Wheldon Protokoll

[Phenom77]

Über Umwege aus Brüssel und dann im Netz nachgeschaut.
Ich meine Bernie, wenn du alle fragst, dann setzen sich die Puzzle Teile automatisch zusammen. Mir wird jetzt so einiges klar auch warum München immer so hoch dosiert therapiert. Es geht nicht um die Keime sondern um die RNASE ( Immunmodulation ) Ausgestattet wird der ganze Wissenprozess dann mit den LTT´s…..
Das ist aber nur meine persöhnliche Meinung.

[teufelchen]

Hallo phenom,

ach ja, die böse RNase, da wäre mir ne schiefe Nase lieber. 😉

Spass muss sein!

Nun aber zurück zum Ernst des Lebens.

Ich bekomme keine Infusionen. Nehme alles in Tablettenform ein. Gluthation, Selenase, Kalziumfolinat, Pascobin, Tracitrans, Colibiogen nehme ich gar nicht. Was ist das eigentlich alles?

GC Maf kennt hier keiner. 🙁

Ich dachte Viren bekommt man nur mit viralen Mittelchen weg. Die AB’s bei Wheldon sind doch antibakteriell?!?

Ansonsten nehme ich folgende Supps zum Wheldon Protokoll ein:
– Q10, Curcuma, Vit. C, Vit. B12, Vit. D, Vit. E, Magnesium, Folsäure, Alpha Liponsäure, L-Carnitin, Probiotikum, Kieselerde oder Biotin, Omega 3, Nachtkerzenöl, Selen, Vit. B Komplex und ACC ( aber nicht so hochdosiert wie empfohlen ).

Bei der Frage, welche Mittelchen die schiefe Nase noch mehr blockieren, da muss ich leider passen. 🙁

Hast Du noch eine Vermutung?

[ilka]

Hi Phenom,

1. Die NK Zellen habe ich nicht messen lassen.

2. Metro und Tini sind beides Bakterizide. Tini soll besser verträglich sein, ich komme damit gut zurecht, außerdem muss ich es nur 2x am Tag nehmen. Tini wird nur aus marktwirtschaftlichen Interessen in der BRD nicht vertrieben, bekommt man problemlos aus den europäischen Ländern.

LG Ilka

[Phenom77]

@Teufelchen Tatsächlich wirken die gen. Antibiotika nachgewiesenermaßen auch virustatisch.

[teufelchen]

Hi, na dann kann ich ja die AB weiterhin mit gutem Gewissen einnehmen. Muss ich nur noch mal die Supplements überdenken, oder was denkst Du?

[Phenom77]

Verträgst die denn alle Nahrungsergänzungsmittel ? Bei mir sind mit der Zeit ein paar Unverträglichkeiten aufgetreten. Deshalb eben die Infusionen.

[teufelchen]

Also zumindest habe ich keine Beschwerden betreffs der Supps. Allerdings frag mich nicht nach den Nebenwirkungen. Was für Unverträglichkeiten hast Du denn?

[Phenom77]

Meine Unverträglichkeiten betreffen überwiegend den Darm. Kann man schwer erklären. Beispiel : nehme ich Vit. C, Vit. B12, Vit. E, Magnesium, Folsäure, Alpha Liponsäure, L-Carnitin, Selenase u.a. oral ein werde ich sehr nervös. Als Infusion treten keine Probleme auf obwohl es die gleichen Mittel sind.

„- ich weiss nicht ob die Einnahme von Vitaminen und Co unterstützend hilft, ich für mich würde die Behauptung aufstellen, „Ja“ es hilft unterstützend, am meisten unterstützen mich dabei Enzyme!“

Darf ich fragen, welche Enzyme das sind ?

Habe hier auch noch etwas sehr gutes zu Minocyclin gefunden :

http://forums.phoenixrising.me/index.php?threads/transient-improvement-from-antibiotics-help-be-troubleshoot.9216/#post-170482

http://www.5goldig.de/Text_Uebersetzer/text-uebersetzen.html

Etliche Studien belegen, das Minocyclin die Replication von Redroviren hemmt. Die Studien wurden überwiegend bei HIV durchgeführt da viele eine Demenz entwickeln und HAART im Nervensystem nutzlos ist.
Bekanntlich schaukeln sich Tetra und Makrolide gegenseit hoch. Das erklärt warum viele MS Patienten und meine Wenigkeit so deutliche Verbesserungen mit Wheldon erfahren.

Hier der Text :
Minocycline: inhibiting NF-KappaB in the brain, inhibiting microglial activation, inhibits HIV replication, protects brains of mice from an MLV (close relative of XMRV). Seems like it would at least help via NF-KappaB inhibition, and if we were really lucky might directly inhibit XMRV replication as it does in HIV. The list of studies documenting one or another neuroprotective feature of minocycline is ridiculously long now but I will limit this to what seems most relevant to XMRV:

J Infect Dis. 2010 Apr 15;201(8):1132-40.
Minocycline attenuates HIV infection and reactivation by suppressing cellular activation in human CD4+ T cells.

Szeto GL, Brice AK, Yang HC, Barber SA, Siliciano RF, Clements JE.
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

Treatment of human immunodeficiency virus (HIV) infection with highly active antiretroviral therapy (HAART) is effective but can be associated with toxic effects and is expensive. Other options may be useful for long-term therapy. The immunomodulatory antibiotic minocycline could be an effective, low-cost adjunctive treatment to HAART. Minocycline mediated a dose-dependent decrease in single-cycle CXCR4-tropic HIV infection and decreased viral RNA after infection of CD4+ T cells with HIV NL4-3. Reactivation from latency was also decreased in a primary CD4+ T cell-derived model and in resting CD4+ T cells from HIV-infected patients. Minocycline treatment resulted in significant changes in activation marker expression and inhibited proliferation and cytokine secretion of CD4+ T cells in response to activation. This study demonstrates that minocycline reduces HIV replication and reactivation and decreases CD4+ T cell activation. The anti-HIV effects of minocycline are mediated by altering the cellular environment rather than directly targeting virus, placing minocycline in the class of anticellular anti-HIV drugs.

PMID: 20205570
Brain Res. 2009 Aug 25;1286:174-84. Epub 2009 Jun 11.
Attenuation of oxidative stress, inflammation and apoptosis by minocycline prevents retrovirus-induced neurodegeneration in mice.

Kuang X, Scofield VL, Yan M, Stoica G, Liu N, Wong PK.
Department of Carcinogenesis, University of Texas, M.D. Anderson Cancer Center, Science Park-Research Division

The ts1 mutant of the Moloney murine leukemia virus (MoMuLV) causes neurodegeneration in infected mice that resembles HIV-associated dementia. We have shown previously that ts1 infects glial cells in the brain, but not neurons. The most likely mechanism for ts1-mediated neurodegeneration is loss of glial redox support and glial cell toxicity to neurons. Minocycline has been shown to have neuroprotective effects in various models of neurodegeneration. This study was designed to determine whether and how minocycline prevents paralysis and death in ts1-infected mice. We show here that minocycline delays neurodegeneration in ts1-infected mice, and that it prevents death of cultured astrocytes infected by ts1 through attenuating oxidative stress, inflammation and apoptosis. Although minocycline reduces virus titers in the CNS of infected mice, it does not affect virus titers in infected mice thymi, spleens or infected C1 astrocytes. In addition, minocycline prevents death of primary neurons when they are cocultured with ts1-infected astrocytes, through mechanisms involving both inhibition of oxidative stress and upregulation of the transcription factor NF-E2-related factor 2 (Nrf2), which controls cellular antioxidant defenses. We conclude that minocycline delays retrovirus ts1-induced neurodegeneration involving antioxidant, anti-inflammation and anti-apoptotic mechanisms.

PMID: 19523933
J Neurovirol. 2008 Oct;14(5):376-88. Epub 2008 Nov 12.
Mechanisms of minocycline-induced suppression of simian immunodeficiency virus encephalitis: inhibition of apoptosis signal-regulating kinase 1.

Follstaedt SC, Barber SA, Zink MC.
Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.

Human immunodeficiency virus (HIV) infection of the central nervous system (CNS) can lead to cognitive dysfunction, even in individuals treated with highly active antiretroviral therapy. Using an established simian immunodeficiency virus (SIV)/macaque model of HIV CNS disease, we previously reported that infection shifts the balance of activation of mitogen-activated protein kinase (MAPK) signaling pathways in the brain, resulting in increased activation of the neurodegenerative MAPKs p38 and JNK. Minocycline treatment of SIV-infected macaques reduced the incidence and severity of SIV encephalitis in this model, and suppressed the activation of p38 in the brain. The purpose of this study was to further examine the effects of minocycline on neurodegenerative MAPK signaling. We first demonstrated that minocycline also decreases JNK activation in the brain and levels of the inflammatory mediator nitric oxide (NO). We next used NO to activate these MAPK pathways in vitro, and demonstrated that minocycline suppresses p38 and c-Jun N-terminal kinase (JNK) activation by reducing intracellular levels, and hence, activation of apoptosis signal-regulating kinase 1 (ASK1), a MAPK kinase capable of selectively activating both pathways. We then demonstrated that ASK1 activation in the brain during SIV infection is suppressed by minocycline. By suppressing p38 and JNK activation pathways, which are important for the production of and responses to inflammatory mediators, minocycline may interrupt the vicious cycle of inflammation that both results from, and promotes, virus replication in SIV and HIV CNS disease.

PMID: 19003592
Bioinformatics. 2007 Oct 15;23(20):2797-9. Epub 2007 Sep 5.
Identification of potential HIV-1 targets of minocycline.

Jenwitheesuk E, Samudrala R.
National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency

Minocycline, a broad spectrum antibiotic, has been discovered to have inhibitory activity against HIV-1 in vitro, but the targets inhibited are unknown. We used a docking with dynamics protocol developed by us to predict the binding affinities of minocycline against seven active sites of five HIV-1 proteins to putatively identify the potential target(s) of minocycline. The results indicate that minocycline has the highest predicted binding affinity against HIV-1 integrase.

PMID: 17804437
PLoS One. 2010 May 7;5(5):e10523.
Proton magnetic resonance spectroscopy reveals neuroprotection by oral minocycline in a nonhuman primate model of accelerated NeuroAIDS.

Ratai EM, Bombardier JP, Joo CG, Annamalai L, Burdo TH, Campbell J, Fell R, Hakimelahi R, He J, Autissier P, Lentz MR, Halpern EF, Masliah E, Williams KC, Westmoreland SV, Gonzlez RG.
AA Martinos Center for Biomedical Imaging and Neuroradiology Division, Massachusetts General Hospital

BACKGROUND: Despite the advent of highly active anti-retroviral therapy (HAART), HIV-associated neurocognitive disorders continue to be a significant problem. In efforts to understand and alleviate neurocognitive deficits associated with HIV, we used an accelerated simian immunodeficiency virus (SIV) macaque model of NeuroAIDS to test whether minocycline is neuroprotective against lentiviral-induced neuronal injury.

METHODOLOGY/PRINCIPAL FINDINGS: Eleven rhesus macaques were infected with SIV, depleted of CD8+ lymphocytes, and studied until eight weeks post inoculation (wpi). Seven animals received daily minocycline orally beginning at 4 wpi. Neuronal integrity was monitored in vivo by proton magnetic resonance spectroscopy and post-mortem by immunohistochemistry for synaptophysin (SYN), microtubule-associated protein 2 (MAP2), and neuronal counts. Astrogliosis and microglial activation were quantified by measuring glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (IBA-1), respectively. SIV infection followed by CD8+ cell depletion induced a progressive decline in neuronal integrity evidenced by declining N-acetylaspartate/creatine (NAA/Cr), which was arrested with minocycline treatment. The recovery of this ratio was due to increases in NAA, indicating neuronal recovery, and decreases in Cr, likely reflecting downregulation of glial cell activation. SYN, MAP2, and neuronal counts were found to be higher in minocycline-treated animals compared to untreated animals while GFAP and IBA-1 expression were decreased compared to controls. CSF and plasma viral loads were lower in MN-treated animals.

CONCLUSIONS/SIGNIFICANCE: In conclusion, oral minocycline alleviates neuronal damage induced by the AIDS virus.

PMID: 20479889
A novel use for an old drug: the potential for minocycline as anti-HIV adjuvant therapy.

Copeland KF, Brooks JI.

J Infect Dis. 2010 Apr 15;201(8):1115-7. No abstract available. PMID: 20205572
JAMA. 2005 Apr 27;293(16):2003-11.
Neuroprotective and anti-human immunodeficiency virus activity of minocycline.

Zink MC, Uhrlaub J, DeWitt J, Voelker T, Bullock B, Mankowski J, Tarwater P, Clements J, Barber S.
Department of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, Md 21205, USA. mczink@jhmi.edu

CONTEXT: The prevalence of human immunodeficiency virus (HIV) central nervous system (CNS) disease has not decreased despite highly active antiretroviral therapy. Current antiretroviral drugs are expensive, have significant adverse effects including neurotoxicity, and few cross the blood-brain barrier.

OBJECTIVE: To examine the ability of minocycline, an antibiotic with potent anti-inflammatory and neuroprotective properties, to protect against encephalitis and neurodegeneration using a rapid, high viral load simian immunodeficiency virus (SIV) model of HIV-associated CNS disease that constitutes a rigorous in vivo test for potential therapeutics.

DESIGN AND SUBJECTS: Five SIV-infected pigtailed macaques were treated with 4 mg/kg per day of minocycline beginning at early asymptomatic infection (21 days after inoculation). Another 6 macaques were inoculated with SIV but remained untreated. Blood and cerebrospinal fluid (CSF) samples were taken on days 7, 10, 14, 21, 28, 35, 43, 56, 70, 77, and 84, and all macaques were humanely killed at 84 days after inoculation, a time that corresponds to late-stage infection in HIV-infected individuals.

MAIN OUTCOME MEASURES: Blood and CSF samples were tested for viral load by real-time reverse transcription-polymerase chain reaction and levels of monocyte chemoattractant protein 1 were quantitated by enzyme-linked immunosorbent assay. The presence and severity of encephalitis was determined by microscopic examination of tissues. Central nervous system inflammation was further assessed by measuring infiltration and activation of macrophages, activation of p38 mitogen-activated protein kinase and expression of amyloid precursor protein by quantitative immunohistochemistry.

RESULTS: Minocycline-treated macaques had less severe encephalitis (P = .02), reduced CNS expression of neuroinflammatory markers (major histocompatibility complex class II, P = .03; macrophage marker CD68 , P = .07; T-cell intracytoplasmic antigen 1, P = .03; CSF monocyte chemoattractant protein 1, P = .001), reduced activation of p38 mitogen-activated protein kinase (P<.001), less axonal degeneration (beta-amyloid precursor protein, P = .03), and lower CNS virus replication (viral RNA, P = .04; viral antigen, P = .04). In in vitro analysis, minocycline suppression of HIV and SIV replication in cultured primary macrophages did not correlate with suppression of activation of p38-mitogen-activated protein kinase pathways, whereas suppression in primary lymphocytes correlated with suppression of p38 activation. CONCLUSIONS: In this experimental SIV model of HIV CNS disease, minocycline reduced the severity of encephalitis, suppressed viral load in the brain, and decreased the expression of CNS inflammatory markers. In vitro, minocycline inhibited SIV and HIV replication. These findings suggest that minocycline, a safe, inexpensive, and readily available antibiotic should be investigated as an anti-HIV therapeutic. PMID: 15855434

[Autor]

Beiträge