Ecklonia cava.Das Superantioxidant? [Beitrag #111841] :: Do., 06 März 2008 09:46 
|
|
|
Ecklonia Cava ist in diversen amerikanischen Foren schon etwas länger bekannt und genutzt.Jetzt trudeln die ersten Berichte ein,die Ecklonia Cava eine unabdingbare Rolle im Kampf gegen den Haarausfall bescheinigen.Grund genug der knuffigen Braunalge einen eigenen Thread zu widmen... 
DHT signalisiert ja bekanntlich den Transforming Growth Factor-Beta.Da Tgf-b nun seinerseits MMP-2,-9 anregt,welche unmittelbar zur Haarfolikeldegeneration führen,ist es wichtig diese zu kontrollieren und niedrig zu halten,jedoch nicht total zu eliminieren und jetzt guckt mal,was ich gefunden habe... 
Life Sci. 2006 Sep 5;79(15):1436-43.
Phlorotannins in Ecklonia cava extract inhibit matrix metalloproteinase activity.
* Kim MM, * Ta QV, * Mendis E, * Rajapakse N, * Jung WK, * Byun HG, * Jeon YJ, * Kim SK.
Marine Bioprocess Research Center, Pukyong National University, Busan 608-737, Republic of Korea.
Matrix metalloproteinase (MMP) inhibitors have been identified as potential therapeutic candidates for metastasis, arthritis, chronic inflammation and wrinkle formation. For the first time here we report a detailed study on the inhibitory effects of phlorotannins in brown algae, Ecklonia cava (EC) on MMP activities in cultured human cell lines. A novel gelatin digestion assay could visualize complete inhibition of bacterial collagenase-1 activity at 20 microg/ml of EC extract during preliminary screening studies. Sensitive fluorometric assay revealed that EC extract can specifically inhibit both MMP-2 and MMP-9 activities significantly (P < 0.001) at 10 microg/ml. In addition, artificially induced activities of MMP-2 and MMP-9 in human dermal fibroblasts and HT1080 cells were inhibited by EC extract in a more or less similar manner to the positive control doxycycline. Even though the expression levels of MMPs differ from one cell type to the other, gelatin zymography clearly revealed that both MMP expression and activity in cells can be inhibited by EC extract. More interestingly, EC extract did not exert any cytotoxic effect even at 100 microg/ml anticipating its potential use as a safe MMP inhibitor.
Ecklonia Cava is significantly more potent than EGCG (Green Tea Extract).
Da Ecklonia Cava auch MMP-1 reduziert,ist es ebenfalls ein wunderbares Anti Aging Mittel.
|
|
Den Beitrag einem Moderator melden
 
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111846 ist eine Antwort auf Beitrag #111842] :: Do., 06 März 2008 10:17 
|
|
|
Über die Bedeutung von Entzündungshemmern habe ich mich ja schon ausgelassen.Dass es für mich ein Hauptbestandteil und gleichzeitig die Nebenerscheinung von Haarausfall ist,bestätigen zumindest diese Publikationen:
Androgenetic alopecia and microinflammation
Yann F. Mahé,PhD, Jean-François Michelet,MSc, Nelly Billoni, MSc, Françoise Jarrousse, BTS , Bruno Buan, BTS , Stephane Commo, BTS, Didier Saint-Léger,PhD and Bruno A. Bernard,PhD
International Journal of Dermatology Volume 39 Issue 8 Page 576 - August 2000
Today, androgenetic alopecia (AGA) is considered to be an alteration of hair growth and/or a premature aging of the pilosebaceous unit with a multifactorial and even polygenic etiology. 1 The fact that the success rate of treatment with either antihypertensive agents, or modulators of androgen metabolism, barely exceeds 30% means that other pathways may be envisioned. The implication of various activators of inflammation in the etiology of AGA has progressively and recently emerged from several independent studies. 2,3,4,5,6,7,8,9,10,11 A fibroplasia of the dermal sheath, which surrounds the hair follicle, is now suspected to be a common terminal process resulting in the miniaturization and involution of the pilosebaceous unit in AGA. 2 8 We review here several observations underlining the possible implication of a slow, silent, and painless process in AGA. Because we think that it should not be confused with a classical inflammatory process, we have called it microinflammation. An early study referred to an inflammatory infiltrate of mononuclear cells and lymphocytes in about 50% of the scalp samples studied. 2 Another more recent study by Jaworsky et al . 3 confirmed an inflammatory infiltrate of activated T cells and macrophages in the upper third of the hair follicles from transitional regions of alopecia (i.e. which are characterized by actively progressing alopecia). This study also reported the occurrence of a developing fibrosis of the perifollicular sheath, together with the degranulation of follicular adventitial mast cells. The miniaturization of the hair follicles was found to be associated with a deposit of so-called "collagen or connective tissue streamers" beneath the follicle, 2,7 as well as a 2 2.5 times enlargement of the follicular dermal sheath composed of densely packed collagen bundles. 3 This thickening of the dermal sheath in progression zones of AGA has also recently been observed in our laboratory using immunohistochemical staining ( Fig. 1 ).
Horizontal section studies of scalp biopsies indicate that the so-called perifollicular fibrosis is generally mild, consisting of loose, concentric layers of fibrotic collagen that must be distinguished from cicatricial alopecia. 4 It is unclear whether or not the fibrosis seen in follicular streamers (stelae or fibrous tracts) is permanent and/or alters the downgrowth of anagen hair follicles. Only 55% of male pattern AGA patients with microinflammation had hair regrowth in response to minoxidil treatment, which was less than the 77% of patients with no signs of inflammation, 4 suggesting that, to some extent, perifollicular microinflammation may account for some cases of male pattern AGA which do not respond to minoxidil. 4 Another study on 412 patients (193 men and 219 women) confirmed the presence of a significant degree of inflammation and fibrosis in at least 37% of AGA cases. 5 The upper location of the infiltrate near the infrainfundibulum 2 7 clearly distinguishes AGA from alopecia areata (AA), the latter disease being characterized by infiltrates in the bulb and dermal papilla zone. 12
The aim of this review is to determine the location and chronology of the microinflammation process within the complex pathophysiology of the human pilosebaceous unit in order to improve the possible approaches for the reduction or prevention of the development of AGA.
Classically, an inflammatory process is ascribed to a central major mediator or pathway. Such a monofactorial vision has been historically well exemplified by the famous interleukin-1 (IL-1) scheme developed by Oppenheim et al . 13 which is still valid even after 13 years. In fact, many inflammatory agents are at the center of a huge array of effects, involving cells, enzymes, adhesion molecules and other biological mechanisms. The identification of the effects of isolated factors is only part of the problem; it may be more important to determine when and where the individual factors are involved in the complex sequence. This pathway has been clearly identified, and several inhibitory anti-inflammatory drugs acting on this aspect of inflammation have been developed and clinically evaluated. 14,15 , 16,17
|
|
Den Beitrag einem Moderator melden
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111847 ist eine Antwort auf Beitrag #111846] :: Do., 06 März 2008 10:18
|
|
|
The cytokine/chemokine side of microinflammation
Why does microinflammation take place in the pilosebaceous unit and for what benefit and purpose? Fig. 2 and Fig. 3 show, in a simplified sequence, that inflammation is a multistep process which may start from a primary event. Let us look at the clues at the "crime scene" of AGA: we observe a perifollicular infiltrate in the upper follicle near the infundibulum. 2 7 This suggests that the primary causal event for the triggering of inflammation might occur near the infundibulum. 3,7 Supporting this point of view, improvement of the inflammatory aspect of AGA has been reported in a pilot study with an antimicrobial lotion. 7 One could speculate that several inhabitants of the scalp, such as the "triad" ( Propionibacterium sp.; Staphylococcus sp.; Malassezia ovalis ) or other members of the transient flora, could be involved in this complex inflammatory process. 7 The presence of porphyrins (produced by Propionibacterium sp.) in the pilosebaceous duct of 58% of AGA patients (compared with 12% of control subjects), which are able to induce the production of complement (C5) chemotactic factor, is considered to be a possible cofactor of this initial pro-inflammatory stress. 6,7 Keratinocytes are also known to respond within minutes to chemical stress, pollutants, UV irradiation or even mechanical stress. 37 Not only are radical oxygen species, 38 NO, 39 PGs, and histamine 40 produced, but also intracellularly stored IL-1 is released 37,41 (see Fig. 2 and step 1 of Fig. 3 ). By itself, this pro-inflammatory cytokine (as well as IL-1 which binds to the same receptor) is able to inhibit the growth of isolated hair follicles in culture in vitro. 9 11 This concentration-dependent inhibition of human hair elongation and survival indicates a high sensitivity to IL-1 of the isolated organ in culture in vitro (IC 50 = 10 pg/mL 11 ). In vivo , transgenic mice which overexpress IL-1 in the basal epidermis and in the outer root sheath of their pelage hair follicles exhibit a spontaneous cutaneous phenotype characterized by a sparseness of hair. 42 As a response to an IL-1 signal, adjacent keratinocytes which express receptors for IL-1 start to engage the transcription of IL-1 responsive genes 41 ( Fig. 3 , step 2). In vitro , following IL-1 stimulation, this transcriptional activation cascade is induced within 6 h in plucked human hair follicles. 11
Alternatively, skin keratinocytes, which may also have antigen presenting capabilities, could theoretically induce T-cell proliferation in response to bacterial antigens. 51 These antigens, once they have been "tagged," are then selectively destroyed by infiltrating macrophages, Langerhans cells, or natural killer cells. 50,52 On many occasions, however, the causal agent persists, resulting in sustained inflammation ( Fig. 3, step 4). This corresponds partly to the situation which has been pictured in the progression zone of roughly one-third of alopecia cases: infiltrating T lymphocytes, together with mastocytes and macrophages, located in the upper perifollicular adventitial dermal sheath perpetuate a local inflammatory stage. 27 This phase of inflammation often results in tissue remodeling, where collagenases, such as matrix metalloproteinase (MMP)-9 (transcriptionally activated by pro-inflammatory cytokines) or MMP-8 (directly produced by infiltrating cells), may play an active role. 5355 Thus, collagenases are suspected to contribute to the tissue changes and the so-called "perifollicular fibrosis" by "preparing" tissue matrix and basal membranes for macrophages and T-cell adhesion. Accordingly, this scenario facilitates the secretion of membrane-anchored cytokines, such as TNF-. 55 Other factors, such as MCP-1, have been directly suspected to contribute to organ fibrosis in an experimental model of renal inflammation. 56 As MCP-1, together with other chemokines, was found to be expressed in human hair follicles in vitro, 11 as well as in the eccrine ducts of sebaceous glands in vivo, 57 it might also be actively involved in the progression of perifollicular fibrosis detected in AGA. 26 The development of perifollicular fibrosis might thus appear as the signature of a disequilibrium between pro-and anti-inflammatory pathways.
|
|
Den Beitrag einem Moderator melden
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111848 ist eine Antwort auf Beitrag #111847] :: Do., 06 März 2008 10:18
|
|
|
Relations between inflammation and steroidogenesis: the missing link
There is no question that androgens are major modulators of hair loss. Recently, it was shown that testosterone inhibited the growth of outer root sheath keratinocytes only when they were cocultured with dermal papilla cells derived from the bald scalp of an adult macaque, 58 reinforcing the hypothesis of an androgen influence on hair growth via the dermal papilla. 59 The potent metabolite of testosterone (i.e. 5-dihydrotestosterone, 5-DHT) is considered as a "culprit". 60 5-DHT is generated from testosterone through the activity of 5-reductase (5-R). Two active isoforms of 5-R, which differ both in tissue site distribution as well as in optimal pH for enzymatic activity, have been identified and cloned. 61,62, 63 While the type II isoform is considered to be the major isozyme in genital tissues, 61 the type I isoform is considered to be the major isoform expressed in skin and in the pilosebaceous unit. 64,65 Isoform II, however, has recently been detected in the inner root sheath of the pilosebaceous unit by immunohistochemistry, 66,67 Northern blotting, 67 and the pH dependence of optimal enzymatic activity. 67 Thus, the contribution of both isoforms in the regression of the pilosebaceous unit is still a matter of debate. Recently, a clinical study using finasteride, a strong inhibitor of 5-RII (and weak inhibitor of 5-RI), showed that intervention in androgen metabolism could, to some extent, modulate the progression of AGA, when the drug was given by the oral route, 68 but not topically. 69 After oral ingestion, an improvement of hair growth was observed, which was associated with a drastic reduction of serum levels of 5-DHT, corresponding to those observed in castrates. 68 Despite such a reduction of circulating 5-DHT levels, however, a number of individuals (60-70%) still remained unresponsive to this treatment, indicating again that simple dysregulation of 5-DHT synthesis levels or a genetic polymorphism of 5-R genes cannot account for all cases of AGA, and a polygenic etiology should be considered. 1
Thus, to date, the only evident link that can be established between androgen metabolism and the complex inflammatory process is sebum production which is controlled by androgens. 70 As sebum harbors a large amount of microorganisms which use lipids as nutrients, 8 it cannot be excluded that, at least for some individuals, androgen metabolism might facilitate the colonization of the sebaceous infundibulum and sebaceous ducts by such microorganisms which may be involved in the first steps of pilosebaceous unit inflammation.
We propose here working hypotheses which do not invalidate the contribution of a hereditary genetic androgen imbalance in AGA, 60 but rather attempt to integrate the neglected microinflammatory aspects of alopecia into the complex etiology of AGA. On the one hand, excessive local and/or endocrine, genetically exacerbated 5-DHT synthesis results in sebaceous gland enlargement; 2,60 as a consequence, some scalps might offer more comfortable niches to harbor the previously mentioned pro-inflammatory microorganisms. 6,7 On the other hand, androgen imbalance and metabolism may be locally exacerbated by pro-inflammatory cytokines. For example, gingival fibroblasts have been reported to modify their androgen metabolism through the action of several growth factors, such as epidermal growth factor (EGF), transforming growth factor beta (TGF-), and the pro-inflammatory cytokines IL-1 and TNF-. 71 Therefore, one could speculate that, once the inflammatory process has been triggered, the androgenetic mechanism of alopecia could subsequently be locally amplified. This upregulation of androgen metabolism by pro-inflammatory cytokines remains, however, to be established at the pilosebaceous unit level.
Our visit to the "crime scene" of AGA yielded many clues ( Fig. 4 ). We know now that, at least in about one-third of cases, the tool which causes the lethal damage is a microinflammatory process. Several factors are present, however, which are suspected to have handled the tool: androgens, microbial flora, endogenous or exogenous stress, genetic imbalance, and possibly others. Although other suspects or tools are likely to be discovered in the future, it cannot be excluded that, for each individual, the causal agent, as well as the sequence of events or combined factors, may be different. The large number of molecules claimed to be active and patented in this field, 89 and their limited efficacy in offering a definite and extensive cure of AGA, confirm that the mechanism of AGA is highly complex. Accordingly, it appears that, due to the complexity and multiple interactivities and cooperations involved throughout the distinct inflammatory pathways (partly described in Fig. 2 ), an anti-inflammatory strategy should be targeted to the appropriate effector(s) at the right moment. For this purpose, we have developed a simple assay to evaluate individuals with potentially affected hair follicles. 11 We observed that plucked hair specimens of 33% of the 116 volunteers evaluated could be classified as highly inflammatory in terms of spontaneous IL-1 production. 11 Consequently, the identification of the "inflammatory alopecic individuals" may help to adapt the right answer to the right cause. Such a selective approach might be valuable for other parameters, such as an imbalance in 11 HSD activity, 5-DHT synthesis, or microorganism colonization. Encompassing individual diversity is thus a prerequisite for appropriately addressing the biological conditions contributing to AGA. Our findings and a review of the literature suggest that inflammation in its diversity is a potentially active player to consider in this approach.
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111866 ist eine Antwort auf Beitrag #111857] :: Do., 06 März 2008 14:38
|
|
|
Pippo,da hab ich mich wahrscheinlich blöd ausgedrückt_6.gifNatürlich habe ich die Nac-leute vor einer zu großen MMP-2 Reduzierung gewarnt,weil für mich nicht klar ist,in wie weit NAC,hochdosiert,wie Tino vorschlug,gegenteilig wirkt.Das dem so ist steht ausser Frage,habe euch ja die Studie mit der Wechselwirkung gepostet.jedoch ist ein zu hoher MMP-2 Spiegel auch nicht das gelbe vom Ei.Mir ging es ja auch mehr hierum: bla bla bla EC extract did not exert any cytotoxic effect even at 100 microg/ml anticipating its potential use as a safe MMP inhibitor. Ich hoffe einfach mal,dass die Herren Wissenschaftler wissen,dass gar keine MMP's schädlich sind.Ausserdem habe ich meine Bauchschmerzen auch hier geäußert...  Ach ja zu Immortals NAC-Empfehlung:kann er ja machen... Er empfiehlt aber längst nicht so viel,wie es laut Tino ratsam wäre....
[Aktualisiert am: Do., 06 März 2008 16:23]
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111881 ist eine Antwort auf Beitrag #111878] :: Do., 06 März 2008 16:29
|
Hammerhaar
Beiträge: 2278 Registriert: April 2007
Power Member ****
Top-User |
| ParkerLewis schrieb am Don, 06 März 2008 16:09 |
@kash.was haben jetzt meine Fotos mit dem Thema zu tun  Macht mich das jetzt,respektive irgendein Thema,in irgendeiner weise weniger glaubwürdig?Wenn dem so wäre,wäre das nicht nur Unverschämt,sondern auch traurig.Wie gesagt ich muss hier weder etwas beweisen,noch folge ich dem Prinzip guilty until proven innocent.Aber gerne verschicke ich Fotos per PN,sollte jemand wirklich daran interessiert sein... ;)Sobald ich diese Morgen oder am Wochenende bearbeitet habe,kannst du mich gerne nochmal per PN anschreiben... ;)Und denk dran,ich glaube fest an deine edlen Motive... Und nun könntest du dich zu Ecklonia Cava äussern...
|
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111926 ist eine Antwort auf Beitrag #111841] :: Do., 06 März 2008 21:09
|
|
|
Falls sich jemand fragen sollte,was Demodex eigentlich sein sollte.Demodex ist eine parasitäre Infektion der Haut und Kopfhaut.Nach Schätzungen sind ca.90 % der Bevölkerung davon betroffen,da sich die kleinen Käfer durch springen von Kopf zu Kopf fortbewegen,sich in den Haarfolikel einnisten und dort ihre Eier legen.Dies kann zu Entzündungen und Haarausfall führen.Allerdings würde ich dem Thema lieber einen eigenen Thread widmen,wenn Interesse bestehen sollte.Ist hier leider noch nie erwähnt worden,wie mir scheint.
http://www.patentstorm.us/patents/7078048-description.html
The present inventors believe that these microbes (demodex) cause an inflammatory reaction, analogous to the inflammation described in connection with inflammation in acne. It is believed that the inflammatory agent is excretia from the mites, a protein shed by the mite, a CD-14 binding protein carried by the mite that activates a TLR (toll-like receptor), or some combination thereof, and the inflammatory reaction is believed to involve AP-1, NF-.kappa.ß, and the subsequent production of MMPs in the skin.
"Accordingly, a treatment that inhibits TLR activation of NF-.kappa.ß and/or that inhibits induction of polymorphonuclear lukocytes would likely aid in the treatment of rosacea.Activation of the TLRs causes NF-.kappa.B to enter the cell nucleus of keratinocyes.
The keratinocytes are thus induced to release chemotactic factors, especially cytokines (IL-1ß, IL-8, IL-10, TNFa). These factors activate the AP-1 and NF-.kappa.B pathways, and NF-.kappa.B activates more IL-1 and TNFa (a cyclical process, such as in FIG. 1 of U.S. Pat. No. 5,837,224 on photoaging due to UV radiation).
The release of these factors causes inflammation, including the recruitment of neutrophils (PMNs; i.e., polymorphonuclear leukocytes) from the blood supply to the area from which the signallying was sent; MMP-8 and elastase are preformed in the neutrophils and so when the neutrophils arrive at the site of the rosacea, these dermal matrix-degrading enzymes arrive at the area.
The cytokines also effect other keratinocytes and fibroblasts (FB), which are resident in the skin, to generate MMPs.
This inflammatory response can directly induce MMPs. The NF-.kappa.ß from the TLR causes cells to produce inflammatory cytokines, such as TNFa, IL-1ß, IL-8, and/or IL-10. TNFa and IL-1ß, acting through NF-.kappa.ß, can induce keratinocytes and fibroblasts to produce MMPs.
The present therapy includes as an adjunct to oral isotretinoin therapy or antimicrobial therapy an inhibitor of NF-.kappa.ß
Curcumin, which inhibits both AP-1 and NF-.kappa.B: Xu et al.
"Curcumin inhibits IL1 alpha and TNF-alpha induction of AP-1 and NF-.kappa.B DNA-binding activity in bone marrow stromal cells," Hematopathol Mol Hematol, vol. 11, no. 1, 1997 8 (pp. 49 62); and Pendurthi et al.,
"The dietary pigment curcumin reduces endothelial tissue factor gene expression by inhibiting binding of AP-1 to the DNA and activation of NF-kappa B," Thromb Haemost, vol. 77, no. 4, 1997 April (pp. 772 82)
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111933 ist eine Antwort auf Beitrag #111929] :: Do., 06 März 2008 21:42
|
|
|
hmm Ausnahmefällen...Ich weiss,dass die Viecher sich von Sebum,DHT und Hormonen ernähern und wenn AGA bedingt,zu viel davon vorhanden ist,können die sich natürlich vermehren und dann werden die zum Problem,verursachen wie gesagt Mikroentzündungen und sorgen für vermehrten Haarausfall.Es wird sogar diskutiert,dass der sogenannte Schorf,den man von der Kopfhaut abkratzen kann kein Talg oder tote Haut,sondern diese toten Milben sind,genau wie die komischen Wölbungen am Endteil eines toten Haares.Die klammern sich dort fest,bevor diese sterben.Sanddornöl,Emu öl und Teebaumöl soll wohl auch dagegen helfen... Aber wie gesagt,wäre ein interessantes Thema für einen neuen Thread
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #111970 ist eine Antwort auf Beitrag #111968] :: Do., 06 März 2008 23:29
|
|
|
Also Pilos,ich finde das langsam eine Frechheit,ich mache mir die Mühe mit dem Thread,versuche Pro und Contra aufzuzeigen,poste Studien und Erfahrungen und du eierst hier wieder mal rum und spamst,dass die Sonne untergeht.Ist doch zum Kotzen.Viele kennen die Amiforen gar nicht,haben weder je was davon gehört noch werden sie es jemals.
Ausserdem kannst du nicht erwarten,dass die User sich durch jeden Thread dort lesen.Wenn ich das mache,mache ich das gerne und stelle die Ergebnisse hier rein,wenn sie mir logisch erscheinen oder ich aus eigener Erfahrung sprechen kann.
Junge,die User hier sind weder dumm noch hirnamputiert und können selbst aus ihren Möglichkeiten wählen und brauchen mit Sicherheit keinen Vormund,wie dich.
Dein Verhalten ist einfach unmöglich und für so was hier einfach untragbar,aber das habe ich dir jetzt schon öfters geschrieben.Wenn ich doch solch ein Schwätzer bin,dann versuch mich doch mal zur Abwechslung sachlich zu demontieren und was konstruktives hier beizusteuern,ausser dein ewiges Gezicke und Geflenne.Ist ja furchtbar...  Ausserdem übernehme ich nicht bloß Sachen von IH,bei vielen Sachen widerspreche ich ihm soagr,siehe Maca,siehe NAC,etc,aber viele Sachen sind auch zumindest diskutierbar und ob ich das dann hier poste oder nicht,lasse ich mir von dir bestimmt nicht vorschreiben.
Das ich mich in jedem Thread mit sowas befassen muss,unmöglich... 
Das zumindest Interesse besteht siehst du alleine schon an den Zugriffen auf dieses Thema,also Pilos wovon habe ich als User des Alopezieforums jetzt mehr,von deinem plumpen Gezeter oder von einer konstruktiven Vorstellung einer neuen Möglichkeit gegen Haarausfall?und da ich ja weiss,dass du dich eh nicht ändern kannst,werde ich dich ab jetzt gekonnt ignorieren,damit das Thema nicht wieder im Nirvana verschwindet,wie du es schon so oft geschafft hast.Das ist hier keine bloße Parker-Pilos Show im Wahlkampf der Republikaner und du bist auch nicht Wishy McWishmop,der nächste Präsident des Forums,also bitte ein bisschen Diskretion...
[Aktualisiert am: Do., 06 März 2008 23:54]
|
|
Den Beitrag einem Moderator melden
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Re: Ecklonia cava.Das Superantioxidant? [Beitrag #112024 ist eine Antwort auf Beitrag #112021] :: Fr., 07 März 2008 11:53
|
|
|
Ahh ja... Na dann freut es mich,dass ich dich wieder einmal zum Lachen bringen konnte ... Und das in dem Forum nicht um an die Wand drängen gehen sollte,dass hast du wahrscheinlich in deiner Weitsicht auch noch nicht ganz mitbekommen,oder?Aber du bist mir wirklich um ein vielfaches überlegen und ich brauche wirklich fünf Accounts,um gegen solch eine Argumentationsflut bestehen zu können... husch husch einen neuen Thread von mir hast du noch übersehen,wo du mir noch kein traditionelles Kommentar kredenzt hast.
Um mal wieder zum Thema zurückzukommen.Scheint so,als wenn Ecklonia Cava auch Caspase 3 runter regulieren und Bax/Bcl-2 hoch regulieren würde.
Edit: liebe 1234567,bevor du hier antwortest,beachte bitte den Thread im Off-topic Forum.Dort gehört unsere "Unterhaltung" nämlich hin.Ich bitte dich also nochmals höflich im Sinne der User und der Gemeinschaft das Gespamme hier zu unterlassen.dankeschön
[Aktualisiert am: Fr., 07 März 2008 12:09]
|
|
Den Beitrag einem Moderator melden
Nächste Seite 
|
|
Suche
Hilfe
Mitglieder
Registrieren
Anmelden
Startseite
NAC-Gegner bleibe ich aber trotzdem,bis einer mir eine Studie unter die virtuelle Nase hält,welche eine sichere MMP-2-9 Regulierung bestätigt... 
Video Schuppen / seborrhoisches Ekzem
