29 August 2011

Mumps Frequencies Version 1.1

Photograph showing child with mumps
See Mayo Clinic article on mumps

Some time ago a child my spouse was caring for came down with a runny nose which the following day became flu like symptoms with a fever. My wife had a pronounced swelling of the parotid gland. Frequencies were looking like a flue frequency set (see previous message below). She thought her lymph glands were swollen, but plate zapping lymph nodes with the frequencies detected did not do much.

A physician friend examined her and thought the swelling was lower on her jaw than the parotid gland. Since she was not noticably ill and mumps can be serious in an adult who was never vaccinated or had mumps, he discounted it. However, when I began treating her, the swelling was definitely above the jaw bone in the location of the parotid gland.

Since I happen to have a homeopathic Mumps nosode, I checked and she tested positive. Within a day or two the Mumps nosode along with some Oscillicosinum and frequency treatment kept her well and eliminated the swelling.

She, of course, infected me with the disease and over the course of a few days, I was able to identify the frequency set. I was never really ill because I detected the frequencies as soon as minor symptoms appeared.

More recently my spouse came back from the orthodontist with a swollen left jaw. After a few days she said it feels like mumps. Sure enough it was. Mumps is very infectious and I had to run frequencies for the whole family.

An upgraded frequency set for mumps is posted on the subscribers list.


27 August 2011

Malaria: Evolutionary Biology

Malaria life cycle illustration.
National Institute of Allergy and Infectious Diseases

The malaria parasite is easily killed by electromagnetic frequencies and there are a number of small pilot projects using zappers in Africa. I've talked with some of the larger nonprofits about expanding these studies as I have seen 100% remission consistently with a few hours of application of exact frequencies. However, the response has been that if a non-profit research institute looked at anything other than conventional drugs they would get all their grants terminated.

It is important to keep up with the latest research on malaria as frequencies can also modify protein production. Virulent forms of this and other diseases (particular viral infections) can kill by evoking an overwhelming immune response. Thus frequencies must modulate immune response through reducing certain protein production as well as kill the pathogen. Those who are intelligent enough to use this technology can at least protect themselves.

Work on malaria frequencies at the recent Frequency Foundation workshop in San Diego has identified several new strains of the malaria parasite. These are available to subscribers as Malaria 2.0 frequencies.


Evolution of virulence in malaria
Bridget Penman email and Sunetra Gupta email
Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK
Journal of Biology 2008, 7:22doi:10.1186/jbiol83

The electronic version of this article is the complete one and can be found online at: http://jbiol.com/content/7/6/22
Published: 28 August 2008 © 2008 BioMed Central Ltd

Abstract
The pathogenesis of severe malarial disease is not yet fully understood. It is clear that host immunopathology plays a central role, and a recent paper in BMC Evolutionary Biology suggests that the ability of the parasite to stimulate interleukin-10 production is a major factor and speculates on its impact on the coevolution of host and parasite.

Minireview
Plasmodium falciparum malaria is responsible for over 1 million deaths each year, mostly in children under the age of 5 living in sub-Saharan Africa. And yet the number of malaria infections which go on to become life threatening is proportionally very small, as the majority of these infections either remain asymptomatic (due to the acquisition of clinical but non-sterile immunity after repeated exposure) or progress to disease without lethal complications [1]. Viewed in an evolutionary context, the existence of severe disease presents a population-level compromise for the parasite between the necessity of bearing factors that increase survival and transmission and the risk that these will stimulate a host immune response that will either curtail the infection or perversely cause the death of the host (thus also spelling the end for the parasite). With the aim of identifying factors that may be relevant in the evolution of this balance, Long et al. in a recent article in BMC Evolutionary Biology [2] have investigated the influence of the inflammatory response on the severity of disease in a rodent model of malaria, and we discuss here how their results may bear on the coevolution of parasite and host, in the context of what is known about the determinants of severe malarial disease in humans.
Factors in the severity of malaria

Severe malaria can be resolved broadly into two different syndromes: cerebral malaria and severe malarial anemia. Cerebral malaria is associated with impaired consciousness and sometimes convulsions and coma, and can leave those who recover with long-term neurological problems. Its pathophysiology is not fully understood but it is probably due to a combination of the obstruction of cerebral capillaries by parasitized cells and an overactive inflammatory response. Severe malarial anemia occurs when the suppression of erythrocyte production, combined with the destruction of red blood cells by the parasite itself, leads to a particularly profound anemia – which can cause shock and respiratory distress. Both syndromes can involve a range of metabolic complications such as acidosis or hypoglycemia [3].

Both host and parasite factors are likely to contribute to the processes leading to severe disease, and Long et al. have examined one possible interaction using mice infected with different clones of the rodent malaria parasite Plasmodium chabaudi chabaudi. Specifically, they have shown that blockade of the receptor for the anti-inflammatory cytokine interleukin-10 (IL-10) has a dramatic impact on time to death of the infected animal, particularly where the infecting parasite clones are normally avirulent. This result certainly implies that IL-10 plays a fundamental role in controlling the inflammatory response to malaria and that its absence can contribute to the demise of the murine host; Long et al. propose that the ability of the parasite to stimulate IL-10 production is a factor determining its relative virulence. However, whether regulation of the inflammatory response by IL-10 actually plays a part in the evolution of parasite virulence remains an open question and requires a careful consideration of the population-level consequences of interactions between host susceptibility and parasite virulence factors.

18 August 2011

Fukushima Radioactive Fallout Frequencies Posted


Fukushima radioactive fallout nears Chernobyl levels

Japan's damaged nuclear plant in Fukushima has been emitting radioactive iodine and caesium at levels approaching those seen in the aftermath of theChernobyl accident in 1986. Austrian researchers have used a worldwide network of radiation detectors – designed to spot clandestine nuclear bomb tests – to show that iodine-131 is being released at daily levels 73 per cent of those seen after the 1986 disaster. The daily amount of caesium-137 released from Fukushima Daiichi is around 60 per cent of the amount released from Chernobyl.
The difference between this accident and Chernobyl, they say, is that at Chernobyl a huge fire released large amounts of many radioactive materials, including fuel particles, in smoke. At Fukushima Daiichi, only the volatile elements, such as iodine and caesium, are bubbling off the damaged fuel. But these substances could nevertheless pose a significant health risk outside the plant.
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Those individuals with a Hadoscan periodically see a radioactive complex in their system that includes uranium, copper, lead, DDT, hexochlorophenol, and castoreum. This causes both internal symptomology and external skin itching and lesions. The most common frequencies for this are posted on the subscribers blog.


17 August 2011

Glutamine Prime: Turbocharge your immune system

4Life Glutamine prime is a new product that will enhance your immune system. Check it out ...

Naegleria fowleri
From Wikipedia, the free encyclopedia

N. fowleri can invade and attack the human nervous system. Although this occurs rarely, such an infection nearly always results in the death of the victim. Naegleria fowleri/nəˈɡlɪəriə/; also known as "the brain-eating amoeba") is a free-living excavate form of protist typically found in warm bodies of fresh water, such as ponds, lakes, rivers, and hot springs. It is also found in soil, near warm water discharges of industrial plants, and minimally chlorinated swimming pools (there is no evidence of this organism living in ocean water) in an amoeboid or temporary flagellate stage. It belongs to a group called the Percolozoa or Heterolobosea. Although not a true amoeba, the organism is often referred to as an amoeba for convenience.


Brain Eating Bug in Lakes Kills Swimmers
See kensavage.com

Naegleria Fowleri living in warm lakes this summer enters the body through the nose and attacks the brain where it feeds on your brain until you die.
Even though encounters with the microscopic bug are extraordinarily rare, it has killed six boys and young men this year. The spike in cases has health officials concerned, and they are predicting more cases in the future.
“This is definitely something we need to track,” said Michael Beach, a specialist in recreational waterborne illnesses for the Centers for Disease Control and Prevention.
“This is a heat-loving amoeba. As water temperatures go up, it does better,” Beach said. “In future decades, as temperatures rise, we’d expect to see more cases.”
According to the CDC, the amoeba called Naegleria fowleri killed 23 people in the United States from 1995 to 2004. This year health officials noticed a spike with six cases – three in Florida, two in Texas, and one in Arizona. The CDC knows of only several hundred cases worldwide since its discovery in Australia in the 1960s.
In Arizona, David Evans said nobody knew his son, Aaron, was infected with the amoeba until after the 14-year-old died on Sept. 17. At first, the teen seemed to be suffering from nothing more than a headache.
“We didn’t know,” Evans said. “And here I am: I come home and I’m burying him.”
After doing more tests, doctors said Aaron probably picked up the amoeba a week before while swimming in the balmy shallows of Lake Havasu, a popular man-made lake on the Colorado River between Arizona and California.

This organism is part of the swine flu parasite set and frequencies are posted on the subscribers blog.

10 August 2011

New Innovation in Frequency Therapy



Sick Indonesians turn to 'railway therapy'

Updated August 04, 2011 06:20:45
Despite warnings from health authorities, some ailing Indonesians are stretching out on railway lines in the belief the tracks give off electrical currents that cure everything from diabetes to high blood pressure.

06 August 2011

Weather Modification Details: HAARP and Chemtrails


Cover

Telomeres and Aging
GERALDINE AUBERT AND PETER M. LANSDORP
Terry Fox Laboratory, British Columbia Cancer Agency, and Division of Hematology, Department of
Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Aubert G, Lansdorp PM. Telomeres and Aging. Physiol Rev 88: 557–579, 2008;
Telomeres play a central role in cell fate and aging by adjusting the cellular response to stress and growth stimulation on the basis of previous cell divisions and DNA damage. At least a few hundred nucleotides of telomere repeats must “cap” each chromosome end to avoid activation of DNA repair pathways. Repair of critically short or “uncapped” telomeres by telomerase or recombination is limited in most somatic cells and apoptosis or cellular senescence is triggered when too many “uncapped” telomeres accumulate. The chance of the latter increases as the average telomere length decreases. The average telomere length is set and maintained in cells of the germline which typically express high levels of telomerase. In somatic cells, telomere length is very heterogeneous but typically declines with age, posing a barrier to tumor growth but also contributing to loss of cells with age. Loss of (stem) cells via telomere attrition provides strong selection for abnormal and malignant cells, a process facilitated by the genome instability and aneuploidy triggered by dysfunctional telomeres. The crucial role of telomeres in cell turnover and aging is highlighted by patients with 50% of normal telomerase levels resulting from a mutation in one of the telomerase genes. Short telomeres in such patients are implicated in a variety of disorders including dyskeratosis congenita, aplastic anemia, pulmonary fibrosis, and cancer. Here the role of telomeres and telomerase in human aging and aging associated diseases is reviewed.

02 August 2011

Longevity Futures: Reverse Aging


Cutting-Edge Natural Product TA-65 Turns On Longevity Gene

Leslie J. Farer
In the past, halting the aging process was the goal of longevity enthusiasts. Now, research shows that it is possible to not just stop, but to reverse some of the infirmities associated with growing older and rejuvenate age-damaged tissues. Ensuring the integrity of telomeres, small segments of repeating DNA at the ends of our chromosomes that decay with time, has the potential to greatly extend youthful vitality and vibrant health. A novel concentrated plant extract known as TA-65 acts at the genetic level to maintain the structure of DNA, restore cellular function, and possibly keep you years younger than your chronological age.

What are Telomeres?

Telomeres are strips of DNA located at the ends of chromosomes. They are composed of a few hundred or more repeats of the nucleotide sequence TTAGGG (1,2) (where T= thymine; A = adenine; G= guanine). They act as protective ‘caps’ preventing loss of DNA, and also guard against fusing, fraying and unraveling of chromosomes, (1,3,4) which can expose and damage the genetic material and cause mutations.
Since investigators in the 1930’s coined the term telomere (from the Greek telos for ‘end’ and meros for ‘part’), a massive amount of research has been undertaken to explore the structure and function of these important chromosomal caps. More than 8,000 scientific papers have been written and the 2009 Nobel Prize in physiology and medicine was awarded to three scientists for their work involving telomeres.

Hayflick’s Fifty Year-Old Observation

Back in the 1960’s, geneticist Leonard Hayflick observed dividing human cells and made an important discovery that had a substantial impact on the future of anti-aging research. But before we examine his finding, let’s look very briefly at cell division, or mitosis ─ a fundamental, genetically-controlled process that enables a cell to duplicate itself, including chromosomes (through the process of DNA replication), to form two identical ‘daughter’ cells. Cell division allows an organism to develop and differentiate into an adult from multiple progressive stages beginning with the initial union of reproductive cells (the germ cells, egg and sperm), and after growth and birth, to construct and repair tissues.
Hayflick reported that human cells cultured under perfect conditions in his lab divided only a finite number of times in a progressive course leading to replicative senescence, (5) when they stop dividing altogether and become dysfunctional (the term senescence is roughly equivalent to ‘aged.’). Once cells have reached their proliferation maximum, or so-called Hayflick limit, they stop functioning properly or die through the process of apoptosis. (1,6,7)
Why do cells stop dividing when they reach their Hayflick limits? Is there a cellular mechanism that monitors and counts each cell division up until the final one? And does Hayflick’s observation have any relevance to aging?
In the early 1970’s, Russian scientist Alexey Olovnikov began to answer some of these questions ─ he made the connection between a DNA replication problem involving telomeres and the limitation on cell division reported by Hayflick.