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Aspasia Tsezou

Publications and source records attributed to Aspasia Tsezou.

9 recordsLinked to original sources
PubMed2006

Stable expression of a neuronal dopaminergic progenitor phenotype in cell lines derived from human amniotic fluid cells.

Cells from human amniotic fluid derived from the fetus are considered a source of multipotent cells. Their properties have not been fully exploited, partially because unlike other embryonic sources such as embryonic stem (ES) cells, cell lines from amniocentesis samples have not been generated. We have established and characterized the properties of eight individual cell lines. Flow cytometry using several cell surface markers showed that all cell lines generated consisted of homogeneous populations that lack HLAII antigenicity. Using a combination of immunocytochemistry, Western blotting, and RT-PCR, we found weak expression of Oct4 and nestin and strong expression of tubulin-betaIII, MAP2, and tau. Specific markers for cholinergic, (nor)adrenergic, and GABAergic neurons or glia were weakly expressed or absent, whereas expression of factors implicated in early induction of dopaminergic neurons, TGF-beta3 and beta-catenin were present. Further analysis showed strong expression of EN-1, c-RET, PTX3, and NURR1 essential for induction and survival of midbrain dopaminergic neurons, TH, AADC, and VMAT2 components of dopamine synthesis and secretion, and syntaxin1A and SNAP-25 necessary for neurotransmitter exocytosis. This phenotype was retained throughout passages and up to the current passage 36. Expression of neuronal and dopaminergic markers in individual AF cell lines was comparable to expression in neurons induced from ES cells and in IMR-32 and SH-SY5Y neuroblastomas. Our data show that cell lines can be derived from subcultures of amniocentesis, and are primarily composed of a population of progenitors with a phenotype similar to that of committed mesencephalic dopaminergic neurons.

Amniotic Fluid↗
PubMed2006

Absence of linkage to chromosomes 6q and 16p in a Greek population with knee osteoarthritis.

Osteoarthritis (OA) is a common age-related debilitating disease of the joints characterized by degeneration of the articular cartilage which leads to joint pain, discomfort, and immobility. Several risk factors have been associated with OA including a genetic predisposition. Specific chromosomal regions have thus far been associated with susceptibility to OA, the strongest being on chromosomes 2, 6, and 16. We hereby report our data on 34 Central Greek knee OA families that were investigated for linkage to the chromosome 6q and 16p susceptibility regions. All affected members had undergone total knee replacement surgery (TKR) at a single large Orthopedics Unit in Central Greece. Nineteen microsatellite markers were selected, 15 for chromosome 6q and 4 for chromosome 16p at a distance of approximately 7 cm. Allele fragment sizes were determined by an automated DNA sequencer using the Fragment Analysis Software. Our results revealed a statistically significant difference in the ratio of affected females to males with knee OA and also showed that there is no evidence of linkage to regions 6q and 16p in a cohort of Central Greek pedigrees with knee OA.

Adult↗
PubMed2006

The canine copper toxicosis gene MURR1 is not implicated in the pathogenesis of Wilson disease.

BACKGROUND: It has recently been demonstrated that the Wilson disease (WD) protein directly interacts with the human homolog of the MURR1 protein in vitro and in vivo, and that this interaction is specific for the copper transporter. The aim of the present study was to clarify the role of MURR1 in the pathogenesis of WD as well as in other WD-like disorders of hepatic copper metabolism of unknown origin. METHODS: Using the single-strand conformation polymorphism (SSCP) method followed by sequencing, we analyzed the 5' untranslated region (UTR) and three exons of the MURR1 gene in three groups of patients: 19 WD: patients in whom no mutations were detected in the ATP7B gene, 53 WD: patients in whom only one mutation in the ATP7B gene was found, and 34 patients in whom clinical and laboratory data suggested a WD-like disorder of hepatic copper metabolism of unknown origin. RESULTS: We detected in these patients six rare nucleotide substitutions, namely one splice-site consensus sequence and one missense and four silent nucleotide substitutions. All substitutions except one were found in the heterozygous state. No difference in the frequencies of the various substitutions was observed between patients and controls. CONCLUSIONS: These data suggest that the MURR1 gene and its protein product are unlikely to play a primary role in the pathogenesis of Wilson disease. More extensive studies with larger numbers of clinically homogeneous patients should be carried out to establish whether nucleotide alterations in the MURR1 gene may have a role in causing WD or WD-like disorders or act as modifying factors in the phenotype variability in WD.

Adaptor Proteins, Signal Transducing↗
PubMed2006

UGT1A1 promoter polymorphism as a predisposing factor of hyperbilirubinaemia in neonates with acute pyelonephritis.

We describe 4 jaundiced neonates with acute pyelonephritis of whom family history was positive for or pointed to Gilbert's syndrome (GS). Uridine diphosphate glucuronosyltransferase 1A1 (UGT-1A1), (TA)7 polymorphism, associated with GS was found in these neonates. We suggest that extended (TA)7 promoter, acting as a predisposing factor, contributes substantially to hyperbilirubinaemia seen in a number of neonates with urinary tract infections (UTIs).

Female↗
PubMed2006

Correlation between radiation-induced telomerase activity and human telomerase reverse transcriptase mRNA expression in HeLa cells.

PURPOSE: To quantify and correlate human telomerase reverse transcriptase (hTERT) mRNA expression with telomerase activity (TA) after ionizing irradiation of HeLa cells. MATERIALS AND METHODS: TA and hTERT mRNA expression were evaluated, at 24-h intervals, in HeLa cells cultured for up to 144 h, before and after treatment with increasing doses of 6 MV photon ionizing radiation (5 - 20 Gy), using the telomeric repeat amplification protocol (TRAP) assay and real-time reverse transcriptase polymerase chain reaction (RT-PCR), respectively. Cell viability was determined using the 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. A prototype phantom was constructed for accurate irradiation of HeLa cells. RESULTS: Treated cells showed a decrease in viability with increasing radiation dose, and a correlation was observed with post-treatment period. TA and hTERT mRNA expression of HeLa cells increased for the first 24 h after irradiation. The maximal increases were approximately two times the un-irradiated cell levels at 24 h post-irradiation, followed by a decrease and a return to the control levels 72 h post-irradiation. The time-course of telomerase activation after 24 h, differed among radiation doses. A dose-dependent G2/M arrest was observed 24 h post-irradiation, along with an increase in polyploidy 48 h post-irradiation and afterwards. CONCLUSION: A correlation between TA and hTERT mRNA expression and a radiation induced cell cycle dependent modification of hTERT mRNA expression was established for the first 24 h post-irradiation.

Cell Survival↗
PubMed2006

Report of novel chromosomal abnormalities in a series of 130 chronic lymphocytic leukemia patients studied by classic cytogenetic analysis.

One-hundred-and-thirty typical, unselected CLL cases were studied by conventional cytogenetic analysis. Seventy-three patients (56.2%) had normal karyotype ('normal sub-group'), while 57/130 patients (43.8%) had abnormal karyotype. Twenty-two of 57 patients (38.6%) carried more than one abnormality. Six novel chromosomal abnormalities were detected in five patients: (i) t(3;13)(q14;q34); (ii) t(Y;11)(q12;q23), del(13)(q12q14); (iii) dic(3;11)(p21;q23); (iv) t(3;5)(q29;q23); (v) t(3;22) (p21;q13); and (vi) t(1;13)(p12;q12). Three of five patients carrying novel translocations had progressive disease. The true biological and clinical significance of novel chromosomal abnormalities remains to be determined.

Aged↗
PubMed2006

Leptin receptor isoforms mRNA expression in peripheral blood mononuclear cells from patients with chronic viral hepatitis.

There is accumulating evidence that leptin has a pleiotropic role in hematopoiesis, immune response, fibrogenesis, and hepatocarcinogenesis. We investigated the expression of leptin and leptin receptor (OB-R) at the protein level by flow cytometry and also quantified by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) the two major leptin receptor isoforms (OB-Rl, OB-Rs) in peripheral blood mononuclear cells (PBMCs) of patients with hepatitis B (HBV; n = 31), hepatitis C (HCV; n = 34), and nonviral liver disease (n = 25), and healthy controls (n = 36), as well as in liver tissues of HBV (n = 8), HCV (n = 7), and healthy individuals (n = 6). Serum leptin levels were measured in all participants (N = 126). We observed significantly lower OB-Rl and OB-Rs mRNA levels in PBMCs of HBV and HCV patients compared with healthy controls and nonviral liver disease patients (P < 0.05). Flow cytometry analysis confirmed the real-time RT-PCR results. Expression of leptin and OB-Rl was significantly increased in viral hepatitis liver tissues compared with healthy tissues (P < 0.01). OB-Rl mRNA levels were not associated with hepatitis patients' clinical status (inactive, chronic hepatitis, or cirrhosis). We also found decreased serum leptin in HBV and HCV patients compared with healthy individuals and the nonviral liver disease group. Leptin was expressed in 3 of 34 HCV (8.8%) and 19 of 25 (76%) nonviral liver disease patients. Moreover, expression of OB-Rl and OB-Rs were associated when all individuals were grouped together (r = 0.78, P < 0.001). In conclusion, our findings may suggest the involvement of the leptin system in the immunopathology of chronic viral hepatitis.

Female↗
PubMed2005

Quantitative determination of human telomerase reverse transcriptase messenger RNA expression in premalignant cervical lesions and correlation with human papillomavirus load.

Expression of human telomerase reverse transcriptase (hTERT) messenger RNA (mRNA) and human papillomavirus (HPV)-16 load were quantified using real-time polymerase chain reaction and correlated with cytological findings and the presence of HPV infection in cervical specimens. Human telomerase reverse transcriptase mRNA expression was evaluated in 15 (20.5%) of 73 specimens of atypical squamous epithelial cells of undetermined significance, in 62 (39.7%) of 156 low-grade squamous intraepithelial lesions (LGSILs), in 49 (96%) of 51 high-grade squamous intraepithelial lesions (HGSILs), and in 9 (20%) of 45 normal samples, whereas viral load was quantified in 52 (89.6%) of 58 samples infected with HPV-16. The mean levels of hTERT mRNA expression were 0.11 in normal tissue, 0.23 in atypical squamous epithelial cells of undetermined significance, 0.75 in LGSILs, and 2.5 in HGSILs. Thus, a significant increase in hTERT mRNA expression was observed with increasing degrees of cervical dysplasia. The HPV-16 load was significantly higher in samples of HGSIL than in those of LGSILs (P < .001). A significant correlation was observed between viral load and quantitative hTERT mRNA expression (r = 0.65; P < .05). Quantitative hTERT mRNA assessment showed 96% sensitivity and 100% negative predictive value for high-grade dysplasia, whereas the specificity and positive predictive value were 72% and 36.2%, respectively. It is suggested that quantitative hTERT has a very high sensitivity and negative predictive value, whereas the observed specificity was moderate, indicating that it cannot be used as a diagnostic marker but may be an adjunct in the management of women with high-grade cervical dysplasia. However, the final diagnosis must rely on the inclusion of clinical evaluation and additional assessment data.

Adult↗