Frequent allelic imbalances including loss of heterozygosity (LOH) and microsatellite instability (MSI) on the short arm of chromosome 3 (3p) have been found in several types of human cancer. This study was designed to identify the tumor suppressor locus (or loci) on 3p associated with tongue squamous cell carcinoma (SCC). Among 16 patients with tongue SCC tested, 7 (44%) of 16 informative cases showed LOH at one or more loci. Deletion mapping of these 16 tumors revealed two discrete, commonly deleted regions on the chromosome arm. Our data support the notion that tumor suppressor gene(s) contributing to the progression of tongue squamous cell carcinoma reside on 3p24 and 3p25.

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The p16/CDKN2 (cycline dependent kinase number 2) gene is known to be one of the negative regulators of the cell cycle. Aberrant 5´CpG island methylation is one of the most important mechanisms of p16/CDKN2 gene promoter region alteration. We studied 8 oral squamous cell carcinoma cell lines and 25 primary tumor tissues for the p16/CDKN2 gene and its expression by PCR-SSCP, MSP, RT-PCR, and immunohistochemical methods to determine the mechanism and the potential biological significance of p16/CDKN2 gene inactivation. In primary tumors, no p16/CDKN2 gene mutations were found by PCR-SSCP. However, hypermethylation of the CpG sites of p16/CDKN2 gene was observed in 48% (12/25) cases of primary tumors and in 50% (4/8) of cell lines. To verify the p16 mRNA expression, we employed RT-PCR and observed decreased or lacked p16 mRNA in 44% (11/25) of primary tumor tissues. In addition, hypermethylation was observed in 6 of the above 11 cases (55%). An immunohistochemistry assay was also performed with the primary tumor tissues, and a semi-quantitative method was used to evaluate the staining intensity of p16 protein. We observed 52% (13/25) negative nucleal staining. When we compared these results with clinicopathological stages, there was no statistical significance. These findings suggest that hypermethylation of p16/CDKN2 promoter region may be associated with p16/CDKN2 gene alteration.

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Behçet's disease is a chronic relapsing vasculitis characterized by recurrent aphthous oral and genital ulcerations with uveitis. Multiple organs can be involved. Entero-Behçet's disease is often uncontrollable, relapsing, and can cause acute intestinal bleeding or perforation. We utilized a combination therapy including 600mg of pentoxifylline per day, in two doses, to treat three female patients and observed the subsequent changes in clinical symptoms, serum C reactive protein levels, and endoscopic findings. In all three patients, clinical symptoms as well as serum C reactive protein levels improved immediately. Endoscopically, lower intestinal lesions were significantly reduced or healed in all of them. Combination therapy including pentoxifylline appears to be clinically effective in the patients with entero-Behçet's disease.

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This case report describes the use of an osseointegrated implant to maximize anchorage in a 24-year-old female orthodontic patient with an Angle Class II, Division 1 malocclusion. Preadjusted edgewise appliance therapy was performed by extraction of only the maxillary first premolars. The osseointegrated implant was placed in the mediansagittal region of the hard palate for maximum orthodontic anchorage and connected to maxillary first molar bands via a transpalatal arch. Total treatment time was 2 years and 8 months. Cephalometric superimposition revealed the achievement of maximum molar anchorage in the maxilla, resulting in satisfactory occlusal and facial improvements. Histological analysis of the implant-bone interface demonstrated that the fixture was successfully osseointegrated. In conclusion, the osseointegrated implant placed in the median-sagittal palate was shown to be an effective orthodontic system that can be used clinically as a rigid intraoral anchorage

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The calcium ion influx through voltage-dependent calcium channels (VDCCs) has a vital role in the control of neurotransmitter release and membrane excitability. The modulation of VDCCs controls the extent of calcium entry and thus provides a way of regulating neuronal function. Prepulse facilitation is a phenomenon in which a strong depolarizing pulse induces a form of the VDCCs that exhibits an increased opening probability in response to a given test potential that persists for several seconds after repolarization. In this study, we have studied the characterization of prepulse facilitation of VDCCs currents (I_Ca) in hamster submandibular ganglion (SMG) neurons, using whole-cell patch clamp recordings. In SMG neurons, application of a strong depolarizing prepulse caused a I_Ca. In 8 SMG neurons, rate of facilitation was 1.1±0.1. The greatest value of prepulse facilitation was obtained with prepulse to +100mV, 10ms duration in this neuron. The magnitude of facilitation was dependent on changing the interval between the -prepulse and the +prepulse and reached a maximum at a interval of 500ms.

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