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    Psychedelics and infection 
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    Bluelighter mr peabody's Avatar
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    Following is a digest of articles and reports that is constantly updated. Jump in!






    HIV and iboga alkaloid congener 18-Methoxycoronaridine (18-MC)


    Edinete Silva, Claudio Cirne-Santos, Izabel Frugulhetti, Bernardo Galvao-Castro, Elvira Saraiva, Martin Kuhne, Dimith Chequer Bou-Habib

    The Iboga alkaloid congener 18-methoxycoronaridine (18-MC) exhibits in vitro leishmanicidal and in vivo anti-addiction properties. In this paper, we describe that 18-MC inhibits HIV-1 infection in human peripheral blood mononuclear cells (PBMCs) and monocyte-derived macrophages. We found that 18-MC inhibits the replication of primary isolates of HIV-1 in a dose-
    dependent manner.

    Introduction

    HIV type 1, the etiological agent of the acquired immunodeficiency syndrome (AIDS), is a global health problem affecting more than 42 million people worldwide. It is estimated that 5 million new infections occurred in 2003, and about 3 million individuals died from AIDS in the same period. HIV-1 persistently replicates in the lymphoid tissues, leading to a progressive deterioration of the immune system, and to a severe clinical outcome of immunosuppression, the foremost characteristic of AIDS. An effective vaccine against HIV-1 infection has not been developed yet.

    Two decades after the discovery of the first cases of AIDS, the clinical use of the abundant antiretroviral repertoire has resulted in an unequivocally favorable effect, decreasing the morbidity and mortality of HIV-1 infection. Treatment with highly active antiretroviral therapy (HAART), a combination of drugs that inhibit the HIV-1 enzymes reverse transcriptase (RT) and protease, promotes a sustained decrease in the viral load and a restoration of the immune response, even in patients who have developed a severe immunosuppression. However, this treatment does not completely eradicate HIV-1 from the infected tissues, and its long-term use is restricted by metabolic disorders and toxicities, emergence of drug-resistant viruses and complex administration. Thus, the search for other antiretroviral compounds is critical, and numerous new anti-HIV-1 agents that target different phases of viral replication cycle are underdevelopment or in clinical trials.

    The Iboga indole alkaloid coronaridine (COR) is found in many species of the plant kingdom. Because of the side effects such as tremor, cerebellar neurotoxicity and bradycardia associated with COR, chemical structure modifications were made to reduce its side effects, which was attained with a methoxylation at carbon-18, resulting in the analogue 18-methoxycoronaridine (18-MC). In preclinical studies, 18-MC exerted few to none of the non-specific or neurotoxic side effects associated with COR administration. We recently reported that the natural alkaloid COR presents an antiparasite activity against Leishmaniaamazonensis, a property showed by 18-MC as well.

    Since many alkaloids have been described as capable of inhibiting HIV-1 infection in vitro, we investigated whether 18-MC is also endowed with antiretroviral properties. We found that 18-MC inhibits HIV-1 replication in human peripheral blood mononuclear cells and in monocyte-derived macrophages, and that this activity is at least partially mediated by reducing the activity of the HIV-1 enzyme reverse transcriptase.

    Results and discussion

    In this paper, we report that the indole alkaloid congener 18-MC inhibits HIV-1 infection, independently of the preferential coreceptor usage of the viral isolates. The infection assays were performed with primary cells acutely infected PBMCs and macrophages) to avoid the genotypic and phenotypic changes that might occur during viral passages in tumor cell lines. We also used primary isolates, which are phenotypically closer to the viral population present in HIV-1-infected patients. In preliminary experiments, we found that the naturally occurring COR decreased the infection in a dose dependent manner. Since 18-MC is an improved molecule of the natural compound COR, presenting little to none of the adverse effects associated with the original molecule, we continued our anti-retroviral studies using the new alkaloid congener 18-MC.

    18-MC mediated a substantial anti-HIV-1 effect in infected PBMCs, regardless of the preferential co-receptor usage of the viral isolates. 18-MC consistently inhibited viral replication,
    with inhibitory levels similar to those reached for the other two phenotypes. AZT, a nucleoside analogue inhibitor of the HIV-1 enzyme reverse transcriptase, blocked viral replication as expected. In some experiments with the X4 isolate, HIV-1-infected PBMCs were cultured for an extended period, and exposed to 18-MC (50 uM) during either three days only, or 10 days. Using this approach, we found that the inhibition of HIV-1 replication was 50% higher when infected cells were treated with 18-MC during the whole period of the assay (10 days), in opposition to a shorter exposure to the compound (3 days). This finding suggests that the optimal anti-retroviral activity may be dependent of the permanent exposure of the infected cells to 18-MC.

    The antiretroviral effect of the alkaloids may be due to their action on different steps of viral replication, such as inhibition of syncytium formation and of the RT activity. Since 18-MC mediates only a moderate dose-dependent RT inhibition, it is possible that other concurrent mechanisms contribute to reduce HIV-1 replication. For example, 18-MC exhibits affinity for k-opioid receptors, and it is known that the k-opioid agonist U50488 inhibits HIV-1 replication in macrophages and lymphocytes. Thus, the anti-HIV activity of 18-MC may also, to some extent, result from its binding to and stimulation of k-opioid receptors. A potential additional mechanism is the reduction of lymphoproliferation, since preliminary experiments performed in our laboratory have shown that 25 uM and 50 uM of 18-MC decreased by 30% and 50% the blastogenesis of PHA-activated PBMCs cultured with IL-2, respectively. This property has been suggested to contribute to the strong antiretroviral activity of mycophenolic acid.

    Our present results warrant further investigation on the mechanisms by which 18-MC decreases HIV-1 replication invitro, in addition to inhibition of HIV-1 reverse transcriptase. Finally, considering that 18-MC demonstrates a vigorous leishmanicidal activity in vitro, its potential therapeutic properties may be uniquely useful for the treatment of HIV-1-infected individuals as well as patients coinfected with Leishmania and HIV-1.

    https://www.arca.fiocruz.br/bitstrea...nti-HIV....pdf

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    Anti-viral effects of Ibogaine

    Dr. Vic Hernandez

    Ibogaine in its administered forms has typically been applied to persons seeking a chemical dependence addiction treatment. The target population not only has had to contend with chemical dependence issues but issues concerning other infections, notably HIV and/or HCV or co-infection. As antidotal and preliminary scientific information is noted concerning Ibogaine treatments, trends suggest potential applications to these pathogens and perhaps others. Medical science has not rigorously pursued investigation into the potential applications of Iboga alkaloids in invitro work, animal studies and human study.

    I am a public health wonk. I have had the luxury of doing what interests me in what I call Public-Health. I get off on effecting and affecting the Publics Health. My work in HIV has concerned oxidative stress and HIV and its contribution to the understanding of pathogenesis and pathophysiology. I've been involved in developing guidelines for physicians treating HIV, trial design and methodology. I have worked on developing practitioner education forums to support understanding and treatment for isolated populations infected with HIV, notably active users. My unique relationship to communities affected by HIV, activism and passion for my work has brought me to unique understandings and relationships that I have brought to other public health work. I received a congressional citation for this work. Working with Lynn Mofenson at the NIH we moved to look at micro-nutrient intervention in HIV non-progressors to affect HIV progression and delay ARV intervention without compromising patient health by allowing HIV to run unabated. The fruits of this work have been born out in the African studies noted in US papers recently. Working with Lynn, Fauzi at Harvard and others, we established a treatment approach that was frowned upon when we started back in 1993 into accepted and respected reality.

    Noted work included the resurrection of Alfa Lipoic Acid as a micronutrient effecting Liver toxicity. It would later be applied to HCV cases. In recent years, needing and wanting a break form HIV, I've worked in the realm of cancer, looking at the role of genetics in identifying trends in non-progressors utilizing non-conventional therapies or no therapeutic interventions. This work has allowed me to look at orthomolecular medicine (effect of micro-nutrients on the biochemistry of the body, pathogen infection, self cells run amuck and wellness and quality of life). Working with colleagues and mentors as Lynn Margulis at U Mass Amherst and Walter Willet at Harvard, I began to understand as Lynn puts it: the symbiosis of medicine, and as Walter puts it, as the effect of the basic building blocks of body systems and their abilities to stay healthy. Why mention this blather, you need to know where I am coming from with this information I am attempting to convey so we can understand where we are all going now and in the future.

    HIV, where are we and what it means

    HIV research and treatment approaches have been checkered and somewhat baffling in approach and far too complex to delve into at this meeting or in this short of time. From a conventional medicine perspective, there are three steps required for HIV to enter cells: Attachment, Binding to a co-receptor, and Fusion of HIV into CD-4 cell. The currently available classes of drugs work to prevent the process of HIV reproducing itself and infecting new cells after HIV enters the CD-4 cell: They are Nucleoside Analogues, Non-nucleoside Analogues and Protease Inhibitors. These drugs have been administered in combination, at varied intervals, and in varying doses to tease out efficacy for the particular viral strain(s) expressed by the patient. Toxicities to body systems and healthy cells require strict and watchful management.

    There is a new class of drugs called Entry Inhibitors which block HIV from entering CD-4 cells. They work by blocking the HIVs ability to enter and infect a cell. Essentially there are two steps to entry of HIV into the CD-4 cell. HIV attaches to the CD-4 cell and then fuses with it. After fusing with the cell, HIV can dump its genetic material into the CD-4 cell, the material it needs to reproduce itself in the CD-4 cell. There are two steps to attachment: attaching to the CD-4 receptor and then to a co-receptor, either CCR5 or CXCR4. Basically how Entry Inhibitors work is first by:

    - Attachment
    - Co-receptor binding
    - Fusion

    Currently available HIV drugs other than Fuzeon, prevent HIV from reproducing once HIV in the cell.

    HIV Super-infection and HIV Drug Resistance. Lets start with HIV super-infection. Studies over the past two years suggest this is a real problem. Super-infection is when a person who has HIV gets infected with a second viral strain of HIV. Super-infection, based on study, occurs 5 to 13 months after estimated date of initial infection. The super-infection strain can be associated with ARV susceptibility and adherence. In some cases, a person can be infected with a drug resistant strain and then become infected with a super-infection wild-type or visa-versa. Initial co-infection cannot be ruled be ruled out. Molecular investigation determines evidence of super-infection coupled with progression and ARV response. The rate of the super-infection based on study hovers somewhere around 6.5% annually. Harm reduction counseling is recommended by the researchers.

    There are some in the medical science community that are trying to link the super-infection to a patient zero that originated from New York. Nonsense! This was tried at the beginning of the HIV/AIDS pandemic by saying that HIV started in North America with a Canadian airline steward. It is impossible to narrow down such a claim. By the way, in that case, it was refuted by the testing of IDU blood samples from the early seventies that had been banked at Beth Israel. HIV was found in those cohorts, long before the Canadian air-steward stuff. At a recent conference, Paul Volberding MD from UCSF noted that the super-infection business hinged on one reliable case and that the bally-who was uncalled for. This should not minimize sound and reliable public health interventions such as safer sex practices.

    Unfortunately, we are learning about HIV pathophysiology and pathogenesis as we go along instead of developing the understanding first. This may deal a blow to 18-MC, if applied to HIV or not.

    Regarding HIV drug resistance, this beast has been rearing its ugly head for some years but it was not until ICAAC in October of 2004 did the rates found seem alarmingly worrisome. Soon after, the media has grabbed a hold on this information. Studies are finding an escalation of HIV drug resistance during primary infection period (shortly after infection). And the resistances vary among drug classes. Drug resistant HIV acquired at time of infection can establish itself as the dominant virus population and become archived in the latent cellular reservoir. This may result in sub-optimal response to ARV interventions and promote the accumulation of mutations and jeopardize already limited treatment options. In further study, HIV drug resistance has been found in 1 of 7 treated in the US of a cohort of 317 in 40 US cities. The prominent resistance was found in the non-nukes class of drugs. Ethnic differences were noted. Latinos and Asian patients had a lower prevalence of reduced susceptibility (6 percent, with Caucasians at 27 percent, and Blacks at 23 percent. There were no gender differentiations or comparisons done. These were among male cohorts.

    HCV and co-infection

    HCV therapeutic interventions are limited in pharmaceutical application (interferon and pegalated interferon [riboviron and interferon]) are limited. There are surfacing reports indicating significant efficacy with TCM. In the co-infected individual, treatment options reduce due to the environment of the liver.

    When Howard approached me with this paper, I read it and got excited. I like new ideas and approaches especially if the science is tight and is respectful of change. No one has the ace card and false hope, especially for patients is highly unethical. Ask David Ho MD at Rockefellers Aaron Diamond Center regarding the premature delivery of HIV cure based on invitro data. After reading the paper Howard shared, the questions flooded through my head and as we talked, he suggested I say a few words. Reluctantly, I accepted. I have been trying to avoid public gigs especially those that risk pissing contests. The paper by Silva et al from Brazil entitled: Anti-HIV-1 Activity of Iboga Alkaloid Congener 18-MC is a significant piece of work. It was an invitro (in lab) study using human cells. The Iboga alkaloid 18-MC was introduced to human Peripheral Blood Mononuclear cells (PBMCs) and monocyte-derived macrophages. The result was the significant inhibition of isolates of HIV-1 in a dose dependent manner.

    The approach of this anti HIV-1 inhibitory activity study went something like this: An invitro study of donor PBMCs cells from healthy donors was executed with monocyte-derived human macrophages isolated from the PBMCs. This was not a formal clinical trial with subjects. Materials and methods seemed valid and reliable. Then HIV-1 primary isolates (3 used) were used. AZT, a nucleoside analogue was used as a control probably because the mechanism of action of 18-MC is as reverse transcriptase inhibitor and AZT is a nucleoside analogue used to affect reverse transcriptase. PBMCs were exposed to viral suspensions of HIV-1 P-24 antigen. Viral replication was assessed by measuring P-24 antigen. Dose ranges went from 12.5 micromolers to 50 micromolers significantly effected HIV proliferation. Time durations varied from 3, 10, 14 and 21 days. A variety of doses, durations were done to observe safety, and effect. Compared to the control (AZT) which was rigorous as expected, 18-MC faired very well. It should be noted that the infection assays were performed with primary cells (acutely infected PBMCs and macrophages) to avoid the genotypic and phenotypic changes that might occur during viral changes that might occur during viral passages in tumor cell lines. They also used primary isolates, which are phenotypically closer to the viral population present in HIV-1 infected patients. Additionally, they looked at the naturally occurring COR and its anti HIV-1 effect and found significant results, but the data was not reported. They did report the indole alkaloid congener 18-MC molecule of the natural COR, presenting little to none of the adverse effects associated with the original molecule in this antiviral study reported. These study design considerations contributed to a tight study with valid and reliable outcomes.

    Basically, 18-MC inhibits HIV-1 replication in human PBMCs and in monocyte-derived macrophages. This antiviral effect of the alkaloids may be due to their action on different steps of viral replication, such as inhibition of syncytium formation and reducing the activity of HIV-1 enzyme reverse transcriptase. So how this applies to the HIV treatment intervention picture is up for grabs. Certainly, further study needs to be done on the mechanisms by which 18-MC decreases HIV replication in vitro, in addition to inhibition of HIV reverse transcriptase. It is worth doing for a number of potential reasons:

    - 18-MC has a lower toxicity profile compared to the drugs in the study control class (nucleoside analogues). And I would venture to say in the other three classes that prevent the process of HIV from reproducing itself and perhaps infecting new cells after HIV enters the CD-4 cell.

    - 18-MC provides a potentially safe ARV therapeutic intervention in less virulent strains of HIV and minimizing toxicities.

    - Co-therapeutic intervention can be matched with micro-nutrient regimens which have been shown in study to delay ARV therapeutic intervention for up to 5 years, notably in women and infected infants.

    - 18-MC, based on its mechanism of action against HIV in comparable drug classes, could be applied to HIV infected pregnant women to affect mother to fetus transmission rates. The studies among these populations used AZT, the control for the 18-MC. I believe 18-MC has a less toxic profile than AZT even thought AZT showed significant interruption of mother to fetus HIV transmission.

    - Given the pharmacodynamics of Iboga alkaloids in the brain, the potential for crossing the blood brain barrier is significant.

    - As mentioned earlier in Dr. Onaivis presentation, the potential of Ibogaine to regulate inflammation (genetically) is significant for persons living with HIV/AIDS where inflammatory states are hallmark.

    I believe it would be cost effective in poorer nations struggling with HIV infection. There are issues here, too.

    - Since this 18-MC affects HIV-1 at reverse transcriptase, such as other classes of drugs, perhaps there is a chance for drug resistance as found in other drugs in that class or a shorter duration to it?

    - Perhaps it can be used in initial therapy in super-infections or drug-resistant strains until it succumbs to those viral expressions.

    - In combination with other drug classes such as nukes, non-nukes and protease, there is a strong potential for side effects. But given their toxicity to body systems and healthy cell lines that the nukes, non-nukes and protease inhibitors have, pairing them up with this group may not be wise. This is dependent on dose levels and state of the patient.

    - Perhaps it can be paired up with the new Entry Inhibitors to provide a well-rounded combination to thwart HIV. This I see as the most promising combination.

    - In the case of co-infection, particularly for those with HIV/HCV infection and dicey livers, this may prove to be questionable. I believe the verdict is not in on and further research is needed.

    - Regarding potential psychedelic effects, it should be noted that Sustiva reports similar side effects (like hypnogocic hallucinations) and has been controlled through a variety of provider and patient interventions.

    What medical science needs to do

    Simple, more study, but the politics of what gets studied and how it gets funded are sad realities. But history has shown us that vigilant activism can effect epistemology, study approach even study design and recruitment. For example, a medical treatment support group comprised of non-active injection drugs users (IDUs) based in the Bronx found the Hypericin study at Bellevue Medical Center in NYC to be of interest. But they found the route of administration (subcutaneous) a bit unwelcoming since it brought up potential triggers to use again. They met with the principal investigator (PI) Fred Valentine MD and persuaded him to add an arm that was orally administered. He agreed and they (the patients) help recruit for the study.

    Since the study was done in Brazil and not in the US, the chances for further investigation are probably more promising. Based on this limited work, an Investigational New Drug (IND) designation can be developed, funding lined up, bring it up with Community Review Boards (CRBs), cultivate interested researchers are among the many avenues medical science must go with this. Working with the Institutional Review Boards (IRBs), who wheel a lot of political power to support pursuit of an Iboga-alkaloid as an anti-viral. This is most effective if you have a PI lined up with a clear focus, good science under his/her belt coupled with sufficient funding source(s).

    What can patients and advocates do?

    I believe there are many things that can be done here, to name a few:

    1. Brainstorm with constituencies of patients in effected populations. Dr. Ken Alper and others have mentioned the comradery of the group having been treated with Ibogaine. These people serve as a constituency who can affect the fast tracking of treatments.

    2. Develop proactive treatment support groups that can be involved in trial design, methodology, trial recruitment, trial implementation, and adherence and compliance issues. For example, I have started HIV/AIDS treatment support groups called AMEN (Attitude, Medications, Exercise, Nutrition). These groups encourage patients to be their own primary healthcare advocate. They are involved in all aspects of patient treatment intervention(s), advocacy, and often times drug development.

    3. Treatment support group can not only promote such objects as patients being their own primary healthcare advocate but also informal researchers. For example, setting up simple databases that encourage the observation of trends of persons taking Ibogaine and the effect on say HCV or HIV. Blood work-up can be a point measure to observe trends.

    4. Cultivate active and fruitful relationships between the treatment support group members and their healthcare providers, especially when it comes to understanding the population of active and non-active users, their medical conditions and predispositions, and above all the dynamic of behavior notably addiction.

    Remember, some of the most profound discoveries and epistemology in medical science came from non-medical/science trained patients and their advocates.

    https://ibogainedossier.com/v_hernandez.html
    Last edited by mr peabody; 19-09-2018 at 12:21.
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    Bluelighter mr peabody's Avatar
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    Antimicrobial activity of P. harmala against MRSA


    Mehdi Goudarzi, Hadi Azimi
    Department of Microbiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran

    Staph aureus, as a major cause of infection in either hospital or within the community, is responsible for a diverse spectrum of human infections and diseases such as pneumonia and bacteremia. This pathogen has an outstanding capability to acquire resistance, especially against methicillin, making it able to persist in the hospitals and the community. Soon after the introduction of penicillin in the 1960s, methicillin resistant Staph Aureus (MRSA) emerged and it has been endemic in hospitals around the world since 1980s. MRSA strains are shown to be able to rapidly develop multi-drug resistance (MDR) although a variety of therapeutic measures, including antibiotic therapy, have been introduced. The emergence and spread of MRSA harboring multi-resistance genes have increased academic burden. Proof caused serious therapeutic problems, and worsened controlling infection in hospitals.

    P. harmala is a medicinal plant used in the Iranian traditional medicine, due to the antimicrobial compounds found in its seeds and roots. The main objective of the study was to investigate the antibacterial activities of P. harmala seeds on MRSA strains. During an 11-month descriptive cross-sectional study, 90 MRSA strains isolated from hospitalized patients in ICU wards were investigated. Micro-broth dilution method was employed to evaluate the antimicrobial effects of the extract on MRSA strains. The results revealed that the P. harmala extract is very effective against MRSA strains isolated from ICU patients and may be useful in treating some of the infections.

    Considering the antibacterial activity of the seed extract of P. harmala against MRSA clinical isolates, it can be concluded that this extract could be exploited as an affordable and available source of therapeutic agents as well as an alternative approach to resistance management. Hence, it can be suggested for the treatment of MRSA infections although it is recommended that more studies be carried out to elucidate the precise bioactive natural compounds that lead to cytotoxicity against HEK 293 cell line.

    https://cdn.neoscriber.org/cdn/serve...ress-15592.pdf

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    Harmaline against Multi-Drug Resistant Escherichia coli


    Multidrug resistance (MDR) is a major challenge in the treatment of infectious diseases. The MDR in urinary tract infection causing bacteria, such as Escherichia coli, has made treatment of UTI very difficult. The aims of the current study were to synthesize a library of harmaline derivatives, and to evaluate their activity against various strains of multi-drug resistance (MDR) E. coli. Harmaline derivatives were synthesized by the reaction of harmaline with various acid halides and anhydrides. These compounds were subjected to susceptibility determination by in vitro MTT assay. The changes in morphology of the bacterial cells after the treatment with harmaline and its derivatives were studied through scanning electron, atomic force and fluorescence microscopy. The current study demonstrated that harmaline, and its derivatives were identified as anti-MDR agents against MDR strains of E. coli. Harmaline and its derivatives were identified as anti-MDR agents against various highly resistant MDR clinical isolates of E. coli. These compounds may serve as the leads for further studies towards the development of treatment against the infections caused by MDR E. coli.

    https://www.ncbi.nlm.nih.gov/pubmed/28124613

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    Cannabis kills MRSA, disrupts Prion Diseases

    Cannabis is a potent antibiotic that can kill Methicillin-Resistant Staphylococcus Aureus (MRSA) and disrupt the progression of prion diseases such as Mad Cow and Creutzfeld-Jakob disease - a medical information resource for doctors sponsored by The Massachusetts Medical Society, publisher of the New England Journal of Medicine.

    Scientists from Italy and the United Kingdom reported in the Journal of Natural Products that the main active ingredient in cannabis, THC, as well as four other pot molecules “showed potent antibacterial activity against six different strains of MRSA of clinical relevance."

    Cannabis also stops prions, a type of protein that can cause neurodegenerative diseases that are invariably fatal. Once prions get into a brain they replicate rapidly and shred brain tissue “resulting in a ‘spongiform’ appearance on post-mortem histological examination of neural tissue."

    In 2007, American and French researchers reported that pot molecule cannabidiol “prevents prion accumulation and protects neurons against prion toxicity” in the Journal of Neuroscience.

    Cannabidiol inhibited prion accumulation in mouse and sheep prion disease cell cultures and inhibited prion formation in the brain of infected mice given injections of CBD. “The authors conclude that CBD likely represents a new class of anti-prion drugs.”

    “These findings are encouraging, as prions are very difficult to kill. According to the National Institute of Neurological Disorders and Stroke, presently there is no FDA-approved treatment that can cure or even control Prion disease.”

    MRSA kills about 18,000 Americans each year and sickens about 94,000.

    https://www.eastbayexpress.com/Legal...prion-diseases

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    Psilocybin against MRSA

    Methicillin-resistant Staphylococcus aureus (MRSA) infection is caused by a strain of staph bacteria that's become resistant to the antibiotics commonly used to treat ordinary staph infections. MRSA is a bacterium responsible for several difficult-to-treat infections in humans. It is also called oxacillin-resistant Staphylococcus aureus (ORSA).

    MRSA is any strain of Staphylococcus aureus that has developed, through the process of natural selection, resistance to beta lactam antibiotics, which include the penicillin's (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins.

    Strains unable to resist these antibiotics are classified as Methicillin-Sensitive Staphylococcus aureus, or MSSA. The evolution of such resistance does not cause the organism to be more intrinsically virulent than strains of S. aureus that have no antibiotic resistance, but resistance does make MRSA infection more difficult to treat with standard types of antibiotics and thus more dangerous.

    The psychedelic mushroom Psilocybe semilanceata has been shown to strongly inhibit the growth of Staphylococcus aureus. An in vitro study showed that the cannabinoids CBD and CBG powerfully inhibit MRSA, in addition to the terpenoid pinene which occurs in cannabis. Cannabinoids (components of Cannabis sativa), including cannabidiol (CBD) and cannabinol (CBN), show activity against a variety of MRSA strains.

    https://www.slideshare.net/arunamdas3/mrsa-2

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    Staph aureus most commonly colonizes the nostrils. The rest of the respiratory tract, open wounds, intravenous catheters, and the urinary tract are also potential sites for infection. Healthy individuals may carry MRSA without symptoms for a few weeks to many years. Patients with compromised immune systems are at a significantly greater risk of symptomatic secondary infection.

    In most patients, MRSA can be detected by swabbing the nostrils and isolating the bacteria found inside. Combined with extra sanitary measures for those in contact with infected patients, screening patients admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the U.S., Denmark, Finland, and the Netherlands.

    About 75 percent of community-associated MRSA infections are localized to skin and soft tissue and usually can be treated effectively. But some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional healthcare-associated MRSA infections. These can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome, and necrotizing ("flesh-eating") pneumonia.

    The psychedelic mushroom Psilocybe semilanceata has been shown to strongly inhibit the growth of Staph aureus, and can also be used to kill and prevent the growth of Staph aureus.

    http://www.wiki30.com/wa?s=Methicill...ococcus_aureus



    Last edited by mr peabody; 20-09-2018 at 07:48.
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    Cannabis oil: Super antibiotic of the future

    “Without urgent, coordinated action by many stakeholders, the world is headed for a post-antibiotic era,” Dr. Keiji Fukuda, the Assistant Director General for the World Health Organization’s Health Security department, said last year after the WHO released its first ever global report on antibiotic resistance. “Common infections and minor injuries, which have been treatable for decades, can once again kill,” he continued, explaining how antibiotic resistant bacteria are now one of the top health concerns of the world.


    Scanning electron micrograph of MRSA on dead human tissue.

    The horrible irony is that the evolution of bacteria into “superbugs” is driven in large part by the antibiotics that were designed to treat them in the first place. Methicillin-resistant Staphylococcus aureus (MRSA) for example, which causes over 10,000 deaths each year according to the Center for Disease Control (CDC), is a direct byproduct of over-using antibiotics, which bred a stronger and more dangerous version of the common Staph aureus bacteria.

    MRSA, which infects open wounds and increases the chance of death in patients by over 60 percent according to the CDC, is now wreaking havoc in hospitals and other facilities where it can spread easily between people in close contact.

    Although MRSA is often associated with those with lowered immune systems, recently there have been outbreaks among healthy populations, including at a New York State high school and even among members of the Buccaneers professional NFL football team – guard Carl Nicks was injured so badly by the infection he had to undergo surgery and ended up losing his place on the team.

    The situation has become so severe that in late 2014, President Obama issued an executive order devoted to combating antibiotic resistant bacteria, which he called “a serious threat to public health and the economy.”

    Obama even allotted $1.2 billion to the annual budget for the establishment of a special task force devoted to the issue, one that would develop an action plan for stopping the fast spread of antibiotic resistant bacteria like MRSA.

    Game changing study

    In 2008, however, a first of its kind study conducted by a team of British and Italian researchers had already found that one of the world’s most commonly cultivated plants could stop MRSA in its tracks: marijuana.

    Specifically, the team tested five of marijuana’s most common cannabinoids against six different MRSA strains of “clinical relevance”, including epidemic EMRSA strains, which are the ones responsible for hospital outbreaks. They found that every single one of the cannabinoids tested showed “potent activity” against a wide variety of the bacteria.

    Cannabinoids are substances unique to the cannabis plant that have wide-ranging medicinal properties: they fight cancer, reverse inflammation and act as powerful antioxidants. Now we know that they are also some of the most powerful antibiotics on earth.


    Professor Giovanni Appendino and Professor Simon Gibbons shocked the medical world
    when they found cannabis compounds that shut down MRSA.


    “Everything points towards these compounds having been evolved by the plants as antimicrobial defenses that specifically target bacterial cells,” said Simon Gibbons, one of the authors of the study and head of the Department of Pharmaceutical and Biological Chemistry at the University College London School of Pharmacy, in a follow up interview in the MIT Technological Review.

    Amazingly, the cannabinoids even showed “exceptional activity” against a strain of the MRSA that had developed extra proteins for increased resistance to antibiotics, showing that cannabis remained effective despite the bacteria’s adaptations.

    “The actual mechanism by which they kill the bugs is still a mystery…” said Gibbons. “I really cannot hazard a guess how they do it, but their high potency as antibiotics suggests there must be a very specific mechanism.”

    The researchers recommend cannabis as the source of new and effective antibiotic products that can be used in institutional settings right now.

    “The most practical application of cannabinoids would be as topical agents to treat ulcers and wounds in a hospital environment, decreasing the burden of antibiotics,” said Giovanni Appendino, a professor at Italy’s Piemonte Orientale University and co-author of the study.

    Since two of the most potently antibacterial cannabinoids were not psychoactive at all and appear in abundance in the common and fast-growing hemp plant, producing the antibiotics of the future could be quick and simple.

    “What this means is, we could use fiber hemp plants that have no use as recreational drugs to cheaply and easily produce potent antibiotics,” Appendino concluded.

    Hidden history of a miracle plant


    But introducing cannabis into the formal healthcare system is nothing new; the plant has been used as medicine by different cultures for millennia. A 1960 paper by Professors Dr. J. Kabelik and Dr. F. Santavy of Palacky University in the Czech Republic entitled Marijuana as a Medicament is perhaps the most comprehensive look at marijuana’s traditional use around the globe ever written. Surprisingly, the authors claim that for most cultures and for most time periods, cannabis was used as an antibiotic and treatment for chronic illnesses first and foremost, while its narcotic use is limited to certain areas and historical periods.

    “All the information obtained from European folk medicine with regard to treatment with cannabis shows clearly that there do not appear to be any narcotic substances in it, or if there are then only in a negligible amount,” the authors claim. “Instead of that, emphasis has been laid on the antiseptic effect, hence on the antibiotic and to a small extent even on the analgetic (analgesic) effect.”

    The same pattern was found in ancient Egypt, where “papyruses point fundamentally to antiseptic use” and in modern African tribes, where the “analgetic, sedative and antibiotic properties of cannabis in internal and external application are well known.”

    In South American folk medicine, marijuana was used for everything from gonorrhea to tuberculosis, according to the paper, and in Southern Rhodesia “it is a remedy for anthrax, sepsis, dysentery, malaria and for tropical quinine-malarial haemoglobinuria.”

    Even as late as the 19th century, cannabis was used by Western doctors to combat serious illnesses at home and abroad. An 1843 article in London’s Provincial Medical Journal, for example, chronicles an Irish doctor’s success in treating both tetanus and cholera in India by using cannabis in the form of crude hemp resin. Both these diseases are caused by bacteria and were major killers at the time.

    A potent and commonly used medicine, cannabis was added to the official U.S. Pharmacopoeia in 1851, where it remained until it was removed in 1942. Coincidentally, the widespread manufacture and use of early commercial antibiotics — like penicillin, which was first isolated in 1929 but not mass produced until 1945 — happened at the same time as cannabis was taken out of medicinal use.

    The next half a century saw the touting of antibiotics as miracle drugs while marijuana came to be almost completely associated with getting “high” — its potent medicinal properties obscured behind a cloud of fear and propaganda.

    It is only in the last couple of decades that the failure of antibiotics and clinical medicine to address a fast growing number of serious illnesses has driven people to rediscover the miraculous healing powers of this ancient plant.

    Shelley’s story

    “Within a few months, Cannabis oil had done what years of antibiotics had failed to do, it had given me my life back,” writes Shelley White in the preface to her recently published book, Cannabis for Lyme Disease and Related Conditions: Scientific Basis and Anecdotal Evidence for Medicinal Use.

    “I most certainly believe it works as an antibacterial,” Shelley told Reset.Me. “I just am not comfortable calling it a cure due to the fact that the disease is so complex and each case is different.” Instead, Shelley says she is “symptom free” after nine years of battling the disease.

    Confusion and mystery surround Lyme disease, which is now the most common vector borne illness in the United States according to the CDC, with 300,000 new cases reported each year. Caused by the spirochete bacteria Borrelia burgdorferi and transmitted through the bite of tick, Lyme is treated by several weeks of antibiotics.

    But the International Lyme and Associated Diseases Society (ILADS) claims that at least 40 percent of Lyme patients end up with long term health problems, known as “chronic Lyme.” Not only has there never been a study that shows that antibiotics successfully treat chronic Lyme, but no accurate tests exist to indicate whether the bacteria has been eradicated or not after treatment, the ILADS website states. For chronic Lyme suffers, life becomes a nightmare without an end in sight.

    “I was completely debilitated, I could not walk or talk and I was in a wheelchair being spoon-fed,” Shelley says in a YouTube video she posted in September of 2013 that chronicles her healing journey with cannabis oil. “I did antibiotics for over a year” she states, “They did not work for me they worked against me.”

    “I took a shot in the dark and started using cannabis oil and it worked,” she explains.

    The video went viral, as for many people who suffer from chronic Lyme, news of a successful treatment is like catching wind of a miracle. It was this response that inspired Shelley to write the book.


    After 9 years of suffering from Lyme disease, Shelley White
    has a new lease on life due to cannabis oil.


    A story of personal healing that is also strongly grounded in scientific research; the book begins with an overview of the antibacterial properties of cannabis. Then, chapter-by-chapter, it looks at evidence supporting the plant’s ability to alleviate every symptom of the disease — from nerve pain and seizures to memory loss and depression.

    Finally, Shelly shares her recipe for homemade cannabis infused coconut and olive oils, which can be made on the stovetop in under a half an hour by anyone with basic cooking skills. The trick is in not heating it over the boiling point to extract as much of the healing properties as possible.

    Medicine for the masses

    It turns out that Shelley’s simple oil extract is possibly the most potent form of marijuana medicine on earth. Olive oil is actually the “optimal choice for preparation of Cannabis oils for self-medication,” states Biologist Dr. Arno Hazekamp of Leiden University in Holland in a 2013 study entitled Cannabis Oil: chemical evaluation of an upcoming cannabis-based medicine.

    The study tested cannabis infused oil olive against several other extraction methods, including the popular solvent based “Rick Simpson” extraction method, which uses either naphtha or petroleum ether, and an ethanol extraction process.

    While the naphtha method did result in a product with the highest THC levels, the olive oil extraction not only yielded the highest overall cannabinoid levels, but higher levels of terpenes than the other processes.

    Terpenes are the essential oil compounds responsible for the distinctly pungent aroma of cannabis. Common strong smelling kitchen herbs like oregano are known for their powerful antibiotic properties, which is due to their terpene content. Volatile and delicate, terpenes can be quickly destroyed when heated too high.

    “It can be concluded that it is not feasible to perform decarboxylation of cannabinoids, without significant loss of terpene components.” Dr. Hazekamp advises. The decarboxylation process, which heats marijuana to a point where the THC becomes psychoactive, happens automatically when cannabis is smoked, meaning tokers are not getting the full benefit of the herb’s medicinal power.

    Likewise, expensive products that rely on processing marijuana, especially those that isolate certain cannabinoids, are also limiting its potential healing power. The terpene beta-Pinene for example, which has been found to be anti-fungal and to synergistically fight MRSA, was completely absent in the naphtha based “Rick Simpson” style cannabis oil tested, which tries to extract as much THC as possible. It remained at high levels in the olive oil extraction however.

    “Retaining the full spectrum of terpenes present in fresh cannabis material should therefore be a major focus during optimal Cannabis oil production,” Dr. Hazekamp concludes. The wide array of cannabinoids and terpenes present in the plant in its natural state are what makes marijuana such a versatile remedy for a variety of conditions and an extremely potent antibiotic.

    And although the White House just lifted many of the restrictions on medical marijuana research that had been in place since the 1990s, it is unlikely that science will ever come up with a more powerful marijuana based product than the simple homemade oil that can be used both topically and internally.

    This means that even with a “post-antibiotic” era looming on the horizon and a growing tide of new mystery illnesses sweeping the land, the super medicine of the future remains right where it has been for most of the past — in nature, freely available for our use.

    http://reset.me/story/marijuana-the-...of-the-future/
    Last edited by mr peabody; 09-09-2018 at 01:56.
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    Iboga congeners coronaridine and its analog 18-Methoxycoronaridine against parasitic Leishmaniasis
    *

    Jan Carlo Delorenzi, Leonardo Freire-de-Lima, Cerli Gattass, Deise de Andrade Costa, Liwen He, Martin Kuehne, Elvira Daraiva

    Leishmaniasis is a parasitic disease found in parts of the tropics, subtropics, and southern Europe. Leishmaniasis is caused by infection with Leishmania parasites, which are spread by
    the bite of phlebotomine sand flies. There are several different forms of leishmaniasis in people. The most common forms are cutaneous leishmaniasis, which causes skin sores, and visceral leishmaniasis, which affects several internal organs (usually spleen, liver, and bone marrow).

    In previous studies, we demonstrated the leishmanicide effect of coronaridine (COR), a natural indole alkaloid isolated from stem bark of Peschiera australis. In this study we show the leishmanicidal effect of Iboga congeners coronaridine and its 18-methoxylated analog, 18-methoxycoronaridine. Both alkaloids revealed a potent leishmanicide effect against Leishmania amazonensis, a causative agent of cutaneous and diffuse cutaneous leishmaniasis in the New World. Despite their potent leishmanicide effect, both alkaloids were neither toxic to murine macrophages nor did they modulate their oxidative or cytokine production responses.

    Leishmaniasis, a disease that affects 12 million people worldwide, presents broad clinical manifestations, ranging from a single localized ulcer to fatal hepatosplenomegaly, depending on the parasite species and the immunological status of the host. Recently, a dramatic increase in leishmaniasis cases was observed, specifically associated with human immunodeficiency virus infection. The drugs currently available for leishmaniasis treatment, pentavalent antimonials, amphotericin B, and pentamidine, present many severe side effects, are expensive, and are frequently ineffective. Furthermore, large-scale clinical antinomy resistance has been reported. All these problems, together with the lack of a safe and effective vaccine, emphasize the importance of the development of new drugs against leishmaniasis.





    Recently, we described the antiparasite effect of coronaridine (COR), isolated from the stem of the Peschiera australis shrub, against Leishmania amazonensis promastigotes and intracellular amastigotes. COR is an iboga-type indole alkaloid found in many species of the plant kingdom. Like others iboga alkaloids, COR was investigated for a wide variety of pharmacological effects, such as antitumor, anti-inflammatory, and bactericidal activities, as well as a stimulatory action on the central nervous system. COR has been studied for its potential antiaddictive properties, showing an effective decrease in morphine, cocaine, ethanol, and nicotine self-administration in laboratory animals analogous to that observed with ibogaine. Because of side effects such as tremor, cerebellar neurotoxicity, and bradycardia associated with ibogaine and COR, an 18-methoxylated COR analog was developed with the goal of reducing adverse effects. In preclinical studies, 18-methoxycoronaridine (18-MCOR) exerted few to none of the side effects associated with ibogaine or COR.

    In this work we describe the antileishmanial activities of the synthetic indole alkaloids COR and its analog, 18-MCOR, against amastigotes of Leishmania amazonensis. The leishmanicidal activities of the synthetic COR and its analog, 18-MCOR, which were similar to the antiparasite effect of the natural COR. The synthetic compounds, like the natural COR, did not induce nitric oxide production, nor did they stimulate the synthesis of interleukin 6 (IL-6), IL-12, and tumor necrosis factor alpha by drug-treated macrophages.

    Besides supporting the anti-leishmanial activity of COR, the results present a congener, 18-MCOR, which effectively kills intracellular amastigotes at when used at concentrations nontoxic to human and murine macrophages. Moreover, the use of ibogaine, a related COR and 18-MCOR compound, as antiaddictive therapy in humans is indicative that COR and 18-MCOR may be safely used for treating leishmaniasis. Other advantages of these compounds are their simple chemical structure and their already-described synthesis, which may facilitate not only their production but also the synthesis of derivatives with increased efficacy for treatment of leishmaniasis.

    *From the article here: https://pdfs.semanticscholar.org/a66...021.1536528169
    Last edited by mr peabody; 19-09-2018 at 12:00.
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    Bufotenine able to block rabies virus infection

    Rabies is a fatal disease that occurs in more than 150 countries, and kills more than 55,000 people every year. It is caused by an enveloped single stranded RNA virus that affects
    the central nervous system, through an infection initiated by the muscular nicotinic acetylcholine receptor, according to many authors. Alkaloids, such as acetylcholine, are widespread molecules in nature. They are present in numerous biological fluids, including the skin secretion of many amphibians, in which they act (together with proteins, peptides and steroids) as protection agents against predators and/or microorganisms. In the present work we describe the effects of bufotenine, which can inhibit the penetration of rabies virus in mammalian cells through an apparent competitive mechanism by the nicotinic acetylcholine receptor.

    Bufotenine is an alkaloid derived from serotonin, structurally similar to LSD and psilocin. This molecule is able to inhibit the rabies virus infection in in vitro and in vivo models, increasing the survival rate of infected animals. Being a very promising molecule for an incurable disease and because of the fact that there is no consensus regarding its neurological effects, this study aimed to evaluate chronic treatment of bufotenine on behavior, pathophysiology, and pharmacokinetics of mice. Animals were daily treated for 21 consecutive days with 0.63, 1.05, and 2.1 mg/animal/day bufotenine and evaluated by open field test and physiological parameters during all the experiment. After this period, organs were collected for histopathological and biodistribution analysis. Animals treated with bufotenine had mild behavioral alterations compared to the control group, being dose-response relationship. On the other hand, animals showed normal physiological functions and no histological alterations in the organs. With high doses, an inflammatory reaction was observed in the site of injection, but with no cellular damage. The alkaloid could be found in the heart and kidney with all doses and in the lungs and brain with higher doses. These results show that the effective dose, 0.63 mg/day, is safe to be administered in mice, since it did not cause significant effects on the animals’ physiology and on the CNS. Higher doses were well tolerated, causing only mild behavioral effects. Thus, bufotenine might be a drug prototype for rabies treatment, an incurable disease.

    From the articles here:
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203886/
    https://www.hindawi.com/journals/bmri/2018/1032638/
    Last edited by mr peabody; 17-09-2018 at 06:02.
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    Understanding Dermaseptin, Kambo’s antiviral peptide that may treat Herpes


    Kambo, the venom of the giant leaf frog 'Phyllomedusa bicolor,' is excreted through its skin. Long used by indigenous tribes for traditional rituals, kambo is administered by applying it onto freshly inflicted burn wounds. Kambo is said to generate an altered state of reality, clear inner sight and a resurgence of long forgotten memories.

    Having suffered personally from oral herpes, finding alternative treatments for this challenging ailment is particularly important to me. For the past ten years, I have experienced the physical pain of outbreaks, the social stigma surrounding the virus, and the concern of passing it on to those I love, especially my children. Luckily, I have a relatively minor strain of the virus and my outbreaks have become more infrequent and manageable. But for those with more aggressive strains, it is paramount to find a cure, efficient suppression system, or vaccine for herpes. Unfortunately, more strains of the virus are becoming resistant to the traditional treatment with Acyclovir and little headway has been made with alternative treatment options. But there is one very promising treatment that comes from an unlikely place: the venom of frogs in the Amazon rain forest.

    Kambo, the medicine made from this venom, contains the peptide Dermaseptin, which has been isolated as a potentially effective antiviral that works against both Herpes Simplex 1 and 2. At the moment, the mechanics of this peptide are still vague, but there are several ways that kambo—or the isolated peptide—may be able to mitigate the effects of herpes and prevent future outbreaks.

    Kambo as a preventative vaccine

    Indigenous tribes traditionally use kambo regularly as a preventative measure throughout pregnancy, childhood, and adult life. This contrasts with how it is currently used in Western society, which usually involves a single treatment or a short series of treatments rather than continual ceremonies. But the continual, preventative approach of indigenous tribes may hold some secrets as to why kambo can reduce the spread of the herpes infection.

    Studies have shown that dermaseptin is most effective against free-herpes viruses as opposed to once the virus has already bonded to nerves. Although it may be able to reduce the amount of herpes once it has attached to a host cell, it works best by preventing the bonding altogether in people who have not already contracted the disease and allowing the virus to be washed out of your system. However, it is unclear how long dermaseptin remains active in the human body after it is administered, which may be why kambo requires multiple, continuous treatments to remain effective.

    And while dermaseptin has been isolated as the most important peptide in kambo when it comes to treating herpes, researchers are still working to understand how much kambo’s other bioavailable peptides could increase the efficiency of dermaseptin by potentially infiltrating target nerves or attacking more mature herpes viruses. As scientists continue exploring how dermaseptin works in conjunction with kambo’s other peptides, they may be able to isolate a combination of peptides that provides a permanent, effective vaccine against herpes.

    Reducing Herpes outbreaks and the spread of Herpes

    Although dermaseptin was shown to be most effective in the early stages of infection, it was still somewhat effective after the virus had attached to nerves. While dermaseptin may not be able to completely eradicate an already established infection, it could potentially prevent the virus from actively reproducing and spreading. This means that, along with preventative treatments, kambo may provide some relief to those currently suffering from herpes, possibly by reducing the number or severity of outbreaks or curbing an outbreak if you catch it early enough.

    If you’re hoping to use kambo to treat a herpes infection, always do so under the guidance of a trained professional. When looking for such a practitioner, it is a good idea to find someone with specific experience treating herpes. They will be more knowledgeable about dose amounts, frequency of application, and location of application—all of which can influence the treatment’s effectiveness. You may also look for a practitioner who utilizes meridian-specific placement, which uses the natural energy flow of the body—based on nerves, muscles, and blood flow—to encourage the kambo to reach specific problem areas. Practitioners with meridian training will likely know the best placement points for kambo to reach the nerves that host herpes in your body.

    Eliminating herpes after exposure

    One of the greatest potentials for kambo as a treatment option against herpes is protecting those who have recently been exposed to the virus. Because it is unclear how long dermaseptin remains active in your body, taking kambo immediately after exposure to herpes may be more effective than using it continuously as a vaccine. However, for this to work, a kambo treatment would need to be pursued before the virus was able to attach to your nerves—within hours or days of exposure. If you think you have been exposed to herpes recently but have not yet experienced an outbreak, you should talk to a kambo practitioner about the possibility of an emergency kambo session. This approach would be best if you had already undergone an initial treatment with kambo and prepared for the experience. After all, kambo can be a somewhat challenging experience physically and can require significant mental preparation before your first ceremony. After you have participated in a ceremony with a trusted practitioner, you will know what to expect and be able to arrange an emergency anti-herpes treatment more quickly.

    Living with herpes is annoying at best and, at its worst, it is painful and isolating. A cure for herpes could help keep the virus under control and prevent future generations from suffering the recurring, endless herpes outbreaks that many in our current generation deal with. Researchers are only beginning to understand how the bio-available peptides in kambo work together to prevent and cure various diseases. While research may eventually lead to a more effective vaccine or treatment that can specifically target herpes, it is a good idea to be aware that traditional kambo treatments may still be able to offer more immediate relief in a variety of forms. To learn more about kambo treatments for herpes, you should talk with a trained kambo professional. And for those located in the San Francisco Bay Area, the staff at Psychedelic Times can help put you in contact with a skilled kambo practitioner.

    https://psychedelictimes.com/traditi...-treat-herpes/
    Last edited by mr peabody; 16-09-2018 at 07:00.
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    Leishmaniasis/HIV co-infection

    As reported above, the Iboga alkaloid congener 18-MC inhibits HIV-1 and may be uniquely useful for treating patients co-infected with Leishmaniasis and HIV.

    A major threat to the control of visceral leishmaniasis (VL) is its interaction with HIV infection. VL has emerged as an important opportunistic infection associated with HIV. In areas endemic for VL, many people have asymptomatic infection. A concomitant HIV infection increases the risk of developing active visceral leishmaniasis by 100 to 2320 times. In southern Europe, up to 70% of cases of visceral leishmaniasis in adults are associated with HIV infection.

    VL/HIV co-infection has important clinical, diagnostic and epidemiological implications. The two diseases are mutually reinforcing: HIV-infected people are particularly vulnerable to VL, while VL accelerates HIV replication and progression to AIDS. The risk of treatment failure for VL is high, regardless of the drug used, and all co-infected patients will relapse – and eventually die – unless they are given anti-retroviral therapy. Indirect methods of diagnosis such as serological tests for VL frequently fail; direct methods such as aspirations (bone marrow, lymph node or splenic) are reliable but are invasive, require skilled microscopy, and have less value in treated and relapsing patients. Further, co-infected patients can serve as human reservoirs, harboring numerous parasites in their blood and becoming a source of infection for the insect vector.

    To date, as many as 35 countries throughout the world have reported cases of VL/HIV co-infection, although most of the published literature concerns the countries of southern Europe. Under-reporting in most endemic areas is due to a lack of facilities to diagnose one or both of the diseases and to poor reporting systems. The fact that VL is not included in the CDC list of opportunistic infections further undermines reporting. In a particularly ominous trend, the spread of HIV infection is bringing the severe visceral form of leishmaniasis to new geographical areas and changing the epidemiology of the disease in dangerous ways.

    Leishmaniasis-HIV co-infected people have a significantly higher chance of developing the full-blown clinical disease, and significantly higher relapse and mortality rates.

    Where leishmaniasis occurs in urban areas, conditions often favour explosive epidemics, thus transforming the disease from a sporadic to an epidemic threat. In persons infected with HIV, leishmaniasis accelerates the onset of AIDS by cumulative immunosuppression and by stimulating replication of the virus. The epidemiological significance of asymptomatic carriers of the parasite has also been amplified by the advent of HIV, as co-infection rapidly activates infection to disease in asymptomatic parasite carriers. Sharing of needles by intravenous drug users contributes to the spread of leishmaniasis in Europe, as well as that of HIV.

    In 1991, WHO established a global surveillance network of 28 institutions, named Leishnet, to document the extent of the problem of co-infection and monitor trends. Initially, the
    sites involved in the network were predominantly European, reflecting the epidemiological situation at the time. A standardized case report form was developed to collect information on demographic, clinical and diagnostic features of the disease. In recent years, the network has expanded to all endemic areas and now includes institutions from Africa, South America and Asia. The network aims not only to monitor epidemiological trends but also to develop guidelines for disease management.

    The number of reported co-infection cases increased rapidly during the 1990s with the spread of the HIV pandemic, increased awareness among reporting institutions, and the
    growing geographical overlap between the two diseases. By 2001, a total of 1911 co-infection cases had been reported, with more than 50% (1099) coming from Spain. Analysis using geographical information systems (GIS) showed that most cases were in coastal urban areas with high population densities. The spatial pattern suggested a progressive ruralization of co-infection cases, as HIV infection spread into rural areas and VL became increasingly periurban. The number of reported cases in southern Europe peaked between January 1996 and June 1998, then decreased steadily until 2001, remaining stable at a low level thereafter. The decrease is attributed to the routine use of ART since 1997.





    In Ethiopia, 535 cases (>90 percent) were reported by the Medecins sans Frontieres VL treatment centre in Kafta Humera district, in the northwestern region of Tigray. They correspond to all co-infection cases treated between 2003 and 2008. In this highly endemic area for VL, the rate of HIV co-infection among VL patients is 15–30%. The position of the area near the Eritrean and Sudanese borders, and its high agricultural activity, attract a high influx of seasonal male migrant workers each year and make it an important transit point for cross-border trade and traffic. The increase in the male population also attracts a high annual influx of commercial sex workers, which probably contributes to the increasing rates of HIV transmission. As in Europe, most of the co-infection cases reported in Africa were in men (94.8 percent).

    http://www.who.int/leishmaniasis/burden/hiv_coinfection/burden_hiv_coinfection/en/
    Last edited by mr peabody; 19-09-2018 at 12:03.
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