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Originally posted by bsl4doc
Did you read the titles of your results?
~MFP
Originally posted by decidedlyundecided
This started out as a bit of a wacky thread,
Originally posted by suzy ryan
Give it some thought, wouldn't some of those who actually suffer from obesity, be pretty angry to find the recent and dramatic viral spread, came out of a lab, maybe even deliberately?
Originally posted by bsl4doc
Patty, please refrain from personally attacking me simply because you have a difference of opinion, especially when you can't provide any information or sources. Ciao!
~MFP
Originally posted by suzy ryan
Well I still think the virus was created and spread through vaccination (remember how it was 'induced' in critters) and though Australia is suddenly catching up with the US, this didn't coincide with fast food or video games etc. but our increased vaccination rate.
Sorry to end OT, but you folk all really need a laugh!
Originally posted by suzy ryan
Hamberglar, you vaccinate against viruses with manipulated viruses, it's very much on topic.
Originally posted by suzy ryanAs to life expectancies, westernised and impoverished nations, cut a huge chunk out of the 'average' age. They are dodgy stats folks like you use to sell the, "only man can save save themselves with science lie".
Originally posted by suzy ryanI'm damn glad my grand and great grand parents didn't try to live down to them.
Originally posted by suzy ryanRubbish every researcher in one post if you must, but when their results fit the drug companies own buried studies (thank God for whistleblowers) you just come across as a "company man", with your rude attempt to kill discussion on this topic.
Originally posted by waffleprime
I am overweight! I blame McDonalds! and Capitalism...or I could just blame myself. its easier.
Originally posted by bsl4doc
Soficrow, those summaries you gave were of articles that I didn't see listed in your original list of articles, so are you admitting that long list was emrely for shock value and of no real value?
The original list came straight from the National Institutes of Health database - the second list was filtered through Google's science for dummies search engine.
Originally posted by bsl4doc
The original list came straight from the National Institutes of Health database - the second list was filtered through Google's science for dummies search engine.
What I was pointing out was that your original list didn't contain any articles relating to obesity and viruses or vaccines, so it was really just a waste of space. Thanks for reading my post though (/sarcasm).
-1: Shan XC, Goodwin PH. Links
Abstract Silencing an ACC oxidase gene affects the susceptible host response of Nicotiana benthamiana to infection by Colletotrichum orbiculare.
Plant Cell Rep. 2006 Jan 6;:1-7 [Epub ahead of print]
PMID: 16397784 [PubMed - as supplied by publisher]
2: Yang K, Shi H, Qi R, Sun S, Tang Y, Zhang B, Wang C. Links
Free Full Text Hsp90 Regulates Activation of IRF-3 and TBK-1 Stabilization in Sendai Virus-infected Cells.
Mol Biol Cell. 2006 Jan 4; [Epub ahead of print]
PMID: 16394098 [PubMed - as supplied by publisher]
4: Gern JE, Brooks GD, Meyer P, Chang A, Shen K, Evans MD, Tisler C, Dasilva D, Roberg KA, Mikus LD, Rosenthal LA, Kirk CJ, Shult PA, Bhattacharya A, Li Z, Gangnon R, Lemanske RF Jr. Links
Abstract Bidirectional interactions between viral respiratory illnesses and cytokine responses in the first year of life.
J Allergy Clin Immunol. 2006 Jan;117(1):72-8. Epub 2005 Nov 28.
PMID: 16387587 [PubMed - in process]
11: Morrison TE, Whitmore AC, Shabman RS, Lidbury BA, Mahalingam S, Heise MT. Related Articles, Links
Abstract Characterization of ross river virus tropism and virus-induced inflammation in a mouse model of viral arthritis and myositis.
J Virol. 2006 Jan;80(2):737-49.
PMID: 16378976 [PubMed - in process]
17: Haller O, Kochs G, Weber F. Related Articles, Links
Abstract The interferon response circuit: Induction and suppression by pathogenic viruses.
Virology. 2006 Jan 5;344(1):119-30.
PMID: 16364743 [PubMed - in process]
Originally posted by suzy ryan
Why are the people with "ham" in their name so rude, insulting, argumentative and belligerent?”
Originally posted by suzy ryan
If you know vacs. and viruses are mother and daughter, why do you insist you can't discuss a relationship?
Originally posted by suzy ryan
I won't go off topic playing the stats. game with you, but poverty, of which America has always had a great deal of, kills people. In that country ALOT of people, and it greatly effects the nations stats.
As a group, America's poor are far from being chronically undernourished. The average consumption of protein, vitamins, and minerals is virtually the same for poor and middle-class children and, in most cases, is well above recommended norms. Poor children actually consume more meat than do higher-income children and have average protein intakes 100 percent above recommended levels. Most poor children today are, in fact, supernourished and grow up to be, on average, one inch taller and 10 pounds heavier that the GIs who stormed the beaches of Normandy in World War II.
Biased source normally, but very well documented this time (footnotes even!)
Originally posted by suzy ryan
Anyway normal, healthy human life, baring accidents and epidemics, that always ran their course and naturally relented anyway, has always been around that 60-70-80, give or take, range. Bad Governance and living/working conditions have always been the greatest shortner of life. Not a lack drugs, that a healthy body doesn't need.
Originally posted by suzy ryan
Something other than 'lifestyle' is making people fatter than ever around the world, and we all don't have the American obsession with corn. We are however, hooked on your drugs.
Mexico probably will surpass the U.S. in obesity rates for the first time next year as the Latin American nation adopts the fast food and sedentary lifestyles of its neighbor to the north.
Read it.
Originally posted by suzy ryan
There's a good thread on that very topic.
Originally posted by bsl4doc
...soficrow, sorry. You need to read the titles of the articles again. I can't find any even somewhat related to viral obesity.
[0024] As used herein the term "exposed to a toxin-forming organism" refers to any patient contact with the toxin, such as direct contact with the toxin-producing organism itself, or by contact with the toxin, produced by the microbial organism. Such contact can occur, for example, by ingestion, inhalation, or contact through skin or mucosal membrane. Such toxin-forming dinoflagellates include but are not limited to Pfiesteria, Ciguatera, and Chattonella. Such toxin-forming fungi include but are not limited to Stachybotrys, Penicillium, Aspergillus, Cladosporium, and Fusarium. Such toxin-forming spirochetes include but are not limited to Borrelia, Treponema, Leptospira, and Denticola. Such toxin-forming protozoa include, but are not limited to Babesia and Plasmodium. Such toxin-forming cyanobacteria include but are not limited to Microcystis, Anabaenopsis and Cylindrospermopsis. Such toxin-forming bacteria include but are not limited to Bacillus, Clostridia, and coagulase-negative Staphylococcus.
United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"
***
* The biphasic change in hypothalamic leptin receptor expression seen during the progression of CDV-induced obesity provides a new paradigm for understanding mechanisms of neuroendocrinological, virus-induced abnormalities.
* ...infection with the obesity-inducing BDV-ob results most likely in neuroendocrine dysregulations leading to the development of an obesity syndrome.
* ...obesity has multiple etiologies
* Viruses can induce progressive neurologic disorders associated with diverse pathological manifestations
Let's take a look at some of the titles in your list...
-1: Shan XC, Goodwin PH. Links
Abstract Silencing an ACC oxidase gene affects the susceptible host response of Nicotiana benthamiana to infection by Colletotrichum orbiculare.
Plant Cell Rep. 2006 Jan 6;:1-7 [Epub ahead of print]
PMID: 16397784 [PubMed - as supplied by publisher]
ACC oxidase is a gene found in plants, not humans or mammals or any other organism other than plants. If you look at the citation entry for that article, you'll see this phrase "Plant Cell Rep. 2006 Jan 6;:1-7". That means it's found in the journal Plant Cell Reproduction. This has nothing to do with viral obesity whatsoever.
2: Yang K, Shi H, Qi R, Sun S, Tang Y, Zhang B, Wang C. Links
Free Full Text Hsp90 Regulates Activation of IRF-3 and TBK-1 Stabilization in Sendai Virus-infected Cells.
Mol Biol Cell. 2006 Jan 4; [Epub ahead of print]
PMID: 16394098 [PubMed - as supplied by publisher]
This article is about the immune responses phosphorylation of IRF-3 and TBK-1, intracellular signal molecules, in response to laboratory controlled sendai virus infection. It focuses on the ability of IRF-3 to control dsRNA regulation. Nothing at all about obesity.
Obesity, diabetes, and cardiovascular disease are the leading causes of morbidity and mortality in industrialized societies. The common thread that links these disorders is dysregulation of lipid metabolism. With the discovery of nuclear receptors that are activated by lipids, a new paradigm has emerged for the transcriptional regulation of metabolic pathways. Included in this group of receptors are the peroxisome proliferator-activated receptors (PPARa, -g, and -d) and the liver X receptors (LXRa and -b). ...PPAR and LXR Mediate Oxidized Lipid Signaling in Macrophages. ...LXRs Link Metabolic and Immune Functions in Macrophages. ...These observations identify the LXR pathway as a common regulator of lipid metabolic and immune functions in macrophages and suggest that LXR ligands may have utility in the treatment of inflammatory diseases. ...Dissection of the TLR3/4 signaling pathway revealed that inhibition of LXR is mediated by the viral response transcription factor IRF3.
Lipid Signaling Pathways in Physiology and Disease
***
An effective immune system requires rapid and appropriate activation of inflammatory mechanisms but equally rapid and effective resolution of the inflammatory state. A review of the canonical host response to gram-negative bacteria, the lipopolysaccharide-Toll-like receptor 4 signaling cascade, highlights the induction of repressors that act at each step of the activation process. These inflammation suppressor genes are characterized by their induction in response to pathogen, typically late in the macrophage activation program, and include an expanding class of dominant-negative proteins derived from alternate splicing of common signaling components. Despite the expanse of anti-inflammatory mechanisms available to an activated macrophage, the frailty of this system is apparent in the large numbers of genes implicated in chronic inflammatory diseases. This apparent lack of redundancy between inflammation suppressor genes is discussed with regard to evolutionary benefits in generating a heterogeneous population of immune cells and consequential robustness in defense against new and evolving pathogens.
Inflammation suppressor genes: please switch out all the lights. J Leukoc Biol. 2005 Jul;78(1):9-13. Wells CA, Ravasi T, Hume DA. Griffith University, Queensland, Australia. PMID: 15774547
***
Mammalian cells respond to virus infections by eliciting both innate and adaptive immune responses. One of the most effective innate antiviral responses is the production of alpha/beta interferon and the subsequent induction of interferon-stimulated genes (ISGs), whose products collectively limit virus replication and spread. Following viral infection, interferon is produced in a biphasic fashion that involves a number of transcription factors, including the interferon regulatory factors (IRFs) 1, 3, 7, and 9. In addition, virus infection has been shown to directly induce ISGs in the absence of prior interferon production through the activation of IRF3. This process is believed to require virus replication and results in IRF3 hyperphosphorylation, nuclear localization, and proteasome-mediated degradation. Previously, we and others demonstrated that herpes simplex virus type 1 (HSV-1) induces ISGs and an antiviral response in fibroblasts in the absence of both interferon production and virus replication. In this report, we show that the entry of enveloped virus particles from diverse virus families elicits a similar innate response. This process requires IRF3, but not IRF1, IRF7, or IRF9. Following virus replication, the large DNA viruses HSV-1 and vaccinia virus effectively inhibit ISG mRNA accumulation, whereas the small RNA viruses Newcastle disease virus, Sendai virus, and vesicular stomatitis virus do not. In addition, we found that IRF3 hyperphosphorylation and degradation do not correlate with ISG and antiviral state induction but instead serve as a hallmark of productive virus replication, particularly following a high-multiplicity infection. Collectively, these data suggest that virus entry triggers an innate antiviral response mediated by IRF3 and that subsequent virus replication results in posttranslational modification of IRF3, such as hyperphosphorylation, depending on the nature of the incoming virus.
Innate cellular response to virus particle entry requires IRF3 but not virus replication. J Virol. 2004 Feb;78(4):1706-17. Collins SE, Noyce RS, Mossman KL. Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5. PMID: 14747536
Full Text
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Chen and his colleagues were seeking a regulatory molecule that would provide a missing link in the activation of two important triggers of the innate immune system -- NF-eB and IRF3. Somehow, these molecules are activated in response to a receptor molecule, called RIG-I, which detects viral genetic material. RIG-I binds to the RNA of viruses such as the influenza virus, hepatitis C virus, West Nile virus and SARS virus. ...The researchers knew the molecule they were seeking was present in a biochemical pathway somewhere between RIG-I and other "downstream" regulatory molecules. They initiated a search for this missing molecule by searching for proteins in the cell that contain a characteristic molecular domain, called a CARD domain, which mediates interactions between different regulatory proteins. Their search yielded a protein, which they called MAVS for mitochondrial antiviral signaling. ...Their experiments revealed that MAVS activated NF-eB and IRF3 in cell cultures.
Cellular power plants also fend off viruses
***
IKK-i(epsilon) overexpression promotes dimerization and nuclear translocation of interferon regulatory factor 3 (IRF3), induces activation of the DNA-binding protein C/EBPdelta and enhances proinflammatory gene induction by transforming growth factor-beta (TGF-beta).
Meeting on the biology and pathology of NF-kappaB
***
Also see: Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism. A novel regulatory mechanism altered in obesity.
Full Text
Cell-line-induced mutation of the rotavirus genome alters expression of an IRF3-interacting protein.
Full Text
4: Gern JE, Brooks GD, Meyer P, Chang A, Shen K, Evans MD, Tisler C, Dasilva D, Roberg KA, Mikus LD, Rosenthal LA, Kirk CJ, Shult PA, Bhattacharya A, Li Z, Gangnon R, Lemanske RF Jr. Links
Abstract Bidirectional interactions between viral respiratory illnesses and cytokine responses in the first year of life.
J Allergy Clin Immunol. 2006 Jan;117(1):72-8. Epub 2005 Nov 28.
PMID: 16387587 [PubMed - in process]
This article is about the development of allergies as a response to cytokines (cellular signal molecules of the immune system) as a result of early life repiratory infections. Nothing mentioned in the journal article in reference to obesity or viral linked obesity.
[0048] We have seen that deficiencies in MSH are commonly seen in patients with elevated levels of pro-inflammatory cytokines associated with exposure to environmental sources of biotoxin production, including indoor toxin forming fungi leading to SBS. The pro-opiomelanocortoid pathway (POMC) generates MSH in the hypothalamus. Leptin is an agonist of cytokine receptors that initiate activity of the POMC. Serum leptin can be measured looking for evidence of reduced receptor activity for the leptin agonist, and thus an elevated level of leptin is a marker of impaired MSH production. The inability of the POMC pathway to make MSH is marked by refractory symptoms, such as obesity and leptin resistance.
United States Patent Application: 0030219400
Sorry, there's no direct link. Go to the US Patent Office website, and search under applications for #0030219400, or "Methods for treating or inhibiting neurotoxin-mediated syndromes"
11: Morrison TE, Whitmore AC, Shabman RS, Lidbury BA, Mahalingam S, Heise MT. Related Articles, Links
Abstract Characterization of ross river virus tropism and virus-induced inflammation in a mouse model of viral arthritis and myositis.
J Virol. 2006 Jan;80(2):737-49.
PMID: 16378976 [PubMed - in process]
This article is about the possible link between viruses and myositis (a swelling of muscles at the joints) and arthritis (a swelling of the joints due to rubbing or wear of cartilage, among other causes). No mention of obesity or viral linked obesity.
...both IL-2 and IL-15 act as chemoattractants for T cells. The two cytokines stimulate the proliferation of NK cells and can synergize with IL-12 to facilitate their synthesis of IFN-γ and TNF-α [31]. Both cytokines induce the proliferation and immunoglobulin synthesis by human B cells stimulated with anti-IgM or CD40 ligand [32]. ...mice made JAK3-deficient by homologous recombination manifest an absence of NK cells and abnormalities of T and B cells but do not have disorders in nonimmunological systems [46]. ...our emerging understanding of the IL-15/ IL-15R system, including the definition of the actions that this cytokine manifests – both those that are shared with IL-2 and those that are distinct – is opening new possibilities for the development of more rational immune interventions directed toward IL-15 and IL-15 receptors that may be of value in the treatment of cancer, the prevention of allograft rejection, the therapy of diseases associated with the retrovirus HTLV-I, and the treatment of autoimmune diseases such as RA.
The contrasting roles of IL-2 and IL-15 in the life and death of lymphocytes: implications for the immunotherapy of rheumatological diseases
17: Haller O, Kochs G, Weber F. Related Articles, Links
Abstract The interferon response circuit: Induction and suppression by pathogenic viruses.
Virology. 2006 Jan 5;344(1):119-30.
PMID: 16364743 [PubMed - in process]
This article is about the role of inteferons (cellular signal molecules specific for certain cells) and their ability to destabilize viral molecules. No mention of obesity or viral linked obesity.
Viruses need to multiply extensively in the infected host in order to ensure transmission to new hosts and survival as a population. This is a formidable task, given the powerful innate and adaptive immune responses of the host. In particular, the interferon (IFN) system plays an important role in limiting virus spread at an early stage of infection. It has become increasingly clear that viruses have evolved multiple strategies to escape the IFN system. They either inhibit IFN synthesis, bind and inactivate secreted IFN molecules, block IFN-activated signaling, or disturb the action of IFN-induced antiviral proteins. The molecular mechanisms involved range from a broad shut-off of the host cell metabolism to fine-tuned elimination of key components of the IFN system. Type I (alpha/beta) IFNs are produced in direct response to virus infection and double-stranded RNA (dsRNA) molecules that are sensed as a danger signal by infected cells. IFNs induce the expression of a number of antiviral proteins, some of which are again activated by dsRNA. Therefore, many viruses produce dsRNA-binding proteins to sequester the danger signal or express virulence genes that target specific components of the IFN system, such as members of the IFN regulatory factor (IRF) family or components of the JAK-STAT signaling pathway. Finally, some viruses have adopted means to directly suppress the very antiviral effector proteins of the IFN-induced antiviral state directed against them. Evidently, viruses and their host's innate immune responses have coevolved, leading to a subtle balance between virus-promoting and virus-inhibiting factors. A better understanding of virus-host interactions is now emerging with great implications for vaccine development and drug design.
Inverse interference: how viruses fight the interferon system. Viral Immunol. 2004;17(4):498-515. Weber F, Kochs G, Haller O. Abteilung Virologie, Institut fur Medizinische Mikrobiologie und Hygiene, Universitat Freiburg, Freiburg, Germany. PMID: 15671747
So, basically, your list is a wash.
I went through and picked a few I thought would be the most interesting reads for me, personally.
If you'd be so kind, could you show me which ones you feel have anything whatsoever to do with obesity in any way?