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“This article reports the chemical components identified in the essential oil from the leaf and stem barks of Polyalthia harmandii (Pierre) Fin. and Gagnep., Polyalthia jucunda (Pierre) Fin. and Gagnep. and Polyalthia thorelii (Pierre) Fin. and Gagnep. The compounds identified in all the samples were alpha-pinene (0.2-3.2%), myrcene (0.3-4.1%), (E)-beta-ocimene (0.2-9.6%), bicycloelemene (0.2-18.0%), beta-elemene

(0.3-4.9%), beta-caryophyllene (0.1-17.8%), germacrene D (4.4-20.1%), bicyclogermacrene (4.2-27.9%) and delta-cadinene (0.2-4.5%). Besides, benzyl benzoate (9.7%) and ishwarane (8.0%), respectively, were the other prominent compounds in the leaf and stem PD0325901 mw of P. harmandii. In addition, delta-3-carene (8.2%), alpha-amorphene (6.5%), beta-phellandrene (5.5%) and beta-pinene (5.1%) were identified in P. jucunda leaf, while sabinene (30.9%) and beta-phellandrene (10.2%) occurred largely in the stem. Moreover, gamma-elemene (22.3% and 12.3%), germacrene D (10.5% and 6.9%) and spathulenol (9.1% and 11.8%) were identified in the leaf and stem of P. thorelii, while alpha-terpinene (7.8%) and

beta-gurjunene (5.2%) were identified only in the leaf oil.”
“Background: Chromosomal imbalances, recognized as the major cause of mental retardation, are often due to submicroscopic deletions or duplications not evidenced by conventional Akt inhibitor cytogenetic methods. To date, interstitial deletion of long arm of chromosome 2 have been reported for more than 100 cases, although studies reporting small interstitial deletions involving the 2q24.1q24.2 region are rare. With the widespread clinical use of comparative genomic hybridization chromosomal microarray technology, several cryptic chromosome imbalances have outlined new genotype-phenotype correlations and isolated a number of distinctive clinical conditions.

Results: here we report on a girl with mental retardation Lonafarnib datasheet and generalized hypotonia. A genome-wide screen for copy number variations (CNVs) using single nucleotide polymorphisms (SNPs) array revealed a 7.5 Mb interstitial deletion of chromosome

region 2q24.1q24.2 encompassing 59 genes, which was absent in parents. The gene content analysis of the deleted region and review of the literature revealed the presence of some genes that may be indicated as good candidate in generating the main clinical features of the patient.

Discussion: the present case represents a further patient described in the literature with an interstitial deletion of chromosome 2q24.1q24.2. Our patient shares some clinical features with the previously reported patients carriers of overlapping 2q24 deletion. Although more cases are needed to delineate the full-blown phenotype of 2q24.1q24.2 deletion syndrome, published data and present observation suggest that hemizygosity of this region results in a clinically recognizable phenotype.