Frictional force between the orthodontic bracket and arch wire during sliding tooth movement is related to many factors, such as the size, shape and material of both the bracket and wire, ligation method and the angle formed between the bracket and wire. There have been clear conclusions drawn in regard to most of these factors, but as to the effect of bracket width on frictional force there are only conflicting studies. This study was designed to investigate the effect of bracket width on the amount of frictional forces generated during clinically simulated tooth movement. Three different widths of brackets (0.018x0.025"standard), narrow (2.40mm), medium (3.00mm) and wide (4.25mm) were used in tandem with 0.016x0.022" stainless steel wire. Three bracket-arch wire combinations were drawn on for 4 minutes on a testing apparatus with a head speed of 0.5mm/min and tested 7 times each. To reproduce biological conditions, dentoalveolar models were designed with indirect technique using a material with similar elastic properties as periodontal ligament (PDL). In addition, to minimize the effect of ligation force, elastomer was used with added resin, which was attached to the bracket to make up for the discrepancies of bracket width. The results were as follows: 1. Maximum frictional force for each bracket-arch wire combination was: Narrow (2.40mm) : 68.09+/-4.69 gmf Medium (3.00mm) : 72.75+/-4.98 gmf Wide (4.25mm) : 72.59+/-4.54 gmf 2. Frictional force was increased with more displacement of wire through the bracket slot. 3. The ANOVA post-hoc test showed that the bracket width had no significant effect on frictional force when tested under clinically simulated conditions (P>0.05)
Elastomers ; Friction* ; Glia Maturation Factor ; Head ; Ligation ; Orthodontic Brackets ; Periodontal Ligament ; Stainless Steel ; Tooth Movement* ; Tooth*

PURPOSE: We evaluated the preoperative clinical factors that affect the surgical outcome of posterior urethral anastomosis (PUA) with a gracilis muscle flap (GMF) to determine which factors predict benefit from the use of the GMF. MATERIALS AND METHODS: This was a retrospective analysis of 49 patients who underwent a delayed PUA with a GMF. A successful clinical outcome was defined as achieving a peak urinary flow rate greater than 15 mL/s at 3 and 12 months postoperatively without evidence of stricture recurrence on a retrograde urethrogram or cystourethroscopy at 3 months postoperatively. Multiple clinical factors were evaluated by use of univariate and multivariate analyses. RESULTS: The outcome of 21 of 49 patients (42.9%) was deemed successful. The mean age of the 49 patients was 37.2+/-13.5 years and the mean follow-up duration was 43.4+/-28.0 months. The length of the urethral defect was significantly shorter in patients with a successful outcome than in patients with an unsuccessful outcome (p=0.010). The outcome differed significantly depending on whether the patients had a previously successful urethroplasty (p=0.036) or whether they had suffered a pelvic bone injury (p=0.012). Multivariate logistic regression analyses revealed that a previous urethroplasty was the only preoperative clinical factor that significantly affected the surgical outcome in PUA with a GMF (odds ratio, 0.218; 95% confidence interval, 0.050 to 0.947; p=0.042). CONCLUSIONS: A history of previous urethroplasty is a preoperative clinical factor that significantly affects the surgical outcome in PUA with a GMF; the procedure is more likely to be successful in patients who have not previously undergone urethroplasty.
Anastomosis, Surgical ; Constriction, Pathologic ; Follow-Up Studies ; Glia Maturation Factor ; Humans ; Logistic Models ; Muscles ; Pelvic Bones ; Recurrence ; Retrospective Studies ; Surgical Flaps ; Urethral Stricture

It is standard practice, whenever a researcher finds a new gene, to search databases for genes that have a similar sequence. It is not standard practice, whenever a researcher finds a new gene, to search for genes that have similar expression (co-expression). Failure to perform co-expression searches has lead to incorrect conclusions about the likely function of new genes, and has lead to wasted laboratory attempts to confirm functions incorrectly predicted. We present here the example of Glia Maturation Factor gamma (GMF-gamma). Despite its name, it has not been shown to participate in glia maturation. It is a gene of unknown function that is similar in sequence to GMF-beta. The sequence homology and chromosomal location led to an unsuccessful search for GMF-gamma mutations in glioma. We examined GMF-gamma expression in 1432 human cDNA libraries. Highest expression occurs in phagocytic, antigen-presenting and other hematopoietic cells. We found GMF-gamma mRNA in almost every tissue examined, with expression in nervous tissue no higher than in any other tissue. Our evidence indicates that GMF-gamma participates in phagocytosis in antigen presenting cells. Searches for genes with similar sequences should be supplemented with searches for genes with similar expression to avoid incorrect predictions.
Animals ; Cell Line ; Cloning, Molecular ; DNA, Complementary ; metabolism ; Databases as Topic ; Expressed Sequence Tags ; Gene Expression ; Gene Library ; Glia Maturation Factor ; genetics ; Humans ; RNA, Messenger ; metabolism ; Rats ; Sequence Analysis, DNA

OBJECTIVETo further study the mechanism of the inhibitory effect of interferon beta-1a (IFN beta-1a) on the activation of human hepatic stellate cell (HSC) LX-2, and to analyze the differences on the protein expression in LX-2 induced by I IFN beta-1a.

METHODSCultured LX-2 cells were treated with 2000 U/ml IFN beta-1a for 48 h. Two-dimensional gel electrophoresis (2-DE) was performed to compare protein patterns of the control (untreated) and IFN beta-1a treated LX-2 and for quantitative and qualitative analyses of protein expression. A rat liver fibrosis model was established and the rats were sacrificed and their various tissues were obtained for the same analyses. Western blotting and RT-PCR were used to validate the expression of the changed proteins after treatment of IFN beta-1a in LX-2 cells and of various tissues of the rats.

RESULTS708 +/- 25 spots were detected in control LX-2 cells and 804 +/- 32 spots in IFN beta-1a-treated LX-2 cells. A match rate of 73%-82% was achieved. The results also showed that 31 protein spots displayed quantitative changes in expression after IFN beta-1a treatment. Of the 31 spots, 21 proteins were identified, of which, one was newly found, two were enhanced in abundance and 18 showed lower expressions. The newly found protein was glia maturation factor beta (GMF beta). The treatment of LX-2 with IFN beta-1a increased the production of GMF beta(GMF beta) protein in comparison with the untreated cells (t=1.81, P < 0.01). The expression of GMF beta protein (1.81 vs 0.10) and mRNA (0.85 vs 0.12) were more in the normal liver tissues than in the cirrhotic liver tissues (t=2.53, 2.13 respectively, P < 0.01). The expressions of GMF beta protein and mRNA were weak in rat heart and lung tissues, however, they were strong in rat liver, kidney, spleen and brain tissues (t=1.91, 1.94 respectively, P < 0.01).

CONCLUSIONThere is a significant difference of protein expression levels between IFN beta-1a untreated and treated LX-2 cells. These proteins, especially GMF beta, may be involved in an inhibition process of IFN beta-1a on activation and apoptosis of LX-2 cells. This proteome study may be useful in further studies of the relationship of IFN beta-1a treatment and human liver diseases.

Animals ; Cell Line ; Female ; Glia Maturation Factor ; metabolism ; Hepatic Stellate Cells ; metabolism ; Humans ; Interferon beta-1a ; Interferon-beta ; pharmacology ; Liver ; cytology ; Liver Cirrhosis ; metabolism ; Proteome ; Rats ; Rats, Sprague-Dawley

OBJECTIVE: This study was designed to examine the pharmaco-dynamic pattern of proteomic expression in cervical carcinoma cells (CaSki cell line; HPV-16 positive) after in vitro treatment by the etoposide. METHODS: We analyzed proteomic profiling in cervical carcinoma cells after etoposide treatment using two-dimensional gel electrophoresis (2-DE) with MALDI-TOF-MS used for protein identification. Then, we tested the several experimental methods for verification and functional identification, including MTT assay, PI staining, DNA fragmentation assay, FDA, FACS and Western blot analysis. RESULTS: Etoposide inhibited the CaSki cervical cancer cell growth in a dose-dependent manner and the optimal concentration of etoposide is 2micrometer(IC50) in the CaSki cervical cancer cells. The etoposide induced apoptosis, as determined by DNA fragmentation assay, FACS, and Western blot. The etoposide increased the protein expression of Fas (Apo-1/CD95), p53, pRb and caspase-3, but decreased the level of Bcl-2 and caspase-3 precursor and subsequently triggered the mitochondrial apoptotic pathway (release of cytochrome c and activation of caspase-9). To this end, we analyzed CaSki cancer cells using 2-DE. Eight proteins (XAP-5, HXC-36, serine/threonine protein phosphatase 2B catalytic subunit, G2/mitotic-specific cyclin B1, T-box transcription factor TBX20, diacylglycerol kinase, amiloride-sensitive amine oxidase, HEF-like protein, ras-related protein Rab-20) were down-regulated and nine proteins (RNA 3'-terminal phosphate cyclase-like protein, late endosomal/lysosomal Mp1 interacting protein, glia maturation factor, replication protein A 14 kDa subunit, mago sashi protein homolog, 14 kDa phosphohistidine phosphatase, protein C14 or f48, cyclin-dependent kinase 4 inhibitior A, retinoic acid-binding protein II) were up-regulated in etoposide-treated CaSki cells when compared with non-treated cells. CONCLUSION: Our results clearly indicate that etoposide induced cell death by apoptosis. These findings may provide insights into the mechanisms underlying the apparent anti-tumoral effects of etoposide.
Apoptosis ; Blotting, Western ; Calcineurin ; Caspase 3 ; Catalytic Domain ; Cell Death ; Cell Line ; Cyclin B1 ; Cyclin-Dependent Kinase 4 ; Cytochromes c ; Diacylglycerol Kinase ; DNA Fragmentation ; Electrophoresis, Gel, Two-Dimensional ; Etoposide ; Glia Maturation Factor ; Human papillomavirus 16 ; Oxidoreductases ; Proteomics ; Replication Protein A ; Transcription Factors ; Uterine Cervical Neoplasms

Brain damage can cause lung injury. To explore the mechanism underlying the lung injury induced by acute cerebral ischemia (ACI), we established a middle cerebral artery occlusion (MCAO) model in male Sprague-Dawley rats. We focused on glia maturation factor β (GMFB) based on quantitative analysis of the global rat serum proteome. Polymerase chain reaction, western blotting, and immunofluorescence revealed that GMFB was over-expressed in astrocytes in the brains of rats subjected to MCAO. We cultured rat primary astrocytes and confirmed that GMFB was also up-regulated in primary astrocytes after oxygen-glucose deprivation (OGD). We subjected the primary astrocytes to Gmfb RNA interference before OGD and collected the conditioned medium (CM) after OGD. We then used the CM to culture pulmonary microvascular endothelial cells (PMVECs) acquired in advance and assessed their status. The viability of the PMVECs improved significantly when Gmfb was blocked. Moreover, ELISA assays revealed an elevation in GMFB concentration in the medium after OGD. Cell cultures containing recombinant GMFB showed increased levels of reactive oxygen species and a deterioration in the state of the cells. In conclusion, GMFB is up-regulated in astrocytes after ACI, and brain-derived GMFB damages PMVECs by increasing reactive oxygen species. GMFB might thus be an initiator of the lung injury induced by ACI.
Animals ; Brain ; metabolism ; pathology ; Brain Ischemia ; complications ; pathology ; Bronchoalveolar Lavage Fluid ; Cell Hypoxia ; physiology ; Cells, Cultured ; Cerebrovascular Circulation ; physiology ; Chromatography, High Pressure Liquid ; Culture Media, Conditioned ; pharmacology ; Disease Models, Animal ; Endothelial Cells ; metabolism ; Gene Expression Regulation ; physiology ; Glia Maturation Factor ; metabolism ; In Situ Nick-End Labeling ; Lung Injury ; etiology ; metabolism ; pathology ; Male ; Neuroglia ; metabolism ; Neurologic Examination ; Peroxidase ; metabolism ; Proteome ; RNA Interference ; physiology ; RNA, Small Interfering ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species ; metabolism ; Tandem Mass Spectrometry