No corium in Fukushima Unit 1 reactor vessel.

The muon scan of the Unit 1 reactor vessel at Fukushima has been completed. No nuclear fuel was fuel in it. No surprise.

According to this article at Simply Info,

TEPCO published the results of the muon scan done by IRID and their cooperating partners. No fuel was found in the reactor vessel of unit 1 Fukushima Daiichi… This was as expected by many (including us) who have been documenting the other evidence that indicated this was the likely case… Also noted on these images was the lack of detectable solid vessel in the bottom head area. The center lower section of the reactor vessel appears to be missing. The uniform dark outline of the reactor vessel is noticeably missing…

The corium has burned through the vessel and has melted through to the basemat and drywell floor. The question is whether it burned through that too, into the soil underneath. I would say this is very likely.

From this long Sandia pdf,

The drywell floor is subdivided into three regions (i.e., cavities) for the purposes of modeling molten-core/concrete interactions (see Figure 20). The first region, which receives core debris exiting the reactor vessel, corresponds to the reactor pedestal floor and sump areas (CAV 0).

Debris that accumulates in CAV 0 can flow out through a doorway in the pedestal wall to a second region representing a 90 degree sector of the drywell floor (CAV 1). If debris accumulates in this region to a sufficient depth, it can spread further around the annular drywell floor into the third region (CAV 2). This discrete representation of debris spreading is illustrated in Figure 20. (p. 64)

It was already assumed that the molten fuel had interacted with the concrete:

The three accidents (i.e., the accidents in Units 1, 2, and 3), while similar in many ways in terms of SBO accident progression, each proceeded to different degrees of core damage, with Unit 1 believed to be the most severely damaged of the three. It is believed that the Unit 1 core damage proceeded to the point of lower vessel head failure that released core materials to the containment cavity where core-concrete interactions likely initiated. Units 2 and 3 are believed to be less damaged. Collectively, the accidents likely reflect varying degrees of core/reactor damage and are therefore an invaluable source of information that can validate/confirm our current understanding of severe reactor accidents and provide new understanding not currently realized in our body of knowledge. (p. 18)

I was already talking about the corium-concrete reaction when I was still posting at the Japan Earthquake scribble. This must have been in early 2011. The corium-concrete reaction liberates all sorts of radionuclides that wouldn’t have been released otherwise, and the concrete particles help spread the radioactive particles into the wind.

Note high levels of Ba-140 and La-140 on March 15-16. Lanthanum-140 is the daughter product of Barium-140… If a TMI-style meltdown occurred, using Dr. Saji’s inventory figures (below), there would have been a 23:1 ratio of I-131 to Te-129m released. The Takasaki figures indicate a 1:2 ratio. The data do not support this scenario…

“This study describes the increase in iodine activity released to the atmosphere during a severe accident due to the radioactive decay of tellurium precursors… here it is seen that the iodine activity in the atmosphere is due disproportionately to I-132. Unlike the longer-lived isotopes, most I-132 (half-life of 2.30 hr.) existing early in the accident will decay before the significant atmospheric releases which follow reactor vessel failure. However, the supply is replenished by the decay of Te-132, which is released in large quantities from the drywell rubble.”

Takasaki is almost 100 miles from the Fukushima plant. Thus most of the I-132 which was released would be decayed. The large amounts of I-132 detected must have come from the decay of Te-132.

From p. 533, “Upon contact, the molten core material (the so-called “corium”) starts to react with the material of the basemat concrete… when the reaction zone is flooded with sump water… the highest temperatures might be reached… the molten-core – concrete interaction is the principal source of the release of the low-volatility fission products to the containment. The volatilization of these elements, such as barium, strontium, lanthanum, and cerium, is strongly supported by the gas bubbles which penetrate through the molten zone.”

Note again the high concentrations of barium and lanthanum, and that of tellurium.

Conclusion: The emissions observed at Takasaki were not due to a TMI-style accident, but one in which corium interacted with concrete and water. This released significant concentrations of barium, lanthanum, and strontium into the atmosphere.

Well, it’s about time they did this scan. It’s only been 4 years.

FUKU+4 HEALTH NOTE: Really nasty hand-foot-mouth rash on my hands and feet. This is from a disseminated enterovirus infection, from a virus I caught almost a year ago. I don’t know what strain or type of enterovirus it is. It has infected the neurons in the brain and spinal cord (thus it is myalgic encephalomyelitis). Minor improvement today… I did a technical thing, added a Mid-p feature to my Fisher’s exact test program for large samples. It is good to know that I can do math and scientific programming again. Things are still dire, though.

Fuku+4. Cancer rates start taking off.

The 4-year anniversary of the catastrophe at the Fukushima Daiichi is upon us. Radioactive emissions into the air and the Pacific Ocean continue, as they apparently will for centuries or millenia.

Radioactive contamination of air, water, and food is causing and will continue to cause cancer, heart disease, and all immune-related disease, including neurological disease, indefinitely.

But there is a latency period, or time lag, between initial radiation exposure and the development of these diseases. This document, issued by the World Trade Center Health Program, officially determines the minimum latency of types of cancers subsequent to the 9/11 disaster in 2001. This determination was stipulated by Congress after the passage of the James Zadroga 9/11 Health and Compensation Act of 2010.

The assessment of minimum latency periods for various types or categories of cancer is straightforward when exposures occur at a single point in time or regularly. However, most human exposures to carcinogens vary significantly over time, making a precise determination of minimum latency periods difficult… Therefore, the Administrator derived minimum latency estimates using several methods based on the best available scientific evidence for each type or category of cancer considered…

4B: Estimates of cancer latency obtained from statistical models used to estimate the lifetime risk of low-level ionizing radiation-related cancers.

The use of a radiation-induced cancer latency estimate is supported by scientific literature indicating shared mechanisms of carcinogenesis that apply to most solid tumors. Furthermore, cancers that may develop as a result of radiation exposure are indistinguishable from those that occur as a result of exposure to other carcinogens.

If multiple estimates of minimum latency based on statistical modeling in epidemiologic studies were available in the scientific literature, the Administrator’s policy is to resolve any uncertainties inherent in this method [Latency Method 4] in favor of the WTC Health Program member by selecting the shortest latency period…

For solid cancers as a group, an estimate of minimum latency of 4 years is available from statistical modeling of risk between exposure to low-level ionizing radiation and solid cancers [Latency Method 4B].

So cancer latency associated with 9/11 dust is the same as cancer latency associated with Fukushima radiation.

The Administrator has selected minimum latencies for the following five types or categories of cancer:

(1) Mesothelioma — 11 years;
(2) All solid cancers (other than mesothelioma, lymphoproliferative, thyroid, and childhood cancers) — 4 years;
(3) Lymphoproliferative and hematopoietic cancers (including all types of leukemia and lymphoma) — 0.4 years (146 days);
(4) Thyroid cancer — 2.5 years; and
(5) Childhood cancers (other than lymphoproliferative and hematopoietic cancers) — 1 year.

So leukemia and lymphoma started developing in some people a few months after 3/11/11. I’m thinking here of Kevin Blanch, who developed AML leukemia in this time frame… though there are many others.

All other childhood cancers (20 years old or less) started developing in March 2012.

Thyroid cancer in adults started developing in September 2013.

All solid cancers in adults start developing NOW.

Solid cancers are all cancers involving solid tumors like breast cancer, colon cancer, lung cancer, liver cancer, etc.

There is nothing hard and fast about this. Some people have developed cancer already, before this minimum latency period. But this is an official number that was developed as a result of a trade-off. These minimum latencies are in stark contrast to latencies of 5, 10, 20 years that are used in medical literature, and skew results to the pro-nuclear side.

But the Fuku+4 point is significant, not just for minimum latencies, but for the point when certain cancer rates start accelerating. Thyroid cancer in Chernobyl children started taking off at the Chernobyl+4 point.

Sickness in general, among Chernobyl liquidators and their children, also significantly rose at the Chernobyl+4 point. This is very simple, the subject is either sick (from anything), or not. The rise in the sickness rates of the children show that this phenomenon was not due to aging.

My research on myalgic encephalomyelitis.

I wanted to get this out there now. Big changes are coming… I have gotten much sicker after the cold weather started, and getting another virus infection. I am moving out of my home soon, and I don’t know how this is possible without significant muscle exertion, which will makes the disease much worse. So massive uncertainty clouds my immediate future.

I still think I will get better after the weather warms up, but right now there is more snow and severe cold in the forecast, and I don’t know when this will happen.

Most of the links are from Facebook. I apologize to those who cannot access it. There is a way to synchronize Facebook posts to this blog, but I am too sick to do it now.

Type I interferons and interferon-gamma in ME. (FB link)

Immunosuppression causes persistence of enteroviral infections in ME, is the foundation of exertion intolerance, and can be reversed by Type I interferon blockers. (FB link)

Enterovirus infections of the central nervous system. (FB link)

Enterovirus infection of the gastrocnemius muscle, IDO, and peroxynitrite. (FB link)

Serotonin, IDO, and reduced tryptophan catabolism in ME. (FB link)

Picolinic acid deficiency in ME and the kynurenine pathway. (FB link)

TGF-beta is released from muscles 24 hours after exercise, and reduces levels of interferon-gamma. (FB link)

TGF-beta reduces NK cell cytolytic activity and MHC I and II expression. (FB link)

Kynurenine as a possible treatment for ME. (FB link)

Dysregulation of the STAT-1 protein in ME. (FB link)

Activin in ME, generated from muscle activity. (FB link)

Caffeine inhibits tryptophan hydroxylase, which is upgraded after exercise. (FB link)

Swimming exercise increases serotonin levels, and decreases corticosterone, interferon-gamma, TNF-alpha, and IDO levels. (FB link)

The TGF-beta autocrine loop in ME. (FB link)

Psychedelics and the desensitization of the 5-HT2A receptor. (FB link)

Exercise-induced reduction of interferon-gamma levels is the cause of post-exertional immune exhaustion in ME. (FB link)

GABA-B positive allosteric modulators are an effective treatment for ME, but are not yet approved by the FDA. (FB link)

List of TGF-beta inhibitors. I have determined that only those medications that use the Smad pathway are effective for ME. (link)

Brief moderate stretching is effective for reducing post-exertional symptoms after exercise. (FB link)

Moderate acute exercise increases TGF-beta, alpha-amylase, and IgA 24 hours after exercise. (FB link)

Noise increases tryptophan hydroxylase levels, which is a factor in noise hypersensitivity in ME. (FB link)

Brown fat, a key player in ME. (FB link)

Follistatin increases muscle mass after exercise, reduces TGF-beta levels via the Smad pathway, and is a myostatin inhibitor. The muscle repair process recruits interferon-gamma from tissues, and is the cause of exertion intolerance. (FB link)

Interferon-gamma deficiency in “chronic fatigue syndrome” – 1990, after the name change from ME. (FB link)

Ionizing radiation exposure is part of the ME disease process, by its generation of peroxynitrite (ONOO-) via radiolysis. (FB link)

Destruction of groups 1 and 3 innate lymphoid cells and the resultant distortion of commensal bacteria is a fundamental aspect of the ME disease process. (FB link)

Psilocybin reduces the activity of the default mode network. The inability to deactivate the DMN is behind the overwhelming neurological and cognitive symptoms in severe ME. (FB link)

Actimmune (interferon-gamma) is an effective treatment for ME. It does not reduce Type I interferon levels, though, which is necessary for a cure. (FB link)

Psilocybin reduces DMN activity by activating the 5-HT2A receptors. The receptors are typically desensitized in ME due to excessive serotonin production. (FB link)

A high-fat diet restores interleukin-22, and also restores the balance of microbiota in the gut. (FB link)

Limbic kindling vs. central sensitization in ME. My response to Leonard Jason’s research. (link)

Ketogenic diet for M.E.: Can it really be this simple? (link)

How ME and radiation sickness has altered my mechanism of thinking. (link)

Origin of M.E. disease process in the immune system. I have found since this, that an enteroviral infection of certain immunoprivileged areas of the brain does the same thing. Any viral, radiotoxic, or other toxic infestation of these brain areas will cause this. It is now known that the upgrade of Type I interferons is behind the dysregulation of the JAK/STAT pathway. (link)