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

Boceprevir Plus Peginterferon Alfa-2a/Ribavirin in Treatment-Naïve Hepatitis C Virus Genotype 1 Patients: International Phase IIIb/IV TriCo Trial

Article full text The full text of this article can be found here. Provide enhanced content for this article If you are an author of this publication and would like to provide additional enhanced content for your article then please contact [email protected]. The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content. Other enhanced features include, but are not limited to: • Slide decks • Videos and animations • Audio abstracts • Audio slides</p

ROCurve for Multiple Logistic Regression (Equation = 0.7049−0.023*(Fasting Plasma Glucose)+0.0188*(HOMA2-IR)−0.084*(HbA1c)+0.0092*(sDPP−4)+0.004*(ASAT)+0.0000072*(ALAT)+0.0004*(gGT)−0.2859*(ASAT/ALAT)+0.0819*(TG). Criterion 0.3712, below: T2D, above: NAFLD).

<p>ROCurve for Multiple Logistic Regression (Equation  = 0.7049−0.023*(Fasting Plasma Glucose)+0.0188*(HOMA2-IR)−0.084*(HbA1c)+0.0092*(sDPP−4)+0.004*(ASAT)+0.0000072*(ALAT)+0.0004*(gGT)−0.2859*(ASAT/ALAT)+0.0819*(TG). Criterion 0.3712, below: T2D, above: NAFLD).</p

Clinical characteristics and the fasting serum DPP-4 activities of healthy individuals (CNTRL) and patients type with 2 diabetes mellitus (2TDM) and non-alcoholic fatty liver disease (NAFLD).

<p>Mean values are indicated in bold letters and (95% Confidence Intervals are indicated in parenthesis).</p><p>*All NAFLD patients, except 9 previously known diabetic individuals underwent a 75g CH OGTT:</p><p>24 NAFLD patients were with normal glucose tolerance (NGT), 4 had either impaired fasting glucose levels or impaired glucose tolerance (“prediabetes”: IFG/IGT), and 11pateint from the NAFLD group were with type 2 diabetes mellitus (28%).</p><p>All patients in the 2TDM group were with normal liver tests and normal liver US morphology (patients with such abnormalities were either excluded from the study or re-classified to the NAFLD group).</p><p>In order to generate non-overlapping groups from the point of diabetes we also analyzed separately the DPP-4 activity in patients with NGT and NAFLD that was (33.08 U/L (95%CI:29.66–36.50) significantly higher in comparison with the 2TDM and also compared to the healthy control group. (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0012226#pone-0012226-g001" target="_blank">figure 1</a>).</p><p>In patients with NAFLD a non-invasive fibrosis score was used to assess the degree of intrahepatic fibrosis as suggested and validated by <i>Angulo et al</i>. (12) Results are as follows:</p><p>No of pts without significant fibrosis (stage 0–2) (NAFLD fibrosis score<−1.455): 29.1.</p><p>Indeterminate (NAFLD fibrosis score−1.455–0.676): 6.</p><p>No of pts with significant fibrosis (stage 3–4) (NAFLD fibrosis score>0.676): 4.</p><p>**23 out of the 82 patients with type 2 diabetes mellitus were treated with insulin – in these cases the HOMA2-IR was calculated using the C-peptide levels.</p><p>***Significant differences were found in certain lipid values using ANOVA with the Newman-Kleus post hoc range test in the 39 patients with NAFLD as follows: NAFLD patients also displayed higher triglyceride (TG) levels (2.41mmol/L, 95%CI:2.04–2.78) than in the CNTRL group (1.12mmol/L, 95%CI:0.65–1.58, p<0.001) and the TG levels in the NAFLD group were non-significantly higher than in the T2DM group (1.94, 95%CI: 1.68–2.2).</p><p>****The LDL-cholesterol was significantly elevated in NAFLD (3.41mmol/L, 95%CI: 3.05–3.77) compared to controls (2.66mol/L, 95%CI: 2.19–3.13, p = 0.012). The HDL cholesterol was significantly lower in both the T2D group (1.30mmol/L, 95%CI: 1.21–1.39, p<0.05) and the NAFLD group (1.28, 95%CI: 1.15–1.40, p = 0.02) then in the healthy controls (1.54, 95%CI: 1.36–1.69).</p><p>*****Metabolic syndrome was both defined as proposed by the NCEP in ATP-III (indicated as NCEP in the table) and as recently suggested by the AHA and IDF the proportion in each study group was calculated using both methods respectively (14, 15).</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

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