Breeding Strategy of Acacia Hybrid (Acacia mangium × A. auriculiformis) to Increase Forest Plantation Productivity in Indonesia

Acacia hybrid (Acacia mangium× A.auriculiformis) shows better growth and wood properties, and tolerance to pest and disease. Currently, acacia hybrid breeding strategy was developed through naturally hybrid selected from trees grown in plantation. However, mass propagation of acacia hybrid using such kind of strategy was not satisfied due to ageing effect. This study was aimed to develop a new acacia hybrid breeding strategy using controlled pollination hybridization technique. The strategy was developed through a series of research: flowering, crossing, hybrid identification, clone multiplication, and clonal test. The results of study showed that the series of research for developing acacia hybrid breeding strategy was achieved. Flowering time synchronization provided a high probability for the success of controlled pollination hybridization. Leaves taxonomy at seedling stage revealed to be an efective way to identify acacia hybrid with acuracy of 92.2%. The acacia hybrid was succesfully propagated using shoot cutting at rate of 78.1%. The best selected clones of acacia hybrid outperformed in height growth at rates of 17.28% over to superior pure parents, which is equivalent to the estimated stand productivity at around 48 m3 ha-1 y-1. The series of research provided a new effective and efficient breeding strategy for acacia hybrid.Keywords: Acacia auriculiformis,  Acacia mangium, acacia hybrid, controlled pollination, breeding strategyDOI: 10.7226/jtfm.19.2.128</p

Caenorhabditis elegans reporter fusion genes generated by seamless modification of large genomic DNA clones

By determining spatial-temporal expression patterns, reporter constructs provide significant insights into gene function. Although additionally providing information on subcellular distribution, translational reporters, where the reporter is fused to the gene coding sequence, are used less frequently than simpler constructs containing only putative promoter sequences. Because these latter constructs may not contain all necessary regulatory elements, resulting expression patterns must be interpreted cautiously. To ensure inclusion of all such elements and provide details of subcellular localization, construction of translational reporters would, preferably, utilize genomic clones, containing the complete locus plus flanking regions and permit seamless insertion of the reporter anywhere within the gene. We have developed such a method based upon λ Red-mediated recombineering coupled to a robust two-step counter-selection protocol. We have inserted either gfp or cfp precisely at the C-termini of three Caenorhabditis elegans target genes, each located within different fosmid clones, and examined previously with conventional reporter approaches. Resulting transgenic lines revealed reporter expression consistent with previously published data for the tagged genes and also provided additional information including subcellular distributions. This simple and straightforward method generates reporters highly likely to recapitulate endogenous gene expression and thus represents an important addition to the functional genomics toolbox

Tumeurs stromales gastro-intestinales familiales (à propos de 2 cas et revue de la littérature)

LILLE2-BU Santé-Recherche (593502101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Heterotopic Gastric Mucosa of the Proximal Esophagus: An Under recognized Entity

Heterotopic gastric mucosa (HGM) is an islet of gastric mucosa within the esophageal mucosa. These lesions can sit throughout the digestive tract and rarely in the upper third of the esophagus. The pathophysiology of HGM remains poorly understood. Our study aims to estimate the prevalence of HGM, clinical signs, endoscopic, microscopic aspects and different epidemiological factors associated. All patients from a single endoscopy center with HGM of the upper third of the esophagus were included over a 5-month evaluation period. All lesions seen in endoscopy were confirmed by histological analysis. The prevalence was 1.3% with a clear male predominance. 80% of patients were symptomatic and received medical treatment, clinical evolution was good. No case of dysplasia was identified and no complication was observed. Due to insufficient data in the evolutionary literature, the management of HGM remains debated and could resemble that of Barett&rsquo;s esophagus for monitoring and therapeutic management, particularly in the event of symptoms or dysplasia

Status epilepticus-induced alterations in metabotropic glutamate receptor expression in young and adult rats

In adult rats, kainic acid induces status epilepticus and delayed, selective cell loss of pyramidal neurons in the hippocampal CA3. In pup rats, kainate induces status epilepticus but not the accompanying neuronal cell death. The precise mechanisms underlying this age-dependent vulnerability to seizure-induced cell death are not understood. Metabotropic glutamate receptors (mGluRs) are developmentally and spatially regulated throughout the hippocampus and are implicated in seizure-induced damage. In the present study we used in situ hybridization to examine possible changes in mGluR expression at the level of the hippocampus after status epilepticus in postnatal day 10 (P10) pup and adult (P40) rats. Status epilepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs. In pup and adult rats, status epilepticus induced a reduction in expression of mGluR2 mRNA in granule cells of the dentate gyrus. This change could lead to augmented glutamate release at mossy fiber synapses on CA3 pyramidal cells and thereby promote hyperexcitation. In pup but not adult rats, mGluR4 mRNA expression was enhanced in CA3 pyramidal neurons. Upregulation of presynaptic mGluR4 in pup CA3 neurons could lead to reduced transmitter release from CA3 axons, including recurrent collaterals, thereby reducing vulnerability of neonatal CA3 neurons to seizure-induced damage. These findings indicate that status epilepticus affects mGluR expression in a gene- and cell-specific manner, and that these changes vary with the developmental stag