patients' peripheral leukocytes. The PCR products were directly sequenced. Screening of ABCC8 and KCNJ11 for mutations revealed abnormalities in the ABCC8 gene in three patients out of 13: homozygosity for the 155del1 mutation, compound heterozygosity for T267-->G/A4612-2-->G, and compound heterozygosity for G4310-->A/R1494Q. No mutations in the KCNJ11 gene were identified. Of the three patients who underwent pancreatectomy, two had identified mutations and one did not have any known mutation. In two patients in whom hyperinsulinism recurred after surgery and in the rest of the children, therapy with either diazoxide or calcium channel blocker proved to be effective in controlling hypoglycemia over the follow-up period. Thus it may be concluded that mutations in the ABCC8 gene were not predictive of the response to drugs. Unidentified mutations in the K-ATP(+) channels other than those screened or other functional abnormalities in these channels may account for the different therapeutic responses

ABCC8 (SUR1) and KCNJ11 (KIR6.2) Mutations in Persistent Hyperinsulinemic Hypoglycemia of Infancy and Evaluation of Different Therapeutic Measures

Persistent hyperinsulinemic hypoglycemia of infancy (PHHI) can occur as a result of mutations in the subunits that form the ATP-sensitive potassium. channel (K-ATP(+)) in pancreatic beta-cells which play a major role in modulating insulin secretion from the beta-cells. Mutations have been shown in the genes for these subunits, namely for the plasma membrane sulfonylurea receptor (SUR1), ABCC8, and its associated inwardly rectifying potassium channel (KIR6.2) KCNJ11 Drugs which act on K-ATP(+) channels, such as diazoxide, seem to need intact ABCC8 to be able to show their effects. Thus, it would be desirable to know the exact locus of the abnormality in the beta-cell to be able to choose the right therapeutic agent or to perform early pancreatectomy. The aim of this study was to search for the correlation between the mutations of the K-ATP(+) channel and the outcome of therapeutic measures in patients with PHHI followed for a duration of 4 months to 7.3 years. Thirteen patients (5 F, 8 M) with PHHI with a median age of 2.5 months (8 days-12.1 years) were included in the study. Therapy for PHHI was initiated either with diazoxide (n = 9) or with calcium channel blocker (n = 4) as the agent of first choice. Three patients unresponsive to drugs underwent 95% pancreatectomy. Mutation analysis Was performed by polymerase chain reaction (PCR) and single strand conformation polymorphism (SSCP) in DNA samples extracted from patients' peripheral leukocytes. The PCR products were directly sequenced. Screening of ABCC8 and KCNJ11 for mutations revealed abnormalities in the ABCC8 gene in three patients out of 13: homozygosity for the 155del1 mutation, compound heterozygosity for T267-->G/A4612-2-->G, and compound heterozygosity for G4310-->A/R1494Q. No mutations in the KCNJ11 gene were identified. Of the three patients who underwent pancreatectomy, two had identified mutations and one did not have any known mutation. In two patients in whom hyperinsulinism recurred after surgery and in the rest of the children, therapy with either diazoxide or calcium channel blocker proved to be effective in controlling hypoglycemia over the follow-up period. Thus it may be concluded that mutations in the ABCC8 gene were not predictive of the response to drugs. Unidentified mutations in the K-ATP(+) channels other than those screened or other functional abnormalities in these channels may account for the different therapeutic responses

[Hypoglycémie hyperinsulinémique persistante du nouveau-né et du nourrisson]

Persistent hyperinsulinemic hypoglycaemia of infancy (PHHI) is the most frequent cause of hypoglycaemia in infancy. Clinical presentation is heterogeneous with variable onset of hypoglycaemia and response to diazoxide, and presence of sporadic or familial forms. Underlying histopathological lesions can be focal or diffuse. Focal lesions are characterised by focal hyperplasia of pancreatic islet-like cells, whereas diffuse lesions implicate the whole pancreas. The distinction between the two forms is important because surgical treatment and genetic counselling are radically different Focal lesions correspond to somatic defects which are totally cured by limited pancreatic resection, whereas diffuse lesions require a subtotal pancreatectomy exposing to high risk of diabetes mellitus. Diffuse lesions are due to functional abnormalities involving several genes and different transmission forms. Recessively inherited PHHI have been attributed to homozygote mutations for the beta-cell sulfonylurea receptor (SUR1) or the inward-rectifying potassium-channel (Kir6.2) genes. Dominantly inherited PHHI can implicate the glucokinase gene, particularly when PHHI is associated with diabetes, the glutamate dehydrogenase gene when hyperammonaemia is associated, or another locus. (C) 1998 Elsevier, Paris