Διαμόρφωση παράκτιας ζώνης και δημιουργία μικρού κέντρου θαλάσσιων ερευνών στον Άγιο Νικόλαο, Αναβύσσου

Στη σύγχρονη εποχή είναι σημαντική η ήπια ανάπτυξη και η προστασία των παράκτιων περιοχών που βάλλονται από την ανθρώπινη παρουσία. Επέλεξα την περιοχή του Αγίου Νικολάου, Αναβύσσου που είναι υψίστου φυσικό κάλλους και όπου εξαιτίας της θέσης της στην Αττική, απειλείται από την άναρχη δόμηση και την τουριστικοποίηση. Η πρότασή μου αφορά την προστασία, την ανάδειξη και την ήπια αξιοποίηση της περιοχής. Ένας στενός λαιμός άμμου ενώνει το νησί του Αγίου Νικολάου με τη στεριά της Αττικής. Ανατολικά του στα λιμνάζοντα νερά του απάνεμου κόλπου, με χρήση φυσικού λιμανιού, συναντούμε έναν σπάνιο βιότοπο. Αρχικά χαράσσεται ένα μονοπάτι που εισέρχεται στον πευκόφυτο λόφο και ενώνει το τελευταίο όριο της Αναβύσσου με τον ʼγιο Νικόλα. Η κίνηση του μονοπατιού δεν είναι συνεχής. Παύσεις και μικροί τοίχοι αντιστήριξης υποδεικνύουν την κατεύθυνση του περιπατητή. Ένα υπαίθριο αναψυκτήριο ελαφριάς κατασκευής βρίσκεται στο σημείο συνάντησης του μονοπατιού με το νερό, ενώ στάσεις με την μορφή κήπων με τοπική βλάστηση συναντιόνται σε όλη την πορεία του. Όταν το μονοπάτι φτάνει στο νερό, αλλάζει μορφή και συνεχίζει ως προβλήτα που το συνδέει με το νησί του Αγίου Νικολάου. Το μονοπάτι συνεχίζει δίπλα από το εκκλησάκι με τους μικρούς κήπους και επιστρέφει πάλι σε αυτό, κινούμενο περιμετρικά του λόφου και διασχίζοντας την κορυφή του. Πέραν όμως των υπαίθριων μονάδων διημέρευσης, το κίνηση του μονοπατιού διακόπτεται από ένα μικρό κέντρο θαλάσσιων ερευνών στην κορυφή ενός λόφου, που ασχολείται με τοπικού ενδιαφέροντος ζητήματα και κυρίως με την προστασία του θαλάσσιου βιοτόπου. Στόχος της επέμβασής μου στην περιοχή είναι να αναδείξω τις αναξιοποίητες μέχρι σήμερα πτυχές και εικόνες αυτού του τόπου. Τα ήπια εγχειρήματα στην τοπογραφία μεταφέρουν δράσεις και ανθρώπους πιο κοντά στην φύση

Serum Dipeptidyl Peptidase-4 Activity in Insulin Resistant Patients with Non-Alcoholic Fatty Liver Disease: A Novel Liver Disease Biomarker

Background: In a cross-sectional study we studied the fasting serum DPP-4 enzymatic activity (sDPP-4) and the insulin resistance index (HOMA2-IR) in gliptin naive patients with type 2 diabetes and in non-alcoholic fatty liver disease (NAFLD) and in healthy controls (CNTRL). Methods and Findings: sDPP-4 was measured by kinetic assay in 39 NAFLD (F/M: 19/20, mean age: 47.42 yrs) and 82 type 2 diabetes (F/M:48/34, 62.8 yrs) patients and 26 (F/M:14/12, 35.3 yrs) controls. Definition of T2D group as patients with type 2 diabetes but without clinically obvious liver disease created non-overlapping study groups. Diagnosis of NAFLD was based on ultrasonography and the exclusion of other etiololgy. Patients in T2D and NAFLD groups were similarly obese. 75 g CH OGTT in 39 NAFLD patients: 24-NGT, 4-IGT or IFG ("prediabetes''), 11-type 2 diabetes. HOMA2-IR: CNTRL: 1.44; T2D-group: 2.62 (p = 0.046 vs CNTRL, parametric tests); NAFLD(NGTonly): 3.23 (p = 0.0013 vs CNTRL); NAFLD(IFG/IGT/type 2 diabetes): 3.82 (p<0.001 vs CNTRL, p = 0.049 vs 2TD group). sDPP-4 activity was higher in NAFLD both with NGT (mean: 33.08U/L) and abnormal glucose metabolism (30.38U/L) than in CNTRL (25.89U/L, p<0.001 and p = 0.013) or in T2D groups (23.97U/L, p<0.001 and p = 0.004). Correlations in NAFLD among sDPP-4 and ALT: r = 0.4637, p = 0.0038 and gamma GT: r = 0.4991, p = 0.0017 and HOMA2-IR: r = 0.5295, p = 0.0026 and among HOMA2-IR and ALT: r = 0.4340, p = 0.0147 and gamma GT: r = 0.4128, p = 0.0210. Conclusions: The fasting serum DPP-4 activity was not increased in T2D provided that patients with liver disease were intentionally excluded. The high serum DPP-4 activities in NAFLD were correlated with liver tests but not with the fasting plasma glucose or HbA1C supporting that the excess is of hepatic origin and it might contribute to the speedup of metabolic deterioration. The correlation among cGT, ALT and serum DPP-4 activity and also between serum DPP-4 activity and HOMA2-IR in NAFLD strongly suggests that serum DPP-4 activity should be considered as a novel liver disease biomarker

Promoter Hypermethylation-Related Reduced Somatostatin Production Promotes Uncontrolled Cell Proliferation in Colorectal Cancer.

BACKGROUND: Somatostatin (SST) has anti-proliferative and pro-apoptotic effects. Our aims were to analyze and compare the SST expression during normal aging and colorectal carcinogenesis at mRNA and protein levels. Furthermore, we tested the methylation status of SST in biopsy samples, and the cell growth inhibitory effect of the SST analogue octreotide in human colorectal adenocarcinoma cell line. METHODS: Colonic samples were collected from healthy children (n1 = 6), healthy adults (n2 = 41) and colorectal cancer patients (CRCs) (n3 = 34) for SST mRNA expression analysis, using HGU133 Plus2.0 microarrays. Results were validated both on original (n1 = 6; n2 = 6; n3 = 6) and independent samples ((n1 = 6; n2 = 6; n3 = 6) by real-time PCR. SST expressing cells were detected by immunohistochemistry on colonic biopsy samples (n1 = 14; n2 = 20; n3 = 23). The effect of octreotide on cell growth was tested on Caco-2 cell line. SST methylation percentage in biopsy samples (n1 = 5; n2 = 5; n3 = 9) was defined using methylation-sensitive restriction enzyme digestion. RESULTS: In case of normal aging SST mRNA expression did not alter, but decreased in cancer (p<0.05). The ratio of SST immunoreactive cells was significantly higher in children (0.70%+/-0.79%) compared to CRC (0%+/-0%) (p<0.05). Octreotide significantly increased the proportion of apoptotic Caco-2 cells. SST showed significantly higher methylation level in tumor samples (30.2%+/-11.6%) compared to healthy young individuals (3.5%+/-1.9%) (p<0.05). CONCLUSIONS: In cancerous colonic mucosa the reduced SST production may contribute to the uncontrolled cell proliferation. Our observation that in colon cancer cells octreotide significantly enhanced cell death and attenuated cell proliferation suggests that SST may act as a regulator of epithelial cell kinetics. The inhibition of SST expression in CRC can be epigenetically regulated by promoter hypermethylation

Exploring Differential Connexin Expression across Melanocytic Tumor Progression Involving the Tumor Microenvironment

The incidence of malignant melanoma, one of the deadliest cancers, continues to increase. Here we tested connexin (Cx) expression in primary melanocytes, melanoma cell lines and in a common nevus, dysplastic nevus, and thin, thick, and metastatic melanoma tumor progression series involving the tumor microenvironment by utilizing in silico analysis, qRT-PCR, immunocyto-/histochemistry and dye transfer tests. Primary melanocytes expressed GJA1/Cx43, GJA3/Cx46 and low levels of GJB2/Cx26 and GJC3/Cx30.2 transcripts. In silico data revealed downregulation of GJA1/Cx43 and GJB2/Cx26 mRNA, in addition to upregulated GJB1/Cx32, during melanoma progression. In three melanoma cell lines, we also showed the loss of GJA1/Cx43 and the differential expression of GJB1/Cx32, GJB2/Cx26, GJA3/Cx46 and GJC3/Cx30.2. The dominantly paranuclear localization of connexin proteins explained the ~10&#8315;90 times less melanoma cell coupling compared to melanocytes. In melanocytic tumor tissues, we confirmed the loss of Cx43 protein, fall of cell membrane and elevated paranuclear Cx32 with moderately increased cytoplasmic Cx26 and paranuclear Cx30.2 positivity during tumor progression. Furthermore, we found Cx43, Cx26 and Cx30 proteins upregulated in the melanoma adjacent epidermis, and Cx43 in the tumor flanking vessels. Therefore, differential connexin expression is involved in melanocytic tumor progression where varying connexin isotypes and levels reflect tumor heterogeneity-related bidirectional adaptive interactions with the microenvironment

Genome-Wide Screening of Genes Regulated by DNA Methylation in Colon Cancer Development

<div><p>Tumorigenesis is accompanied by changes in the DNA methylation pattern. Our aim was to test a novel approach for identification of transcripts at whole transcript level which are regulated by DNA methylation. Our approach is based on comparison of data obtained from transcriptome profiling of primary human samples and in vitro cell culture models. Epithelial cells were collected by LCM from normal, adenoma, and tumorous colonic samples. Using gene expression analysis, we identified downregulated genes in the tumors compared to normal tissues. In parallel 3000 upregulated genes were determined in HT-29 colon adenocarcinoma cell culture model after DNA demethylation treatment. Of the 2533 transcripts showing reduced expression in the tumorous samples, 154 had increased expression as a result of DNA demethylation treatment. Approximately 2/3 of these genes had decreased expression already in the adenoma samples. Expression of five genes (<em>GCG</em>, <em>NMES-1</em>, <em>LRMP</em>, <em>FAM161B</em> and <em>PTGDR</em>), was validated using RT-PCR. <em>PTGDR</em> showed ambiguous results, therefore it was further studied to verify the extent of DNA methylation and its effect on the protein level. Results confirmed that our approach is suitable for genome-wide screening of genes which are regulated or inactivated by DNA methylation. Activity of these genes possibly interferes with tumor progression, therefore genes identified can be key factors in the formation and in the progression of the disease.</p> </div

Significant correlation (r = 0.5295; p = 0.0026) between the HOMA2-Insulin resistance index and the fasting serum DPP-4 enzymatic activity in NAFLD patients.

<p>Significant correlation (r = 0.5295; p = 0.0026) between the HOMA2-Insulin resistance index and the fasting serum DPP-4 enzymatic activity in NAFLD patients.</p

Significant correlation (r = 0.3827; p = 0.019) between the liver disease biomarker γGT and the fasting serum DPP-4 enzymatic activity after logarithmic transformation in NAFLD patients.

<p>Significant correlation (r = 0.3827; p = 0.019) between the liver disease biomarker γGT and the fasting serum DPP-4 enzymatic activity after logarithmic transformation in NAFLD patients.</p

Significant correlation (r = 0.4087; p = 0.0120) between the liver disease biomarker ALT and the fasting serum DPP-4 enzymatic activity after logarithmic transformation in NAFLD patients.

<p>Significant correlation (r = 0.4087; p = 0.0120) between the liver disease biomarker ALT and the fasting serum DPP-4 enzymatic activity after logarithmic transformation in NAFLD patients.</p