Non Malignant radiogenic disease 8 Cytokines.

http://www.eje-online.org/content/133/6/660.extract

“Cytokines and the endocrine system. I. The immunoendocrine network

Thomas Mandrup-Poulsen,
Jørn Nerup,
Jesper I Reimers,
Flemming Pociot,
Henrik U Andersen,
Allan Karlsen,
Ulla Bjerre and
Regine Bergholdt

Excerpt

The cytokines interleukin 1 (IL-1), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) are the main common denominators that elicit the acute phase response, a generalized host reaction caused by a variety of pathological processes, i.e. infection, inflammation, tissue injury, neoplastic diseases and physical and psychological stress. It is characterized by activation of the immune system and associated changes in neurological, metabolic and endocrine functions (1), irrespective of the diverse underlying pathological conditions. As the classical hormones, cytokines have both autocrine, paracrine and endocrine effects. However, in contrast to hormones, cytokines do not appear to have any homeostatic importance, but are almost exclusively induced and liberated in tissues and to the circulation in association with cellular injury. Further, cytokines exert their action at lower molar concentrations than most hormones (10−12 to 10−15 mol/l), and their actions are potentiated by several other cytokines. …” end quote.

http://physrev.physiology.org/content/79/1/1.long Regulation of the Hypothalamic-Pituitary-Adrenal Axis by Cytokines: Actions and Mechanisms of Action

ANDREW V. TURNBULL and
CATHERINE L. RIVIER

http://www.ncbi.nlm.nih.gov/pubmed/17032631

Int J Radiat Biol. 2006 Sep;82(9):686-97.
Effect of gamma radiation on cytokine expression and cytokine-receptor mediated STAT activation.
Han SK, Song JY, Yun YS, Yi SY.
Source

Laboratory of Radiation Immunology, Korea Institute of Radiological and Medical Sciences, Nowon-ku, Seoul.
Abstract
PURPOSE:

The expression of cytokine mRNA and their related transcription factors was examined in order to assess the effects of gamma radiation on the immune function of murine splenocytes.
MATERIALS AND METHODS:

Splenocytes were collected from seven-week-old female Balb/c mice, and then irradiated at a dose of 5 Gy of 60Co gamma-ray at a dose rate of 1.394 Gy/min. Total RNA was extracted from both irradiated and non-irradiated splenocytes at 1/2, 1, 3, 6, and 24 h and analysed by reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS:

The mRNA level of interferon (IFN)-gamma, which is a Th1-type (T helper cell type 1) cytokine, was reduced after 3 h post-irradiation, whereas the interleukin (IL)-2 mRNA in the naïve splenocytes had no significant changes within the 24 h after irradiation. Moreover, IFN-gamma and IL-2 mRNA expression in concanavalin A (Con A, 2.5 mug/ml) activated-splenocytes was significantly reduced by gamma irradiation. On the other hand, the mRNA level of the Th2 type (T helper cell type 2) cytokines, such as IL-4, IL-5 and IL-10, was increased both in naïve and activated splenocytes, and pro-inflammatory cytokines were also rapidly induced in response to irradiation in naïve splenocytes. Interestingly, gamma irradiation had no effect on transforming growth factor (TGF)-beta mRNA expression. Moreover, the mRNA levels of the leucine zipper trqnscription factor c-Maf and GATA binding protein-3 (GATA-3), which regulate IL-4 and IL-5 transcription, were found to have been up-regulated. However, the mRNA coding for interferon regulatory factor (IRF)-1, which is involved in IFN-gamma production, was reduced 6 h post-irradiation. The level of signal transducers and activators of transcription (Stat)-1 and Stat-4 phosphorylation, which are activated by IFN-gamma and IL-12, respectively, was significantly reduced by gamma irradiation, but IL-4 receptor mediated Stat-6 activation remained unchanged.
CONCLUSIONS:

These results suggest that gamma irradiation may play a role in Th1 and Th2 cytokine expression, via regulation of the level of cytokine-mediators through transcriptional modulation and Stat signaling. These results are helpful to understand general profile of cytokine expression in response to gamma irradiation. end quote.

http://www.ncbi.nlm.nih.gov/pubmed/17379094

Exp Hematol. 2007 Apr;35(4 Suppl 1):96-104.
Radiation-induced alterations in cytokine production by skin cells.
Müller K, Meineke V.
Source

Bundeswehr Institute of Radiobiology, Munich, Germany.
Abstract

Ionizing radiation exposure of skin results in a cutaneous radiation reaction comprising all pathophysiological reactions and clinical symptoms in irradiated skin. Biological responses of skin occur in a characteristic temporal pattern and mainly depend on radiation quality, dose rate, total dose, and cellular conditions. Immediately after irradiation, production of cytokines by skin cells is initiated and continues as a cascade during all stages of the cutaneous radiation syndrome leading to progressive late symptoms, the predominant of which is fibrosis. Cytokines are important signaling molecules mediating communicative interactions both locally between different cell types within dermal tissues and distantly between organs. Although during recent years much progress has been made in dissecting the complex cytokine network, the role of cytokines in the pathophysiology of the cutaneous radiation reaction is only beginning to be elucidated. Previous studies indicate that the major cytokines in the response of skin cells to ionizing radiation include IL (interleukin)-1, IL-6, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta, and the chemokines IL-8 and eotaxin. In this paper, existing data on the radiation-induced modulation of cytokine expression by skin cells are reviewed.

end quote

http://www.ncbi.nlm.nih.gov/pubmed/16166805

Neuroimmunomodulation. 2005;12(5):255-69.
Cytokine dysregulation, inflammation and well-being.
Elenkov IJ, Iezzoni DG, Daly A, Harris AG, Chrousos GP.
Source

Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, Washington, D.C., USA.
Abstract

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis, health, and well-being. Like the stress response, the inflammatory reaction is crucial for survival and is meant to be tailored to the stimulus and time. A full-fledged systemic inflammatory reaction results in stimulation of four major programs: the acute-phase reaction, the sickness syndrome, the pain program, and the stress response, mediated by the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Common human diseases such as atopy/allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro- versus anti-inflammatory and T helper (Th)1 versus Th2 cytokine balance. Recent evidence also indicates the involvement of pro-inflammatory cytokines in the pathogenesis of atherosclerosis and major depression, and conditions such as visceral-type obesity, metabolic syndrome and sleep disturbances. During inflammation, the activation of the stress system, through induction of a Th2 shift, protects the organism from systemic ‘overshooting’ with Th1/pro-inflammatory cytokines. Under certain conditions, however, stress hormones may actually facilitate inflammation through induction of interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha and C-reactive protein production and through activation of the corticotropin-releasing hormone/substance P-histamine axis. Thus, a dysfunctional neuroendocrine-immune interface associated with abnormalities of the ‘systemic anti-inflammatory feedback’ and/or ‘hyperactivity’ of the local pro-inflammatory factors may play a role in the pathogenesis of atopic/allergic and autoimmune diseases, obesity, depression, and atherosclerosis. These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health. These hypotheses require further investigation, but the answers should provide critical insights into mechanisms underlying a variety of common human immune-related diseases.

Copyright (c) 2005 S. Karger AG, Basel

PMID:
16166805
[PubMed – indexed for MEDLINE]

end quote.

http://www.ncbi.nlm.nih.gov/pubmed/14737921

Biol Res Nurs. 2004 Jan;5(3):203-10.
Levels of fatigue compared to levels of cytokines and hemoglobin during pelvic radiotherapy: a pilot study.
Ahlberg K, Ekman T, Gaston-Johansson F.
Source

Sahlgrenska Academy, Göteborg University, Faculty of Health Caring Sciences, Institute of Nursing, Department of Oncology, Gothenburg, Sweden. karin.ahlberg@vgregion.se
Abstract

Cancer-related fatigue (CRF) is a prevalent and distressing symptom experienced by patients during cancer therapy. One proposed mechanism for the development of fatigue is the increased secretion of proinflammatory cytokines and/or the development of anemia. The major purpose of this pilot study was to investigate the levels of fatigue and cytokines during radiation therapy and determine whether there was a correlation between the two. A secondary purpose was to explore the relationships among hemoglobin values, cytokines, and fatigue. Participants included 15 women diagnosed with uterine cancer, who received curative external radiation therapy. Fatigue was assessed by a self-report instrument (Multidimensional Fatigue Inventory [MFI-20]) and hemoglobin and cytokines (Il-1, Il-6, and TNF-alpha) were measured before, during, and after radiotherapy. The degree of fatigue increased during radiotherapy without a significant change in IL-1, IL-6, or TNF-alpha levels. There was no significant correlation between changes in general fatigue and the changes in IL-1 and TNF-alpha. There was a significant negative correlation between the change in IL-6 and general fatigue. The hemoglobin levels did decrease significantly during radiotherapy, but there was no significant correlation between general fatigue and hemoglobin after 3 weeks of therapy or after the completion of therapy. In conclusion, pelvic radiotherapy in women with uterine cancer is associated with increased fatigue. There were no significant relationships between anemia or cytokine levels and fatigue. The pathogenesis of fatigue during radiation therapy remains to be elucidated.

PMID:
14737921
[PubMed – indexed for MEDLINE]

http://clincancerres.aacrjournals.org/content/15/17/5534.full.pdf

2009;15:5534-5540. Published OnlineFirst August 25, 2009.
Clin Cancer Res

Julienne E. Bower, Patricia A. Ganz, May Lin Tao, et al.

Therapy for Breast and Prostate Cancer
Inflammatory Biomarkers and Fatigue during Radiation
Purpose:
Biomarkersofradiation-inducedbehavioralsymptoms,suchasfatigue,havenot
been identified. Studies linking inflammatory processes to fatigue in cancer survivors led
us to test the hypothesis that activation of the proinflammatory cytokine network is asso-
ciated withfatigue symptoms during radiation therapy for breast and prostate cancer.
Experimental Design:
Individuals withearly-stage breast (
n
= 28) and prostate cancer
(
n
= 20) completed questionnaires and provided blood samples for determination of
serum levels of interleukin 1
β
(IL-1
β
) and IL-6 at assessments conducted before, during,
and after a course of radiation therapy. Serum markers of proinflammatory cytokine
activity, including IL-1 receptor antagonist and C-reactive protein, were examined in
a subset of participants. Random coefficient models were used to evaluate the associ-
ation between changes in cytokine levels and fatigue.
Results:
As expected, there was a significant increase in fatigue during radiation treat-
ment.ChangesinserumlevelsofinflammatorymarkersC-reactiveproteinandIL-1recep-
tor antagonist were positively associated withincreases in fatigue symptoms (
P
s < 0.05),
although serum levels of IL-1
β
and IL-6 were not associated withfatigue. These effects
remained significant (
P
s < 0.05) in analyses controlling for potential biobehavioral con-
founding factors, including age, body mass index, hormone therapy, depression, and
sleep disturbance.
Conclusions:
Results suggest that activation of the proinflammatory cytokine network
and associated increases in downstream biomarkers of proinflammatory cytokine activ-
ity are associated withfatigue during radiation therapy for breast and prostate cancer.
(Clin Cancer Res 2009;15(17):5534

40) end quote, again, the most likely source of a similar study involving internally contaminated individuals who are healthy is in the miltary record, open or secret. The first act of the Manhattan Project in relation to the then rapid discovery of the fission products list was to contract Hamilton to inject the substance into animals. Fatigue in animals may be difficult to discerne. Hamilton used rodents and gold fish, others used beagles. The nuclear veterans and A bomb survivors were the human cohorts. Other than this people suffering serious disease
were the medical cohort.

http://www.cfids-cab.org/MESA/Pall.pdf

Post-radiation syndrome as a NO/ONOO

cycle,
chronic fatigue syndrome-like disease
Martin L. Pall
*
School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4234, USA
Received 9 May 2008; accepted 12 May 2008
Summary
Post-radiation syndrome is proposed to be chronic fatigue syndrome (CFS) or a chronic fatigue syndrome-
like illness, initiated by exposure to ionizing radiation. This view is supported by the nitric oxide/peroxynitrite (NO/
ONOO

) cycle mechanism, the putative etiologic mechanism for CFS and related illnesses. Ionizing radiation may
initiate illness by increasing nitric oxide levels via increased activity of the transcription factor NF-JB and consequent
increased synthesis of the inducible nitric oxide synthase. Two types of components of the nitric oxide/peroxynitrite
cycle have been studied in post-radiation syndrome patients and shown to be elevated. The symptoms and signs of
post-radiation syndrome and its chronicity are similar or identical to those of chronic fatigue syndrome and can be
explained as being a consequence of nitric oxide/peroxynitrite cycle etiology. While the data available to test this view
are limited, it provides for the first time a comprehensive explanation for post-radiation syndrome.
c
2008 Elsevier Ltd. All rights reserved

for study purposes : ” The complex chronic symptoms have
typically been found in persons both shortly after
exposure and continuing for years after such expo-
sure. Pastel
[7]
described the symptoms as includ-
ing ‘‘fatigue, sleep and mood disturbances,
impaired memory and concentration and muscle
and/or joint pain’’.
end quote.

There is little doubt in my mind that the condition as described is a strong warning to authorities that the confinement of symptomology due to acute radiation syndrome (radiation sickness) only is insufficient. Confining radiation fatique only to radiation administrated in medical treatments is like wise inadequate. For it is plain that right now many thousands of people in the former Soviet Republics suffer the condition.
The indications are that people in Japan are suffering the same syndrome as a result of the nuclear failure there.

Given the readiness in which the medical profession accepts the cytokine mediated radiation fatigue response as being a biochemical fact, it appears extremely cruel of world nuclear authorities, including its associated medicos (if you can call them that) to quickly pull out their copies of DSM IV and ascribe a mental condition to civilian victims of nuclear disaster, whereas in hospitals around the world treating doctors are thoroughly familiar with this aspect of the radiation response.

In relation to internal emitters, the cytokine response is a bio chemical response which may explain aspects of the physical signs and symptoms of radiation exposure listed in my old Army notes.

The Cytokine storm is explained by Wikipedia at http://en.wikipedia.org/wiki/Cytokine_storm “A cytokine storm, or hypercytokinemia is a potentially fatal immune reaction consisting of a positive feedback loop between cytokines and immune cells, with highly elevated levels of various cytokines.”

Below that, there is the chronic health problems seen in US Downwinders. The chronic conditions may escalate into fatal episodes, as described by Carole Gallagher at http://americangroundzero.blogspot.com.au/2011/01/commemorating-60th-anniversary-of-first.html

For this post of mine, the relevant bit of Carole’s post begins halfway down her page: “…About five years after that memorable trip to Salt Lake with PV#1, I made an appointment to photograph one of the subjects of the federal study conducted at the University of Utah of downwinders for thyroid disease, and met Della Truman from West Jordan, Utah, then a southern suburb of Salt Lake City. Years of “thyroid storms,” as her son, Jay, described them, had accelerated her metabolism to the point where her life was unbearable. The nodules on her thyroid had thus created chronic heart problems due to her chaotic metabolism, and other health difficulties…….” The piece ends at Della’s funeral.

I’ll leave it for the idiots at US DOE Low Dose to figure out what part of the bomb test fallout was beneficial to Della.

4 Responses to “Non Malignant radiogenic disease 8 Cytokines.”

  1. CaptD Says:

    It is sad that just the language makes it easy for the nuclear information to be hidden for people…
    Someone needs to write:
    A Dummies Guide To N☢T Getting Irradiated!

  2. nuclearhistory Says:

    ha ha Capt D. See, being a non-doktor, the industry will say I’m not qualified to write about such things, So all I can do is cite the medical literature. The endocrine system is a system which is intimately involved in the radiation response. And the cytokine releases include substances which are intimately linked to disease. Such as endocrine and metabolic disorders, and to heart and circulatory system disease.

    The Japanese authorities, rather than evacuate properly, are prepared to wear the health effects suffered by people. Protecting the nuclear industry by denying effects and condemning people who break through into the awareness of the media by accusing such people as being “weak minded”. Cytokine release is stated above by the qualified source as an organic cause of depression. Instead of throwing the DSMIV manual at the people, it is the nuclear industry gurus who pretend to have an informed consent they do not have, who should be examined for socio pathology in my opinion.

    Fukushima Diiachi is not a hospital. It is a broken nuclear power complex. From March 2011 on we have though, heard a stream of “medical” prognostications from nuclear industry. If there is not informed consent, there is no patient. If there is patient there is no medicine, just a breach of Nuremberg. As pointed out the Adivsory Committee for Human Radiation Experiments which advised the US President in 1994.

    If there is no medical need for an exposure, then its ain’t medicine.

    The Fukushima Diiachi disaster is not like a CT scan. As they claimed in March 2011 and claim still.
    There is no benefit from reactor disasters, and that has been repeatedly demonstrated.

  3. Bobby1 Says:

    The increase in pro-inflammatory cytokines due to radioactive exposure causes atherosclerosis, which is the #1 killer in industrialized countries.

    “One of the paradigm shifts in our understanding about atherosclerosis in the last decade is the development of the concept that it is potentially caused by a chronic inflammation. When considering the role of cytokines in inflammation related to atherosclerosis it is important to distinguish between local inflammation within the plaque microenvironment and systemic inflammation, as evident by acute-phase protein production and circulating proinflammatory mediators. Locally produced proinflammatory mediators with atherogenic activity include IFN-gamma, TNF-alpha, IL-1, IL-8, IL-12, IL-18, and monocyte chemotactic protein-1 (MCP-1). Systemic mediators and markers of inflammation include IL-6, IL-8, and CRP. Increased IL-6 is associated with elevated fibrinogen levels, which leads to an increased tendency to thrombosis, independent of the effects of IL-6.”

    http://instructional1.calstatela.edu/eporter/BIOL520/Literature/Calcagni%20et%20al%202006.pdf

  4. Bobby1 Says:

    Cellular immunity refers to the ability of the immune system to target and kill cells that have been infected with an antigen. Humoral immunity refers to targeting, killing or removing organisms and antigens in the interstitial fluid between the cells.

    Cellular immunity refers to a pro-inflammatory, anti-allergic Th1 response. Humoral immunity refers to an anti-inflammatory, pro-allergic Th2 response.

    If an isotope is water-soluble, it will promote a Th2 humoral response. If it is insoluble, it will promote a Th1 cellular response.

    Cesium is water-soluble, plutonium is water-insoluble.

    The type of immune response depends in part on the solubility of the radioactive substances the individual is exposed to.

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