1,458 karma · joined July 5, 2020
I don’t know which parts are true or false, but that’s right in the post, and makes complete sense.
It's just shy of full-time (to withhold benefits), but not exactly the same thing as a side gig. And you're bent over a barrel.
So, a quick rebuttal to this trash blog post recounting a trash publication. This is a cut-and-paste from a real rebuttal (Dore & Chignol, Fertility & Sterility, 2012), transcribed here for easy browsing. Link at the end:
"We think that the evidence presented in this article cannot support the claim that the observed effects are non-thermal and caused by exposure to a Wi-Fi radiofrequency electromagnetic field."
1. Keeping constant the temperature under the computer by an air conditioning system is not sufficient to ensure homo-geneity of the temperatures within the experimental area, be-cause the heat source from the laptop is not homogenous itself, and to exclude that there is no local variation in the samples temperatures. If the exposure design can be justified by the desire of being as close as possible to the actual conditions of use of a lap-top computer, the dosimetry used in these experiments is much too simplistic. There is no indication of the homogeneity of the field under the laptop, which may greatly depend upon the location of the Wi-Fi antenna within the computer.
2. The control samples,‘‘kept in another room away fromany computers or electronic devices,’’were not actually keptunder identical conditions. A more suitable experimental de-sign would have been a sham exposure design in which con-trol samples would have been exposed under the sameactively working computer, but with its Wi-Fi emission turned off.
3. Moreover, Avendano et al. state that‘‘[radiofrequency electromagnetic waves] from mobile phones may cause DNA damage’’and that‘‘research has shown negative consequences of electromagnetic fields on biological mechanisms,’’and they cite in support of their contention a highly controversial article(cite2). Genotoxicity of radiofrequencies is not a matter of opinion: radiofrequency energy absorption cannot break DNA molecules, and it should be kept in mind that there is no known biologically plausible mechanism by which non-ionizing radio waves of low energy can disrupt DNA(cite3). Recently, while classifying radiofrequency electromagneticfields (RF-EMF) as‘‘possibly carcinogenic to humans’’(group2B), the International Agency for Research on Cancer Working Group reached the overall conclusion that there is only weak mechanistic evidence relevant to RF-EMF–induced cancer in humans(cite4)
The conclusion of the rebuttal: "There is a serious message behind our rebuttal. Citing Avendano et al.(cite1) among the evidence of an association between Wi-Fi exposure and a genotoxic effect on humans perm would demonstrate how studies with an erroneous methodology can be used to support important public health claims and also the weakness of the evidence purporting to demonstrate a non thermal effect of Wi-Fi RF."
cite2: Diem et al. 2005 Non-thermal DNA break-age by mobile-phone radiation (1800 MHz) in human fibroblasts and in trans-formed GFSH-R17 rat granulosa cells in vitro.
cite3: Moulder at al. 2005, Mobile phones, mobil ephone base stations and cancer: a review.
cite4: Baan et al. 2011, Carcinogenicity of radiofrequency electromagnetic fields
Some basic neuro papers have found that it's directly neurotoxic.
Others have found that it exacerbates the neurotoxicity of certain other compounds (e.g., lead).
And other studies have found that pthalate exposure increases urinary output of quinolinic acid, a neurotoxic metabolite of the tryptophan metabolic pathway to which pthalates are structurally similar.
This suggests a couple of things: (1) that pthalates are neurotoxic via the excitotoxic pathway that quinolinic acid acts through, and (2) that pthalates induce higher quinolinic acid production (we've confirmed this is true in humans).
Essentially, we've confirmed pthalates to be neurologically harmful in a number of animal studies, found a candidate pathway, and confirmed that that pathway is in fact affected in the prediction direction in humans experimentally exposed to higher doses of pthalates.
(That last bit slipped by the ethics boards because there are meds that already include pthalates, so patients were randomized to get higher- or lower- pthalate containing formulations of the med, which were otherwise equivalently dosed.)
It's a pretty reasonable conclusion at this point, if one isn't already wedded to the idea of the compound's safety.
We could call these people researchers, in honor of their tenacity in scrutinizing and re-scrutinizing their work and the work of others. And when their work impacts the health of the many, maybe we could use mass communications technology to share it.
Pie in the sky, I know.
Let’s not overstate the findings here.
Intelligent people were having intelligent debates.
The grand-parent comment to which I am replying describes near-instant addiction in the context of an opioid prescribed for pain control.
2. Kaiser Health News
No, the 'vast majority' do not. I've supervised medical grade opioid administration to more than a few people, both acutely and chronically, and *folks without a pre-existing substance use problem* do not often develop one, especially if it's over the short term. The idea that "I give you an opioid and then BAM I want more!" is highly divergent from my clinical experience.
Do you have a source for this assertion? I'm just a physician with a particular specialty in medically managed (as opposed to procedurally managed) pain, and I've never seen a "I took it once and was instantly addicted." I don't mean to undercut your subjective experience, but I've seen a few folks on pain killers, and if what you described was more common than "very rare", I would have by now.
The delay in registration is for deaths that occur up until the week-end update; it is a one-week retrospective potential bump. The fall to baseline in Israel began three weeks ago, and has shown a continuous and steady slope.
You spoke too late, and I hope you issue a correction.
That said, their statistics regarding the symptomatic case rate speak for themselves.
Your comment is surprisingly true! And utterly out of context.
As of today, Israel's deaths - both for the 65-and-overs and all-ages - is nearly down to its historical normal range, per your link.
Going back two weeks there was a huge peak at a z-score of 9.7; and going back eight weeks it was at a statistically anomalous low, at a z-score of -2.2.
I'd be tempted to point out the period of the low was the high holidays; the enormous deflection to positive slope started a week after the high holidays, and continued for three weeks. So, you know, "a bunch of people broke all quarantine for the high holidays and new year and did their level best to stay home rather than go to the doctor, and caused a giant spike, which has receded as the cases associated with that spike calmed down."
That's not the vast majority of law, though.
It also helps a lot with sterility.
The staging is just ("just") a reflection of the primary cancer mass, which is really predictive of outcomes. It's generally not directly related to whether these sorts of satellite tumors form, since the above advances. It's mostly at this point a historical point of "this is part of how we figured out how cancer works," and ties into the rationale for some of the now-standard treatments.