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26 août 2011 5 26 /08 /août /2011 12:50

 

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Presssion artérielle cible : 140 pour tout le monde, y compris les patients âgés

Publié le 25/08/2011 Partager sur Twitter Partager sur Facebook Imprimer l'article Envoyer à un confrère Réagir à l'article Enregistrer dans ma bibliothèque Reduire Agrandir


La plupart des recommandations invitent à réduire la pression artérielle (PA) chez l’hypertendu non diabétique et non coronarien à moins de 140 mmHg. Cependant, comme le signale par exemple la société européenne de cardiologie, les preuves manquent dans plusieurs groupes de patients : les hypertendus non compliqués, les hypertendus de grade 1 et surtout les hypertendus âgés.

C’est pour remédier à ces manques que les résultats de l’étude en double aveugle FEVER qui a randomisé 9 711 Chinois hypertendus ont pu être ré-analysés par sous-groupe. Cette étude avait démontré que réduire la PA en moyenne à 138 mmHg par un traitement plus intensif apportait un bénéfice significatif en termes de protection cardio-vasculaire en comparaison avec un groupe traité moins intensivement et chez qui la PA moyenne était à 142 mmHg. L’étude avait inclus des patients jeunes et vieux, ainsi que des patients avec ou sans diabète et atteints ou non de pathologies vasculaires.

La réduction du risque cardio-vasculaire a été recherchée dans différents groupes. Le risque de survenue d’un accident vasculaire cérébral a été moindre dans le groupe traité intensivement, que les patients aient présenté au départ une hypertension non compliquée (-39 %, p=0,002), une PA systolique à la randomisation <153 mmHg (-20 %, p=0,03) ou qu’il s’agisse de patients âgés (-44 %, P <0,001). De telles réductions également significatives (en moyenne entre -29 et - 47 %) ont été également retrouvées, que ce soit pour l’ensemble des évènements cardio-vasculaires ou pour la mortalité totale. Baisser la pression systolique à moins de 140 mmHg a permis de prévenir 2,1 (hypertendus non compliqués) à 5,2 (patients âgés) événements cardiovasculaires tous les 100 patients traités sur 3,3 ans.

Cette étude vient renforcer les recommandations, l’objectif est donc bien de ramener la pression à moins de 140 mmHg que les patients soient porteurs d’une hypertension non compliquée ou modérée ou bien qu’ils soient âgés.



Benoît Tyl

 

Zhang Y et coll. Is a systolic blood pressure target <140 mmHg indicated in all hypertensives? Subgroup analyses of findings from the randomized FEVER trial. Eur Heart J 2011;32 (12): 1500-1508.

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24 août 2011 3 24 /08 /août /2011 09:14

 

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Potential applications of curcumin and its novel synthetic analogs and nanotechnology-based formulations in cancer prevention and therapy

Murielle Mimeault and Surinder K Batra

 

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Chinese Medicine 2011, 6:31 doi:10.1186/1749-8546-6-31

Published: 23 August 2011

Abstract (provisional)

Curcumin has attracted great attention in the therapeutic arsenal in clinical oncology due to its chemopreventive, antitumoral, radiosensibilizing and chemosensibilizing activities against various types of aggressive and recurrent cancers. These malignancies include leukemias, lymphomas, brain, melanoma and skin, lung, prostate, breast, ovarian, liver, gastrointestinal, pancreatic and colorectal epithelial cancers. Curcumin mediates its anti-proliferative, anti-invasive and apoptotic effects on cancer cells, including cancer stem/progenitor cells and their progenies, through multiple molecular mechanisms. The oncogenic pathways inhibited by curcumin encompass the members of epidermal growth factor receptors (EGFR and erbB2), sonic hedgehog (SHH)/GLIs and Wnt/beta-catenin and downstream signaling elements such as Akt, nuclear factor-kappa B (NF-kappaB) and signal transducers and activators of transcription (STATs). In counterbalance, the high metabolic instability and poor systemic bioavailability of curcumin limit its therapeutic efficacy in human. Of great therapeutic interest, the selective delivery of synthetic analogs or nanotechnology-based formulations of curcumin to tumors, alone or in combination with other anticancer drugs, may improve their chemopreventive and chemotherapeutic efficacies against cancer progression and relapse. Novel curcumin formulations may also be used to reverse drug resistance, eradicate the total cancer cell mass and improve the anticarcinogenic efficacy of the current anti-hormonal and chemotherapeutic treatments for patients with various aggressive and lethal cancers.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

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23 août 2011 2 23 /08 /août /2011 20:13

 

 

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La baisse du cholestérol n’a pas d’influence sur la progression des calcifications coronaires

Publié le 23/08/2011

 

L’extension des calcifications coronaires que l’on peut détecter et mesurer par différentes méthodes est corrélée à l’importance de l’athérosclérose et prédit le risque de survenue d’un événement clinique. Il a donc été proposé de pratiquer des séries de scanners de détection de ces calcifications pour d’une part surveiller la progression de l’athérosclérose et d’autre part évaluer les effets des traitements hypolipémiants. Cependant, plusieurs études ont rapporté des résultats contradictoires quant à l’influence de la cholestérolémie et des traitements hypolipémiants sur le changement des calcifications coronaires. Certaines études ont, en effet, retrouvé une forte corrélation entre cholestérolémie et calcifications et ont démontré qu’une baisse de la première entraînait une diminution de la progression des secondes. D’autres études, au contraire, n’ont retrouvé aucun lien entre les deux.
 
Pour y voir plus clair, une équipe a décidé de mettre en place une étude de suivi sur plusieurs années. Ils ont enrôlé 510 patients coronariens stables (âge moyen 63 ± 9 ans). Au départ, 372 patients étaient traités, alors que 138 autres ne l’étaient pas. Ils ont tous bénéficié d’un scanner spiralé tous les 2 ans pendant en moyenne 5,6 ans.

Le taux de cholestérol a diminué dans les deux groupes, mais, comme on pouvait s’y attendre, cette baisse a été plus prononcée chez les patients qui recevaient un traitement hypolipémiant. L’évolution du score calcique total a été similaire dans les deux cas. Les modifications de la cholestérolémie n’ont pas été associées à celle des calcifications coronaires au cours du suivi : le score calcique a ainsi augmenté de 501±63 dans le quartile supérieur de changement de cholestérolémie ainsi que de 358±44, 403 ±41 et 480±56 dans les 3 suivants (p =0,2). Par ailleurs, il n’a pas été noté de corrélation entre cholestérolémie au départ et score calcique de base. De nouvelles lésions calciques ont été diagnostiquées chez plus du quart des patients (132 soit 28,2 %) sans différence significative entre les 2 groupes. En analyse multivariée, les seuls prédicteurs de changement du score calcique ont été ce même score calcique au départ (p <0,001), l’indice de masse corporelle (p=0,007) et l’âge (p=0,006).

Dans cette étude, qui mélange plusieurs types d’hypolipémiants, les changements au long cours de la cholestérolémie n’ont pas eu d’influence sur les calcifications coronaires.



Dr Benoît Tyl

 

Tenenbaum A et coll. Long-term changes in serum cholesterol level does not influence the progression of coronary calcification. International Journal of Cardiology 2011 ; 150 : 130–134

 

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16 août 2011 2 16 /08 /août /2011 10:44

 

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The Proteasome Inhibitor MG132 Reduces Immobilization-Induced Skeletal Muscle Atrophy in Mice

Annabelle Z Caron email, Sonia Haroun email, Elisabeth Leblanc email, Frederic Trensz email, Chantal Guindi email, Aziz Amrani email and Guillaume Grenier email

BMC Musculoskeletal Disorders 2011, 12:185doi:10.1186/1471-2474-12-185


Published: 15 August 2011

Abstract (provisional)

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Background

Skeletal muscle atrophy is a serious concern for the rehabilitation of patients afflicted by prolonged limb restriction. This debilitating condition is associated with a marked activation of NFkappaB activity. The ubiquitin-proteasome pathway degrades the NFkappaB inhibitor IkappaBalpha, enabling NFkappaB to translocate to the nucleus and bind to the target genes that promote muscle atrophy. Although several studies showed that proteasome inhibitors are efficient to reduce atrophy, no studies have demonstrated the ability of these inhibitors to preserve muscle function under catabolic condition.

Methods

We recently developed a new hindlimb immobilization procedure that induces significant skeletal muscle atrophy and used it to show that an inflammatory process characterized by the up-regulation of TNFalpha, a known activator of the canonical NFkappaB pathway, is associated with the atrophy. Here, we used this model to investigate the effect of in-vivo proteasome inhibition on the muscle integrity by histological approach. TNFalpha, IL-1, IL-6, MuRF-1 and Atrogin/MAFbx mRNA level were determined by qPCR. Also, a functional measurement of locomotors activity was performed to determine if the treatment can shorten the rehabilitation period following immobilization.

Results

In the present study, we showed that the proteasome inhibitor MG132 significantly inhibited IkappaBalpha degradation thus preventing NFkappaB activation in vitro. MG132 preserved muscle and myofiber cross-sectional area by downregulating the muscle-specific ubiquitin ligases atrogin-1/MAFbx and MuRF-1 in vivo. This effect resulted in a diminished rehabilitation period.

Conclusion

These finding demonstrate that proteasome inhibitors show potential for the development of pharmacological therapies to prevent muscle atrophy and thus favor muscle rehabilitation.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

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9 août 2011 2 09 /08 /août /2011 08:15

 

 

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Mortelle, la spondylarthrite ankylosante ! Prise en charge précoce par anti-inflammatoires

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Publié le 03/08/2011 JIM.fr


       

 

La spondylarthrite ankylosante ( SPA) est un rhumatisme inflammatoire chronique affectant principalement les articulations sacro iliaques et le rachis.

Une mortalité accrue au cours de cette maladie a été constatée dès 1950 et est en rapport avec des conséquences directes de la maladie telles que fractures et subluxations cervicales mais également avec l’association possible à une aortite, une fibrose pulmonaire, ou une amyloïdose.

Les études de cohortes actuellement disponibles datent du milieu du siècle dernier et ont été menées rétrospectivement.

Les auteurs de ce travail ont réalisé une étude chez 677 malades (511 hommes et 166 femmes)  atteints de SPA. Tous les sujets suivis à l’hôpital universitaire «  university hospital of northern Norway » depuis 1977 ont été inclus et appariés pour l’âge, le genre et le lieu de résidence à 3 sujets contrôles issus de la population générale.

Le délai moyen de diagnostic de la SPA dans cette cohorte était de 9 ans (déviation standard DS 7) et le suivi moyen de 31,9 ans (DS 11,3).

Un sous groupe de 360 malades inclus entre les années 1998 et 2000 a été analysé dans une étude prospective parallèle  avec un suivi de 10 ans afin d’évaluer les facteurs de risques de surmortalité.

Sur la période de suivi, ont été constatés 98 décès, 89 hommes et 9 femmes (mortalité de 14,5 % chez les malades). Le ratio standardisé de mortalité totale (RSM) était de 1,61 (IC 95 % 1,29 à 1,93). Il différait entre les hommes  et les femmes et n’était significativement augmenté que chez les hommes (1,63 vs 1,38 p < 0,001).

La cause la plus fréquente de décès était une pathologie cardiovasculaire (40 %  des causes : coronaropathie, anévrysme aortique, pathologie valvulaire,) puis les maladies néoplasiques ( 26,8 %) et infectieuses (23,2 %).

Les facteurs de risque indépendants associés à une moindre survie étaient un retard au diagnostic de SPA ( OR 1,05), une C reactive proteine (CRP) élevée (OR 2,68), un handicap au travail (OR 3,65) et la non utilisation d’anti-inflammatoires non stéroidiens (OR 4,35).

La CRP est une mesure directe de l’activité de la maladie. Les facteurs de risques de mortalité retrouvés sont tous des marqueurs plus ou moins directs de l’activité de la maladie . Ces résultats laissent entrevoir l’importance d’une détection rapide de la maladie et d’une prise en charge précoce par anti-inflammatoires ainsi que l’intérêt d’une vigilance accrue quand aux facteurs de risque cardiovasculaire chez ces malades.

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La spondylarthrite ankylosante (pelvispondylite rhumatismale, spondylose rhizomélique)

 

[?] Qu'est-ce que c'est ?

C'est une maladie inflammatoire chronique qui touche le rachis et les articulations sacro-iliaques. Deuxième des grands rhumatismes inflammatoires chroniques par sa fréquence et sa gravité, elle est quand même dix fois moins fréquente que la polyarthrite rhumatoïde et n'atteint que 0,1 à 0,2 % de la population. Elle représente 85% des rhumatismes des hommes de moins de 30 ans.
Le sujet présente dans 90 % des cas l'antigène HLA B27.

Dans 10 à 20% des cas, la maladie est associée à une autre affection :

  • Un syndrome oculo-urétro-synovial (OUS) ;
  • Une maladie intestinale chronique ;
  • Un rhumatisme psoriasique...

[?] Les signes de la maladie

La spondylarthrite ankylosante débute entre 20 et 40 ans par des douleurs au bas des reins (lombalgies) ou des douleurs dans les fesses dans la moitié des cas. Ces douleurs ne sont pas calmées par le repos mais au contraire sont plus importantes la nuit et le matin au réveil. Elles résistent à l'aspirine.

D'autres fois, les symptômes révélateurs sont :

  • Une sciatique ;
  • Des douleurs rachidiennes ;
  • Une arthrite périphérique ;
  • Une douleur inflammatoire du talon.

L'arthrite sacro-iliaque est constante : ce sont des douleurs fessières irradiant vers l'arrière des cuisses et pouvant simuler des douleurs de sciatique.
Les douleurs lombaires sont fréquentes, accompagnées de raideur surtout matinale, ainsi que les douleurs thoraciques. L'articulation manubri-sternale est douloureuse. Des douleurs du cou sont possibles. Si les hanches sont souvent touchées, toutes les articulations peuvent être atteintes y compris les doigts et les orteils qui sont gonflés.

Les autres signes sont :

  • Une iritis ou uvéite antérieure (oeil rouge douloureux non larmoyant soulagé par les corticoïdes) ;
  • Une urétrite non gonococcique (ou une cervicite chez la femme) ;
  • Une diarrhée aiguë contemporaine de l'arthrite ;
  • Une sacro-iléite à la radiographie ;
  • La présence de l'antigène HLA B27 ;
  • L'amélioration remarquable des douleurs par les AINS.

Une insuffisance aortique peut être associée.

[?] Evolution de la maladie

La maladie évolue par poussées. La spondylarthrite ankylosante bloque progressivement les articulations du bas du dos. Dans les cas les plus sévères, elle va jusqu'à souder la colonne vertébrale en un seul bloc. L'évolution se fait en 10 à 20 ans par poussées qui touchent successivement toutes les articulations.

[?] Examens et analyses complémentaires

La radiologie montre des images d'arthrites.
Les lésions sacro-iliaques sont typiques : élargissement de l'interligne, flou articulaire...
Les lésions rachidiennes débutent à la charnière dorsolombaire. Il existe des images d'ossification intervertébrale (syndesmophytes) et une calcification des ligaments intervertébraux. Au maximum est réalisée l'image radiologique de "colonne de bambou".
Sur le plan biologique, la vitesse de sédimentation est accélérée pendant les poussées. L'antigène HLA B27 est retrouvé dans 90 % des cas.

[?] Diagnostic différentiel

  • Le mal de Pott ;
  • La polyarthrite rhumatoïde ;
  • La sacro-coxalgie ;
  • Les spondylodiscites ;
  • la brucellose ;
  • L'épiphysite vertébrale…

[?] Traitement

Le traitement repose sur le repos, la rééducation fonctionnelle et les médicaments:
Le repos est indispensable, en particulier au moment des poussées.
La kinésithérapie active avec gymnastique respiratoire et posturale est également très importante pour éviter des déformations.
Les médicaments sont déterminants dans le traitement de la crise et éventuellement dans le traitement de fond de la maladie.

  • Les anti-inflammatoires non stéroïdiens (AINS) sont utilisés en première ligne lors des poussées.
  • Une association antalgique de paracétamol et de dextropropoxyphène est parfois prescrite en complément lorsque les AINS seuls sont insuffisants pour réduire la douleur due à l'inflammation.
  • Un traitement local sous forme d'infiltration (injection intra-articulaire) de corticoïdes ou une synovitorthèse (injection intra-articulaire de substances chimiques visant à détruire la membrane synoviale enflammée) sont aussi parfois pratiqués.
  • Dans certains cas (cas très sévères ou pathologie associée : psoriasis, rectocolite hémorragique, etc.), un traitement de fond peut être prescrit. Il est basé sur la prise de salazopyrine ou de méthotrexate ou d'azathioprine ou de ciclosporine.

Pour les formes de la maladie qui sont très déformantes et ankylosantes, un recours à la chirurgie orthopédique peut s'avérer nécessaire.

Dr Lyonel Rossant, Dr Jacqueline Rossant-Lumbroso.

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9 août 2011 2 09 /08 /août /2011 07:50

 

 

 

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Malattia dipendenti pubblici: i nuovi controlli per le assenze targate Brunetta

brunettaDALL’ITALIA. Una nuova circolare relativa alle assenze per malattia negli uffici della Pubblica amministrazione: è il provvedimento emesso dal ministro della P.a. e dell’innovazione tecnologica, Renato Brunetta, con l’obiettivo di chiarire le novità introdotte di recente dalla Manovra economica varata dal governo, poi convertita nella legge 111/2011 il 15 luglio scorso.

La circolare 10/2011 riguarda le modalità con cui le amministrazioni dovranno organizzare il controllo sulla malattia, il regime della reperibilità ai fini del controllo e delle procedure previste per giustificare le assenze dei dipendenti pubblici: visite, terapie, prestazioni sanitarie ed esami diagnostici.
Le disposizioni riguardano anche il personale il cui ordinamento segue le norme pubblicistiche ovvero professori e ricercatori universitari, magistrati, avvocati dello Stato, militari e forze di polizia, diplomatici e prefetti, vigili del fuoco, dirigenti delle carceri.

Punto centrale nel nuovo iter sarà la valutazione del dirigente responsabile ai fini della decisione di effettuare una visita di controllo, con l’obiettivo di prevenire sia l’assenteismo che eventuali cattive condotte da parte dei dipendenti, da valutare esclusivamente in base a criteri oggettivi.
La visita di controllo dovrà essere sempre disposta, in particolare, se il dipendente si assenta nei giorni che precedono o seguono i giorni non lavorativi.

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5 août 2011 5 05 /08 /août /2011 17:45

 

 

 

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Quelle est la part du dépistage organisé dans la baisse de la mortalité par cancer du sein ?

Publié le 05/08/2011 Partager sur Twitter Partager sur Facebook Imprimer l'article Envoyer à un confrère Réagir à l'article Enregistrer dans ma bibliothèque Reduire Agrandir


Les décès par cancer du sein diminuent régulièrement dans la plupart des pays d’Europe de l’Ouest et du Nord, en Amérique du Nord et en Australie. Après plus de 20 ans de pratique de dépistages systématiques par mammographie, il est toutefois difficile de déterminer, dans cette réduction de la mortalité, la part liée à une détection plus précoce et celle qui est due à une meilleure prise en charge de la maladie. Selon certains auteurs, une participation d’au moins 70 % aux campagnes de dépistage devrait assurer une réduction de 25 % de la mortalité.

Une analyse rétrospective utilise un moyen original pour vérifier cette assertion et essayer de faire la part des choses. Les auteurs ont apparié des pays voisins ayant le même type de système de soins et de facteurs de risque, mais où la systématisation du dépistage était instituée à plusieurs années de distance. Ont été ainsi appariées l’Irlande du Nord (Royaume Uni) et la République d’Irlande, la Hollande et la Belgique, enfin la Suède et la Norvège.

De 1989 à 2006, les décès par cancer du sein ont diminué de 29 % en Irlande du Nord et de 25 % en République d’Irlande. Le dépistage systématique était institué dès les années 90 en Irlande du Nord et se maintient autour de 75 % depuis 1995, alors qu’il est mis en place seulement en 2002 en République d’Irlande, atteignant 78 % de couverture en 2008.

En Hollande, le programme de dépistage est initié dès 1989 et trouve sa vitesse de croisière, aux alentours de 79 % de couverture en 1997. Entre 1989 et 2006, les décès par cancer du sein baissent de 25 %. Dans le pays voisin, la Belgique, le dépistage était laissé à la discrétion des patientes et des médecins jusqu’en 2001et le programme mis en place ensuite atteindra un taux de participation relativement faible, de 59 % en 2005. La baisse de la mortalité par cancer y sera, entre 1989 et 2006, de 20 % en Wallonie et de 25 % en Flandres.

Enfin en Suède un programme de dépistage est institué en 1986 et atteint une couverture maximale en 1997, alors que chez les voisins Norvégiens le dépistage systématique se met en place seulement en 1996. La diminution de la mortalité sera de 16 % en Suède et de 24,1 % en Norvège.

Force est de constater qu’il existe de grandes similitudes entre pays voisins dans les taux de diminution des décès par cancer du sein, malgré des écarts importants dans les dates de mise en place des programmes de dépistage. Pour les auteurs cette inadéquation soutient l’hypothèse selon laquelle le dépistage systématique ne jouerait peut-être qu’un rôle mineur dans la baisse constatée de la mortalité par cancer du sein. Les progrès thérapeutiques et l’efficacité accrue des différents systèmes de soin sont pour eux les explications plus probables de cette baisse.



Dr Roseline Péluchon

 

Autier P et coll.:Breast cancer mortality in neighbouring European countries with different levels of screening but similar access to treatment: trend analysis of WHO mortality database. BMJ 2011;343:d4411 doi: 10.1136/bmj.d4411. http://www.bmj.com/content/343/bmj.d4411.full.pdf

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RAPIDA AZIONE INTRAPRESA DALL'AMBASCIATA D'ITALIA E DAL GOVERNO MONEGASCO, IN MENO DI DUE MESI, DOPO L'ACCORDO RAGGIUNTO IL 12 MAGGIO 2011 CON GIUSEPPE RUOCCO, DIR.GEN. DEL MINISTERO DELLA SALUTE ITALIANO.

 

 

15juillet-0190.JPG

A centro dell'immagine Stéphane Valeri, Ministro della Salute ed Affari Sociali del Principato con, alla sua destra, l'Ambasciatore d'Italia Antonio Morabito ed alla sin. il Ministro degli Affari Esteri, José Badia, durante la presentazione dell'accordo alla stampa monegasca ed ai rappresentanti dei frontalieri italiani.

 

 

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Da sin. l'Ambasciatore Antonio Morabito ed il Ministro Stéphane Valeri. 

 

 

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I rappresentanti del sindacato dei frontalieri con le autorità monegasche ed italiane.

 

Assistenza sanitaria nel Principato di Montecarlo per i lavoratori frontalieri italiani.  

 

 

Grazie al coordinamento dell’Ambasciata italiana i connazionali potranno beneficiare delle strutture sanitarie del Principato e non solo per le “urgenze. Durante la conferenza stampa del pomeriggio, al Palazzo di Governo, presenti l’ambasciatore italianoAntonio Morabito, con Stephane Valeri, Ministro della Salute ed Affari Sociali e José Badia, Ministro degli Affari Esteri del Principato è stAta illustrata la normativa che si rifà e rende operativo l’art.10 della Convenzione bilaterale di sicurezza sociale del 1982.

 

 

 

I lavoratori frontalieri italiani potranno ora beneficiare delle strutture sanitarie del Principato di Monaco, oltre che in caso di urgenza (come già in atto), anche per esami e visite a livello specialistico... Saranno sufficienti una prescrizione del medico di famiglia italiano, e la relativa autorizzazione preventiva dell’istituzione competente del luogo di lavoro.

 

E’ questo il considerevole risultato in risposta alle esigenze degli oltre 4.000 lavoratori, a tutela della loro salute, ed a debita considerazione della loro particolare condizione occupazionale: risultato che risolve di fatto lo “status quo” di trattamento differenziato e disparità rispetto ai lavoratori francesi o italiani residenti nei comuni limitrofi a quello monegasco.

La sostanziale “novità” si deve all’azione diplomatica dell’Ambasciata italiana a Montecarlo, da  dieci mesi retta da Antonio Morabito, che assieme al Ministro della Salute monegasco Stephane Valeri, fattivo e determinante interlocutore, è riuscito a portare avanti un tavolo di concertazione tra le parti interessate alla questione (in primis il dott. Giuseppe Ruocco Direttore Generale Rapporti Internazionali del Ministero della Sanità Italiana, poi la Regione Liguria, il Direttore della ASL1 della  Provincia di Imperia Antonio Rossi, le Casse sociali monegasche, il Centro Ospedaliero “Princesse Grace”).


“In sintesi – ha spiegato nel pomeriggio in conferenza stampa al palazzo del Governo monegasco, l’ambasciatore – l’intesa consiste in una più attenta interpretazione dell’art.10 della Convenzione bilaterale di sicurezza sociale, concordata nel corso della riunione della Commissione mista italo-monegasca, organizzata dall’Ambasciata italiana lo scorso 12 maggio. L’intesa, ad incidenza finanziaria neutra per entrambi i Paesi, opera negli spazi già previsti dalla citata Convenzione, e non necessita di modifica delle attuali disposizioni”.

.

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Obésité : même combat après 70 ans

Publié le 03/08/2011 Partager sur Twitter Partager sur Facebook Imprimer l'article Envoyer à un confrère Réagir à l'article Enregistrer dans ma bibliothèque Reduire Agrandir


Si le risque de surmortalité dû au surpoids ou à l’obésité semble unanimement établi à l’âge mûr, les études chez les plus âgés sont divergentes, jusqu’à conclure à un effet protecteur. L’excès de graisse corporelle demeure-t-il un FR de mortalité après 70 ans en l’absence de pathologie associée ?

Une cohorte de 6 030 adventistes californiens n’ayant jamais fumé, indemnes de pathologies cardio-vasculaires et cancéreuses, a été constituée en 1958, réévaluée en 1974 et suivie jusqu’en 1986.

L’analyse de la variation du poids a été adjointe à celle de l’IMC pour mieux prendre en compte l’accroissement de la masse grasse chez les personnes âgées. Mille trois cent cinquante deux décès ont été identifiés. Les sujets ayant un IMC dans le quartile inférieur (<20,6 chez les femmes et 22,3 chez les hommes) mangeaient moins de viande, étaient plus actifs et présentaient moins de pathologies chroniques. Le risque de décès y était plus faible chez les hommes (de 32 %, 30 % en cas de poids stable, soit moins de 5 kg de variation), même à la 9ème décennie. Chez les femmes le risque maximal se retrouvait dans le quartile supérieur (augmenté de 59 %, et en cas de poids stable de 49 %). La survie au cours de la 9ème décennie diminuait pour les IMC supérieurs à 22,3 chez les hommes, 27,4 chez les femmes et tout sujet à l’IMC supérieur à 27 et ayant pris du poids au cours des 29 ans de suivi. Pour ces IMC l’espérance de vie des hommes dont le poids était resté stable entre 75 et 99 ans était amputée de 3,7 ans et le risque de mortalité accru de plus de 100 %. Chez les femmes l’espérance de vie diminuait de 2,1 ans et la mortalité augmentait de 41 %. En cas de gain de 10 à 19 kg le risque de décès était multiplié par 1,52 chez les femmes et 1,89 chez les hommes. Une prise de poids survenue entre 65 et 74 ans était associée à un risque majoré de 397 % (facteur de 4,97) alors qu’il n’était « que » de 62 % (facteur de 1,62) en cas de constitution avant 65 ans.

Cette étude va à l’encontre de multiples autres travaux peut-être en raison de la durée de suivi, du style de vie des recrutés ou de leur absence d’antécédents. La différenciation du gain et de la stabilité de poids permet de contrôler le facteur de confusion qu’est l’amaigrissement lié à une pathologie. L’IMC optimal diffère selon le sexe : entre 75 et 99 ans, il est de moins de 22 chez les hommes et de 27 chez les femmes (reflet d’une imprégnation œstrogénique supérieure). Des sites de stockage différents pourraient également expliquer cette divergence. L’augmentation de la consommation de viandes est reliée à une prise de poids, un accroissement du risque de diabète et une réduction de l’espérance de vie de 3,6 ans dans cette population.

Une analyse de la perte de poids et des caractéristiques de la masse grasse restent à faire.



Dr Anne Bourdieu

 

Singh PN et coll. Does excess body fat maintained after the seventh decade decrease life expectancy? J Am Geriatr Soc 2011; 59: 1003-11.

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A 6-month depot formulation of leuprolide acetate is safe and effective in daily clinical practice: a non-interventional prospective study in 1273 patients

Ulf W Tunn email

BMC Urology 2011, 11:15doi:10.1186/1471-2490-11-15

 
Published: 29 July 2011

Abstract (provisional)

Background

Testosterone stimulates growth in many prostate tumours. The established GnRH analogue leuprolide acetate is incorporated in a novel biodegradable polymer matrix (Atrigel(R) delivery system), that can be administered to reduce testosterone levels in men with advanced hormone-dependent prostate cancer. This novel formulation is available as a 1-, 3- and most recently 6-month depot (Eligard(R) 45 mg). The latter was shown to lower and maintain safe and effective serum testosterone suppression in a clinical study.

Methods

A non-interventional study to confirm the efficacy and safety of 6-monthly leuprolide acetate (Eligard(R) 45 mg) in routine urological practice was performed in Germany. Data were obtained from 1273 patients under the care of 634 urologists, and were analysed descriptively. Concentrations of PSA and serum testosterone were documented at the baseline visit and at 6 and 12 months following 6-monthly leuprolide acetate. The participating physicians were also asked to assess the efficacy, tolerabilty and handling of 6-monthly leuprolide acetate.

Results

Serum concentrations of PSA and testosterone were decreased substantially within 6 months of initial 6-monthly leuprolide acetate administration. At 12 months, median reductions of 96% (to 0.5 ng/ml) in PSA, and 90% (to 8.9 ng/dl) in serum testosterone, were observed. Further PSA and serum testosterone decreases were also observed in a subpopulation of patients who switched to 6-monthly leuprolide acetate from other GnRH analogues. Physicians rated 6-monthly leuprolide acetate as easy to use, and patients reported good tolerability. Adverse events occurred in 9% of patients; the majority were not serious. In particular, low rates of hot flushes were reported.

Conclusions

This non-interventional study showed that the reliable reduction of PSA and testosterone levels demonstrated in previous clinical studies of twice-yearly leuprolide acetate can also be achieved in routine clinical practice. This study also confirmed good tolerability of 6-monthly leuprolide acetate in routine clinical use and received positive appraisal from physicians.

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Lotta alle droghe: la via dei vaccini contro le dipendenze

drogheDALL'ITALIA. Nella lotta alle droghe ha assunto un ruolo importante la ricerca su dei vaccini capaci di curare le dipendenze

Procedono a tal fine le sperimentazioni negli Stati Uniti, come ha affermato il direttore dell’istituto di ricerca statunitense Nida (National Institute on Drug Abuse), Nora Volkow, intervenuta a Palazzo Chigi alla presentazione di un accordo di collaborazione con il Dipartimento delle politiche antidroga italiano. "La scienza può fornire strumenti sempre più all’avanguardia contro la droga: un esempio sono i vaccini - ha dichiarato Volkow. Negli Stati Uniti - sono in sperimentazione sull’uomo due prodotti, uno contro la dipendenza da nicotina e uno contro quella da cocaina. In fase di studio su modello animale sono invece un vaccino contro l’abuso di metanfetamine e uno contro la dipendenza da eroina”

“È importante individuare precocemente il problema e offrire terapie precoci alle persone tossicodipendenti – ha aggiunto l’esperta – sia per la dipendenza che per l’infezione da Hiv. Penso che la collaborazione tra Nida e Dpa porterà grandi vantaggi a tutta la comunità scientifica e ai pazienti”.
Quanto alle droghe leggere, Volkow ha evidenziato: “la cannabis ha un principio attivo più potente che in passato. Aumenta il numero delle persone che diventano dipendenti e che finiscono in pronto soccorso per le conseguenze della cannabis. È inoltre una droga ‘gateway’, cioè cancello d’entrata verso la dipendenza da sostanze più pesanti. La definizione di ‘droga leggera’ è ormai inadeguata: fu formulata quando non si sapeva quanto potesse nuocere”, ha concluso.

www.sanitaincifre.it

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Pourquoi toujours autant de cancers invasifs du col utérin malgré le dépistage ?

 

Le Dr. Viola Polena, de l'équipe du JIM (Journal International de Médecine) confirme l'article du Prof. F. Borruto

 

Borruto

Prof. Franco BORRUTO

 

Le dépistage et le traitement des lésions précancéreuses du col utérin (cervical intraepithelial neoplasia CIN) ont réduit significativement l’incidence de ce cancer et sa mortalité. Cependant, malgré l’installation de programmes de dépistage dans certains pays développés, de trop nombreux cas de cancers invasifs sont encore observés.

Au Pays Bas, un programme national de dépistage (NCSP) a été mis en place en 1988 et malgré une diminution importante de l’incidence du cancer du col, il y a encore 600 à 700 nouveaux cas de cancer invasif diagnostiqués annuellement. Les facteurs susceptibles d’influencer le nombre de nouveaux cas sont multiples, allant du taux de femmes dépistées et de l’intervalle entre les dépistages aux erreurs de diagnostic.

 

depistagecarac photo 1    Dans ce contexte, une étude effectuée dans la région de Nijmegen au Pays Bas a analysé l’histoire du dépistage pour des femmes présentant un cancer invasif du col utérin (n=401) et ré-analysé les frottis classés normaux pendant les 5 ans précédant le diagnostic afin de comprendre pourquoi le dépistage n’a pas empêché la survenue de ces cancers.

Parmi les 401 femmes incluses, 67 % (269) avaient reçu au moins une invitation pour participer au NCSP. La moitié (201) ne s’y étaient finalement pas soumises, soit du fait de leur âge, soit parce qu’elles n’avaient tout simplement pas répondu. Un tiers des patientes ne faisaient en effet pas partie des groupes d’âge ciblés par le NCSP : 22 % (87) étaient plus âgées que l’âge limite supérieur (> 60 ans) et 11 % (45) trop jeunes (< 30 ans). Dix sept pour cent des femmes n’avaient jamais répondu aux invitations du NCSP.

Parmi les 201 patientes qui avaient suivi le NCSP, 85 (42 % des 201) avaient eu au moins un frottis pendant les 5 années précédant le diagnostic du cancer du col (intervalle de dépistage = 5 ans) soit au total 136 frottis déclarés normaux. Or  98 de ces 136 frottis ont été revus et seulement 39 % ont été considérés comme vraiment normaux après la relecture.

Les adénocarcinomes étaient plus fréquents chez les femmes les plus jeunes (26,7 %) par rapport aux femmes dans la cible du NCSP (19,7 %) et aux femmes les plus âgées (11,5 %). Par contre, il y avait davantage de stades avancés (stade IIB ou supérieur) chez les patientes les plus âgées (54 %) comparativement aux femmes les plus jeunes (18 %) et aux femmes du groupe d’âge ciblé par le NCSP (11 %) (p<0,001). Enfin parmi les patientes  concernées par le NCSP, 13,1 % des femmes dépistées régulièrement présentaient des stades IA de la maladie, contre 7,4 % de celles dont le dépistage était irrégulier (p=0,123).

Seulement 40 % (107) des 269 femmes dans la cible du NCSP avaient été dépistées selon les recommandations de ce programme (frottis tous les 5 ans de 30 à 60 ans) ; 35 % avaient été dépistées irrégulièrement, et 25 % n’avaient pas répondu aux invitations du NCSP. Parmi les 107 femmes dépistées régulièrement, un diagnostic de cancer du col avait été posé pour 36 d’entre elles dès la première consultation de dépistage.

En conclusion, les résultats de cette étude indiquent que les nouveaux cas du cancer du col utérin sont dus aux facteurs suivants : 1. la non-participation au programme de dépistage ; 2. les limites d’âge trop étroites prévues pour le NCSP ; 3. la sensibilité médiocre des tests de dépistage liée aux erreurs de prélèvement et/ou d’interprétation.

Les taux d’incidence et de mortalité pourraient être améliorés, d’une part en réévaluant les limites d’âge (30 et 60 ans) pour le dépistage et  l’intervalle entre les dépistages (5 ans), et d’autre part en améliorant le taux de participation au programme de dépistage et la sensibilité des tests.

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Anti-cancer natural products isolated from Chinese medicinal herbs
 

CANCERimages.jpg 


 

© 2011 Tan et al. ; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
http://www.biomedcentral.com/
 

 

Chinese Medicine
© 2011 Tan et al. ; licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
 

 

Anti-cancer natural products isolated from Chinese medicinal herbs
 

 

Wen Tan 1, 2 §, Jinjian Lu 1, 2, 3 §, Mingqing Huang 1, 2, 4, Yingbo Li 1, 2, Meiwan Chen 1,
2, Guosheng Wu 1, 2, Jian Gong 1, 2, Zhangfeng Zhong 1, 2, Zengtao Xu 1, 2, Yuanye
Dang 1, 2, Jiajie Guo 1, 2, Xiuping Chen 1, 2 *, Yitao Wang 1, 2 *
1 State Key Laboratory of Quality Research in Chinese Medicine, University of
Macau, Av. Padre Toma's Pereira S.J., Taipa, Macao SAR, China
2 Institute of Chinese Medical Sciences, University of Macau, Av. Padre Toma's
Pereira S.J., Taipa, Macao SAR, China
3 College of Life Sciences, Zhejiang Chinese Medical University, 548 Binwen Rd.,
Binjiang Dist., Hangzhou 310053, Zhejiang, China
4 College of Pharmacy, Fujian University of Traditional Chinese Medicine, No.1
Huatuo Rd., Shangjie University Town, Fuzhou 350108, Fujian, China
 

 

§ These authors contributed equally to this work
 

 

* Corresponding authors:
Xiuping Chen and Yitao Wang
State Key Laboratory of Quality Research in Chinese Medicine
University of Macau
Av. Padre Toma's Pereira S.J.
Taipa, Macao SAR
China
Email addresses:
WT: ya87501@umac.mo
JJL: jinjian.lu@163.com
MQH: hmq1115@126.com
YBL: ya77504@umac.mo
MWC: chenmeiwan81@163.com
GSW: wuguosheng1983@gmail.com
JG: yb07513@umac.mo
ZFZ: ma86935@umac.mo
ZTX: xuzengtao@gmail.com
YYD: dangyuanye@163.com
JJG: mb05828@umac.mo
XPC: xpchen@umac.mo
YTW: ytwang@umac.mo
 

 

Abstract
In recent years, a number of natural products isolated from Chinese herbs have been
found to inhibit proliferation, induce apoptosis, suppress angiogenesis, retard
metastasis and enhance chemotherapy, exhibiting anti-cancer potential both in vitro
and in vivo. This article summarizes recent advances in in vitro and in vivo research
on the anti-cancer effects and related mechanisms of some promising natural
products. These natural products are also reviewed for their therapeutic potentials,
including flavonoids (gambogic acid, curcumin, wogonin and silibinin), alkaloids
(berberine), terpenes (artemisinin, β-elemene, oridonin, triptolide, and ursolic acid),
quinones (shikonin and emodin) and saponins (ginsenoside Rg3), which are isolated
from Chinese medicinal herbs. In particular, the discovery of the new use of
artemisinin derivatives as excellent anti-cancer drugs is also reviewed.
Background
Surgery, chemotherapy and radiotherapy are the main conventional cancer treatment
often supplemented by other complementary and alternative therapies in China [1].
While chemotherapy is one of the most extensively studied methods in anti-cancer
therapies, its efficacy and safety remain a primary concern as toxicity and other side
effects of chemotherapy are severe. Moreover, multi-drug resistant cancer is even a
bigger challenge. Medicinal herbs are main sources of new drugs. Newman et al.
reported that more than half of the new chemicals approved between 1982 and 2002
were derived directly or indirectly from natural products [2]. Some active compounds
have been isolated from Chinese medicinal herbs and tested for anti-cancer effects.
For example, β-elemene, a compound isolated from Curcuma wenyujin Y. H. Chen et
C. Ling (Wenyujin), is used as an anti-cancer drug in China. For this study, we
searched three databases, namely PubMed, Scopus and Web of Science, using
keywords “cancer”, “tumor”, “neoplastic” and “Chinese herbs” or “Chinese
medicine”. Publications including research and review papers covered in this review
were dated between 1987 and 2011, the majority of which were published between
2007 and 2011. Chinese herb-derived ingredients, including flavonoids, alkaloids,
terpenes, quinones and saponins, were found.
Gambogic acid (GA)
GA (Figure 1A) is the principal active ingredient of gamboges which is the resin from
various Garcinia species including Garcinia hanburyi Hook.f. (Tenghuang) [3]. GA
has various biological effects, such as anti-inflammatory, analgesic and anti-pyretic [3]
as well as anti-cancer activities [4, 5]. In vitro and in vivo studies have demonstrated
its potential as an excellent cytotoxicity against a variety of malignant tumors,
including glioblastoma, as well as cancers of the breast, lung and liver. GA is
currently investigated in clinical trials in China [6-8].
GA induces apoptosis in various cancer cell types and the action mechanisms of GA
remain unclear. Transferrin receptor (TfR) significantly over-expressed in a variety of
cancers cells may be the primary target of GA [4]. The binding of GA to TfR in a
manner independent of the transferrin binding site, leading to the rapid apoptosis of
tumor cells [4]. Proteomics analysis suggests that stathmin may be another molecular
target of GA [9]. The importance of the role of p53 in GA-induced apoptosis remains
controversial [5,10]. Furthermore, GA antagonizes the anti-apoptotic B-cell
lymphoma 2 (Bcl-2) family of proteins and inhibits all six human Bcl-2 proteins to
various extents, most potently inhibiting myeloid cell leukemia sequence 1 (Mcl-1)
and Bcl-B, as evidenced by a half maximal inhibitory concentration (IC50) lower than
1μM [11]. Moreover, GA also influences other anti-cancer targets, such as nuclear
factor-kappa B (NF-κB) [12] and topoisomerase IIα [13].
GA causes a dose-dependent suppression of cell invasion and inhibits lung metastases
of MDA-MB-435 cells in vivo through protein kinase C (PKC)-mediated matrix
metalloproteinase-2 (MMP-2) and matrix metallopeptidase-9 (MMP-9) inhibition [8].
GA also exhibits significant anti-metastatic activities on B16-F10 melanoma cancer
cells partially through the inhibition of the cell surface expression of integrin α4 in
C57BL/6 mice [14].
Notably, the combination of GA with other compounds enhances their anti-cancer
activities [15-17]. For example, He et al. [15] reports that proliferative inhibition and
apoptosis induction are much more visibly increased when Tca8113 cells are treated
with combined GA and celastrol, indicating that the combination of GA and celastrol
can be a promising modality for treating oral squamous cell carcinoma. Another study
showed that GA in combined use with 5-fluorouracil (5-FU) induced considerably
higher apoptosis rates in BGC-823 human gastric cells and inhibited tumor growth in
human xenografts [16]. Furthermore, low concentrations of GA were found to cause a
dramatic increase in docetaxel-induced cytotoxicity in docetaxel-resistant
BGC-823/Doc cells [17]. Magnetic nanoparticles of Fe3O4 (MNPs-Fe3O4) were
reported to enhance GA-induced cytotoxicity and apoptosis in K562 human leukemia
cells [18].
Curcumin
Curcumin (Figure 1B) is the main active flavonoid derived from the rhizome of
Curcuma longa (Jianghuang), with its dry herb weight consisting of up to 3.08%
curcumin [19]. Curcumin has been used to treat cardiovascular disease, inflammation
and arthritis [20]. Epidemiological studies have found that incidence of several
cancers is low in India where curcumin is widely consumed, suggesting that curcumin
intake plays a role in cancer prevention [21]. Other studies have also indicated that
curcumin inhibits cell proliferation and survival in breast cancer, colon cancer,
prostate cancer, gastric cancer, leukemia, lymphoma and melanoma [20]. Curcumin
induces cell apoptosis through complex intrinsic and extrinsic pathways. Curcumin
binds to more than 30 different protein targets, including transcript factors (NF-κB
and activator protein-1), growth factor receptors [epidermal growth factor receptor
(EGFR), human epidermal growth factor receptor 2 (HER2)], kinases
[mitogen-activated protein kinase (MAPK), PKC and protein kinase A (PKA)],
inflammatory cytokines [tumor necrosis factor (TNF) and interleukins], cell
cycle-related proteins (p53 and p21), matrix metalloproteinases (MMPs) and
urokinase plasminogen activators (u-PA) [20, 22, 23]. Daily oral administration of
curcumin suppresses metastasis in breast, colon, lung and medulloblastoma cancers.
The suppression involves the regulation of metastatic proteins, such as vascular
endothelial growth factor (VEGF), MMP-2, MMP-9 and intercellular adhesion
molecules [24, 25].
Curcumin induces non-apoptotic cell death, such as autophagic cell death, which
involves the degradation of the cell’s own components through lysosomal machinery
[23]. In vitro and in vivo studies have demonstrated that curcumin induces autophagic
cell death, as evidenced by the immunoreactivity of microtubule-associated protein
light chain 3 (LC3) in myeloid leukemia cells. The action mechanism is attributed to
the inhibition of the Akt/mammalian target of rapamycin/p70 ribosomal protein S6
kinase pathway and activation of extracellular signal-regulated kinase 1/2 by
curcumin in malignant glioma cells [26, 27]. In addition, autophagic inhibitor
bafilomycin A1 suppresses curcumin-induced cell death [28]. Another type of
non-apoptotic cell death induced by curcumin is paraptosis which is observed in
malignant breast cancer cells but not in normal breast cells. Curcumin induces
paraptotic events (eg the promotion of vacuolation accompanied with mitochondrial
and/or endoplasmic reticular swelling and fusion) and decreases the level of paraptotic
inhibitor protein AIP-1/Alix [29]. These paraptotic events are attributed to superoxide
anion and proteasomal dysfunction [29].
Curcumin reduces toxicity induced by anti-cancer agents [30], sensitizes
chemo-resistant cancer cells and demonstrates synergic effects with different
chemotherapeutic agents such as doxorubicin, 5-FU, paclitaxel, vincristine,
melphalan, butyrate, cisplatin, celecoxib, vinorelbine, gemcitabine, oxaliplatin,
etoposide, sulfinosine, thalidomide, suberoylanilide hydroxamic acid, dasatinib and
bortezomib [30]. Prior administration of curcumin reduces the DNA damage and
oxidative stress induced by cyclophosphamide (CXC) [31], improves uroprotective
efficacy in the CXC hemorrhagic cystitis model [32] and suppresses early lung
damage in CXC-treated rats [33]. Curcumin alleviates the side effects of mitomycin
C, as evidenced by decreased lipid peroxidation and DNA damage [34]. Furthermore,
curcumin reduces weight loss and improves kidney function and bone marrow
suppression in animal studies [35]. When combined with oxaliplatin, curcumin
decreases the proliferative capacity of oxaliplatin-resistant cell lines and enhances the
cytotoxicity of oxaliplatin in an in vitro oxaliplatin-resistant model [36]. Additionally,
curcumin protects healthy cells against radiation and sensitizes tumor cells to
radiation therapy [37, 38].
Clinical trials have been or are currently being conducted to evaluate the tolerance,
safety, pharmacokinetics and efficiency of curcumin as well as its combination
therapy with current anti-cancer drugs [39]. A phase I clinical trial found no
dose-limiting toxicity in patients treated with an oral-dose of up to 8g/day of
curcumin. The recommendation is seven consecutive doses (6g/day) of curcumin
every three weeks in combination with a standard dose of docetaxel [40].
Improvements in biological and clinical responses were observed in most treated
patients [40]. A phase II trial of gemcitabine-resistant pancreatic cancer found
chemotherapeutic drugs in combined use with curcumin to be sufficiently safe,
feasible and efficient. While the bioavailability of curcumin is relatively poor, two out
of 21 patients in the phase II trial showed clinical biological responses; one patient
exhibited marked tumor regression coupled with a significant increase in serum
cytokine levels [41, 42].
Wogonin
Wogonin (Figure 1C) is one of the flavonoids isolated from Scutellaria baicalensis
Georgi (Huangqin), with its dry herb weight consisting of up to 0.39mg/100mg of
wogonin [43]. Wogonin has been widely used in the treatment of various
inflammatory diseases owing to its inhibition of nitric oxide (NO), prostaglandin E2
and pro-inflammatory cytokines production, as well as its reduction of
cyclooxygenase-2 (COX-2). In vitro studies [44-48] have shown wogonin to possess
cytostatic and cytotoxic activities against several human tumor cell lines.
Wogonin induces apoptosis through the mediation of Ca2+ and/or inhibition of NF-κB,
shifting O2
- to H2O2 to some extent; H2O2, in turn, serves as a signaling molecule that
activates phospholipase Cγ. Ca2+ efflux from the endoplasmic reticulum is then
regulated, leading to the activation of Bcl-2-associated agonist of cell death [44].
Wogonin may also directly activate the mitochondrial Ca2+ channel uniporter and
enhance Ca2+ uptake, resulting in Ca2+ overload and mitochondrial damage [44].
Furthermore, wogonin induces cell type-dependent cell cycle inhibitions in cancer
cells, such as those observed in human cervical carcinoma HeLa cells at the G1 phase
[48] and in THP-1 cells at the G2/M phase [46] respectively. Unlike the inhibitory
effect of baicalein and baicalin on normal human fetal lung diploid TIG-1 cells [46],
wogonin imposes minor or almost no toxicity on normal peripheral T cells [44],
TIG-1 cells [46] and human prostate epithelial cells [47]. This selective inhibition of
wogonin is due to a high expression of L-type voltage dependent Ca2+ channels in
cancer cells [44]. In addition, wogonin suppresses VEGF-stimulated migration and
tube formation in HUVEC by inhibiting VEGF receptor 2 (VEGFR2) instead of
VEGFR1 phosphorylation [49].
The synergistic effect of wogonin on chemotherapy drugs, such as etoposide, has also
been investigated. Wogonin significantly improves etoposide-induced apoptosis in
cancer cells in a similar capacity as the typical P-glycoprotein (P-gp) inhibitors
verapamil and cyclosporine A [50-52]. However, other P-gp substrates, such as
doxorubicin and vinblastine, do not show any synergistic effect [52]. Similar effect
was also found when combination treatment with 5-FU in human gastric MGC-803
cells and in MGC-803 transplanted nude mice [53]. The underlying mechanisms
might be due to its pro-apoptotic effect and inhibition of NF-κB nuclear translocation
activity [53].
Anti-inflammatory and anti-viral activities of wogonin may also contribute to tumor
prevention [54]. Wogonin is a good anti-cancer candidate due to its broad toxicities to
various types of tumor cell lines and the low toxicities to normal tissues, as well as the
synergistic effects.
Silibinin
Silibinin (Figure 1D), a mixture of flavonoids derived from Silybum marianum
(Shuifeiji), is therapeutically used for the treatment of hepatic diseases in China,
Germany and Japan. Silibinin has effects on many cancers, such as prostate, colon,
bladder and lung cancers [55,56], particularly the migration, invasion and metastasis
of cancer cells [57]. In a transgenic adenocarcinoma of the mouse prostate (TRAMP)
mouse model, silibinin inhibits tumor growth, progression, local invasion and distant
metastasis [56]. Silibinin induces both death receptor-mediated and
mitochondrial-mediated apoptosis in human breast cancer MCF-7 cells [58]. Silibinin
also reduces hepatocellular carcinoma xenograft growth through the inhibition of cell
proliferation, cell cycle progression, as well as phosphatase and tensin homolog/P-Akt
and extracellular signal-regulated kinase (ERK) signaling. These effects induce
apoptosis and increase histone acetylation and superoxide dismutase-1 (SOD-1)
expression on human hepatocellular carcinoma xenografts [59]. Not only does
silibinin inhibit primary prostatic tumor progress but also protects against
angiogenesis and late-stage metastasis. Therefore, silibinin may have a potential for
improving survival and reducing morbidity in prostate cancer patients [60].
Silibinin exerts anti-cancer activity mainly by blocking cell cycle progression and
induces G1 cell cycle arrest in a dose- and time-dependent manner in large cell
carcinoma H1299 and H460 cells and bronchioalveolar carcinoma H322 cells [61].
Silibinin modulates the protein levels of cyclin-dependent kinases (CDKs; 4, 6 and 2),
cyclins (D1, D3 and E), and CDK inhibitors (p18/INK4C, p21/Waf1 and p27/Kip1) in
a differential manner in the above-mentioned cell lines [61]. Silibinin also regulates
multiple cellular proliferative pathways in cancer cells, including receptor tyrosine
kinases (RTKs), androgen receptors, signal transducers and activators of transcription
(STATs), NF-κB [62]. Moreover, silibinin inhibits the constitutive activation of
STAT3 and causes caspase activation and apoptotic cell death in human prostate
carcinoma DU145 cells [63].
The combined use of silibinin with 1,25-dihydroxyvitamin D3 promotes the
expression of both differentiation-promoting and -inhibiting genes in acute
myelogenous leukemia cells and the latter can be neutralized by a highly specific
pharmacological inhibitor, suggesting the therapeutic potential of silibinin [64].
Berberine
Berberine (Figure 1E) is an isoquinoline alkaloid isolated from Coptidis Rhizoma
(Huanglian), which is a Chinese medicinal herb for heat dissipation and
detoxification, with its dry herb weight consisting of up to 7.1mg/100mg of berberine
[65]. Berberine has diverse pharmacological activities [66-70] and is especially used
as an antibacterial and anti-inflammatory gastrointestinal remedy in China [71].
Berberine has anti-proliferative effects on cancer cells has been documented [72-78].
Multiple targets of berberine have been identified, including mitochondria, DNA or
RNA, DNA topoisomerases, estrogen receptors, MMPs, p53 and NF-κB [74, 79-82].
Berberine exerts cytotoxicity and inhibits telomerase and topoisomerase in cancer
cells by specifically binding to oligonucleotides or polymorphic nucleic acid and by
stabilizing DNA triplexes or G-quadruplexes [81,83,84]; the electrostatic interactions
may be quantified in terms of the Hill model of cooperative interactions [85].
Cell cycle regulation is a common target mechanism in anti-cancer therapies. A
low-dose (12.5–50μM) berberine treatment induces G1 phase arrest whereas doses
higher than 50μM induce G2 phase arrest in mouse melanoma K1735-M2 and human
melanoma WM793 cells [86]. Moreover, 50μM berberine decreases cyclin B1 levels
and induces cycle arrest at the G1 phase in human lung cancer H1299 and A549 cell
lines [75]. Even in anoikis-resistant human breast cancer MDA-MB-231 and MCF-7
cells, 10 or 20μM doses of berberine is superior to 5 or 10nM of doxorubicine
respectively by inducing cell cycle arrest at the G0/G1 phase [87].
In human breast cancer MCF-7 cells, berberine induces apoptosis through a
mitochondrial dependent pathway by increasing the Bcl-2-associated X protein
(Bax)/Bcl-2 protein ratio, activating caspases and inducing poly (ADP-ribose)
polymerase (PARP) cleavage [76]. These apoptotic processes also occur in human
tongue squamous carcinoma cancer-4 and human glioblastoma T98G cells [73, 88].
Accumulation of berberine on mitochondrial membranes alters the binding between
adenine nucleotide translocator and bongkrekic acid, thereby inducing depolarization
and fragmentation which may contribute to mitochondrial respiration inhibition and
mitochondrial dysfunction [89]. In the p53-expressing human neuroblastoma
SK-N-SH and p53-deficient SK-N-MC cells, the role of p53 in berberine’s
anti-neoplastic function is highlighted by the cytotoxic effects and apoptotic gene
expression accompanied by caspase-3 activation [72].
In addition to apoptotic alteration induced by berberine, recent findings are about
anti-cancer mechanisms that have a higher propensity to cause autophagy. Berberine
induces autophagic cell death in human hepatocellular liver carcinoma cell lines
(HepG2) and MHCC97-L cells, which may be diminished by cell death inhibitor
3-methyladenine through beclin-1 activation and mammalian target of rapamycin
(mTOR) signaling pathway inhibition [90]. In addition, berberine also modifies LC3,
an autophagic marker, in human lung cancer A549 cells, indicating that autophagy
may play a crucial role in berberine-induced cancer cell death [91].
Berberine also inhibits tumor metastasis and invasion. For example, berberine inhibits
12-O-Tetradecanoylphorbol 13-acetate (TPA)-induced cell migration and blocks
prostaglandin E (EP) receptor 4 agonist-induced migration by reducing EP receptors 2
and 4 in A375 and Hs294 cells [92]. Even at low doses, berberine suppresses Rho
GTPase activation and induces migration and motility inhibition in HONE1 cells [93].
Berberine also inhibits Rho kinase-mediated Ezrin phosphorylation at Thr (567) in
5-8F cells, leading to a 51.1 % inhibition of tumor metastasis to the lymph nodes in
vivo [94]. A combination of As2O3 (5μM) and berberine (10μM) inhibit the formation
of a cell confluent layer by blocking PKCα and ξ, consistent with reduced levels of
myelocytomatosis oncogene (Myc), Jun proto-oncogene, metallothionein 1-MMP and
MMP-2 [95].
Berberine enhances chemo- and radio-sensitivity, implying its potential as an adjuvant
in cancer therapy. Combined with chemotherapy drugs such as cisplatin or As2O3,
berberine exhibits significant cytotoxicity in HeLa and SH-SY5Y cells compared with
monotherapy [96, 97]. When combined with γ radiation, the apoptotic effect is
significantly enhanced in HepG2 cells [98]. Berberine also alleviates
chemo-resistance by down-regulating overexpressed transformed mouse 3T3 cell
double minute-2 and activating p53 in acute lymphoblastic leukemia cells [99].
Berberine’s poor bioavailability makes it less likely to be an independent anti-tumor
agent [100-102]. Berberine is nevertheless a potential natural compound for
alternative cancer therapy.
Artemisinin and its derivatives (ARTs)
Artemisinin (Figure 1F) is an active terpene of the Chinese medicinal herb Artemisia
annua L. (Huanghuahao) used in China to treat malaria and fever. ARTs, such as
dihydroartemisinin (DHA) and artesunate (Figure 1G), exhibit anti-cancer activities in
vitro and in vivo [103-106]. DHA is one of the main metabolites of ARTs and
artesunate is a semi-synthesized derivative of ARTs; both compounds exhibit
anti-cancer potentials.
The anti-cancer potential of ARTs has been demonstrated in various cancer cells
including those of leukemia and other cancer cells of breast, ovary, liver, lung,
pancreas and colon [104, 105]. The selective anti-cancer potential of ARTs was
related with the expression of different molecules such as c-MYC, cdc25A, EGFR,
γ-glutamycysteine synthetase (GLCLR) [105, 106]. ARTs also exert anti-cancer
effects in vivo in multiple cancer types [103, 107, 108]. For example, either DHA or
artesunate has anti-cancer activity against pancreatic cancer xenografts [107, 109].
The anti-cancer mechanism of ARTs is likely to be related to the cleavage of the
iron- or heme-mediated peroxide bridge, followed by the generation of reactive
oxygen species (ROS) [110-112]. According to Efferth et al. [113], CCRF-CEM
and U373 cells are sensitive to a combined treatment of ARTs and iron (II)-glycine
sulfate or holotransferring. Pretreatment with deferoxamine mesylate salt (an iron
chelator) visibly reduces DHA-induced apoptosis in HL-60 leukemia cells [104].
The anti-cancer potential of ARTs is possibly connected to the expression of TfR.
The synergism of artesunate and iron (II)-glycine sulfate co-treatment is unsuitable
for all types of tumor cells [114]. Endoplasmic reticulum stress is partially involved
in some cases of ARTs-mediated anti-proliferation [115, 116].
ARTs induce cell cycle arrest in various cell types [103, 115, 117]. For example,
DHA and artesunate effectively mediate G1 phase arrest in HepG2 and Hep3B cells
[103]. DHA reduces cell number in the S phase in HCT116 colon cancer cells
[115]. Interestingly, DHA also arrests the G2 phase in OVCA-420 ovarian cancer
cells [117]. Thus, ART-mediated cell cycle arrest is possibly cell type dependent.
ARTs also induce apoptotic cell death in a number of cell types, in which the
mitochondrial-mediated apoptotic pathway plays a decisive role [104, 106]. For
instance, DHA enhances Bax and reduces Bcl-2 expression in cancer cells
[103,107]. DHA-induced apoptosis is abrogated by the loss of Bak and is largely
reduced in cells with siRNA-mediated downregulation of Bak or NOXA [118].
However, DHA activates caspase-8, which is related to the death receptor-mediated
apoptotic pathway in HL-60 cells [104]. DHA enhances Fas expression and
activates caspase-8 in ovarian cancer cells [119]. DHA also enhances death receptor
5 and activates both mitochondrial- and death receptor-mediated apoptotic
pathways in prostate cancer cells [120]. ARTs-induced apoptosis in cancer cells
may involve p38 MAPK rather than p53 [103, 104].
ARTs inhibit angiogenesis which is a vital process in metastasis [121-124]. DHA
inhibits chorioallantoic membrane angiogenesis at low concentrations and decreases
the levels of two major VEGF receptors on HUVEC [122]. Conditioned media from
K562 cells pre-treated with DHA inhibits VEGF expression and secretion in chronic
myeloid leukemia K562 cells, leading to angiogenetic activity decrease [121,124].
Artemisinin inhibits cell migration and concomitantly decreases the expression of
MMP2 and the αvβ3 integrins in human melanoma cells [125]. ARTs also regulate
the levels of u-PA, MMP2, MMP7 and MMP9 all of which are related to metastasis
[126].
ARTs exert synergistic effects with other compounds. Combination of DHA and
caboplatin significantly reduces the development of ovarian cancer as compared with
DHA only [119]. Combined use of DHA or artesunate with gencitabine inhibits the
growth of HepG2 and Hep3B transplanted tumors [103]. Supra-additive inhibition of
cell growth in some glioblastoma multiforme cells is observable when artesunate is in
combined use with EGFR inhibitor OSI-774 [127]. DHA not only up-regulates death
receptor 5 expression but also cooperates with TNF-related apoptosis-inducing ligand
(TRAIL) to induce apoptosis in human prostate cancer cells [120]. Therefore, either
used alone or in combination with other compounds, ARTs are promising compounds
for chemotherapy.
β-elemene
Elemene (Figure 1H) is a sesquiterpene mixture isolated from more than 50 Chinese
herbs and plants, such as Curcuma wenyujin Y. H. Chen et C. Ling (Wenyujin) [128].
Elemene is mainly composed of β- and δ- and γ-elemene, with β-elemene accounting
for 60 %–72 % of all three isoforms. β-elemene exerts anti-cancer potential in brain,
laryngeal, lung, breast, prostate, cervical, colon and ovarian carcinomas [128-130].
Elemene shows synergistic effects in combination with other chemotherapeutic drugs
[131], leading to the blockade of cell cycle progression by modulating the G2 cell
cycle checkpoint and inducing G2/M arrest in human non-small cell lung cancer
(NSCLC) and ovarian carcinoma cells while inducing G0/G1 phase arrest in
glioblastoma cell lines through phosphorylation of p38 MAPK [129, 130, 132]. In
NSCLC cells, β-elemene induces cell arrest at the G2/M phase by increasing
phospho-Cdc2 (Tyr15) and p27/Kip1, and by decreasing phospho-Cdc2 (Thr161) and
cyclin B1. Moreover, elemene reduces the expression of Cdc25C, activates Cdc2 and
increases Chk2 [129]. β-elemene combined with cisplatin also mediate G2/M cell
cycle arrest in chemo-resistant ovarian carcinoma cells through down-regulation of
cyclin B1 and Cdc2 by elevating the levels of phosphorylation of Cdc2, Cdc25C, p53,
p21/Waf1, p27/Kip1 and GADD45 [130]. β-elemene also induces
mitochondrial-mediated apoptosis in prostate cancer and NSCLC cells [128, 129].
Combining β-elemene with cisplatin, docetaxel and taxanes significantly increases its
inhibitory effect in androgen-independent prostate carcinoma DU145 and PC-3 cells,
as well as in NSCLC H460 and A549 cells [131]. β-elemene enhances cellular uptake
of taxanes due to the alteration of cell membrane permeability may partly account for
its synergistic effects with taxanes [131]. Elemene inhibits the growth of human
epidermoid and thyroid cancer cells in vivo [133], and passes through the blood-brain
barrier [134], suggesting its potential for treating cerebral malignancy.
β-elemene has been approved by China’s State Food and Drug Administration as a
second class innovative drug and is prescribed as an adjuvant drug for some tumor
therapies in China.
Oridonin
Oridonin (Figure 1I) is a diterpenoid isolated from Rabdosia rubescens (Hemsl.) Hara
(Donglingcao), with its dry raw herb consisting of up to 0.35 % of oridonin [135].
Rabdosia rubescens (Hemsl.) Hara has long been used to treat sore throat, tonsillitis,
and esophageal cancer by native residents of Henan Province. Oridonin was included
in the Chinese Pharmacopoeia in 1977. Main chemical constituents of Rabdosia
rubescens (Hemsl.) Hara are ent-Kaurene diterpenoids, which have multiple
biological activities, such as anti-inflammatory, anti-bacterial and anti-tumor effects.
Oridonin significantly inhibits tumor cell proliferation, induces cell cycle arrest and
promotes cell death. In anti-proliferation tests, different cell lines exhibited similar
sensitivity to oridonin with an IC50 of about 40–80μM after 24 hours of treatment
[136-141]. Oridonin induces G2/M cell cycle arrest by up-regulation of heat shock 70
kDa protein 1, serine-threonine kinase receptor-associated protein, translationally
controlled tumor protein, stress-induced phosphoprotein 1, trifunctional purine
biosynthetic protein adenosine-3 and inorganic pyrophosphatase as well as
down-regulation of poly(rC)-binding protein 1 [142] in a p53-independent and
p21/Waf1-dependent manner [143]. Induction of apoptosis contributes to
oridonin-induced cell death, mainly through mitochondrial-mediated pathways. The
up-regulation of Fas, Fas ligand (FasL) and Fas (TNFRSF6)-associated via death
domain (FADD) expression, as well as the down-regulation of pro-caspase-8
expression suggests that the activation of the Fas/FasL pathway may also be partially
involved in oridonin-induced apoptosis [144]. Possible downstream responses include
the induction of loss of mitochondrial transmembrane potential [145], the activation
of several caspases [136,146], the down-regulation of Bcl-2, the up-regulation of Bax
and Bid [136,147] as well as the promotion of cytochrome c release [147] and PARP
cleavage [148]. However, the regulation of Bcl-xL and participation of caspase-3/9
remain controversial [136,143,146,148-150]. Oridonin-induced intracellular ROS
formation may be an initiator of this process [143, 151]. Other proteins may also be
involved in oridonin-induced cell cycle arrest and apoptosis; these proteins include
ERK [144, 152], p38MAPK [149], insulin-like growth factor 1 receptor [153], EGFR
[154], NF-κB [155], as well as p16, p21/Waf1, p27/Kip1 and c-MYC [156]. Oridonin
induce cell death by affecting the balance of apoptosis and necrosis. In A375-S2 cells,
low concentrations (34.3μM) of oridonin induce p53 and ERK-dependent apoptosis
whereas high concentrations (137.4μM) induce necrosis [146]. In L929 cells, oridonin
induces a caspase-independent and mitochondria- or MAPK-dependent cell death
through both apoptosis and necrosis [139, 149]. Similar results are also observed in
A431 cells [154]. Oridonin also induces simultaneous autophagy and apoptosis in
MCF-7 [157] and HeLa cells [138]. This autophagy may be attributed to the
inactivation of Ras, changes in mitochondrial membrane potential [158], activation of
PKC, Raf-1 or c-jun N-terminal kinase (JNK) signaling [141] and even NF-κB
signaling pathways [159]. Inhibition of autophagy is attributed to apoptotic
up-regulation because oridonin-induced apoptosis augmentation is accompanied by
reduced autophagy [138] whereas oridonin-induced autophagy inhibits ROS-mediated
apoptosis by activating the p38 MAPK-NF-κB survival pathways in L929 cells [160].
Oridonin inhibits DNA, RNA, and protein syntheses [161], decrease telomerase, as
well as down-regulate human telomerase reverse transcriptase mRNA expression
[162]. The in vivo anti-tumor activities of oridonin have been demonstrated in
different tumors such as Ehrlich ascites carcinoma, sarcoma-180 solid tumors and in
leukemic mice models [163,164].
Triptolide
Triptolide (Figure 1J) is a diterpenoid triepoxide and the principal active ingredient of
Tripterygium wilfordii Hook. f. (Leigongteng) used in Chinese medicine to treat
inflammation and autoimmune diseases [165]. Triptolide exhibits potent
anti-inflammation, immunomodulation and anti-tumor activities [166-170]. Triptolide
exerts multiple effects on apoptosis, angiogenesis, metastasis and drug-resistance
[166-170].
Triptolide is active in pro-apoptosis in diverse tumor cell types including ovarian
cancer [166], myeloma [167], myeloid leukemia [168], thyroid carcinoma [169] and
pancreatic tumor cells [170]. Many in vitro and in vivo studies have tried to elucidate
the potential mechanism of triptolide; however, conclusions have been inconsistent.
Triptolide seems to induce apoptosis via different pathways in various cell lines. For
example, triptolide induces apoptosis by the overexpression of cytomembrane death
receptor in a caspase-8-dependent manner in pancreatic tumor [170] and
cholangiocarcinoma cells [171]. Triptolide also promotes apoptosis in leukemic and
hepatocarcinoma cells by the mitochondrial-mediated pathway [172, 173].
Triptolide is a potent inhibitor of tumor angiogenesis in a zebrafish embryo model and
demonstrates potent activities against vessel formation by nearly 50 % at 1.2μM
[165]. In a xenograft model, triptolide (0.75mg/kg/day) blocks tumor angiogenesis
and progression in a murine tumorigenesis assay possibly correlated with the
down-regulation of proangiogenic Tie2 and VEGFR-2 expression [174]. In vitro
studies have shown that triptolide inhibits the proliferation of HUVEC. A chick
embryo chorioallantoic membrane test shows that triptolide inhibits angiogenesis as
well. Triptolide impairs VEGF expression in thyroid carcinoma TA-K cells and
down-regulates NF-κB pathway activity; the target genes of triptolide are associated
with endothelial cell mobilization in HUVEC [165]. The down-regulation of NF-κB
signaling [175], in combination with the inhibition of VEGF expression [176], may be
the anti-angiogenesis action of triptolide.
Furthermore, triptolide inhibits tumor metastasis, reducing basal and stimulated colon
cancer cell migration through collagen by 65 % to 80 % and decreasing the expression
of VEGF and COX-2 [174]. Triptolide inhibits the expression of multiple cytokine
receptors potentially involved in cell migration and cancer metastasis, including the
thrombin receptor, CXCR4, TNF receptors and TGF-β receptors [174]. Triptolide also
inhibits interferon-γ-induced programmed death-1-ligand 1 surface expression whose
up-regulation is an important mechanism of tumor immune evasion in human breast
cancer cells [177]. Triptolide inhibits the experimental metastasis of melanoma cells
to the lungs and spleens of mice [178]. Moreover, triptolide inhibits the migration of
lymphoma cells via lymph nodes, a result which may be related to its
anti-proliferative effects and blockage of the SDF-1/CXCR4 axis [179].
Triptolide enhances the anti-neoplastic activity of chemotherapy [180, 181]. The
combination index-isobologram indicates that the effect of triptolide on 5-FU is
synergistic on colon carcinoma [180]. In a tumor xenograft model, the combined
effects of triptolide (0.25mg/kg/day) and 5-FU (12mg/kg/day) on the growth of colon
carcinoma are superior to those of individual agents [180]. Triptolide is synergistic
with other anti-cancer agents or therapies including hydroxycamptothecin [181],
idarubicin, AraC [182], TRAIL [183] and ionizing radiation [184]. These results
indicate the therapeutic potential of triptolide in treating cancer.
Ursolic acid (UA)
UA (Figure 1K) is a ubiquitous pentacyclic triterpenoid compound from many plants
such as Ligustrum lucidum Ait. (Nuzhen). UA exerts proliferation inhibition in human
ovarian cancer CAOV3 cells and doxorubicin-resistant human hepatoma R-HepG2
cells [185,186]. UA disrupts cell cycle progression and induces necrosis in a clonal
MMTV-Wnt-1 mammary tumor cell line [187]. Eight novel UA derivatives with
substitutions at positions C-3, C-11, and C-28 of UA show cytotoxicity to some
degree in HeLa, SKOV3 and BGC-823 in vitro; only one derivative exhibits more
potent cytotoxicity than UA [188].
UA induces apoptosis via both extrinsic and intrinsic signaling pathways in cancer
cells [189]. In PC-3 cells, UA inhibits proliferation by activating caspase-9 and JNK
as well as FasL activation and Akt inhibition [190]. A significant proliferation
inhibition and invasion suppression in both a dose- and time-dependent manner is
observed in highly metastatic breast cancer MDA-MB-231 cells; this inhibition is
related to the down-regulation of MMP2 and u-PA expression [191]. Moreover, UA
reduces IL-1β- or TNF-α-induced rat C6 glioma cell invasion and inhibits the
interaction of ZIP/p62 and PKC-ζ [192]. Nontoxic UA concentrations inhibit vessel
growth in rat aortic ring and down-regulate matrix MMPs such as MMP2 and MMP9
[193]. In other cancer cell lines, such as Hep3B, Huh7 and HA22T cells, UA exerts a
potential anti-angiogenic effect by decreasing HIF-1α, VEGF and IL-8 gene
expression [194].
Shikonin
Shikonin (Figure 1L) is a natural anthraquinone derivative isolated from the roots of
Lithospermum erythrorhizon (Zicao) and exerts anti-tumor effects mainly by
inhibiting cell growth and inducing apoptosis. The underlying molecular mechanisms
vary with cell types and treatment methods. Shikonin induces apoptosis in a classic
caspase-dependent pathway in cervical, bladder and melanoma cancer cells. [195-198].
Shikonin induces necroptosis regardless of the drug concentration in
caspase-3-negative MCF-7 cells [199]. Different concentrations of shikonin induce
either apoptosis or necroptosis, and necroptosis converts to apoptosis in the presence
of Nec-1 in HL-60 and K562 cells [200]. The growth inhibition and apoptosis induced
by shikonin in some cancer cells may be attributed to the inactivation of NF-κB
activity or increasing Annexin V signal and CD95 (Fas/APO) expression [201, 202].
Shikonin also induces apoptosis via ROS production in osteosarcoma and
Bcr/Abl-positive CML cells [203, 204].
Several different mechanisms contribute to the anti-cancer activities of shikonin. For
example, shikonin suppresses proteasomal activities thereby inhibiting tumor growth
in both H22 allografts and PC-3 xenografts [205]. Shikonin also inhibits
topoisomerase II [206] and down-regulates ER2 and activates NFE2-related factor 2
as an anti-estrogen agent in human breast cancer [207, 208]. Shikonin modulates an
estrogen enzyme by down-regulating the expression of steroid sulfatase which is
important for estrogen biosynthesis [205]. Shikonin inhibits tumor invasion via the
NF-κB signaling pathway in human high-metastatic adenoid cystic carcinoma cells
[209]. Therefore, shikonin may directly or indirectly inhibit or modulate
disease-related cellular targets in cancer.
Emodin
Emodin (Figure 1M) is a natural anthraquinone derivative isolated from Rheum
palmatum L. (Zhangyedahuang), with its dry raw herb consisting of up to
0.20mg/100mg of emodin [210]. Emodin exerts anti-tumor activity against various
human cancers [211]. Emodin induces cell cycle arrest and apoptosis in cancer cells
[212-214] and the oxidative injury acts upstream of anti-proliferation. Emodin inhibits
IL-6-induced Janus-activated kinase 2/STAT3 pathways and induces apoptosis in
myeloma cells via the down-regulation of Mcl-1 [213]. Emodin down-regulates
androgen receptors and inhibits prostate cancer cell growth [215]. Moreover, emodin
stabilizes topoisomerase II-DNA cleavage complexes, thereby inducing DNA
double-strand breaks [216]. The suppression of excision repair cross complementation
1 (ERCC1) and Rad51 expression through ERK1/2 inactivation is vital in
emodin-induced cytotoxicity in human NSCLC cells [217].
Emodin inhibits basic fibroblast growth factor (bFGF)-induced proliferation and
migration in HUVEC and VEGF-A-induced tube formation [218]. Emodin inhibits
tumor cell migration through suppression of the phosphatidylinositol
3-kinase-Cdc42/Rac1 pathway [219]. The disruption of the membrane lipid
raft-associated integrin signaling pathway by emodin may inhibit cell adhesion and
spreading [220].
Emodin sensitizes chemotherapy associated with ROS production [221, 222]. In
combined use with cisplatin, emodin elevates ROS generation and enhances
chemosensitivity in DU-145 cells, accompanied by the down-regulation of MDR1
expression and suppression of HIF-1α transactivation [223]. Emodin enhances the
sensitivity of gallbladder cancer SGC996 cells to platinum drugs via glutathione
depletion and multidrug resistance-related protein 1 down-regulation [224]. The
mechanisms of the synergistic effects of emodin with cisplatin or gencitabin may be
attributed to the emodin-induced down-regulation of ERCC1 and Rad51 expression,
respectively [225,226]. These results suggest that emodin may be used as an adjuvant
to enhance the anti-cancer effects of chemotherapeutic agents.
Ginsenoside Rg3
Extracted from Panax ginseng C.A. Mey. (Renshen) and Panax quinquefolius L.,
Araliaceae (Xiyangshen), ginsenoside Rg3 (Figure 1N) is a biologically active
component with both in vitro and in vivo anti-cancer activities [227, 228]. The
anti-proliferative mechanism of ginsenoside Rg3 is associated with the inactivation of
NF-κB [229, 230], modulation of MAPKs [231] and the down-regulation of
Wnt/β-catenin signaling [232]. Ginsenoside Rg3 affects the ephrin receptor pathway
in HCT-116 human colorectal cancer cells [233]. The anti-proliferative mechanism of
ginsenoside Rg3 is also associated with the molecules of mitotic inhibition, DNA
replication, repair, and growth factor signaling [234].
Ginsenoside Rg3 inhibits the proliferation of HUVEC and suppresses the capillary
tube formation of HUVEC on a matrigel at nanomole scales in the presence or
absence of VEGF. Ginsenoside Rg3 attenuates VEGF-induced chemo-invasion of
HUVEC and ex vivo microvascular sprouting in rat aortic ring. bFGF-induced
angiogenesis may be abolished by ginsenoside Rg3 [227]. In lung metastasis models
of ovarian cancer, ginsenoside Rg3 decreases the number of tumor colonies in the lung
and vessels oriented toward the tumor mass [235]. This effect may be partially due to
the inhibition of angiogenesis and the decrease in MMP9 expression [235].
Ginsenoside Rg3 increases the efficacy of cancer chemotherapy. Combined treatments
with ginsenoside Rg3 enhance the susceptibility of colon cancer cells to docetaxel,
paclitaxel, cisplatin and doxorubicin; the mechanism of such an enhancement is
related to the inhibition of the constitutively activated NF-κB [229]. A similar
phenomenon has been observed in prostate cancer cells, in which the combination of
ginsenoside Rg3 and docetaxel more effectively induces apoptosis and G1 cell cycle
arrest, accompanied by the inhibition of NF-κB activity [230]. Low-dose
administration of cyclophosphamide (CTX) with ginsenoside Rg3 increases the
efficacy of targeting the tumor microvasculature and the two-drug combination
treatment results demonstrate the longest patient survival rates [236]. Ginsenoside Rg3
combined with gemcitabine not only enhances the efficacy of tumor growth
suppression and survival prolongation, but also decreases VEGF expression and
microvessel density in tumors [228].
Conclusion
Natural products such as GA, curcumin, β-elemene et al. derived from Chinese
medicinal herbs are potential candidates for anti-cancer therapeutic drugs.
Abbreviations
5-FU: 5-fluorouracil; AIF: apoptosis inducing factor ; AP-1: activator protein-1;
ARTs: artemisinin and its derivatives; ATRA: all-trans retinoic acid; bFGF: basic
fibroblast growth factor; CDKs: cyclin-dependent kinases; CTX: cyclophosphamide
DHA: dihydroartemisinin; DPD: dihydropyrimidine dehydrogenase; EGFR:
epidermal growth factor receptor; ERK1/2: extracellular signal-regulated kinase 1/2;
FasL: Fas ligand; GA: gambogic acid; HDMEC: human dermal microvascular
endothelial cells; HUVEC: human umbilical vascular endothelial cells; ICAM-1:
intercellular cell adhesion molecule-1; IL-1β: interleukin-1β; LC3: light chain 3;
MMP2: matrix metalloproteinase-2; MMP9: matrix metalloproteinase9; MRP1:
multidrug resistance-associated protein 1; NF-κB: nuclear factor-kappa B; P-gp:
P-glycoprotein; PI3K: phosphoinositide 3-kinase; ROS: reactive oxygen species;
STAT: signal transducer and activator of transcription; STS: steroid sulfatase; TfR:
transferrin receptor; TPA: 12-O-tetradeca noylphorbol-13-acetate; TRAMP:
transgenic adenocarcinoma of the mouse prostate; UA: ursolic acid; u-PA: urokinase
plasminogen activators; VCAM-1: vascular cell adhesion molecule-1; VEGF:
vascular endothelial growth factor; VEGFR1:vascular endothelial growth factor
receptor 1; VEGFR2: vascular endothelial growth factor receptor 2
Competing interests
The authors declare that they have no competing interests.
Authors’ contributions
WT, JJL, MQH, YBL, MWC, GSW, JG, ZFZ, ZTX, YYD and XPC wrote the
manuscript (WT wrote berberine; JJL wrote GA and ARTs; MQH wrote emodin and
ginsenoside Rg3; YBL wrote cucurmin; MWC wrote silibinin; GSW wrote shikonin;
JG wrote wogonin; ZFZ wrote β-elemene; ZTX wrote triptolide; YYD wrote UA;
XPC wrote oridonin. ). JJG drew the chemical structures in Figure 1. WT, JJL and
XPC revised the manuscript. YTW designed and supervised this work. All authors
read and approved the final version of the manuscript.
Acknowledgements
The work was supported by the grant (029/2007/A2) from the Science and
Technology Development Fund of Macau Special Administrative Region, China and
supported in part by the National Natural Science of China (No. 81001450) awarded
to JJL.

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LA CONTROVERSE AUTOUR DU PAPILLOMAVIRUS

 

 

 borrutoDSC 3217 

Le Prof. Franco BORRUTO, au centre de l'image

 

Il y a quelques jours, le quotidien Le Monde a publié un article qui remet en cause la vaccination antipapillomavirus.

 

Ce journal note en effet que « deux jeunes femmes se disant victimes d’effets secondaires du Gardasil ont envoyé une demande d’indemnisation à la commission régionale de conciliation et d’indemnisation des accidents médicaux de Lyon». Le quotidien rappelle en outre que les deux vaccins contre ce cancer (Gardasil et Cervarix) « figurent sur la liste des 77 médicaments placés sous surveillance» par l’Afssaps ». 

 

Nous avons interpellé à ce sujet le Professeur Franco BORRUTO, qui a intégré l'équipe dirigée par le Professeur TREISSER au CHPG  de Monaco. 

 

 

 borrut 

LE PROF.BORRUTO AVEC LE  PROF. HARALD ZUR HAUSEN, PRIX NOBEL POUR LA MEDECINE 2008 POUR AVOIR DECOUVERT LE RÔLE I CARCINOGENETIQUE DE L' HPV

 

 

LM- Professeur qu’en pensez-vous ?Pouvez-vous nous donner votre opinion,et si c’est possible,quelques explications et éléments scientifiques nécessaires à la connaissance de la situation :est-ce qu’ une vaccination peut réduire sensiblement le nombre de  cancers de l’utérus ?

 

Je pense vraiment  qu’«aussi longtemps que le rapport entre les bénéfices et les risques sera favorable, il faudra poursuivre la vaccination. Pour l’instant, celui-ci est largement favorable ». En ce qui concerne les rapports de l’Afssaps, ils «n’ont pas permis d’établir l’existence de graves effets secondaires. Compte tenu du nombre de vaccinations, certaines coïncidences surviennent. L’investigation médicale doit vérifier s’il existe un lien de causalité qui incriminerait les vaccins. Pour le moment, ce lien n’est absolument pas démontré. Par contre, les bénéfices, eux, sont bien connus. Actuellement 900 femmes meurent chaque année en France du cancer du col de l’utérus. Or 97% de ces cas pourraient être évités, à condition d’effectuer correctement deux choses : d’une part la vaccination, d’autre part le dépistage ».

 

 

CHARLENE (5)A

 

  AVEC S.A.S. LA PRINCESSE CHARLENE DE MONACO ET LE PROF. RENE FRIEDMAN

 

Le virus du papillome humain aussi appelé HPV est considéré comme une cause principale du cancer de l'utérus.

Les femmes sexuellement actives devraient impérativement  effectuer le Pap test selon une frequence de 1 à 3 ans, déterminée par leur gynécologue : il s'agît  d'une analyse qui permet de mettre en évidence la présence éventuelle de lésions cervicales et les infections ;elles peuvent être  cause majeure du cancer du col.

Pour les adolescents  non sexuellement actifs un vaccin existe.

La vaccination est désormais considérée comme sûre, bien tolérée et capable de prévenir les lésions provoquées par   deux souches virales à haut risque(16,18) responsables de la plupart des cas de menace pour la santé des femmes, de sorte que maintenant, de nouvelles recherches semblent indiquer que la vaccination peut également être utile pour les femmes plus matures.

 

La vaccination ne remplace pas le dépistage par frottis. Le test de Papanicolaou est encore indispensable pour toutes les femmes.

 

Comme cela arrive souvent quand il s'agit de vaccination, les opinions sont parfois contradictoires entre partisans et opposants. La vaccination est désormais présentée comme une occasion importante pour les adolescentes d'aujourd'hui, les femmes de demain, et dès lors est l'outil considéré comme un plus pour la prévention. L'administration du vaccin pour les femmes adultes, semble être la réponse à des données qui montrent que de nombreuses femmes ne subissent pas le test de Papanicolau .

 

Le virus du papillome humain, également appelé HPV, est considéré comme une cause de cancer de l'utérus. Le HPV est très stable, probablement identique a ceux existants il y a des milliers d’années ;il n’est donc pas comparables à d’autres virus, par exemple a ceux responsables de la grippe.

 

Tous les cancers sont causés par l’infection HPV  au niveau du col. Il y a une centaine de types de virus du papillome humain  divisés et numérotés en HPV à faible risque, qui attaquent la peau (6, 11, 42, 43, 44) et en HPV à risque élevé, qui attaquent les muqueuses (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59,68).On estime que plus de 70%des femmes contractent une infection génitale à HPV au cours de leur existence, mais que la grande majorité de ces infections est susceptible de disparaître spontanément en quelques mois à cause de leur système immunitaire.

 

C’est seulement lorsque l’infection virale à haut risque HPV persiste sur une longue periode que cette infection peut devenir oncogène,et dans une minorité de cas, le développement d'une tumeur maligne  peut  apparaître sur  une periode longue de plusieurs années..

 

LM- Mais quels sont les symptômes du virus du papillome humain  et comment se transmet-il ?

 

Les HPV - sont transmis  non seulement par des rapports sexuels lors d'un contact étroit,de peau à peau.

(Pas besoin de pénétration, le préservatif ne protège pas).

 

Très peu de femmes infectées par le VPH vont développer un cancer du col: le virus est donc seulement l'une des causes du cancer, mais il est une cause nécessaire. Presque toutes les femmes atteintes de cancer sont en fait atteintes d’abord par  l'infection à HPV du col utérin.

 

D'autres facteurs déclencheurs sont: les mauvaises habitudes comme le tabagisme, l'alimentation déséquilibrée et d'une teneur faible en vitamines, une mauvaise hygiène personnelle, la promiscuité sexuelle, de nombreuses grossesses, des antécédents familiaux de cancer du col utérin. 

 

Dans le cas du cancer du col, les premiers stades sont généralement asymptomatiques. Ce n'est qu'après cette période que l'on peut avoir des saignements anormaux, lourds et nauséabonds, des pertes vaginales, des douleurs au bas du ventre ou du dos, du sang dans l'urine, une douleur dans l'acte d'uriner.

 

La seule stratégie efficace contre les virus du papillome humain est la prévention.

 

Il convient de noter que le vaccin ne protège pas seulement du cancer du col, mais aussi d'autres maladies. Je fais allusion à des cancers oro-pharyngés et les cancers de la tête et du cou ainsi que de l'anus, du pénis et de la vulve. On pense aussi  avoir même un rôle dans la survenue de maladies auto-immunes et inflammatoires telles que la sclérose en plaques et la polyarthrite rhumatoïde. Arme souveraine contre cet ennemi de la santé des femmes, appelé papillomavirus,  la vaccination est déjà effectuée sur une grande échelle depuis 2007 en faveur de la nouvelle génération d'adolescents.

Le HPV16 est un virus à haut risque qui favorise la prolifération des cellules cancéreuses. Ces tumeurs se développent principalement chez les jeunes accros à la cigarette et l'alcool, qui sont des facteurs de risque majeur de ces cancers »,« Les oropharynx liés au cancer du VPH sont d'environ 25-30% en Europe et 40 - 50% en Amérique du Nord. Ces tumeurs ont un meilleur pronostic et peuvent à l'avenir supporter un traitement moins agressif. " 

La vaccination est utile non seulement pour les adolescentes, mais aussi pour  les femmes ayant déjà eu des rapports sexuels : des données existent ,et démontrent qu’il y a un intérêt à vacciner les femmes jusqu’à l’âge de 45 ans.

Envisageable comme  une opération majeure de protection de la santé publique,  la vaccination généralisée devrait être faite par un personnel spécialisé, spécifiquement formé, gérée par la santé publique et confiée à des mains compétentes.

Ce n'est pas un argument que l'on fera valoir, uniquement parce qu'il est à la mode.

Aujourd'hui, 13 pays de l'UE - dont l'Italie et la France - et 18 dans le monde entier ont adopté un protocole et ont reconnu le problème.

Il ya deux types de vaccin :le bivalent et le quadrivalent.

Le premier vaccin  couvre les deux souches de virus les plus impliquées, le second couvre également deux autres souches, moins « dangereuses » mais responsables d’autres lésions (le verrues et les condylomes).

La réponse immunitaire protectrice avec le vaccin bivalent est renforcée du fait que le bivalent contiens un adjuvant.

 

LM- Quelle est la durée de validité du vaccin?

 

Nous avons des donnèes demontrant que   8,4 ans après  vaccination par le vaccin bivalent, la validité clinique est toujours bonne. Le vaccin est considéré comme efficace et   une étude récente publiée dans le « Lancet » par une équipe d'Australie le démontre,il prévient les lésions du col utérin qui sont la principale cause du cancer du col. Le risque de tomber gravement malade est  abaissé de façon drastique.
Selon les informations scientifiques disponibles, la vaccination contre le VPH est sécuritaire, bien tolérée et peut prévenir presque tous les cas, la survenue d'une infection persistante des deux souches de virus dangereux pour la santé des femmes. Pour les adolescents sexuellement actifs, le vaccin semble montrer sa pleine efficacité Le 'Victorian Registry » des services de cytologie, une véritable base de données, a montré que les filles de moins de 18 ans qui  ont été vaccinées ont  moins de 38% de chances de développement de métaplasie (lésions précancéreuses) au col de l'utérus.

Toutes les femmes devraient avoir régulièrement, cependant, le test PAP, ce qui est recommandé à partir de 25ans et jusqu’à 64 ans, afin de faire un diagnostic précoce des lésions et infections dangereuses pour la santé,à long terme.

 

LM - Y a-t-il des contre-indications à la vaccination?

 

Des effets secondaires ont parfois été observés comme rougeurs, fièvre, et céphalées. Globalement, plus de 32 millions de doses ont été distribuées, et des contrôles précis ont révélé seulement une douzaine de réactions indésirables: un pourcentage très insignifiant. 

Donc créer des doutes et des alarmes injustifiés  est une procédure irresponsable parce que seuls des travaux scientifiques peuvent démontrer l’efficacité ou non de la vaccination .  

 

Qui dit le contraire ne dit pas la vérité !

 

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Come combattere l'ansia

ansia_1DAL MONDO. L’ansia è uno stato mentale che, mediante determinati segnali fisici ed emozionali, segnala la presenza di un pericolo imminente interno o esterno all’individuo; di per sé l’ansia è quindi una reazione normale, fisiologica e adattativa che ogni persona sperimenta nel corso della sua esistenza funzionale a mobilitare le energie e le risorse per far fronte alle difficoltà.

L’ansia non è più adattiva ma patologica quando diviene invece una sintomatologia cronica disturbante e disorganizzante che, al contrario dell’ansia-segnale, impedisce un funzionale e soddisfacente adattamento agli eventi. Come combattere l'ansia?

Combattere l’ansia: non significa eliminarla. Chi sperimenta un disturbo d’ansia - un problema di attacchi di panico, agorafobia o uno stato d’ansia generalizzato ad esempio – si percepisce in qualche modo sopraffatto e dominato dalla propria ansia che, benché riconosca come eccessiva e irrazionale, non riesce a gestire né a controllare. Il desiderio di combattere l’ansia deriva proprio da questo: percepire l’ansia come un problema “altro da sé” che vada in qualche modo aggredito ed eliminato alla stessa stregua di un batterio si una malattia infettiva.

Ebbene, combattere l’ansia significa in realtà, più propriamente, non eliminarla – nessuno vive senza provare ansia – ma ridimensionarla in modo che le proprie reazioni ansiose agli eventi divengano via via più selettive e misurate. In questo modo combattere l’ansia significa in realtà riconoscerla non come un demone fuori di noi ma, al contrario, come una funzione al nostro servizio di cui possiamo prendere il comando, una risorsa importante che ci segnala potenziali difficoltà e ci aiuta ad attivarci in maniera appropriata alla soluzione dei problemi. Un livello di “attivazione” adeguato è infatti indispensabile per concentrarsi e ottimizzare le proprie prestazioni (un esame, una gara sportiva, un colloquio di lavoro eccetera…), sono livelli troppo elevati (o troppo bassi) ad essere disfunzionali perché in tal modo l’ansia non è più uno stato che segnala un problema ma è di per se stessa un problema che ostacola invece che favorire l’adattamento agli eventi.

Combattere l’ansia: quali possibilità terapeutiche. Per combattere l’ansia, nel caso di veri e propri disturbi, può essere utile intraprendere un percorso psicoterapeutico o psicodinamico incentrato sui conflitti psicologici interni che l’ansia esprime o cognitivo comportamentale incentrato sulla ristrutturazione delle idee e credenze irrazionali alla base delle proprie reazioni ansiose. In alcuni casi per combattere l’ansia la psicoterapia può essere affiancata da una terapia farmacologica che aiuti la persona a gestire l’aspetto sintomatologico.

In tutti i casi, può essere di beneficio combattere l’ansia anche attraverso tecniche di rilassamento, come il Training Autogeno, che, lavorando su uno stato di calma e di riequilibrio tra mente e corpo, aiutano ad eliminare tensioni corporee legate all’ansia (come le cefalee muscolo-tensive) e aiutano la persona a costruirsi e a ritrovare un proprio spazio interno di tranquillità con se stessa.

Cristina Rubano www.crescita-personale.it

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Telepatia: funziona davvero?

telepatiaDAL MONDO. Come possiamo sapere se ciò che abbiamo percepito è stata una vera comunicazione telepatica? O semplice immaginazione, qualcosa che ci pare di aver udito?

Per riconoscere una vera trasmissione telepatica è necessaria un po' di pratica. Non esercizi duri, estenuanti. Dobbiamo solo essere certi e sicuri di ciò che vogliamo ancora ottenere, di ciò che possiamo avere, di ciò che abbiamo sempre saputo e di ciò di cui abbiamo sempre avuto bisogno.  'Tele' significa 'lontananza'; 'patìa' vuol dire 'sofferenza'. Soffrire per la lontananza. Non è dunque solo ciò che è bello e piacevole che viene trasmesso, ma anche il negativo, il dolore ed è probabile anche che ciò che si è percepito come reale, quel 'qualcosa' che abbiamo sentito, compaia prima che la comunicazione arrivi.

'Sappiamo' che 'quella' telefonata recherà il messaggio che una persona cara ha cessato di vivere. 'Sappiamo' di avere intrapreso la strada sbagliata. E, ancora, 'sappiamo' che 'quella' persona che abbiamo appena incontrato, avrà una certa importanza nella nostra vita. Nelle situazioni di estrema necessità ci fidiamo delle nostre percezioni telepatiche. Nella vita di ogni giorno ci lasciamo pervadere dai nostri pensieri, sensazioni, emozioni e sentimenti e da quelli dei nostri simili. È questo il passo più importante perché tu riesca a sfruttare al meglio le tue capacità telepatiche nella vita quotidiana: quando pensi, fallo con concetti chiari e lineari.

Cerchi una nuova abitazione? Stabiliscine prima il posto, le dimensioni, la luminosità, la cucina, il bagno. Rifletti a lungo, fino a che non avrai una visione chiara di ciò che cerchi. Poi esci e comincia a cercare. Non perderai molto tempo e potrai spiegare esattamente ciò di cui hai bisogno. E troverai la tua casa. Dovrai fare dei compromessi, magari il bagno è un po' più piccolo di come lo volevi. La vista non proprio eccezionale. Ma in fin dei conti è quello che cercavi.

Concentrati e trova un posto tranquillo per 'chiedere' al tuo corpo cosa gli piacerebbe mangiare oggi. Alleggerisci prima la tua mente da tutte le idee preconcette sul cibo buono e salutare. Prendi in considerazione quello che il tuo corpo ti comunica. Magari sotto forma di immagini o di parole.

Se questo ti sembra inizialmente troppo complicato, recati presso il settore frutta e verdura di un centro commerciale e soffermati su cosa compreresti volentieri di tua spontanea volontà. Ti renderai anche conto di quello che sicuramente non vorresti. Questo esempio di comunicazione telepatica arriva direttamente a te attraverso il tuo stesso corpo. Bada che la comunicazione telepatica alla tua domanda sia rapida e immediata. Non appena dovessero comparire un 'se' e un 'forse', non si tratterebbe già più di una comunicazione telepatica.

La telepatia è la cosa più naturale del mondo. È un processo in corso cui non siamo soliti dare importanza. La telepatia è sempre qui, con noi quando comunichiamo con noi stessi. Non esiste comunicazione che non venga trasmessa anche telepaticamente con tutti gli ausili sia fisici che materiali come la voce, il linguaggio del corpo, il telefono, la tastiera, la matita. Ogni comunicazione ha luogo sul piano spirituale, sottile e le parole, i gesti e la mimica ne solo l'espressione materiale, tangibile. Si potrebbe paragonare all'aria o al cielo in un giorno d'estate. L'aria non si vede - eppure è lì, qualcosa di sottile ed etereo.

Nell'aria c'è anche acqua, che noi non vediamo, fino a che non si scioglie. Il raffreddamento dà origine al vapore, acqua distribuita in minuscole goccioline da cui nascono le nubi. È questo il il fenomeno della compressione. E anche questo possiamo vederlo. Non è che l'aria sia in un mistico luogo lontano e qui sono visibili solo le nuvole. Entrambi sono sempre presenti.

Lo hanno riconosciuto fisici del calibro di Max Planck che affermava: “Non esiste la materia di per sé. Tutta la materia prende origine, ed esiste, solo a causa di una forza che porta gli atomi ad oscillare, tenendoli insieme, a formare quello che è il sistema solare microscopico dell’atomo. Poiché nell’universo non esiste una forza intelligente, né eterna, dobbiamo considerare uno spirito cosciente ed intelligente dietro questa forza. Questo spirito è la base di tutta la materia”.

Spirito e materia non sono dunque due mondi distinti e separati, ma un unico mondo, inestricabilmente intrecciati e interdipendenti. Solo il punto di vista dal quale ha luogo l'osservazione cambia, se si parla alternativamente di Materiale e di Spirituale. Non possiamo negare la differenza che c'è tra osservare la foto di un bosco bellissimo e passeggiare a piedi nella foresta. Quando siamo nella foresta, assorbiamo queste correnti rassicuranti (flussi di tranquillità) e tutta l'energia che è negli alberi. Non lo vediamo a occhio nudo, ma lo percepiamo spiritualmente. Mentre guardiamo una fotografia, possiamo ricordarci di una passeggiata fra gli alberi. Ma la percezione non sarà altrettanto forte come se noi fossimo lì.

Se la telepatia è dunque la cosa più normale del mondo, quando riceviamo e inviamo le nostre comunicazioni telepatiche, perché non riusciamo a dominarle? Perché non facciamo come gli aborigeni australiani presso i quali la telepatia è più potente che da noi. Loro 'chiamano a casa' senza bisogno di un telefono cellulare, per dire che hanno ucciso un canguro!

Ci sono molte ragioni per cui ci siamo evoluti al punto in cui siamo oggi. Nel tentativo di potenziare le nostre capacità telepatiche, incontriamo molte barriere ed ostacoli. Si può leggere nel pensiero? E vogliamo davvero che qualcuno riesca a farlo? Come i pregiudizi, anche tutto ciò che sta accadendo intorno a noi, ci sta portando a fare maggiore affidamento sulla telepatia.

Chi intraprende la via del ritorno, supererà gradualmente questi ostacoli, sperimentando una differenza nella qualità della vita che non aveva mai conosciuto prima.

Affermava - a questo proposito - Albert Schweizer: “Siano legati per affinità e un comune destino, a tutto ciò che vive. La vera etica richiede che noi non solo ci incoraggiamo a vicenda. Tutta la vita è un mistero. Tutta la vita ha valore. Solo quando riconosciamo e affermiamo la nostra affinità con tutti gli esseri viventi, l'uomo possiede la vera umanità”.

Luzia Janett www.ilcambiamento.it

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10 juillet 2011 7 10 /07 /juillet /2011 08:03

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ROYAL MONACO RIVIERA WEB MAGAZINE

 

 

MEDICINE & CHINESE TRADITIONAL MEDICINE

 

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Luigi Mattera is a certified by CERFPA (St. Laurent du Var-France) in HOMEOPATHY & ZUO TUINA MASSAGE OF TRADITIONAL CHINESE MEDICINE - Online certificate from TEXAS CHIROPRACTIC COLLEGE (Pasadena-Texas 2007) in CHIROPRACTIC SPORTS & CHIROPRACTIC TREATMENT OF GOLF INJURIES


 

 

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Anti-inflammatory effects of Chinese medicinal herbs on cerebral ischemia

Shan-Yu Su and Ching-Liang Hsieh

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Chinese Medicine 2011, 6:26 doi:10.1186/1749-8546-6-26

Published: 9 July 2011

Abstract (provisional)

Recent studies have demonstrated the importance of anti-inflammation, including cellular immunity, inflammatory mediators, reactive oxygen species, nitric oxide and several transcriptional factors, in the treatment of cerebral ischemia. This article reviews the roles of Chinese medicinal herbs as well as their ingredients in the inflammatory cascade induced by cerebral ischemia. Chinese medicinal herbs exert neuroprotective effects on cerebral ischemia. The effects include inhibiting the activation of microglia, decreasing levels of adhesion molecules such as intracellular adhesion molecule-1, attenuating expression of pro-inflammatory cytokines such as interleukin-1beta and tumor necrosis factor-alpha, reducing inducible nitric oxide synthase and reactive oxygen species, and regulating transcription factors such as nuclear factor-kappaB.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production.

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8 juillet 2011 5 08 /07 /juillet /2011 13:30

 

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ROYAL MONACO RIVIERA WEB MAGAZINE

 

 

MEDICINE & CHINESE TRADITIONAL MEDICINE

 

LUIGIpass.jpg

Luigi Mattera is a certified by CERFPA (St. Laurent du Var-France) in HOMEOPATHY & ZUO TUINA MASSAGE OF TRADITIONAL CHINESE MEDICINE - Online certificate from TEXAS CHIROPRACTIC COLLEGE (Pasadena-Texas 2007) in CHIROPRACTIC SPORTS & CHIROPRACTIC TREATMENT OF GOLF INJURIES


 

 

PRESENTS:

Welcome to BMC Urology published by BioMed Central BMC Urology is an open access journal publishing original peer-reviewed research articles in all aspects of the prevention, diagnosis and management of urological disorders, as well as related molecular genetics, pathophysiology, and epidemiology. BMC Urology (ISSN 1471-2490) is indexed/tracked/covered by PubMed, MEDLINE, CAS, EMBASE, Scopus and Google Scholar.

 

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Bilateral ureteropelvic disruption following blunt abdominal trauma: Case report

Fumiaki Iwase email, Yoshibumi Miyazaki email, Tastuho Kobayashi email, Hiroko Kikuchi email and Kiyoshi Mastuda email

BMC Urology 2011, 11:14doi:10.1186/1471-2490-11-14

 
Published: 7 July 2011

Abstract (provisional)

Background 

Ureteral injury occurs in less than 1% of blunt abdominal trauma cases, partly because the ureters are relatively well protected in the retroperitoneum. Bilateral ureteral injury is extremely rare, with only 10 previously reported cases. Diagnosis may be delayed if ureteric injury is not suspected, and delay of 36 hours or longer has been observed in more than 50% of patients with ureteric injury following abdominal trauma, leading to increased morbidity.

Case presentation

A 29-year-old man was involved in a highway motor vehicle collision and was ejected from the front passenger seat even though wearing a seatbelt. He was in a preshock state at the scene of the accident. An intravenous line and left thoracic drain were inserted, and he was transported to our hospital by helicopter. Whole-body contrast-enhanced computed tomography (CT) scan showed left diaphragmatic disruption, splenic injury, and a grade I injury to the left kidney with a retroperitoneal haematoma. He underwent emergency laparotomy. The left diaphragmatic and splenic injuries were repaired. Although a retroperitoneal haematoma was observed, his renal injury was treated conservatively because the haematoma was not expanding. In the intensive care unit, the patient's haemodynamic state was stable, but there was no urinary output for 9 hours after surgery. Anuresis prompted a review of the abdominal x-ray which had been performed after the contrast-enhanced CT. Leakage of contrast material from the ureteropelvic junctions was detected, and review of the repeat CT scan revealed contrast retention in the perirenal retroperitoneum bilaterally. He underwent cystoscopy and bilateral retrograde pyelography, which showed bilateral complete ureteral disruption, preventing placement of ureteral stents. Diagnostic laparotomy revealed complete disruption of the ureteropelvic junctions bilaterally. Double-J ureteral stents were placed bilaterally and ureteropelvic anastomoses were performed. The patient's postoperative progress was satisfactory and he was discharged on the 23rd day.

Conclusion

Diagnosis of ureteral injury was delayed, although delayed phase contrast-enhanced CT and abdominal x-rays performed after CT revealed the diagnosis early. Prompt detection and early repair prevented permanent renal damage and the necessity for nephrectomy.

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