22 results on '"Vogiatzi T"'
Search Results
2. Implant failure predictors in the posterior maxilla: a retrospective study of 274 consecutive implants
- Author
-
Friedberg, J. R., Vogiatzi, T., and Ioannidou, E.
- Published
- 2006
3. Alpha-synuclein and protein degradation: O28
- Author
-
Vekrellis, K., Emmanouilidou, E., Vogiatzi, T., Ikonomopoulos, S., and Stefanis, L.
- Published
- 2006
4. Prosthodontic complications in a prospective clinical trial of single-stage implants at 36 months.
- Author
-
Duncan JP, Nazarova E, Vogiatzi T, and Taylor TD
- Abstract
PURPOSE: The present material reports on prosthodontic complications in a trial of 51 patients with prostheses supported by single-stage implants over a period of 36 months. MATERIALS AND METHODS: One hundred eighty-six single-stage implants were placed in 51 patients over a 3-year period in 2 carefully controlled prospective clinical trials. Nineteen of the patients (103 implants) were completely edentulous and restored with a maxillary complete denture and a mandibular fixed-detachable complete prosthesis. Single metal-ceramic crowns or fixed partial dentures were fabricated for the remaining 32 patients (83 implants). The fixed restorations were either screw-retained or cemented. RESULTS: All patients/implants were followed for a minimum of 3 years. Complications in the edentulous patients included fracture of denture teeth, fracture of the maxillary denture, and occlusal screw loosening. Occlusal screw loosening and loss of the resin composite access plug were the only complications observed in the patients treated with screw-retained restorations. No complications were found in the patients restored with cemented restorations on solid abutments. DISCUSSION: Problems with prostheses were very common in the completely edentulous patients (13 of 19 patients encountered complications), possibly a result of increased bite force or inadequate laboratory technique. Tooth fractures were seen more frequently in men than in women. Complications occurred in only 5 of the 32 partially edentulous patients. CONCLUSION: Complications were associated with laboratory-related procedures rather than the implant system itself. [ABSTRACT FROM AUTHOR]
- Published
- 2003
5. Implant prosthodontics: current perspective and future directions.
- Author
-
Taylor TD, Agar JR, and Vogiatzi T
- Published
- 2000
6. Association of allelic loss at the FHIT locus and p53 alterations with tumour kinetics and chromosomal instability in non-small cell lung carcinomas (NSCLCs)
- Author
-
Garinis, GA Gorgoulis, VG Mariatos, G Zacharatos, P and Kotsinas, A Liloglou, T Foukas, P Kanavaros, P and Kastrinakis, NG Vassilakopoulos, T Vogiatzi, T Field, JK and Kittas, C
- Subjects
neoplasms - Abstract
The FHIT gene, located at the FRA3B fragile site of chromosome 3p14.2, encodes a 16.8 kD homologue of the yeast enzyme diadenosine tetraphosphate (Ap(4)A) hydrolase, Frequent allelic losses at this region in various malignancies, including non-small cell lung carcinomas (NSCLCs), imply that FHIT may represent a tumour suppressor gene (TSG), Increasing evidence suggests that multiple TSG impairment has a synergistic effect on tumour growth. The present study of 67 NSCLCs investigated the allelic imbalance (AIm) within the FHIT locus and its relationship with p53 abnormalities, kinetic parameters [proliferative activity or proliferation index (PI) and apoptotic index (AI)], and ploidy status of the carcinomas. Allelic imbalance at FHIT was observed in 35 out of 55 informative (heterozygous: H) cases (64%), Similar frequencies of loss of heterozygosity (LOH) were noticed among squamous cell lung carcinomas and adenocarcinomas, The high percentage of AIm in stage I tumours (71%) is indicative of its relatively early involvement in NSCL carcinogenesis. No association was found between LOH at FHIT, kinetic parameters, and ploidy status of the tumours, Concurrent loss at FHIT and p53 overexpression [FHIT(LOH)/p53(P)] was the most frequent pattern and was observed in 39% of the informative cases. The latter pattern was not associated with smoking, supporting the hypothesis that in patients with a history of tobacco exposure, FHIT allelic loss may not be a consequence of p53 checkpoint defects, but the outcome of tobacco-induced mutagenesis. Statistically significant differences in the presence of FHIT(LOH)/p53(P) and FHIT(LOH)/p53(N) patterns were noted at the proliferative and apoptotic level, whereas ploidy was similar amongst all groups, implying that mild-type (wt) p53 may play a safeguard role against altered I;HIT function. However, the possibility of a masking effect from wt p53 cannot be excluded, since the FHIT(LOH)/p53(P) profile demonstrated a higher growth index (GI = PI/AI mean value ratio) than FHIT(H)/p53(P) (32 vs. 8), although this was not significant. Further studies are needed in order to elucidate the role of FHIT and its relationships with other cell-cycle regulatory molecules involved in NSCL carcinogenesis. Copyright (C) 2000 John Wiley & Sons, Ltd.
- Published
- 2001
7. Association of allelic loss at the FHIT locus and p53 alterations with tumour kinetics and chromosomal instability in non-small cell lung carcinomas (NSCLCs)
- Author
-
Garinis, G. A., Gorgoulis, V. G., Mariatos, G., Zacharatos, P., Kotsinas, A., Liloglou, T., Foukas, P., Kanavaros, P., Kastrinakis, N. G., Vassilakopoulos, T., Vogiatzi, T., Field, J. K., and Kittas, C.
- Subjects
Male ,Ploidies ,DNA, Neoplasm/analysis ,Loss of Heterozygosity ,Carcinoma, Non-Small-Cell Lung/*genetics/metabolism/pathology ,Middle Aged ,Cell Division/genetics ,Survival Rate ,Genes, p53/*genetics ,Apoptosis/genetics ,Humans ,Neoplasm Proteins/metabolism ,Female ,Proteins/*genetics ,Tumor Suppressor Protein p53/metabolism ,Acid Anhydride Hydrolases ,Aged ,Follow-Up Studies ,Lung Neoplasms/*genetics/metabolism/pathology - Abstract
The FHIT gene, located at the FRA3B fragile site of chromosome 3p14.2, encodes a 16.8 kD homologue of the yeast enzyme diadenosine tetraphosphate (Ap(4)A) hydrolase. Frequent allelic losses at this region in various malignancies, including non-small cell lung carcinomas (NSCLCs), imply that FHIT may represent a tumour suppressor gene (TSG). Increasing evidence suggests that multiple TSG impairment has a synergistic effect on tumour growth. The present study of 67 NSCLCs investigated the allelic imbalance (AIm) within the FHIT locus and its relationship with p53 abnormalities, kinetic parameters [proliferative activity or proliferation index (PI) and apoptotic index (AI)], and ploidy status of the carcinomas. Allelic imbalance at FHIT was observed in 35 out of 55 informative (heterozygous: H) cases (64%). Similar frequencies of loss of heterozygosity (LOH) were noticed among squamous cell lung carcinomas and adenocarcinomas. The high percentage of AIm in stage I tumours (71%) is indicative of its relatively early involvement in NSCL carcinogenesis. No association was found between LOH at FHIT, kinetic parameters, and ploidy status of the tumours. Concurrent loss at FHIT and p53 overexpression [FHIT(LOH)/p53(P)] was the most frequent pattern and was observed in 39% of the informative cases. The latter pattern was not associated with smoking, supporting the hypothesis that in patients with a history of tobacco exposure, FHIT allelic loss may not be a consequence of p53 checkpoint defects, but the outcome of tobacco-induced mutagenesis. Statistically significant differences in the presence of FHIT(LOH)/p53(P) and FHIT(LOH)/p53(N) patterns were noted at the proliferative and apoptotic level, whereas ploidy was similar amongst all groups, implying that wild-type (wt) p53 may play a safeguard role against altered FHIT function. However, the possibility of a masking effect from wt p53 cannot be excluded, since the FHIT(LOH)/p53(P) profile demonstrated a higher growth index (GI=PI/AI mean value ratio) than FHIT(H)/p53(P) (32 vs. 8), although this was not significant. Further studies are needed in order to elucidate the role of FHIT and its relationships with other cell-cycle regulatory molecules involved in NSCL carcinogenesis. J Pathol
- Published
- 2001
8. Altered expression of the cell cycle regulatory molecules pRb, p53 and MDM2 exert a synergetic effect on tumor growth and chromosomal instability in non-small cell lung carcinomas (NSCLCs)
- Author
-
Gorgoulis, VG Zacharatos, P Kotsinas, A Mariatos, G and Liloglou, T Vogiatzi, T Foukas, P Rassidakis, G Garinis, G Ioannides, T Zoumpourlis, V Bramis, J Michail, PO and Asimacopoulos, PJ Field, JK Kittas, C
- Abstract
Background: Recent in vitro studies provide evidence that the cell cycle molecules pRb, p53 and MDM2 form a tightly regulated protein network. In this study, Mle examined the relationship of this protein network in a series of non-small cell lung carcinomas (NSCLCs), with the kinetic parameters, including proliferative activity or proliferation index (PI) and apoptotic index (AI), and ploidy status of the tumors. Material and Methods: A total of 87 NSCLCs were examined using immunohistochemical and molecular methods in order to estimate the status of the pRb-p53-MDM2 network. The kinetic parameters and the ploidy status of the tumors were assessed by in situ assays. The possible associations between alterations of the network, kinetic parameters and ploidy status of the carcinomas were assessed with a series of statistical methods. Results: Aberrant expression of pRb (Ab) and overexpression of p53 (P) and MDM2 (P) proteins were observed in 39%, 57%, and 68% of the carcinomas, respectively. The comprehensive analysis revealed that concurrent alterations in all three cell cycle regulatory molecules were the most frequent pattern, pRb(Ab)/p53(P)/MDM2(P); this “full abnormal” phenotype represented approximately 27% of the cases. This immunoprofile obtained the highest PI/AI value; whereas, the “normal” phenotype was the lowest one (p = 0.004). Furthermore, the pattern pRb(Ab)/p53(P)/MDM2(P) acquired the highest PI (p < 0.001) and lowest AI (p < 0.001) scores. Interestingly, the groups of carcinomas with impaired expression of one or two molecules attained PI/Al ratio values clustered in a narrow range placed in the middle of the scores exhibited by the “normal” and “full abnormal” phenotypes. These tumors had significantly lower AI, but similar PI values, compared with those noticed in the normal pattern. Ln addition, it was observed that the pRb(Ab)/p53(P)/ MDM2(P) phenotype was also significantly associated with aneuploidy (p = 0.002) and a tendency was observed when the expression of two components was altered (p = 0.055). Conclusions: Our findings suggest that simultaneous deregulation of all members of the pRb-p53-MDM2 network confers an additive effect on tumor growth. The apoptotic pathway seems to be more susceptible to its defects than the cell proliferation machinery. The findings of the ploidy analysis, which are in parallel with those regarding the proliferative activity and the apoptotic rate study, further support the concept that these molecules constitute a tightly regulated network participating in cell cycle control and chromosomal stability.
- Published
- 2000
9. Expression of p16(INK4A) and alterations of the 9p21-23 chromosome region in non-small-cell lung carcinomas: Relationship with tumor growth parameters and ploidy status
- Author
-
Mariatos, G Gorgoulis, VG Zacharatos, P Kotsinas, A and Vogiatzi, T Rassidakis, G Foukas, P Liloglou, T and Tiniakos, D Angelou, N Manolis, EN Veslemes, M Field, JK and Kittas, C
- Abstract
The 9p21-23 chromosome region harbors a number of known and putative tumor-suppressor genes (TSGs). The best characterized gene in this area is p16(INK4A) (CDKN2A). Alterations of its product have been observed in various malignancies, including non-small-cell lung carcinomas (NSCLCs). We earlier investigated the mechanisms underlying p16(INK4A) inactivation. In the present study, we examined, in a series of 87 NSCLCs, its relationship with the kinetic parameters [proliferation index (PI) and apoptotic index (AI)] and the ploidy status of the tumors. In addition, we extended our previous LOH analysis of the 9p21-23 region by examining flanking areas of p16(INK4A). Aberrant p16 expression was observed in 41.4% of the carcinomas. A significant association was found with increased PI (p = 0.037), but not with apoptosis. Aneuploid tumors were more frequently correlated with abnormal p16 staining (p = 0.05), A high frequency of allelic imbalance (AIm) was noticed at: the D9S161 (51.3%) and D9S157 (64.5%) loci, which lie approximately 4cM centromeric and 7cM telomeric, respectively, to CDKN2A, Abnormal p16(INK4A) expression was strongly correlated with Aim at D9S161 (p = 0.004). Allelic losses at D9S157 occurred more frequently in early stages (p = 0.018) and were significantly associated with deletions at D9S161 (p = 0.035). We conclude that, in a sub-set of NSCLCs, (i) abnormal p16 expression contributes to tumor growth mainly by increasing the proliferative activity in the initial stages of carcinogenesis; (ii) the association with aneuploidy merely reflects the impact of aberrant p16 on proliferative activity; and (iii) other putative TSGs possibly reside within the 9p21-23 region that possibly co-operate in certain cases with CDKN2A in the development of NSCLCs. (C) 2000 Wiley-Liss, Inc.
- Published
- 2000
10. Allelic imbalance at the 5q14 locus is associated with decreased apoptotic rate in non-small cell lung carcinomas (NSCLCs). Possible synergistic effect with p53 gene alterations on apoptosis
- Author
-
Gorgoulis, VG Mariatos, G Manolis, EN Zacharatos, P and Kotsinas, A Liloglou, T Vogiatzi, T Tsagkaraki, A and Kokotas, S Tsoli, E Alchanatis, M Sfikakis, PP and Asimacopoulos, PJ Field, JK Kittas, C
- Abstract
Deletions in the 5q14 region have been described in a variety of neoplasms, such as testicular germ cell tumors, ovarian, gastric and lung cancer. The high frequency of allelic losses observed in this region implies the presence of putative tumor suppressor gene(s) (TSGs). In the present study, we investigated in a series of 56 non-small cell lung carcinomas (NSCLCs) the allelic imbalance (Alm) within the 5q14 region, employing the D5S644 marker, and its relationship with p53 abnormalities, the kinetic parameters [proliferation index (PI) and apoptotic index (AI)] and the ploidy status of the carcinomas. AI at D5S644 was found at a frequency of 51.2%. The rather high percentage of Alm in stage I tumors suggests an early involvement in NSCLC development. LOH at 5q14 was associated with decreased AR in lung tumors insinuating the presence of a putative TSG(s) (P = 0.008). Simultaneous alterations of both p53 and D5S644 locus were the most frequent pattern observed (37.5%). Cases demonstrating this profile also exhibited a marked decrease in AI (P = 0.001). These findings imply a synergistic mechanism of co-operation between different TSGs. However, proliferation activity was dependent only on p53 status, leading to the assumption that the putative TSG(s) present at 5q14 may probably be involved in normal apoptotic procedures. Further studies are needed to identify the candidate gene(s). (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
- Published
- 2000
11. Allelic imbalance at the 5q14 locus is associated with decreased apoptotic rate in non-small cell lung carcinomas (NSCLCs). Possible synergistic effect with p53 gene alterations on apoptosis
- Author
-
Gorgoulis, V.G, primary, Mariatos, G, additional, Manolis, E.N, additional, Zacharatos, P, additional, Kotsinas, A, additional, Liloglou, T, additional, Vogiatzi, T, additional, Tsagkaraki, A, additional, Kokotas, S, additional, Tsoli, E, additional, Alchanatis, M, additional, Sfikakis, P.P, additional, Asimacopoulos, P.J, additional, Field, J.K, additional, and Kittas, C, additional
- Published
- 2000
- Full Text
- View/download PDF
12. Association of allelic loss at the FHIT locus and p53 alterations with tumour kinetics and chromosomal instability in non-small cell lung carcinomas (NSCLCs)
- Author
-
Garinis, G.A., Gorgoulis, V.G., Mariatos, G., Zacharatos, P., Kotsinas, A., Liloglou, T., Foukas, P., Kanavaros, P., Kastrinakis, N.G., Vassilakopoulos, T., Vogiatzi, T., Field, J.K., and Kittas, C.
- Abstract
The FHIT gene, located at the FRA3B fragile site of chromosome 3p14.2, encodes a 16.8 kD homologue of the yeast enzyme diadenosine tetraphosphate (Ap4A) hydrolase. Frequent allelic losses at this region in various malignancies, including non-small cell lung carcinomas (NSCLCs), imply that FHIT may represent a tumour suppressor gene (TSG). Increasing evidence suggests that multiple TSG impairment has a synergistic effect on tumour growth. The present study of 67 NSCLCs investigated the allelic imbalance (AIm) within the FHIT locus and its relationship with p53 abnormalities, kinetic parameters [proliferative activity or proliferation index (PI) and apoptotic index (AI)], and ploidy status of the carcinomas. Allelic imbalance at FHIT was observed in 35 out of 55 informative (heterozygous: H) cases (64%). Similar frequencies of loss of heterozygosity (LOH) were noticed among squamous cell lung carcinomas and adenocarcinomas. The high percentage of AIm in stage I tumours (71%) is indicative of its relatively early involvement in NSCL carcinogenesis. No association was found between LOH at FHIT, kinetic parameters, and ploidy status of the tumours. Concurrent loss at FHIT and p53 overexpression [FHIT(LOH)/p53(P)] was the most frequent pattern and was observed in 39% of the informative cases. The latter pattern was not associated with smoking, supporting the hypothesis that in patients with a history of tobacco exposure, FHIT allelic loss may not be a consequence of p53 checkpoint defects, but the outcome of tobacco-induced mutagenesis. Statistically significant differences in the presence of FHIT(LOH)/p53(P) and FHIT(LOH)/p53(N) patterns were noted at the proliferative and apoptotic level, whereas ploidy was similar amongst all groups, implying that wild-type (wt) p53 may play a safeguard role against altered FHIT function. However, the possibility of a masking effect from wt p53 cannot be excluded, since the FHIT(LOH)/p53(P) profile demonstrated a higher growth index (GI=PI/AI mean value ratio) than FHIT(H)/p53(P) (32 vs. 8), although this was not significant. Further studies are needed in order to elucidate the role of FHIT and its relationships with other cell-cycle regulatory molecules involved in NSCL carcinogenesis. Copyright © 2000 John Wiley & Sons, Ltd.
- Published
- 2001
13. Altered expression of the cell cycle regulatory molecules pRb, p53 and MDM2 exert a synergetic effect on tumor growth and chromosomal instability in non-small cell lung carcinomas (NSCLCs)
- Author
-
Gorgoulis, V. G., Zacharatos, P., Kotsinas, A., Mariatos, G., Liloglou, T., Vogiatzi, T., Foukas, P., Rassidakis, G., Garinis, G., Ioannides, T., Zoumpourlis, V., Bramis, J., Michail, P. O., Asimacopoulos, P. J., John Field, and Kittas, C.
- Subjects
Lung Neoplasms ,Base Sequence ,Neoplasms. Tumors. Oncology ,Gene Expression ,Nuclear Proteins ,Apoptosis ,Proto-Oncogene Proteins c-mdm2 ,Aneuploidy ,Genes, p53 ,Diploidy ,Models, Biological ,Retinoblastoma Protein ,Carcinoma, Non-Small-Cell Lung ,Proto-Oncogene Proteins ,Tumor Cells, Cultured ,Humans ,RNA, Messenger ,RNA, Neoplasm ,Genes, Retinoblastoma ,Tumor Suppressor Protein p53 ,Alleles ,Cell Division ,DNA Primers ,Research Article - Abstract
BACKGROUND: Recent in vitro studies provide evidence that the cell cycle molecules pRb, p53 and MDM2 form a tightly regulated protein network. In this study, we examined the relationship of this protein network in a series of non-small cell lung carcinomas (NSCLCs), with the kinetic parameters, including proliferative activity or proliferation index (PI) and apoptotic index (AI), and ploidy status of the tumors. MATERIAL AND METHODS: A total of 87 NSCLCs were examined using immunohistochemical and molecular methods in order to estimate the status of the pRb-p53-MDM2 network. The kinetic parameters and the ploidy status of the tumors were assessed by in situ assays. The possible associations between alterations of the network, kinetic parameters and ploidy status of the carcinomas were assessed with a series of statistical methods. RESULTS: Aberrant expression of pRb (Ab) and overexpression of p53 (P) and MDM2 (P) proteins were observed in 39%, 57%, and 68% of the carcinomas, respectively. The comprehensive analysis revealed that concurrent alterations in all three cell cycle regulatory molecules were the most frequent pattern, pRb(Ab)/p53(P)/MDM2(P); this "full abnormal" phenotype represented approximately 27% of the cases. This immunoprofile obtained the highest PI/AI value; whereas, the "normal" phenotype was the lowest one (p = 0.004). Furthermore, the pattern pRb(Ab)/p53(P)/MDM2(P) acquired the highest PI (p < 0.001) and lowest AI (p < 0.001) scores. Interestingly, the groups of carcinomas with impaired expression of one or two molecules attained PI/AI ratio values clustered in a narrow range placed in the middle of the scores exhibited by the "normal" and "full abnormal" phenotypes. These tumors had significantly lower AI, but similar PI values, compared with those noticed in the normal pattern. In addition, it was observed that the pRb(Ab)/p53(P)/MDM2(P) phenotype was also significantly associated with aneuploidy (p = 0.002) and a tendency was observed when the expression of two components was altered (p = 0.055). CONCLUSIONS: Our findings suggest that simultaneous deregulation of all members of the pRb-p53-MDM2 network confers an additive effect on tumor growth. The apoptotic pathway seems to be more susceptible to its defects than the cell proliferation machinery. The findings of the ploidy analysis, which are in parallel with those regarding the proliferative activity and the apoptotic rate study, further support the concept that these molecules constitute a tightly regulated network participating in cell cycle control and chromosomal stability.
14. Assessing the physical condition of waterlogged archaeological leather
- Author
-
Malea, Ekaterina, Vogiatzi, T., Watkinson, David, Malea, Ekaterina, Vogiatzi, T., and Watkinson, David
15. Effect of orthodontic extraction of mandibular premolars on third molar angulation after treatment with fixed appliances : A cross-sectional study.
- Author
-
Di Giovanni T, Vogiatzi T, Koretsi V, Walsh T, Silikas N, and Papageorgiou SN
- Subjects
- Humans, Female, Male, Adolescent, Cross-Sectional Studies, Treatment Outcome, Mandible diagnostic imaging, Radiography, Panoramic, Orthodontic Appliances, Fixed, Tooth, Impacted diagnostic imaging, Tooth, Impacted surgery, Risk Factors, Molar, Third diagnostic imaging, Molar, Third surgery, Bicuspid surgery, Bicuspid diagnostic imaging, Tooth Extraction
- Abstract
Purpose: Orthodontic treatment involving premolar extractions might improve the angulation of lower third molars, which are the teeth most often impacted. This study analyzes the impact of first/second lower premolar extraction during orthodontic therapy on the angulation of mandibular third molars., Methods: A total of 120 patients treated non-extraction (n = 40), with extraction of first (n = 40), or second lower premolars (n = 40) were included. The mesiodistal angulation of lower third molars relative to the adjacent tooth and their developmental stage were evaluated from posttreatment orthopantomograms. Between-group differences were statistically evaluated at a significance level of 0.05., Results: The orthopantomograms of 120 patients (51% female) with a median age of 15.2 years at the time of debonding were evaluated after a mean treatment duration time of 2.9 years. No difference (P > 0.05) was seen between the average angulation of the lower third molars of the right (mean = 24.4°, standard deviation [SD] 13.6°) and the left side (mean = 23.6°, SD 14.1°). No differences in the angulation of the lower third molar were found between the non-extraction and extraction groups for the right (P = 0.44) or the left side (P = 0.22). Likewise, no differences were found when comparing the first and second premolars for the right (P = 0.26) or the left side (P = 0.10). Premolar extraction was associated with an advanced root development stage of the right third molar (odds ratio 7.1; 95% confidence interval 1.1-48.1; P = 0.04), with no differences between extraction of the first or second premolar (P = 0.10)., Conclusion: Orthodontic treatment involving premolars extractions might be associated with a small acceleration in root development, but not with the angulation, of lower third molars., (© 2023. The Author(s).)
- Published
- 2024
- Full Text
- View/download PDF
16. Effect of field of view (FOV) positioning and shielding on radiation dose in paediatric CBCT.
- Author
-
Vogiatzi T, Menz R, Verna C, Bornstein MM, and Dagassan-Berndt D
- Subjects
- Child, Cone-Beam Computed Tomography methods, Humans, Phantoms, Imaging, Radiation Dosage, Spiral Cone-Beam Computed Tomography, Thermoluminescent Dosimetry
- Abstract
Objective: To investigate the effect of two different large field of view (FOV) positions in the vertical dimension and shielding (thyroid collar and eyeglasses) on the effective dose and the local doses of various sites of the craniofacial complex., Methods: Organ doses and effective doses were calculated based on the measured doses using 27 pairs of thermoluminescent dosemeters in a paediatric tissue-equivalent of a 10-year-old anthropomorphic phantom. The large FOV of the 3D Accuitomo F170 CBCT scanner was used to image parts of the craniofacial complex. Six protocols were performed: (A) cranial position without shielding; (B) cranial position with shielding; (C) caudal position without shielding; (D) caudal position with shielding, (E) similar to C with 360
0 rotation and (F) similar to D with 360° rotation. Measurements were obtained in duplicate, and the relative δ value (%) was applied to compare the average doses between the protocols., Results: Changing the FOV position from cranial to caudal without using shielding resulted in an increase of the effective dose of 18.8%. Use of shielding in the caudal position reduced the dose by 31.6%. Local absorbed dose of the thyroid had the most relevant impact on calculation of the effective dose, followed by oesophagus, bone marrow and bone surfaces, especially when comparing the different protocols., Conclusions: Application of shielding devices for thyroid in combination with a most caudal positioning of FOV led to the lowest local absorbed doses as well as the effective dose in a child phantom model.- Published
- 2022
- Full Text
- View/download PDF
17. Condylar resorption in orthognathic patients after mandibular bilateral sagittal split osteotomy: a systematic review.
- Author
-
Mousoulea S, Kloukos D, Sampaziotis D, Vogiatzi T, and Eliades T
- Subjects
- Humans, Malocclusion surgery, Mandible surgery, Mandibular Osteotomy methods, Orthognathic Surgical Procedures adverse effects, Orthognathic Surgical Procedures methods, Osteotomy, Sagittal Split Ramus methods, Research Design, Rotation, Bone Resorption etiology, Mandibular Condyle pathology, Mandibular Osteotomy adverse effects, Osteotomy, Sagittal Split Ramus adverse effects
- Abstract
Objective: To systematically search the literature and assess the available evidence regarding the incidence and quantification of condylar resorption following bilateral sagittal split osteotomy (BSSO) of the mandible in orthognathic patients., Search Methods: Electronic database searches of published and unpublished literature were performed. The reference lists of eligible studies were hand searched for additional studies., Selection Criteria: Randomized clinical trials (RCTs), prospective, and retrospective studies with patients of any age that underwent BSSO were included., Data Collection and Analysis: Study selection, data extraction, and risk of bias assessment were performed individually and in duplicate., Results: One RCT, 3 prospective, and 10 retrospective studies were included in this review. The lack of standardized protocols and the high amount of heterogeneity precluded a valid interpretation of the actual results through pooled estimates. There was a substantial consistency among studies, however, that young, female patients with mandibular deficiency and high mandibular plane angle, submitted to surgical counterclockwise rotation of mandibular segments, were more prone to a higher risk for condylar resorption after BSSO. The level of evidence was found to be low given the high/serious risk of bias in all included studies., Conclusions: Condylar resorption should be taken into account as a potential postsurgical complication after BSSO. However, its incidence and quantification need precautious interpretation owing to the low level of evidence and the high heterogeneity of studies. Additional high-quality prospective research assisted by 3D imaging technology is needed to allow more definitive conclusions., Registration: Study not registered., Conflict of Interest: None., (© The Author 2016. Published by Oxford University Press on behalf of the European Orthodontic Society. All rights reserved. For permissions, please email: journals.permissions@oup.com)
- Published
- 2017
- Full Text
- View/download PDF
18. Incidence of anatomical variations and disease of the maxillary sinuses as identified by cone beam computed tomography: a systematic review.
- Author
-
Vogiatzi T, Kloukos D, Scarfe WC, and Bornstein MM
- Subjects
- Humans, Maxillary Sinusitis diagnostic imaging, Mucocele diagnostic imaging, Nasal Mucosa diagnostic imaging, Nasal Polyps diagnostic imaging, Anatomic Variation, Cone-Beam Computed Tomography methods, Maxillary Sinus diagnostic imaging, Paranasal Sinus Diseases diagnostic imaging
- Abstract
Purpose: To analyze available evidence on the incidence of anatomical variations or disease of the maxillary sinuses as identified by cone beam computed tomography (CBCT) in dentistry., Materials and Methods: A focused question was developed to search the electronic databases MEDLINE, EMBASE, the Cochrane Oral Health Group Trials Register, and CENTRAL and identify all relevant papers published between 1980 and January 19, 2013. Unpublished literature at ClinicalTrials.gov, in the National Research Register, and in the Pro-Quest Dissertation Abstracts and Thesis database was also included. Studies were included irrespective of language. These results were supplemented by hand and gray literature searches., Results: Twenty-two studies were identified. Twenty were retrospective cohort studies, one was a prospective cohort study, and one was a case control study. The main indication for CBCT was dental implant treatment planning, and the majority of studies used a small field of view for imaging. The most common anatomical variations included increased thickness of the sinus membrane, the presence of sinus septa, and pneumatization. Reported sinus disease frequency varied widely, ranging from 14.3% to 82%. There was a wide range in the reported prevalence of mucosal thickening related to apical pathology, the degree of lumenal opacification, features of sinusitis, and the presence of retention cysts and polyps. More pathologic findings in the maxillary sinus were reported in men than in women, and the medial wall and sinus floor were most frequently affected., Conclusion: CBCT is used primarily to evaluate bony anatomy and to screen for overt pathology of the maxillary sinuses prior to dental implant treatment. Differences in the classification of mucosal findings are problematic in the consistent and valid assessment of health and disease of the maxillary sinus.
- Published
- 2014
- Full Text
- View/download PDF
19. Abberant alpha-synuclein confers toxicity to neurons in part through inhibition of chaperone-mediated autophagy.
- Author
-
Xilouri M, Vogiatzi T, Vekrellis K, Park D, and Stefanis L
- Subjects
- Animals, Cell Line, Down-Regulation, Humans, Lysosomes metabolism, PC12 Cells, Parkinson Disease metabolism, RNA, Small Interfering metabolism, Rats, alpha-Synuclein genetics, Autophagy, Molecular Chaperones metabolism, Neurons metabolism, alpha-Synuclein metabolism, alpha-Synuclein toxicity
- Abstract
Background: The mechanisms through which aberrant alpha-synuclein (ASYN) leads to neuronal death in Parkinson's disease (PD) are uncertain. In isolated liver lysosomes, mutant ASYNs impair Chaperone Mediated Autophagy (CMA), a targeted lysosomal degradation pathway; however, whether this occurs in a cellular context, and whether it mediates ASYN toxicity, is unknown. We have investigated presently the effects of WT or mutant ASYN on the lysosomal pathways of CMA and macroautophagy in neuronal cells and assessed their impact on ASYN-mediated toxicity., Methods and Findings: Novel inducible SH-SY5Y and PC12 cell lines expressing human WT and A53T ASYN, as well as two mutant forms that lack the CMA-targeting motif were generated. Such forms were also expressed in primary cortical neurons, using adenoviral transduction. In each case, effects on long-lived protein degradation, LC3 II levels (as a macroautophagy index), and cell death and survival were assessed. In both PC12 and SH-SY5Y cycling cells, induction of A53T ASYN evoked a significant decrease in lysosomal degradation, largely due to CMA impairment. In neuronally differentiated SH-SH5Y cells, both WT and A53T ASYN induction resulted in gradual toxicity, which was partly dependent on CMA impairment and compensatory macroautophagy induction. In primary neurons both WT and A53T ASYN were toxic, but only in the case of A53T ASYN did CMA dysfunction and compensatory macroautophagy induction occur and participate in death., Conclusions: Expression of mutant A53T, and, in some cases, WT ASYN in neuronal cells leads to CMA dysfunction, and this in turn leads to compensatory induction of macroautophagy. Inhibition of these lysosomal effects mitigates ASYN toxicity. Therefore, CMA dysfunction mediates aberrant ASYN toxicity, and may be a target for therapeutic intervention in PD and related disorders. Furthermore, macroautophagy induction in the context of ASYN over-expression, in contrast to other settings, appears to be a detrimental response, leading to neuronal death.
- Published
- 2009
- Full Text
- View/download PDF
20. alpha-synuclein degradation by autophagic pathways: a potential key to Parkinson's disease pathogenesis.
- Author
-
Xilouri M, Vogiatzi T, Vekrellis K, and Stefanis L
- Subjects
- Animals, Humans, Lysosomal-Associated Membrane Protein 2 genetics, Lysosomal-Associated Membrane Protein 2 metabolism, Lysosomes metabolism, Molecular Chaperones metabolism, Parkinson Disease metabolism, Rats, Autophagy, Neurons metabolism, Parkinson Disease etiology, alpha-Synuclein metabolism
- Abstract
The neuronal protein alpha-synuclein is thought to be central in the pathogenesis of Parkinson's disease (PD). Excessive wild type alpha-synuclein levels can lead to PD in select familial cases and alpha-synuclein protein accumulation occurs in sporadic PD. Therefore, elucidation of the mechanisms that control alpha-synuclein levels is critical for PD pathogenesis and potential therapeutics. The subject of alpha-synuclein degradation has been controversial. Previous work shows that, in an assay with isolated liver lysosomes, purified wild type alpha-synuclein is degraded by the process of chaperone-mediated autophagy (CMA). Whether this actually occurs in a cellular context has been unclear. In our most recent work, we find that wild type alpha-synuclein, but not the closely related protein beta-synuclein, is indeed degraded by CMA in neuronal cells, including primary postnatal ventral midbrain neurons. Macroautophagy, but not the proteasome, also contributes to alpha-synuclein degradation. Therefore, two separate lysosomal pathways, CMA and macroautophagy, degrade wild type alpha-synuclein in neuronal cells. It is hypothesized that impairment of either of these two pathways, or of more general lysosomal function, may be an initiating factor in alpha-synuclein accumulation and sporadic PD pathogenesis.
- Published
- 2008
- Full Text
- View/download PDF
21. Wild type alpha-synuclein is degraded by chaperone-mediated autophagy and macroautophagy in neuronal cells.
- Author
-
Vogiatzi T, Xilouri M, Vekrellis K, and Stefanis L
- Subjects
- Animals, Cerebral Cortex metabolism, Humans, Lysosomal-Associated Membrane Protein 2, Lysosomal Membrane Proteins genetics, Lysosomal Membrane Proteins metabolism, Mesencephalon metabolism, Mice, Molecular Chaperones metabolism, PC12 Cells, Parkinson Disease genetics, Rats, Rats, Wistar, alpha-Synuclein genetics, Autophagy genetics, Molecular Chaperones genetics, Neurons metabolism, Parkinson Disease metabolism, alpha-Synuclein metabolism
- Abstract
Alpha-synuclein (ASYN) is crucial in Parkinson disease (PD) pathogenesis. Increased levels of wild type (WT) ASYN expression are sufficient to cause PD in humans. The manner of post-transcriptional regulation of ASYN levels is controversial. Previously, we had shown that WT ASYN can be degraded by chaperone-mediated autophagy (CMA) in isolated liver lysosomes. Whether this occurs in a cellular and, in particular, in a neuronal cell context is unclear. Using a mutant ASYN form that lacks the CMA recognition motif and RNA interference against the rate-limiting step in the CMA pathway, Lamp2a, we show here that CMA is indeed involved in WT ASYN degradation in PC12 and SH-SY5Y cells, and in primary cortical and midbrain neurons. However, the extent of involvement varies between cell types, potentially because of differences in compensatory mechanisms. CMA inhibition leads to an accumulation of soluble high molecular weight and detergent-insoluble species of ASYN, suggesting that CMA dysfunction may play a role in the generation of such aberrant species in PD. ASYN and Lamp2a are developmentally regulated in parallel in cortical neuron cultures and in vivo in the central nervous system, and they physically interact as indicated by co-immunoprecipitation. In contrast to previous reports, inhibition of macroautophagy, but not the proteasome, also leads to WT ASYN accumulation, suggesting that this lysosomal pathway is also involved in normal ASYN turnover. These results indicate that CMA and macroautophagy are important pathways for WT ASYN degradation in neurons and underline the importance of CMA as degradation machinery in the nervous system.
- Published
- 2008
- Full Text
- View/download PDF
22. Expression of p16(INK4A) and alterations of the 9p21-23 chromosome region in non-small-cell lung carcinomas: relationship with tumor growth parameters and ploidy status.
- Author
-
Mariatos G, Gorgoulis VG, Zacharatos P, Kotsinas A, Vogiatzi T, Rassidakis G, Foukas P, Liloglou T, Tiniakos D, Angelou N, Manolis EN, Veslemes M, Field JK, and Kittas C
- Subjects
- Aged, Alleles, Apoptosis, Carcinoma, Non-Small-Cell Lung genetics, Carcinoma, Non-Small-Cell Lung pathology, Carcinoma, Squamous Cell metabolism, Cell Division, Cyclin-Dependent Kinase Inhibitor p16 genetics, Female, Gene Expression Regulation, Neoplastic, Humans, Immunoenzyme Techniques, Immunohistochemistry, Lung Neoplasms genetics, Lung Neoplasms pathology, Male, Middle Aged, Survival Analysis, Carcinoma, Non-Small-Cell Lung metabolism, Chromosomes, Human, Pair 9 genetics, Cyclin-Dependent Kinase Inhibitor p16 biosynthesis, Genes, p16 genetics, Loss of Heterozygosity, Lung Neoplasms metabolism, Ploidies
- Abstract
The 9p21-23 chromosome region harbors a number of known and putative tumor-suppressor genes (TSGs). The best characterized gene in this area is p16(INK4A) (CDKN2A). Alterations of its product have been observed in various malignancies, including non-small-cell lung carcinomas (NSCLCs). We earlier investigated the mechanisms underlying p16(INK4A) inactivation. In the present study, we examined, in a series of 87 NSCLCs, its relationship with the kinetic parameters [proliferation index (PI) and apoptotic index (Al)] and the ploidy status of the tumors. In addition, we extended our previous LOH analysis of the 9p21-23 region by examining flanking areas of p16(INK4A). Aberrant p16 expression was observed in 41.4% of the carcinomas. A significant association was found with increased PI (p = 0.037), but not with apoptosis. Aneuploid tumors were more frequently correlated with abnormal p16 staining (p = 0. 05). A high frequency of allelic imbalance (Alm) was noticed at the D9S161 (51.3%) and D9S157 (64.5%) loci, which lie approximately 4cM centromeric and 7cM telomeric, respectively, to CDKN2A. Abnormal p16(INK4A) expression was strongly correlated with Alm at D9S161 (p = 0.004). Allelic losses at D9S157 occurred more frequently in early stages (p = 0.018) and were significantly associated with deletions at D9S161 (p = 0.035). We conclude that, in a sub-set of NSCLCs, (i) abnormal p16 expression contributes to tumor growth mainly by increasing the proliferative activity in the initial stages of carcinogenesis; (ii) the association with aneuploidy merely reflects the impact of aberrant p16 on proliferative activity; and (iii) other putative TSGs possibly reside within the 9p21-23 region that possibly co-operate in certain cases with CDKN2A in the development of NSCLCs., (Copyright 2000 Wiley-Liss, Inc.)
- Published
- 2000
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.