text:
How does sleep prevent our eyes from drying out?
If we don't sleep for about 16 hours, our eyes start to get dry, and no amount of eye drops helps. You use eye drops and then you're dry 10 minutes later.
However, after you've slept for 8 hours, your eyes can go another 16 or so hours without drying out.
What specifically happens to our eyes during sleep that prevents them from drying out in the next 16 hours after sleep?
Are there any research papers explaining the mechanics of all this?
The reason I am asking about this is in order to understand whether there are any connections between nasal and eye moisturization.
There's a condition called empty nose syndrome, in which people with reduced nasal turbinates suffer from a range of symptoms and a lot of them have to do with their nose getting dry.
Here's a CT scan of a person suffering from empty nose syndrome in one nostril. As you can see, one of their turbinates has been reduced, and the other one looks normal.

There's something called "the nasal cycle", it's a phenomenon where turbinates swell up on one side at a time in order to "rest", according to wikipedia. Here's a picture illustrating the nasal cycle:

As you can see from the picture, one nostril of this person is mostly closed, due to cavernous tissue being swollen. It is not a disease, it is actually how our nose normally works.
Of course, if you have reduced nasal turbinates, like in the first picture, it is impossible to properly close the nasal airway and expect it to "rest", so that it can start producing moisture again.
Does that mean that our nasal turbinates work in the same way as our eyes do? They have to be closed for a while in order to properly produce moisture?
As I've mentioned before, when your eyes are dry, you can moisturize them, and then they're dry 10 minutes later... It seems to be the same with empty nose syndrome patients. It seems to me that in order to restore normal moisture in the nose we need to have it closed for several hours. I think it is so, but I'd like to first find out why our eyes need to be closed in order to rest. So, I want to find the parallels between nasal and eye moisturization.

When we don't sleep we force our eyes open, blinking less to stay awake and focused. Less blinking means less eye hydration. I've never heard about what you say, can you provide any references to learn about that 16 hours awake limit?

@MarioZ I'm using rough estimates of my own findings. I only mention it because there are 24 hours in a day. Normal sleep should be about 8 hours, that means that we stay awake for 16.

Regarding our eyes getting dry at the end of the day, when we're tired, I think it's common. You can google it. If people don't sleep much, for example, their eyes are red...


text:
In the lysogenic cycle, does the provirus split from the cell's main genetic material for replication?
In a diagram of the lysogenic cycle sent by my instructor in a video, it shows the provirus splitting from the cell's main DNA when the dormancy period ends and the viral DNA is "activated". Is this how it happens, or was he just trying to illustrate the activation?
I guess a better way of phrasing this would be, is the viral DNA replicated as part of the cell's normal DNA, or is it replicated separately?
Thanks!
evamvid

When the virus is integrated into the hosts genome (and becomes a provirus) it is replicated with the cell genome, since it is now part of it. When the provirus gets activated (this happens by changes in the host's environmental conditions or health), it will get transcribed.
This is followed by the translation of the viral proteins which then leads to a cell which exclusively produces viruses until its resources are exhausted and the cell gets destroyed.

source: Stack Exchange

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

sort: votes


text:
Why did eukaryotic cells develop?
If eukaryotic cells can survive in extreme conditions, then why are their still prokaryotic organisms?

This is essentially the same as another question that was just submitted - have you tried looking at some textbooks?

The question suggests that you might want to have a look at Understanding Evolution (UC Berkeley), a free online introductory course to evolutionary biology.

I am not quite sure I understand the relationship between the title and the content of the post. Also, I suppose you meant "evolved" rather than "developed".

Are you thinking that eukaryotes are so competitive that it seems weird to you that procaryotes would not be outcompeted and get extinct. Do I understand you correctly?

It is like asking if humans are so advanced, then why do gorillas exist. Basically, all lifeforms are different survival strategies and none is "better" than the other (whatever exists is good enough for this environment). Please go through the website that Remi mentioned. It explains the evolution basics nicely and in easy words which even a high-schooler can understand. If you have specific doubts related to evolution then please feel free to ask (but make an effort from your side before asking others). I let your other question be but I have to put this on hold.

As far as I understand your question, the "development" of eukaryotic cells can be linked to the endosymbiotic theory Symbiogenesis.
This diagram only depicts a possible trajectory of evolution which is still unknown.

A cell that respired anaerobically took in a bacterium that respired aerobically, supplying both itself and the larger cell with energy in the form ATP. This created a competitive advantage for the larger cell because aerobic respiration is known to be more efficient than anaerobic respiration. Unhurriedly, the aerobic bacteria evolved into mitochondria and the larger cell into a heterotrophic eukaryote.
A heterotrophic cell took in a smaller photosynthetic bacterium, which supplied it with organic compounds, thus making it an autotroph. The photosynthetic prokaryote evolved into chloroplasts and the larger cell into photosynthetic eukaryotes.

Do we know which aerobic bacteria evolved into mitochondria? Do they still exist?

@CountIblis Ancestors of mitochondria belong the the group of α-proteobacteria. Many free-living bacteria of this clade still exist.

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


text:
Can soap kill cockroaches and/or ants? If so, how?
Is it possible to use dishwashing soap as an alternative insecticide? How would that and what are the components of the dishwashing soap that would kill the insect?

please read the help pages before posting questions

I'm not completely confident that the aforementioned post is a duplicate, because the question explicitly asks "Why do cockroaches burst from soapy water?" While this question explicitly asks "Can soap kill cockroaches and/or ants?"
The short answer to your question is yes.
According to this website:

The soapy water kills [cockroaches] by forming a thin film over the
  roach's breathing pores that stays in place due to surface tension,
  causing the roach to suffocate.

Ants are killed in a similar manner (see this archived Reddit post).
For a more scientific read, check out this paper: Behavioral Responses and Mortality in German Cockroaches (Blattodea: Blattellidae) After Exposure to Dishwashing Liquid.


text:
Is a bone marrow transplant limited by sex?
Can a female patient get transplanted with bone marrow of a male donor and vice versa?

Well, I guess it's possible because graft rejection/acceptance is based on MHC/hla which are not dependent on sex.

Short answer: Yes. Because in almost all cases of organ transplant, the organ recipient will be administered immunosuppressive drugs.
There is some literature on the effect of sex on the outcomes. I have included two hints here.
from: http://www.nature.com/bmt/journal/v35/n6/full/1704861a.html
The impact of the donor gender on outcome in HLA-identical sibling donor hematopoietic stem cell transplantation for multiple myeloma was studied in a retrospective registry study of 1312 patients (476 male to male (M → M); 334 female to male (F → M); 258 male to female (M → F); 244 female to female (F → F) reported to the European Group for Blood and Marrow Transplantation (EBMT). The best overall survival (OS) from the time of transplantation was found in F → F (median 41 months) with no significant difference between other groups (median 25 months in M → M, 18 months in F → M, 19 months in M → F) despite a significantly higher nonrelapse mortality in F → M. This was due to a significantly lower relapse rate (REL) in F → M compared to all other groups. Before 1994, OS was poorer in F → M than in M → M, which improved to similarity from 1994 onwards (median 29 months in M → M and 25 months in F → M). The reduced REL contributed to this improvement in F → M indicting a sex-specific graft vs myeloma effect. Therefore, a female donor is as good as a male one for male patients, while for female patients gender disparity is a negative factor for outcome.
from: https://www.broadinstitute.org/news/1386
"It's been clear for some time that bone marrow transplants involving a female donor and a male patient pose a higher risk of GVHD," said Bradner. "This ‘sex mismatch' arises from genes that are carried on the male-specific Y chromosome and are therefore present in males but not in females..."

Anyone can be a donor ir recipient in hla markers are same or a close match. A female donor over 45 who has had 2 or more kids is the worst donor choice. This is because when a woman is pregnant the blood cells get good at attacking foreign blood from the baby. When the blood is given to the recipient there will be higher likelihood of gvh bc the blood will attack the host. By bone marrow, it’s really stem cells, baby blood cells. Once transplanted they replicate and are the new blood and immune system. My donor was my brother. 15+ years ago.

Thank you for your contribution.  It could be improved by adding a reference to a source for the donor pregnancy-history effect.


text:
Does alpha-amylase from different species have different *optimal* conditions?
Do the optimal conditions for the enzyme isoforms differ between species? Specifically, do the optimal pH and temperature for alpha-amylase differ for that enzyme produced by B. lichiniformis and A. orzyae.

They may differ as different organisms have evolved to live in different environments.


text:
Why are published chromosome counts for polyploids often incorrect by an integer multiplication factor of the original diploid like count?
Why are published chromosome counts (done using techniques such as root smashes) for polyploidy flowering plants often incorrect by a multiplication factor of 2 or 3 from the original diploid like count?
When published chromosome counts for some polyploidy orchid and rhododendron species were updated such counts showed a multiplication of the original more diploid like count rather than a incremental refinement to a slightly more accurate count already in the polyploidy range.
See Ploidy Orchids
In rhododendron multiple counts of 26 chromosomes for R. austrinum, atlanticum, and luteum have been updated indicating a number of chromosomes for these three species is closer to 52 chromosomes.
Is there something about the way a polyploidy flowering plant species undergoes meiosis or mitosis that causes such miscounting to be the chromosome count for closely related diploids?

Your questions do not make sense. Please provide specific examples, i.e. In species x, which chromosomes in that species, etc. The answers will be different based on the organism. Also please use quantifiable terms as a lot and a little are completely subjective. Getting an additional copy of even a part of a chromosome in a human can be lethal during development, others can survive, but lead to dosage dependent conditions. In plants, they can likely sustain polyploidy, but there are probably examples that would be lethal as well.

Also you could provide links to the studies that you are referring to that generated your questions in the first place. If these are unpublished findings then providing the relevant data for others to evaluate the questions would be productive.

@AMR The question now is specific to flowering plants such as orchids and rhododendron.

The question now makes sense, unfortunately I now very little about plant genetics, other than green wrinkled peas and purple or white flowers, etc... Hope someone with knowledge on the subject gets back to you.... My intuition would say however, in your example of 26 to 52, than the plant is completing S phase of mitosis and then stopping, or the cells are multinucleated, sort of like human muscle cells, but again, that is strictly speculation and not based on a knowledge of the subject of the question.


text:
What's the point of glycolysis in fermentation?
In order to initiate glycolysis, 2 ATP are necessary. In the glycolytic process, you generate an additional 4 ATP, which results in a net gain of 2 ATP.
If you don't undergo glycolysis, however, then you have an extra 2 ATP not being used. If you do glycolysis, you still got only 2 ATP. Am I missing something here?

replace "ATP" with "money" and you have a financial system - they do plenty well :)

Turning 2 ATP into 4 ATP isn't good?

you said that glycolysis generates net 2 ATP. That means 2 ATP in excess of what you started with. Plus @Chinmay and Satwik's answers

Suppose the cellular pool has $x$ATP before starting glycolysis. In the initial phosphorylation steps, we use up two ATP to get the total tally at $(x-2)$ATP. The following steps yields $4$ ATP which brings the final total to $(x+2)$ATP.
Assuming the cell is performing fermentation, the two additional $NADH$ formed will not be contributing to any ATP gain. And hence we earn a total of $2$ ATP in excess of the already existing amount.

Actually, the NADH contributes to ATP gain in many fermentative systems.

@ChinmayKanchi You might be correct. But I guess the OP's concern is limited to cases where substrate base phosphorylation is the only source of ATP.

Remember that glycolysis yields 2 NADH as well as 2 net ATP. This NADH can be used to a terminal electron acceptor to produce an end product with a net gain of ATP. End-products of fermentation can include lactate, acetate, butyrate, propionate and ethanol, all of which generate different amounts of additional ATP.
The exact pathways involved vary according to the organism, but anywhere between 1 (or even 0.5) and 4 additional ATPs can be generated, even without the involvement of oxygen. In the case of aerobic respiration of course, the NADH feeds into the electron transport chain and yields ATP.
EDIT: It's perhaps worth noting that the 2 ATP is gained. See @SatwikPasani's answer for the math.


text:
How are non-glucose sugars metabolized in the body?
In my biology book's section on disaccharide metabolism and glycolysis, it states that sugars other than glucose must be acted upon to enter glycolysis. Let's take sucrose as an example. Sucrose is hydrolyzed in the small intestine by sucrase. The resulting fructose and glucose are absorbed and transported to the liver via the portal vein. My question concerns the fate of fructose.
To undergo glycolysis, the book states that fructose is converted into either fructose-6-phosphate (F6P) or fructose-1-phosphate (F1P). Let's say it is converted to F1P. Aldolase splits this into dihydroxyacetone phosphate and D-glyceraldehyde. Triose kinase then converts D-glyceraldehyde to glyceraldehyde-3-phosphate, a glycolytic intermediate. Where is this occurring in the body? Are we still in the liver? I can't imagine that all the fructose we consume is undergoing glycolysis in the liver. To leave the liver as a sugar, it would have had to been converted to glucose, right?
In classes I've taken, I've been told that sugars that enter the liver are pretty much all converted to glucose. Once they are converted to glucose, they can be distributed to the rest of the body, stored as glycogen, etc. If we are going straight from fructose to F1P to a glycolytic intermediate, we couldn't have left the liver. How is such a transformation even useful? Anyone care to shed some light on this?

Where is this occurring in the body?

Almost totally in the liver.

To leave the liver as a sugar, it would have had to been converted to glucose, right?

Correct, but it's not a direct conversion.
Fructose is metabolized almost completely in the liver in humans, and is directed toward replenishment of liver glycogen and triglyceride synthesis...
...Increased concentrations of DHAP and glyceraldehyde-3-phosphate in the liver drive the gluconeogenic pathway toward glucose-6-phosphate, glucose-1-phosphate and glycogen formation. It appears that fructose is a better substrate for glycogen synthesis than glucose and that glycogen replenishment takes precedence over triglyceride formation. Once liver glycogen is replenished, the intermediates of fructose metabolism are primarily directed toward triglyceride synthesis.
So, Fructose is almost entirely made into something else first, and then that something (Glycogen or the Glycerol from triglycerides) gets broken down into Glucose or an intermediate.
Fructose stays in the liver because Fructokinase has a pretty low Km (0.5 mM) compared to Glucokinase (12mM) for Fructose, so almost all of the Fructose that enters the liver is phosphorylated into F1P - which cannot leave.


text:
Biosafety Level 1 (BSL-1) surrogate viruses that show greatest similarity to SARS-CoV-2
I would like to know if there are any viruses that show high similarity to SARS-CoV-2 (particularly in terms of structure) that are very safe to use (i.e., classified as BSL-1).
For example, an avian coronavirus would be good to use but it is BSL-2. Ideally, I would need BSL-1.
Ideally if there were any corona type viruses that were BSL-1 or those which have distinguishing features with proteins emanating from an outer lipid membrane similar to SARS-CoV-2 .
I am particularly interested in finding a virus with similarity to the protruding S1 spike in SARS-CoV-2 (see image).

Can you be more specific about 'structure' and 'similarity'. Do you mean similarity in RNA sequence, protein sequence, function, pathogenicity etc?

Good question! Thanks for your comment. I mean in terms of its most outer appearance/structure. e.g., anything with a similar protruding protein stricture on its outer membrane.

I added an image too to illustrate that I am interested mainly in any similar viruses that have similar outer protein structures.

To be further specific. I'm thinking in terms of how it would interact with a (generic) surface. So any virus that is classified as BSL-1 that is similarly covered in protruding protein and/or would interact with a given surface (be that a window, door or even a host cell) in a similar manner.

What you're looking for is a suitable surrogate. For H1N1 the surrogate used was MS2 coliphage. I recommend going onto https://viralzone.expasy.org/294 and looking at the coronaviridae family. Then find viruses in this family and go onto the atcc website and see what classification BSL a certain strain of the virus is (be careful not to confuse it with genomic RNA from the virus). Adenoviruses with spike cloned onto them (what astra zeneca is doing) could also be an option, but last I checked this was only BSL2. Maybe Orthomyxoviridae (family of influenza) might have some genetically modified.

Thanks for this info! Very useful. I am not a biologist by training. Navigating this space effectively is a little difficult to me as much of the terminology is alien to me. I'm suprised a suitable surrogate has not already been identified. In my case, I'm after a safe and suitable surrogate which is representative of the coronaviridae family in general based on its outer protein conformation. Any other suggestions?

Some specific examples would be awesome if anyone can provide some? even if you are not very sure. it would be a big help. thanks

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


text:
Is Valerian extract a diuretic or an antidiuretic?
I am trying to determine if valepotriates (valerian extract) is a diuretic or an antidiuretic. Some individuals take valerian as an herbal supplement for anxiety disorders. Some individuals claim that valerian extract can act as a diuretic, while others claim that it is an anti-diuretic. I am trying to determine which it is - diuretic or antidiuretic?

I couldn't find credible sources on the effect of valerian on the kidneys. One case report mentions hyponatrema (due to excessive diuresis), but relates it to excessive water consumption instead.

where have you seen these claims that is has diuretic or anti-diuretic properties?

Without a source, this question is unclear.

There is one study that I can find that has been cited in the medical literature that examines individuals taking valerian extract for generalized anxiety disorder. In this paper, there do not appear to be any claims that valerian has any diuretic or anti-diuretic properties. However, that's not to say that those properties don't exist. Additionally, there is no indication that the extract is associated with hyponatremia or hypernatremia, which are two other signs of disorders affecting salt/water balance. Overall, it sounds like if there is a diuretic or anti-diuretic effect of valerian, it is not well-described (yet).

The Natural Medicines Database monograph for Valerian includes a pooled adverse effects analysis of more than 20 clinical trials with Valerian for various indications.  No diuretic effects were identified in any trials.
Natural Medicines Database monographs are available by subscription only and are considered by the vast majority of healthcare professionals to be the gold-standard source for any natural supplement, herbal or food supplement evidence-based information.  www.naturaldatabase.com
Professional Opinion (Pharmacist):
The specific mechanism of Valerian is unknown.  Valerian is possibly effective for insomnia and it is suggested that it is also helpful for anxiety, depression and stress (insufficient reliable evidence to rate).  A large number of pharmaceutical products that have similar uses (tri-cyclic antidepressants, mirtazapine, trazodone) can cause urinary retention, sedation and dry mouth by anticholinergic effects.  If I had to guess whether it would have diuretic or antidiuretic properties, I would go with antidiuretic effects secondary to anticholinergic effects.

Welcome to BiologySE - thanks for your answer. It would definitely strengthen your answer if you could add some links to the database that you mention so other users can read about your answer. Also, you may want to check out the help center for how to write a good answer for some additional pointers - it will help you gain more reputation points in the community. Link: http://biology.stackexchange.com/help


text:
What is the circulation that allows for nutrient absorption and excrete of metabolic wastes in humans?
Pulmonary veins carry oxygenated blood from lungs to heart, while pulmonary arteries carry deoxygenated/CO2 rich blood from heart to lungs. On the other hand, systemic arteries carry oxygen-rich blood from the heart to other parts of the body and likewise systemic veins carry CO2-rich blood from all the parts of body back to the heart and lungs. This makes sense to me, since oxygen and CO2 are used and generated in metabolic processes, respectively, and need to be transported to and from the lungs/systemic tissues continuously.
However, what I do not quite understand is what blood vessel carry absorbed nutrients from the intestine to other parts of body? Also, what blood vessels carry other metabolic wastes from the peripheral cells to the kidney for excretion?
Any reference/link to basic working of blood circulation would be helpful.

If you do a bit of research into "mesenteric circulation" (choose one with the stomach) and "renal circulation" on Google images, it should give you all the information you need.

Your first sentence is incorrect. Please [edit] your post and clarify.

This question always intrigued me, but i didn't think about it much. Time to study, and learn :D


text:
Can anyone identify this dragonfly spotted outside of Boston, MA?
Can somebody identify this dragonfly please? It was seen about 15 miles west of Boston.

This dragonfly? I see two of them, one eating the other.

Yes...I interrupted lunch for the greed darner. Not sure what the other one is, you really can't see it.

It is a male Green Darner.
Pretty common in general, especially in the US.


text:
Can you knockout a gene specifically in the dorsal root ganglion in adult mammals?
Since the dorsal root ganglion is so small, would that be easier than the entire body?

Welcome to BiologySE - do you know how to make a whole body gene knockout? Or perhaps a tissue specific knockout? Those might be better questions to ask because then you'll understand why the size of a particular tissue or organ that matters, but rather the gene expression of a particular organ. There are a number of review articles on gene knockout techniques, I would recommend you read one of those and then post a more specific question that would be more helpful.

what is the exact problem you want to solve?

It requires two genetic constructs to create a conditional KO organism. One parent with a transgene that expresses a DNA recombinase (such as Cre) after the promoter of a gene that is ONLY expressed in your tissue of interest. The other parent contains a modified gene of interest to be removed in the presence of said DNA recombinase but is fully functional otherwise.
Therefore, the ability to target a Knockout to a specific tissue is dependent on identifying a gene that is only expressed in the tissue of interest.
It is actually easier to create a whole animal KO, but because gene products can have different functions temporally in development and in different tissues, a whole animal KO may be lethal, whereas removing it in a specific tissue may not be and allows study of the effects of said removal.
Thus, if your gene of interest were lethal when removed from whole organism, AND you know of a gene that is only expressed in the DRG, you would have incentive to see if a CKO animal could be made.
A brief search on Cre Lox technology will bring up 1000's of images and articles.
Here is one and a nice illustration:

@Hamham just a note on this technique... this technique works well but you can control the timing of the knockout... that is, if you want to make some mice and then induce the expression of the Cre enzyme in the adult animal (if you have an inducible-Cre system) you can do that; however, if the Cre is expressed in embryos during development then the gene will be missing from birth and may have a different phenotype compared to if the gene knockout is induced in an adult animal.

@VanceLAlbaugh Can the "if you want to make some mice" part be switched to "if you catch some wild mice"? Aka, Unlike the picture above, I can just use any mouse without transgenic parents and induce the gene knockout in it...? Thanks!

@Hamham No, this wouldn't be successful with wild mice - you have to use laboratory mouse strains for which DNA sequence information is known. As indicated above, the idea is to breed one strain of mouse that has loxP sites flanking the gene of interest to another strain that expresses a tissue/cell-specific Cre recombinase enzyme. There are other technologies to do knockout (like CRISPR https://en.wikipedia.org/wiki/CRISPR ); but again, this is to begin breeding mice, not to knockout a gene in an adult mouse


text:
Can the respiratory quotient be calculated from a formula or must it be measured directly?
I found the following question on the Respiratory quotient:

A normal human diet has a  Respiratory quotient (RQ) of approximately 0.85. Given that pure oxidation of fatty acids has a Respiratory quotient (RQ) of 0.7 and pure oxidation of carbohydrates has Respiratory quotient (RQ) of 1, can one determine the fraction between the amount of oxygen used for aerobic respiration of the fat and the amount used for aerobic respiration of the carbohydrates?

My solution:
$$\text{glucose} + \ce{O_2} + \text{fat} + x \, \ce{O_2 \rightarrow} \ce{CO_2} + 0.7x \, \ce{CO_2} \, + \ce{H2O}$$
Note that I haven't balanced the equation excepted for $\ce{O_2}$ and $\ce{CO_2}$ where I added coefficients based on the given RQ. This equation gives $$\text{RC}_{total}=\frac{1+0.7x}{1+x} = 0.85$$
Hence $1+0.7x=0.85(1+x)$, which gives $x=1$, so the amount of oxygen used for Aerobic respiration of the fat and the amount used for Aerobic respiration of the carbohydrates is equal.
Is this correct?

Note: This is not really homework, but a question that can be seen as a more challenging problem. There are unfortunately no solutions for the challenge problems.

I'm not sure I follow the point of your question? are you just trying to be able to calculate a theoretical RQ based on the theoretical values for oxidizing 100% fat versus 100% glucose? - - - if that is the case, I don't think that's possible - (also, you have ketogenic and glycogenic amino acids that also can be oxidized that will also alter the RQ)


text:
Can a dead tree root still draw water?
Can a tree whose roots have died due to whatever reason, let's say due to ringing, still draw water up? I personally doubt so but I believe that since all forms of conducting water up a plant requires only passive actions, such as root pressure or capillary action, and that having a dead tree root will not result in leaves dying, hence transpiration can still take place. Is it hence derived that a tree is able to continue taking up water even if their roots died, or, does it depend on the woodiness of the tree?
Edit: I still got no answer

It can draw a littly bit of water up, but without leaves the evaporation rate is minimal. im guessing that an live oak drinks a cubic meter every day in the summer, and a dead oak will evaporate 1 liter or so, wood becomes just a sponge.

I mean like since its just the roots that died,  the leaves havent died yet so transpiration can still take place?

Root pressure and capillary action are only able to raise water against gravity about 8 feet. You need transpiration to pull the water molecules the rest of the distance up the tree to the canopy. Xylem is dead anyway, even in a perfectly healthy plant.

From observation, trees are going to die if their roots die.  (Although with some you can induce new root growth on cuttings.)  Far more likely is that the leaves & trunk will die (or be broken/cut off), and new shoots will sprout from the living roots.


text:
Estimated cost for diy biohacking
How much would it cost (more precise the better) if i wish to start a diy bio lab in my own house. Assuming that all I want is a functional set and to create maybe simple things like glowing bacteria/glowing fish/deadly virus（jk)

are you talking about just combining premade store bought genes or or do you need to be able to discover new ones.

@John probably making my own? Since I dont think i know where i can acquire new genes

you can buy them in catalogues, I have actually done the glowing bacteria combination a dozen times with high school students.

@charles, true but it is a question I doubt anyone but a biological scientist could answer. However it might be better placed in world building.

@John You're not wrong, but I think that would place it better on a chat forum than on here.

I don't understand the down votes; this question has a clear answer that seems to show the question is reasonable. It may not be "fancy biology" but this appears to be a real thing.

" ... you can get started for around $500 or less with a little improvisation and patience." -- How to Set Up Your Own DIY Bio Lab
The $500 is pretty minimal and you won't get much done with that -- they mention other equipment (like a PCR machine) -- and you'd need to be extremely handy to be able to build all the equipment by hand.  More likely you're looking at thousands or several thousands of dollars.
Several sites give guidance:

A How-To For DIYbio Lab Equipment
Genome at Home: Biohackers Build Their Own Labs

Getting reagents may not be easy; I don't know how readily companies sell to individuals.
Don't forget that some experiments may require approval by animal care committees etc, unless you want to be arrested for animal abuse.
You might look into biohacker collectives, which are shared spaces where multiple "hackers" can use common equipment.

I was certain these would all turn out to be joke links, but wow this is a thing! Are  PRC reagents for example controlled substances, or once you have a machine, can you just order them from Amazon? (err, I mean Aldrich)

PCR reagents aren't controlled (as far as I know) -- there's nothing toxic about them -- but the companies that carry them aren't used to dealing with individuals, so you might have a hard time ordering them.


text:
Why do humans transport glucose but not sucrose like plants?
The reason why plants transport sucrose rather than glucose is due to the fact that it is more efficient and that nearby cells would not take up all the glucose too quickly.
Hence the plant convert glucose to sucrose before transporting them throughout the plant.
However, why is that humans and other animals all transport glucose in their bloodstreams? Why is it that they do not convert glucose to sucrose before transporting them since, as mentioned above, it would be more efficient?

Short answer digestion and absorption.
Animals have to digest sucrose into it's component sugars before it can be absorbed. Turning it back into sucrose afterwards would take energy and have no real benefit so it has had no reason to evolve.
The real question is why do plants make sucrose, and the answer is by living at a much slower pace,As you mentioned it is has slower uptake on the cellular level which is fine for plants but a detriment for more energy demanding animals. Stability is the other concern, sucrose is a lot more stable than glucose, animals are burning through glucose as fast as they can release it from storage so it doesn't matter how stable it is, whereas plants keep it around for longer and move it slower so it has a chance to breaks down on the way which would be a problem. Sucrose is more chemically stable than glucose and slightly more favorable osmotically (takes less water to dissolve the same energy value of sucrose than glucose) Both of these reasons make it more beneficial for plants to convert the sugars to sucrose, (if starch was water soluble they would likely only convert it to that.) They do this right at the end of photosynthesis then break it down just as it is being used in respiration so the energy investiture is minimal, while for animals they would be spending energy to break it down (digestion), then energy to put it back together, then energy to break it down again for respiration, its two extra steps for no benefit.
Just as a extra you can see why animals would evolve to break it down for absorption since as has been mentioned glucose is easier to absorb, whereas plants don't have to worry about extracting it from anything.

Short answer: Because sucrose is a pain.
Sucrose = glucose + fructose bound together. Obviously, a larger molecule has the disadvantage of inherent decreased cell membrane permeability except if you're using transporter constructs.
Glucose metabolism largely comes standard across human cells. Meanwhile, sucrose must first be split into glucose and fructose, then the fructose must largely be metabolized in the liver (https://en.wikipedia.org/wiki/Fructose#Fructose_metabolism).


text:
Golden Brown Flying beetle identification
Bug (probably a beetle) flew into my house tonight with golden body and black stripes. I live in pacific asia.

.

Pacific Asia could be a bit vague as a location. As well if you can specify the season (you just saw it now or few month ago) and what kind of habitat your living (urban area, jungle, desert and so on).

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


text:
Why is sedimentation rate significant for a ribsome
When we take a look at biology textbooks (Campbell,  Pearson etc), they will only mention the difference between eukaryotic and prokaryotic ribosome sedimentation rates. Why is sedimentation rate numerically important for ribosomes and not for other organelles like the mitochondria or the nucleus?

It’s important insofar as the ribosomes are named after their sedimentation rate.

Summary

Ultracentrifugation was necessary to identify and ribosomes, and characterize them on the basis of their size. The method does not allow an absolute measurement of molecular mass, but uses a relative quantitation as sedimentation coefficient, expressed in Svedberg Units (S).
Nuclei and mitochondria were characterized by light microscopy and, being much larger than ribosomes, sediment at speeds which do not require an ultracentrifuge and would not be resolved in an ultracentrifuge.
Nuclei and mitochondria vary in size, so their size is not a defining property for them. Ribosomes from one source all have the same size, which may differ from that of ribosomes from other sources in a definitive manner.
Ribosomes are composed of smaller subunits, which are assembled from precursor particles of a different size. They occur in larger complexes on mRNA (polysomes). These forms of different but specific size can be separated and characterized by on the basis of size in the ultracentrifuge — i.e. by their sedimentation coefficient.

Amplification and examples

Prokaryotic monoribosomes (e.g. E. coli) have a sedimentation value
of 70S, the cytoplasmic monoribosomes of eukaryotes (e.g. rat) 80S,
and those of mammalian mitochondria between 50 and 60S. The values may differ for different eukaryotes and prokaryotes, but are constant for one species, reflecting the constant ribonucleoprotein composition of the particles.
All ribosomes have two subunits — a large subunit (50S and 60S for the prokaryotes and eukaryotes mentioned, respectively) and a small subunit (30S and 40S). The subunits are identified by ultracentrifugation, which is also used to separate them preparatively. Hence it is natural that their S values should be used to name them.
The formation of ribosomal subunits from RNA and protein involves sequential addition of proteins. The different sized intermediates at different stages can be differentiated by their sedimentation, and it is natural to refer to them by their S values.
Ultracentrifugation is also used to separate and characterize the ribosomal RNAs in a similar manner.

Bibliography
The Wikipedia entry on ribosomes corroborates some of the factual data I have presented.

The Svedberg unit is measurement used to characterize the ribosomal subunits. And it represents  rate of sedimentation in centrifugation process instead of size.
But every organelle and sub-cellular material has its own sedimentation rate. On basis of this characteristic, differential centrifugation technique works.
In case of ribosomes, it may be used so that it becomes easy to differentiate between different subunits.
(Via:  https://www.britannica.com/science/ribosome)


text:
What sort of fish is this?
Just saw a meme online with this fish on it. Is this a real fish? Can some aquatic expert identify this for us?

That is a blue parrotfish (Scarus coeruleus):

(photo: Marc Tarlock via Wikimedia Commons)

Mgk - C'mon. Parrotfish are AMAZING! Some of them can change sexes as adults! They are responsible for most of the sand on earth! They are good eating! You can actually hear them crunching coral when snorkeling! Surely you can say more than "this is a parrot fish." (Can you tell I like parrot fish?)


text:
Can humans go to hibernation?
Like squirrel undergoes hibernation during unfavourable periods if we induced the hibernation causing pitutary hormones in the human blood stream, can humans go to hibernation?

This is unclear. You ask if we can go into hibernation, then say if we induced hibernation. Those are two different things. What exactly are you asking? If your question is, "Can metabolism slow down during times of decreased food," then please ask that. If your question is, "Can we manipulate hormones to cause metabolism slow down during times of decreased food," then please ask that.

Humans cannot hibernate. There are a number of reasons why we would not expect them to do so.
Hibernation is thought to be an evolutionary adaptation to cold temperatures, and food scarcity, (perhaps also predator avoidance). Humans evolved in tropical regions with an abundance of food, and are also considered apex predators. There was thus no evolutionary pressure.
If we were to induce sleep with the relevant pitutary hormones. Humans would likely die, if they do not have any life support.


text:
Are there predefined implantation sites in mammalian uterus?
  I do surgical embryo transfer of genetically modified (microinjected) mouse embryos (at 1 or 2 cell stage). As most of the constructs are new, we expect that it may affect birth rate. In case there are no or very low number of pups born we try to investigate at what stage the problem occurs. I dissect the embryo recipients on day 21(+48 hrs to make sure that we don't sacrifice a mouse that is late to litter down). Sometimes I find dark, gelly, regularly interspaced structures on the mesenterial side of the uterus. Initially, I thought them to be implantation sites of the embryos that have been subsequently resorbed for some reason. Until I found similar structures in mice that haven't been mated with male. My question is: are there anatomically predefined sites in an uterus that embryos can invade? Are my dissections just a waste of time and yield no valuable data?

I haven't been able to verify this, but if the gelly on the outside of the uterus looks at all like endometrial tissue, might you be seeing mice with endometriosis? In humans, there are no special implanttation sites, just highly probable to low probability. The embryo can implant anywhere it "touches down". Where it implants does influence the probability of carrying to term, though.

Hi, It is inside the uterine horn's wall, where placentas are formed. It seems to be connected to the blood vessel branches. Basically it looks very structured and be there for the purpose. I dissected one of this thinghs and it looks (100x magnification) like very dense capillary network.

Ah, thanks. I know of no similar anatomical structures in humans. It's strange, though, that you find them only on some female mice (is that correct?) I, too, in your place would have thought them influenced by the embryo(s), since the embryo has the ability to alter the architecture of it's implantation site, especially with regard to vascularization. Odd to find them on non-mated mice. I wish I could help.

Just had a thought; when you find them in unmated mice, look at the ovaries for visible corpus lutea. It may be anatomically normal but cyclical.

I started to believe that it is anatomical feature. The problem is that I talked to many people including vet surgeon, people doing research on embryology etc and nobody gave me the clear answer.

Keep an open mind. You might have made a discovery. :)


text:
Why would the citrulline content of the watermelon be so high?
Citrulline is a non-proteinogenic amino acid (that is, citrulline is an amino acid that is not coded for in mRNA), and it is an important metabolic intermediate in the Urea Cycle. The Urea Cycle is critical for nitrogen (e.g. ammonia) excretion in humans as well as other mammals.
Citrulline is an interesting amino acid, given its vital function in the Urea Cycle, but also because it has such a high concentration in the watermelon. The name citrulline is actually derived from citrullus vulgaris, which is the Latin word for watermelon.
A notable fact about the watermelon is that the watermelon is the only food known to have such high content of citrulline. There are NO other foods that have such high endogenous levels of this amino acid.
As a physiologist citrulline is very interesting metabolically, but I wonder why the watermelon would have such a high concentration? Why would that occur? Would high citrulline content offer some type of competitive advantage to the watermelon in terms of out-competing other plants? As biologists, we usually think about things from a teleologic perspective in order to make sense of the world around us. With that perspective, is there a logical reason that citrulline would be so enriched in the watermelon? It seems very odd that it would be the only plant with notable quantities.

I am just a novice undergrad in biology and am a poor student and probably way off base. My chemistry is also really bad. But I read via the wikipedia page that citrulline is a " precursor to producing nitric oxide". I feel like i am using "ad hoc" logic but i also read Nitric Oxide can be responsible for retaining water (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC116475/) and for disease prevention via cell death (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1810256/). Sorry if im way off base, but I always try and make an effort to answer questions, even if I am lost myself.

@RoSiv, you may not have been that far off, though I think it is likely related to seed development and germination. Google Scholar for Seed Development and Citrulline and Seed Development and Nitric Oxide. I would check Cantaloupe and Cucumbers, things that maintain their seeds in the pulp of the fruit.

@AMR I like your thinking along with Ro Siv, but unlike watermelon - cantaloupe and cucumbers have very little citrulline... I'm trying to understand why watermelon in particular would have such high concentrations of citrulline compared to all the other known fruits/veggies - seems strange but there must be some type of reason

One of the things I saw was that it was concentrated in the rind. Look to see if watermelon has homologs to PADI4... Maybe it has Multiple gene duplications that are all active... or check its overall arginine distribution in its genome... Maybe its reading frames code for an inordinate amount of arginine when compared to other plants.

Asking why things happen evolutionary is a bit misleading. One can guess pretty well (for example, skunk cabbage being thermogenic gives it a distinct advantage as it flowers when few other plants can compete for pollinating insects) but the answer, ultimately, is that for some reason, this is how it came to be. May be as simple as an accidental duplication of a particular gene, whatever. But "why" is in this case probably only a guess in an evolutionary perspective.

@anongoodnurse I agree with what you are saying - I come from a medical/mammalian background and citrulline is very interesting from a scientific perspective... I posted the question and tagged it with "botany" to see if anyone with plant expertise might be able to rationalize an explanation for what all that citrulline might be doing - it seems odd that only watermelon has that high of a citrulline content. It might just be one of those biological mysteries - but I wanted to see if anyone might have some good ideas. I think this is a great forum for asking and can't find an explanation for it

Good question. I don't know the answer, but there are several examples of specific amino acids accumulating in certain tissues also in animals. One hypothesis is that is it advantageous for specific cells to specialize in storing one amino acid (as opposed to all cells storing all of them) because a high intracellular amino acid concentration can shift equilibria of related reactions and thus interfere with metabolism. For example, it might be advantageous to store citrulline in a tissue that does not have urea cycle activity.

Also, keep in mind that present-day watermelons are not evolved in nature, but bred by humans.  So observed traits might not be advantageous to the melon, but to us.  Maybe high citrulline makes for tasty melons  ;-)

I can see a pretty outlined role for citrulline in nitrogen metabolism. A couple articles that caught my eye may point toward a role for citrulline in the rind that pulls toxins out of the flesh: l-Citrulline: An active corrosion inhibitor component of watermelon rind extract for mild steel in HCl medium, and A fixed bed column study for the removal of Pb2+ ions by watermelon rind.

@Roland I happened to run across the answer to this question according to some molecular botanists  (and will post). Just happened to run across it by chance while doing some other work for a book chapter - you were exactly correct! The reason for high citrulline is an "evolutionary hold-over" from wild watermelons that isn't really needed in our agricultural society nowadays.

According to molecular botanists and plant physiologists, watermelon is the only plant that is known to contain significant amounts of citrulline. Interestingly, it appears that the reason for this tremendous enrichment in citrulline stems from the environment in which wild watermelons naturally thrived hundreds of years ago prior to the development of agriculture.
According to botanists, drought is one of the most severe stresses to which a plant can be exposed. Drought generates a high level of free radicals and oxidative stress, in part because plants maintain their photosynthetic machinery even in the face of severe drought. A number of investigators have shown that different plants have unique molecular mechanisms/systems to allow them to tolerate such harsh conditions and oxidative stress.
Wild watermelon plants inhabit the Kalahari Desert in Botswana, where the annual rainfall is less than 2 cm. Despite the minimal rainfall, the watermelon (a xerophyte) can tolerate the extreme conditions well with an exceedingly high drought tolerance. Surprisingly, this tolerance to intense drought conditions by watermelon plants even persists despite a sub-optimally developed root system. In the case of the watermelon, citrulline is overproduced in the leaves (and apparently the rest of the plant) and citrulline acts as the major hydroxy radical scavenger that allows wild watermelon to tolerate the drought-induced oxidative stress. From this same source (Annals of Botany - link below), there are also other proteins that may also be involved in these mechanisms as well. Even though the citrulline content is predominately used in the leaves to buffer oxidative stress, it appears that it secondarily accumulates in the melon itself.
Note: The image below is from Annals of Botany paper in the links below - it is OPEN ACCESS, which is why I posted the picture and included the reference link. You can clearly see the before and after pictures of drought and how the watermelon leaves appear minimally changed, unlike the radish and cucumber leaves.

See below for some interesting Papers about citrulline, watermelon, and mechanisms of drought-resistance:
Ann Bot. 2002 Jun;89 Spec No:825-32.
Citrulline and DRIP-1 protein (ArgE homologue) in drought tolerance of wild watermelon.
FEBS Lett. 2001 Nov 23;508(3):438-42.
Citrulline, a novel compatible solute in drought-tolerant wild watermelon leaves, is an efficient hydroxyl radical scavenger.

It seems to me that this is a teleological explanation for "why" ("because it suited it's growth in certain regions") as opposed to an objective reason ("because it contains multiple copies of a certain gene for the [etc.] found in plants originating in x region."). I dunno, maybe not. Maybe just me.

@anongoodnurse agreed, teleologic indeed - not my area of expertise but i happened to run across it working on a book chapter (go figure) - I would love someone with a plant background to answer who might have more insight

http://www.watermelon.org/Contact Maybe they will be able to give you the contact of a botanist that studies the plant in detail... One interesting fact I didn't know is that the rind is edible as well, and that is where most all of the citrulline is found.

Also it also appears that the citruilline pathway uses Ornithine instead of Arginine as the human pathway does. But there only appeared to be a single Ornithine cyclodeaminase gene. http://www.icugi.org/cgi-bin/ICuGI/genome/search.cgi

@AMR heard back from watermelon.org... actually send me some scientific studies about the benefits of citrulline, but no idea about why it is enriched in watermelon - FYI


text:
What is the first recorded unambiguous case of childhood cancer?
I can't seem to find any references to childhood cancer going far back. I am asking for the first verifiable instance of childhood cancer.

Kindly add some references as well

What? ..........

Verified how..?

"Cancer" is a huge range of diseases. Some are not uncommon in children. Others are rare/undocumented. This question is unclear or too broad until it is narrowed down.

Osteosarcoma is mostly a disease of teenagers and it leaves characteristic changes in the bone.  Sometimes archaeologists find such bones.
I found this

Malignant primary bone tumours were very rare in antiquity and
  continue to be rare in modern populations. The earliest known case
  affected a male Celt (about 800–600 BC) who was about 15 years old and
  lived in what is now Switzerland.1 The lesion is a neoformed bone mass
  at the level of the metaphysis of the humerus, whose gross pathology
  and radiographic aspect are consistent with a possible osteosarcoma or
  chondrosarcoma. A few additional cases of malignant primary bone
  tumours have been mentioned in literature. A possible osteosarcoma of
  the pelvis has been reported in a young individual from Ancient Egypt,
  dating to about 250 AD,92 and a well-documented case of osteosarcoma,
  with the typical radiographic “sunburst” pattern, has been observed in
  the femur of a native Peruvian dating to 800 BP (Fig. 4).93 Possible
  additional cases of osteosarcoma have been reported in a young female
  femur from the prehistoric population of Oahu in Hawaii,94 in a
  zygomatic bone from the French Middle Ages,95 in a 17th century
  mandible from West Virginia,96 in a young male from the Saxon
  necropolis of Standlake, England97 and in medieval skulls from the
  Czech Republic98 and France.99

http://onlinelibrary.wiley.com/doi/10.1002/ijc.20610/full
But if you want "described" meaning a contemporary of the child wrote down what he saw, I found this by John Abernathy in 1804.

from https://archive.org/details/surgicalobservat1804aber
Surgical observations : containing a classification of tumours, with cases to illustrate the history of each species : an account of diseases which strikingly resemble the venereal disease : and various cases illustrative of different surgical subjects
by Abernethy, John, 1764-1831
Percival Pott was an English surgeon who is remembered for his realization that the job of chimney sweeping puts men at risk for development of scrotal cancer.  Mostly these were grown men but among cases described was an 8 year old; this in 1808.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1037746/?page=3
I am pleased that my find in Abernathy's and Pott's works predates the earliest listed in this 1937 review of pediatric cancer, which gives a date of 1819 for description of tumors in the eye of a 3 year old.
[Dargeon, J Pediatrics 1937].   Dr Dargeon did not have Google.
  (http://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-S0022347639800415/first-page-pdf)
ADDENDUM:  An earlier find yet:
from http://onlinelibrary.wiley.com/doi/10.1002/cncr.25000/full
A note from history: the first printed case reports of cancer.
Hajdu SI. Cancer. 2010 May 15;116(10):2493-8. doi: 10.1002/cncr.25000.
He describes the work of Theophilus Boneti, whom in 1700 published a book of many hundreds of case reports accumulated from the previous 150 years.  Included was a case of retinoblastoma (I could not tell what year it was from):

In the fourth case, the patient was a 5-year-old girl who presented
  with a fungous (soft) tumor of the right eye. After a short period of
  observation, a similar tumor was detected in the left eye. Both tumors
  invaded the meninges with adhesion to the brain. Boneti did not say
  so, but this youngster must have had bilateral retinoblastoma.

That puts the earliest solid description of a cancer in a child at 1700.


text:
What kind of bug did I squish?
I saw a bug swimming through my carpet, and promptly squished it. I had never seen this kind of bug before, and wanted to find out what it is, so that I can assess it's danger to my house and family, and know how to responsibly take care of it. However, my dog gobbled it up before I could take a photograph, so all I have to go by is a mental image:

1.5-2.5 inches long (3-6cm)
2-3 segmented body, with a smaller head, and over 3/4 of it's length was the back segment
Mandibles/Pincers at one end of the body (I can't remember which)
I think it only had 6 or so legs.
The dog made a disgruntled face when she ate it, so I think it could have tasted badly, or bit/stung her tongue as she ate it.
I believe it was two colors, with a pale colored section and a reddish-brown section, although I can't remember their locations.

I live in the Northwestern US, and have three trees on my lot: two maples and a boxelder. The house was built in 1954 and has a crawlspace foundation.

Did it look like this? https://en.wikipedia.org/wiki/Devil%27s_coach_horse_beetle

Or possibly https://en.wikipedia.org/wiki/Earwig?

@arboviral it looked more like an earwig, I'm familiar with those, but it was at least twice as long as any I've seen, and the coloring was different.

Okay; I can't think of anything obvious but if you can add details of the colouring that might help others.

@arboviral -  I've added in what I can remember about color

this i going to be very hard without pictures! some beetle larvae have "pincers" in front, maybe check out some carabid larvae?


text:
Are these statements about the effectiveness of condoms in preventing HIV transmission reconcilable?
Can the following statements be reconciled:

Condoms form an essentially impermeable barrier to HIV
Sexual activities other than penetration carry a very low risk of transmission
The consistent use of condoms reduces the risk of HIV transmission to about a fifth of what it would otherwise have been (source: Am Fam Physician. 2004 Oct 1;70(7):1268-1269 as summarized at aafp.org/afp/2004/1001/p1268.html)

Obviously the effectiveness of condoms is going to depend on them being used correctly, but surely they are not used so incorrectly that the effectiveness drops as much as these statements imply - assuming all 3 statements are correct, is there a more plausible explanation?

I'm voting to close this question as off-topic because it is not about biology but an attempt to start a discussion either on scientific logic or some hobby horse issue.

No, it is a genuine request for help understanding the numbers. The one fifth comes from Am Fam Physician. 2004 Oct 1;70(7):1268-1269 as summarized at http://www.aafp.org/afp/2004/1001/p1268.html. It is expressed as 80% effectiveness but I was hoping that the contrast with the other two statements would be clearer if I expressed it as a reduction in risk. The other statements can be found on any number of apparently reliable sites. Is the risk of transmission virtually nil, as the first and second statements imply, or is it 20% of whatever it would be if you were not using condoms?

Then please put this info in your question.

Please see  https://skeptics.stackexchange.com/q/3167/24840

Thanks for the reference anongoodnurse - I don't seem to be able to rate it as useful, I guess because I'm a newb.

Note that those three statements are also approximately equivalent to pregnancy risk in the context of vaginal intercourse:

Condoms form an essentially impermeable barrier to sperm
Sexual activities other than penetration carry a very low risk of pregnancy
The use of condoms has an annual failure rate around 15%, i.e. on average 15/100 couples using exclusively condoms will conceive in a year

There are dozens of sources that reconcile these issues, and it all comes down to the failure rate and misuse rate of condoms. Even the source you cite talks about this explicitly, so I'm not sure why you still have a question about it that isn't already answered there.

It's because the discrepancy seems too large to be explained that way. Failure of the condom itself is rare: http://www.thebody.com/content/art2436.html. Unintended pregnancies are overwhelmingly due to user failure, which is overwhelmingly non-use rather than incorrect use (ibid). The study cited previously excluded couples reporting less than 100% use. Given the pregnancy statistics, incorrect use is not a plausible explanation for a 20% rate of failure to protect (same whether per act or per year). Did the couples misreport consistency of use, or is there something else going on?

The answer may be that the per year multiplier only approximates the per act multiplier when the risk involved in unprotected sex is very small. The probability of HIV transmission through unprotected sex, given a serodiscordant couple, seems to be much lower than the probability of conception, given a couple in the normal fertility range, so the same rate of failure per act may translate into a very different rate per year.

Yes, the annual multiplier is almost the same for HIV transmission as for conception at about 0.2, which sounds as though it makes sense until you realize that it corresponds to a per act failure rate of about 0.2 in the case of HIV and about 0.1 in the case of conception (as best I can calculate it), and that the failure rate for conception includes cases where the couple didn't actually use a condom whereas - if we accept what the study participants reported - the failure rate for HIV does not. If condoms themselves are equally effective, the annual failure rates should differ significantly.

@Riedt Oops, I read the paper you linked incorrectly, though it seems like you might have too; they are not taking about a 20% rate of failure but rather a 80% reduction. The actual rate of failure they are talking about is 1% per year. You also seem to be missing the very important statement in the abstract of the paper: Consistent use is defined as using a condom for all acts of penetrative vaginal intercourse. Because the studies used in this review did not report on whether condoms were used correctly for every act of intercourse, effectiveness and not efficacy is estimated.

No, I realize that. What I mean by 20% failure is 20% failure of protection, not 20% transmission. It's the same as an 80% reduction in risk. I have commented on your second point below.

No, they are not reconcilable unless we assume either that serodiscordant couples are very much more likely to use condoms incorrectly than seronegative couples, or that the effectiveness of a condom in terms of protecting against HIV is very much more easily compromised by incorrect use than its effectiveness in terms of preventing conception. It is difficult to assess whether it is more plausible that participants in the studies analyzed in Am Fam Physician. 2004 Oct 1;70(7):1268-1269 reported that they had used condoms consistently (which was defined for the purposes of the analysis as meaning "always") when in fact they had only used them sometimes. This would make the third statement unreliable. While that is a possibility, it is wise to be extremely careful storing handling and using condoms (don't keep them in your wallet, for example) and to make sure that it is your own that are used. It is extremely unwise to assume that as long as you are using a condom for vaginal sex, you do not need to be concerned about your partner's HIV status.

I commented this in response to your comments on my own answer, but I'll add it here as well: Consistent use is defined as using a condom for all acts of penetrative vaginal intercourse. Because the studies used in this review did not report on whether condoms were used correctly for every act of intercourse, effectiveness and not efficacy is estimated. I'd also add that by posting this poorly thought-out answer in addition to your original question suggests that some users' suspicions that you are here to rant rather than ask a question is validated.

I am sorry to have given you that impression. It is not the case at all. I am at risk and am trying to quantify the risk and the extent to which it can be reduced. I am aware of the statement you quote in italics - in fact that is largely what gives rise to the discrepancy I have been trying to understand. Are you perhaps reading it as saying that the study does not report on whether condoms were used for every act? It does not mean that, it means that the couples reported using them for every act (meeting the definition) but we don't know whether they used them correctly.

Hopefully it is clear that I am looking to explore this in the abstract, from an academic perspective. I am not asking for medical advice. I only mention my own circumstances because I don't know how else to allay the suspicions you mention.


text:
Which plasmid can express T7 RNA polymerase in mammalian cells?
Does anyone know what plasmid could express T7 RNA polymerase in mammalian cells, I would like to transfect it with other plasmid containing Gene Of Interest under control of T7 promoter. Thanks a lot!


text:
Question on the concept of mitochondrial Eve
My question is about the very definition of this common ancestor.
Why shouldn't be the mother of mitocondrial Eve the real Eva m (and so on to grand grand ...mother)? All I know on the subject comes from Wikipedia. My question comes from the idea that mitochondrial DNA is passed from mother to daughter. I do not see where to stop back in time.
Please consider that here I am not asking for details or controversies. Just the significance of mitochondrial Eve.

I don't really understand your question. What do you call Eva m exactly? The MRCA of all of today's mitochondria in humans? What do you call real Eva m?

It is mitochondrial Eve,  not Eva and is sometimes abbreviated mt-Eve or mt-MRCA (see the wiki article)

As the Wikipedia article says:

In human genetics, the Mitochondrial Eve (also mt-Eve, mt-MRCA) is the matrilineal most recent common ancestor (MRCA) of all currently living humans

Note the use of the words "most recent".  The mother and grandmother of the actual Mitochondrial Eve were living before Mitochondrial Eve, and thus are less recent than she is.

Thanks. I somehow skip that. I am amazed by this. How it comes that we are not from 2, 3 , n ... maternal lines ? I just discovered it yesterday and makes me wonder.


text:
Is urban beekeeeping harmful or are there good practices to follow?
I have found several newspaper articles on how good could be urban beekeeping both for the bees and for agriculture.
Today I read this one: Urban beekeeping is harming wild bees saying that urban beekeeping is harming wild pollinators. I did not find a direct link to the paper, but it is probably referring to Conserving honey bees does not help wildlife. Unfortunately I only have access to the summary of the paper.
Are there good practices that could be followed to practice urban beekeeping without harming wild life (for example avoid placing hives close to a forest...) or is it harmful in any case?

Did you read the article?  Did you read the article cited in the article?  Did you read the comments?

@swbarnes2- I couldn't find the original. Did you? I'd be interested in reading it.

@swbarnes2 I could not access the cited paper. Today I finally managed to download the paper cited in the article. It looks like the problem (if real) has little to do with urban beekeeping and more relevant for beekeeping in protected areas.

AFAIK, any monoculture or similar practice by humans reduces the diversity of resources available to wild animals... That said, compared to pesticide use, which is massively depleting wild insects found rurally, beekeeping is of much lesser concern.

You can sidestep the entire issue and raise native bees, https://www.sare.org/publications/managing-alternative-pollinators/chapter-five-bumble-bees/raising-bumble-bees/

Beekeeping in urban areas often require that beekeepers supplement their colonies with feed since urban areas have, on average, very little forage available to sustain a colony year-round. There are usually very little in terms of wildlife (or wild pollinators) when it comes to urban settings. In contrast, suburban areas would have more to offer as there are often backyard gardens and unmanicured lawns that could provide food throughout the season.
The wild pollinators within suburban to rural areas are probably under the biggest threat from managed colonies, but the impact is also usually very difficult to assess. Even with the limited range of managed colonies forage (around 5km), there's usually not enough of the colonies stretched out across a wide area in such big numbers that it would out-compete with other wild pollinators. The wild pollinators are often solitary, with much greater foraging capacity. As such, they would just move away from any competing resource if they're unable to defend it themselves until the threat subsides.
Regardless of the location (urban, suburban or rural), best practices still include protecting your colonies against diseases and pests. If you don't you may end up losing your colony, or spreading diseases to other colonies or wild pollinators. Probably the most significant threat nowadays globally (except for Australia) would be Varroa Destructor. So, best practices here would include keeping on top of these mite loads to avoid it from spreading and/or overrunning your colony.
As reference, here is a visual capture of the article:


text:
COVID-19 deaths by year of birth?
Are there (global, country, etc.) data of COVID-19 deaths (or hospitalization) by year of birth? I was able to found them only by "age group", the meaning of this being usually an interval of 5 to 15 years, but I'm interested in smaller intervals.
Why I am interested? We know that the severity of this illness increases with age, and in fact increases a lot with ages around 70. If this increasing is more o less locally constant (that is, the first derivetive does not vary much in any interval of a few years) or at least the second derivative is more o less locally constant, we can think that maybe age on its own is a factor risk. But if there is a rapid increasing in one, two or three (consecutive) years and then a smaller slope (that is, a sort of "jump"), it is possible that there are (instead/also) other factors: maybe an exposition of this aged people to something during their lives that younger people don't lived, or some other thing that we don't know yet. So we need to know with more detail ages of hospitalization, deaths, or other sign of severity.

Data are usually binned in broad age groups partly because that's all the detail that's useful in some context, and because access to more detailed data often involves access to strongly controlled, personally identifiable information.
This preprint (full disclosure: I'm a co-author) gives information in 2-year bins for COVID in Ontario, e.g. this graph of the fraction of known infections (KI) hospitalized, and fraction of hospitalizations that resulted in survival, by (2-year) age group.
It looks pretty smooth, although if you squinted hard you might be able to convince yourself there were some breakpoints, e.g. between [60-61] and [62-63] in hospitalization or between [62-63] and [64-65] in survival (although I doubt these impressions would stand up to a formal statistical analysis ...)

Thank you. Indeed these curves seem pretty smooth. There is another break (in hospitalization) between [68-69] and [70-71] (of a different nature, since it is preceeded by a higher slope) but this one seems very small in the curve of deaths in the preprint. Very interesting paper!


text:
Book on data science talking about both DNA and RNA
I do not have any eductatin in biology, I am a mathematician. However I am reading a book in data science, and am trying to understad an example involving, DNA, mRNA and genes.
From what I understand we have these concepts:
DNA: This is the double helix molecule that makes up our genetic code. The helix is long and consists of a long code, and the code is made up of four molcules and the order in which the molecules occur is the code
Gene: This is different parts of the DNA.
RNA: This is similar to the DNA, but is a single helix. It also consists of four molecules, but one molecule is different from the DNA.
The relevant text is this:

Question:
The author  want to measure the amount of genes in a cell by measuring the amount of RNA in that gene? However a gene is something that is in DNA? So by this logic something that is in the DNA consists of RNA, but as I noted above, RNA and DNA are built up of 4 molecules, but one differ, so how can this be?

The concept here is which genes are being "read"/ transcribed into mRNA in that cell/tissue.  From Nature.com: "Even though nearly every cell in an organism's body contains the same set of genes, only a fraction of these genes are used in any given cell at any given time. It is this carefully controlled pattern of what is called "gene expression"  that makes a liver cell different from a muscle cell...(The article is very easy to understand and helpful!)

@anongoodnurse Thank you very much! I found this in your article very helpful: "Remember, in order to activate a gene, a cell must first copy the DNA sequence of that gene into a piece of mRNA known as a transcript. Thus, by determining which mRNA transcripts are present in a cell, scientists can determine which genes are expressed in that cell at different stages of development and under different environmental conditions. " I think this answers my question. :) If you want you can put this as an answer, and I will accept.

Unfortunately this is very much a basic biology question, which means it falls under the homework policy, and means it will be closed.

Yes, it's a good article and explains gene expression very well. Thanks for the offer, but I only answer in comments when I know the question will be closed, and think the OP can use a bit of help. :) (I stink at math, so maybe someday, you'll pay it forward for someone like me.)


text:
What arthropod is in the picture?
I am from Philippines and I found this in my room.
This arthropod has 6 legs and have a bit long Chelicerae like spiders that can fold to hold its food. It's about half an inch long. It also looks like a
scorpion but I could not find anything like it on the internet. Thank you!
I've also noticed that it can jump and it also produced spider silk.

It is not a pseudoscorpion as those would have 8 legs and then the two front large pincers. This is most likely a kind a jumping spider where the two large front legs count as two of the 8 legs.
Depending on your geography (not given in the question), this looks to resemble a jumping spider in the genus Chalcolecta (or some regional variant of that based on where you are). Hard to see any detail (like eyes and body segments) from your photos. But have a look at some of these and see if any of them match your specimen. Here are some pics of C.prensitans and C.simon.

This is actually the closest one. I noticed that it can jump and produces silk like a spider. However, the tip of its abdomen does bend sometimes.


text:
What is the C765-Gal4 driver?
What is a gene driver and what does C765 stand for? Is Gal4 a transcription factor?
Source: "Dynamics of Dpp Signaling and Proliferation Control"

C765 is a transgenic Drosophila strain that has a specific Gal4 expression pattern ("embryonic salivary glands and larval wing and leg discs").
Gal4 is a transcription factor from yeast which binds an upstream activating sequence (UAS) and also happens to function in other species (like flies). In the Gal4/UAS system, a strain expressing Gal4, under the control of a tissue specific promoter or a minimal promoter in an enhancer trap, is crossed with a strain expressing a gene of interest flanked at the 5' end by the UAS. The F1 generation will thus express the gene of interest tissue specifically (ie only in the tissue(s) expressing Gal4).

[source]

Further reading:
Phelps CB, Brand, AH. 1998. Ectopic Gene Expression in Drosophila Using Gal4 System. Methods 14(4):367-379.


text:
What's the frequency resolution of the human ear?
I was thinking about audio compression (namely mp3), that "filters" out sound that we would not likely hear.

The MP3 lossy audio data compression algorithm takes advantage of a perceptual limitation of human hearing called auditory masking.
  from: http://en.wikipedia.org/wiki/MP3

I've also checked the wiki entry for auditory masking, and found this:

If two sounds of two different frequencies are played at the same time, two separate sounds can often be heard rather than a combination tone. The ability to hear frequencies separately is known as frequency resolution or frequency selectivity. When signals are perceived as a combination tone, they are said to reside in the same critical bandwidth.

My question is how much is this critical bandwidth or what's the smallest frequency difference we can perceive as two different tones, if you wish. Let's assume that both tones are equally loud, are coming from the same direction and distance and we are in a quiet room - so basically we eliminate as much noise and affecting phenomenons as possible.
As @ sanchises pointed out (thank you again!) in the comment section the frequency resolution is 3.6Hz between 1 and 2kHz. But since perception threshold is a function of the pitch of the sound I'd assume that the ability to resolve two tones would change with pitch too. Does anybody have any data on that? For example resolution X pitch graph.

possible duplicate of What are the lower and upper hearing limits of the human ear?

Just googling 'frequency resolution human ear' yields the wikipedia page on Psychoacoustics: Frequency resolution of the ear is 3.6 Hz within the octave of 1000 – 2000 Hz.

@Dane Not a duplicate; this question is about resolution, not range.

@Dane - I"m aware of the lower and upper bounds of human hearing, my question is not about that. I've specifically linked that my question is linked is related to auditory masking and the critical bandwidth.

@sanchises - I've googled many things, yet not the most obvious :S I got stuck around audio compression, and forgot to take a step back....

@poka.nandor - don't hold back on shooting at my answer - no worries :) Good question, and hard to answer! Feel free to criticize.

I would also ask - especially given the context of the question - whether there's any sort of training effect.  Certainly I can perceive a difference between classical music compressed with MP3, and the same piece at full CD resolution.  Which itself involves some downsampling compression: I recall that when CDs first came out, some audiophiles claimed to hear a quality difference between them and an analog recording, though I never could.

The frequency limen, or frequency resolution can be determined in various ways using psychophysical measures. You refer to a simultaneous method, in which two (or more) frequencies are presented at the same time. This has consequences for the test as different frequencies are perceived with different perceived loudness under constant sound pressure levels, meaning that additional cues are present besides pitch cues.
One carefully controlled study Zwicker et al (1957) in this regard defined the critical band basically as "those frequencies where no intensity summation occurs", meaning that adding those frequencies (below or above the center frequency) do not result in differences in loudness perception (as expressed in acoustic threshold of the center frequency). This method nicely prevents loudness summation cues by deploying them in the criterion. This article shows the following picture (after Zwicker et al. (1957)):

The critical band (upper graph) is dependent on frequency, and ranges from 0.1 kHz to >2 kHz.
The markedly lower difference limen of 3.6 Hz as touched upon in the comments may have been obtained using an alternative psychophysical test where the test frequency is modulated by another frequency (bottom graph). This procedure is based on adding a frequency to a certain sinusoidal stimulus, basically resulting in a single stimulus instead of two (or more). This procedure is technically not defined as a critical band and indeed results in a difference limen of ~3.5 hz and up. The other graph plotted in the figure is a masking procedure (middle plot), which basically determines the physiological overlap between frequencies in the cochlea in the intensity domain by determining the amount of masking from one frequency by another.
NB: The authors worked with headphones so no effects of direction.
Reference
Zwicker et al. JASA 1957; 29: 548-57

I guess you had to dig really deep to find this paper.... thank you!

I think you have already gotten ur question answered. The human auditory system has the resolution of 640 different frequencies, so dividing the hearing frequency range by this you could see the smallest frequency. although the bandwidth is not constant in the whole range (100 for frequencies below 500 Hz and 0.2f for frequencies above 500 Hz). Also, the auditory system of ours has a dynamic resolution of less than 1 dB.
hope I got it right :)

It is important to add references to improve the quality of the answer.


text:
Do antigen presenting cells present only antigens they have receptors for?
As APCs  take up whole virus or bacteria  their receptors may be restricted to antigens "they have receptors vor", i.e. those antigens that are on the outside of virus or bacteria. Put simply: do they uptake "inner" antigens their receptor doesn't contact with AND, then, present them?
It should make sense for antigen presenting cells - APCs - to present only antigen that can be used for recognition. In other words: why should APC present antigens to T-cells if these cannot use such kind of antigen  to recognize and attack cells because those antigens are part of inner structural proteins that do not show on the external surface?
That may be different with B cells/MHC2.
Admittingly, this question is awkwardly put, as it should be known to any advanced learner that the APC's, the antigen-presenting-cells of the immune system have very broad receptor specifity. So there should be no antigen at all "they do not have receptors for" - same s for B cells as a wohl class or set.
I have not found any  or textbook passage on  B-cells taking up, via B-cell-receptor, "inner" antigens that come as cell debris. But then, the B-cell receptor in fact is a receptor in terms of my question. Which interestingly makes it seem a possibility that macrophages and dendritic cells have receptors that do not recognize any inner structural protein that comes as cell debris.
Having gone through and read Kuby, Janeway, Roitt on immunology, my understanding  is that not each and  every antigen of a  virus will find its way to the MHC complex on the cell membrane of antigen presenting cells. If that is correct,  how could eukaryotic cells possibly differentiate between antigen of viruses they present and those they would not? Do they present not "all sorts" of antigen but only those "they have receptors for" (awkwardly said)?
Regarding  "normal" cells of the body  that become infected and are not part of the immune system, do, for instance, CoV-19 infected body cells  present only the spike protein on MHC1?  The spike is the antigen they "have receptor for".
So any antigen that cannot be considered antigen to a receptor and becomes presented would answer my question to the negative. If so, is there any selection within that set of "inner" antigens ("non-uptake antigen").

"On MHC II, do cells present only antigen they have receptors for?"
Thank you for boiling your question down to its essence. The answer is no. Professional antigen-presenting cells (APCs) such as macrophages, dendritic cells, B cells, etc., which present peptides in the context of the major histocompatibility complex (MHC) Class II to CD4+ Thelper cells, initially obtain the source proteins through non-specific phagocytosis. Receptor binding doesn't necessarily have anything to do with it, unless you're looking specifically at B cells and antigen's binding to the B cell receptor (BCR) before being endocytosed.

From immunology.org
Where you might be confused about receptors is that only some of the peptides generated by cathepsin-mediated proteolysis in the phagocytic endosome have high-enough structural affinity to bind the MHC II receptor by displacing the CLIP fragment and being exported to the cell surface.

Very valuable advice on Clip "selection", thanks!Part of my "confusion" may be derived from viewing MHC as a kind of receptor. Anyway, question above may lead to better awareness of receptors that exist inside the cell - they do exist -, and MHC looks like one - which is, as it occurs to me writing this - as an unspecific one, like the others!

... considerung "CLIP" in the context of "crosspresentation". Still cryptic, it's just a new look at things. If MHC were "some" receptor - then answer would go like: yes, of course, why you ask. - -  "Clip" to me denotes position at handing over of antigen betw. 2 "receptors", new view. –
See, for instance,   to illustrate Ciminski, "...findings show that bat IAV HAs make use of the major histocompatibility complex class II proteins of different vertebrate species to gain entry into host cells, ...".

Sorry, one more and last: not so trivial to see MHC as a "receptor", as one got to know: 1. there are "inner cell" receptors, and 2nd consider your word "affinity" in "enough structural affinity". To paraphrase: there are, do exist, antigens which there is no affinity for. There are antigens there seems to be no receptor for. Jokingly: no demo to/for/of them... no chatting: no mad demo for those.