Imaging characteristics of slow-growing soft tissue chondroma of the tongue: A case report.

INTRODUCTION: Extraskeletal soft tissue chondroma (STC) is a rare benign tumor. Soft-tissue chondromas rarely occur in the oral cavity. In this study, we aimed to confirm a slow-growing tongue mass using magnetic resonance imaging. PATIENT CONCERNS: A 60-year-old woman presented with a painful, slow-growing tongue mass that had persisted for 17 years. Intraoral examination revealed a pedunculated mass covered with mucosa on the right side of her tongue. DIAGNOSIS: CT and MRI revealed a lobulated heterogeneously enhancing mass without calcification. Compared with previous images obtained 17 years prior, the mass presented slow growth, more prominent enhancement, and lobulated contour. Histopathological examination confirmed the presence of STC. INTERVENTIONS: Excision of the mass surrounding normal tissue was performed under general anesthesia. OUTCOMES: During 1-year follow-up period, no recurrence was observed. CONCLUSIONS: In this study, STC lesions were slow-growing, and changed from weakly homogeneous enhancement and clean margins to markedly heterogeneous enhancement and lobulated margins over time.

Enhanced culturing of adipose derived mesenchymal stem cells on surface modified polystyrene Petri dishes fabricated by plasma enhanced chemical vapor deposition system.

Mesenchymal stem cells (MSCs) have received considerable attention as therapeutic cells for regenerative medicine and tissue engineering, because of their ability to replace damaged cells or regenerate surrounding cells. There are many technical difficulties in the mass production of high-quality stem cells because the stem cells must maintain an efficient proliferative cell state during in vitro culture. The results of this study show that plasma surface-modification enhanced significantly the culture of adipose-derived mesenchymal stem cells (ASCs) on the polystyrene (PS) Petri dishes. Ar, O2 , pyrrole, and 4,7,10-trioxa-1,13-tridecanediamine (TTDDA) were used as the gas and/or precursors for plasma modification. Specifically, surfaces of PS Petri dishes, coated with plasma polymerized pyrrole (ppPy) and plasma polymerized TTDDA (ppTTDDA) were found to contain amine and carboxyl functional groups, respectively. Ar and O2 plasma-treated PS Petri dishes have similar culture abilities (±1.2 times) to commercially available tissue culture polystyrene (TCPS) dishes, and PS Petri dishes coated with ppPy and ppTTDDA have significantly enhanced culture abilities (2.4 times) at 96 hr compared with TCPS dishes. Western blotting was performed using antibodies against stem cell marker proteins to confirm the stemness properties of stem cells, in the sense that the expressions of the antibody proteins such as CD44, CD73, and CD105 in plasma modified samples were similar to or higher than those in TCPS dishes.

Study on Effects of Carrier Gas Flow Rate on Properties of Low Dielectric Constant Film Deposited by Plasma Enhanced Chemical Vapor Deposition Using the Octamethylcyclotetrasiloxane Precursor.

In semiconductor industry, low-dielectric-constant SiCOH films are widely used as inter-metal dielectric (IMD) material to reduce a resistance-capacitance delay, which could degrade performances of semiconductor chips. Plasma enhanced chemical vapor deposition (PECVD) system has been employed to fabricate the low-dielectric-constant SiCOH films. In this work, among various parameters (plasma power, deposition pressure, substrate temperature, precursor injection flow rate, etc.), helium carrier gas flow rate was used to modulate the properties of the low-dielectric-constant SiCOH films. Octamethylcyclotetrasiloxane (OMCTS) precursor and helium were injected into the process chamber of PECVD. And then SiCOH films were deposited varying helium carrier gas flow rate. As helium carrier gas flow rate increased from 1500 to 5000 sccm, refractive indices were increased from 1.389 to 1.428 with enhancement of mechanical strength, i.e., increased hardness and elastic modulus from 1.7 and 9.1 GPa to 3.3 and 19.8 GPa, respectively. However, the relative dielectric constant (k) value was slightly increased from 2.72 to 2.97. Through analysis of Fourier transform infrared (FTIR) spectroscopy, the effects of the helium carrier gas flow rate on chemical structure, were investigated. It was thought that the increase in helium carrier gas flow rate could affect the density with changes of chemical structure and composition. In conclusion, regulation of helium carrier gas flow rate can effectively modulate k values and mechanical strength, which is needed for IMD material in semiconductor fabrication possess.

Plasma Polymerized SiCOH Films from Octamethylcyclotetrasiloxane by Dual Radio Frequency Inductively Coupled Plasma Chemical Vapor Deposition System.

We have fabricated porous plasma polymerized SiCOH (ppSiCOH) films with low-dielectric constants (low-k, less than 2.9), by applying dual radio frequency plasma in inductively coupled plasma chemical vapor deposition (ICP-CVD) system. We varied the power of the low radio frequency (LF) of 370 kHz from 0 to 65 W, while fixing the power of the radio frequency (RF) of 13.56 MHz. Although the ppSiCOH thin film without LF had the lowest k value, its mechanical strength is not high to stand the subsequent semiconductor processing. As the power of the LF was increased, the densities of ppSiCOH films became high, accordingly high in the hardness and elastic modulus, with quite satisfactory low-k value of 2.87. Especially, the ppSiCOH film, deposited at 35 W, exhibited the highest mechanical strength (hardness: 1.7 GPa, and elastic modulus: 9.7 GPa), which was explained by Fourier transform infrared spectroscopy. Since the low-k material is widely used as an inter-layer dielectric insulator, good mechanical properties are required to withstand chemical mechanical polishing damage. Therefore, we suggest that plasma polymerized process based on the dual frequency can be a good candidate for the deposition of low-k ppSiCOH films with enhanced mechanical strength.

Post-treatment with oxcarbazepine confers potent neuroprotection against transient global cerebral ischemic injury by activating Nrf2 defense pathway.

Oxcarbazepine (OXC), a voltage-gated sodium channel blocker, is an antiepileptic medication and used for the bipolar disorders treatment. Some voltage-gated sodium channel blockers have been demonstrated to display strong neuroprotective properties in models of cerebral ischemia. However, neuroprotective effects and mechanisms of OXC have not yet been reported. Here, we investigated the protective effect of OXC and its mechanisms in the cornu ammonis 1 subfield (CA1) of gerbils subjected to 5 min of transient global cerebral ischemia (tGCI). tGCI led to death of most pyramidal neurons in CA1 at 5 days after ischemia. OXC (100 and 200 mg/kg) was intraperitoneally administered once at 30 min after tGCI. Treatment with 200 mg/kg, not 100 mg/kg OXC, significantly protected CA1 pyramidal neurons from tGCI-induced injury. OXC treatment significantly decreased superoxide anion production, 4-hydroxy-2-nonenal and 8-hydroxyguanine levels in ischemic CA1 pyramidal neurons. In addition, the treatment restored levels of superoxide dismutases, catalase, and glutathione peroxidase. Furthermore, the treatment distinctly inhibited tGCI-induced microglia activation and significantly reduced levels of pro-inflammatory cytokines (interleukin-1ß and tumor necrosis factor-α). In particular, OXC treatment significantly enhanced expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream protein heme oxygenase-1 in ischemic CA1. The neuroprotective effects of OXC were abolished by brusatol (an inhibitor of Nrf2). Taken together, these results indicate that post-treatment of OXC can display neuroprotection against brain injuries following ischemic insults. This neuroprotection may be displayed by attenuation of oxidative stress and neuroinflammation, which can be mediated by activation of Nrf2 pathway.

The relationship between low survival and acute increase of tumor necrosis factor α expression in the lung in a rat model of asphyxial cardiac arrest.

Cardiac arrest (CA) is sudden loss of heart function and abrupt stop in effective blood flow to the body. The patients who initially achieve return of spontaneous circulation (RoSC) after CA have low survival rate. It has been known that multiorgan dysfunctions after RoSC are associated with high morbidity and mortality. Most previous studies have focused on the heart and brain in RoSC after CA. Therefore, the aim of this research was to perform serological, physiological, and histopathology study in the lung and to determine whether or how pulmonary dysfunction is associated with low survival rate after CA. Experimental animals were divided into sham-operated group (n=14 at each point in time), which was not subjected to CA operation, and CA-operated group (n=14 at each point in time), which was subjected to CA. The rats in each group were sacrificed at 6 hours, 12 hours, 24 hours, and 2 days, respectively, after RoSC. Then, pathological changes of the lungs were analyzed by hematoxylin and eosin staining, Western blot and immunohistochemistry for tumor necrosis factor α (TNF-α). The survival rate after CA was decreased with time past. We found that histopathological score and TNF-α immunoreactivity were significantly increased in the lung after CA. These results indicate that inflammation triggered by ischemia-reperfusion damage after CA leads to pulmonary injury/dysfunctions and contributes to low survival rate. In addition, the finding of increase in TNF-α via inflammation in the lung after CA would be able to utilize therapeutic or diagnostic measures in the future.

Revision Total Hip Arthroplasty Using Tantalum Augment in Patients with Paprosky III or IV Acetabular Bone Defects: A Minimum 2-year Follow Up Study.

PURPOSE: The purpose of this study is to report the short-term outcomes of revision total hip arthroplasty (THA) using tantalum augments in patients with severe acetabular bone defects. MATERIALS AND METHODS: We retrospectively analyzed 15 revision THAs performed in 15 patients using tantalum augments between June 2010 and December 2013. Acetabular bone defects were Paprosky type IIIA in 7 hips, type IIIB in 7, and type IV in 1. The causes of revision surgery were aseptic loosening in 12 hips and deep infection in 3. Revisions were first in 1 hip, second in 3, and third in 11. Six patients were male and 9 female with a mean age of 59 years (range, 48-75 years). Mean follow-up was 29 months (range, 24-48 months). RESULTS: Mean Harris hip score was improved from 34 points (range, 12-54 points) preoperatively to 84 points (range, 38-90 points) at final follow-up. On the final follow-up radiographs, there were 12 hips (80.0%) with stable fixation of the acetabular cup, 2 (13.3%) with secondary stability after mild acetabular protrusion, and 1 (6.7%) with radiolucency around the acetabular cup without mechanical symptoms. Complications included one patient with acute hematogenous infection managed by surgical debridement and long-term antibiotic therapy. There were no cases with nerve palsy or dislocation during the follow-up period. CONCLUSION: The present study showed satisfactory clinical and radiographic outcomes of revision THA using tantalum augments due to severe acetabular bone defects of Paprosky type III or IV at a minimum follow-up of 2 years.

High union rates of locking compression plating with cortical strut allograft for type B1 periprosthetic femoral fractures.

PURPOSE: Unified classification system (UCS) type B1 periprosthetic femoral fractures are associated with many complications, and management decisions continue to be controversial. The purpose of this study was to evaluate outcomes of UCS type B1 periprosthetic femoral fractures treated by locking compression plating with strut allograft augmentation. MATERIALS AND METHODS: We retrospectively reviewed 17 consecutive UCS type B1 periprosthetic femoral fractures treated by open reduction and internal fixation using a lateral locking compression plate supplemented with an anterior cortical strut allograft. There was one man and 16 women with an average age of 74 years (range, 57-92 years). All had a cementless hip arthroplasty, and eight of the arthroplasties were revisions. RESULTS: The mean duration of follow-up was 28 months (range, 12-74 months). All 17 fractures healed successfully at a mean of 20 weeks (range, 12-30 weeks). The mean post-operative Harris hip score was 86 points (range, 77-95 points). No mechanical complications such as failure of plate or screws and malalignment were noted. According to the graft-remodeling classification of Emerson et al., a partial bridging was observed in nine and a complete bridging in eight. Two patients required a removal of the plate due to irritation of the iliotibial band. No femoral stem loosening or deep infection was observed. CONCLUSION: Our findings indicate that open reduction and internal fixation of UCS type B1 periprosthetic femoral fractures using a lateral locking compression plate supplemented with anterior cortical strut allograft provides adequate mechanical stability of fracture fixation and enhances the fracture healing.

Integrated high-resolution array CGH and SKY analysis of homozygous deletions and other genomic alterations present in malignant mesothelioma cell lines.

High-resolution oligonucleotide array comparative genomic hybridization (aCGH) and spectral karyotyping (SKY) were applied to a panel of malignant mesothelioma (MMt) cell lines. SKY has not been applied to MMt before, and complete karyotypes are reported based on the integration of SKY and aCGH results. A whole genome search for homozygous deletions (HDs) produced the largest set of recurrent and non-recurrent HDs for MMt (52 recurrent HDs in 10 genomic regions; 36 non-recurrent HDs). For the first time, LINGO2, RBFOX1/A2BP1, RPL29, DUSP7, and CCSER1/FAM190A were found to be homozygously deleted in MMt, and some of these genes could be new tumor suppressor genes for MMt. Integration of SKY and aCGH data allowed reconstruction of chromosomal rearrangements that led to the formation of HDs. Our data imply that only with acquisition of structural and/or numerical karyotypic instability can MMt cells attain a complete loss of tumor suppressor genes located in 9p21.3, which is the most frequently homozygously deleted region. Tetraploidization is a late event in the karyotypic progression of MMt cells, after HDs in the 9p21.3 region have already been acquired.

Unfavorable prognosis of CRTC1-MAML2 positive mucoepidermoid tumors with CDKN2A deletions.

The CRTC1-MAML2 fusion oncogene underlies the etiology of mucoepidermoid salivary gland carcinoma (MEC) where it confers a favorable survival outcome as compared with fusion-negative MEC. While these analyses suggested that detection of CRTC1-MAML2 serves as a useful prognostic biomarker, we recently identified outlier cases of fusion-positive MEC associated with advanced-staged lethal disease. To identify additional genetic alterations that might cooperate with CRTC1-MAML2 to promote disease progression, we performed a pilot high-resolution oligonucleotide array CGH (aCGH) and PCR-based genotyping study on 23 MEC samples including 14 fusion-positive samples for which we had clinical outcome information. Unbiased aCGH analysis identified inactivating deletions within CDKN2A as a candidate poor prognostic marker which was confirmed by PCR-based analysis (CDKN2A deletions in 5/5 unfavorable fusion-positive cases and 0/9 favorable fusion-positive cases). We did not detect either activating EGFR mutations, nor copy number gains at the EGFR or ERBB2 loci as poor prognostic features for fusion-positive MEC in any of the tumor specimens. Prospective studies with larger case series will be needed to confirm that combined CRTC1-MAML2 and CDKN2A genotyping will optimally stage this disease.

Low-penetrant RB allele in small-cell cancer shows geldanamycin instability and discordant expression with mutant ras.

Certain kindreds with low-penetrant (lp) retinoblastoma carry mutant alleles which retain partial tumor suppressor activity and we previously showed that these alleles exhibit defective, temperature-sensitive binding in yeast. To investigate the molecular basis for incomplete penetrance, we studied three recurrent lp alleles and observed approximately 50% of wildtype activity measured by (i) phosphorylation at key regulatory sites, S780, S795, S807/S811, (ii) transcriptional co-activation, and (iii) 'flat-cell' differentiation in mammalian cells in vivo. In addition, we studied a small-cell carcinoma that is homozygous for the R661W allele providing the first analysis of the effect of a naturally occurring lp allele in a human tumor. While we detected abundant expression of the R661W protein, we noted marked instability of both endogenous and recombinant R661W following treatment in vivo with the Hsp90 inhibitor, geldanamycin and stabilization of R661W following heat shock. In addition, we observed a discordant phenotype in the tumor cells with induction of p16 and loss of cyclin D1 consistent with a null RB status combined with homozygous expression of mutant ras which had not been reported previously for RB (-) small-cell cancer. These findings show that a recurrent missense lp allele retains greater functional activity in vivo than predicted from earlier in vitro assays, proposing a role for stabilizing chaperone-like activity in vivo. In addition, these data suggest that reversible protein instability and the requirement for a cooperating mutation may provide a stochastic explanation for the molecular basis of incomplete penetrance in kindreds carrying these alleles.

Mect1-Maml2 fusion oncogene linked to the aberrant activation of cyclic AMP/CREB regulated genes.

Malignant salivary gland tumors can arise from a t(11;19) translocation that fuses 42 residues from Mect1/Torc1, a cyclic AMP (cAMP)/cAMP-responsive element binding protein (CREB)-dependent transcriptional coactivator, with 982 residues from Maml2, a NOTCH receptor coactivator. To determine if the Mect1-Maml2 fusion oncogene mediates tumorigenicity by disrupting cAMP/CREB signaling, we have generated in-frame deletions within the CREB-binding domain of Mect1/Torc1 for testing transformation activity and have also developed a doxycycline-regulated Mect1-Maml2 mammalian expression vector for global gene expression profiling. We observed that small deletions within the CREB-binding domain completely abolished transforming activity in RK3E epithelial cells. Further, we have shown that the ectopic induction of Mect1-Maml2 in HeLa cells strongly activated the expression of a group of known cAMP/CREB-regulated genes. In addition, we detected candidate cAMP-responsive element sites within 100 nucleotides of the transcriptional start sites of other genes activated by Mect1-Maml2 expression. In contrast, we did not observe alterations of known Notch-regulated target genes in these expression array profile experiments. We validated the results by reverse transcription-PCR in transfected HeLa, RK3E, and H2009 lung tumor cells and in mucoepidermoid cancer cells that endogenously express the fusion oncopeptide. Whereas overexpression of components of the cAMP pathway has been associated with a subset of human carcinomas, these data provide a direct genetic link between deregulation of cAMP/CREB pathways and epithelial tumorigenesis and suggest future therapeutic strategies for this group of salivary gland tumors.

Loss of the Smad3 expression increases susceptibility to tumorigenicity in human gastric cancer.

Loss of the tumor suppressive effect of transforming growth factor-beta (TGF-beta) has been commonly found at later stages in carcinogenic progression. Although the genes encoding TGF-beta receptors and Smads have been found genetically altered in certain human cancers, no mutation in Smad3 has been observed. Therefore, suppression of Smad3 expression may mediate key oncogenic properties of TGF-beta. First, we observed that 37.5% of human gastric cancer tissues showed low to undetectable levels of Smad3 and that in nine human gastric cancer cell lines examined, two showed deficient Smad3 expression. Introduction of Smad3 into human gastric cancer cells that did not express Smad3, restored TGF-beta responsiveness: induction of p21 and p15 gene expression, and growth inhibition in response to TGF-beta. Furthermore, these Smad3-expressing cells showed markedly decreased and delayed tumorigenicity in vivo. These findings suggest that Smad3 expression may have a critical role in tumor suppression in the early stages of gastric carcinogenesis.