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Ubiquitination 15 is live.

Discussion in 'Factor X' started by Jack Kruse, May 29, 2015.

  1. Jack Kruse

    Jack Kruse Administrator

  2. Nittygrittydanny

    Nittygrittydanny New Member

    We used Ozone gas generators in smoke restoration work to kill odors deep in things chemicals couldn't remove. The chamber always had a unique smell after we vacated the gas.
     
  3. Jack Kruse

    Jack Kruse Administrator

    Ozone gas is no bueno for breathing.......
     
  4. Nittygrittydanny

    Nittygrittydanny New Member

    We opened the chamber after exhausting the gas outside when the cycle was over. We knew if the chamber had a leaky seal because people coughed near it and the ozone smell was stronger.

    I had folks try to sell me an Alpine Aire system years ago. It was part of a multi-level sales gig. Glad I knew what was up with the hazzard!
     
  5. Josh

    Josh Gold

    We could obliviously scale this down to alterations in ones internal environment that change these dynamics endogenously.
     
  6. Josh

    Josh Gold


    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4063847/
     
  7. Josh

    Josh Gold

  8. Josh

    Josh Gold

    Nitric Oxide Gut 2004.jpg

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782592/
     
    Paleodocteur likes this.
  9. Josh

    Josh Gold



    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372352/ NOGUT2015.jpg
     
  10. Josh

    Josh Gold

    [​IMG]

    Figure 79.2.— Urea cycle and associated pathways: (1) carbamoyl phosphate synthetase I activating system and (2) orotate forming system. The blue line separates two compartments: (1) mitochondrial and (2) cytoplasmatic. Enzymes found inside the mitochondria: NAGS: N- Acetylglutamate synthetase (carbamoyl phosphate synthetase I activating system); CPS Ii: carbamoyl phosphate synthetase I inactivated; CPS Ia: carbamoyl phosphate synthetase I activated; OTC: ornithine transcarbamylase. Enzymes found in the cytoplasm: CPS II: carbamoyl phosphate synthetase II (orotate forming system); AS: arginosuccinate synthetase; AL: arginosuccinate lyase.

    http://pediatricneuro.com/alfonso/pg79.htm
     
  11. yewwei.tan

    yewwei.tan Gold

    Ubiquitin needs Sulfur (cysteine) to be activated (E1).
    Then needs more Sulfur (cysteine) to be conjugated (E2).
    Then needs to reduce Nitrogen to be ligated (through an E3, resulting in bonding to a Lysine Residue forming an isopeptide bond, or to an Amine group) ;).

    Reminder: The wavelength of absorbance for a peptide bond is 190–230 nm. (same with isopeptide bond)


    [​IMG]
     
    David Limacher and Josh like this.
  12. The air we breath
    Acute coronary syndrome don't happen too often in a regular practice.

    Back when I was still in my Beloved Polluted Capital, two patients had an MI the same year … what were the odds that they both happened on pollution peak day?

    redflow.jpg
     
    David Limacher likes this.
  13. Reading your blogs and Stephanie Seneff paper shed a new light on how it happened.
     
  14. I always "felt" off on pollution peak days, so I suspected there was a neurological aspect to it too.
    I was the odd one. My non asthmatic colleagues didn't feel anything special but they would agree that there was an increase of consults during the peaks.

    When I was offered to participate in a Public Health panel to revise air pollution alert guidelines, I was happy to help.

    Then I told them about the neurologic effects , and the Experts chuckled…

    I knew I couldn't tell them I "felt" it or that my mood was low or that I had compulsive binge eatings on pollution days…
    So I told them "TNF alpha , UFP mechanistic models , Milano UFP vitiated air rat studies …."
    Confirmation bias?
    They said "bring the studies" ( mind you they were Ze Experts..)
    So I did.
    And then we left the Beautiful City of Light.
     
    cinnamon and David Limacher like this.
  15. I had brains to protect.
    Two years later , despite the fears and hurdles, I still believe it was the right thing to do.

    PLoS Med. 2015 Mar; 12(3): e1001792.
    Published online 2015 Mar 3. doi: 10.1371/journal.pmed.1001792
    PMCID: PMC4348510
    Association between Traffic-Related Air Pollution in Schools and Cognitive Development in Primary School Children: A Prospective Cohort Study

    Abstract
    Background
    Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development.

    Methods and Findings
    We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). Chronic traffic air pollution (elemental carbon [EC], nitrogen dioxide [NO2], and ultrafine particle number [UFP; 10–700 nm]) was measured twice during 1-wk campaigns both in the courtyard (outdoor) and inside the classroom (indoor) simultaneously in each school pair. Cognitive development was assessed with the n-back and the attentional network tests, in particular, working memory (two-back detectability), superior working memory (three-back detectability), and inattentiveness (hit reaction time standard error). Linear mixed effects models were adjusted for age, sex, maternal education, socioeconomic status, and air pollution exposure at home.

    Children from highly polluted schools had a smaller growth in cognitive development than children from the paired lowly polluted schools, both in crude and adjusted models (e.g., 7.4% [95% CI 5.6%–8.8%] versus 11.5% [95% CI 8.9%–12.5%] improvement in working memory, p = 0.0024). Cogently, children attending schools with higher levels of EC, NO2, and UFP both indoors and outdoors experienced substantially smaller growth in all the cognitive measurements; for example, a change from the first to the fourth quartile in indoor EC reduced the gain in working memory by 13.0% (95% CI 4.2%–23.1%). Residual confounding for social class could not be discarded completely; however, the associations remained in stratified analyses (e.g., for type of school or high-/low-polluted area) and after additional adjustments (e.g., for commuting, educational quality, or smoking at home), contradicting a potential residual confounding explanation.

    Conclusions
    Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development.
     
  16. nonchalant

    nonchalant Silver

    We would be driving back to Dallas from a week of summer camping, and it was so depressing to see the yellow-brown haze over the city.
     
  17. nonchalant

    nonchalant Silver

    In the previous blog you asked
    Looks like mitochondrial magnetism would be equivalent to our earth's magnetosphere, to deflect nnEMF. Then the mitos would need clouds... How about pigments? Do mitochondria have protective pigments, like in the back of the retina in our eyes? Or is it up to the cell membrane to cloud over?
     
  18. The flow? the circulating hydric plasmic flux, in and around the cell, in and around the layers of cells, in and around our organs, in and around our bodies. If any.
     
  19. Jack Kruse

    Jack Kruse Administrator

    they have frequency specific pigments as you will soon learn
     
    David Limacher likes this.

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