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Can people be bred for tameness in a similar way to Russian foxes?
Russian foxes were selectively bred for tameness. Can a similar process happen to humans, under the right conditions — say, extreme political pressure to obey ?

Do you understand how the process works for a fox (or anything else for any other trait, for that matter)? Think about what the prerequisites are and what the process is.

Cages and a basic test for friendliness. I know this has dark resonances for humans and their history - I'm not advocating it, I'm asking if it is a process that happens already. I should maybe change the question to "Have" instead of "Can".

If a trait is genetically influenced, has variation, and affects production of progeny, it can be selected on, naturally or artificially. So if there is variation in human tameness with a genetic cause (unlikely to have been studied specifically as 'tameness'), and people who are not tame are killed or otherwise prevented from reproducing, then yes, you would select for tameness. You won't be able to get a rigorous result for the more specific questions your question seems to imply or that you've mentioned in a comment.

OK so thinking about the selection within societies I suppose we're looking back at the beginning of social stratification and law - favouring obedience and punishing disobedience. Sometimes this is highly ruthless and lethal - the USSR would be one example of this. But the activities of Stalin & co were quite brief. But do the selection processes of dictators select for tameness or aggression ? Dictatorships seem to reward both the aggression (on the government side) and obedience (on the citizenry side) simultaneously. OK good thanks you've prompted me to reconsider on this.

Harpending wrote about it.

define tameness in respect to a human. Less likely to get violent, already is being selected for.

OK how to define it. Good question. In foxes it is friendliness to another species. That wouldn't count for human-human tameness. It's also submission to authority and control - for the foxes that is to the species which cages it. So I would call human tameness a propensity to obey, be friendly towards, rule makers. The law or ruling class.
I read that Russian foxes become tame in six generations. Call a human generation 25 years, and make a huge assumption (probably not true) that humans adapt as quickly, then that would be about 150 years. Some social systems and religions are much older.

@JimmyWiddle If you're using your actual name, be careful, for you're getting close to verboten ideas. Religion civilizing people is indeed an old phenomenon that seems foreign to moderns. Of course, this implies that if Alice's ancestors and Bob's ancestors spent centuries under different religions, then Alice and Bob may be very, very incompatible. Forcing Alice and Bob to live under the same laws and under the same social norms may be a fool's errand.

I hadn't thought of that, but I see what you mean. Yeah that could be a hot potato !
I think the foxes are tame to humans generally, not just Russian humans with a certain language, appearance and smell. Would it be different for humans ? I expect this has been considered already, given the authoritarian political regime under which the fox experiments were started, and maybe the reason it was conducted on the quiet out in the sticks.

@JimmyWiddle In humans, tameness to humans in general and tameness to humans of the same family / clan / tribe / race would be an interesting distinction. If I recall correctly, Dmitry Belyayev was working at the Institute of Cytology and Genetics in Akademgorodok — the Soviet version of Los Alamos.

@JimmyWiddle You may want to read this.

Quote from Slavoj Zizek, would seem to imply that the search for human tameness genes is ongoing. "I visited China five years ago I got in a conversation with some big shot from their Academy of Biogenetics. I mean biogenetic department of their Academy of Sciences. And he gave me the program of goals of biogenetics in China. A kind of a programmatic text which pretty much terrified me. It opens up the text with something like the goal of biogenetics in the People’s Republic of China is to regulate the physical and the psychic welfare of Chinese people. My God, what does that mean?"

@JimmyWiddle Einstein himself had some naughty thoughts.

Setting aside the eugenic implications of what are you suggesting (short answer: yes it is theoretically possible, but no it is practically impossible), a more interesting observation is that evolutionary anthropologists think that humans might have "self-domesticated" during our evolutionary history.
There is a wide literature on this topic, but a recent paper summarizes the main ideas and addresses the question from a genomic point of view. Theofanopoulou and coauthors find credible genomic evidence for similar patterns of genetic evolution in humans and other domesticated animals.

Good yes I was wondering about the natural neotony of humans over time. But the eugenics - I was wondering if it already happened unconsciously, for instance through the communist era in Russia and various other times and places where people have been selected by political or religious systems.
As I understand it the foxes showed signs of change in about 10 generations. In human terms that's somewhere around 250 years I think. Whether there is an equivalence between human and fox generations is part of my question, really.

@kmm What do you mean with practically impossible?

@Marzipanherz From an implementation (practical) perspective, breeding humans will not work. If there is heritable variation, it can be selected on. Actually doing that selection on humans is impossible.

@kmm I was thinking, whether something like this might have happend (unintentionally) already: Think of an isolated culture (an island, for example) that prevents non-tame people from getting children (via prison or death penalty). If such a culture has been/is stable for enough generations and assuming that tameness in human was heritable....

@kmm There are practical ways that artificial selection can be done in humans (This is a different question from whether it should be done). A country which is a welfare society could, for example, make IVF with embryo selection free and legal. When some portion of the variation of trait X is understood genetically (such as from GWAS), then you can select directly at the embryo level. For example, a procedure could be that a couple made 10 fertilized eggs, and then you can select the egg that has the highest probability of high/low X.


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Why are bats the source of dangerous coronavirus pandemics?
Why do coronaviruses come from bats?
I mean, why precisely coronaviruses and not (for instance) herpesviruses?
It looks like bats host more zoonotic viruses (per species) than rodents, although they don't develop any sign of disease.
The article above says that rodents host more zoonotic viruses than bats overall (68 against 61), but at the same time most of the latest pandemics originated from bats.
It also seems that bats could be involved in the maintenance of ebola viruses.
My question is: why did these major pandemics originate from bats and not from rodents, although rodents host more zoonotic viruses overall?
We should also take into consideration that human-rodent interaction is usually more likely than human-bat interaction, except for people who consume bats (like Chinese people; this would (partially) explain why both SARS and 2019-nCoV developed in China).

There is lots of discussion of this in the literature, but I think no solid answers: https://scholar.google.ca/scholar?hl=en&as_sdt=0%2C5&q=bat+virus+reservoir+physiology&btnG=

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Why not bats?  .

I think your first link answers that question as well as anyone here can: they're highly mobile, have long lifespans that facilitate chronic viral infections, surpress their immune systems during hibernation, and often live in large groups that enable viruses to spread quickly between individuals.

Theory: When they fly, bats raise their body temperatures similar to those seen in other mammals that have a fever (100 to 106 degrees Fahrenheit)... Perhaps the viruses are primed to thrive in humans because bat fevers can overcome human fever temperatures. Perhaps a bat fever temperature is 110, if one of you has access to a feverish bat and a mini temperature gage.

keep in mind many of our viruses come from other many species, (dogs, birds, swine, bats, rats, cows), this particular one just happened to come from a bat.

@John I knew that, my question is why bats' viruses are deadlier than the others

they are not, viruses from bats are no worse than viruses from any other animal. Every spill over virus is a roll of the dice.

The preponderance of links between bat and human pathogens has led to a debate about whether bats disproportionately contribute to emerging viral infections crossing the species barrier into humans (26–30). Given the diversity of the Chiroptera order (Figure (Figure1),1), we may simply see more bat viruses because there are so many (>1,300) species of bats (31). However, even when accounting for the fact that they make up ~20% of extant terrestrial mammals, bats are overrepresented as reservoir hosts of pathogens with a high potential for spilling into human populations (32, 33). In fact, no known predictors that have been described to impact the likelihood of crossing the species barrier, including reservoir host ecology, phylogenetic relatedness to humans or frequency of reservoir-human contact, explain this pattern (32). Thus, why bats are such a frequent source of pathogenic human viruses remains a tantalizing mystery.

--Going to Bat(s) for Studies of Disease Tolerance
Other references that debate whether bats are special, generally conclude that they might somehow be, and argue about causes, include

Brook CE, Dobson AP. Bats as ‘special’ reservoirs for emerging zoonotic pathogens. Trends Microbiol. (2015) 23:172–80. This may be the best of the group, going into more detail and including more recent data
Dobson AP. Virology. What links bats to emerging infectious diseases? Science (2005) 310:628–9.
Wang LF, Walker PJ, Poon LL. Mass extinctions, biodiversity and mitochondrial function: are bats ‘special’ as reservoirs for emerging viruses? Curr Opin Virol. (2011) 1:649–57.
Olival K, Epstein JH, Wang LF, Field HE, Daszak P. Are bats exceptional viral reservoirs? In: Aguirre AA, Ostfeld R, Daszak P, editors. editors. New Directions in Conservation Medicine. Oxford, UK: Oxford University Press; (2012). p. 195–212.
Luis AD, Hayman DT, O'Shea TJ, Cryan PM, Gilbert AT, Pulliam JR, et al. . A comparison of bats and rodents as reservoirs of zoonotic viruses: are bats special? Proc Biol Sci. (2013) 280:20122753.

The following paper proposes that the bat borne viruses evolve to rapidly-transmit as a response to their robust immune systems:

We carried out virus infectivity assays on bat cell lines expressing induced and constitutive immune phenotypes, then developed a theoretical model of our in vitro system, which we fit to empirical data. Best fit models recapitulated expected immune phenotypes for representative cell lines, supporting robust antiviral defenses in bat cells that correlated with higher estimates for within-host viral propagation rates. In general, heightened immune responses limit pathogen-induced cellular morbidity, which can facilitate the establishment of rapidly-propagating persistent infections within-host. Rapidly-transmitting viruses that have evolved with bat immune systems will likely cause enhanced virulence following emergence into secondary hosts with immune systems that diverge from those unique to bats.

Accelerated viral dynamics in bat cell lines, with implications for zoonotic emergence, eLife Sciences (2020)

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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.

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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.

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)

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What is the meaning of the word "Ligandable" in "ligandable proteome"?
I see "ligandable proteome", "ligandable proteins" and "ligandable targets" an awful lot.
But really I don't know what exactly the word "ligandable" means?
Is that it means, for example, "ligandable proteins" means proteins have ligands?
Thank for your help.

Can you please add some references that use the terms "ligandable proteome", "ligandable proteins" and "ligandable targets"?  Context helps elucidate meaning.

In biochemistry, ligand is usually taken to mean a substance which binds to a larger molecule such as an enzyme or other protein, thereby forming a larger complex.  The study of ligand binding has been important for pharmaceuticals, particularly in ligand-based drug design.
The term ligandability (and hence ligandable) seems to have come into significant use with a paper by Edfeldt, Folmer, and Breeze in which they say:

In recent years, the term druggability has increasingly been adopted to describe the ability of a protein target to bind small molecules with high affinity; however, we believe the term ‘ligandability’ is more appropriate for this purpose. Although ligandability is a requirement for finding drugs for a particular target, it is not a guarantee that such ligands will make good drugs.

So, ligandable usually refers to the capability of a molecular target of drug design to bind small molecules.  A ligandable proteome would then be a set of proteins capable of binding small molecules.

Thank you for identifying the culprits. I believe there is a special place in hell reserved for such as they.

Woah, I couldn't thank you enough. It really helps me a lot. Now, I get exactly what it means.

Ligand is borrowed from Latin ligandus, imperative verb tense of ligo (“bind, bandage, unite”), From Proto-Indo-European *leyǵ- (“to bind”).
You can find it in many words in English, French, Spanish, i.e. Liaison which means "to link, to associate"
In chemistry, it means: An ion, molecule, or functional group that binds to another chemical entity to form a larger complex.
Ligand is a latin scientific word which means "to link, to associate, to bind together" so you can just substitute the text books for one of those words. European scientists often know 500 or 1000 latin and greek word constructions like that. Words like Astro, Geo, Bio, logos, Con, anti, which are used commonly in science.
https://www.google.com/search?q=rely+etymology&oq=rely+etymology&aqs=chrome..69i57j0.4031j0j9&sourceid=chrome&ie=UTF-8

So, in conclusion, "ligandable proteins" means that proteins have an ability to link, right?

yes that's correct


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Does a reproductively successful male have the same genetics as a reproductively successful female?
Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?
However, I've heard that in humans today, males don't like rich females while females like rich males. Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't. Females and males also played very different roles in society. Also, successful males often don't spend much time taking care of children and spend more time making them, while successful females spend more time taking care of them. This suggests that successful males are genetically different than successful females? I'm an amateur in biology, so correct me if I'm wrong.

One important thing that the logic of your question seems to be completely missing is that, at least for humans and many other species, no male has the same genetics as a female. In humans and related species, males have one X and one Y chromosome whereas females have two X chromosomes.

What difference does it make though? Isn't the only difference that being female decreases or increases the degree of some of the traits that a male would have and vice versa? Or are the interactions more complicated than this?

Because the traits expressed by males and females are not the same.

So your're saying that an aggressive male wouldn't necessarily make a relatively aggressive female? I somehow don't believe that.

Evolutionarily, using humans as an example, it would make sense that a successful female would produce successful male offspring. If a successful female produced male offspring that weren't successful, the female also wouldn't be successful by definition and would, through evolution, stop being desired by males. Therefore, females are selected for by their ability to produce successful males and thus successful male genes must be the same as successful female genes?

That assumption is wrong. Of course the best thing for an individual's reproductive success is to have as many successful offspring as possible regardless of gender, but in the real world there are sometimes tradeoffs. If an individual had a trait that made, say, their female offspring a lot more successful but mildly impaired their male's offspring's success, the advantage to the female offspring might outweigh the disadvantage to the male and the trait might get passed on, even though it produced male offspring that weren't very successful.
Here is a paper apparently exploring the concept in seed beetles:
http://rspb.royalsocietypublishing.org/content/early/2009/12/21/rspb.2009.2026

However, I've heard that in humans today, males don't like rich females while females like rich males.

You've heard that of humans, have you? Are you sure what you heard actually applied to all humans, and not the humans in one specific society? You say "humans today", do you mean "anatomically modern humans" or "people in the 21th century"?
You really ought to investigate this kind of thing you hear before drawing all-encompassing conclusions about biology or evolution from them. Maybe you were assuming that "in humans, males don't like rich females while females like rich males" was consensus biology; if so, well, it isn't. And given that it isn't, we can't answer your questions based on such a vague claim; you should give a source that explains more precisely what exactly is being said there.

Also, from what I've read, lascivious females used to be looked down upon in the past while lascivious males weren't.

Same thing; I'll also highlight the "in the past" when your previous sentence talked about "today". Evolution works on the scales of hundreds and thousands of generations. Why would you assume evolutionary explanations for social trends that, by your own words apparently, have changed recently?

This suggests that successful males are genetically different than successful females?

In order for those things suggest that, you would need: 1) to establish reliably that the differences you talked about exist, 2) to establish that they have a probable biological basis; one way of establishing this could be to show that they are universal across human cultures, geography and history. If they aren't then it's more likely the explanation is cultural than biological, and 3) to establish that the biological difference is related to individuals being successful, as opposed to being random variation (which happens a lot in evolution).

competition between male and female genes is known to exist in some species, in the most extreme case sien in some mice genes on Y chromosomes that actually prevent X carrying sperm from forming properly.

Before I read this I thought biology was simple stuff. But does this answer my question?

@dan-dan I tried to answer your question, so I think so... Do you feel this doesn't answer your question, and if so can you say what's missing?


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What is this plant with hardened fruits on the beach in Mozambique?
We saw these near the Barra and Tofinho beaches in the Inhambane province in Mozambique, in July. They were hard and leathery and dry to the touch, long past something resembling edible fruit.
Anybody have an idea what they might be? (just curious)

Edited: Here is some context around the tree.

I will take a guess that it is Ficus racemosa which is found in that area. More info. If you have pictures of the rest of the tree that would be helpful.

Thanks for the suggestion. I added a context image, and one can see that they are indeed clustered around a trunk, as with Ficus racemosa.

Interesting.  Looks to be a very small specimen or one that is broke-off and making its last stand (my first thought was "where is the rest of the tree?).  These can be very large trees but maybe it is in an exposed area and relatively small or young.


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What change would you expect in phospholipid orientation of the membrane if the enviornment were mostly heptane?
The external and internal environment of the cell is basically water, thus phospholipids organize themselves the way they do (bilayer). If the environment were to magically become mostly heptane, how would the phospholipid orientation change?
Phospholipids maintain their structure in the cell membrane because of the hydrophilic heads and the hydrophobic tails. Much unlike water, Heptane (CH3-CH2-CH2-CH2-CH2-CH2-CH3) is non polar and thus would not cause the heads to present themselves on the outer bilayer and the tails to tuck themselves away.
Because heptane is non polar, I wouldn't expect there to by any hydrogen-bonding going on, so I don't think that we would see an "inverted bilayer". I could be wrong though.
My thought - the cell membrane would cease to exist, I can't think of what would hold it together, but that seems a bit out there.
Thoughts?

Is this a homework question? If so note that the SE Biology policy on homework questions indicates it should be tagged as such.

Yes, this is a homework question. I'll go ahead and tag.  Also not really looking for an outright answer, more just guidance on my current train of thought. Which... do you have any?
Also, I feel like I've met all the rules. https://biology.stackexchange.com/help/homework

I agree that you have followed the rules. Your answer that the membrane would cease to exist seems most reasonable to me, but I suppose you are expected to think about the polar and non-polar parts of the phospholipid and which would orient itself to the hydrophobic heptane. I hate this sort of question, because this only works if you assume that the membrane is still surrounding a cell with an aqueous interior and the membrane still exists. I assume your instructor knows this is so, but you or I would not, which is not fair on you (I don't care).


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Net electrical load of a peptide
I have to determine the electrical charge of the next peptide chain:
C - E - H - P
I know that this page is not there to raise doubts about this style, but I have looked for resources on the Internet and find nothing. Please explain to me how to determine the net load according to pH and the isoelectric point, so that I can take this as an example.
My teacher told me to get the necessary data from this table:

Thank you very much for the link, it gives me the solution. But, I still don't know how to do it on my own.


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Difference in time tick spends on host based on feeding location
Does the time a tick remains on a host, and the 'health' of a tick vary depending on the location where it feeds on the host? Do they change locations on the host to find a better environment?
I recently realized that what I thought was a skin blemish on our dog was in fact a tick (it was there for weeks-- our dog gets occasional skin growths on her head and perhaps I have been distracted). This tick was on her snout-- and dog ticks most commonly attach to the head, neck and ears.  Ticks frequently get ticks on their head and ears because they stick their head (snouts!) into everything. Apparently, different species will stay and feed for different durations (7-10 days for many, but male American Dog Ticks can remain on the host for an indefinite period of time alternately feeding and mating.  This made me think-- how does finding a very exposed part of a host (snout) affect the health of a tick and the duration of their time on the host? At some point might they decide they need to find a better habitat and move?

Can't be answered the way it's asked; what species of tick? It has nothing to do with bone, and a lot to do with skin thickness. Dog ticks "fall" onto victims, so scalp will be common for people, scalp/back/neck for deer, etc. (Your source refers humans.) Deer ticks are mostly on the ground, and crawl up, so leg/groin are good places. Your dog probably had this tick, gotten from sniffing the ground. They're small, and dog nose epidermis is thin (despite appearances), so they'll dig right in. Thin epidermis means capillaries are near the surface, so within reach for small ticks.

@anongoodnurse Thanks for info & guidance on revising my question. Perhaps it still needs help, and I'm assuming it is a dog tick (I don't actually know).

Dog ticks are big, even the nymphs. It would be very surprising if you didn't notice a dog tick on your dog's nose, because they're big, and when engorged, they are so distended it's disgusting (I don't like ticks.) And no, they don't move around after they've started feeding, maybe because a fully engorged tick can't walk. They drop to the ground and lay eggs. I've read some of what you refer to.

BTW, read carefully. Your article (which I just read) stated male ticks alternately feed and mate; females become engorged. Male ticks do not become engorged. Which further complicated your question.


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Common english name for tissues which are separated from the blood by blood-tissue barriers
Which general term is used to denote such organs/tissues as: brain, testis, thymus etc., which are separated from the blood by blood-tissue barriers?

I am not aware of any umbrella term: the barriers for each are not identical, the function and reasons for the barriers are not the same.
Often these organs are referred to as "immune privileged" because one of the important consequences of the separation is that immune responses in each of those organs are different than in the rest of the systemic circulation, even though this is of course not the only significance of blood-tissue barriers. The meaning of the term has also shifted a bit, though, and I still see different definitions in different places (for example, the Wikipedia definition is not the one I would use). As a consequence, it is easy to argue that some like the thymus should not be considered immune privileged, so my umbrella suggestion would be to just avoid umbrella terms.


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plant dormancy in different locations
Say plant x has a dormancy period of y in location z, for instance in Sweden. We bring this plant to another location z', say France. Are there any results with respect to if/how the dormancy period would change? (I would assume such observations would be of interest to understand how plants adapt to/can cope with climate change.)

Not really clear what you want.  Do you mean dormancy of seeds, of bulbs &c, of the kinds of perennials that die back to the ground, or trees & shrubs that lose their leaves but keep the aboveground parts?  It's also a quite complex question.  There's more going on than just winter dormancy, e.g. plants of mediterranean-type climates that go dormant in the hot, dry summer.

My question was more in the direction took by the answer of @Jonathan Moore; that is, i was missing the notion of "vernalisation". With this, i found an article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4532801/ which answers even more my question.

It might depend on the signal that the seed uses to end dormancy. Some seeds require 'vernalisation', that is a prolonged period of low temperatures, for them to germinate successfully.  If they don't have the cold period, they don't germinate because they 'think' that they haven't had winter yet.
Dormancy can also depend on the conditions that the parent plant lived under, so it is quite possible that if two plants were grown in different environments, their seeds would have differences in dormancy. This study looked at that effect in the 'model plant' Arabidopsis thaliana:
Donohue K., Dorn L., Griffith C., Kim E., Aguilera A., Polisetty C. R., Schmitt J. Environmental and genetic influences on the germination of Arabidopsis thaliana in the field. Evolution. 2005;596(1):740–757.
This paper gives a good review of Seed Dormancy and Germination in Arabidopsis from a few years ago:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243337/#i1543-8120-70-1-1-b60


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Does consistency in minor allele frequency of a SNP across populations imply selection?
If a particular SNP has very similar MAF value across multiple largely non-overlapping populations, with the assumption of no gene flow between the populations over many generations, would that then suggest that there is a selective pressure that is keeping the MAF stable in these populations?
Are there methods to test that can parse out the drift and selection effects in such cases?
Also, does it matter in this context if the MAF value is high or low - since I believe a low MAF SNP is more likely to disappear than a high MAF one?
Thanks in advance for any insight.

Your are not saying but I would assume you are specifically interested in cases of balancing selection?

I would assume you would need a vast number of independent populations and/or small population sizes in order to be able to deduct from the constance of an allele frequency alone that balancing selection is at play.

Yes that was what I was meaning to, sorry for not being very clear...do you know of any literature or probabilistic methods that can deduce if balancing selection is at work versus random drift. Thanks for your answer.

No, I am afraid I don't know of any literature on the subject. I would tend to think though that with population genetic data only, it will be very hard to get a good signal of balancing selection but I might be wrong.


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How is AMP "recharged" to become ATP in a cell?
I understand that after the translation stage of ribosomal protein synthesis, tRNA molecules are floating in the cytoplasm without attached amino acids until they find the correct aminoacyl tRNA synthetase enzyme which revitalizes them.
However, in this process the enzyme takes an ATP molecule and returns an AMP (not ADP) molecule. It's been my understanding that an ATP's energy is normally harnessed via removing a single phosphate group and leaving an ADP molecule. Processes like respiration and photosynthesis deal with the conversion of ATP to ADP and vice versa. I understand that in removing the extra phosphate group to get an AMP more energy is released, but that also means that more energy has to be used to convert the AMP to ATP.
Does the cell convert the AMP to ADP, which will ultimately become ATP in respiration, or does the cell use some retrofitted respiration/metabolism to revitalize the AMP?
I would expect the first option but it would take energy (most likely from an ATP) and I would expect the amount of energy released from an ATP becoming an ADP to be different from the amount of energy released from an ADP becoming an AMP (so an ATP becoming an ADP would take more or less energy than would be required to make an AMP become an ADP, leading to inefficiencies). The other possibility (that I can see) is that the AMP is just used as a nucleotide in DNA and RNA, but I don't think that the numbers add up there. I've looked around but I can't find an answer.
So how do cells convert AMP to ATP? Also I was told that the ATP to ADP conversion is the general power-conversion. Is that not the case, or is this just some rare occurrence when AMPs are involved in power conversions?

Are you interested here in plant cells, animal cells, etc? Bare in mind for many cell types, ADP are largely converted to ATP by ATP-synthase, but AMP plays a crucial homeostatic roll, and coupled to adenylate kinase, helps to, accoring to this article, optimize the ATP-synthase process (I believe they're studying plant cells there).

I'd be interested to learn about AMP conversions in both plant AND animal cells, but I'll settle for whichever is more common (as in whichever one that uses AMP molecules more frequently).

Your statement about AMPs possibly being used in DNA/RNA synthesis is wrong, those are built with nucleotide triphosphates, including ATP, TTP, UTP, CTP, and GTP. Nucleic acid synthesis is similarish to your tRNA question because each triphosphate loses 2 phosphates when added to the growing DNA/RNA chain. If the chain is ever broken up, the nucleotides are released as monophosphates.

@user137 Nucleotides do, in fact, have only one phosphate group. Molecules like ATP and GTP have three. Nucleotides have ONE phosphate group, a ribose sugar, and a nitrogenous base

@jacob Nucleotide vs Nucleoside is just being pedantic. The point is that three phosphates go in, 2 get thrown out. See this image

@jacob It was an obvious typo, since "nucleotide triphosphates" would contain four phosphate groups.

AMP is first converted to ADP in the reaction
AMP + ATP $\leftrightarrow$ 2 ADP
catalyzed by adenylate kinase. So one phophate group is transfered from ATP to AMP, resulting in two ADP molecules. The ADP formed is then used to synthesize ATP as usual, by the mitochondrial ATP synthase or by the glycolysis enzymes.
For other nucleotides and deoxynucleotides, the monophosphate form NMP are usually phosphorylated to NDP using ATP, catalyzed by various kinases. For example, UMP and CMP is handled by the enzyme CMPK. Note that this is essentially the same type of reaction as adenylate kinase.
Regarding the energetics, the above reaction is only slightly favorable (at equal reactant concentrations) with $\Delta G=-2.6$ kJ/mol. In most cells, ATP concentration is much higher than ADP though, which helps drive the adenylate kinase reaction forward. See this site where you can investigate the energetics more closely.

Roland, where the ATP is found if it is not synthesized (оxidative phosphorylation needs ADP for synthesis of ATP)?

@AlexanderBestavashvili, I'm not sure I understand you question, but there is plenty of ADP, since most reactions that hydrolyze ATP produce ADP. The adenylate kinase reaction just takes care of the more rare case where AMP is produced instead of ADP.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Why don’t plant cells need centrioles?
I’ve just learned about cell division and I noted that plant cells don’t have centrioles but still undergo cell division. I’ve read a few documents about it and wondered why plant cells don't have centrioles.
How is it that plant cells can divide without centrioles?

Welcome to Biology.SE! It is expected that you will demonstrate that you have done some research on your own before asking questions here — a quick search turns up this: https://biology.stackexchange.com/questions/10210/how-do-plant-cell-divide-without-centrioles ——— Please also take the time to take the tour and then the help pages starting with How to Ask questions on this site. Thanks!


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Can you name this plant that likes shade on Asturias?

This was located in the Turón valley on Mieres, Asturias, Spain. Usually, I find this plant in shadowy, not too illuminated spots, although I'm not sure if that's important or simply coincidence. This picture is from yesterday 16th February 2019. The plant is lower than knee high, so let's say a maximum of 30cm tall maybe.

You have found a helleborus, possibly helleborus viridis.
https://en.m.wikipedia.org/wiki/Helleborus_viridis

Seeing that there's even a common name for it in Asturian (yerbunegru) I think you identified it perfectly :D Thank you


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Are all endocrine glands associated with common human feelings?
I was looking at endocrine glands and found it interesting that a few of them have some very understandable feelings/mentalities associated with them.  In particular:

Gonads: arousal/romance
Pancreas: hunger (glucose)
Adrenal glands: fight or flight
Pineal gland: sleepiness (melatonin)

Of course, there is a lot more complexity to how these glands work and what they do, but I find the notion of being able to empathize with a part of the body interesting.
As a counter-example, if something is wrong with my spleen, there may be feelings associated with that (ie pain), but they aren't so profound as things like hunger, fear, and arousal.
Anyways, my curiosity here is: do all endocrine glands have a feeling associated with them?
Here's the list of all glands:

Pituitary gland
Thyroid gland
Parathyroid glands
Adrenal glands
Pancreas
Gonads
Pineal gland

Also, I know this is a silly question, but please bear with me here.  It's piqued my interest, and I just want to fulfil some curiosity.

You may not be able to feel or be aware of the actions of all endocrine glands at the time they occur.
The parathyroid gland secretes parathormone, which affects calcium absorption in the intestine, kidneys and bones, phosphate excretion in the kidneys and vitamin D production in the kidneys. I'm not sure if one can feel these actions or its consequences.
The adrenal cortex secretes aldosterone, which maintains sodium and potassium blood levels, which is related to blood pressure and urine excretion. It also secretes cortisol, which affects glucose utilization, fat breakdown and inflammation and affects the actions of some other hormones, but within normal physiological range, you don't feel these effects. Cortisol is also known as a stress hormone, but its actions are much more subtle (on the level of metabolism) than those of adrenaline (heart rate, excitement). Saying that, cortisol secretion can be related to sleep and appetite. There is a lot of speculation how it might affect mood or "energy levels" (adrenal fatigue).
There are many gastrointestinal hormones (gastrin, secretin, cholecystokinin, ghrelin), some of which affect digestion, some peristalsis and some appetite and you may not be consciously aware of all of that.
Some pituitary gland hormones (ACTH, TSH, FSH, LH) stimulate the secretion of hormones from other glands (adrenal, thyroid, gonades) and some (growth hormone, ADH, oxytocin) act directly on organs - I don't think you can say that you can feel these effects.
Some hormones have effects on other hormones (cortisol > adrenaline ; thyroxine > growth hormone, etc.), so it may not always be possible to pinpoint which feeling is directly related to which hormone.
Common human feelings related to hormone secretion:

Excitement or stress response, including fast heart rate and breathing and anxiety: short term response: adrenaline; long-term response: cortisol
Appetite: ghrelin, leptin, adiponectin, cholecystokinin, insulin, glucagon-like peptide, gastrointestinal peptide...
Sexual drive: sex hormones, mainly testosterone and estradiol
Sleepiness: melatonin, cortisol
Depression: cortisol, sex hormones (mainly in women)

The point of this answer is to show that some of your feelings can be simply affected by hormones, which are note some ultimate forces, and that being aware of that can help you to control them to some extent.


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How do plant cell divide without centrioles?
Most plants do not have centrioles, so what organelle enables them to multiply?

There are many different ways to make a spindle in plant cells:

Mitotic spindles may be organized at centriolar centrosomes (only in final divisions of spermatogenesis), polar organizers (POs), plastid MTOCs, or nuclear envelope MTOCs (NE-MTOCs).

Of these, only the latter has been observed in angiosperms (flowering plants). For more info (and the source of the quote), see Brown & Lemmon, "The Pleiomorphic Plant MTOC: An Evolutionary Perspective"

Plant cells without centrioles build special vesicles from their Golgi apparatus which are important for cell division.
This website has a nice comparison of different modes of cell division. Look for "Cytokinesis by Phragmoplasts" to get to the relevant part. Phragmoplasts are not exactly a replacement for centrioles, but the whole process is a little different.

Spindle formation in plants is very different from most other eukaryotes owing to the fact that plant cells lack centrosomes or spindle pole bodies, which act as the microtubule organizing centers in animal cells. The evolutionary advantage that animal cells gain due to the presence of centrosomes is the ability to direct drastic changes in their shapes during mitosis. On the other hand, plant cells have a rigid cell wall that does not undergo any major changes in shape during mitosis; and the cell wall itself can organize many of the microtubules that form the spindle during mitosis.

Please add some references to your answer.

Animal cells under go cell division in two phases karyo-kinesis and cyto-kinesis.
During cell division (anaphase) the chromosomes are pulled away by structures called microtubule's which are formed by centrioles , just before this the centrioles line up on two opposite sides of the cell . in plant cells microtubules are made by the Golgi bodies. Animal cells are much evolved than plant cells that's why they have centrioles . Spindle formation is very much different in plant cells than in animal cells due to the absence of centrioles .

Welcome to Biology.SE! Please add some references to your answer.


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What makes synapses stay "fixed"?
What makes synapses not move or pre- and postsynaptic cells neither touch nor move away from each other? I mean the synaptic cleft is a gap between the pre- and postsynaptic cells that is about 20 nm wide (according to Wikipedia), so what makes it of that width? Are there some protein fibers anchored in both pre- and postsynaptic cells? Or do the glial cells keep them at that (often temporarily) fixed position? What prevents them from being displaced by the slightest movement of the body? I'm talking obviously about the chemical synapses.
Thanks in advance for the answer.

Synapses are held together by adhesion molecules, like cadherins and neuroligins/neurexins, so they aren't just loose adjacent membrane, they are securely anchored in place.
The adhesion molecules serve both a structural and regulatory role, being important for synapse formation and plasticity.
Missler, M., Südhof, T. C., & Biederer, T. (2012). Synaptic cell adhesion. Cold Spring Harbor perspectives in biology, 4(4), a005694.


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How to promote acorn maturation
I have acorns from an oak tree. They look like:

but I would like to speed up their maturation so they split and I can separate the caps:

How can I speed up this maturation process?

I am not sure but my instinct is to put them in a dry place with a lot of sun.

I would suggest putting them in the ground and watering them (Factors affecting acorn production and germination and early growth of seedlings and seedling sprouts).

Good idea, but in particular I'm not looking to grow a tree, rather to dismantle the acorn.

Sorry. Apparently I misunderstood you. It seems to me that you should leave them to dry (but that's just my feeling). Good luck...


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How does blood pressure substantially drop in the capillaries and arterioles?
Is this due to increased frictional resistance which decreases the velocity of the blood? You would think using Bernoulli's principle that the velocity of blood in the capillaries would increase due to the decrease in pressure but the inverse is true.

There are two main reasons why the pressure in the capillaries is lower than in the big arteries:

Arteries are elastic - they increase in diameter with every pulse, so the blood pressure is falling as the blood is moving along.
The total cross-sectional area of the capillaries is greater than the one of the big arteries.

Biology-pages.info

The pressure of arterial blood is largely dissipated when the blood
  enters the capillaries. Capillaries are tiny vessels with a diameter
  just about that of a red blood cell (7.5 µm). Although the diameter of
  a single capillary is quite small, the number of capillaries supplied
  by a single arteriole is so great that the total cross-sectional area
  available for the flow of blood is increased. Therefore, the pressure
  of the blood as it enters the capillaries decreases.


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Are All Taxonomic Groups Uniquely Named?
The Linnaean classification system classifies and groups organisms into taxonomic groups: Kingdom, Phylum, Class, etc. Obviously, a clade at any taxonomic level is uniquely determined by its classification at this level and all its parents in the hierarchy, e.g., Kingdom = Bacteria, Phylum = Firmicutes, Class = Clostridia uniquely identifies a group of bacteria. But is this group also uniquely identified by just Clostridia? Or are there situations where two Phylums might both contain Classes with the same name?
Since Genus & Species are typically used to identify organisms, I would assume that combinations of these at least are unique. As @Jam pointed out in the comments, Species alone is not enough. Note, however, that I am not asking about the binomial name for a species - I am asking about uniqueness among higher levels of aggregation, such as Class, Order, and Family.

The simple answer to your question is 'no' because many species share the name 'vulgaris'. But whether all genuses and classes are uniquely named, I'm not sure.

Possible duplicate of How many species can have the same scientific name? and What instances are there in which two species share the same binomial name?

Possible duplicate of What instances are there in which two species share the same binomial name?

Duplicate voters: note OP has now made explicit that the question is only about taxon rank higher than species.

There are quite a few biological homonyms (especially at the genus level, which apparently you aren't asking about).  At the family taxonomic level, the Interim Register of Marine and Nonmarine Genera (IRMNG) currently lists 100 family names which are used for two or more distinct taxa.

Are there any homonyms between taxa above family rank: classes, phyla, types?


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Do some birds really clean themselves using wet leaves?
While researching native shrubs to put in my garden for bird habitat, I read that some birds will take advantage of bushes to clean themselves by rubbing themselves against a wet leaf after rainfall (emphasis below is mine).

Water: Birds that sip nectar from the flowers on shrubs will enjoy the liquid refreshment, and larger shrub leaves will collect small amounts of water that different birds may sip. Birds may even rub against damp leaves for a quick bath.
  --The Spruce, "Shrubs for Birds"

I've been unable to find any reference to this from further search on the internet, though - the only cleaning strategies I've found written about are puddle bathing, dust bathing, and anting. Is this strategy of cleaning with wet leaves something that actually happens in nature, or just a product of a gardening website's imagination? Is there another process that could be misinterpreted by an observer here?
If this is real, I would love to read more about it, or even find a picture or video of the behavior.

Yes, birds do clean themselves using wet leaves. It is called leaf bathing. Mainly small birds do it but this behavior can be observed in big birds too.

Leaf bathing is the term used when birds make use of the water droplets accumulated on large leaves to bathe. The water in this case came from the rain but it may well come from dew, condensed fog or even from the garden sprinkler or water hose.
Leaf bathing was first reported by L.F. Baptista. In 1971 he observed a Rufous-crowned Sparrow (Aimophila ruficeps) bathing on leaves of an eucalyptus in Berkeley, California.
https://besgroup.org/2007/03/05/leaf-bathing/

Here is a video of an olive-backed sunbird having a leaf bath:
https://www.youtube.com/watch?v=23M6nsLNCFs
I've created a short animated gif from the video also:

Further sources:

Mass leaf bathing of sunbirds
https://besgroup.org/2008/02/25/mass-leaf-bathing-of-sunbirds/
Tomás, X., Senar, J. C., 2021. Leaf bathing in ring-necked parakeets Psittacula krameri. Arxius de Miscel·lània Zoològica, 19: 131-133, DOI: https://doi.org/10.32800/amz.2021.19.0131
Beat about the Bush: Birds
by Trevor Carnaby - Google Books

My god that's adorable.


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Balancing selection vs introgression?
Balancing selection can maintain polymorphisms in natural populations for extended periods of evolutionary time. However, in this paper, Dannemann et al. 2016 identify three archaic haplotypes in the modern human genome that are due to adaptive introgression. Why can we exclude that haplotypes III, IV and VII (the introgressed haplotypes) have remained in the human gene pool since the split between modern humans and Neanderthals because of balancing selection?

I'm closing this question because based on a discussion in the comments it seems that the premise of the question is a homework assignment that isn't reproduced here.

Balancing selection and positive selection are not mutually exclusive. Neither are balancing selection and negative selection. Sickle cell is a classic example where there is negative selection against the homozygote for the sickling mutation, and positive selection for the heterozygote. The result is that there both alleles are maintained in the population under balancing selection.

Thank you. I understand that both balancing and positive selection can occur together (along with introgression). In the paper, the authors present evidence for positive selection of the archaic haplotypes. However, I'm wondering if there is conclusive evidence to exclude balancing selection in this case? (The question comes from a homework assignment, so balancing selection is already presumed to be excluded...)

There is nothing in the paper about balancing selection being excluded. Are you saying that the only reason you think it's excluded is because a homework assignment is telling you this?  Also, you keep mentioning introgression along with selection--those two terms need not be related at all. Introgression in the absence of selective signatures is common.

Yes, the question assumes it's excluded which is why I'm wondering what evidence can be drawn from the paper for that? From what I understand, introgression and balancing selection can leave similar genomic signatures so it would be difficult to distinguish between the two of them.


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Do epigenetics determine the proteins a cell produces and therefore it's function?
I'm having trouble understanding what epigenetics is in a simple sense.
How I imagine it is that if we had 2 twins with identical DNA and we let them live we will see that they'll develop differently. Their DNA will stay the same (unless the DNA gains mutations, which could lead to cancer...) but their epigenetic tags will differ. These epigenetics tags determine the execution of parts of the DNA and the way the twins live their lives determine how the tags will be distributed. It's hard for me to find an example.
Another way I think of epigenetics is for example the cells in the muscles have a specific epigenetic tags to produce the specific proteins needed to create the muscle and the cells in the skin for example have different tags, produce different proteins which produce the skin.
Is my understanding of epigenetics anywhere close to the truth?

Short answer: Yes, epigenetics play a role in determining gene expression, therefore protein expression and function.
Lifestyle factors like diet, smoking, alcohol consumption, and stress can change one's epigenome. A historical example of this might be the Dutch Hunger Winter of 1944-45; there is evidence that after the parents' generation suffered during World War II, the children who were conceived during this time and exposed in utero to famine had different epigenetic marks than their siblings who were conceived not during the famine.
Epigenetic regulation is also essential for cell differentiation in vivo and in vitro. Embryonic stem cells undergo many changes to their epigenome in order to become mature cells. One interesting example for further reading is the transcription factor NeuroD1, which binds to targets in the DNA to cause widespread changes in gene expression that are specific to neurons, and commits cells to a neuronal fate. It doesn't bind to thousands of neuronal genes; instead, it causes a "ripple effect" thanks to epigenetic mechanisms.
Longer answer: Epigenetic marks are added to the genome for many reasons, including the two you just listed, and I think it is helpful to understand what happens at a molecular level in order to understand "why" we have them and to better visualize what the epigenetic marks ("tags") are. This might help you to think of better examples on your own.
DNA spends most of its time wrapped around proteins called histones. A complex of DNA and histones is called a nucleosome. DNA-in-nucleosomes is called chromatin. Chromatin can then either be "loose" (called euchromatin) or "compact" (called heterochromatin). There are more detailed ways to define how accessible chromatin is, but this is the basic idea. Intuitively, loose chromatin is more easily accessible and the genes there can be transcribed actively. Compact chromatin is less active.
The looseness of chromatin is determined by how closely the nucleosomes interact, which is controlled by the histones' molecular properties. Whether or not the histone proteins interact to make the chromatin compact, or repel each other to make the chromatin loose, depends on what modifications they possess. These modifications are added by histone-modifying enzymes.
Histone-modifying enzymes are regulated by transcription factors (i.e. during the process of differentiation) as well as signals generated by extrinsic factors (i.e. during the organism's lifetime). The balance of activating and silencing activity is what adds and removes these marks to give a cell its individual epigenome.
So, in simple terms, epigenetic marks determine how accessible different parts of the DNA are, and a whole lot of factors (like cell identity and lifestyle) can determine where those epigenetic marks are.

The question makes no mention of epigenetic marks. It is very clearly put — has two parts, neither of which mentions epigenetic marks, and neither of which you answer, although you say the answer is yes. It isn’t.

@David, although the answer uses "marks" and the question uses "tags", the two are both used for epigenetic modifications, I believe synonymously.

@mgkrebbs — You miss the point. The poster gives two examples of what he thinks epigenetics may mean. One, for which he states he knows no examples is dangerous anti-science. I will put this in an answer when I get home.

@David - I added some references to support the two examples. I still think that it's very hard for a beginner student to think of examples of epigenetics without having a physical picture of epigenetic modifications, which is why I chose to explain epigenetic marks (tags).


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Why does water stress lead to alkalinity of xylem sap in plants?
I was reading this book: Plant Physiology and Development, Sixth Edition by Lincoln Taiz, Eduardo Zeiger, Ian M. Møller, and Angus Murphy when this doubt came to my mind. Abscisic acid, the stress hormone, works to prevent water loss from a plant. Its mechanism of action requires the xylem sap of the plant to be alkaline. I can't figure out how water stress in the plant body causes alkalinisation of the xylem sap. The section in the book stated as follows:-

During the early stages of water stress,however, the pH of the xylem sap becomes more alkaline,increasing from about pH 6.3 to about pH 7.2.
  Stress-induced alkalinization of the apoplast favors formation of the dissociated form of abscisic acid, ABA–, which does not readily cross membranes. Hence, less ABA enters the mesophyll cells, and more reaches the guard cells via the transpiration stream.

I'd be grateful if anyone out there can help.

According to recent studies, drought stress does not consistently lead
to increases in the pH of xylem sap. One article which discusses
interspecies differences is Vit Gloser, et al., "The dynamics of
xylem sap pH under drought: a universal response in herbs?," Plant and
Soil 409, nos. 1-2 (2016): 259-272.
As to what may have prompted the textbook authors to assert this, see an
earlier article by two of the coauthors of the Gloser essay: Sally
Wilkinson and William J. Davies, "Xylem sap pH increase: a drought
signal received at the apoplastic face of the guard cell that involves
the suppression of saturable abscisic acid uptake by the epidermal
symplast," Plant Physiology 113 (1997): 559-573. Wilkinson and Davies
summarize an earlier study: "Hartung and Radin (1989) found that the pH
of xylem sap from water-stressed Phaseolus vulgaris roots increased
from control levels of 6.3 to 7.2." (560)

Welcome to Biology.SE! It would be very helpful if you could elaborate on your answer.  For example: How do changes in the cation/anion ratio affect the pH?  Also did you mean to say that lower nitrate uptake causes the cation/anion ratio to decrease? ——— You may also wish to take the time to go through the [tour] and the help pages starting with [Answer] questions effectively on this site. Thanks!

Pls elaborate. Don't just give references


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Can animals that rely heavily on sonar sense colour?
Apparently there're species around as rely heavily on sonar to sense the world around them.
E.g. Bat, Dolphin, Whale ...
The humans, and other terrestrial beings in a lighted world are capable of distinguishing colour in varying degrees of acuity. Is this ability to sense colour in our environment applicable to species (terrestrial, avian, and marine) that rely heavily on sonar?

Are you asking whether they can see color with their eyes, or whether they can detect the properties of an object that would reflect light in the "red" wavelength with reflected sound waves?

Any animal using sound cannot sense color though sonar directly, though these animals are not entirely blind and can probably see colors in the infrared we can't.

Even on the darkest night there is some light around and all bats use this. Old World fruit bats have colour vision, which is useful to them as they are often quite active in daytime, roosting on trees in exposed positions, rather than tucked away in dark crevices like most microbats, which can see only in black-and-white.

Dolphins have additional senses in addition to seeing they can sense electrical fields.  So if an animal has its eyes covered, they will seem to be able to do things you would not expect.  Its not the same as seeing the color though.
Such animals using sonar can additionally sense density and hardness as well as other material attributes which would cause the acoustic properties of the material as well as movement.

A hard-bodied insect produces a different quality of echo from one with a soft body, so bats can distinguish between some different groups of insects in this way. They can also determine the size of the object.

What's really interesting is that even human beings can experience this unusual sense.  Blind people have learned to echolocate by making clicks with their mouth, and there is a movement to teach this skill.
Anyone can try it.  In just an hour or two I was able to tell how close I was to a wall, whether the wall was concrete.  I couldn't play video games (2:20 on the link) or see colors though.

Dolphins, seals and other sea mammals have a monochromatic view, only a green photoreceptor.
http://brain.mpg.de/fileadmin/user_upload/images/Research/Research_Units/Peichl/2001_MPG_whales_and_seals_EN.pdf
Most mammals have bichromatic B.G vision:
The evolution of trichromatic color vision in primates occurred as the ancestors of modern monkeys, apes, and humans switched to diurnal (daytime) activity and began consuming fruits and leaves from flowering plants.
Wiki evolution of color vision (see top ref to main article)
Humans see R.G.B. and bats see G.B.UV.
Some birds, shrews, tenrecs and rats can use simpler echolocation. (wiki)
Birds R.G.B.UV have five types of cones including four single cones, which support tetrachromatic color vision and a double cone, which is thought to mediate achromatic motion perception.
Rats Grey-UV (Rattus norvegicus) have two classes of cone, one containing an ultraviolet (UV)-sensitive photopigment and the other housing a pigment maximally sensitive in the middle (M) wavelengths of the visible spectrum.
Reindeer can see UV.
UV vision isn't possible with big eyes:
...the eyes of smaller birds were more UV transparent than the eyes of larger birds. This means that small birds, such as songbirds, can take full advantage of ambient UV light, while larger birds, such as swifts and raptors, block a lot of the UV light from reaching the retina.
"If you want to be highly UV sensitive — be a UV specialist — you have to be small," Lind said. "For me, that is quite thrilling because it means that your perception of the world is dependent on your physical size."
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0006390

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How does water buffer a sudden drop in temperature?
A property of water is that it is slow to heat and cool. According to my biology book, some energy from an increase in temperature would spent breaking hydrogen bonds, so that temperature does not rise too fast - helping a cell to maintain homeostasis.
As far as I can tell, this answer does not explain how a drop in temperature would be slowed down by water in a cell. How does water slow down heat loss? Is it just because it is difficult for the heat that is already inside the cell to leave?

This question is about physics rather than biology or biochemistry.

I agree with Marta, this belongs on the Physics SE.

Speaking as a Physics.SE mod I'm sufficiently at sea to not know if this is a good question for our site. Ultimate Gobblement, could you clarify the question a bit?

Are you wanting more than the high specific heat capacity of water meaning that it is a good store of energy, which it releases to keep cooling objects warm (as your question suggests) as a result of thermodynamics?

I know this is probably more a physics question, but I think it is related to biology. If someone would like to move the question, then feel free to. I have edited it so hopefully my question makes more sense now.

I think the updated question is a much better fit for this site, as you put it in a biological context. I think Rory's answer is the right one, perhaps he could expand it into a full answer?

Biologists should still know about statistical thermodynamics.

From pure biophysical viewpoint the question
"Why does water buffer sudden temperature changes?" can be answered in the following way:
Water has relatively high specific heat capacity. This is the measure of the energy required to raise the temperature of one kilogram of a substance by one kelvin without a change of state occurring. "Relatively high" means that water can absorb more energy without noticeable (for the cell) increase in temperature.
Here are some heat capacity values from the above-linked Wikipedia article:

Animal (incl. human) tissue   3500 Jkg-1
  Water at 25 °C    liquid  4181.3 Jkg-1
  Methanol  liquid  2597 Jkg-1
  Ethanol       liquid  2440 Jkg-1
  Paraffin  wax solid   2500 Jkg-1
  Graphite  solid   710 Jkg-1

Water has relatively high thermal conductivity. This means that the absorbed heat is quickly distributed over the complete cell volume, leveling down the focal temperature increases in cell. Here are again some values for comparison:

Water 0.6 Wm-1K-1
  Wood 0.2  Wm-1K-1
  Paper 0.05  Wm-1K-1
  Glycerol 0.3 Wm-1K-1

The follow-up questions:
"Why does water have relatively high heat capacity?" and "Why does water have relatively high thermal conductances?" are not within the scope of this site. However, here exactly comes your explanation with hydrogen bonds in play (from Wikipedia):

Hydrogen-containing polar molecules like ethanol, ammonia, and water
  have powerful, intermolecular hydrogen bonds when in their liquid
  phase. These bonds provide another place where heat may be stored as
  potential energy of vibration, even at comparatively low temperatures.
  Hydrogen bonds account for the fact that liquid water stores nearly
  the theoretical limit of 3 R per mole of atoms, even at relatively low
  temperatures (i.e. near the freezing point of water).


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Do telomeres appear at just one end of the chromosome?
I have just studied DNA Replication for my Biology Class and I have this question that leaves me stuck, though I have tried to figure it out myself.
During telomere replication, I am aware Telomerase elongates the 3' end of the template strand on both molecules and then DNA repair Polymerase comes in to fill in the gap that could not be previously synthesised after the last primer.
After this is complete, we would have the T-loop formation and Shelterin complex arrangement to protect these ends and form what we know as telomeres. However, if we take both DNA molecules, this only happens at one end of each of them, right? As the other end would correspond to the leading strand.
So I am confused: do telomeres just appear at one end of the chromosome?

The term "leading strand" only makes sense in the context of a gene. Both strands can contain genes, it only depends on where is the promoter. I think this is where your confusion comes from. So, correcting your question you were probably looking for to the 5'->3' strand and the 3'->5' one. As both ends have both strands (one's 5'->3' is the other's 3'->5'), yes, telomeres appear at both ends.

Ah, okay, I see. In my class, we did not see any specificity as to replication being made about a gene but rather as a whole strand, so I just figured that for a 5'->3' strand, every left replication fork would give rise to a continuously synthesised strand and the right one to a lagging one.

This answer might help you (if you’re still interested in getting help 2 years later). You’re right that this has nothing to do with genes.

This is a great question!  The issue- the "paradox" of replication of linear chromosomes- of trying to filling in the unreplicated region (an overhanging 3' end) should technically be an issue only for one 3' end of each chromosome on any round of replication, as one new 3' end is produced by leading stand synthesis, and the other- the one with the issue- by lagging strand synthesis. However, both ends will have telomeres, they simply trade off being the end with the issue, in each round of replication.  Or you could say, in a single round of replication, one sister will have an issue at the right end end, and the other sister will have the issue at the left hand end.

Welcome. Can you add sources?


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How does Bernoulli’s Principle apply to the cardiovascular system?
Below are graphs which illustrate the cross-sectional area, velocity, and fluid pressure through each vascular segment of the cardiovascular system.

It makes sense that velocity and cross-sectional area should be inversely related graphically (by the equation of continuity, ($v_1A_1=v_2A_2$). However, Bernoulli’s principle states that where velocity is high, pressure is low, and vice versa. However, in the graph above, clearly pressure is decreasing as you move away from the aorta, regardless of velocity.
I can understand how the pressure in capillaries will be higher than those in venules, since a higher pressure in capillaries would accelerate the blood as it moves into the venules with a lesser total cross-sectional area. This agrees graphically, since, past the purple stripe, the pressure curve decreases as the velocity curve rises. Yet the mean arterial pressure in the aorta and arteries seems to violate the relationship between velocity and pressure stated in Bernoulli’s principle. What is there to make of this?
(Image taken from Campbell Biology, 10th edition)

Bernoulli's principle can be a little tricky when applied to the cardiovascular system, but it still holds true across the entire system. You mention a good point that the relationship doesn't seem quite right at the aorta or arteries, because of the constant fluctuation of pressure between systolic and diastolic without a significant change in diameter of the vessel. Remember that this is due to the pulsatile flow of blood from the heart, and has nothing to do with Bernoulli's principle. If the flow was constant (i.e. not pulsatile) then the pressure would be constant as the diameter of the vessels is constant. As the diameter of the vessels begins to decrease the velocity would increase to maintain a constant value.
As you mention, Bernoulli's principle describes how the product of area and velocity of flow must be constant across a system. When the total surface area of the system increases, the pressure decreases as well as flow. It is important to remember that even though the capillaries are so small and individually high resistance (which you would think according to Bernoulli's principle should increase the velocity), you are effectively adding an innumerable number of these very small resistors in parallel (not in series) and the resistance overall (and subsequently pressure + flow) decreases greatly.
When adding resistance in series the total resistance is additive and it adds up quickly! $$R_{Total} = R_1 + R_2 + R_3$$
While resistance in parallel adds the reciprocal of the resistor, meaning that as more resistors (or capillary pathways) are added the total resistance continues to decrease because of the following relationship: $$\frac{1}{R_{Total}} = \frac{1}{R_1}+\frac{1}{R_2}+\frac{1}{R_3}$$
The parallel resistance stuff was difficult for me to grasp when I was a student, because it never seemed to make sense in my mind that the resistance significantly decreased when you added all these small capillaries. One of my physiology professors described it well when he said, "Think of adding resistance in parallel, in the way that capillary beds and other vessels are in the cardiovascular system, like giving the blood another place to go." If the blood has more places that it can go, then it's easier to see why resistance falls so much when you add a bunch of extra places for the blood to flow.

I think there are several things that keep Bernoulli's principle from being straightforwardly applied.
First, Bernoulli's principle would help us calculate the pressure exerted by the blood on the walls of the vessels, but that's not what blood pressure measures. Blood pressure measures the amount of force that has to be applied to stop the blood from flowing forward. There's some relationship between the two, but it's not clean.
Second, the branching makes the surface area calculations different from a single pipe. The arteries have more cross-sectional area than the aorta, but they have have much, much more surface area-- way more of a difference than a single pipe with those cross-sectional characteristics would have.
So Bernoulli's principle does mean that blood is exerting more pressure on the surface of the arteries and arterioles than it is in the aorta. However, pressure is force per unit area, and there's much more area in the smaller vessels, so the pressure in any single vessel is less.

I love this question, and there is a number of things to unpack.
Exactly where we are measuring a pressure in that circut matters. We usually measure a persons BP in the brachial artery, so relatvely on the left side of your picture.
Here, we can consider the pressure to be part of a simple circut, where Pressure = Resistance * Flow (ohms law).
Vasoconstriction of artieroles further downstream could be considered to be increasing resistance. This results in an increase in pressure at the level of the arteries and specifically, where we measure it at the brachial artery.
(As a side note: it doesnt overly matter at this level that the distal system is in parallel. For simplicity, vasoconstriction will still increase the overall resistance. In a parallel system, increasing all or most of the resistors still increases the overall circuit resistance)
==========================================================
If we were to look at what is happening in the microvasculature, its a very very different kettle of fish, and much more akin to what you are describing with Bernoulli's principle.
In areas subject to vasoconstriction, there is indeed a decrease in pressure. This means there is less perfusion at that area (due to a decrease in hydrostatic pressure, see starling forces).
In areas not subject to vasoconstriction, there is a relative increase in pressure and therefore an increase in perfusion.
This about why this matters - We want to keep perfusion high in places that need blood (the brain, the kidneys), so they will stay relatively dilated. Conversly, if we dont need to perfuse our muscles, we can direct blood away from them and perfuse other organs preferentially by constricting their blood vessels.
Its probably worth noting as well - the resistance happens PRIOR to the capillaries. Capillaries dont change size. The artieroles and meta-arterioles do but the pressure before and after them does change and the pressure will be lower in areas that have undergone constriction.
To make matters more complicated however (read on at your peril);
If we also apply Ohms law at the level of the microvasculature and we consider this to be a parallel circuit, consider that increasing resistance will also lead to a decrease in flow. This is "shunting", where blood will flow preferentially to areas of less resistance. This extra flow 'would' (with an ideal fluid and non-compliant vessel), increase flow and decrease pressure. However, blood does not behave like an ideal fluid, and its viscosity prevents its speed from increasing as you'd expect. Moreover, the blood vessels tend to expand with the increased blood volume, increasing the radius of the vessel which significnatly decreases speed and overall actually probably increases its pressure (since radius is SUPER important in determining speed).
NB: This is STILL a huge oversimplification of a complex physics system - we havnt even touched on the effect of gravity and columns of water (is the perfusion pressure in our feet HUGE??!)
Happy learning!


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Identification of UK insect

We found this in our UK garden! Any ideas? Not sure if it had/has wings.
It has a segmented tail and 6 legs. It’s about 2 inches/ 8cm long.

It would be helpful to include more information about exactly where in the UK you found this and what kind of habitat.

That;s the last stage of the dragonfly in the pond, where it eats even tadpoles probably. It climbs out and emerges as a dragonfly, waits for it's wings to dry and flies away.

If you look at reeds and grass next to ponds at this time of year, you are bond to see many of those.

That looks like the cast off outer layer of a dragon fly nymph§:

The following resources may be helpful to get a more precise identification:
https://www.fba.org.uk/sites/default/files/EA_specid/ea_specid_mod_8.pdf
https://british-dragonflies.org.uk/odonata/species-and-identification/

§Note: As pointed out by Arthur J. Frost this is actually the exoskeleton left behind when a dragonfly nymph molted and became an adult.

More properly, the OP is what's left of a dragonfly nymph; the adult had emerged and flown off some time prior.

indeed -Exuvieae of a Anisopera dragonfly.
https://en.wikipedia.org/wiki/Exuviae


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Why are veins not blocked by plaques?
In my textbook, it is written that atheromatous plaques block the artery. This leads to heart attack and and heart failure. But my question is why do the plaques only block arteries and not the veins? Do the plaques also block the veins?

Atherosclerosis can develop in high pressure systems, such as arteries, and not in low pressure systems, such as veins. It is high blood pressure that can damage the lining of the blood vessel and initiate the process of atherosclerosis.
BUT, atherosclerosis can develop in veins that have been used as grafts instead of arteries, for example, in a coronary artery bypass surgery.
Springer: Atherosclerosis:

In this regard, we may note that atherosclerotic lesions do not
  develop in the veins in their normal environment of low pressure and
  high flow, but that the lesions do develop when the veins are used as
  arterial bypass grafts where they are subjected to high pressure.
  Similarly, atherosclerotic lesions develop in the pulmonary arteries
  only in pulmonary hypertension.


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What is the number of DNA strands per cell?
I wonder if each cell possess only one strand of DNA which according to my book is more than "7 feet" long(if uncoiled), then why does human has 46 chromosomes which are actually coiled chromatin (DNA wrapped around histone proteins)? Does DNA break into parts and form 46 chromosomes during cell division (I am just guessing I am not sure about it)?

I think you are misusing the term "strand". "filament" instead? Or perhaps, you have the "chromatin string" in mind? Can you clarify it in your question, please?

I am referring to DNA molecule (entire chain of polypnucleotide) or you can say how many chains of deoxy ribonucleic acid are found in each cell?

Referring to this picture https://en.wikipedia.org/wiki/DNA#/media/File:Lambda_repressor_1LMB.png the DNA molecule is composed of the red strand and the blue strand.  A chromosome is composed of one DNA molecule or two DNA strands.

So that means if one chromosome is composed of one DNA molecule and there are 46 chromosomes therefore 46 DNA molecules are present in each DNA. Right?

Yes, in each diploid human cell there are 46 molecules of DNA

I agree with this formula , because each Chromtid contain only one DNA then 1 chromosome contains 2 DNA it means that 46 chromosome contains 92 DNA..... Then what about MMitochondria which has its own DNA

Put it this way according to my understanding. Every human cell has 23 pairs of chromosomes and every pair contains 2 seperate DNA molecules. That means every human cell contains 2 X 23 = 46 separate molecules. So human genome means actually decoding 46 DNA molecules. That's all

Human cells contain 23 pairs of chromosomes (46 chromosomes in total).
Each chromosome is formed by 2 strands of DNA tied by hydrogen bonds to each other making the classic  DNA double helix (double-stranded DNA). So, in total there are 46*2=92 strands of DNA in each diploid human cell! Gametes contain half of the chromosomes, so half of the strands as well.

Ah yeah, if you consider each plus and minus as a strand then the number doubles, good point!

@JoeHealey — although the OP probably was misusing strand, and his major concern was how many copies of each dsDNA chromosome there were.

Each chromosome is present twice in every cell (excluding sperm and eggs, where only one of each is acquired in meiosis). So yes, that is 46 'strands' of DNA wrapped around histones as you said.
During mitosis each chromatid is replicated, and then in anaphase the sister chromatids are separated in to each daughter cell.
Any basic high school/university text book will have a good diagram of this.

So you mean human cell have 46 DNA strands which are coiled to form chromosomes?

Yes exactly (with the exception of the gametes as I mentioned, which are haploid rather than diploid).


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Identification of store-bought succulent plant
I bought this succulent in the Bronx Botanical Garden Shop, but it was unlabeled. On the photo it is about 4" high:

Can anyone help identify this? Could this be Echeveria haagai? It's indoors in NYC.

Please provide your location as well as where you obtained the specimen. Thank you.

The only reason I have any clue as to what this could be is because I have one that looks exactly like it and, in a stroke of sheer genius, I wrote the name on the bottom of the pot. I think it is some member of x Pachyveria, which are intergeneric hybrids of Pachyphytum and Echeveria. Because there are so many, determining the exact cultivar may prove difficult. Mine is "Blue Pearl" and it looked very similar until it's untimely demise.
You can check out this website to see some different varieties. Actually, some of the Pachyphytum look pretty close too.
Compare w/ x Pachyveria "Cheyenne" (source):

and x Pachyveria "Little Jewel" (source):


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How does vasoconstriction increase the pressure of blood?
Is the increase of pressure due to the decrease in volume? Wouldn't the decrease in volume push the components of blood closer to one another resulting in an increase of repulsive forces, thus increasing pressure? Or is the increase in pressure due to the heart pumping the blood with more force in order to maintain blood flow?

Because pressure is inversely proportional to area. If you consider a pipe, if you squeeze it's tip to decrease it's area you'll observe that the velocity of water flow becomes high due to high pressure. Same is with blood in veins.


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How to confirm secondary structure formation of Precursor miRNA on gel?
I want to fold precursor-miRNA into its secondary structure and then confirm it on gel. At first, I heat it in annealing buffer at 95°C for 5 minutes and cool down slowly. Then I run it on gel but the samples are at same position as the original dilution.

What kind of gel are you using? pre-miRNA will mostly from hairpin loops (I guess), which don't change the overall size of the RNA by much (it's still linear, now just a bit 'shorter' but therefore 'wider'). I'd guess you need a relatively high percentage gel (native and probably better poly-acrylamide), with custom markers for your size-range)

Your question looks incomplete. For e.g. you haven't mentioned how many minutes at 95°C. Please [edit] your question to all necessary details. I advise that you provide the full protocol that you are using.

My gel is 18 % polyacrylamide ( 40% acrylamide; 1M Tris, 1M Hepes, 1M EDTA, 1M MgCl2, TEMED and APS) in 1X Hepes (containing 1M Tris, 1 mMEDTA, 30mM MgCl2)

 Disclaimer: Although I have attempted northern blots for miRNA, I haven't actually done the kind of experiment you are talking about.
First of all you need controls.

A negative control: a same length RNA that will not fold (you can introduce some mutations in your pre-miRNA sequence to disrupt the base pairing). You can use the miRNA secondary structure prediction tools for rationally designing such controls.
A positive control: perhaps a folded pre-miRNA that is crosslinked. Frankly, I haven't come across anyone using such crosslinking agents to study RNA secondary structure. I had however, seen some old papers on this topic (Wagner and Garrett, 1978, Rabin and Crothers, 1979). You may also try some conditions (salt concentrations etc) under which the RNA will fold (studied using biophysical assays).

Now, you cannot run agarose gels. You would need long polyacrylamide gels ~15%. You also need to use the right buffers. 0.5-1x TBE supposedly works. You may want to run your sample in two conditions: denaturing (with 8M urea) or non-denaturing. You can refer to this protocol (Petrov et al. 2013).
Your positive control should migrate faster than the negative control. If your RNA is folded (fully or partially) it should migrate between the positive and negative controls in the non-denaturing gel. In the denaturing gel, your RNA should migrate at the same level as the negative control. Positive control (if it works) should not be affected by urea.
Also, the gel heats up during electrophoresis which in turn can dentature RNA. You may want to run the non-denaturing gel in the cold room.
Having said all this, I would advise that instead of putting in so much effort in gel based assay you can use more sensitive equipment to study RNA folding. There are many biophysical studies on in vitro RNA folding. You can check them out.