Detection of human papillomavirus DNA in intraosseus ameloblastoma

Human Papillomavirus (HPV) infection has been shown as a risk factor in oral carcinogenesis. The association between HPV and benign and malignant neoplasm of oral mucosa, especially surface epithelium-derived tumors, is well established. The role of HPV in pathogenesis of odontogenic cysts and tumors has been published in few articles. The aim of this study was detection of HPV in Iranian patients with intrabony ameloblastoma and investigation of specific risk factors associated with ameloblastoma. One hundred intrabony ameloblastoma and 50 age-sex matched samples as controls were evaluated by polymerase chain reaction for the detection and typing of HPV. Fisher exact and chi square tests were used to assess the data. HPV DNA was detected in 32% of patients and 10% of controls. HPV-6 was the most prevalent genotype (31.6%) in infected cases. It was followed by HPV-11 (12.5%), HPV-16 (12.5%) and HPV-31 (3.1%). We found a significant association between presence of HPV and location of tumor (p = 0.02), traumatic history (p = 0.03) and ododontic therapy (p = 0.01). These findings indicated that HPV-6 probably is one of the most important etiologic agents in causing intraosseous ameloblastoma in Iranian population. © 2006 Academic Journals Inc., USA

A semi-dominant mutation in the general splicing factor SF3a66 causes anterior-posterior axis reversal in one-cell stage C. elegans embryos.

Establishment of anterior-posterior polarity in one-cell stage Caenorhabditis elegans embryos depends in part on astral microtubules. As the zygote enters mitosis, these microtubules promote the establishment of a posterior pole by binding to and protecting a cytoplasmic pool of the posterior polarity protein PAR-2 from phosphorylation by the cortically localized anterior polarity protein PKC-3. Prior to activation of the sperm aster, the oocyte Meiosis I and II spindles assemble and function, usually at the future anterior pole, but these meiotic spindle microtubules fail to establish posterior polarity through PAR-2. Here we show that a semi-dominant mutation in the general splicing factor SF3a66 can lead to a reversed axis of AP polarity that depends on PAR-2 and possibly on close proximity of oocyte meiotic spindles with the cell cortex. One possible explanation is that reduced levels of PKC-3, due to a general splicing defect, can result in axis reversal due to a failure to prevent oocyte meiotic spindle microtubules from interfering with AP axis formation

Attention-deficit/hyperactivity disorder (ADHD) association with the DAT1 core promoter -67 T allele

Association between attention deficit hyperactivity disorder (ADHD) and the 10-repeat allele of a polymorphism (a 40 bp variable number of tandem repeats) in the dopamine transporter gene (DAT1) has been reported by several groups. In this study, we examined whether either allele of the DAT1 core promoter -67 functional polymorphism is associated with ADHD in a case/control study. The allele and genotype frequencies of the polymorphism were studied in 110 patients and 120 controls, which were matched on the basis of sex, age and ethnicity. The genotype frequencies in the patients group were as follows: AA 19.2; AT 65.2; TT 15.4 vs. the genotype frequencies in the control group: AA 47.5; AT 43.3; TT 9.2 �2 = 20.73, df = 2, P � 0.0001. The T allele of the -67A/T polymorphism revealed an �1.56-fold excess in the patients group comparing with the controls �2 = 14.50, df = 1 (P � 0.001). For the first time, these findings provide tentative evidence of the contribution of the DAT1 gene core promoter polymorphism to the etiopathophysiology of ADHD at least in the Iranian population that we have studied. Further work is warranted to confirm this finding and to assess its generalization to other ethnic groups. © 2006 Elsevier B.V. All rights reserved

Reversed polarity of P0 asymmetric cell division in <i>or430</i>ts zygotes.

<p>Time-lapse DIC images of wild type (A) and <i>or430</i>ts mutants (B–D), showing <i>or430</i>ts embryos with reversed (B), symmetric (C) and normal (D) cell division. Arrows indicate polar bodies. (E–G) Time-lapse confocal images of P₀ mitotic spindle orientation in wild-type and <i>or430</i>ts zygotes expressing a GFP fusion to ß-tubulin (and a GFP fusion to PIE-1 in F that labels P granules and cytoplasmic PIE-1)). Vertical lines in each image indicate 50% egg length. (H) P₀ mitotic spindle orientations in wild-type and <i>or430</i>ts zygotes (each n = 22). (I) P₀ cleavage furrow position along AP axis in wild-type (n = 26) and <i>or430</i>ts zygotes (n = 30). (J) Pronuclear meeting site along AP axis in wild-type (n = 22) and <i>or430</i>ts zygotes (n = 22). (K) Maximum P₀ mitotic spindle length in wild-type and <i>or430</i>ts zygotes (n = 22). (L) Duration of P₀ mitosis from pronuclear meeting to cleavage furrow ingression in wild-type and <i>or430</i>ts zygotes (each n = 22). In this and subsequent figures, t = 0 corresponds to pronuclear meeting.</p

Identification of <i>repo-1(or430</i>ts<i>)</i> causal mutation in the SF3a66 <i>C. elegans</i> ortholog F11a10.2.

<p>(A) Schematic of <i>repo-1</i> map position on chromosome IV and partial amino acid sequences of predicted proteins in wild-type and <i>or430</i>ts F11a10.2/<i>repo-1</i>, and in fly, human and fission yeast orthologs. Location of <i>tm4961</i> deletion indicated; whole genome sequencing of <i>repo-1(or430</i>ts<i>)</i> revealed no sequence changes in the neighboring gene, <i>lex-1</i>, which also is disrupted by the <i>tm4961</i> deletion (data not shown). (B) Loss of polarity reversal after RNAi knockdown of F11a10.2 in <i>repo-1(or430</i>ts<i>)</i> mutants, and in <i>repo-1(tm4961)/repo-1(tm4961)</i> mutants, assessed by measuring P₀ cleavage furrow position. Note that the single embryo with an apparent reversal in <i>repo-1(tm4961)</i> mutants may represent an example of a posteriorly positioned polar body, which occurs at low frequency in wild-type embryos. WT and <i>or430</i>ts data are same as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0106484#pone-0106484-g001" target="_blank">Figure 1I</a>. L4440 refers to the empty vector used as a negative control for feeding RNAi.</p

PKC-3 opposes and oocyte meiotic spindles promote AP axis reversal in <i>repo-1(or430</i>ts<i>)</i> zygotes.

<p>(A) Time-lapse confocal images of wild-type and <i>or430</i>ts oocyte Meiosis I and II in zygotes expressing GFP and mCherry fusions to ß-tubulin and Histone2B; t = 0 at ovulation. (B) P₀ cleavage furrow position along AP after reducing <i>pkc-3</i> gene dosage. P = 0.006 for an independent t test to compare the difference of the furrow position for <i>or430</i> versus <i>or430; pkc-3(−/+)</i>. (C) P₀ cleavage furrow position along AP axis after RNAi knockdown of <i>lin-5</i> and <i>unc-116</i>. P = 0.285 for an independent t test to compare the difference of the furrow position for <i>or430</i> versus <i>or430; unc-116(RNAi); lin-5(RNAi)</i>. WT and <i>or430</i>ts data in (B) and (C) are same as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0106484#pone-0106484-g001" target="_blank">Figure 1I</a>.</p

AP axis reversal in <i>repo-1(or430</i>ts<i>)</i> zygotes.

<p>(A) Time-lapse confocal images of wild type and <i>or430</i>ts zygotes expressing GFP fusions to ß-tubulin and PAR-2. (B) Time-lapse confocal images of wild type and <i>or430</i>ts zygotes expressing GFP fusions to ß-tubulin and PIE-1. (C) Kymographs of pseudocleavage furrow movement in wild-type zygotes and its absence in <i>or430</i>ts zygotes. Time in seconds before pronuclear meeting for both wild-type and <i>or430</i>ts are shown in wild-type images. (D) Quantification of GFP: PAR-2 levels in wild-type (n = 10) and <i>or430</i>ts (n = 10) zygotes; see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0106484#s4" target="_blank">Materials and Methods</a> for details. (E) Location along AP axis of P0 cytokinesis furrow ingression in wild-type and mutant zygotes. Arrows indicate polar bodies. P<0.001 for an independent t test to compare the difference of the furrow position for <i>or430</i> versus <i>or430; par-2(RNAi)</i>. Data for WT and <i>or430</i>ts are same as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0106484#pone-0106484-g001" target="_blank">Figure 1I</a>.</p