What is the "lifecycle" of an average eschar and what types of cells are involved in each stage? (after some deliberation in the comments, I've decided to make the question more general)

An eschar or "dry scab" often forms at a site of injury over a large cut or sore.

It seems as though the healing scab portion binds more strongly to the other scab cells than to those of the surrounding healthy tissue initially, as evidenced by the ability to remove the scab en masse without disturbing the edges of the actual wound (in surgical debridement or when the area is "picked" at).  Then, the eschar bonds then bonds more strongly with the edges of the wounds (so it's more difficult to remove), and then finally, the underlying newly formed skin seems to push it off completely.

Does this accurately describe the "lifecycle" of a common dry scab, or are there other well defined stages in the process?  What types of cells (platelets in the beginning?  epithelials at the end?) are involved with each stage of the process?

Response to cutaneous tissue damage occurs is several distinct but overlapping phases. First an scab is formed as the blood is 'allowed' to clot. A matrix is formed as the platelets adhere to one another, which contracts and 'dries' (forces out the serum) to form a scab. This process clearly happens prior to tissue regeneration/formation to reduce further blood loss.

Fibrinogen

In response to damage to blood vessels a signaling cascade is initated that results in the massive production of fibrin, which is deposited at the site of wounding and subsequently forms blood clots by activating platelets and stabilising the matrix by cross-linking (see PDB's protein of the month 2006).

So this is why clots do not appear to be attached to the surrounding tissue; the fibrin causes the blood to form a matrix that is very tightly bound to itself. Only after clot formation does the tissue remodeling occur, and it is during this stage that the scab will 'bind' more stongly to the surrounding tissue.

The Cell Types and Processes of Wound Healing

This figure (from (Li, 2007)) shows the various stages that occur and cells that are involved in acute wound healing  (wounds such as burns and cuts that heal "in a timely fashion");


Unidentified insect seen in southern UK, near North Downs This creature was seen in southern UK, near North Downs, just this weekend.
https://youtu.be/5VJYOrMJXaQ

Though it might resemble a woolly aphid (https://dengarden.com/gardening/Woolly-Aphids-Whats-that-Fluffy-White-Stuff-on-my-Tree). I'm more certain that it is a mealy bug instead (https://puffycarrot.com/little-fuzzy-white-bugs/). the fact that it is not on a plant is what confuses me since both these species are usually living on plants which is where they grow.
here is some images i found that look almost identical to the photo you have and give other angles to the species, you can compare it with the images in the other links:
https://www.flickr.com/photos/unique127/2539022716/
https://www.ecosia.org/images?q=white+furry+insect#id=DDEE9FF71839419EF585778C7DA8F1E1545E98D1


Converting Ensembl Compara gene tree DNA alignment to corresponding amino acid alignment I have Ensembl compara gene tree alignments (Compara.gene_trees.57.fasta.gz downloaded from ftp://ftp.ensembl.org/pub/release-57/emf/ensembl-compara/homologies/) in nucleotide format. According to documentation, it says that the file "contains the peptide alignment for every genetree in fasta format".

I was wondering what might be a handy tool to obtain the corresponding amino acid alignments from the file.

Thanks,

Ikram

As a general rule, both within and without the world of bioinformatics, public FTP sites contain README files tat explain what each file offered by the FTP server contains. The file README.protein_trees states:

Compara.gene_trees.{release}.emf.gz
                        contains the peptide alignment for every genetree in emf alignment format
Compara.gene_trees.{release}.fasta.gz
                      contains the peptide alignment for every genetree in fasta format

This means that both Compara.gene_trees.57.emf.gz and Compara.gene_trees.57.fasta.gz contain the protein alignments. I had a quick look at the files and it looks like Compara.gene_trees.57.fasta.gz actually contains nucleototide sequences but Compara.gene_trees.57.emf.gz does indeed contain a protein alignment:
$ zgrep -m 1 AAAAASAAAT Compara.gene_trees.57.emf.gz.crdownload
SAAA-AHS-AGTAAAAA--AA--AAAAASAAAT-ASAATAI-SASSA-ASAAT-V----AAASVAA-HAFAS---ASAAASAAAAA-TIVAAAAX-SAASIYSAAAA-YAA--AASAS-ASAASAS-ASAASSSSSARS-AAS

So, to answer your question, the file you want is the .emf.gz one.


Clonidine's adrenonergic nature? I am little confused here.
I used the term adrenoagonist and sympatholytic to describe the compound.
However, my teacher says that the correct term here is adrenomimetic -term.

My understanding of Terms

Adrenoagonist says that to bind to adrenoreceptor which prolongs the effect of NE in receptor.
Sympatholytic - inhibition of postganglionic fibers of sympathetic nervous system
Adrenomimetic - mimic effects of sympathetic nerve stimulation on pre- / postganglionic fibers.

I still think clonidine is sympatholytic i.e. adrenolytic (not adrenomimetic).

How can clonidine be adrenomimetic?
Why not adrenolytic?

Clonidine is an agonist on the α2 receptor... but then again norepinephrine is also an agonist on the α2 receptor. Then the physiologic ligand of the a2 receptor, norepinephrine is autocrine (meaning it is released from a cell then binds on a receptor on the same cell) causing negative feed back and it inhibits further release of norepinephrine from the neuron thus preventing overstimulation. Clonidine is quite specific to the α2 receptor and it doesn't really stimulate α1/β1/β2. Given a situation  where only the α2 receptor is stimulated and none of the other epinephrine receptors, you would have a net decrease of sympathetic effects since the amount of norepinephrine being released is begin decreased by the stimulation of the α2 receptor on the presynaptic membrane of the sympathetic neuron. Hence clonidine is an α2 agonist that is sympatholytic

I have no clue what the difference are between these

agonist vs mimetic
adreno vs sympatho


Are PVC&PET bacteria found inside homes? I am interested in weather PVC and PET eating bacteria can be found inside people's homes. The PET consuming ones were found in or near plastic waste dumps or in the ocean, but would they also have adequate conditions in people's domiciles or they require specific things like the plastic being constantly in contact with water or earth?

I am mainly interested in the probability/possibility of PET eating bacteria being found in domestic spaces.

If you read the Wikipedia article carefully, and the recent article in PNAS on improving the enzymes responsible for TET degradation, it is evident that Ideonella sakaiensis is the only example so far known of a bacterium that can use PET as an energy source. As it is a Japanese marine bacterium it will not be found in “domestic spaces”.

The requirement for an aqueous environment is presumably related to the need for the enzymes the bacterium secretes to gain access to the plastic and the products of the digestion to be reabsorbed, and perhaps also for access to essential nitrogen, not present in the plastics. The rarity of bacteria that have evolved this facility presumably relates to the ‘difficulty’ of the chemistry — or its difference from that involved in degrading other carbon sources — although there is some similarity to cutinase, the enzyme in certain fungi that can digest the cuticle of plants.


What really causes the toxicity of wrongly-thawed meat? (Note: I've seen multiple related questions over at Cooking.SE, but I'm looking for a scientific explanation, not cooking advice!)

I've been researching this for a couple of hours but the more I read, the less I seem to understand the situation. Many sources claim that thawing meat in warm water is wrong and that I should instead opt for cold water to prevent bacteria from growing and producing toxins. I found a wide variety of toxin-producing bacteria that can live and reproduce in meat, such as Escherichia coli, Salmonella, Corynebacterium diphtheriae, Listeria monocytogenes and Clostridium botulinum.

There are two things I don't understand:

If I thaw the meat quickly, the bacteria have less time to reproduce before I cook the meat. This is especially true for Listeria monocytogenes which seems to be able to quickly reproduce in cooler temperatures. Why is it bad to thaw meat in warm water?
If the sources I've read are true, it leads me to believe that Listeria monocytogenes is not a bigger issue than the other species of bacteria growing in the meat. I suspect that bacteria compete for resources and that it is probably only one of them that is the main factor in making a piece of meat toxic for consumption even after cooking. What is the primary cause of meat toxicity?

Or is it possible that I've been overanalyzing the situation and the exponential relationship between bacterial growth and temperature is the main reason?

This is a really fascinating question and got me reading stuff all through the night. If my response seems tl;dr, then please skip to the fourth paragraph.

From what I've found in literature, it may be the case that prolonged exposition to certain temperature ranges may prove lethal to some pathogens. Shortening this time or shifting the temperature may cause suboptimal death rate of microbes. El-Kest et al. have found that Listeria monocytogenes would be most effectively killed by 5 to 6 freeze-thaw cycles with 35 degrees C as the thawing temperature and -18 degrees as the freezing temperature. Freezing at -198 degrees proved way less successful in killing the bacteria. This suggests that not only the thawing temperature and rate have the influence on microbial diversity in meat but also the actual temperature of storage!
Here is the link to the publication by El-Kest et al.: http://jfoodprotection.org/doi/pdf/10.4315/0362-028X-55.8.639?code=fopr-site

Freezing rate also has a significant influence. If freezing occurs slowly, ice crystals will mostly appear mainly outside cells with rapid freezing having the exact opposite effect. It is quite logical why it happens: spots within the food that are freezing will slowly make the unfrozen surroundings rich in ions and osmotically active substances, the water will gradually seep out from bacterial cells to the surroundings and subsequently freeze up. (https://books.google.pl/books?id=o6kJCAAAQBAJ&pg=PA25&lpg=PA25&dq=Inactivation+by+cold.+In+Inhibition+and+Inactivation+o+f+Vegetative+Microbes.&source=bl&ots=zlH-dMFiqo&sig=AfglM7piuvMnjI3q3JV0ovHy-FE&hl=pl&sa=X&ved=0ahUKEwjS-6fAypTYAhWiJJoKHe-gDJAQ6AEIQTAE#v=onepage&q=Inactivation%20by%20cold.%20In%20Inhibition%20and%20Inactivation%20o%20f%20Vegetative%20Microbes.&f=false)
From that perspective slow freezing is more likely to get microorganisms killed, as there is no cold-shock response and the cells do not become desiccated prior to freezing.

Now, let's look at the big question: why can't we use warm water to thaw meat. As one of the commenters pointed out, there is something called "danger zone" in frozen food safety, in fact USDA keeps talking about it all the time. This might be counterintuitive but by rapidly increasing the temperature in outer layers of meat, you will quickly provide microbes with ideal conditions for cellular division. As time progresses each next layer will be infested by bacteria from the outer layer as well as those that will just start undergoing cellular division, and so on, and so on, until you reach the very center. You end up with a pretty nice bunch of bacteria throughout your meal, though you shouldn't probably worry to much about it, unless you like your meat half-raw.

What happens during cold-water thaw or refrigerator thaw is different because you essentially increase the temperature of each consecutive layer but without providing enough thermal energy to give microbes a near-optimal temperature for intensive cellular division. Sure, they will start dividing anyway but to a much lesser degree. The temperature increase is not rapid therefore there is no abrupt resumption of life-cycles of microbes. Think of it as waking up on a cold winter day vs. warm, pleasant summer morning.

Still, you can use hot-water thaw safely if you're dealing with thin cuts of meat, if fact USDA approves it: http://onlinelibrary.wiley.com/doi/10.1111/j.1750-3841.2010.02037.x/full

Further reading:

https://www.fsis.usda.gov/shared/PDF/Big_Thaw.pdf
https://link.springer.com/content/pdf/10.1007/978-1-4615-5975-7_10.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662152/

Now, regarding your second question, I'll mostly answer from my own experience. We used to test meat in our microbiology lab during studies and we tested different kinds of meat. Teachers who teach the subject for 10+ years, when asked, admitted that there is generally a pattern of how many bacteria and what types of bacteria populate different kinds of meat, so there is no safe way to say that there is a single major pathogen that is responsible for food poisoning from meat in general. I'd say what's most dangerous are exotoxins produced by those bacteria, e.g. botulinum toxin is the most potent toxin known to mankind and Clostridium botulinum loves to populate meat stored at room temperature. Listeria is a popular example because of its great survivability in cold temperatures. But it really depends on the kind of meat and even on the specific batch of meat. You simply never know what you'll get with it.

Either way, you were not just overanalyzing the topic. There are really many factors to the quality of food preparation safety, especially when it comes to meat. To summarize:

Hot-water thaw can be used for thin slices of meat (I still use it for bigger slices as well, but only if I'm certain I'll fry the meat very thoroughly)
Cold-water thaw is better due to lower probability of serious bacterial infestation, especially recommended for thicker slices of meat
Freezing as well as thawing rate both influence meat quality
Freezing temperature cannot be too low, nor too high to ensure optimal death count of certain species of bacteria
Meat toxicity is generally caused by pathogenic bacteria that multiplied within or were previously present (e.g. due to improper meat handling by the producer), in most cases due to the toxins produced by the bacteria

Hope I helped a bit :)

[EDIT]
There was a request in the comments to include some more info about the toxins produced by food-borne pathogens. There's a good review here:
https://www.ncbi.nlm.nih.gov/pubmed/8750662 (not sure if paywalled though, I'm using library internet right now). You could group those toxins into 4 arbitrarily defined groups:

heat-liable enterotoxins – these generally can be destroyed in the process of cooking or frying; produced by Salmonella spp., E. coli, Campylobacter spp., Vibrio cholerae (yes, this one causes cholera)
heat-stable enterotoxins – these cannot be efficiently removed by heat preparation of food; produced by Yersinia enterolytica and some strains of E. coli
Shiga-Like toxins – they resemble verotoxin of Shiga spp.; produced by E. coli O157:H7 (this strain is very pesky, as it induces hemorrhagic diarrhea and kidney failure)
Unique toxins – some bacteria produce unique toxins, e.g. Bacillus cereus, Clostridium botulinum, Clostridium perfringens

Generally E. coli strains have many subtypes of heat-stable as well as heat-liable enterotoxins and some strains have other types of toxins like the O157:H7. The name "enterotoxins" refers to toxins that are secreted by microorganisms targeting intestines and generally they are cytotoxic, which essentially means they cause cell lysis of the host. Mechanisms of action are varying, e.g. cholera toxin triggers a cascade of reactions that overdrive CFTR channels (chloride ion transporters) and alters osmotic balance, which macroscopically manifests itself by a production of characteristic watery stool.

Worth noticing: some of those pathogens require other factors to cause disease, e.g. Vibrio cholerae requires a toxin-coregulated pilus to be pathogenic and some even do not produce any toxins directly (for instance Listeria monocytogenes overdrives lysosomes and doesn't let them take the bacterium apart, then it spreads from cell to cell by the means of actin filaments).

In the context of detox diets, there is a large dispute going on about their effectiveness whatsoever. I'd recommend confronting these two articles, which, to me are well written:
https://link.springer.com/chapter/10.1007/978-3-319-49929-1_33
http://onlinelibrary.wiley.com/doi/10.1111/jhn.12286/full
Some animal models have indeed shown some anti-toxic effects of certain foods, other researchers argue that most of the toxins eventually get to the liver and get broken down. The liver does its job pretty well, so running for two weeks on a "kale juice" would be a bad idea. People seem to forget that usually the dose is the poison: if you ingest highly diluted cyanide, it won't harm you, while drinking 7-8 liters of water at once could kill. Switching to an unbalanced, monotonous diet could be actually detrimental to health a lot more than those minuscule amounts of food-borne toxins ingested. The best way to live a healthy life is still: move, eat well and diverse, follow food safety guidelines, take care of your physical and mental health.


Vitamins that could help "make us smarter"? I was at Sprouts health store and saw a lot of vitamins/herbs that claimed to be "Study Aids" etc, so if there is any basis to it, where exactly does it hold truth? And are these supplements safe?

Are there vitamins that make us smarter?

Vitamins are micronutrients required in small quantities for normal human metabolism. Extra high (supra-physiological) doses do not generally result in improved performance. Of course, if one is deficient in certain vitamins (e.g. Vit B-1 deficiency causing Wernicke-Korsakoff encephalopathy), taking a vitamin can restore normal function. However, with adequate access to a normal diet, you are unlikely to be deficient. Commonly cited exceptions include:

strict vegans (Vit B12)
alcoholics (thiamine (B1), folate)
cultures highly dependent on maize as a staple (niacin (B3))

In people with a normal diet, taking additional vitamin supplements is usually not helpful.* (An exception may be Vitamin D depending on whom you talk to, but this is unrelated to cognitive performance.)

There have been scattered studies showing some benefit of various plant extracts and other “natural” substances. Studies such as this one about Bacopa monniera do demonstrate benefit. However, many such studies are of limited value due to sponsorship by the makers of supplements and publication in journals with questionable quality of peer review. This meta-analysis reviewing the effects of phosphatidylserine, phosphatidylcholine, citicoline, piracetam, vinpocetine, acetyl-L-carnitine, and antioxidants reached a more guarded conclusion:

  for most of the "brain-specific" nutrients we review, some mildly suggestive effects have been found in preliminary controlled studies

Note that most of the substances discussed thus far are not vitamins but rather amino acids, more complex plant extracts, or — in the case of caffeine — a synthetic crystalline xanthine alkaloid. These sorts of things are commonly included in supplements found at health stores. As for vitamins specifically, this large randomized controlled trial found no effect of multivitamin and mineral supplementation on cognitive function.

What component of Cognitive Supplements are active?

The answer is usually caffeine. Caffeine is cheap, widely available, and markedly improves short-term cognitive and physical performance. By modulating adenosine activity in the central nervous system, it improves alertness, prevents impairment in neuro-plasticity associated with sleep deprivation, potentiates synaptic transmission in animal models, and may slow neurodegeneration in certain disease states.

This review article looked at ”enhancement supplements” containing taurine, guaraná, ginseng, glucuronolactone, B-vitamins, and other compounds  as well as caffeine and concluded:

  there is an overwhelming lack of evidence to substantiate claims that components of [energy supplement drinks], other than caffeine, contribute to the enhancement of physical or cognitive performance.

To your question,

  Are these supplements safe?

You should look at the ingredients. If it is caffeine, the answer is: usually. However, it is not recommended for those with insomnia, anxiety, palpitations, or who are underweight. As for other components of these, you need to read the label and do your research. As mentioned in the footnote, vitamins themselves are not without the possibility of harm at supra-physiological doses. For other components the danger is likely uncertain and under-researched.

*For those interested in the vitriol around this subject, check out this series of editorials that followed the paper linked above. Quoting the first of these:

   In conclusion, β-carotene, vitamin E, and possibly high doses of vitamin A supplements are harmful. Other antioxidants, folic acid and B vitamins, and multivitamin and mineral supplements are ineffective for preventing mortality or morbidity due to major chronic diseases. Although available evidence does not rule out small benefits or harms or large benefits or harms in a small subgroup of the population, we believe that the case is closed— supplementing the diet of well-nourished adults with (most) mineral or vitamin supplements has no clear benefit and might even be harmful. These vitamins should not be used for chronic disease prevention. Enough is enough.


Why do humans have 46 chromosomes? Humans have approximately 25000 genes. Why are these genes on 46 chromosomes? Why not 40 or 50?

According to this article, no one knows; it's an "evolutionary mystery." As a general rule, closely related species generally have a similar number of chromosomes, and the number typically increases with the complexity of the species. However, the actual number varies wildly.

The author also points, out,

  Each egg or sperm gets 23 chromosomes (half of each pair). Which
  chromosome they get in the pair is totally random. When you do the
  math, this comes out to 10 trillion different possible combinations.
  If we had only one pair of chromosomes, the number drops to 4.


Do xylem vessels in roots have lignin? I learned that water enters xylem vessels in the roots after absorption by osmosis, but also that xylem cells are impregnated with lignin that doesn't allow water to pass through them to prevent water loss. Does that mean xylem cells in roots of plants aren't impregnated with it?

We have to consider the main function of lignin in xylem vessels, which is providing mechanical support for the plant. For the parts of plant above the ground, the stem where the xylem is located has to counteract the gravitational force pulling the plant down. Here's where lignin comes in to strengthen the xylem to support the plant. Remember that this is for many land plants.

Compare this to creepers, vines and aquatic plants. Lignin is absent or only present in small amounts as for creepers and vines, they have another external support, while for aquatic plants, it's weight is distributed on the surrounding water apart from the stem.

Now we can liken the case for aquatic plants to the xylem vessels in the roots of land plants. The roots of land plants are firmly anchored in the soil, and the plant's weight is distributed along the roots and soil, not just on the central root (for tapped roots). Hence there is not a need for lignin in roots of land plants.

And yes there are perforations in lignin as mentioned by @Always Confused, hence water can still enter the xylem vessel even when lignin is waterproof.


Are there animals who do things just for pleasure like humans? In a debate my father said that only humans do things that are not directly linked to survival(painting, playing musical instruments, singing etc). He said that this is because we are "special" and not like other animals on the planet.

I said that this is only because we have much more developed brain than other animals. But now I'm also interested in one question.

Are there animals who do similar things(not exactly same, of course) not for mating/survival but just because they like it?

I see that Gerardo has said effectively what I was going to: animals don't do things because they have reasoned out that these things will help them survive; they engage in behaviors because these behaviors lead to reward circuitry response and animals who find general categories of behavior rewarding have tended to survive better. Sometimes behaviors that are not directly related to survival trigger the same circuitry.

(P.S.: this is exactly what is happening in humans, too.)

Masturbation is one example, as above; so are animals that 'adopt' either conspecific or heterospecific juveniles who don't belong to them, which is not uncommon in many species. (Barn cats in particular do this often; aside from all the cute Youtube pictures of cats who think ducklings are kittens, it's very common for queens with kittens about the same age to co-nurse them.) You can argue that sociality and taking pleasure in altruistic activities with no immediate personal benefit is a survival adaptation, but that's not a calculation the animal is consciously making at the time.

Animals often have strong aesthetic preferences, especially for conspecifics; female and male animals often prefer traits that don't have anything obvious to do with survival in potential mates, and there is an entire discipline of sexual selection in biology devoted to teasing out why. It's worth noting, however, that in many species it turns out that females have preferences that vary widely for a number of traits, and that female preferences do not always line up to male reality...

Outside of naturalistic social behavior, numerous examples of elephants and chimpanzees creating drawings or paintings in their enclosures without any conscious reinforcement from their keepers have proved interesting reading. There are also examples of animals who keep "pets", including the famous case of Koko the gorilla and her pet kittens. You may find this article, with descriptions and citations of several animals who may or may not be engaging "art" for its own sake, to be a useful read.


What is the Edward O. Wilson fuss about? I have just read this article on E. O. Wilson and I don't understand what the difference is between what he is arguing and "standard" natural selection.

I read "the extended phenotype" some years ago and from what I vaguely remember that argued that everything about selection comes down to genes: they are the units of what is inherited and drive everything else (and their reach can be quite surprising).  At first glance that seems inconsistent with the article, since it mentions "group selection".  But when you read the details it includes things like

  Group selection begins when a colony of creatures develops a behaviour
  that gives it a competitive advantage over other groups. Initially,
  this could be down to a random genetic mutation.

which sounds like it's gene-based too (and examples seem to come from ants and the like which I thought were closely genetically-related across a colony too...).

So what is the fuss about?  And how will it be resolved?

Maybe the difference is easier to explain in terms of some difference between mathematical models?  If so, that's fine (I hope - it might make more sense than jargon in a field I am unfamiliar with ;o).

[Is this too "general public" for this site?  Apologies if so.]

After reading the article, the fuss is about this:

In currently accepted theory Eusociality or "kin selection" explains altruistic behavior (the sacrifice of yourself or resources you control for the betterment of something else besides you) by relating the act to the amount of genetic information passed on.

The relevant equation is Hamilton's rule:

                                                                $rB > C$

C is the cost to the actor (the person giving up resources). B is the number of others involved, and r is the relationship value to the actor in terms of genetic similarity.

So if you and two full-siblings (who each share on-average 50% of your genome) and a bus comes straight at the group, and you have the capability to push them out of the way while dying yourself, kin selection suggests you shouldn't because the genetic cost is equivalent. You eliminate yourself from the gene pool, and save the equivalent of yourself for future generations (2 x 1/2 = 1).

However, if you and three siblings were in the situation, then it's evolutionarily advantageous to be altruistic. You would die (a cost of 1), but you would save the equivalent of 1.5x your genome (3 x 1/2 = 1.5) to pass on to future generations.

Thus, communal and social behaviors like those of ants basically boil down to: Everybody is so closely related that spending resources to help your kin is essentially spending resources to ensure the majority of your genome survives (which is the big point of evolution, after all).

Wilson's argument, what I can glean from the small brief of the study and the article, is that you don't need the relatedness equation to explain altruistic behavior in social situations (basically the row is he's saying the currently accepted theory is wrong). All you need to start with is a genetic mutation somewhere along the line that causes the offspring to stick close to home. Once you have a few generations that don't leave the nest, you start to develop social behavior that results in altruism because you've gone from selfish individuals to a group setting.

The article and Wilson don't give any more insight other than altruism apparently develops spontaneously from the formation of groups. Simply being social is the explanation for why some individuals will give resources to others to ensure the success of the others.

Whether or not Wilson is correct isn't really discussed. He openly admits to needing a lot of research, some of which is being performed.


Do blood cells immediately die after leaving the body? I am wondering, do blood cells die right after they leave the body?

No. If they did, blood transfusions wouldn't be possible (or they would require some sort of direct body-to-body system).

Red cells collected can be stored under refrigeration for over a month. See for example the description of what happens to donated blood from the Red Cross. Platelets don't last quite as long, but they also survive for some time in the right conditions. Of course, some cells die during storage, but there is no instantaneous die-off once cells leave the body.


Are there known genome sequencing issues in E. coli? Despite the fact that the human genome project was declared "complete" in 2001, there are even now still gaps due to difficult-to-sequence regions of the genome such as telomeres and centromeres. Only last year was the first entirely complete chromosome sequence produced.
Telomeres and centromeres, however, are specific to eukaryotes.  Are there similar challenges with prokaryotes? A recent publication on a gapless E. coli sequence implies that there are indeed typically gaps, but I can't tell whether this indicates any systematic challenges, as with the human genome.
Thus, my question: are there known genome sequencing issues that currently make it difficult to acquire complete genome sequences from common lab strains such as E. coli?

Generally, gaps in genomes occur due to failure of de novo assembly -- the DNA can be sequenced accurately, but cannot subsequently be placed into a contiguous assembly due to alignment ambiguity with adjacent sequences.  In eukaryotes, telomeres and centromeres are difficult to assemble from short reads because they are highly repetitive. In bacteria, repetitive regions of the genome can cause similar problems when assembling from short reads.  Such regions include CRISPR arrays, integrated mobile elements (e.g. transposons), and gene duplications.1,2
So, what made a short-read no-gap assembly of E. coli strain C difficult, specifically? Alignment of the original short-read assembly 3 to the long-read reference 4 with Mauve 5 gives positions and length of gaps.

The first gap in the ordered short-read assembly (left-most red line in the figure) occurs at position 15,085 in the first contig and is 320 bp long. Looking at the same region in the long-read assembly, this closely corresponds to a 236 bp tandem repeat (CTGG × 59) at position 14,848. The authors of the short-read paper used 150 bp paired-end MiSeq reads to create their assembly, which, after adapter trimming, would likely not give enough sequence context flanking the repeat region to span it with a single read, thus creating a gap. This is just one example, and the rest of the gaps could also be repeats or other aforementioned mobile elements.

Treangen TJ, Abraham AL, Touchon M, Rocha EP. Genesis, effects and fates of repeats in prokaryotic genomes. FEMS Microbiol Rev. 2009 May;33(3):539-71.
Ricker N, Qian H, Fulthorpe RR. The limitations of draft assemblies for understanding prokaryotic adaptation and evolution. Genomics. 2012 Sep;100(3):167-75.
https://www.ncbi.nlm.nih.gov/nuccore/MNKV00000000
https://www.ncbi.nlm.nih.gov/nuccore/CP029371
Darling AC, Mau B, Blattner FR, Perna NT. Mauve: multiple alignment of conserved genomic sequence with rearrangements. Genome Res. 2004 Jul;14(7):1394-403.


What type of ants are these? I live in NYC and these fellas started popping out near my computer screen and desk. They don't seem interested in food as my sister usually leaves candy wrappers around. They however are stinky, I tried to catch one with a tape and I can smell the odors they give off like 4 inches away. They got these stingers on their butt so I think they could be a species of fire ant. They're also really tiny. As shown on a q tip here.

(click to enlarge)

Finally could these be bites? They are really itchy and I get them overnight.

They should be Red Imported Fireants.
https://en.wikipedia.org/wiki/Red_imported_fire_ant


Identification of unknown bagworm (Singapore) This bagworm was found in Singapore (near McRitchie Reservoir) some time in June 2012.

This is the plant from which the bagworms were obtained:

A few examples of the bagworms:

The bagworm when dissected out of its bag:

Is the plant Banana (looks similar)? If so, the bagworm (Psychidae) Kophene cuprea could be a possibility, since it is considered a pest on banana (Mosich & Larsen, 1978). The larval case is also supposed to be conical, but I cannot find an online picture for comparison.


Does ethanol destroy RNase? I've gotten conflicting advice on this: some people believe one can remove RNase contamination simply by spraying the bench, pipettes, gloves, etc. with ethanol. Others think ethanol does not destroy RNase and special reagents are needed to prevent RNase contamination.

So does ethanol remove RNase contamination? If not, what reagent does?

I think the protocols to clean glassware take no chances and just care about RNA degradation rather than targeting one class of enzymes.

EtOH is supposed to denature RNAse and any other proteins on the surface.

Other chemicals such as Diethylpyrocarbonate  (DEPC) used to wash glassware kill all biochemical activity by reacting with nucleophilic moieties in the protein (-OH, -SH -NH(2/3) ).   (See comments below for more.)

These treatments are followed by heating at 300-450 F for 2-4 hours.  This is not a specific RNAse decontamination - all biological activity is killed.

RNAse activity is not assessed by specific detection of a particular enzyme, but rather judged by the degradation of an RNA sample in the lab environment.  So specific inhibition isn't worthwhile - any protein that might interact with and degrade RNA is called an RNAse in these protocols.


Phosphorylation-Dephosphorylation : ATP-driven VS spontaneous Is protein dephosphorylation most commonly spontaneous (without need of ATP)? I came across some papers that mention it, as well as the opposite case (ATP-driven), but I can't figure out which is common or which is rare.

In the case of protein phosphorylation, I would say ATP is always needed since it provides the phosphate? Or could you have a spontaneous phosphorylation using free phosphates that float around?

I am aware that in the end, pretty much everything is possible, so I am more looking for likelihood. What is commonly accepted, wide spread, and what may happen but is rare.

First, I would like to clarify what is meant by "spontaneous". In chemistry, thermodynamically favorable reactions ($\Delta G < 0$) are indeed termed spontaneous because they will eventually occur, regardless of how slowly. But if transition states are unfavorable (high energy barrier), the reaction rate can be extremely slow --- millions of years in some cases. For example, combustion of wood is highly favorable and, chemically speaking, it is spontaneous. But that doesn't mean trees are unstable and likely to catch fire any minute.

Most biologists would probably call a reaction "spontaneous" only if it actually happens on a reasonable time scale, perhaps on the order of hours, depending on the context. So the terminology is a bit messy. But neither chemists nor biologists would call a molecule "unstable" if it has a reasonable half-life, I think.

Now for the actual questions. Dephosphorylations are typically not ATP-driven, because breaking the P-O bonds is usually favorable already (although I'm sure there exceptions). However, the reaction is typically too slow to be useful to cells, so it is not "spontaneous" in this sense, and therefore needs to be catalyzed by phosphatases. A typical example is alkaline phosphatase which dephosphorylates a wide range of proteins and other substrates.

Phosphorylation requires a phosphate source of course, but also an energy source, because forming P-O bonds is not a favorable reaction on its own (the reverse of the above). So adding a lone phosphate would not be favorable, but transfering one from ATP is much better, because this simultaneously involves breaking a P-O bond in ATP, "freeing up" energy to drive the reaction.

Finally, an interesting point is that ATP itself is actually a quite stable molecule, with a half-life of about two weeks. So ATP hydrolysis is not "spontaneous" in the biologist's sense, and enzyme catalysis is required (kinases). In fact, the combination of a high "energy content" and good stability is probably key to the role of ATP as an energy currency in cells: if ATP was indeed unstable, it would randomly phosphorylate everything. Stability means enzyme catalysis can be used to control phosphorylation events. Truly unstable compounds are never used by cells, because their reactivity causes damage and toxicity.


Why does the chance of having a baby with Down's syndrome increase with the age of the mother? Down's syndrome occurs when either the egg or the sperm cell contain on extra chromosome 21. To my understanding, women are born with all the egg cells in place already, so there's no further cell divisions, and thus no further chance of having one cell with an extra chromosome.

Now, the chance of having a baby with Down's syndrome increase with age:

  At maternal age 20 to 24, the probability is one in 1562; at age 35 to 39 the probability is one in 214, and above age 45 the probability is one in 19

Why is this so, when the egg cells are complete at birth?

The frequency rises with maternal age due to a peculiarity of meoisis
  in female mammals.  Meiosis is originated in the fetal ovary,
  arresting at metaphase I with the homologous  chromosomes aligned for
  segregation. Cells remain in this state until the time of ovulation,
  often  decades later in humans. The longer cells remain in the
  arrested state, the greater the chance  that there will be a
  nondisjunction event when meiosis resumes.

Source : http://www.madsci.org/posts/archives/2005-07/1121714807.Ge.r.html

I think you have the misconception that egg cells have completed meiosis by the time female is born. This is not true ( as indicated above in the answer). At birth, they are in metaphase I , after puberty, each month some of them divide further but only one survives and get arrested at metaphase II . Only after fertilization is the meiosis complete.


Using PGAL10 promoter to overexpress specific yeast genes: How to? I was reading a poster about expression boosting for Artemesinin production in yeast and it had this line:

  PGAL1
  and PGAL10 have been used for the
  overexpression of all genes from the mevalonate
  pathway.

What exactly does this mean? I suppose these are promotors? http://www.yeastgenome.org/locus/S000000224/overview

But how exactly does one use them during cloning to boost expression?

Say that you wanted to over-express ERG10, the gene coding for the first enzyme in the MVA pathway. How does one go about using PGAL10 to do this during the cloning steps?

Link to the poster: https://ddd.uab.cat/pub/tfg/2014/119349/TFG_narcisferrerledo.pdf

You're right about them being promoters, although it would be useful if you posted the link to the source of the sentence that you cite, so that we can read exactly how they are being used.

A fairly common way to study genes that aren't consistently highly expressed is to place them under the control of a strong promoter; that is, a promoter that is recognized by transcription factors in such a way that its linked gene is almost always expressed.

This is exactly what this group did in this paper, to study some features of yeast metabolism. In this case, the genes that they were interested in studying were cloned into a vector that was then inserted into yeast cells that lacked that gene. This way, the researchers knew that any expression of their gene of interest came from the vector and was driven by the pGAL1 promoter.

Similarly, if ERG10 was your gene of interest, this might be a strategy that you could adopt to study it.


Confusion about the duration of different phases of the cell cycle such as G1, G2 & S We all know that normally most of our cells (which are alive and have nuclei - except for cells such as "stem cells", "red blood cells", etc) spend most of their lives in interphase.
But the Interphase itself is also composed of other parts, other stages, including G1, S, and G2.
Is the staying duration of the most human cells in each stage(G1,G2 & S) is comparable to the other stage?
For example, is it true to say that:

"Most human cells, which have the ability to divide(passing the cell cycle), spend most of their lives on stage G1 than S phase or vice versa."?

Usually, which stage is the longest or shortest?
It is quite clear that the G1 is normally longer that G2 and as far as I know the G2 is the shortest stage in interphase, but what about G1 and S?
Is stage S usually longer than G1?
Is there any information?

It depends on the conditions, cell type or state of the cell.

I don't think anyone here can do better justice to the question for a beginner than this web page.

To show you why your answer is not answerable, by way of example: some cells exit the cell cycle and enter a stage called G0. This can be a permanent state for some cells, or, for instance, others may return to the cycle if they receive (external) signals.

Here is a very loose approximation, circles are to scale with respect to cycle time. Notice, for instance, the human circle is for an immortalized cell line under laboratory conditions, rather than for cells in your body. A neuron (brain) or an enterocyte (gut) have vastly different cell cycle states, so it's impossible to give you a single straight answer without misleading you totally.

Bonus food for thought: notice that the fraction of time cells spend on G1, S, G2 and mitosis is also different between different cell types.

Bonus food for thought #2: In fruit fly embryos (pictured bottom right in the above picture), you have an extreme example of unconventional (non-textbook) cycling. Rather than synthesizing new cytoplasmic materials, the size of the developing embryo is constant except for the replication of the genetic material. This happens in the growing larva for ~10 cell divisions, in thousands of cells. One of these cycles takes about 8 minutes to complete fully. That's an impressive time to copy a genome; most* bacteria can't do it this quickly!

(*any that I am aware of)


Why does a coconut have exactly three "holes"? Why do coconuts have exactly three "holes", as seen in this picture?

A theory says:
As coconut is a sibling of palm, somehow long time ago, three palms were in a same husk. Based on evolution theory, it's how the coconut was born in the world with three holes.

Reference:

"Why does a coconut have exactly three eyes?", Quora

The three "holes" are the result of the 3 carpels in coconut flowers, and three carpels is typical of the family Arecaceae (Palms). The "holes" are actually germination pores, where one is usually functional and the other two are plugged. The new coconunt shoot will emerge from the functional, open, germination pore.

For further info and pictures, see this webpage or the paper Morphological and anatomical studies of the coconut (Smit 1970, link to pdf), which holds a wealth of information.


What is the morphological difference between Leydig cell in human and pig? The pig is only an example, just an animal. Leydig cells have protein inclusions (Reinke crystals) that are mostly made of crystallised lipofuscin. They are secretory inclusions i.e. cells formed in secreting cells.

An example of Leydig cell in pig's testicle:

My teacher told me that there is a difference in the existence of some cells between humans and animals.
However, I cannot find such a difference. I have not been provided a slide of human Leydig cell so I have not been able to compare.

What is the morphological difference between Leydig cell in human and pig?

Perhaps what your teacher meant was not so much a difference in Leydig cell morphology, but in interstitial tissue morphology, ie. tissue which occupies the space in between seminiferous tubules. Leydig cells are its most interesting component, others being small blood vessels (a lot of them), nerves and connective tissue (mostly fibroblasts, mastocytes, lymphocytes and macrophages). In different species interstitial tissue looks differently, for example:

Leydig cells form clumps around blood vessels, and are surrounded by fibroblasts (which makes them more difficult to isolate) in guinea pig, but not in mice or rat;
in human a lot of interstitial tissue is extracellular matter, Leydig cells are not so frequent, but more active;
and, last but not least, in pig, there is little extracelluar matter and a lot of Leydig cells that are very easily isolated (and produce large amounts of estrogen).

I found all this in some old lecture notes; I couldn't dig up any sensible reference, though.


qPCR: do both primers have to contain a GC-clamp in order to be effective? I'm developing software which, among other things, designs primers pairs (forward and reverse) for qPCR. In my research on various properties, I read about GC-clamps and I understand the basics of it I think. There is still something unclear to me.

Do both primers in a pair need to have a GC-clamp in order for it to be effective? Or does one GC-clamp in, let's say the forward primer, just increases specificity, and both primers containing a clam increasing it even more?

You can have GC-clamps (3' terminal G/C) in both primers; this may overall improve the PCR efficiency. However you should take care not to put too many G/Cs. This may lead to stabilization of primer pairs, leading to formation of primer-dimers. Also see this post: When designing primers how important is the GC clamp?

GC-clamps are not always essential and you should look at other parameters too.


Do "shooting" animals exist? The well-known cartoon imagery of porcupines shooting their quills at opponents in a fight is just that: a silly cartoon concept that isn't real.  But it makes me wonder, does that mechanism exist elsewhere in nature?
Are there any animals whose bodies produce solid projectiles that are used as launched/thrown weapons?  (Not looking for liquid ranged weapons such as skunk spray, bombardier beetles, etc.)

A good exemple should be the “harpoon” in cone snails (Conidae), which is created from a modified tooth inside their proboscis.

(Cone snail with proboscis, from KQED.org)
The harpoon is launched at prey at close distance, and is used to poison and stun prey, and later to pull them in. According to high-speed camera capture the harpoon is launched in just 200 microseconds, with an acceleration similar to a gun. The “harpoon“ structure is also very similar to a human made harpoon (see picture below)

(from KQED.org, Courtesy Manuel Jimenez Tenorio, Universidad de Cádiz)

(from KQED.org, Courtesy Joseph Schulz, Occidental College)
These harpoons are not re-used, and a cone snail can have up to 20 harpoons at different stages of development (see Cone snail toxicity).
It is also worth noting that the harpoon and its venom is a potent defence weapon also against humans. One cone snail can contain poison to kill about 700 people, and people stung by cone snails can get severely injured or even die (fatality reported to 15-75% according to Kapil et al, see below).
If you would include use of tools, in projectile use/shooting animals, apes and elephants are known to use stones as throwing weapons (see wiki-page linked below).
Sources:
https://www.kqed.org/science/1923898/watch-these-snails-stab-fish-and-swallow-them-whole
wikipedia: projectile use by non-human organisms  (with other examples of projectile use)
Kapil S, Hendriksen S, Cooper JS. Cone Snail Toxicity. [Updated 2020 Sep 3]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. www.ncbi.nlm.nih.gov


Why don't mosquitoes evolve towards muting themselves? Quite certainly, muted mosquitoes would be much more effective as far as their blood-sucking pursuits are concerned, since mosquito sound is predominantly responsible for sealing their fate (between the two palms of the hand). Muting themselves would certainly reduce the chances of being caught in the act. For instance, unless you notice by looking, leeches go undetected for long periods because there isn't any obvious sound emanating from them.

Thus, reasoning says - this should be favorable from the point of view of evolution, unless there is a some indispensable purpose served by this sound, which can not be otherwise served. This page seems to suggest that this is so from the point of view of mating. In fact, quoting verbatim:

  Since female mosquitoes are larger, they flap their wings slower, and males know it. They use the distinctive pitch of the females' buzz to recognize them. Louis M. Roth, who studied yellow fever mosquitoes for the U.S. Army during World War II, noticed that males ignored females whenever the females were quietly resting, but whenever the females were flying, and therefore buzzing, the males wanted to mate with them. The males even wanted to mate with recordings of female mosquitoes or tuning forks that vibrated at the same pitch.

But mating signals could also be of other forms, like some chemicals secreted (I envisage something like pheremones). Why is making sound so important? Why can't this noise be either less intense, or lie outside the audio range for humans (their targets)?

Your question is really good, but in actuality, they do evolve towards muting themselves, actually, they have pretty much done "most of the work":

It is assumed that microscopic scales along veins and wind margin
play an important role as a silencer as downs on the flight feather of owl.

From this we can assume that the effectiveness of these scales are high, as they had plenty of time to evolve; thus the other factor they should alter to make them quieter is the frequency of their flapping $f$, which can be calculated from the following equation:

$$f=K m^{-1/6}$$

where $m$ is the mass of the animal and $K$ is the proportionality constant. The resulting number is around several hundred hertz (Remi.b observed a value around 440 Hz)

There are two options for them, either increasing the frequency up until our ear is incapable of hearing it which would be impossible as even the highest flapping frequency can hardly exceed 1000 Hz, which is nowhere near the required 20,000 Hz. By increasing their body mass they could decrease the frequency but the needed 15-20 Hz is pretty low compared to the actual several hundred, thus it would likely need a complete body structure change which is not something to happen in the near-future.

An another solution might be a different strategy in flying. Gliding attacks might pay off really well (that's why owls on the other hand can't be heard during flight), but even though there are some insects capable of such[1], it would need an immerse amount of time, not talking about the problems that might arise from the bumping into of our body.

I don't think that the mating signaling would be indispensable from an evolutionary perspective, but this statement of mine can't be proved.

These are the physical/biological difficulties of the problem, here is one from an evolutionary aspect: They are not likely to have experienced a strong selection against this feature, as most of the possible victims are incapable of doing much against a mosquito due to the absent of hands (and tails are seldom enough to stop them). The first possibly blood-sucking mosquito was found to be living 79 million years ago, while animals that might be able to "seal their fate" are much more recent, while not even having success most of the time.

https://www.jstage.jst.go.jp/article/jsmec1997/43/4/43_4_895/_pdf
http://www.geologica-acta.com/pdf/aghv3501a12.pdf
http://www.physics.emory.edu/faculty/weeks//lab/papers/jwang-arf05.pdf


Why do spiders make their web near the ceiling and near a light source? Why do spiders make their webs near the ceiling and near light sources ?
Is their an advantage for spiders in doing that? For example do they catch more insects when their web is near a light source because prey insects are drawn to it, hence giving those spiders with a well-lit web a better chance of survival?

Because many insects (their food) are attracted to light. This attraction is called phototaxis.

Hypotheses for why insects are attracted to light

The leading hypothesis for why so many insects are attracted to light is that before artificial existed, insects were using the light from the moon in order to navigate. They would keep themselves at a given angle relative to the light source in order to navigate straight.
Another hypothesis is the presence of light indicates that the pathway is clear.
A third hypothesis is that some insects may confuse artificial light source with the other sex. This appeared to be true for moths for example

These three hypotheses are not mutually exclusive.

How do spiders chose their habitats

For more information about the abilities of spiders to find a good habitat, have a look at this very interesting answer.


"Acellular" designation for organisms Why do some biologists refer to single-celled organisms such as Amoeba and Paramecium as
acellular (i.e., without cells) rather than unicellular (i.e., one cell)?

From Wikipedia:

Some biologists refer to wholly syncytial organisms as "acellular" because their bodies contain multiple nuclei which are not separated by cell walls.

As Albano pointed out, "cell walls" should probably be "cell membranes".

Paramecium and some types of amoeba like the Chaos genus have multiple nuclei so they fall under this definition.


Theoretically, what technique would one use to modify a virus so that it only affected a subset of the population? I'm writing a novel and i would like to know some of the equipment and techniques involved with modifying a virus.

Is it feasible for a virus to be engineered to only affect certain people? It doesn't have to be possible, only sound like i know what i'm talking about. I have been trying to research the subject but nothing i have found will tell me the basics of what is involved with virus modification.
Thanks.

Yes, it is possible and probably you won't need many literary artifices to make it work.

Essentially viruses are what is technically called "obligate intracellular parasites".
Parasites because they cannot grow by themselves, they need a host cell from which they "steal" the intracellular machinery to replicate; intracellular because they grow inside cells; and obligate because they cannot reproduce outside their target cell.

Now, each virus has its "favourite cell" to infect. For instance HIV targets a type of lymphocytes (cells of the immune system), other viruses may only target bacteria (these are called bacteriophages) and so on.

How is this specificity achieved? Well, to put it simply, viruses "anchor" to specific proteins (or other molecules) that are sitting on the membrane of their target cells and that allows them to go in. If a cell does not have that specific protein, then the virus cannot infect it.

So, in your story, maybe the target population will have a mutation in their genome that will modify a certain protein. You could then (fictionally) construct a virus that specifically targets cells expressing that protein and you're set!

The virus construction part is just standard molecular biology, really.

A few things to read:
http://en.wikipedia.org/wiki/Genetic_engineering
http://en.wikipedia.org/wiki/Genetically_modified_virus
http://en.wikipedia.org/wiki/Viruses <--this explains a lot


Why do some trees hold their leaves through fall and winter? Why do some species of oak (Quercus spp.) retain their leaves through fall and winter?  I've found that these leaves are called marcescent leaves. There must be some benefit that the tree gains from this because it seems like it would increase the possibility of limb damage due to snow accumulation on the leaves.

The trait might not necessarily allow for an advantage, but a few possibilities have been proposed:

Nutrient return to the soil when needed in the spring
Less palatability to grazing animals

Source:

 http://northernwoodlands.org/articles/article/why-do-some-leaves-persist-on-beech-and-oak-trees-well-into-winter


Why are children and adults so different? In many animal species, juveniles aren't just smaller versions of adults. In mammals, the contrast is not as spectacular as in species that undergo metamorphosis, but still quite noticeable.

For example, puppies have shorter limbs and flatter faces than adult dogs. Fawns are coloured differently than adult deer, and males do not start growing antlers until they reach sexual maturity. There are behavioural differences as well: habituation is much stronger and faster in juveniles. In humans, children have different proportions than adults and lack secondary sexual characteristics. But why? Wouldn't it be simpler to form a small version of the adult and grow linearly?

Why delay sexual maturity in the first place?
Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
Why the different body proportions?
Why lose play behaviour and learning ability as adults?

I'm interested in mammals in general and humans in particular.

GREAT QUESTIONS!!!
Why delay sexual maturity in the first place?
-I believe it is also related to "the best-used" of resources. Firstly, it is unnecessary and impossible for children to have sex (biologically and evolutionarily), they don't have the physicality to sustain sexual intercourse or the ability to bear a children inside their body. Secondly, it is to focus resources on growth. Children uses lots of energy on growth. Human body does amazing jobs on allocating body resources or material so that we are in the best shape possible. If they don't do sex, they can focus more on growth.

Why tie sexual maturity to a host of other changes? For example, why aren't babies born with adult hair patterns? (Yes, because hair growth responds to sexual hormones, but the response could be different.)
- This one is a hard one. I believe it is just how biologists categorize human growth. We can study how human bodies develop in each stage, which is I believe it's really important on morphology.

Why the different body proportions?
-Evolutionary advantages!!! It is believed that baby has a greater head portion than adult. That's why people say children learn better than adults. Human values their brains more than other organs of the body, developing intellectual capacity as early as possible allows them to win in natural selection.

Why lose play behaviour and learning ability as adults?
If I understand you correctly, you are asking why adults lose their play behaviour and learning ability as they grow up. For learning ability, I believe it is caused by degeneration, just like the other organs of the heart. We have a mortal body and so once the body hits its maximum growth capacity, it will start going downhill unfortunately. For play behaviour, I believe it is a human behavioural changes due to life experience, social expectation and peer interaction. We lose interest of 'games' as we grow up because they are considered to be childish, silly and not useful.


Why is glycerol supplied/used as 87% solution? While preparing glycerol stocks of my transformed bacterial cells (DH5alpha) the protocol I had to follow was that I would make one 50% glycerol stock (500µl culture, 500µl glycerol 50%) and another 87% glycerol stock (850µl bacterial culture, 150µl glycerol 87%). 87 seems to be a very specific number. Any particular reason why 87% glycerol concentration is used?

Typically, a glycerol stock will have a final concentration of 10-20% of glycerol. Glycerol is highly viscous. Pipetting higher concentrations of glycerol is difficult (especially for smaller volumes). Therefore a lower concentration such as a 50% solution (works for me) is convenient: add 300µl to 700µl of bacterial culture.

Regarding 87%: some vendors provide 87% glycerol along with anhydrous (>99%) glycerol. The reason is probably the same: it is easier to pipette 87%.

From a vendor's website:

  Glycerol is a component of several buffers, media or reagents in
  biological research. It is supplied as glycerol anhydrous or 87 %, the
  latter containing 13 % water. Both glycerols are from the same
  quality, the 87 % glycerol has the advantage of a lower viscosity.
  Anhydrous glycerol can be pipetted with difficulty only, especially at
  low temperatures.

But the question is why 87% and not 90 or 80? See Michal et al. (2017)  for a relationship between viscosity and concentration of glycerol-water mixtures.

Another graph plotted from the data given in the document mentioned by iayork in the comments. Different coloured lines denote data at different temperatures (in °C). Original data from: The properties of ordinary water substance. Compiled by N. E. Dorsey, New York (Reinhold), 1940.

So I am guessing that 87% must have been optimal beyond which the viscosity just shoots up rapidly with a small increase in concentration. I wish to reiterate that this is just my guess. I could not find a authoritative (in fact any) reasoning on why precisely 87% glycerol is (or was historically) supplied.


What is "multiple" myeloma? Multiple myeloma, commonly referred to as myeloma, is a cancer of the plasma cells found in the bone marrow.(source)

Is there any significance in calling myeloma as "MULTIPLE" myeloma?

J. Von Rustizky, a Russian pathologist working in the laboratory of Friedrich von Recklinghausen (1833–1910) in Strassburg in 1873, introduced the term “multiple myeloma.” At autopsy, a 47-year-old patient examined had eight separate tumors of bone marrow, which Von Rustizky called “multiple myelomas,” and he noted that the nucleus of the tumor cells was located in the periphery of the cell membrane — a morphology highly suggestive of plasma cells.

source: Kyle, RA, Steensma, DP (2011) History of multiple myeloma. Recent Results Cancer Res., 183: 3-23

From the same item:

  The most commonly recognized [first documented] case is that of Thomas Alexander McBean, a highly respectable tradesman from London in 1850. Mr. McBean excreted a large amount of protein that was described by Henry Bence Jones in the middle of the 19th century. Jones was a well-known physician and made many contributions to medicine.

The Bence Jones protein is in fact an immunoglobulin light chain. Purified Bence Jones protein were sequenced by FW Putnam, and
variations between patients were some of the first clues to the existence of the variable regions of immunoglobulin molecules.


What is the purpose of the brown louver-like structure on the underside of a mushroom? On the underside of the cap of a mushroom is a structure with many brown leaves closely spaced together like slats or a louver.

What is the purpose of this structure?

These thin, closely-spaced structures are commonly called gills (in more formal contexts a gill is called a lamella).  Our most familiar mushrooms have gills, but there are other species that do not have structures of this form.

Photo by Jason Hollinger via WikiMedia.org

The gills exist for reproduction. Mushrooms spread by producing tiny spores that disperse on air currents.  (In fact the entire mushroom structure exists for this purpose; the main part of the organism, a fungus, is a diffuse web under the ground or other substrate.)

Mushroom spores develop on surface tissues so that they can be released into the air.  The gills evolved to provide more surface area so that more spores can be produced and released (up to twenty times the area of the supporting surface).  The gill spacing is important because the spores are shot out of the surface, are slowed by air resistance, and then fall downwards from between the gills. (Source: Why mushrooms form gills: efficiency of the lamellate morphology)


How can individual strands of coat hair have only a single color when considering codominance? I understand how codominance works. We have two (or more) alleles for one gene, neither having dominance over the other. They are both expressed independently, which means that different phenotypes are visible simultaneously. However, I'm not sure how it really works when we take, say, coat color. If both alleles are active, assuming each one produces a different pigment for each color, that means there are both pigments in a cell. What I see explained is that, if you look closely, each hair has a different color, and when you see it from far away, it gives the impression that the coat is made of one single color. But how can one hair have the same color all throughout? How can the different pigments be aggregated like this? As in, how is it that they do aggregate like this?

The terms dominance/recessivity, additivity, co-dominance, incomplete dominance, etc... express a relationship between genotypes and phenotypes but the mechanism behind this relationship is not being defined by these terms.

There might be a large number of mechanisms associating genotypes at a given locus with phenotypes. There is, in general, no reason to expect a mechanism of relationship of dominance at a given locus to be similar to that at another locus. In other words, there is no general mechanism leading to dominance/recessivity, additivity, co-dominance, incomplete dominance, etc...

On top of that, the actual mechanism in specific cases leading to particular genotypes - phenotype association are often unknown and I don't think we have good knowledge about what mechanisms could be more common or even how to categorize such mechanisms.

You might want to have a look at the posts

Why are some genes dominant over others? What is the mechanism behind it?
Evolution of dominance

or some papers such as

Llaurens et al. (2009)

In general, it appears suggested that one needs to know the specifics of the biological pathway to be able to predict dominance relationships and gene interaction network (see Llaurens et al. (2009)).


Is Thyroxine a hormone? I have read the phrase 'T3 is three to four times more potent than T4' several times both in books and websites. But isn't T4 a prohormone of T3? Why do then these sources talk about its potency as a hormone(I suppose)?

It is necessary to distinguish between classical and non-classical actions of thyroid hormones.

Classical action involves nuclear THR (or TR) receptors (TR alpha1, TR beta1, TR beta2). They are activated by T3, 3,5-T2, TRIAC and 3,5-DIAC, and blocked by rT3 and rTRIAC. T4 and TETRAC hardly have an effect on nuclear thyroid hormone receptors, but they are converted in the periphery and in target tissues by deiodinases to T3 and 3,5-T2, and TRIAC and 3,5-DIAC, respectively. From the classical perspective, T4 and TETRAC are therefore prohormones and not hormones in the narrower sense.

Non-classical action denotes binding of thyroid hormones to integrin receptors on the cell membrane. The resulting non-genomic actions may be directly mediated by T4 and TETRAC and don't require deiodination. From the non-classical perspective T4 and TETRAC are hormones sensu stricto.

Figure from Hoermann et al. 2015 (CC BY license)

References

Hoermann R, Midgley JE, Larisch R, Dietrich JW. Homeostatic Control of the
Thyroid-Pituitary Axis: Perspectives for Diagnosis and Treatment. Front
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Why do my tomatoes start to rot on the same fruit part? I observe a phenomenon for many years now. I observe it on a wide diversity of tomatoes produced all over Europe and Northern Africa that are sold at my local supermarket.

When I keep my tomatoes at ambient temperature around 20 to 25 degrees celsius, they deteriorate after a variable time, usually starting a five to fifteen days after I bought them. Nothing abnormal so far.

However, I observed that the mold pattern of virtually all these tomatoes is the same. It almost always starts a few millimeters from the junction where the tomato was attached to its branch, forming a ring on the top of the fruit.

I have thought why this could happen and my main hypothesis is that when they are grown the sun hits the top of the tomatoes (except where it is attached to the branch, obviously) and some ultraviolet radiation might weaken the tomato resistance in some way. The other reasonable hypothesis, although I cannot think of a definite mechanism, is that gravity would favor this polarized degradation. I have other hypotheses but they are too far a stretch, I believe.

So what is really happening?

I am a biologist, just not into botany or agriculture, so feel free to go technical and not just oversimplify.

Mold spores float around everywhere in the air, in your home and on farms. They are also likely found on the surfaces of farm equipment used for harvesting (shears, knives, etc.). Grey mold can infect tomato leaves and stems where there are lesions, such as those introduced when harvesting fruit, when cutting the fruit off at the stem. This could happen wherever such spores can find ingress between the farm, produce distributors, the market, and your home.

Cite: https://content.ces.ncsu.edu/botrytis-gray-mold-of-tomato


What is the mechanisms responsible for downregulation or loss of MHC-1 expression on the surface of cancer cells？ Downregulation or loss of MHC-1 expression on the surface of cancer cells generally have been thought to be involved in the mechanism of immune escape.
It seems to be very attractive but I don't know the mechanisms of downregulation or loss of MHC-1 at cancer cells. Would you tell me the molecular mechanism,

There is no single mechanism (as you'd expect, since there is no evolutionary relationship between different individuals' cancers).  The most common mechanisms are various forms of mutations, ranging from point mutations in single MHC molecules to large deletions of the MHC locus. Mutations in genes involved in antigen processing, that are not themselves part of the the MHC locus (e.g. TAP, b2-microglobulin), are also fairly common.  Epigenetic changes are also not uncommon.  There are several reasonably recent reviews, including

MHC Class I Antigen Processing and Presenting Machinery: Organization, Function, and Defects in Tumor Cells
Different regulation of MHC Class I antigen processing components in human tumors
The escape of cancer from T lymphocytes: immunoselection of MHC class I loss variants harboring structural-irreversible “hard” lesions


Spider Identification Illinois I noticed a really huge, beautiful web on my porch last week, and tonight, I discovered its resident. I'm thinking it's an Araneus diadematus (Cross Orbweaver), but I was hoping for some confirmation.

Can anyone confirm this or offer a better suggestion?

This is very likely an araneid (or Orb-weaver spider) in the family Araneidae.

Without further evidence, it's hard to narrow down to a species.

One possibility:

Neoscona crucifera (Hentz orbweaver, spotted orbweaver or barn spider)

 Source: Will Cook 2001

 Source: Wikipedia

Description:

Relatively variable in color (and sometimes pattern), but is usually rusty-red or golden orange color.

This site suggests females are reddish-brown to brown and males are lighter brown with the sides of the carapace nearly black.

Dorsal abdomen is brown and hairy; abdomen underside = black, with two white spots
The epithet crucifera refers to the cross-like pattern on their back
Legs have alternating light and dark brown bands.

Size: females = 9.5-19 mm long; males = somewhat smaller
Web: very large (up to 0.61 m diameter) and often on buildings and other man-made structures
Range: Eastern/Central USA + Mexico

According to Will Cook,

  Several other species of Neoscona are confusingly similar...Other species usually have a bolder pattern.

We can rule out Neoscona domiciliorum because Illinois is west of its range and the colroation is different. [Source].


Aligning multiple sequences in heterogeneous group I have a list of ~200 DNA sequences, representing probably 50 different genomic regions but they're all mixed up. For example, if I have seq1, seq2.... seq10, seq1 might align to seq3 and seq8, but be completely unrelated to the others.

There are also some differences in the lengths sampled, so the above example might represent:

Seq1-------------------------------------------------

Seq3----------------------   seq8-----------------

Such that seq3 and seq8 don't align to each other, but both align to seq1

So what I'd like to do is go through and somehow generate a list of groups of sequences that align to each other, as well as the alignments. eg:

Group 1

Seq1-------------------------------------------------

Seq3----------------------   seq8-----------------

Group 2

seq2------------------------------------

.       seq6-----------------------------

.   seq7--------------------------xxxxxx

Group 3... etc

Trying ClustalW or MUSSLE to align everything doesn't work (or takes an unreasonable amount of time), I'm guessing because there are so many sequences that don't align at all. I tried making a custom BLAST database and then BLASTed each sequence against it, but then I get multiple hits for the same alignment (with the group 2 example above, seq2:seq6, seq2:seq7, seq6:seq2, seq6:seq7, seq7:seq2 and seq7:seq6 all get returned as 6 unique hits, when they should be grouped together.

My current coding knowledge is fairly basic, but I'm willing to read docs and figure stuff out, I just don't want to reinvent the wheel.

Edit2:
Really, the grouping is the important part - once I have the groups, I can do the alignment separately with little effort. I'd just like to have groups where each sequence is in a single group.

You can try this:

BLAST each sequence to every other sequence (pairwise).
Every alignment (with some defined cutoff) denotes a connection.
Map all connections.
If a sequence is connected to some other directly or indirectly, it falls in a group. Put all the sequences that seq1 aligns to, in Group-1, then go to the alignments of these sequences; put all the sequences that these align to again in Group-1; so keep populating the group like this.

Methodology:

Install standalone blast (if you don't have many sequences then you can run online BLAST as well)
Make a blast database from your sequences using makeblastdb
Align these sequences against the database. If you are using online BLAST use BL2seq (align two sequences). It is much better and convenient to use standalone. You can also mention if you want plus-plus or plus-minus or both alignments. You might in some cases want only either of the two.
In the standalone BLAST you can specify the output format (which fields to include etc- the format you choose just depends on your requirements).

A tabular output format looks something like this:

# BLASTN 2.2.27+
# Query: TCONS_00036712 gene=XLOC_017996
# Database: ../nt_db/nt
# Fields: query id, subject id, % identity, alignment length, mismatches, gap opens, q. start, q. end, s. start, s. end, evalue, bit score
# 1014 hits found
TCONS_00036712  gi|191174875|emb|CU655970.6|    95.54   202 9   0   423 624 16680   16479   8e-85    324
TCONS_00036712  gi|51491599|gb|AC144709.2|  95.02   201 10  0   424 624 28443   28243   1e-82    316

Ignore the commented (#) lines; the first field is query ID, the second is the subject ID and there is an alignment between the two; the other fields provide information about the alignment (You can choose these fields).

For parsing I use a fast and easy scripting language called awk which is included in all UNIX based systems. It is also available for windows in GNUWin32 package.

What you have to do is check the first two fields and update the group.

# MakeGroups.awk

BEGIN{FS="\t"}     # Declaring Field separator as Tab

!($1 in grp){          # Check if the seq is a parent group. If not...
    k=1
    for(i in grp){
        if($1 in grp[i]){    # Check if the seq is part of any other groups
            parentgrp[$1]=i
            if(!($2 in grp[i]))   # Check if the second field i.e subject already present in the parentgroup
                grp[i][$2]        # if not assign the second field to the parent group
            k=0
            break    # stop checking further
        }
    }
    if(k==1)        # There is no parent group with this label and the seq is not a part of any other group
        grp[$1][$1] # Make a group with the query-id as the label and add this query to this group.
}

$1 in grp{
    if(!($2 in grp[$1]))
        grp[$1][$2]    # If the second field is not a part of the group with first field as label then assign it to that
}

END{
    for(i in grp){
        x++
        print "Group-"x"\n----------"
        for(j in grp[i])
            print j
    }
    print "\n"
}

Run this script like this in the terminal:
gawk -f MakeGroups.awk blastalignmentfile.txt

Note: This script contains multidimensional arrays. It will not work with all versions of awk. Use gawk version >4.0.

As swarnbes mentions in their answer, there are faster algorithms which do this kind of stuff and are used for sequence assembly. What many of them do is to make a graph (networks called deBruijn graphs), where each connection is an alignment, and compute an Eulerian Path. See this review by Pavel Pevzner for details. Overlapping sequences form contigs and you can easily trace back which sequence came from which contig (which you can call a Group). Each contig/Group is a disjoint deBruijn sub-graph.


Are vertebrate wings and fins considered vertebrate limbs? I have come across many articles which seem to suggest (but do not explicitly state) that limbs refer to arms and legs. My confusion stems from the fact that does the term vertebrate limb also include vertebrate wings and vertebrate fins or only refer to arms and legs of vertebrates. I would be grateful for clarification.

A simple google definition states that it does include the wings of birds however I would like to know if this is also the case in evolutionary biology or not.

I also refer you to this article
Yano, T., & Tamura, K. (2013). The making of differences between fins and limbs. Journal of Anatomy, 222(1), 100–113.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552418/

Are vertebrate wings and fins considered vertebrate limbs?

Based on other articles I have read wings are included in the definition of limbs but I am not sure whether fins are included.

There is no alternative definition of "limb" in evolutionary biology. Legs, arms, wings and fins are all limbs. Note that a prehensile tail can also be called a limb. From wikipedia > limb

  A limb (from the Old English lim), or extremity, is a jointed, or prehensile (as octopus arms or new world monkey tails), appendage of the human or other animal body.

You can have a look at Cohn et al. (1997), where the term limb is used to refer to legs, arms, wings and fins.

Apparently some authors (as OP has shown examples in the comments) use the term differently. I think it is always made clear so as to not yield to any possible confusion. If you've ever been confused, you might want to let us know which article got you confused.


What is this small insect called? It is about 1-2 mm long. It also can fly and it stays on the wall.

Location: Lebanon.

It looks to me like a cigarette beetle- they can infest many different types of products so I would definitely check everything carefully. Here's the link I used as a source, you can find more info here: https://www.orkin.com/other/beetles/cigarette-beetles/


Does alcohol really do more damage to the body of a child compared to an adult? Beside the fact that children and teens (people under the age of 18 year) usually have less body weight than the average adult, is there a   biologically fundamental difference between the damage done to their bodies compared to an adult when drinking alcohol?

I often read that their organs are still developing and thus alcohol will do more damage, but has this actually been proven?

As is stated in this article by Hiller-Sturmhöfel and Swartzwelder from the National Institute on Alcohol Abuse and Alcoholism, there are ethical issues surrounding research on human subjects that preclude direct testing, however studies in model mammals and observational studies do find that "adolescence is a unique stage of brain development which is particularly sensitive to the disrupting effects of alcohol."

A research review by Tapert, Caldwell, and Burke, also finds that studies support the conclusions that alcohol use by adolescents and young adults has a negative effect on cognitive abilities.

Hope that begins to provide you with an answer to your question.


How does sodium in one's diet affect blood pressure? Due to high blood pressure, my doctor has recommended I go on a low-sodium diet.  So, that got me wondering what it is about sodium that drives this recommendation?

What does sodium do to a body that, by its presence or absence, affects blood pressure in humans?

The basic reason is osmosis, the tendency of solutes to move from an area of high concentration to one of low concentration across a permeable barrier. So, ingesting large amounts of salt results in a high sodium concentration in the blood stream. This in turn causes water to enter the blood vessels by osmosis. More water in the blood means a greater volume of liquid and, therefore, higher blood pressure.

This process occurs primarily in the kidneys, specifically in the part of the nephron called the loop of henle (the image below was taken from wikipedia and is originally from Grey's Anatomy):

With low salt concentrations, water exits the loop and is retained by the body. When sodium concentration is high, the opposite occurs, water enters the blood stream by osmosis and increases blood pressure.


Is the brain functionally symmetrical? I understand that each half of the human brain handles different parts of our thinking. Left brain, right brain, that whole topic.

But in pictures, the brain is always depicted as having symmetrical structure. I'm curious about that. I realize that it might be silly to expect such a complex tool to be truly symmetrical, so my question is:

Is the brain functionally symmetrical or not? By functionally, I'm referring to whether the specialized groups within the brain all exists on both sides or rather each side contains different components.

No. For instance, Broca's area exists only in the frontal lobe of one hemisphere, usually the left. (it's responsible for speech, btw)


Phenotype-Genotype for multi-hybrid crosses It's generally easy to figure out genotype and phenotype frequencies using a Punnett square for monohybrid and Dihybrid crosses. But what about situations involving 5 or 6 traits? Is there a simpler way to get about this?

As a sample problem:
If we have two organisms crossed, one with genotype AaBBcCddEe and the other with genotype aaBBccDdEe (lowercase is recessive and upper case is dominant), how many individuals would have the genotype AaBBCcDdEE?

In my opinion, the easier way is dealing with each trait separately, as if it was a simple monohybrid cross, and writing down each result:

Aa x aa → $\frac{1}{2}$ Aa;
BB x BB → 1 BB;
Cc x cc → $\frac{1}{2}$ Cc;
dd x Dd → $\frac{1}{2}$ Dd;
Ee x Ee → $\frac{1}{4}$ EE;

Now, simply multiply all the results:

$\frac{1}{2} * 1 * \frac{1}{2} * \frac{1}{2} * \frac{1}{4}$ → $\frac{1}{32}$

I don't know about your country, but in my country of birth all secondary books have a chapter for monohybrid cross and another chapter for dihybrid cross. I don't like that, it creates a nonexistent separation and it makes (some) students memorize concepts. Linkage apart, I like to say to my students to do not mind about dihybrid, trihybrid, tetrahybrid etc crosses, just treat them as individual monohybrid crosses combined.


Blood circulation and blood pressure in different tissues The volume of blood coursing the blood circulation is approximately five litres. A typical vein will stretch about eight times as much as corresponding artery. Because veins have high capacitance, large changes in blood volume have little effect on arterial blood pressure.
If the volume rise or falls, the elastic walls stretch or recoil, changing the volume of blood thus blood pressure in the nervous system.

What else tissues can we consider?
I am interested in blood circulation and blood pressures in different tissues.

I'm not sure I understand your question very well-maybe try and rephrase it? As another example, low blood pressure in the kidneys is sensed by the juxtaglomerular apparatus which secretes renin into the circulation. Renin converts angiotensinogen (released by the liver) into angiotensin I. Angiotensin I is then converted into angiotensin II by angiotensin converting enzyme (this is the target of anti-hypertensives called ACE inhibitors) secreted by the lungs. Angiotensin II is a potent vasoconstrictor which directly increases the blood pressure (and hence glomerular filtration rate).  Angiotensin II also causes the release of aldosterone which acts on the kidneys to re-absorb salt and water again all facilitating an increase in blood pressure. I hope I've answered your question, if not please edit the question so it very clear.


Why do some animals have 8 Limbs (e.g. Spiders, Octopuses)? Octopuses have 8 tentacles, spiders have 8 legs.

Is there something special about 8? It seems like an animal that needs 360° mobility has 8 legs.

No, there is nothing special about eight legs. You have species with two legs (humans), four legs (most mammals), six legs (insects), eight legs (spiders), ten legs (lobsters), and many more legs (millipedes, centipedes).


Are all quadrupeds edible? I wonder if all quadrupeds (or, mammals, at least), are edible?

From what I have collected, even down to fish, everything is edible apart from being sick or infected, and, apart from some glands secreting (deliberately, as far as this term makes sense in evolution) poisonous molecules.

This is (if correct), in stark contrast to plants, where frequently many parts of the plant contains poisons. (It has some logic: plants can't run away or mechanically fight back.)

Q: Are all quadrupeds edible?

An additional bonus on: WHY?

Edible by whom? Lets assume humans.

Yes all quadrpeds are edible though you may not want to eat every part.

For example, the scent glands of a skunk, or the quills of a porcupine are repulsive or impossible to eat. Also, some organs, like the liver of a polar bear, which accumulates vitamin A to toxic (to humans) levels.

It's impossible to say why this is so, since we can't prove why evolution occurs one way or another. What you suggest about mobility is reasonable, but not universal, since the poisonous puffer fish is able to move.


Can one type of bacteria cause several diseases? If yes.
Does it change its shape in every disease, or does it remain in the same shape and cause several diseases?

Yes, one type of bacteria can cause multiple diseases.  For example:

"Rheumatic fever is caused by group A Streptococcus. This bacterium causes strep throat or, in a small percentage of people, scarlet fever. It’s an inflammatory disorder." [https://www.healthline.com/health/rheumatic-fever#causes].

The difference is in how the individual's immune system responds to the infection (and how the infection is treated).  Everyone responds a bit differently to the same infection.


Short, concise, practical manual for doing experimental biology I am am physical scientist working in biology, and have recently started doing experiments. I would like a manual akin to "Numerical Recipes", but for the lab: straight forward, easy instructions on how to do the (100) most basic biology experiments - PCR, cloning, etc. I realize that a lot of these depend on kits, and specific equipment, but it seems like there still should be something that would give you the outline of how to do these experiments. Does anyone know of a resource like this?

Molecular Cloning is updated and in its 4th edition.  Every lab used to have it.  Its comprehensive, but really no book could be complete.


Could a man be proved positive for a pregnancy test? From the question: Could a man be proved positive for a pregnancy test?. I don't mean if a man could be pregnant but if he runs a pregnancy test, it is possible for it to come out positive?

Pregnancy test, just like any test, has some non-zero false positive rate. So yes, of course a test could be positive when a man pees on it.

Pregnancy tests work by detecting the presence of a hormone called Beta-HCG. This hormone is produced by both genders but is produced in much higher dose during early pregnancy. Teenagers also produce a relatively high dose of Beta-HCG which can eventually inflate the false positive rate.

It just so happen that tumours from a particular type of testicular cancer also excrete Beta-HCG (see this blog post from the American Cancer Society). If your question arises from a personal experience, then I would strongly recommend that you talk about it with your doctor.


Where did Neanderthals and Denisovan Man come from? Neanderthals, Denisovans and our species (Homo sapiens) are commonly cited as closely related subspecies, even interbreeding with each other. Yet our species theoretically didn't migrate out of Africa until about 60,000 years ago, whereas Neanderthals were living in Europe a few hundred thousand years ago. Did they evolve out of Homo habilis, which migrated out of Africa before our species?

This suggests that Neanderthals must have evolved from Homo sapiens (or perhaps Homo habilis) stock in Africa before migrating out of Africa to Europe. However, conventional wisdom suggests that Neanderthal morphology was shaped by Ice Age Europe.

One possibility is that they evolved into a distinct subspecies in Africa, then migrated into Europe, where continuing evolution turned them into the familiar Neanderthals. But wouldn't this mean that Homo sapiens (the ancestor of Neanderthals) then migrated out of Africa hundreds of thousands of years ago?

Is this simply a question that hasn't been resolved, or is there a popular theory that explains the origin of Neanderthals and Denisovans?

The topic is reviewed in a freely available Nature article, from which the figure below (I have added the labels ‘Hominid’ and ‘Human’) is taken. As can be seen it is thought that the lines leading to the ancestor of Neanderthals/Denisovans and that leading to modern humans diverged  before humans had left Africa; and that the lines leading to Neanderthals and Denisovans split from their common ancestor subsequently.

You will notice that the article refers to “modern humans”, rather than Homo sapiens, presumably because this terminology is confusing, whereas the picture is clear.


Why is it that guttation is most commonly observed in the morning? Knowing that guttation occurs through a plant's hydathodes due to root pressure forcing liquid water out of the leaves, I am curious as to why so many small drops of water are observable on plants in the morning. Could this potentially have to do with the moisture in the air at night vs day? Since humidity tends to increase at night?

Thanks in advance!

Guttation is commonly seen at night and early morning. Plants release excess of water via the guttation. During day time as the transpiration rate increases, excess of water is released via transpiration and hence guttation decreases. Also due to high temperature these small droplets are quickly evaporated during day time.


Human Digestion of Cellulose? Most animals can digest the cellulose in grass because of the anaerobic bacteria called Fibrobacter succinogenes living in their rumen (gut). The bacteria produces the enzyme cellulase and is therefore able to break down the β-Glucans(1,4) glycosidic bond in the cellulose. Animals like cows and giraffes grow up to be very large simply on a diet of grass!

Is there a way for humans to ingest the Fibrobacter succinogenes bacteria and be able to digest cellulose?

This isn't a complete answer, but searching Google Scholar for "Fibrobacter succinogenes human" I found this paper:

The cellulose-degrading microbial community of the human gut
varies according to the presence or absence of methanogens

The abstract of which begins this way:

  Cellulose-degrading microorganisms involved in the breakdown of plant cell wall material in the human gut remain rather unexplored despite their role in intestinal fermentation. Microcrystalline cellulose-degrading bacteria were previously identified in faeces of methane-excreting individuals, whereas these microorganisms were undetectable in faecal samples from non-methane excretors. This suggested that the
  structure and activity of the cellulose-degrading community differ in methane- and non-methane-excreting individuals.

Note also in Table 1, Fibrobacter succinogenes is one of the strains that seem to have been detected, so that answers the part of your question that seems to ask if humans can incorporate those bacteria into their gut fauna: yes, some already do.

This suggests to me that:

some humans do have a limited ability to digest cellulose through their gut bacteria, though this ability is probably limited enough that "humans can't digest cellulose" can still be considered true in the large scheme of things,
the challenge in digesting cellulose isn't so much getting the gut bacteria in there, but providing them with an environment where they will thrive and digest a lot of cellulose. This is probably where the specialized gut structures of ruminants come in; it becomes not so much a matter of digesting cellulose, but of digesting it well enough that you can live off of it. I'm guessing this is also related to the differences the paper found between people who excrete methane and those who don't but I wasn't able to figure out what that was supposed to be related to (is it a cause or an effect of the presence of certain gut bacteria? is it related to diet, genes, something else? I couldn't find that information in the paper though I didn't read every word)
according to the paper there isn't much research done into this.
the paper gives no info as to how significant those cellulose-digesting bacteria are to the host's energy balance, which I imagine is what you're really interested in. Is it significant, is it too small to be noticeable, does the host even benefit at all calorie-wise? They don't address that question in the paper.