Most of the SSRs had lower PIC value (less than 0.30) and the maximum PIC value was observed for JGM_A281, JGM_A326 (0.63) followed by JGM_B300 (0.62), JGM_B361 (0.58), JGM_A244 (0.55), JGM_B595 (0.55) and JGM_B176 (0.55). The genetic similarity coefficient among the accessions off. curcas and one accession off. integerrima ranged from 0.11 to 0.92 with an average of 0.57 +/- 0.31. The phenogram classified all the 7 accessions off. curcas in one cluster and the J. integerrima remained as an out group. The BLASTX analysis of SSR containing sequences showed maximum similarity of 50% with Ricinus communis (Euphorbiaceae) followed by Populus trichocarpa (22%), Vitis
vinifera (16%) and Arabidopsis spp. (4.5%). This study may enrich the validated repertoire of SSR markers in J. curcas and could be used in various genetic buy PP2 studies including construction of linkage map, diversity analysis, and QTL/association mapping. (C) 2013
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“Background: Iron supplementation is recommended during pregnancy to meet the needs of the rapidly growing fetus. However, its intake is associated with the generation of destructive Alpelisib free radicals, i.e., oxidative damage to the fetal brain. Folic acid supplementation is needed during pregnancy to reduce the risk of neural tube defects. Hypothesis: Intake of folic acid can ameliorate the morphological features of cell damage in the striatal tissue (brain of neonatal rats) associated with the intake of iron. Objectives and methods: To test this hypothesis, an animal model (pregnant Albino rats) was established. The animals were divided into three groups: group A, control animals treated with saline only; group B, animals treated with iron gluconate; and group C, animals
treated concomitantly with iron gluconate and Buparlisib nmr folic acid. The striatal brain tissues of the neonates were examined for features of cellular damage, using immunohistological and ultrastructural methods. Results: The authors found significant variations among the three groups. The intake of iron (group B) and its deposition in the striatal tissue (neurons and glial cells) was associated with changes indicative of both cellular injury and regeneration. The former includes neuronal apoptosis and necrosis, and destruction of the organelles, including the mitochondria, endoplasmic reticulum, Golgi apparatus, and lysosomes of the neurons and glial cells. The latter includes microgliosis, astrogliosis, upregulation of glial fibrillary acidic protein, and inducible nitric oxide synthase. These changes were absent in the striatal tissue of the control group (group A) and in animals treated concomitantly with both iron gluconate and folic acid (group C). Conclusion: Intake of folic acid can protect the neonatal striatal tissue against iron-induced oxidative stress damage.