text:
What disposition means in the context of registering clinical studies?
I was diving into the AACT database, and in the studies table I had noticed some columns containing the term disposition such as:

disposition_first_submitted_date
disposition_first_submitted_qc_date (qc means quality control)
disposition_first_posted_date
disposition_first_posted_date_type

and I do not know what disposition means in this context.
Additional information
The AACT database contains the same data as ClinicalTrials.gov, but in a relational databse, so it is a database of all clinical trials made in the US, but also has international studies.
Every row in the studies table represents a clinical study.
Here is the first 5 rows where the disposition_first_submitted_date is not null, alongside the header:
|nct_id                                                                                |nlm_download_date_description                                                                       |study_first_submitted_date|results_first_submitted_date|disposition_first_submitted_date|last_update_submitted_date|study_first_submitted_qc_date|study_first_posted_date|study_first_posted_date_type                                                                        |results_first_submitted_qc_date|results_first_posted_date|results_first_posted_date_type                                                                      |disposition_first_submitted_qc_date|disposition_first_posted_date|disposition_first_posted_date_type                                                                  |last_update_submitted_qc_date|last_update_posted_date|last_update_posted_date_type                                                                        |start_month_year                                                                                |start_date_type                                                                                |start_date|verification_month_year                                                                             |verification_date|completion_month_year                                                                               |completion_date_type                                                                                |completion_date|primary_completion_month_year                                                                       |primary_completion_date_type                                                                        |primary_completion_date|target_duration                                                                                |study_type                                                                                |acronym                                                                                |baseline_population                                                                                |brief_title                                                                                |official_title                                                                                |overall_status                                                                                |last_known_status                                                                                |phase                                                                                |enrollment |enrollment_type                                                                                |source                                                                                |limitations_and_caveats                                                                             |number_of_arms|number_of_groups|why_stopped                                                                                |has_expanded_access|expanded_access_type_individual|expanded_access_type_intermediate|expanded_access_type_treatment|has_dmc|is_fda_regulated_drug|is_fda_regulated_device|is_unapproved_device|is_ppsd|is_us_export|biospec_retention                                                                                |biospec_description                                                                                |ipd_time_frame                                                                                |ipd_access_criteria                                                                                |ipd_url                                                                                |plan_to_share_ipd                                                                                |plan_to_share_ipd_description                                                                       |created_at         |updated_at         |
|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|--------------------------|----------------------------|--------------------------------|--------------------------|-----------------------------|-----------------------|----------------------------------------------------------------------------------------------------|-------------------------------|-------------------------|----------------------------------------------------------------------------------------------------|-----------------------------------|-----------------------------|----------------------------------------------------------------------------------------------------|-----------------------------|-----------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------|----------------------------------------------------------------------------------------------------|-----------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|---------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-----------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-----------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|--------------|----------------|----------------------------------------------------------------------------------------------------|-------------------|-------------------------------|---------------------------------|------------------------------|-------|---------------------|-----------------------|--------------------|-------|------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|----------------------------------------------------------------------------------------------------|-------------------|-------------------|
|NCT00684515                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2008-05-22                |2014-05-09                  |2008-10-09                      |2018-08-22                |2008-05-22                   |2008-05-26             |Estimate                                                                                |2014-07-28                     |2014-07-29               |Estimate                                                                                |2009-10-21                         |2009-10-22                   |Estimate                                                                                |2018-08-22                   |2018-09-21             |Actual                                                                                |September 21, 2006                                                                                |Actual                                                                                |2006-09-21|August 2018                                                                                |2018-08-31       |November 8, 2007                                                                                |Actual                                                                                |2007-11-08     |November 8, 2007                                                                                |Actual                                                                                |2007-11-08             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Trial to Assess the Safety of Vorapaxar in Japanese Subjects With Cerebral Infarction (P05005; MK-53|Phase II Study of SCH 530348 in Subjects With Cerebral Infarction                                   |Completed                                                                                |                                                                                |Phase 2                                                                                |90         |Actual                                                                                |Merck Sharp & Dohme Corp.                                                                           |                                                                                |3             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |http://engagezone.msd.com/ds_documentation.php                                                      |Yes                                                                                |https://www.merck.com/clinical-trials/pdf/ProcedureAccessClinicalTrialData.pdf                      |2020-02-26 08:06:42|2020-02-26 08:06:42|
|NCT00684203                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2008-05-22                |2014-05-09                  |2008-10-09                      |2017-03-31                |2008-05-22                   |2008-05-26             |Estimate                                                                                |2014-07-28                     |2014-08-15               |Estimate                                                                                |2009-10-21                         |2009-10-22                   |Estimate                                                                                |2017-03-31                   |2017-05-05             |Actual                                                                                |December 1, 2006                                                                                |Actual                                                                                |2006-12-01|March 2017                                                                                |2017-03-31       |October 1, 2007                                                                                |Actual                                                                                |2007-10-01     |October 1, 2007                                                                                |Actual                                                                                |2007-10-01             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Trial to Assess the Safety and Effects of Vorapaxar in Japanese Subjects With Acute Coronary Syndrom|Phase II Study of SCH 530348 in Subjects With Acute Coronary Syndrome                               |Completed                                                                                |                                                                                |Phase 2                                                                                |120        |Actual                                                                                |Merck Sharp & Dohme Corp.                                                                           |                                                                                |5             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 08:06:46|2020-02-26 08:06:46|
|NCT00452426                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2007-03-26                |2010-10-06                  |2008-10-16                      |2010-12-30                |2007-03-26                   |2007-03-27             |Estimate                                                                                |2010-12-30                     |2011-01-25               |Estimate                                                                                |2008-10-22                         |2009-10-02                   |Estimate                                                                                |2010-12-30                   |2011-01-25             |Estimate                                                                                |March 2007                                                                                |                                                                                |2007-03-31|December 2010                                                                                |2010-12-31       |October 2007                                                                                |Actual                                                                                |2007-10-31     |October 2007                                                                                |Actual                                                                                |2007-10-31             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Effectiveness of a Computer-Assisted Personalized Sedation (CAPS) Device for Propofol Del|Multi-center Pivotal Clinical Trial to Compare the Safety and Effectiveness of Procedural Sedation i|Completed                                                                                |                                                                                |Phase 3                                                                                |1000       |Actual                                                                                |Ethicon Endo-Surgery                                                                                |                                                                                |2             |                |                                                                                |false              |                               |                                 |                              |true   |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:15:02|2020-02-26 09:15:02|
|NCT00318214                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2006-04-24                |                            |2008-12-04                      |2012-05-24                |2006-04-25                   |2006-04-26             |Estimate                                                                                |                               |                         |                                                                                |2009-11-05                         |2009-11-09                   |Estimate                                                                                |2012-05-24                   |2012-06-01             |Estimate                                                                                |June 2006                                                                                |                                                                                |2006-06-30|May 2012                                                                                |2012-05-31       |February 2008                                                                                |Actual                                                                                |2008-02-29     |February 2008                                                                                |Actual                                                                                |2008-02-29             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Efficacy Study of MRE0094 to Treat Large, Single or Multiple, Chronic, Neuropathic, Diabe|                                                                                |Terminated                                                                                |                                                                                |Phase 2                                                                                |16         |Actual                                                                                |Pfizer                                                                                |                                                                                |2             |                |The study had poor enrollment with only 16 patients randomized across 19 study centers over an¶    1|false              |                               |                                 |                              |false  |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:56:26|2020-02-26 09:56:26|
|NCT00312364                                                                                |ClinicalTrials.gov processed this data on February 25, 2020                                         |2006-04-06                |                            |2008-12-04                      |2012-05-24                |2006-04-06                   |2006-04-10             |Estimate                                                                                |                               |                         |                                                                                |2009-11-05                         |2009-11-09                   |Estimate                                                                                |2012-05-24                   |2012-06-01             |Estimate                                                                                |December 2005                                                                                |                                                                                |2005-12-31|May 2012                                                                                |2012-05-31       |December 2007                                                                                |Actual                                                                                |2007-12-31     |December 2007                                                                                |Actual                                                                                |2007-12-31             |                                                                                |Interventional                                                                                |                                                                                |                                                                                |Safety and Efficacy Study of MRE0094 to Treat Chronic, Neuropathic, Diabetic Foot Ulcers            |                                                                                |Completed                                                                                |                                                                                |Phase 2                                                                                |322        |Actual                                                                                |Pfizer                                                                                |                                                                                |              |                |                                                                                |                   |                               |                                 |                              |       |                     |                       |                    |       |            |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |                                                                                |2020-02-26 09:58:37|2020-02-26 09:58:37|

I suspect disposition in this context is not about the subjects leaving the study or the drug interacting with the patients. If I have to guess: it means the beginning of the study.


text:
Origins of the body mechanics theory
In physical therapy and occasionally in sports coaching, there's often a precise description of the mechanics of what happens during the movement (which muscles are engaged, which joint moves where etc). I couldn't find any information on where that knowledge comes from - observation and "probing" for engagement alone would not be enough as some muscles are tiny and/or hidden under bigger ones. So, how was the theory developed?
Example: how do we know these are the muscled that perform external rotation (at the shoulder, for instance) ? https://en.m.wikipedia.org/wiki/List_of_external_rotators_of_the_human_body What tells us every single one is necessary? What tells us another one isn't involved?
(please let me know if this is better suited for a different StackExchange)

Its funny that one of the first uses of electricity was to test muscles from donor corpses.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
How do Apes get their Omega 3s in the wild given so few plant sources? Are they able to convert it to DHA?
Given so few plant sources(around 6-7) of ALA, how do Apes get ALA in the wild?
Are they able to convert it into DHA in satisfactory amounts?

I am not sure they as much as a human, at least their brain is smaller afaik. and humans need is mostly for the membrane of brain cells. Another thought that from cardiovascular perspective you can compensate the missing omega-3 with omega-9. At least I have pretty good LDL/HDL ratio and I eat mostly omega-9 from olives instead of omega-3. We don't have sea nearby...

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
When does LH surge actually occur?
I’ve seen many textbooks saying that LH surge occurs in the Follicular phase while others say it occurs in the Ovulatory phase.
I’ve tried googling this, only to end up knowing two things:
1) It occurs 2-3 days before ovulation and 2) It occurs in Ovulatory phase.
Doesn’t that two contradict each other?
If you see the hormonal variation graph, LH surge occurs somewhere between follicular phase and Ovulatory phase. This is quite confusing.
So, at what phase does LH surge actually occur?

Some graphs about the ovarian cycle mention only the follicular phase and luteal phase, and the ovulation just as a point in time, not a phase, for example, here:

Source: Differencebetween.com
In this case, the LH surge starts in the follicular phase and peaks at ovulation or shortly before it.
Some other graphs also show the "periovulatory" phase (or "ovulatory phase" or just "ovulation" as a phase):

Source: Nature - Scientific Reports
In this graph, LH surge starts few days before ovulation, so in the follicular phase and peaks in periovulatory phase.

The first half of the menstrual cycle is comprised by the menstrual
  and follicular phases during which time estrogen levels are low
  (menstrual phase) and rise (follicular phase) and ends with the
  periovulatory phase in which follicular stimulating hormone (FSH) and
  luteinizing hormones (LH) peak.

Now, these graphs are still confusing, but Merck Manual defines the ovulatory phase by the surge of LH and FSH:

The ovulatory phase begins with a surge in luteinizing hormone and
  follicle-stimulating hormone levels.

In conclusion, LH surge occurs in the ovulatory phase, if the source mentions it as a separate phase, and if not, it occurs in the follicular phase.

This pathway makes more sense when viewed in an evolutionary context.  Many other animals experience induced ovulation, where various stimuli associated with copulation triggers the release of the egg.  For example, in fish and cats, the male may bite the back of the female's neck to help induce ovulation.  Whatever stimuli are received, they are pieced together by neurons that respond by secreting GnRH from the hypothalamus.  GnRH is routed via the hypophyseal portal system (a blood vessel) directly to the anterior pituitary to trigger LH and FSH production.  So what in humans seems like a slow and cyclic hormonal cycle is adapted from a rapid reflex response to sensation.
As a result, the LH and FSH surge does occur very close to the end of the follicular phase.  It has the 'intended' result of causing ovulation immediately afterward.  The follicle bursts, the egg is released, and by definition the part that remains is the corpus luteum - so the physical act of ovulation starts the luteal phase.
I see there's a rule about citations: see
https://en.wikipedia.org/wiki/Induced_ovulation_(animals)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6101186/
http://www.ansci.wisc.edu/jjp1/ansci_repro/lec/lec_25_dog_cat/lec25out.htm


text:
How many times has SARS-CoV-2 mutated?
According to
Coronavirus has mutated at least once

The novel coronavirus that has infected thousands of people across the
  world may have mutated at least once — meaning there may be two
  different types of the virus causing illnesses, a new study conducted
  by Chinese scientists suggests.
Scientists with Peking University’s School of Life Sciences and the
  Institut Pasteur of Shanghai in a preliminary study found that one
  strain — type “L” —  of the virus was more aggressive and accounted
  for about 70 percent of the strains analyzed. The second — type “S” —
  was less aggressive and accounted for about 30 percent of analyzed
  strains.

But also several webpages theorized the virus has mutated before passing from animals to humans.
This page What we know about the Wuhan virus says

This virus belongs to a family of viruses known as coronaviruses.
  Named for the crown-like spikes on their surfaces, they infect mostly
  bats, pigs and small mammals. But they mutate easily and can jump from
  animals to humans

and

Where did the new coronavirus come from? The new virus likely came
  originally from bats, scientists say. It isn’t known exactly where or
  how it jumped to humans, though. Viruses from bats often infect
  another mammal first and then mutate to become more transmissible to
  humans.

though

Coronaviruses can also jump directly to humans, without mutating or
  passing through an intermediate species.

Is something more known about this? Is it possible the virus has mutated twice in a period of time of months?

How many times has the virus mutated? As many times as it has replicated in a host. Viruses mutate every generation. Most of these mutations are "neutral" in the sense that they do not confer new evolutionary advantages or disadvantages. They likely do not even give a different phenotype. But they are mutations nonetheless.

This coronavirus is a RNA and tries to replicates lots of times with lots of bad replications. Is it any wonder that some successes are  mutations?

Can we please start calling it Covid-19 instead of corona? Corona is a family. SARS, MERS, Covid, all coronas. Questions like this are going to be a pain with the next outbreak in a few years.

@Mast I'm not sure it will be too much of a problem in the future. The media have locked onto this being called "Corona" and so I think it probably is appropriate to use "Corana" as this allows the majority of people to immediately know what is being discussed. Using "Covid-19" as well wouldn't hurt though.  And if a new outbreak occurs in the future the media may well call it "Corona" again or they may  latch onto a new term for the new outbreak.

@Mast If you want to be technical, the name of the virus is SARS-CoV-2; COVID-19 is the name of the disease caused by that virus.

@Charles Fine with me, as long as we stop with the corona-this, corona-that.

Unfortunately, the answer is "too many times."

This question makes a number of incorrect assumptions and I don't have time to correct them. The short answer is that the virus has mutated probably hundreds of times since it entered humans in late 2019.
The lower figure on the NextStrain.org ncov page, "Diversity", shows the known mutations that have been identified so far. As I look at it now, there are maybe 100-200 shown there, but that will change daily and I can't be bothered to count them.
Is it possible the virus has mutated twice in a period of time of months? Of course it is. That's what we expect from coronaviruses. It would be shocking if it did not.
The default assumption (based on a vast amount of experience with coronaviruses and many other viruses) is that these mutations are neutral and do not affect the virus in terms of fitness, virulence, or transmissibility in any way; they are occasionally useful in tracking sources, but unless you have spent a lot of time looking at virus phylogenetic trees for several years, your interpretations of these mutations are almost certainly wrong.
An example of people making claims based on unfamiliarity with virus evolution is the "two different types of the virus" claim. That claim is addressed by MacLean and colleagues in their Response to “On the origin and continuing evolution of SARS-CoV-2”. Summary:

Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations

MacLean et al.'s "Response" to Tang et al.'s paper gives this stronger summary: "Given these flaws, we believe that Tang et al. should retract their paper, as the claims made in it are clearly unfounded and risk spreading dangerous misinformation at a crucial time in the outbreak."

The default assumption as described here The default assumption (based on a vast amount of experience with coronaviruses and many other viruses) is that these mutations are neutral and do not affect the virus in terms of fitness, virulence, or transmissibility in any way has been proven wrong at least three times by SARS-CoV-2: The mutation D614G, the Alpha variant, and the Delta variant came with significantly improved fitness and show an ongoing adaption to the new human host of the virus.

I don't think you understand what "default assumption" means.

I added this as a caveat for the readers. And probably in the case of a zoonotic virus hitting mankind rather recently, this default assumption is profoundly wrong, as the virus is still in the process of adaption to its new host. At least, the huge increases in transmissibility have caught leading virologists such as C. Drosten as bad surprises.


text:
If someone with "XO" is one of the identical twins with the other twin as male, then what would the sex chromosome of the other twin be?
A more complete question: If someone with sex chromosome of XO is one of the monozygotic twins with the other twin as phenotypically male, then what would the sex chromosome of the other twin be?
I had heard that both XXY and XY is possible. Is it true?

"XO" (an unpaired X chromosome) is characteristic of Turner syndrome.  The Wikipedia article https://en.wikipedia.org/wiki/Turner_syndrome provides a typical image - a woman with a fairly distinctive broadness of the neck.  The phenotype is described as female, though of course gender identity can be unpredictable for anyone.
For the other monozygotic twin to be phenotypically male, the most likely explanation is a Y chromosome - a Y chromosome that was lost in all or many of the cells of the XO woman.
A set of monozygotic twins with one XXY and one XO would be very surprising - in other words, with the twins differing by two chromosomes - would be very surprising.  But nothing is truly impossible in biology.  And ... this may be such a reference, but I didn't look at the full text to make sure: https://www.ncbi.nlm.nih.gov/pubmed/27315788


text:
Do Angiotensin II Receptor Blockers (ARBs) or other factors control the level of ACE2 expression? [coronavirus receptor]
Because ACE2 is used by SARS-NCoV-2 to enter the cell, I am curious what factors determine its expression.  Interestingly, myocardial infarction increases ACE2 expression in the heart in an animal model ( https://www.ncbi.nlm.nih.gov/pubmed/15671045 ).  The paper found no significant effect from ramipril, an ACE inhibitor, but I don't think I can assume ARBs would work the same way.  (I am suspicious they might increase it based on the increase in the product Ang(1-7) level - https://www.nature.com/articles/hr200974 )  Note that soluble sACE2 can bind cells that did not produce it, by an RGD independent association with integrin beta 1.
Anything that influences the amount of ACE2 on cell surfaces is a useful answer.

I should follow up with some things I've found.  As a starting point, the normal expression pattern is available at https://onlinelibrary.wiley.com/doi/pdf/10.1002/path.1570 - note the staining of simple squamous epithelium in the alveoli and the endothelia of blood vessels.  Another paper details a sharp decrease in expression with age in rats, but I don't know if that extends to humans.
For regulation of expression, I was surprised to see that Google Scholar actually provides a very good assortment of search results, easier to work with than PubMed, which were topped by the MI regulation I described in the question.  Additionally https://onlinelibrary.wiley.com/doi/abs/10.1002/path.1670 (yes, that IS a different link) describes ACE2 expression in renal disease but not in normal kidney.  ACE2 expression correlated with proteinuria, but negatively with GFR. https://link.springer.com/article/10.1007/s00125-008-0988-x  There are discordant notes in some other situations: for example, subtotal nephrectomy decreased ACE2 expression in a way that was partially prevented by ramipril. https://portlandpress.com/clinsci/article/118/4/269/68827/Reduction-in-renal-ACE2-expression-in-subtotal
The mRNA and protein are both described in atherosclerotic lesions: https://onlinelibrary.wiley.com/doi/abs/10.1002/path.2357
In the lungs https://jvi.asm.org/content/79/23/14614.short describes a positive correlation with differentiation state in airway epithelium.  The regulation by HIF-1 alpha in hypoxia seems of special importance: https://journals.physiology.org/doi/full/10.1152/ajplung.90415.2008 but it is complicated (both positive and negative).
ACE2 is also expressed at high levels in placenta during pregnancy - at least in rats. https://journals.physiology.org/doi/full/10.1152/ajpregu.90592.2008
Last but not least, pharmacologic data is reviewed at https://link.springer.com/content/pdf/10.1007/s11906-008-0076-0.pdf which describes up-regulation of ACE2 by angiotensin II receptor blockers, ACE blockers, and mineralocorticoid receptor blockers.  This includes the common drugs lisinopril and losartan.  (see also https://onlinelibrary.wiley.com/doi/full/10.1111/jcmm.12573 ) Unfortunately the paper did not report substances inhibiting ACE2 expression.  But https://journals.physiology.org/doi/full/10.1152/ajpheart.00239.2008 reported that high glucose (!) or PKC inhibitors could reduce ACE2 expression.  (but the high glucose was causing kidney injury, which as described above could mean more ACE2...)  The anti-diabetes drug liraglutide increased ACE2: https://academic.oup.com/endo/article/156/10/3559/2422879  To top it all off?  SARS itself decreases ACE2 expression, and this might be part of the process injuring the lungs: https://www.nature.com/articles/nm1267
This is by no means a complete survey, and there is much I don't understand.  The relationship between ACE2 biology and the emerging COVID-19 risk groups seems apparent - as is the urgent need for research to determine which manipulations to ACE2 expression have positive versus negative effects on the prognosis of that disease.
Update: a NEJM podcast today described this biology as 'complicated' link.  It is clearly of interest, but still under investigation.  For example, losartan is presently the subject of two clinical studies news, presumably these ClinicalTrials

Perhaps take a look at the GeneCards record for ACE2 (https://www.genecards.org/cgi-bin/carddisp.pl?gene=ACE2), which contains annotations for regulatory regions (e.g., enhancers and promoters) which contain transcription factor binding sites. TFs could potentially bind to these regions to regulate the expression of this target. ChIP-seq data can help lend experimental support.

Thanks for the suggestion - I found a link there to https://europepmc.org/article/MED/15151696 which shows an increase in HUMAN heart conditions.  The transcription factor sites, well... it's hard to be sure what is meaningful.  It seems very easy to start chasing daydreams.  MITF is in monocyte-derived lineages, and macrophages produce ACE2, so ...?  But it seems like that site is everywhere.

A lot of pathways may be redundant or constitutive. I'm not sure if a deeper dive into papers related to knock-out or knock-down mutants related to ACE2 regulation (or upstream) may help? http://regulatorynetworks.com may be of interest.

It might be useful to know about the physiological role of ACE2 and its product Angiotensin (1-/). If 1 to 7 is good for you, why not over-express. Also, I wonder about some general theory on "over-expression of hormone receptors".

Over-expression of ACE2 in case of ACE inhibition has been found: Carlos M Ferrario et al.,  Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2, https://pubmed.ncbi.nlm.nih.gov/15897343/
These findings seem to be confirmed by findings that vice versa,  in the opposite situation  of high levels of AngiotensinII  downregulation of ACE2 occurs:
Deshotels MR, Xia H, Sriramula S, Lazartigues E, Filipeanu CM: Angiotensin-II mediates angiotensin converting enzyme type 2 internalization and degradation through an Angiotensin-II type I receptor-dependent mechanism. Hypertension 2014; 64: 1368–75 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231883/
Two studies, however,  apparently did not find any down- or upregulation, which is in line with the reference you cited:

Ramchand J, Patel SK,  et al., Elevated plasma angiotensin converting enzyme 2 activity is an independent predictor of major adverse cardiac events in patients with obstructive coronary artery disease. Plos One 2018; 13: e0198144
Walters TE, Kalman JM, et al., Angiotensin converting enzyme 2 activity and human atrial fibrillation (...) Europace 2017; 19 (8): 1280–7

As your question seems to be unsettled here is my individual opinion:
The feedback circle you suggest makes sense as a mechanism of  upregulation (more product leads to more production). Why not have more input if output can be made and has been generated in larger and larger amounts? However, there also is "demand or no demand" down the cascade. A large amount of product that accumulates  thus may signal a lack of its being needed - I'd cast my vote for down-regulation of the expression of input receptors, as I'd vote for "we have enough". So contrary to your answering your question I'd suggest a high amount of product Angotensin (1-7) might cause a down-, not upregulation of ACE2.
Over-expression of receptors, to my knowledge, explains drug addiction and getting used to medication.
If in surplus of ligand hormone (in that case Angiotensin II) all receptors are "filled", it makes sense to  broaden the basis and up regulate expression of ACE2. Thus,   a block of ACE (not ACE2!) by ace-inhibitors would not lead to overexpression which seems coherent with the results of  the study on blood pressure medication you cited.
Interestingly, there is an alternative pathway of ligand transformation, and an alternative product of ACE2, it's Angiotensin (1-9). It think it is a possibility that those ACE2 cells do  over-express that are engaged in the modification of AT 1-9, not AT II, as ACE-inhibitors ("beta blockers" in German) do not address or inhibit renin production which should remain elevated. Renin becomes Angiotensin I, the alternative ligand of ACE2. However, downward that alternativ pathway, it's ACE again that transforms, and its being inhibited dampens "demand".

Your post starts out by seeming to answer the OPs question including a relevant reference. I was prepared to say good job and upvote at that point. However, you then continue with text that appears to be speculative if not entirely fictional and stop including references. Are you trying to rescue your initial speculation by tacking on something like a real answer at the beginning? No matter how much you love your ideas this isn't the place for them. (Also note that "beta blockers" is not German.) Please take the [tour] and read through the [help] starting with [Answer] and [edit] accordingly.

By " your post starts out by seeming..." you refer to my edited newer version (yes, I see, 5 hours ago). So, yes indeed, no misleading as introduction. It's intension to be polite, I remember deleting "contrary" to what you suggest and refere in your answer. So without saying I think reputabel references that come to diverging conclusions that are just the opposite of each other should give the right here and now to speak up with an opinion that is frankly declared as such. Feel free to down vote. You clearly say that this is not the place for my "ideas"?

To lyersome: Also note that "Betablocker" is German, yes, it is. Are you German, too? (By the way, I can tell you you wouldn't want to say "betablockers" with an s if you want the plural.

To lyersome, again: are you offended by my clumsy use of English when I said "Here is my own personal answering"? Sorry for that, it sure aint etzetera. What I find annoying that I feel peer reviewed without peer or editor taking up on verifying if indeed there are divergent studies (which I - it's up to you as administrator of this place I happily admit to you - think is a legitimate basis to offer one's own thought. Are you serious: this is not the place for my own ideas?

To lyersome: I have revised according to your criticism as far as I could get me. Even this I "Write to the best of your ability" :-). Citation meant to be some proof of me having read your recommended help page on how to write a good answer. There, I could not find anything in favour of your point that answers should not contain any own ideads (what's more, if they are clearely declared as personal knowing, it seems just the contrary, it surely is and should be encouraged - the more if there really is no or diveregent authority!)


text:
Poor Hygiene vs. Cross-species transmission?
Did a poor hygiene at wet Chinese markets add anything to equation to trigger critical mutation of COVID-19 helping it to transmit the virus from bats/pangolins to humans?
If not, would it spread to humans anyway (even if those markets were clean and spotless) since people over there were in frequent contact with such viruses (right before preparing those wild animals as meals), which would give the virus enough time for necessary adjustment/mutation?

Even though I mentioned COVID-19, I think the question could be
  generally applied to any mutation of a virus right before it transmits
  from animals to humans. It happened many times in our past and I am
  quite confident there are many researches out there related to this
  topic.

I'm specifically interested in deciphering whether poor hygiene on those wet markets helps propelling such cross-species transmission.
Could it be the virus was already transmittable to humans whilst it was still in those bats/pangolins without any prior mutation whatsoever?
Please elaborate. Thanks.

I just discovered this most recent study that fully answers my question.
The reason appears not to be related with the hygiene itself, but the high stress level of animals that are put into cages close to humans. Therefore, the hygiene level seems irrelevant for such virus transmission from animals to humans, as long as it doesn't increase the stress level of each individual animal:
Global shifts in mammalian population trends reveal key predictors of virus spillover risk


text:
Human Immune Response to COVID-19 Virus
I have tried to find an answer to this but have not found anything after multiple attempts.
The question on the table is if the human body is able to produce an immune response to the COVID-19 virus if one has been exposed? This would apply most specifically to persons that have been tested positive but have "survived" (i.e. not having succumbed to the serious lung complications that have caused deaths for some persons).
A follow on question that comes from this is if the human body is able to mount a suitable defense does the current practice of keeping people in quarantine for two weeks allow for this defense to reach full effectiveness?

I would think if you recover at all, that signifies some kind of immunity, short-term or not. Otherwise, the virus would just keep replicating, methinks.

We probably won't really know for certain until we have time to gather more data from survivors. However, infection with existing coronaviruses (including SARS-CoV, genetically very similar to the COVID-19 virus SARS-CoV-2; ref. https://www.nature.com/articles/s41564-020-0695-z) suggests that those who are infected and survive may develop temporary immunity (ref. https://www.statnews.com/2020/02/04/two-scenarios-if-new-coronavirus-isnt-contained/):

The toll of a seasonal-flu-like coronavirus also depends on immunity — which is also scientifically uncertain. Exposure to the four endemic coronaviruses produces immunity that lasts longer than that to influenza, Webby said, but not permanent immunity. Like respiratory syncytial virus, which can re-infect adults who had it in childhood, coronavirus immunity wanes.
“Everyone, by the time they reach adulthood, should have some immunity to some coronavirus,” said Tim Sheahan, a coronavirus researcher at University of North Carolina’s Gillings School of Global Public Health. But because it doesn’t last, older people can get reinfected. The elderly also have a higher death rate from coronaviruses such as SARS and MERS, a pattern 2019-nCoV is following.
“There is some evidence that people can be reinfected with the four coronaviruses and that there is no long-lasting immunity,” Dr. Susan Kline, an infectious disease specialist at of the University of Minnesota. “Like rhinoviruses [which cause the common cold], you could be infected multiple times over your life. You can mount an antibody response, but it wanes, so on subsequent exposure you don’t have protection.” Subsequent infections often produce milder illness, however.

It might also be possible that someone was infected with two different strains of SARS-CoV-2 and did not develop immunity from the first infection. But it could have also been a continuation of the first infection, or testing error. Without virus sequence data, it was not possible to determine what happened for certain (ref. https://www.wired.com/story/did-a-woman-get-coronavirus-twice-scientists-are-skeptical/):

What could be worse than getting the pneumonia-like illness now known as Covid-19? Getting it twice.
That’s what Japanese government officials say may have happened to a female tour bus guide in Osaka. The woman was first diagnosed with Covid-19 in late January, according to a statement released by Osaka’s prefectural government Wednesday. She was discharged shortly after, once her symptoms had improved. A subsequent test came back negative for the virus. Three weeks later she returned with a sore throat and chest pain and tested again. For a second time, she tested positive for Covid-19.
News reports detailing the case raised the possibility that people may not be developing immunity to the new coronavirus, even after they’ve recovered. But several infectious disease specialists say there’s not enough data to support that conclusion. Another possibility is that the virus subsided and flared up again. (Some viruses tend to do that.) Or the test was simply wrong.

If someone was infected twice, comparing the genomic sequences of the virus over time would have helped determine that with more certainty.

Macaque monkeys seem to develop immunity. If they try to reinfect the monkeys 28 days after the first time they are infected with SARS-CoV-2, same strain both times, they do not get sick.
https://www.livescience.com/monkeys-cannot-get-reinfected-with-coronavirus-study.html
(Not a link to the actual study.)


text:
Why is the thyroid gland in the neck?
The neck seems like an odd place for it. All other neck anatomy must interface between the head and abdomen (trachea, esophagus, circulation, spine etc).
Surprisingly I have not been able to find any explanation for the thyroid’s location.

Why does the neck "seem a vulnerable place"? If you get a neck injury, the thyroid is the least of your worries. Especially in fish (the thyroid evolved early in vertebrate evolution).

You’re right. I removed that part.

I don't understand the downvotes, I think it is a valid question. Maybe people cannot face that they have no idea. :D

Almost certainly not the pituitary proximity hypothesis. Simple counter-examples include the adrenal gland (ACTH-cortisol axis), liver (GH-IGF1 axis) and  the gonads (LH/FSH axis).

Tib is referring to the theory that the the thyroid must be close to the pituitary to respond to TSH stimulation. I have since removed that theory from my original question.

@Doug I don't think so. We are talking about hormones and to be regulated by hormones you don't have to be close to the source, they travel with the blood. Maybe this way it can answer in 1 min instead of 5 mins, but I don't think that makes a real difference. Maybe you would freeze to death easier if it were be lower, but that is just a guess. I think the real answer is something totally different and we should read more about the evolution of this organ.


text:
Where does the "para" in parasitism come from
He there.
So in biology there is the concept of parabiosis, that describes a relationship where one part experiences a positive side effect and the other one has no disadvantages because of that. The "para" shows, that only a half of the organisms experiences this advantage.
Then I asked myself: Where does the "para" in parasitism come from? Is it because only one of the two sides experiences the exploitation? And if so: Is there a term for a relationship, where 2 organisms exploit each other, so basically an equivalent of parabiosis and symbiosis, but for parasitism?
~Okaghana

What exactly is the question here? The title doesn't really match the text, and the text seems to have several different questions in it, all of which are rather vague. The title question isn't biology-related, it's an etymological question.

Had a small typo in there, Now I'd say the title matches. And I would argue that although the question is about the origins of a word, it fits more in a biology forum than a ethymologic forum.

Welcome @Okaghana. For future reference, you're asking about the history or origin of the word, so on pedantic grounds it'd be better suited in an etymological forum. I disagree with the close vote for 'needs more focus', it is a clear, focused question. A little off topic surely, but it's been answered well and I think we should leave it at that.

"exploiting each other" would be a negative-negative interaction, i.e. competition.  If both members of an interaction harm each other, it would be hard to maintain symbiosis (close association). A positive-positive interaction would be mutualism (and there are lots of mutualistic symbionts)

Welcome to SE Biology. Please complete your reading of the Tour, where you will see that this site is concerned with questions about biological problems, not about the etymology of biological terms, which can usually be found in on-line English dictionaries.

The prefix para- means beside; adjacent to.
Parasite (from Etymonline):

"a hanger-on, a toady, person who lives on others,"...from Greek
  parasitos "one who lives at another's expense, person who eats at the
  table of another," especially one who frequents the tables of the
  rich and earns his welcome by flattery, from noun use of an adjective
  meaning "feeding beside," from para- "beside."

So, in the word parasitism, para- refers to the relation of a parasite to its host.

But the poster could have found the answer to this English Language question himself if he had done the research that this site requires before posting an off-topic question. Answering such questions is easy, but it attracts more rubbish to this site. The Help on answering questions makes it clear that not all questions deserve an answer.


text:
Do organisms use detergents to fight off viruses?
Common advice against contracting bacteria or viruses is to wash your hands because soap dissolves the viruses' shell. Does any organism exploit this effect to protect against infection, e.g. by having detergents in their mucous membrane? If not, why not?

I think that only works on enveloped viruses.

To answer your question, consider why soap is effective against bacteria and viruses.  The chemistry of detergents allows them to interrupt the lipid layer that surrounds cells and some viruses.  Viral envelopes, in particular, tend to be composed of host-derived phospholipids and proteins.  So, if an organism were to synthesize a detergent to fight off a pathogen, that detergent would pose a threat to the producing organism, as well.

Edit - most air-breathing animals produce a pulmonary surfactant in their alveolar cells, though the purpose of these molecules is lung function and cell size regulation, not immunity.

@user1136, Yes, insomuch that antimicrobial peptides are membrane-disrupting molecules.  Some bacteria even produce charged peptides for this purpose.  But the OP's question specifically referred to soap / detergent, which I take to mean amphipathic molecules with lipid-like and ionic components

Possibly?
I note that the body of your question refers to bacteria as well as viruses.
The following review discusses the antimicrobial effects of amphipathic bile salts, including a detergent-like mechanism:
Urdaneta V, Casadesus J. 2017. Interactions between bacteria and bile salts in the gastrointestinal and hepatobiliary tracts. Front Med 4:163.

Bile acids are surface active, amphipathic molecules, and their detergent activity damages cell membranes. Not surprisingly, many bile-sensitive mutants of both Gram-negative and Gram-positive bacteria carry mutations that impair membrane integrity. Likewise, electron microscopy studies have described a shrunken phenotype in Propionibacterium freudenreichii cells exposed to bile. Enzymatic assays in E. coli, Clostridium perfringens, and Lactobacillus acidophilus have shown that bile causes leakage of intracellular material. Factors that influence the severity of membrane disruption are as follows:
(i) Concentration of bile, high concentrations will dissolve membrane lipids, causing leakage and cell death. Low concentrations of bile may have more subtle effects on membrane fluidity and permeability by altering membrane-bound proteins or increasing trans-membrane divalent cation flux. Low levels of bile can also alter the hydrophobicity of the cell surface.
...

I haven't looked into this deeply, so I'm not sure how pronounced these effects are in vivo. There are other mechanism by which bile salts exhibit antimicrobial effects (also discussed in the review). Another review suggests that bile salts may have a similar, detergent-like effect on enveloped viruses:
Bertok L. 1977. Physico-chemcial defense of vertebrate organism: the role of bile acids in defence against bacterial endotoxins. Perspect Biol Med 21:70-76.

Attention should be called to the possibility that the detergent effect of bile acids as a physico-chemical defense mechanism may not be confined to protection against bacterial endotoxins. Theiler has noted that yellow fever virus and other arthropod-borne viruses are inactivated by mixing them with bile or sodium deoxycholate. However, the viruses of poliomyelitis, murine encephalomyocarditis, and Coxsackie virus are resistant to bile acid treatment. These observations have become a significant means of virus classification; viruses have been divided into two large groups, one being sensitive and the other resistant to sodium deoxycholate. The potential pathogenic and prophylactic significance of these observations has not been suggested heretofore. It is concluded that only those viruses with lipoprotein coating (peplon) are sensitive to this detergent action under in vitro conditions. Those with no such covering are resistant. The examination of the effect of bile acid on Aujeszky virus of the herpes group has demonstrated in vivo that bile acids do have the capacity to protect the organism from such viruses.

There is also a model for the mechanism of amphipathic antimicrobial peptides that involves a detergent-like action:
Bechinger B, Lohner L. 2006. Detergent-like actions of linear amphipathic cationic antimicrobial peptides. Biochim Biophys Acta 1758:1529-1539.

Whereas detergents at very low detergent-to-lipid ratios can have a neutral effect on model membranes, or can even result in their stabilization, openings might form temporarily at intermediate concentrations, and membrane disintegration becomes apparent at higher peptide-to-lipid ratios. Disintegration of the bilayer takes into account the loss of the membrane barrier, dissipation of the transmembrane electrochemical gradient, loss of cytoplasmic constituents and concomitantly interference with the energy metabolism of living cells, all being observed also with antimicrobial peptides.


text:
Role of Prevalence in Estimating Coronavirus Mortality
Let there be a sample of 10,000 people.
100 of them have a fever. You test them for COVID19 and they all come out positive.
5 of them die, 9 of them end up in intensive care.
The estimated mortality is 5%, and estimated intensive care rate is 9%.
What about the 9,900 asymptomatic people who did no get tested?
Scenario A: All 9,900 asymptomatic people would test negative for COVID19.
Scenario B: All 9,900 asymptomatic people would test positive for COVID19 because of a combination of high rate of asymptomatic carriers and high false positive rate.
End result:
Scenario A: true mortality rate is 5% and true intensive care rate is 9%.
Scenario B: true mortality rate is 0.05% and true intensive care rate is 0.09%.
the numbers are fictitious, but the point is simple - we can't estimate mortality without knowing the prevalence
Question:
Where are we right now between scenario A and scenario B? Or put another way, are there any ongoing studies/reports which take into account this factor?

Update, using real numbers:
Italy has a 250 cases/1mil pop (0.025% of the population tested positive)
That’s 15k cases, and 1k deaths (7%).
Scenario A - the remaining 99.975% are 100% Covid-free:
Mortality is 7%.
=> If 100% of the planet is infected, 490mil die.
Scenario B - the remaining 99.975% are asymptomatic, but positive Covids:
Mortality rate is 0.0001%.
=> If 100% of the planet is infected, 7k die.

I think you're talking (setting aside false-positive/low-specificity testing problems for the moment) about the difference between infection fatality ratio (IFR, fraction of infected people who die from disease) and the case fatality ratio (CFR, fraction of clinically defined "cases" who die from disease). The difference between these two depends completely, as you suggest, on the difference between the population that gets infected and the population that is defined as a "case" (which could vary a lot: is it people who have a cough? fever & cough? request testing? are admitted to the hospital? are admitted to the ICU?).
Because most of the people aboard the Diamond Princess cruise ship were tested (3063/3711), we can have a reasonably good idea of the fraction infected (unlike the usual scenario where most asymptomatic cases are never noticed). The authors of this (not yet peer-reviewed) study concluded that:

the all-age cIFR on the Diamond Princess was 1.2% (0.38–2.7%) and the cCFR was 2.3% (0.75–5.3%)

(where 'c' in cIFR and cCFR stands for 'corrected'; these are estimates that account for the fact that we don't yet know the outcome for all patients).
Other issues to think about:

sensitivity and specificity of testing (false positive/negative rates)
variation with/adjustment for age (discussed in the paper)
variation by medical/social context (e.g. Wuhan vs Iran vs places where cases are caught early and the medical infrastructure isn't overwhelmed)

Russell et al., "Estimating the infection and case fatality ratio for COVID-19 using age-adjusted data from the outbreak on the Diamond Princess cruise ship". https://cmmid.github.io/topics/covid19/severity/diamond_cruise_cfr_estimates.html

Comments are not for extended discussion; this conversation has been moved to chat.


text:
Can viruses stabilize and increase the shelf life of wine and other foods?
When you make wine, you use the yeast Saccharomyces cerevisiae to ferment sugary juices. After you're done, you want to avoid them doing anything by using some chemicals etc. There are also other living things (especially bacteria) that can ruin your wine or food during storage. For example, there are bacteria that would turn your wine into vinegar.
Have viruses been identified that infect and kill the bacteria that spoil wine or other foods?

For an example of background reading that could help you improve your questions I found this freely available paper.

There is at least one bacteriophage ("phage") that targets bacteria that spoil wine:

The Gluconobacter phage GC1 is a novel member of the Tectiviridae family isolated from a juice sample collected during dry white wine making. The bacteriophage infects Gluconobacter cerinus, an acetic acid bacterium which represents a spoilage microorganism during wine making, mainly because it is able to produce ethyl alcohol and transform it into acetic acid.

This particular linked paper does not say anything about usage of bacteriophages as a food preservative or for food safety, but there is interest in using bacteriophages for this general application, as an alternative to the use of antibiotics in food production.
Phages are everywhere. Craig Venter went out on his yacht and scooped up a bunch for one of his papers. Phage therapy may end up augmenting or replacing antibiotics, which would be good for us humans as many disease-causing bacteria have developed or are developing resistance to them.

Phage are quite specific though. It would be difficult putting together a cocktail that could kill all of the many bacteria that might spoil a particular food.


text:
Could total 2020 flu deaths be low due to Covid19 countermeasures?
A working assumption is that Covid19 countermeasures will also reduce seasonal flu transmission and mortality.
Could this effect be so large that the 2020 total global deaths from both causes will be lower than the annual expected deaths from seasonal flu alone ?
I understand global seasonal flu mortality is around 40k/month

This seems too speculative to me - do you possibly have a citation for this "working assumption"?

Contact minimisation will reduce all pathogen transmission. Are there references to the contrary ? https://royalsocietypublishing.org/doi/full/10.1098/rsif.2009.0302.focus

In the regions where they heavily restricted public events, closed schools, etc. because of COVID-19, it's very likely there will be lower flu incidence and mortality. The problem is how to prove that, because the incidence of flu differed grossly from year to year in past years when there were no countermeasures.

This is a question and answer site for problems about biological processes. Such problems should be capable of being answered objectively. Questions about the expected effect of a current epidemic of one disease on the future mortality caused by another disease are not about biological problems in terms of this site and are only capable of speculative opinions. Your question is therefore off-topic. Some reputable sources concerning the current coronavirus pandemic can be found here.

@cumfy if they don't go down after all this fuss it will be embarrassing. I have to go to the bathroom when my nose itches just so I can wash before scratching it. Gonna be annoyed if that doesn't save anyone, covid 19 or not.

@David I'm sorry this epidemiological question isn't to your taste. Viral transmission mechanisms, their efficiency and analysis of their variation and sequelae between similar viruses is a central topic in epidemiology. Many statistical inferences can be drawn from carefully recorded epidemic data.

@cumfy — Please read what I have written — it is not a matter of taste. I explained that your question only admitted of speculative answers and was therefore off-topic according the standards of this site. You post here without even finishing reading the Tour (you lack the corresponding badge), never mind the Help on asking questions where this is laid out. New contributors are welcome to SE Biology, but they are expected to read and follow the "rules".


text:
Ratio of bleach to water required to disinfect COVID-19?
I am confused about the needed ratio of bleach to water required to disinfect COVID-19 from surfaces.
The guide on CDC states that: https://www.cdc.gov/coronavirus/2019-ncov/community/home/cleaning-disinfection.html

Diluted household bleach solutions can be used if appropriate for the surface. Follow manufacturer’s instructions for application and proper ventilation. Check to ensure the product is not past its expiration date. Never mix household bleach with ammonia or any other cleanser. Unexpired household bleach will be effective against coronaviruses when properly diluted.
Prepare a bleach solution by mixing:
5 tablespoons (1/3rd cup) bleach per gallon of water or
4 teaspoons bleach per quart of water

This is a 2% ratio. My problem is that it is not clear what "bleach" means. Chemically I guess it's Sodium hypochlorite. What's not clear is that what is the strength of the solution I can buy in shops.
Wikipedia states that bleach in stores can be anything between 3-25%.
Does CDC recommend the final strength of Sodium hypochlorite : water to be 2% or "bleach in stores" : water to be 2% (which can be anything between 0.06% - 0.5%
Disregarding this confusing CDC direction: What is the scientific recommendation for the required sodium hypochlorite : water ratio needed for disinfecting COVID-19 from surfaces?

Just a note: bleach can discolor surfaces...

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. Although I understand your concern about the coronavirus outbreak, your question is not about the biology of the disease but about personal or public hygiene and therefore is off-topic.  I advise you to consult more appropriate reputable sources of information, some of which are listed here.

Perhaps I can help answer your microbiology question which is really about SARS-CoV-2 which is an enveloped mRNA virus. There is a lot of misunderstanding about SARS-CoV-2 and the medical disease it causes, COVID-19. The confusion is understandable as this is a novel coronavirus with a high rate of transmission & people around the globe are still in a learning curve about it. It's important to understand how to decimate SARS-CoV-2 whenever possible. I'm an RDN & years ago I went to grad school on an Allied Health Traineeship thanks to citizens of the U.S.A. Although now retired, as well as having been a clinician, I'm a former prof. I believe in giving back to society which has supported me.
Many pieces in the press unfortunately use terms of SARS-CoV-2 and then COVID-19 interchangeably, which they should not. This adds to public confusion. Keep in mind that disinfection in this instance pertains to decimation of the virus SARS-CoV-2 per se.
Cleaning should precede disinfection. Disinfection is biocidal elimination on fomite surfaces of microorganisms, in this instance SARS-CoV-2. After applying disinfecting dilution be sure to allow it adequate action time and then allow surface to air dry.
When CDC says to use “5 tablespoons (aka 1/3 cup) bleach per gallon of water” or “4 teaspoons bleach per quart of water” that is in effect 1000 ppm. CDC guidance assumes household bleach concentration to be 5-6.25%, even though most NaOCl manufacturers int the U.S.A. went to 8.25% back around 2012-2013. Check any bottle you have (or box it came in) for the NaOCl concentration for that batch of bleach. When first manufactured concentration is higher, but over time actual available free chlorine level drops and adequate potency passed by 1 year out from manufacturing date. If stored at higher room temperature, cut that down to 6 months which is more realistic. Adequate 1000 ppm of NaOCl for enough time (minimum 1 minute) can kill SARS-CoV-2.  If the non-porous fomite surface happens to be a countertop where inadvertently later food might be placed on, then after first cleaning, then disinfecting, be sure to rinse with potable H2O, then use a sanitizing solution dilution and allow to air dry.
See: "COVID-19 – Disinfecting with Bleach" from Michigan State U Center for Research on Ingredient Safety which will explain how to read date code of manufacturing on a household bleach (NaOCl) bottle and how much bleach to add to cold water in order to reach what is effectively a 1000 ppm dilution if bleach is still ‘fresh enough’ aka adequate concentration in bottle as purchased. The bleach concentration bottle code information can be read as follows (quoted or paraphrased from article):
Example: code E619337.
●First two characters E6 identify the company facility that manufactured the bleach.
●Second two numbers 19 tell the year the company manufactured the bleach.
●Last three numbers 337 tell the day of the year the company manufactured the bleach.
So, code E619337 tells us this bottle of bleach was manufactured at facility E6 in 2019 on the 337 day of the year (using a Julian calendar), which is December 3.
This bottle of bleach technically expires one year from December 3, 2019, so it needs to be used or disposed of by December 2, 2020.
Similarly a  product code A420027 tells us the product was manufactured at facility A4 in 2020 on the 27 day of the year, which is January 27. The product expires one year from January 27, 2020, so it needs to be used or disposed of by January 26, 2021.
Adjust the Julian calendar keeping in mind the year as 2020 is a leap year.
From experience using test strips with bleach concentrate dilutions, often that expiration timeline is closer to 6 months (commercial settings open bottle only 1 month).
canr.msu.edu/news/covid-19-disinfecting-with-bleach
Public Health Ontario has an online "Chlorine Dilution Calculator" to help anyone determine how much NaOCl  "household" bleach of a given concentration level to add to how much safe tap water to achieve a certain ppm of diluted chlorine sol'n. One can calculate sanitizing or even disinfecting diluted chlorine sol'n levels using the online calculator. Although the site is in Canada, they kindly include both English and Metric units. https://www.publichealthontario.ca/en/health-topics/environmental-occupational-health/water-quality/chlorine-dilution-calculator
Advisement of 1000 ppm for a NaOCl dilution based on publication:
Kampf, G. et al. Persistence of coronaviruses on inanimate surfaces and their inactivation with biocidal agents. Journal of Hospital Infection, Volume 104, Issue 3, 246 - 251 (March 2020). https://doi.org/10.1016/j.jhin.2020.01.022
Fomite transmission (contact w/ inanimate or nonpathogenic object surface transmission exclusive of food components) reduction via biocidal agents such as 0.1%-0.5% NaOCl aka 1000-5000 ppm. “...Human coronaviruses on inanimate
surfaces can be effectively inactivated by surface disinfection procedures with 62-71% ethanol, 0.5% hydrogen peroxide or 0.1% sodium hypochlorite within 1 minute.” from pre-print https://doi.org/10.1016/j.jhin.2020.01.022
Edit: The question is really about disinfecting for SARS-CoV-2, the mRNA virus which causes COVID-19 in humans.
The edit is to:
1) Clarify the actual question, which deals w/ microbiology relating to SARS-CoV-2, not a medical disease condition COVID-19;
2) Acknowledge that the press has incorrectly used the two different terms interchangeably creating public confusion & explain why many professionals are responding in forums around the world trying to clear up that confusion by providing accurate information;
3) Include current full rather than shortened links to details of NaOCl disinfection of SARS-CoV-2 with enough detail that if links are later unavailable readers will still know what to do.

Wow, thanks for this comment! I have changed the accepted answer to yours!

I think Stackexchange doesn't like bit.ly links, it's better to write them out full or use the markdown editor. Hopefully someone will come over and fix the links.

If anyone is having difficulty w/ bit.ly links, for COVID-19 – Disinfecting With Bleach just go to: https://www.canr.msu.edu/news/covid-19-disinfecting-with-bleach ; then for Public Health Ontario online "Chlorine Dilution Calculator" just go to: http://www.publichealthontario.ca/en/ServicesAndTools/Tools/Pages/Dilution-Calculator.aspx ; hope that helps.

Welcome to Biology.SE! First, while this looks like a good answer it is to a question that is off-topic for this site (because it is a personal medical question — see [help/on-topic]) and it would be better to leave such questions unanswered. Second, for future posts please include the complete reference information since links can (and do) break. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

In addition, comments are ephemeral on this site, so updates should be made by making an [edit] of your original post.

I have also been frustrated by use of percentages in protocols when making dilutions of stock bleach.  It's helpful to look at the product labels, as they often have dilution factors for different uses as well as concentrations in parts per million.
I have a bottle of Clorox brand concentrated bleach sitting next to me, and the label says this solution is 8.25% sodium hypochlorite.  The label also says that 8.25% sodium hypochlorite yields 7.85% available chlorine, and that 4 oz. of this product in 1 gallon of water yields 2,400 ppm chlorine, implying that the stock concentration is 76,800 ppm if 1 gallon (128 oz.) is the total volume or 79,200 ppm if the 1 gallon is added to 4 oz. (that is, 132 oz. total).  For simplicity, let's say that the stock solution is 78,500 ppm so that 1% available chlorine is exactly 10,000 ppm chlorine.
The CDC website cites a study that states 200 ppm chlorine is sufficient to inactivate 25 different viruses.  Sadly, I cannot find the text of that study.  Here's the citation:
Klein M, DeForest A. The inactivation of viruses by germicides. Chem. Specialists Manuf. Assoc. Proc. 1963;49:116-8.
So, using the low end of your given values, a 3% stock solution of bleach will have ~2.85% available chlorine, following the yield ratio above.  Diluting 5 tbsp. (2.5 oz.) of this stock in 1 gallon of water (total volume 130.5 oz.), as recommended, will yield ~0.05% available chlorine, or 500 ppm, which is sufficient for viral inactivation.
Edit - a bulletin from Clorox (PDF, cached HTML) states that 2400 ppm available chlorine is recommended for disinfecting hard, nonporous surfaces.  The bulletin also lists enveloped and non-enveloped viruses against which this product is effective (at the "99.9%" level), including Human Coronavirus (Strain 229E, ATCC VR-740)

The World Health Organization states[*]:

1:100 dilution of 5% sodium hypochlorite is the usual recommendation. Use 1 part bleach to 99 parts cold tap water (1:100 dilution) for disinfection of surfaces.

They say most household bleach solutions contain 5% sodium hypochlorite (50 000 ppm available chlorine), which does seem to be the typical concentration in the U.S.  The recommended dilution yields 0.05% sodium hypochlorite (or 500 ppm available chlorine).
That same source page has a few helpful points to guide usage.  Most importantly they point out: "Do not use bleach together with other household [cleaning agents], because this reduces its effectiveness and can cause dangerous chemical reactions. For example, a toxic gas is produced when bleach is mixed with acidic detergents, ... and this gas can cause death or injury. If necessary, use detergents first, and rinse thoroughly with water before using bleach for disinfection."  The latter is important because they also say "Organic materials inactivate bleach; clean surfaces so that they are clear of organic materials before disinfection with bleach."
[*] World Health Organization. "Infection Prevention and Control of Epidemic- and Pandemic-Prone Acute Respiratory Infections in Health Care" (2014), "Annex G - Use of disinfectants: alcohol and bleach".

That page seems to only link for influenza viruses, nothing COVID-19 specific.

@hyperknot, that page is part of a large document not about influenza, but about "Pandemic-Prone Acute Respiratory Infections" (exactly what we're facing).  Of course it doesn't mention SARS-CoV-2 (the virus that causes COVID-19) since it was written in 2014. It does mention the SARS-CoV virus, the cause of the 2003 SARS epidemic (and  a close relative of the virus causing COVID-19).  In any case, pretty much all types of virus particles are all vulnerable to harsh chemicals like bleach.


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Breakdown of functional human genome by organ/What fraction of the functional human genome is devoted specifically to brain functioning?
Of course, there won't be a precise known answer to the question, as it is not even known precisely what percentage of the genome is functional in the first place - but I am still looking for research.
The book "Principles of Neural Design" claims that "20% of our genome is devoted to coding neural signaling molecules". This seems not only vague, but also suspect to me, as that is more than the fraction of DNA that is known to have a function in the first place - maybe they meant only protein-coding genes?
One hears a lot about the human brain as "the most complicated object in the universe" etc., but I would like to put a number of that and compare the genetic complexity needed to express it to that needed for other body parts.

The complexity of the brain is not necessarily related to the amount of genome involved. Humans have much more complex brains than rodents and yet mostly share the same proteins with only relatively minor modifications.

I think that depends on the definition of "complexity". In terms of "amount of data needed to describe an instance of the system", I agree - but then, counting the degrees of freedom, a rock could have a higher complexity than a human brain. What I was getting at is "amount of data needed to recreate the system" (further restricting to "biological data", not the experiences the brain bases its learning on or randomness), and if the human brain doesn't need much more "code" than a mouse brain, these would indeed be similar according to the definition I am interested in.

I agree with your assessment of that statement as vague. At best, it's a gross oversimplification. For one thing, neurotransmitters are not directly encoded by genes. However, this online fact-sheet published by the NIH state, "at least a third of the genes in the human genome are primarily expressed in the brain." Still a bit vague, but slightly less so. Obviously not a proper answer, hence the comment format.
https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Genes-Work-Brain


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How do you go from virus infection to disease?
I heard on the radio a few days ago1 a discussion on viruses and diseases (go figure why :)).
The guest was very precise in how the virus enters a cell, how its RNA merges with the cell's one and how it turns the cell into a "virus factory" (roughly speaking).
The question which was not accurately answered was "and so what? how does this makes someone actually sick?"
One of the points vaguely confirmed by the virologist (following a question from the journalist) was that the immune response of the body (notably the raised temperature) was what we perceived as the disease.
Since their time was short, there were no more deliberations on that interesting point.
My question: what happens that turns the "virus replication" activity into disease? I understand that the raised temperature is a direct effect of the immune system fighting these foreign bodies (the virus) but there are other effects such as headache, cough, etc.
Are all of these a consequence of the immune system fighting back? Or is the virus changing the way the cells function, and therefore they fail at their intended activity?

1 French radio France Culture, the guest was Olivier Schwartz, director of the Dept of Virus and Immunology of the Institut Pasteur, link to the podcast (in French, obviously)

This question is very general and seems more appropriate to SE Medical Sciences.

In viral infections, the disease (on the cell/tissue level) is mainly due to immune response that results in inflammation, for example, of the throat mucosal lining, which can trigger symptoms, such as dry cough.
Each symptom has its own trigger. For example, in flu:

The mucous membranes lining the nasal and sinus cavities can become
  inflamed when infected with the flu virus. This results in increased
  pressure around the eyes and face, which may lead to a magnified
  headache (National Headache Foundation).

and

The immune reaction to the viral infection and the interferon response
  are responsible for the viral syndrome that includes high fever,
  coryza, and body aches (StatPearls).

How viruses cause symptoms is a broad question - it depends on the virus and exact symptom, so just few more examples:

In viral pneumonia, immune response triggers inflammation in the lung alveoli, which can result in shortness of breath (StatPearls).
In AIDS, HIV virus destroys CD4 lymphycites and thus impairs cell-mediated immunity, which makes the infected person vulnerable for infections, so most symptoms are from those infections, for example, oral thrush due to overgrowth of Candida yeasts in the mouth (MerckManual).

Viruses usually do not cause disease or symptoms by merely changing the function of the cells, but by damaging them, so it's more about "injury" than just a changed function. The damage of the cells and the viruses themselves trigger inflammation and most of symptoms usually originate from it.

Thank you very much. Does that mean that the functions of the cell themselves are not degraded to the point of a malfunction? In other words, if a cell is supposed to work in a certain way and a virus comes in - the activity of the cell is not significantly impaired? (which could lead to something not being produced, or over produced, or something else being produced instead (beside the virus replica))

@WoJ, It's more about damage of the cell, which is worse than impaired function. I expanded my anser a bit.


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How is honey not toxic to our epithelial cells?
Being a supersaturated solution of sugar, honey pulls the water out of cells it comes in contact with via osmosis - killing the cells. It also contains the inactive enzyme glucose oxidase, which when diluted with water activates and then converts glucose into gluconic acid and hydrogen peroxide - both of which are bad news for cells.
Honey also likely contains an antibiotic protein Bee Defensin-1, which is also bad news for bacteria. I didn't yet look into how it works so I don't know if it affects our epithelial cells.
Then some honey types (manuka) contain Methylglyoxal. Damage by methylglyoxal to low-density lipoprotein through glycation causes a fourfold increase of atherogenesis in diabetics. [1] Methylglyoxal binds directly to the nerve endings and by that increases the chronic extremity soreness in diabetic neuropathy.[2][3]
How is it safe to eat?

Because the lining of the stomach guards the component cells from acid, osmotic stress, and all sorts of other nasty stuff, while digestive enzymes make short work of any food proteins that they encounter.

What about the esophagus and mucosa of the mouth?

I'll change my initial comment into a real answer.
The human digestive tract has evolved to allow us to be broadly omnivorous, safely consuming a wide range of vegetable, animal, and mineral-based foods. While honey can be damaging to exposed cells, the epithelial cells lining the digestive tract are not exposed like the endothelial cells that line the circulatory system. Eating honey is not the same as injecting it into your veins.
A layer of mucous covers the cells of the digestive tract from mouth to colon and provides both lubrication as well as protection to the cells underneath it. It is protective to varying degrees against such challenges as acid, osmotic stress, mechanical damage, and foreign microorganisms. Additionally, the cells themselves are layered and are continually being sloughed off and regenerated, so even if the mucosal lining isn't 100% effective, damaged cells will be replaced fairly quickly.
Food quickly travels from the mouth through the esophagus to the stomach, not allowing enough time for osmotic stress or enzymes to damage anything to any significant degree. (Obviously, if you swallow something extremely harsh like bleach, lye, or concentrated acid, that's a different story.)
Once in the stomach, a food like honey is diluted by the digestive juices and any other food or drink already present -- it's not like the stomach is totally empty and globs of honey can just sit in direct contact with cells for an extended period of time, allowing for osmotic or enzymatic damage. Digestive enzymes and the acidic environment quickly attack proteins and other substrates, so even if the glucose oxidase can become activated, it will be cleaved by proteases into inactive fragments long before damaging levels of H2O2 can build up.
Low-density lipoprotein (LDL) is found in the bloodstream, not in the digestive tract, so any methylglyoxal present in food would need to be actively transported into the blood to do any damage. The work in the paper you cited was done completely in vitro, with no evidence that MG-mediated glycation as a result of eating honey actually occurs in people.
Many foods we commonly eat would appear to be dangerous to our bodies in one way or another, yet we have evolved strong mechanisms to minimize harm. However, it's pretty clear that some foods are damaging in various ways over time, so we still need to moderate what we eat. I don't know if honey (or certain kinds of it) is one of those foods, so more research is needed.

What an answer. By the time I got through it, you answered several subsequent questions that popped up:) Amazing!


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Are prions a recent biological phenomenon?
Is there evidence to suggest whether prions have existed for a large portion of evolutionary history, played a role in evolutionary history, or could they actually be a recent biological technology invented by mother nature? Is there evidence or biochemical data that prions may predate cells?

Knock-out experiments on non-pathological prion proteins ("PrP") show damage to neurons. So there is evolutionary pressure to conserve their sequence and expression. Mutations to PrP and related regulatory regions appear to be deleterious and the organism will not likely get to reproduce.
A paper here explores this question and demonstrates empirically that pathology-causing prions — normal PrP that refolds into a form that causes disease — themselves undergo selection pressure:

In summary, prions show the hallmarks of Darwinian evolution: They are subject to mutation, as evidenced by heritable changes of their phenotypic properties, and to selective amplification, as documented by the emergence of distinct populations in different environments.

To the extent that organs susceptible to aberrant prions have undergone evolution, one could infer from this that prions themselves would be under selection pressure to adapt, as their host environment changes.
Further, there is another paper that discusses sequence-level similarity of PrP between clades:

The presence of the human and mouse PrP genes within conserved syntenic groups (Sparkes et al. 1986) and the presence of aPrP gene in chicken (Gabriel et al. 1992) argue that the PrP gene existed before the speciation of mammals. In mammals, DNA sequences of the ORFs encoding PrP generally exhibit ∼90% similarity. As expected, the degree of similarity at the amino acid level increases to >95% when PrPs of different primates are compared (Schätzl et al. 1995) but is much lower when human PrP is compared with that of a marsupial (∼70%) (Windl et al. 1995). An even lower degree of homology is found when human PrP is compared with that of the chicken (∼30%) (Harris et al. 1989; Gabriel et al. 1992). Attempts to find PrP-related genes in lower eukaryotes have, to date, been unsuccessful (Oesch et al. 1991).

There is an estimation of 600M years of evolutionary distance between humans and chickens, back to their common ancestor:

The last common ancestor of birds and mammals (the clade Amniotes) lived about 310 – 330 million years ago, so 600 million years of evolutionary time in all separates humans from Aves, 300 million years from this common ancestor to humans, plus 300 million years from this ancestor to birds.

This would suggest to me that PrP has been around for a while, at least 330M years and probably longer, and that aberrant and pathological folds of PrP would have been evolving since (along with PrP, itself).

Update: note that prion-like proteins have now been discovered in Archaea.
Note that prion proteins are an important component of yeast natural history.
If they are shared between yeast, amniotes, and Archaea (which branched off at least a billion years ago), one could argue that prions are:

Extremely ancient (>1 billion years since that split).
a phenomenon that arises spontaneously in proteins. There is some support for this, see e.g. here.

If prions arise spontaneously in proteins, then it is reasonable to assume that they have been around as long as proteins have been made in any diversity (e.g. since the origin of cellular life).

A wise biologist told me once that, if some biochemical event is energetically feasible, it will likely happen. Protein folding, TF binding, whatever.