Non-Syndromic Familial Unerupted Teeth: A Rare Contidion

A tooth that remains unerupted beyond the normal time of eruption and fails to erupt is called an impacted tooth. Maxillofacial surgeons encounter the problem of impacted teeth very often. Usually, impacted teeth involve the permanent dentition and they are rare in the primary dentition. Impaction of a primary tooth is a very rare entity. These rare cases are seen more frequently in primary second molars, followed by the order of the lower and upper centralincisor, lateral incisor and the canine teeth. Evolutionary and hereditary factors may cause uneruption. In this report, three cases of impacted primary teeth that belong to same familial members are presented. Father and sons. We extracted boy’s teeth but father refused treatment

Genomic alterations in low-grade, anaplastic astrocytomas and glioblastomas.

RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are.To extend our understanding of potential stepwise genetic alterations that may underlie tumor progression from low-grade astrocytomas to glioblastomas, histopathologic and comparative genomic hybridization analyses were performed on tumor specimens from 68 primary lesions, including 40 glioblastomas, 10 anaplastic and 18 low-grade astrocytomas. The number of aberrations per case increased towards the higher grade tumors (grade II: 1.66+/-1.49; grade III: 2.80+/-1.68; grade IV: 3.02+/-1.07; F=6.955, p=0.002). A gain of 7/7q was common and the most frequently seen aberration in low-grade astrocytomas, whereas loss of 10q was the most frequently seen anomaly in anaplastic astrocytomas and glioblastomas. Chromosome 7p amplification was only detected in glioblastomas. Chromosome 10/10q deletion and combination of 1p, 19q and 17p deletions were specific to high-grade astrocytic tumors. Sequences of chromosome 7 and 10 seem to have pivotal roles in the biology of human gliomas. The genomic copy deletions of chromosomes 1p and 19q might provide an alternative mechanism in the genesis of astrocytomas

Is there a genetic predisposition for Turkish patients with sarcoidosis in the 329-bp region containing the BTNL2 rs2076530 polymorphism?

Background/aim: Sarcoidosis is a complex, multifactorial immune disorder with unknown etiology. A single nucleotide polymorphism (G -> A, rs2076530) in the butyrophilin-like 2 (BTNL2) gene results in a truncating protein formation. It has been previously reported that this variation may be a risk factor for sarcoidosis in certain ethnic groups. This study was conducted to determine whether there is any genetic predisposition for the BTNL2 rs2076530 polymorphism in the 329-bp region in Turkish patients with sarcoidosis

Erken Başlangıçlı Koroner Arter Hastalığında MiRNA Profili Farklı mı?

Objective: MicroRNAs have been explored as potential biomarkers for many pathological processes including coronary artery disease. In this study, we aimed to compare the circulating levels of selected atherosclerosis-associated miRNAs in patients with a history of early-onset coronary artery disease with that of age- and sex-matched healthy controls and older patients with late-onset coronary artery disease. Methods: Study population consisted of 30 patients with early onset coronary artery disease, 31 age- and sex-matched healthy controls, and 30 patients with late-onset coronary artery disease. Plasma levels of 13 microRNAs (endothelial cell-related miR-126, -92a/b; vascular smooth muscle cell-related miR-145; inflammation-related miR-16, -21, -125b, -146a/b, -147b, -150, -155; lipometabolism-related miR-27b, -122, -370) were evaluated by using real-time polymerase chain reaction. Results: In patients with early onset coronary artery disease, plasma expressions of the -lipometabolism-related miR-27b, miR-122; inflammation-related miR-125b, miR-146a/b, miR-147b, miR-150, miR-155; and VSMC-related miR-145 were significantly downregulated and endothelial cell-related miR-126 was significantly upregulated compared to age- and sex-matched healthy controls. Circulating microRNA profile of patients with early onset coronary artery disease was also different from that of older patients with late-onset coronary artery disease. Plasma levels of miR-21, miR-27b, miR-122, miR-125b, miR-146b, miR-147b, and miR-155 were lower and plasma levels of miR-16 and miR-92a were higher in patients with early onset coronary artery disease compared to older patients with late-onset coronary artery disease. Conclusion: MicroRNAs are promising biomarkers for early onset coronary artery disease

Investigation of key miRNAs and target genes in bladder cancer using miRNA profiling and bioinformatic tools

Despite the association of several miRNAs with bladder cancer, little is known about the miRNAs' regulatory networks. In this study, we aimed to construct potential networks of bladder-cancer-related miRNAs and their known target genes using miRNA expression profiling and bioinformatics tools and to investigate potential key molecules that might play roles in bladder cancer regulatory networks. Global miRNA expression profiles were obtained using microarray followed by RT-qPCR validation using two randomly selected miRNAs. Known targets of deregulated miRNAs were utilized using DIANA-TarBase database v6.0. The incorporation of deregulated miRNAs and target genes into KEGG pathways were utilized using DIANA-mirPath software. To construct potential miRNA regulatory networks, the overlapping parts of three selected KEGG pathways were visualized by Cytoscape software. We finally gained 19 deregulated miRNAs, including 5 ups-and 14 down regulated in 27 bladder-cancer tissue samples and 8 normal urothelial tissue samples. The enrichment results of deregulated miRNAs and known target genes showed that most pathways were related to cancer or cell signaling pathways. We determined the hub CDK6, BCL2, E2F3, PTEN, MYC, RB, and ERBB3 target genes and hub hsa-let-7c, hsa-miR-195-5p, hsa-miR-141-3p, hsa-miR-26a-5p, hsa-miR-23b-3p, and hsa-miR-125b-5p miRNAs of the constructed networks. These findings provide new insights into the bladder cancer regulatory networks and give us a hypothesis that hsa-let-7c, hsa-miR-195-5p, and hsa-miR-125b-5p, along with CDK4 and CDK6 genes might exist in the same bladder cancer pathway. Particularly, hub miRNAs and genes might be potential biomarkers for bladder cancer clinics