ΦαρμακοΤρίμματα Κατάθλιψη. Μετά-Prozac εποχή Posted: 05 Aug 2012 02:56 PM PDT

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Κατάθλιψη. Μετά-Prozac εποχή Posted: 05 Aug 2012 02:56 PM PDT Στην ιστορία των φαρμάκων λίγα ήταν εκείνα που έτυχαν ενθουσιώδους αποδοχής όπως η λευκή-πράσινη κάψουλα που περιείχε υδροχλωρική φλουοξετίνη, η χημική ουσία γνωστή με την εμπορική ονομασία Prozac(Ladose). Το 1988 ένα χρόνο μετά την έγκριση από την Υπηρεσία Τροφίμων και Φαρμάκων(FDA), στις ΗΠΑ είχαν εκδοθεί 2.469.000 συνταγές για το Prozac. Το 2002 ανέβηκαν σε πάνω από 33 εκατομμύρια. Το 2008 τα αντικαταθλιπτικά ήταν στην τρίτη θέση μεταξύ των πιο συνταγογραφούμενων φαρμάκων στις Ηνωμένες Πολιτείες.Φτάνοντας στο 2012, τα ίδια αντικαταθλιπτικά που είχαν προκαλέσει τόσο ενθουσιασμό, έγιναν τα μαύρα πρόβατα της μοντέρνας ψυχοφαρμακολογίας, σκευάσματα υπερεκτιμημένα και υπερσυνταγογραφημένα, τυπικό δείγμα μιας κουλτούρας που αναζητά γρήγορη λύση σε πολύπλοκα ψυχικά προβλήματα. Στην πραγματικότητα οι ίδιες αρχές βάση των οποίων αυτά τα φάρμακα λειτουργούν, έχουν τεθεί υπό αμφισβήτηση. Τα νευρικά κύτταρα, οι νευρώνες, επικοινωνούν μεταξύ τους μέσω χημικών σημάτων που ονομάζονται νευροδιαβιβαστές οι οποίοι μπορούν να έχουν διαφορετικές μορφές: όπως σεροτονίνη, ντοπαμίνη ή νορεπινεφρίνη. Για δεκαετίες η επικρατέστερη θεωρία ήταν ότι τα αντικαταθλιπτικά λειτουργούσαν αυξάνοντας τα επίπεδα της σεροτονίνης. Πίστευαν ότι στον εγκέφαλο των ατόμων που πάσχουν από κατάθλιψη το σήμα της σεροτονίνης κατά κάποιο τρόπο είχε εξασθενίσει λόγω της χημικής ανισορροπίας στους νευροδιαβιβαστές. Και πως το Prozac(Ladose) και το Paxil(Seroxat) μπορούσαν να αυξήσουν αυτά τα επίπεδα μεταξύ των νευρικών κυττάρων ενισχύοντας αυτά τα σήματα - δυναμώνοντας σαν ένα μεγάφωνο την επικοινωνία μεταξύ των κυττάρων. Ωστόσο αυτή η θεωρία είχε επικριθεί ευρέως. Έχει όμως στην πραγματικότητα ξεπεραστεί η υπόθεση της σεροτονίνης σχετικά με τη κατάθλιψη; Τα αποτελέσματα των τελευταίων ερευνών έχουν επιβεβαιώσει ότι στην πραγματικότητα ο ρόλος της σεροτονίνης παραμένει καθοριστικός για τη διάθεση ακόμα και αν ο μηχανισμός δράσης της είναι περισσότερο εντυπωσιακός από όσο μπορούμε ποτέ να φανταστούμε. Το Prozac το Paxil και το Zoloft πιθανόν να μην είναι τα θαυματουργά φάρμακα που πιστεύαμε στο παρελθόν, μας έχουν βοηθήσει όμως να καταλάβουμε τι είναι η κατάθλιψη και πως μπορούμε να την αντιμετωπίσουμε. Η σύγχρονη αντίληψη της σχέσης μεταξύ της κατάθλιψης και των χημικών ουσιών στον εγκέφαλο γεννήθηκε σχεδόν τυχαία στα μέσα του προηγούμενου αιώνα. Το φθινόπωρο του 1951 οι γιατροί του Sea View Hospital του Staten Island οι οποίοι χρησιμοποιούσαν στη θεραπεία ασθενών με φυματίωση ένα νέο φάρμακο, την ιπρονιαζίδη, παρατήρησαν μια ξαφνική αλλαγή στη διάθεση και τη συμπεριφορά των ασθενών τους. Οι θάλαμοι νοσηλείας, συνήθως σκοτεινοί και αθόρυβοι γεμάτοι ασθενείς που έμοιαζαν απαθείς και ετοιμοθάνατοι "ήταν φωτισμένοι από ευτυχισμένα πρόσωπα ανδρών και γυναικών" όπως χαρακτηριστικά έγραψε μια δημοσιογράφος μετά από επίσκεψη της στο νοσοκομείο. Όταν το περιοδικό Life έστειλε ένα φωτογράφο στο νοσοκομείο, στα πλαίσια σχετικής έρευνας, οι ασθενείς δεν ήταν καθηλωμένοι στα κρεβάτια τους αλλά έπαιζαν χαρτιά και χόρευαν στους διαδρόμους. Μερικά εκατοντάδες χιλιόμετρα νοτιότερα οι ασθενείς του νοσοκομείου Dukes ζούσαν μια τελείως αντίθετη εμπειρία. Το 1954 είχε συνταγογραφηθεί σε μια γυναίκα 28 ετών το Rauxidin(Ρεσερπίνη) για τη ρύθμιση της αρτηριακής της πίεσης. Μετά από κάποιους μήνες επέστρεψε στο νοσοκομείο παραπονούμενη ξεσπάσματα κλάματος, νωθρότητα και λήθαργο. Αισθανόταν άχρηστη, απελπισμένη και γεμάτη ενοχές. Μερικούς μήνες αργότερα, εκείνο το αίσθημα κενού είχε μετατραπεί σε επιθετικότητα. Αυτή η αίσθηση δυστυχίας παρέμεινε μέχρι ως ότου οι ασθενείς δεν σταματούσαν να παίρνουν το φάρμακο. Σε ένα άλλο νοσοκομείο μια ασθενής στην οποία χορηγήθηκε το ίδιο φάρμακο αποπειράθηκε να αυτοκτονήσει. Πολλά άτομα εισήχθησαν σε ψυχιατρικά τμήματα και νοσοκομεία και υπεβλήθησαν σε ηλεκτροσόκ για να μειώσουν τα συμπτώματα. Οι ψυχίατροι και οι φαρμακολόγοι έδειξαν ενδιαφέρον για αυτά τα περίεργα περιστατικά. Αναρωτήθηκαν πως είναι δυνατόν δύο φάρμακα φαινομενικά άσχετα μεταξύ τους, να προκαλούν τόσο βαθιές και αντίθετες επιδράσεις στην διάθεση. Ήταν περίπου εκείνη την περίοδο όπου οι επιστήμονες ανακάλυψαν ότι ο εγκέφαλος ήταν "βυθισμένος" σε ένα υγρό χημικών ουσιών. Στις αρχές του αιώνα άρχισαν να αναρωτιούνται πως τα νευρικά κύτταρα επικοινωνούσαν μεταξύ τους. Στα τέλη της δεκαετίας του 60' είχε πλέον αποδειχτεί ότι τα σήματα μεταξύ των νευρώνων μεταφέρονταν μέσω διάφορων χημικών ουσιών συμπεριλαμβανομένου και του νευροδιαβιβαστή σεροτονίνη. Οι επιστήμονες αναρωτιόνταν αν ήταν δυνατόν η ιπρονιαζίδη και η ρεσερπίνη να αλλοιώνουν τα επίπεδα κάποιου νευροδιαβιβαστή, αλλάζοντας τα σήματα στο εσωτερικό του εγκεφάλου και κατά συνέπεια τη διάθεση. Ήταν αυτό που ακριβώς συνέβαινε. Η ρεσερπίνη που προκαλούσε το αίσθημα θλίψης, μείωνε δραστικά τη συγκέντρωση της σεροτονίνης και άλλων νευροδιαβιβαστών με τους οποίους είναι συνδεδεμένη στενά. Τα φάρμακα που προκαλούσαν εφορία όπως η ιπρονιαζίδη αντιθέτως προκαλούσαν αύξηση στη συγκέντρωση της σεροτονίνης. Αυτές οι πρώτες ανακαλύψεις οδήγησαν τους ψυχίατρους να διατυπώσουν μια καινούργια υπόθεση για την αιτία και την αντιμετώπιση της κατάθλιψης - ήταν το αποτέλεσμα μιας χημικής ανισσοροπίας των νευροδιαβιβαστών: υπό φυσιολογικές συνθήκες στον εγκέφαλο η σεροτονίνη ταξίδευε μπρος - πίσω μεταξύ των νευρώνων διατηρώντας τη ψυχική διάθεση σε ισορροπία, ενώ αυτό δε συνέβαινε στον εγκέφαλο εκείνων που έπασχαν από κατάθλιψη. Ο συγγραφέας Andrew Solomon χαρακτήρισε τη κατάθλιψη ως "απώλεια αγάπης". Οι γιατροί του νοσοκομείου Duke είχαν παρατηρήσει σε πραγματικό χρόνο την εμφάνιση αυτής της απώλειας στους ασθενείς τους: σταδιακά μειωνόταν η αγάπη για τον ίδιο τους τον εαυτό(ενοχές, ντροπή, τάσεις αυτοκτονίας), η αγάπη για τους άλλους(απόδοση ευθυνών, επιθετικότητα) και τέλος η ίδια η ανάγκη για αγάπη(λήθαργος, εσωστρέφεια, απάθεια). Αλλά σύμφωνα με τους επιστήμονες όλα αυτά αποτελούσαν μόνο τα εξωτερικά συμπτώματα της κακής λειτουργίας των νευροδιαβιβαστών. Η απώλεια αγάπης ήταν η απώλεια χημικών ουσιών. Η θεωρία αυτή επιβεβαιώθηκε και με την ανακάλυψη νέων ειδικών φαρμάκων που προκαλούσαν αύξηση στη συγκέντρωση της σεροτονίνης. Το πρώτο από αυτά το Zimelidine(Normud) δημιουργήθηκε από ένα Σουηδό ερευνητή τον Arvid Carlsson. Ακολουθώντας το παράδειγμα του η φαρμακολόγοι επικέντρωσαν τις προσπάθειες και χρησιμοποίησαν τους διαθέσιμους πόρους στην έρευνα για φάρμακα που ενισχύουν τη συγκέντρωση σεροτονίνης, και έτσι γεννήθηκαν με γρήγορη διαδοχή όλοι οι νέοι "γίγαντες" στον κόσμο των αντικαταθλιπτικών. Το Prozac δημιουργήθηκε το 1974, το Paxil εμφανίστηκε το 1975 και το Zoloft τo 1977(τα εμπόρικά τους ονόματα δόθηκαν μερικά χρόνια αργότερα). Για να καταλάβουμε όμως αν η απουσία σεροτονίνης προκαλεί κατάθλιψη πρέπει να ξέρουμε αν στον εγκέφαλο των ατόμων που πάσχουν από αυτήν την ασθένεια, τα επίπεδα της σεροτονίνης ή των μεταβολιτών της σεροτονίνης(που παράγονται από την αποσύνθεση της) είναι στη πραγματικότητα πιο χαμηλά. Το 1975 μια ομάδα παθολόγων πραγματοποίησαν αυτοψίες σε μερικούς καταθλιπτικούς ασθενείς για να κάνουν μετρήσεις. Τα πρώτα συμπεράσματα έμοιαζαν να επιβεβαιώνουν τη θεωρία: οι καταθλιπτικοί ασθενείς έτειναν να έχουν μειωμένα επίπεδα σεροτονίνης. Όμως το 1987 μερικοί Σκανδιναβοί ερευνητές επανέλαβαν το πείραμα με νέα εργαλεία μετρήσεων και διαπίστωσαν ότι στους καταθλιπτικούς ασθενείς τα επίπεδα σεροτονίνης ήταν ψηλότερα. Νέα πειράματα δεν έκαναν άλλο από το να επιβεβαιώσουν αυτή την αντίθεση. Σύμφωνα με κάποια test οι καταθλιπτικοί ασθενείς είχαν χαμηλότερα επίπεδα σεροτονίνης, ενω σύμφωνα με άλλα υψηλότερα, για άλλα δεν υπήρχε καμία διαφορά. Τι θα συνέβαινε όμως αν διεξήγαγαν το αντίστροφο πείραμα; Το 1994 σε μια ομάδα εθελοντών του πανεπιστημίου McGill στο Μόντρεαλ χορηγήθηκε ένα μείγμα χημικών ουσιών που χαμήλωνε τα επίπεδα της σεροτονίνης. Οι γιατροί παρατήρησαν τις αλλαγές στη διάθεση τους καθώς τα επίπεδα μειώνονταν. Ακόμα και όταν η σεροτονίνη δεν υπήρχε πλέον καθόλου, το μεγαλύτερο μέρος των ατόμων δεν παρουσίαζε σημαντικές αλλαγές στη διάθεση. Με μια πρώτη ματιά αυτές οι μελέτες μας κάνουν να σκεφτούμε ότι δεν υπάρχει καμία σχέση μεταξύ σεροτονίνης και κατάθλιψης. Αλλά από το πείραμα McGill προέκυψε ένα σημαντικό γεγονός: η μείωση των επιπέδων της σεροτονίνης δεν παρήγαγε κανένα αποτέλεσμα σε υγιείς εθελοντές που δεν υπέφεραν πότε από κατάθλιψη, ενώ παρήγαγε εντυπωσιακά αποτελέσματα σε άτομα που είχαν οικογενειακό ιστορικό κατάθλιψης. Σε αυτά τα άτομα όταν τα επίπεδα της σεροτονίνης μειώνονταν η διάθεση χειροτέρευε σημαντικά. Μια παλαιότερη έκδοση αυτού του πειράματος, που πραγματοποιήθηκε στο Yale το 1990, είχε αποτελέσματα περισσότερο ανησυχητικά. Όταν οι ασθενείς που έπασχαν από κατάθλιψη και ακουλουθούσαν είδη θεραπεία με χορήγηση φαρμάκων όπως το Prozac έπαιρναν ένα μείγμα ουσιών που χαμήλωνε τα επίπεδα της σεροτονίνης έπεφταν συχνά σε βαθιά καταθλιψη. Άλλα πειράματα έδειξαν πως αν όχι όλοι οι ασθενείς με κατάθλιψη παρουσίαζαν χαμηλότερα επίπεδα σεροτονίνης, για εκείνους που είχαν τάσεις αυτοκτονίας αυτό ήταν σίγουρο. Στα τέλη της δεκαετίας του 80' έγιναν κάποιες μελέτες για να επαληθευτούν τα αποτελέσματα του Prozac σε καταθλιπτικά άτομα. Διαπιστώθηκε πως συγκριτικά με placebo το φάρμακο μείωνε τα συμπτώματα της κατάθλιψης. Συνήθως η διάγνωση της κατάθλιψης γίνετε χρησιμοποιώντας μια τυποποιημένη σκάλα συμπτωμάτων. Συνολικά κάποιοι ασθενείς παρουσίασαν σημαντική βελτίωση από κλινικής απόψεως ακόμα και αν τα αποτελέσματα ήταν συνήθως πολύ μικρά και άλλαζαν από test σε test. Στην πραγματική ζωη ακόμα και αυτές οι μικρές αλλαγές μπορούσαν να είναι πολύ σημαντικές: η μείωση του άγχους, των ενοχών και το τέλος των τάσεων αυτοκτονίας. Για άλλους όμως ασθενείς οι αλλαγές ήταν οριακές. Ίσως το πιο σημαντικό στοιχείο που προέκυψε από αυτά τα test ήταν το πιο υποκειμενικό: το 74% των ασθενών δήλωνε ότι αισθανόταν καλύτερα από τη στιγμή έπαιρνε τα αντικαταθλιπτικά. Στα τέλη της δεκαετίας του 80', ένας νευρολόγος με το όνομα Fred Cage άρχισε να ενδιαφέρεται για ένα ζήτημα που αρχικά έμοιαζε μακρινό με το πρόβλημα της κατάθλιψης: μπορεί ο ανθρώπινος εγκέφαλος ενός ενήλικα να παράγει νέα εγκεφαλικά κύτταρα; Την εποχή εκείνη οι νευροβιολόγοι ήταν πεπεισμένοι ότι στον εγκέφαλο ενός ενήλικα δεν υπήρχε ανάπτυξη και δεν γεννιόντουσαν πια νέα νευρικά κύτταρα, πως όταν τα νευρικά κυκλώματα δημιουργούνταν για μία φορά κατά τη διάρκεια της παιδικής ηλικίας παρέμεναν σταθερά και αμετάβλητα. Αν όμως οι νέοι νευρώνες αντικαθιστούσαν τους παλιούς,οι αναμνήσεις δεν θα έπρεπε να χαθούν; Ο Cage και άλλοι επιστήμονες επανεξέτασαν παλιά ευρήματα και ανακάλυψαν ότι στην πραγματικότητα στα ποντίκια, στους αρουραίους και στα ενήλικα ανθρώπινα όντα σχηματίζονται νέοι νευρώνες αλλά μονάχα σε δύο ειδικές περιοχές του εγκεφάλου: στον οσφρητικό βολβό όπου καταγράφονται οι οσμές, και στον ιππόκαμπο το όργανο που ελέγχει τη μνήμη και που είναι λειτουργικά συνδεδεμένο με τις ζώνες του εγκεφάλου που ελέγχουν τα συναισθήματα. Για να ανακαλύψουν αν υπάρχει κάποια σχέση μεταξύ των συναισθημάτων και της γέννησης των νευρώνων στον ιππόκαμπο ο Cage και οι συνεργάτες του άρχισαν να μελετούν τα ποντίκια κάτω από συνθήκες stress. Όταν τα ποντίκια υποβάλλονται σε χρόνιο stress, είτε γιατί το περιβάλλον τους ξαφνικά αλλάζει είτε γιατί τα κρεβάτια τους μετακινούνται, παρουσιάζουν συμπτώματα άγχους ή απάθειας και γίνονται λιγότερο δραστήρια, όλα στοιχεία που ταυτίζονται με την κατάθλιψη στον άνθρωπο. Η ομάδα του Cage ανακάλυψε ότι σε αυτά τα ποντίκια η παραγωγή νευρικών κυττάρων στον ιππόκαμπο μειωνόταν. Φαινόταν επίσης ότι συνέβαινε και το ακριβώς αντίθετο. Όταν τα ποντίκια τοποθετούνταν σε ένα περιβάλλον με περισσότερα ερεθίσματα που συνήθως περιείχε λαβύρινθους, υλικό για την κατασκευή της φωλιάς και για παιχνίδι γίνονταν ενεργητικά και δραστήρια. Εξ ερευνούσαν περισσότερο μάθαιναν γρηγορότερα και έψαχναν την ευχαρίστηση. Τα ερεθίσματα πρακτικά λειτουργούσαν σαν αντικαταθλιπτικά. Όταν ο Cage εξέτασε τον εγκέφαλο αυτών των τρωκτικών που δέχτηκαν περισσότερα ερεθίσματα, συνειδητοποίησε ότι στον ιππόκαμπο γεννιόντουσαν περισσότεροι νευρώνες. Στο πανεπιστήμιο Columbia ένας άλλος επιστήμονας ο Rene Hen εντυπωσιασμένος από τις μελέτες του Cage μαζί με τους συνεργάτες του άρχισαν να ερευνούν τη σχέση μεταξύ του Prozac και της ανάπτυξης νευρώνων. Στα ποντίκια o σχηματισμός νέων νευρώνων απαιτεί δύο με τρείς εβδομάδες, σχεδόν ο ίδιος χρόνος που χρειάζεται για να αρχίσουν τα αντικαταθλιπτικά φάρμακα να έχουν αποτελέσματα. Ήταν δυνατόν τα αποτελέσματα του Prozac και του Paxil να συνδέονταν με την ανάπτυξη των νευρώνων και όχι μόνο με τη συγκέντρωση σεροτονίνης; Ο Hen άρχισε να χορηγεί Prozac στα πειραματόζωα του. Μετά από κάποιες μέρες η συμπεριφορά τους άλλαξε: τα συμπτώματα άγχους μειώθηκαν και τα πειραματόζωα γίνονταν πιο δραστήρια. έψαχναν για τροφή σε διαφορετικά μέρη και υιοθετούσαν αμέσως νέες συμπεριφορές. Οι νέοι νευρώνες εμφανίζονταν στον ιππόκαμπο στο ίδιο σημείο που είχε παρατηρήσει ο Cage στα δικά του πειράματα. Όταν όμως ο Hen μπλόκαρε τη δημιουργία των νευρώνων στον ιππόκαμπο, η τάση των πειραματόζων να είναι πιο δραστήρια εξαφανίστηκε. Με άλλα λόγια τα θετικά αποτελέσματα του φαρμάκου εξαρτώνταν από τη γέννηση νευρικών κυττάρων στον ιππόκαμπο. Το 2011 ο Hen και οι συνεργάτες επανέλαβαν αυτό το πείραμα αυτή τη φορά σε ομάδα πιθήκων. Στους πιθήκους το χρόνιο stress δημιουργεί συμπτώματα παρόμοια με αυτά της κατάθλιψης στους ανθρώπους. Ακόμα περισσότερο από τα ποντίκια οι πίθηκοι κάτω από stress χάνουν το ενδιαφέρον τους για κάθε ευχαρίστηση και γίνονται απαθείς. Όταν μέτρησε τη δημιουργία των νευρώνων στον ιππόκαμπο αυτών των ζώων, ο Hen διαπίστωσε ότι ήταν μειωμένη. Όταν αντιθέτως χορήγησε στους πιθήκους ένα αντικαταθλιπτικό, διαπίστωσε ότι τα συμπτώματα της κατάθλιψης μειώνονταν και πως οι νευρώνες άρχισαν να δημιουργούνται ξανά. Μπλοκάροντας την ανάπτυξη νευρικών κυττάρων το Prozac δε λειτουργούσε πια. Τα αποτελέσματα των πειραμάτων του Hen έχουν σημαντικές επιπτώσεις για τη ψυχιατρική και τη ψυχολογία.Τα αντικαταθλιπτικά όπως το Prozac και το Zoloft, σύμφωνα με τον Hen μπορούν να ανεβάσουν προσωρινά τα επίπεδα της σεροτονίνης στον εγκέφαλο αλλά η δράση τους είναι ορατή μόνο όταν γεννιούνται νέοι νευρώνες. Η κατάθλιψη είναι μια πολύπλοκη ασθένεια που μπορεί να έχει διαφορετικές μορφές και αιτίες. Όπως αποδεικνύουν οι κλινικές μελέτες, μόνο ένα μέρος των ασθενών που πάσχουν από βαριά κατάθλιψη ανταποκρίνεται στη θεραπεία με αντικαταθλιπτικά που ενισχύουν τη συγκέντρωση της σεροτονίνης. Οι διαφορετικές αντιδράσεις στα φάρμακα μπορούν επίσης να οφείλονται σε διαφορές στα βιολογικά "μονοπάτια". Σε κάποια άτομα θα μπορούσαν να εμπλέκονται και διαφορετικοί νευροδιαβιβαστές από τη σεροτονίνη. Σε άλλους οι μεταβολές στον εγκέφαλο θα μπορούσαν να προκληθούν από βιολογικούς παράγοντες διαφορετικούς από τους νευροδιαβιβαστές. Και τέλος σε κάποιους οι χημικοί και βιολογικοί παράγοντες θα μπορούσαν να μην είναι αναγνωρίσιμοι. Για παράδειγμα η κατάθλιψη που σχετίζεται με τη νόσο του Parkinson μοιάζει να έχει ελάχιστη σχέση με τη σεροτονίνη. Η επιλόχειος κατάθλιψη είναι ένα τόσο ιδιαίτερο σύνδρομο έτσι ώστε είναι δύσκολο να φανταστούμε πως οι νευροδιαβιβαστές ή η γέννηση νευρώνων στον ιππόκαμπο μπορούν να διαδραματίσουν τον καθοριστικό ρόλο σε αυτό. Οι νέες θεωρίες δεν εξηγούν επίσης για πιο λόγο η ψυχοθεραπεία λειτουργεί με κάποιους ασθενείς και όχι με άλλους, και γιατί μιλώντας με έναν θεραπευτή και λαμβάνοντας παράλληλα αντικαταθλιπτικά μπορεί να έχουμε καλύτερα αποτελέσματα. Για να μελετήσουμε το άγνωστο σύμπαν της ψυχικής διάθεσης και των συναισθημάτων τα μέσα που διαθέτουμε είναι λίγα. Μπορούμε μονάχα να συνδυάζουμε χημικές ουσίες και να ενεργοποιούμε ηλεκτρικά κυκλώματα, ελπίζοντας έμμεσα να κατανοήσουμε τη δομή και τη λειτουργία του εγκεφάλου μέσα από τα σχετικά αποτελέσματα. Με τη πάροδο του χρόνου, αυτές οι νέες θεωρίες για τη κατάθλιψη πολύ πιθανόν μπορούν να οδηγήσουν στη δημιουργία νέων αντικαταθλιπτικών. Αυτά τα φάρμακα θα κάνουν το Prozac και το Paxil, να μοιάζουν ξεπερασμένα. Τα σημερινά αντικαταθλιπτικά δεν πρέπει να θεωρούνται κατάκτηση της ιατρικής αλλά τεχνολογικές ανακαλύψεις, και είναι αυτές οι τεχνολογικές ανακαλύψεις που μας επέτρεψαν να ξεκινήσουμε να κατανοούμε κάτι για τον εγκέφαλο μας και τη βιολογία αυτής της μυστηριώδης ασθένειας που προσβάλει τον άνθρωπο. Πηγή:           Siddhartha Mukherjee http://www.nytimes.com/ http://www.internazionale.it/           Internazionale, 26 Giugno/5Luglio 2012, N.95           Εικόνες, Benoit Paille FarmakoTrimmata    Depression. After-Prozac era Posted: 05 Aug 2012 02:56 PM PDT In the history of drugs were those few who were enthusiastic acceptance as the white-green capsule contains fluoxetine hydrochloride, a chemical known by the brand name Prozac (Ladose). In 1988, one year after approval by the Food and Drug Administration (FDA ), U.S. 2,469,000 issued prescriptions for Prozac. In 2002 rose to over 33 million. In 2008, antidepressants were in third place among the most prescribed drugs in the United States. Arriving in 2012, the same antidepressants that had caused so much excitement, were the black sheep of modern psychopharmacology, and overestimated ypersyntagografimena formulations, typical of a culture that looks fast solution to complex mental health problems.  In fact the same principles on which these drugs work, have been questioned.  The nerve cells, neurons, communicate through chemical signals called neurotransmitters which can have different forms: as serotonin, dopamine or norepinephrine. For decades, the prevailing theory was that antidepressants worked by increasing serotonin levels. They believed that the brains of people suffering from depression serotonin signal somehow been impaired due to chemical imbalance in neurotransmitters. And how Prozac (Ladose) and Paxil (Seroxat) could increase these levels between nerve cells by enhancing these signals - dynamonontas as a speaker to communicate between cells. However this theory has been widely criticized.  But it has actually surpassed the serotonin hypothesis of depression?  The results of recent surveys have confirmed that in fact the role of serotonin remains crucial for the disposal even though the mechanism of action is more impressive than we can ever imagine. To the Prozac Paxil and Zoloft may not be the miracle drugs we thought before, but have helped us to understand what depression is and how to treat it.  The modern understanding of the relationship between depression and chemicals in the brain was born almost by accident in the middle of last century. In the fall of 1951 the doctors of Sea View Hospital in Staten Island who used to treat TB patients a new drug, the iproniazidi, noticed a sudden change in mood and behavior of their patients. The ward, usually filled with dark and silent patients seemed apathetic and dying "was illuminated by happy faces of men and women" as a features reporter wrote after a visit to the hospital. When Life magazine sent a photographer to the hospital, in relative research, patients were not stuck in their beds, but they played cards and danced in the aisles.few hundred kilometers south of the hospital patients Dukes lived a completely opposite experience. In 1954 he was prescribed to a woman 28 years Rauxidin (reserpine) to regulate blood pressure. After some months he returned to hospital complaining crying spells, drowsiness and lethargy. He felt useless, hopeless and full of guilt. A few months later, that empty feeling had become aggressive. This sense of misery as they remained until the patients stopped taking the drug. In another hospital where a patient was administered the same drug attempted suicide. Many people admitted to psychiatric hospitals and underwent electroshock to reduce symptoms.  Psychiatrists and pharmacologists have shown interest in these strange occurrences. They wondered how can two seemingly unrelated drugs, to cause such profound and adverse effect on mood. It was about that time where scientists discovered that the brain was "immersed" in a liquid chemicals. At the beginning of the century began to wonder how nerve cells communicate with each other. In the late 60's had now been shown that signals between neurons were transferred through several chemicals including the neurotransmitter serotonin. Scientists wondered if it was possible iproniazidi reserpine and altering levels of a neurotransmitter, changing the signals inside brain and thus the mood. It was exactly what was happening. The reserpine to cause a feeling of sadness, greatly reduce the concentration of serotonin and other neurotransmitters by which tied closely.  The drugs that caused the IRS as iproniazidi instead caused an increase in the concentration of serotonin. These discoveries led the first psychiatrists to formulate a new hypothesis for the cause and treatment of depression - was the result of a chemical imbalance of neurotransmitters: in normal brain serotonin traveled forth - forth between neurons maintaining a balance of mind while this does not happen in the brain of those suffering from depression. The writer Andrew Solomon described the depression as "loss of love." Doctors Hospital Duke had observed in real time the occurrence of this loss in their patients: decreased progressively love for their own self (guilt, shame, suicidal), love for others (accountability, aggression) and end of the very need for love (lethargy, introversion, apathy). But according to scientists all these were only the outward symptoms of malfunctioning neurotransmitters. The loss was the loss of love, chemicals.  This theory was confirmed with the discovery of new specific drugs that cause an increase in the concentration of serotonin. The first of these, Zimelidine (Normud) created by a Swedish researcher, the Arvid Carlsson. Following the example of the pharmacologist focused their efforts and use available resources to research drugs that enhance serotonin concentration, and thus were born in quick succession all new "giants" in the world of antidepressants. The Prozac was established in 1974, appeared in 1975, Paxil and Zoloft The 1977 (the trade name given some years later).  But to understand whether the absence of serotonin causes depression we need to know if the brains of people suffering from this disease, the levels of serotonin or serotonin metabolites (derived from the decomposition of) is actually lower. In 1975 a group of pathologists conducted autopsies on some depressed patients to make measurements. The preliminary findings seemed to confirm the theory: the depressed patients tended to have lower levels of serotonin. But in 1987 some Scandinavian researchers repeated the experiment with new measurement tools and found that in depressed patients, serotonin levels were higher. New experiments did other than to confirm that opposition. According to a test depressed patients had lower levels of serotonin, while according to other higher, for others there was no difference.  What would happen if the reverse experiment conducted?  In 1994 a volunteer group of McGill University in Montreal was a mixture of chemicals that lower levels of serotonin. Doctors noticed changes in their mood and reduced levels. Even when serotonin no longer existed at all, most people did not show significant changes in mood. At first glance these studies make us think that there is no relationship between serotonin and depression. But the experiment showed a McGill important fact: the lowering of serotonin did not produce any effect in healthy volunteers when they did not suffer from depression, and produced impressive results in people who had family history of depression. These people when serotonin levels decreased significantly worsened the mood. An earlier version of this experiment, conducted at Yale in 1990, was more alarming results. When patients suffering from depression and akoulouthousan types of therapy with drugs like Prozac were taking a mixture of substances that lower levels of serotonin often fell into deep depression. Other experiments showed that although not all patients with depression had lower levels of serotonin, for those who were suicidal, it sure was.  In the late 80's were some studies to verify the effects of Prozac to depressed people. It was found that compared with placebo the drug reduces symptoms of depression. Usually the diagnosis of depression become a standard ladder using symptoms. Altogether some patients experienced significant improvement of clinical, even if the results were usually very small and change from test to test. In real life, even these small changes could be very important: the reduction of anxiety, of guilt and the end of suicide. For other patients but the changes were marginal.  Perhaps the most important element that emerged from these test was the most subjective: 74% of patients say they feel better than when he was taking antidepressants.  In the late 80's, a neurologist named Fred Cage became interested in an issue that initially seemed far away with the problem of depression: Can an adult human brain produce new brain cells?  At that time, neurobiologists were convinced that an adult brain development and there was not born any more new nerve cells, that when the neural circuits created once during childhood remained stable and unchanged. But ifthe new neurons replace the old, memories should not be lost?  The Cage and other scientists have reviewed old findings and discovered that in fact in mice, rats and adult human beings form new neurons, but only in two specific areas of the brain: the olfactory bulb, where smells are recorded, and the hippocampus, which controls the instrument memory and that is functionally connected areas of the brain that control emotions.  To find out if there is any relationship between emotions and the birth of neurons in the hippocampus Cage and his colleagues began studying the rats under conditions of stress. When the mice subjected to chronic stress, either because their environment changes suddenly or because their beds are moved, they show symptoms of anxiety or apathy and become less active, all items are identified with depression in humans. Cage's team discovered that these mice to produce nerve cells in the hippocampus decreased. It seemed that was exactly the opposite. When the mice were placed in an environment with more stimuli that usually contained mazes, material for building the nest and become active play and active. By investigating more and learn faster searching pleasure. The stimuli practically functioned as antidepressants. When Cage examined the brains of these mice that received more stimulation, she realized that most were born hippocampal neurons.  At Columbia University, another scientist Rene Hen impressed by his studies with Cage and his colleagues began to investigate the relationship between Prozac and development of neurons. In mice o formation of new neurons requires two to three weeks, almost the same amount of time it takes to start antidepressant medication have an effect. Was possible the effects of Prozac and Paxil have been linked with the development of neurons and not only on concentration Serotonin?  The Hen began granting Prozac in the guinea pigs. After some days the behavior changed: the anxiety symptoms decreased and the animals become more active. searching for food in different places and have adopted new behaviors immediately. The new neurons in the hippocampus appeared at the same point that was noticed by Cage's own experiments. But when the Hen blocked the creation of neurons in the hippocampus, the tendency of peiramatozon be more active disappeared. In other words, the positive effects of the drug depended on the birth of nerve cells in the hippocampus.  In 2011 the Hen and colleagues have repeated this experiment, this time a group of monkeys. In monkeys, chronic stress creates symptoms similar to depression in humans. Even more than the mice, monkeys under stress lose interest for every pleasure and become apathetic. When measured the creation of neurons in the hippocampus of these animals, the Hen found that they were reduced. When monkeys instead granted an antidepressant, found that symptoms of depression decreased and that the neurons began to arise again. Blocking the development of nerve cells in Prozac was not working anymore.  The experimental results of Hen have important implications for psychiatry and psychology. Antidepressants such as Prozac and Zoloft, according to the Hen may temporarily raise levels of serotonin in the brain but the effect is visible only when new neurons are born .  Depression is a complex disease that can have different forms and causes. As demonstrated by clinical studies, only a fraction of patients suffering from severe depression responds to treatment with antidepressants that enhance the concentration of serotonin. Different reactions to drugs may also be due to biological differences in "paths". In some people could be involved in the different neurotransmitters serotonin. In other changes in the brain could be caused by biological factors other than neurotransmitters. And finally some of the chemical and biological agents could not be identifiable. For example, the depression associated with Parkinson's disease seems to have little to do with serotonin. The postpartum depression is a syndrome so special so it is difficult to imagine how the neurotransmitters or the birth of neurons in the hippocampus may play a decisive role in this. The new theories also explain why most of the psychotherapy work with some patients and not others, and why talking to a therapist and taking antidepressants also can have better results.  To study the unknown universe of mood and emotions our resources are few. We just want to combine chemicals and energize electrical circuits, implicitly hoping to understand the structure and functioning of the brain through the results. With time, these new theories of depression could very likely lead to the creation of new antidepressants. These medications will make Prozac and Paxil, to look outdated. Current antidepressants should not be considered medical conquest but technological breakthroughs, and these technology breakthroughs have allowed us to begin to understand something about our brains and biology this mysterious disease that affects humans.  Source:  Siddhartha Mukherjee  http://www.nytimes.com/ http://www.internazionale.it/ Internazionale, 26 Giugno/5Luglio 2012, N.95  Pictures, Benoit Paille

Amnesty International Urgent Action - EXECUTION LOOMS FOR SAEED SEDEGHI - Index Number: MDE 13/056/2012 Date Published: 3 August 2012

 

Human Chain Project

#IRAN: FURTHER INFORMATION: 
#EXECUTION LOOMS 4 #SAEED__SEDEGHI Plz Take Action & RT 

Amnesty International Urgent Action 

Index Number: MDE 13/056/2012
Date Published: 3 August 2012

EXECUTION LOOMS FOR SAEED SEDEGHI

Saeed Sedeghi, a shop worker sentenced to death for a drugs offence, appears to be at imminent risk of execution. He was transferred from Tehran’s Kahrizak detention centre to Ghezel Hesar Prison in Karaj on 1 August, where he could be executed at any time.

On 28 July 2012, Saeed Sedeghi was brought before Branch 30 of Tehran’s Revolutionary Court, where he was required to sign a document, apparently informing him that his death sentence was going to be implemented. Saeed Sedeghi’s lawyer was not present. Saeed Sedeghi had previously made an application to the Amnesty and Clemency Commission. He was never formally told of the outcome of this application, but given what happened in court on 28 July, it appears to have been rejected.

Saeed Sedeghi had an unfair trial, on 26 May 2012, before Branch 30 of Tehran’s Revolutionary Court, where he was represented by a state-appointed lawyer.

This lawyer had had no contact with Saeed Sedeghi, or access to his casefile, before the trial. The court sentenced him to death on 2 June 2012 for participating with three other men in the purchase and possession of 512 kg of methamphetamine. Saeed Sedeghi was also ordered to pay a fine of two million rials (approximately US$163) and sentenced to 20 lashes for individual possession of 21 grams of the drugs opium and marijuana.

Please write immediately in
Persian, Arabic, English or your own language:

Urging the Iranian authorities not to carry out the flogging or execution of Saeed Sedeghi, and to commute his death sentence, and that of anyone else on death row;
Calling on them to ensure Saeed Sedeghi is given immediate and regular access to any medical attention he may require, his family and a lawyer of his own choosing:

Acknowledging that the authorities have a right to prosecute anyone for offences connected to the production and supply of illegal drugs, but pointing out that drugs offences do not meet the threshold of “most serious crimes” to which the death penalty must be restricted under international law, and that death sentences should not be mandatory.

PLEASE SEND APPEALS BEFORE 14 SEPTEMBER 2012 TO:

Leader of the Islamic Republic
Ayatollah Sayed ‘Ali Khamenei
The Office of the Supreme Leader
Islamic Republic Street – End of Shahid Keshvar Doust Street, Tehran, Islamic Republic of Iran
Email: info_leader@leader.ir
Twitter: "#Iran leader @khamenei_ir: halt execution of Saeed Sedeghi”. Use the hashtag: #saeedsedeghi
Salutation: Your Excellency

Head of the Judiciary
Ayatollah Sadegh Larijani
[care of] Public relations Office
Number 4, 2 Azizi Street
Vali Asr Ave, above Pasteur Street intersection
Tehran, Islamic Republic of Iran
Email: bia.judi@yahoo.com 
(Subject line: FAO Ayatollah Sadegh Larijani) or info_leader@leader.ir
Salutation: Your Excellency

And copies to:

Secretary General, High Council for Human Rights
Mohammad Javad Larijani
High Council for Human Rights
[Care of] Office of the Head of the Judiciary, Pasteur St., Vali Asr Ave. south of Serah-e Jomhouri, Tehran 1316814737, Islamic Republic of Iran
Email: info@humanrights-iran.ir
(subject line: FAO Mohammad Javad Larijani

Also send copies to 
diplomatic representatives accredited to your country.

Please check with your section office 
if sending appeals after the above date. 

This is the first update of UA: 165/12. 

Further information: http://www.amnesty.org/en/ library/info/MDE13/035/ 2011/en

ADDITIONAL INFORMATION

Saeed Sedeghi was arrested along with three other men in Tehran on 29 November 2011 for possession of the synthetic drug methamphetamine. Until his transfer to Ghezel Hesar Prison, he had been held in Kahrizak detention centre, in southern Tehran. Saeed Sedeghi had told his family that he was tortured or otherwise ill-treated, including having several teeth knocked out while in Kahrizak detention centre.

Iran has one of the highest rates of drug addiction in the world; in May 2011 the Head of the Law Enforcement Force, Esma’il Ahmadi-Moghaddam, said that there were probably more than two million users of illegal drugs in the country. It is also second only to China in the number of executions carried out each year.

In 2011, of some 600 executions recorded by Amnesty International from both official and unofficial sources, 488 were for drugs offences – a staggering 81 per cent.

For more information, see Addicted to death: executions for drugs offences in Iran (MDE 13/090/2011), 15 December 2011, http://www.amnesty.org/en/library/info/MDE13/090/2011/en So far in 2012, at least 121 of the 178 executions acknowledged by the Iranian authorities have been for drug-related offences. Amnesty International has received credible reports of 94 other executions which were not officially acknowledged, mostly of people convicted of drugs offences.

The Interior Minister stated in October 2010 that the campaign against drug trafficking was being intensified, and the Prosecutor-General stated that month that new measures had been taken to speed up the judicial processing of drug-trafficking cases, including referring all such cases to his office. 

Under Article 32 of the Anti-Narcotics Law, those sentenced to death for drugs offences do not have the right to appeal, as their convictions and sentences are merely confirmed by either the President of the Supreme Court or the Prosecutor-General. In practice, it seems that many such death sentences are referred to the Prosecutor-General. 

This contravenes Article 19 of the Law on Appeals, under which all death sentences are open to appeal, as well as Article 14 (5) of the International Covenant on Civil and Political Rights (ICCPR), which states that “everyone convicted of a crime shall have the right to his conviction and sentence being reviewed by a higher tribunal according to law”.

In December 2010, amendments to the Anti-Narcotics Law extended the scope of the death penalty to include additional categories of illegal drugs (including methamphetamine - “crystal meth”), possession of more than specified amounts of which carries a mandatory death sentence. 

The UN Human Rights Committee has stated that “the automatic and mandatory imposition of the death penalty constitutes an arbitrary deprivation of life, in violation of Article 6(1) of the ICCPR, in circumstances where the death penalty is imposed without any possibility of taking into account the defendant's personal circumstances or the circumstances of the particular offence”.

Under Article 6 (2) of the ICCPR, to which Iran is a state party, “sentence of death may be imposed only for the most serious crimes”. UN human rights mechanisms, including the Special Rapporteur on extrajudicial, summary, or arbitrary executions and the Human Rights Committee, have concluded that the death penalty for drug offences fails to meet the condition of "most serious crime". 

The UN High Commissioner for Human Rights and the director of the UN Office on Drugs and Crime have likewise expressed grave concerns about the application of the death penalty for drug offences.

Names: Saeed Sedeghi
Gender m/f: m

urther information on 
UA: 165/12 Index: MDE 13/056/2012 Issue Date: 3 August 2012

SOURCE : Amnesty International 

Australia's unknown Schapelle - August 5, 2012 REPORTER: Mike Willesee PRODUCER: Mick O’Donnell In a crowded prison in Peru, a young Australian sits singing songs about freedom.

http://au.news.yahoo.com/sunday-night/features/article/-/14437155/australias-unknown-schapelle/

 

Australia's unknown Schapelle

Enlarge photo

 

August 5, 2012

REPORTER: Mike Willesee

PRODUCER: Mick O’Donnell

In a crowded prison in Peru, a young Australian sits singing songs about freedom.

27-year-old Bronwyn Kay Atheron is four years into a 14-year sentence for drug trafficking after she was busted at Lima airport with a suitcase full of cocaine.

Peru has overtaken Colombia as the number one exporter of cocaine worldwide. Much of the cocaine that comes into the United States, Europe and now Australia is being directly attributed to the mountains of Peru.

Sunday Night travelled to Lima’s Santa Monica Prison to meet this young Australian woman whose troubled life drew her into the deadly international drug trade.

Unlike Schapelle Corby’s much publicised plight, Bronwyn’s story has never been told. In interviews in prison with Sunday Night’s Mike Willesee, Bronwyn told of the cartel who hired her, set her up, then betrayed her. She was a drug mule sacrificed so a more lucrative shipment could be smuggled through safely.

Born in Cowra, Central NSW, Bronwyn said she suffered sexual abuse as a child and left home at the age of 16. A year later she gave birth to a baby boy called Shamaya.

”He really was an angel. I breast fed him two and a half years and I woke up every morning to his beautiful smile and his shiny eyes,” she said.

While in the care of his father, Bronwyn’s then-three-year-old son suffered a constricted bowel and died suddenly.

 

 

“I’m not saying that everyone that has bad things happen to them are going to end up in jail, but it’s like I was on the path of destruction because I was messed up and I was broken and because I needed love,” she told Willesee.

A few months later Bronwyn was raped. Six months after that she was diagnosed with HIV.

“I lost hope in my life…What more bad can actually happen to me? I was all messed up.”

In a bid to escape her problems, Bronwyn left Australia, and in a café in Pretoria, South Africa, she was befriended by members of a Nigerian drug syndicate.

“In under a year my son had died, I got raped and found out I had HIV. That’s the most full-on stuff that can happen to you; of course I could easily make the worst decision of my life.”

In the overcrowded prison Bronwyn shares a tiny cell measuring three metres square with three other women. During one of Sunday Night’s visits, we watched her sing as part of a choir in the courtyard, alongside best friend Deidre – a Canadian also jailed for cocaine smuggling.

Bronwyn looked well enough and put on a brave front, but her 14-year jail term may be a death sentence because of difficulties getting access to the HIV medications she needs to stay healthy.

Sunday Night put Bronwyn in touch with Dr Emilia Fishman, a highly regarded lawyer who’s now appealing for clemency and is confident she can at least secure a reduction of her sentence.

 

 

Sadly, Bronwyn’s story is not unique. Each year, hundreds of foreigners are arrested in Peru for drug offences. In January this year an Australian man died at Lima Airport when cocaine leaked in his stomach.

Supporters of Bronwyn's plight have set up a website and a Facebook group for those who'd like to write to her or offer help.

Pussy Riot trial 'worse than Soviet era' Judge refuses to allow 10 defence witnesses while lawyer claims women are being tortured with lack of food and sleep Miriam Elder in Moscow guardian.co.uk, Friday 3 August 2012 19.29 BST

http://www.guardian.co.uk/world/2012/aug/03/pussy-riot-trial-russia

 

Pussy Riot trial 'worse than Soviet era'

Judge refuses to allow 10 defence witnesses while lawyer claims women are being tortured with lack of food and sleep

• Miriam Elder in Moscow
• guardian.co.uk, Friday 3 August 2012 19.29 BST

Pussy Riot band members: from left, Nadezhda Tolokonnikova, Yekaterina Samutsevich and Maria Alyokhina in court. Photograph: Aleshkovsky Mitya/Corbis

By the end of the first week of Pussy Riot's trial, everyone in the shabby Moscow courthouse was tired. Guards, armed with submachine guns, grabbed journalists and threw them out of the room at will. The judge, perched in front of a shabby Russian flag, refused to look at the defence. And the police dog – a 100lb black Rottweiler – no longer sat in the corner she had occupied since the start of Russia's trial of the year, but barked and foamed at the mouth as if she were in search of blood.

The trial of the three band members, jailed since March after performing a "punk prayer" against Vladimir Putin in Moscow's main cathedral, has been about more than the charges brought against them – formally, hooliganism motivated by religious hatred. In five days of testimony, lawyers and witnesses have laid bare the stark divide that has emerged in Russian society: one deeply conservative and accepting of a state that uses vague laws and bureaucracy to control its citizens, the other liberal bordering on anarchist and beginning to fight against that state with any means it can.

The court is dominated by a glass cage that holds the three women – Maria Alyokhina, who has emerged as their unofficial spokeswoman; Nadezhda Tolokonnikova, whose chiselled features have made her the band's unofficial face; and Yekaterina Samutsevich, who sits in a corner of the cage looking every bit the disgruntled punk.

After five days' sitting in the cage, some days for 10 hours at a time, the women appear exhausted. Violetta Volkova, one of their lawyers, said they were being tortured – denied food and adequate sleep. After a week of being dismissed and lectured by the judge, she could no longer hide her anger. On Friday, as the judge, Marina Syrova, denied yet another defence objection, Volkova began to shout.

Syrova, her glasses forever perched perfectly in the middle of her nose, answered tartly: "You're losing the frames of dignity."

"Those frames long haven't existed here," Volkova replied, seething.

According to Pussy Riot's lawyers, Russia has revived the Soviet-era tradition of the show trial with its case against the group. "Even in Soviet times, in Stalin's times, the courts were more honest than this one," lawyer Nikolai Polozov shouted in court. Outside, during a rare break, he explained: "This is one of the most shameful trials in modern Russia. In Soviet times, at least they followed some sort of procedure."

In one week, Syrova has refused to hear nearly all the objections brought by the defence. One objection claimed that exactly the same spelling errors were found in several witness statements, implying they were falsified.

The prosecution was allowed to call all its witnesses, mainly people who were inside the church at the time of the performance or who had viewed a video of it on YouTube. They answered questions like: "What does your Orthodox faith mean to you?", "Was the women's clothing tight?" and "What offended you about their balaclavas?"

One witness said she heard music during the band's performance in the Cathedral of Christ the Saviour, although footage shown in court showed the women singing with no live instruments. The music was added later to their viral video clip, "Virgin Mary, Chase Putin Out!"

"What kind of music did you hear?" asked the defence. "It wasn't classical – and it wasn't Orthodox," the witness replied.

The defence, meanwhile, tried to call 13 witness, including opposition leader Alexey Navalny and celebrated novelist Lyudmila Ulitskaya. Syrova only allowed them to call three. The prosecution launched the questioning of all its witnesses with the same question: Are you an Orthodox believer? When the defence tried to ask the same question of one of its three witnesses, Syrova shouted: "Question stricken."

The defence knows they are fighting a losing battle in a judicial system that is notoriously politicised. But the media battle remains. Pyotr Verzilov, Tolokonnikova's husband, has spent the trial perched in the seat closest to his wife's cage. He tweets furiously, and constantly checks how often his message is spread.

On Friday, three men climbed on to a ledge across from the courtroom windows, wearing white, purple and green balaclavas and shouted "Freedom to Pussy Riot!". There have been reports of imitation stunts carried out in other cities in Russia.

"At first, after the [anti-Putin] protests started in December, the authorities got scared that they had lost control," Polozov said. "Now they've recovered and have started to react – and the trial against Pussy Riot is the clear first step."

Every day as the trial begins, dozens of journalists gather on the stairs outside the court, repeating a tradition launched with the second trial of Mikhail Khodorkovsky, the oil tycoon and Putin foe, which was held in the same room.

Amid the crush stands Samutsevich's father and Alyokhina's mother, Natalya.

"My daughter and I had very different views about politics," Alyokhina said. "But this trial is bringing them closer."

Putin said this week that the women should not be judged "too harshly". They face up to seven years in jail if convicted but their lawyers took Putin's comments as a signal that they would not receive the full sentence. A verdict is expected next week.

New push to free convicted drug smuggler Schapelle Corby CLEMENTINE CUNEO The Daily Telegraph August 04, 201212:00AM

http://www.news.com.au/national/new-push-to-free-convicted-drug-smuggler-schapelle-corby/story-fndo4bst-1226442532955

 

New push to free convicted drug smuggler Schapelle Corby

• CLEMENTINE CUNEO
• The Daily Telegraph
• August 04, 201212:00AM

Australian drug smuggler Schapelle Corby. Picture: AFP Source:AFP

Nervous wait for Corby parole news

Schapelle is 'no longer afraid'

Corby seeks government help

CONVICTED drug smuggler Schapelle Corby could be released on parole in just two weeks, if a letter from the federal government supporting her bid is viewed favourably in Indonesia.

Corby's family has welcomed the letter from the Australian government as "great and exciting news".

The government yesterday confirmed a letter supporting Corby's parole application was being prepared. If it is met favourably by Indonesian authorities, Corby could be eligible to apply for release in just two weeks.

The Department of Foreign Affairs refused to say whether the letter would provide a guarantee that Corby will adhere to a strict set of conditions that would likely be imposed for her parole.

"It would be premature and inappropriate to discuss the details," a DFAT spokesman said. A Corby family spokeswoman said: "This is great and exciting news which we are thankful for." It is understood Corby, 35, would live with her sister Mercedes in Bali to serve her parole time.

Corby, who was caught in 2004 attempting to import 4.1kg of marijuana into Bali in her bodyboard bag, will be eligible to apply for parole if a recommendation that another six months be shaved from her sentence is approved.

Her 20-year sentence was slashed by five years in May after she won an appeal for clemency from Indonesian President Susilo Bambang Yudhoyono. A fresh recommendation for another six-month cut, if approved as expected, and combined with more than two years in remissions she has already received, will mean Corby would have served two-thirds of that sentence. Under Indonesian law, prisoners who have served two-thirds of their sentence are eligible to apply for parole.

Gusti Ngurah Wiratna, the governor of Bali's notorious Kerobokan jail where Corby has been imprisoned for eight years, said a guarantee would be crucial to a successful parole application.

"There are stages that must be gone through like hearing by correctional observer . . . guarantee from the family, and if she has undergone two-thirds of sentence or not, as well as a guarantee from the (Australian) embassy," Mr Wiratna said.

If she fails to win parole, the earliest Corby could walk free from Kerobokan jail is mid-2015, so long as she continues to win the maximum remissions each year.

The development comes amid resentment in some quarters in Indonesia after a clemency decision in May.

JOHNNIE LEE SAVORY Coalition Seeks DNA Testing For Man Who Insists He's Innocent of Murders That Occurred When He Was 14

http://www.law.northwestern.edu/cwc/newsandevents/Savory.html

 

JOHNNIE LEE SAVORY

Coalition Seeks DNA Testing For Man Who Insists He's Innocent of Murders That Occurred When He Was 14

Johnnie Lee Savory (Photo: Jennifer Linzer)

CHICAGO - Johnnie Lee Savory, 45, spent two-thirds of his life behind bars for a double murder that he says DNA testing can prove he did not commit.

The trouble is that, even though Illinois law guarantees the right to DNA testing when it is relevant to a claim of actual innocence, the courts have denied that right in Savory's case.

As a result, Savory is asking Illinois Governor Rod Blagojevich to order the testing, which would be paid for privately, at no cost to the taxpayers.

And today Savory was joined in his quest for DNA testing by a broadly based coalition of supporters — including five former U.S. Attorneys, 30 former prisoners who were exonerated by DNA, authors John Grisham and Studs Terkel, and arrays of business, religious, and civil rights leaders, academics, defense lawyers, and past and present and public officials.

Letters signed by the supporters — 212 in all — were released today at a press conference in the offices of the Center on Wrongful Convictions at Northwestern University School of Law.

Lawyers from the Center and the Chicago law firm of Jenner & Block took on the Savory case five years ago at the behest of the late U.S. District Court Judge Prentice H. Marshall, who in retirement had taken an interest in the case and had come to believe that Savory was innocent.

Although the lawyers succeeded in obtaining Savory's release on parole on December 19, 2006, on-going efforts to obtain DNA testing through the courts have not succeeded. With those remedies exhausted, Savory's only hope of proving his innocence lies with Governor Blagojevich before whom a petition for executive clemency based on innocence is pending.

It is in that context that Savory's supporters are asking the governor to order the testing. There is precedent for that — Governor James R. Thompson did it in 1988 in the case of Gary Dotson, who as a result became the first person ever to be exonerated by DNA. Since that case, DNA has exonerated 209 additional wrongfully convicted prisoners nationally, including 25 more in Illinois.

Johnnie Savory, an African-American, was twice convicted by all-white juries of the murders of teenagers James Robinson, Jr. and Connie Cooper, who were found stabbed to death in their Peoria home on January 18, 1977. The second conviction, which is the only one that matters now, rested primarily on the testimony of three informants who claimed that Savory had talked about committing the crime in their presence. Two of the informants eventually recanted, stating that the conversations in fact had not occurred.

The physical evidence in the case — a bloody pair of pants seized from Savory's home, fingernail scrapings from both victims, head hairs found in the victims' hands and bathroom sink, and a pocket knife with a blood-like stain on it that the prosecution theorized was the murder weapon.

The blood on the pants was of the ABO type shared by Johnnie, one of the victims, and, importantly, Savory's father, who testified that the pants were his. The pants were several sizes too big for Johnnie, and his father had suffered an injury at work consistent with the positioning of the blood. (Actually, the father was treated at a hospital, where there were records that would have corroborated his testimony, but that the defense did not present.)

The fingernail scrapings were said to be of no evidentiary value, and nothing regarding them was presented at the trial. Nor was anything presented regarding the hairs. The knife was entered into evidence, but the stain on it was so minute that it could not be determined whether it was blood. Most if not all of these items should be amenable to DNA testing with today's state-of-the-art technology.

Not only could the requested DNA testing exonerate Savory but it also could identify the real killer of James Robinson and Connie Cooper.

The five former U.S. Attorneys who support Johnnie's request for DNA testing are Samuel K. Skinner, Thomas P. Sullivan, Dan K. Webb, Anton Valukas, and Scott Lassar. They were represented at the press conference by Sullivan, a Jenner & Block partner and chairman of the Advisory Committee of the Center on Wrongful Convictions.

The broad range of the group is perhaps best illustrated by the names of Skinner, who was Secretary of Transportation and White House Chief of Staff under President George H.W. Bush, and Abner J. Mikva, White House Counsel under President Bill Clinton. Among other names indicative of the diversity are those of Noam Chomsky, a retired MIT professor who has characterized his personal visions as "fairly traditional anarchist ones," and Richard A. Epstein, a Distinguished Service Professor of Law at the University of Chicago known for libertarian views. Religious leaders among the signatories include Roman Catholics, Protestants, Jews, Muslims, and Greek Orthodox. Among business leaders on the list is Lester Crown, president of Henry Crown & Co.

The 30 former prisoners exonerated by DNA were represented at the press conference by Kenneth Adams, one of the defendants in the Ford Heights Four case. They languished a total of 434 years behind bars for crimes they did not commit. Four of them were on death row — Kirk Bloodsworth, in Maryland, Rolando Cruz, in Illinois, Ray Krone, in Arizona, and Curtis Edward McCarty, in Oklahoma.

The letter to which the exonerated lent their names notes that many of them would still be in prison and some of them might have been executed if they had been denied DNA testing, and ends with a simple plea to the governor on Savory's behalf — "We beseech you to do the right thing."

Chicago Sun-Times Story

Chicago Tribune Story

Chicago Daily Law Bulletin

Letter to Governor Rod Blagojevich

Letter from Exonerated to Governor Rod Blagojevich

Excerpts from Johnnie L. Savory's Clemency Petition