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What is the consensus, if it exists, on the (absence of) biological effects of artificial sweeteners?
I tried to Google (and PubMed) the question, but it seems to be fairly polarized debate and there does not seem to be a consensus as to whether sweeteners like asparatme, acesulfame etc. have meaningful biological effects.
Some studies point to molecular effect with little to no explanations about their relevance for health, and since statistical significance and size effects are quite different things, question remains unanswered.

If the scientific research papers can't provide a clear answer to this, then likely there is no consensus effect known. Whether this is interpreted that as 'no actual effect whatsoever' or 'we have't looked deep enough' is up to you I guess.

I remember checking out a lot of papers on the subject at some point and most of them report a slightly impaired glucose intake insuline response as the only side effect of chronic artificial sweeteners consumption. Also another conclusion was soda with these sweeteners does help weight loss but not as much as not drinking any kind of soda at all. I can try to search for the papers later again


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Resting membrane potential in cells
My textbook says “Among K+, Na+ and Cl-, K+ contributes to the resting membrane potential the most, because it has the greatest permeability across the membrane.”
I agree with this, but I’m just curious: why is the equilibrium potential of Cl- (-75mV) closer to the resting membrane potential (-70mV) than that of K+ (-90mV)?

This is only true because the chloride concentration happens to be slightly less negative than potassium, therefore the weighted (by permeability) average of all the other ions is near the reversal potential for chloride.
Even if you assume the permeability of every ion except sodium and potassium is zero (i.e., if chloride doesn't contribute at all), you will end up with a resting potential near chloride's reversal potential.

source: Stack Exchange

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

sort: votes


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What is the reason behind that sometimes when I see new thing I feel that I have already seen them?
I have googled it and I found that it is, because of good memory, but how it can be due to good memory as it didn't happen before. It happened to me many times, that I feel that the scene which is happening now, has already happened to me in my past. But it was a new scene in my life, so why does I feel like this? How is it possible that a same scene happens twice?. What is the reason behind it, that we feel something twice in our lives.

What you are talking about is a déjà vu, the feeling of familiarity even though the situation is not familiar at all. It is, in fact, a very common phenomenon. A high percentage of people report having had déjà vus. It is nevertheless hard to put a number to it, because the experiences and déjà vu definitions might be different. I have found numbers between 60 and 90% of the population.
The claim that this is a sign of a good memory is related to the view, that a déjà vu is not a false memory, because you actually realize that the situation should be unfamiliar to you (also mentioned here).
But how do déjà vus happen? There are several theories...
It seems clear that déjà vus are associated with activity in the temporal lobe (on the side of the brain). That's where memory is processed, especially episodic memory (things that happen - in contrast to learning a skill). People with epilepsy often report déjà vus right before a seizure that starts in the temporal lobe.
One theory, put forward in this paper, says that the memory and feeling of familiarity are processed in different areas and there is a false activation of the familiarity area during a déjà vu. The brain is not always working proberly, e.g. false sensations can happen, like hallucinations. So, the false activation of that familiarity center could give us the sense of familiarity in an unfamiliar situation.
Similar to this is the idea, that there might be a mismatch between perception and memory formation. When something we are experiencing right now is "leaking" into our memory due to false activation, we think that this has happened in the past. There is a problem with this explanation: despite having a strong feeling of familiarity during a déjà vu, people fail to give any context to when this previous event happened or which other events have preceded it. So, it doesn't seem to be perceived as a memory.
Another explanation could be a false combination of the experience with something that is loosely connected to it (like planning the trip, watching a movie with a similar scene, etc.). Our brain always tries to connect experiences. It might falsely identify something you've seen in pictures or read in a book as a real experience.
As you see, we still struggle to explain the phenomenon. It is caused by some error in the way our brain perceives a situation, writes or retrieves memory or processes familiarity. This error might be a wrong activation or wrong timing or the like.

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


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Why are bed bugs attracted to Carbon Dioxide?
All over the Internet it says bed bugs are attracted to Carbon Dioxide. This is why they congregate around beds. Your bed is the only place you are stationary for long enough periods of the day to exhale enough Carbon Dioxide. So, I grant that there seems to be a consensus that they are in fact attracted to Carbon Dioxide. But, why? Certainly they're not breathing it. (Are they?) I was under the assumption that all animals are aerobic.

Can you please some link for the space on "all over the internet"?

For the second part of the question: No, the bed bugs do not breathe carbondioxide and especially do not use it for respiration. Instead, carbon dioxide environment is used to kill the begbugs - "Elevated CO2 levels cause insect spiracles to remain open, resulting in death from water loss" - Nicolas G. Sillans D.. 1989. Immediate and latent effects of carbon dioxide on insects. Annu. Rev. Entomol.  34: 97–116.

@dmishra https://www.bedbugsupply.com/blog/treatments/truth-diy-bed-bug-traps/, https://www.terminix.com/blog/education/what-attracts-bed-bugs/, https://www.ncbi.nlm.nih.gov/pubmed/24020296, https://www.epa.gov/bedbugs/bed-bug-myths

It's nothing to do with what they breath, they're attracted to carbon dioxide because it's generally a good indication of the presence of a larger organism (such as a person) so they're simply following the "scent" (for want of a better euphemism) to their food (in this case you, or whoever happens to be in the bed), the traps in your links just take advantage of this to trap and kill them.


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Are the chemical constituents of human bodily fluids similar to sea water?
I have heard a comparison of human bodily fluids to sea water from various sources in the past. The most notable was a teacher who claimed, if I remember correctly, embryonic fluid is comparable in chemical content to sea water. I am wondering if this claim has any scientific basis. If not, is there another bodily fluid known for this characteristic? I tried doing some google searches and did not find any supporting evidence. If this is a myth, has anyone else heard such a claim and how it may have begun?

I also remember the teacher adding a disclaimer that it was not just any sample of sea water, rather an average or maybe seawater in the open ocean. She implied this comparison did not necessarily apply to various "sea water" bodies like bays or coastal areas.

Let's just consider mineral salts, since obviously sea water does not contain animal proteins or cells, and (fortunately) our bodies don't contain phages, micro-algae etc.
Sea water is very salty; on average about 0.5mol/L of NaCl (the main salt dissolved in sea water).
On the other hand, human biological fluids like plasma and the intracellular space are at least 2-3 times more dilute.
Unless some other human bodily fluids are exceptionally salty, it seems that there is a pretty big difference and it is not very accurate to say that bodily fluids and sea water have close chemical compositions.
There are not many fluids that are very close from bodily fluids in term of composition. Popular culture tells the tale of emergency transfusions of coconut water during WWII, but that's not supported by medical literature; even though more recently, in exceptional emergency cases, it has been reported to be possible as a short term solution because of the similarity of osmolarity between plasma and coconut water.

I'd guess the teacher was just making the broad comparison that bodily fluids and seawater can both contain $\ce{Na+, K+, Cl-}$ even if they're not at the same concentrations or the only constituents of those fluids.

Yes, I was meaning chemicals, ie minerals, or just elements, and not to include specifically other biological organisms. @Jam what you are saying sounds similar to what the teacher said. I think she did refer to those elements specifically.


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Lambda red recombination without electroporation
All protocols that I found about Lambda red recombination are using Electroporation as a method to introduce (inject) the homologous DNA (usually a PCR products or a linear dsDNA) to the E.coli cell. Can I use chemical method (CalCl2 + PEG) and heat shock method instead ?

Rubidium chloride method and the Inoue's method of making chemical competent cells give higher efficiency than the CaCl₂ method.

@WYSIWYG thank you for this info. But "Rubidium" sounds very strange to me. if it not popular, as I might think it will expensive than CaCl2 .

It is certainly more expensive than calcium chloride. Rubidium an alkali metal and you can check out the protocol for RbCl competent cell preparation, here. It also uses other salts. These salts may be slightly more expensive than CaCl₂ (because these metals are rarer) but would still be cheaper than buying an electroporator and the cuvettes.

@WYSIWYG Thank you alot. But any evidence that RbCl will work with lambda red recombination? If electroporate is just firing a high voltage between 2 electrode, I'm planning to purchase a high voltage generator module on Ebay, edit it a bit and put it directly to a plastic tube. Will be much cheaper?

You can make a DIY electroporator but I don't think an Ebay product will work that well (you'll just end up wasting more time). You need to generate a pulse and you need to have proper electrodes. I have not worked with lambda red. This site says that recombination rate is less than 1:10000. You can get efficiency of ~10⁷/µg with RbCl method which means you should get ~10³ colonies. You can use a selectable marker to select the positive cells.

Since Lambda red recombination is a rare event you want to have to have a good transformation efficiency, thus electroporation would be your best choice. Also since the expression of the recombination system usually needs growing bacteria at 42º you will probably inhibit the expression of the recombination machinery with the chemical method.

Thank you for answer. Because electroporator is so expensive so I'm finding a more cheaper protocol.


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Do garden bird feeders harm wild birds?
I enjoy watching birds at a garden bird feeder but have started feeling guilty that it is having a negative impact on the birds. For example this study recently showed that birds in the UK have longer beaks than their European cousins because bird feeders are more common there. This led me to google for more info and several sites list numerous potential negative effects of feeding wild birds from altering their migration patterns to increased spread of diseases.
Should I feel guilty or are bird feeders just a drop in the ocean compared to all the other ways humans are changing the environment?

A good question but not easy to answer and I am not sure it's even in scope for a gardening forum.

It is important  to regularly clear, wash and sterilize feeders to reduce risk of infection, but whilst I do have a nut feeder, I've switched to using half coconut shells  filled with fat/seed/grains. No longer beaks required for those, and the birds will go to that in preference to the nut feeder(I;m in the UK). They don't last long so risk of infection is very low. But don't forget the ground feeders like robins... scattering sunflower  seeds or similar is useful for those. And you could just switch to feeding them during winter and early spring instead of year round, which is what I do.

The serious problem is that birds get dependent on the feeders when food is scarce : Then the people don't consistently put food in it . This is especially true of humming bird feeders as hummers do not have the energy reserves to search for natural food.

I had posted an answer that was probobly the best one your getting but it was deleted for not being scientific (as if most questions in life are answered scientifically). No one in this world is really capable of answering this question and if they say they are their lying. They could say it changes the ecology so no but they can't prove that changing the ecology is morally or ethically incorrect. The OP's question was: "should she feel guilty" that's a theological question not something that can be answered scientifically, morons.


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The Tun state of a tardigrade
I was wondering How long does it take for a tardigrade to enter and exit the Tun state?
I'm doing a thesis on tardigrades for my B.S in biology and I haven't come along any information in the primary literature talking about how long roughly, it takes to enter the tun state in cryptobiosis. I understand that it takes a couple hours for it to pop back up again, but what about entering?


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Are humans the only primates being engaged in group sex?
There are quite many examples of humans being involved in group sex. I won't say it is a common thing and won't say whether it is "natural" or "cultural" (but "cultural" only means induced to majority by minority).
What I'm asking is if there are any other primates being involved in group sex (or how is it called in biology?). Under "group sex" I mean a sexual intercourse where several males or females can see other males and females being involved in sex too, right as they themselves are.

I haven't looked this up specifically, but bonobo's are sort of literally crazed sex monkeys - I'd be surprised if they don't do this.

@Nicolai Their sex has 13 seconds duration. I'm not sure another male or female has time even to come there.


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Are $DCX^{-}PSA-NCAM^{+}$ neurons the result of adult neurogenesis in human being?
A recent study by Sorrells et al. (2018) has stirred a debate whether human being really do have adult neurogenesis in hippocampus or not.
In a following paper- Adult hippocampal neurogenesis: a coming-of-age story, HG Kuhn, T Toda, FH Gage have criticized the original study by stating that

while Sorrells et al. did count $DCX^{+}PSA-NCAM^{+}$ cells as
  adult-born neurons; they did not count $DCX^{-}PSA-NCAM^{+}$ as the
  same, claiming that the latter exhibited more mature morphological
  features based on their criteria. However, the developmental time
  course of adult-born neurons in the human dentate gyrus has not been
  clearly characterized, and neurons in higher mammals take at least six
  months to fully mature (Kohler et al., 2011).

My Question is- are the $DCX^{-}PSA-NCAM^{+}$ neurons really the result of adult neurogenesis, as claimed in the second paper? Or are Sorrells et al. correct in calling only those neurons adult born that respond to both the markers (DCX,PSA-NCAM).

What answer are you looking for beyond what's in those papers? I.e., why do you think they've overlooked something that is decided in the field rather than there being disagreement? One of them is advocating a more stringent criterion, that's it.

@bryankrause the authors of the two papers are making contradictory claims, and supporting their claims with reason. One of them claims that the markers can give false positive results by identifying glia cells as new born neurons. The others claim otherwise. I need opinion of others on this disagreement, some arguments, facts and perhaps link to some sources, so that this can help me understand the situation more clearly.

Right, which is the purpose of the commentary by Kuhn et al: they note that Sorrells is being more conservative than previous work in their definitions and that "the developmental time course of adult-born neurons in the human dentate gyrus has not been clearly characterized" - in other words, if Sorrells et al criteria is right, their conclusion is right, if their criteria is wrong, their conclusion is wrong. It's hard to do these studies because there aren't many human brains available to chop up.

Kuhn isn't claiming "otherwise" they are claiming "unclear"; similarly Sorrells isn't claiming "does give false positive" they are claiming "could" - uncertainty is normal on the edges of knowledge, if it wasn't then those wouldn't be the edges.


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Why are vaccines containing attenuated microorganisms preferable to those containing dead microorganisms instead?
My teacher said it more closely resembles a real infection but I didn't get that.

could you define 'preferable' for your question. There are pros and cons to both, which is why both exist...

It's not necessarily true that attenuated vaccines are "preferable" to killed vaccines. It's a case by case basis. In some cases one or the other simply isn't possible or practical. It may not be possible to make a vaccine that's attenuated enough, for example. Or a killed vaccine may not be effective.
Here are some pros and cons of attenuated vaccines:

more likely to follow the natural path of infection, so there might be more immunity at the specific site of infection. For example, attenuated vaccines against gut pathogens might drive gut-specific immunity.
Might replicate in the host so that the actual amount of antigen seen by the host is greater than the amount delivered -- so you can deliver a much smaller dose to get similar immunity
Might cause more inflammation. Inflammation can drive a much stronger immune response because the body "thinks" it's being attacked by a dangerous pathogen

Cons:

Might cause more inflammation. Inflammation can cause tissue damage or local pain
May be less safe. Replicating in the host may give the opportunity to mutate and become more dangerous
May be more fragile. A killed vaccine could be relatively temperature stable, while an attenuated vaccine might need to be kept in a very narrow temperature range so it doesn't die and become ineffective. That might make it difficult to use in, say, developing countries

There are many more points that could be made but the overall picture is that attenuated vaccines might be more effective but more dangerous. Attenuated vaccines that are used today have been shown to be safe as well as effective, and killed vaccines that are in use have been shown to be effective as well as safe, so these are concerns during development of new vaccines, not in use of present ones.


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

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

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

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

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

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

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


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How is the electrical potential difference distributed between two stimulating electrodes?
Suppose I set the voltage value of an isolated stimulator with a floating ground. I place one electrode above the spinal cord (positive) and the other placed subcutaneously far away from the spinal cord (negative). The circuitry within the stimulator will operate in such a way that the electrical potential difference between these two electrodes is the value I specify.
The stimulator can fix the electrical potential difference between the two electrodes in multiple ways:

Hold the positive electrode's potential constant while changing the negative electrode's potential.
Hold the negative electrode's potential constant while changing the positive electrode's potential.
Adjusting both electrode potentials using a rule.

Although each of these ways can fix the voltage between the electrodes, they do not have equal effects on the biological environment that the electrodes are placed in. Going back to my example, if the stimulator obeys 1, I would expect a larger effect to be induced local to the spinal cord, in contrast to 2, which would would have a greater effect in the subcutaneous area. This is because there is an initial heterogenous charge distribution.
How should I assume my stimulator is fixing the potential difference between my electrodes?

The situation is quite reminiscent of a Voltage clamp experiment (Fig. 1), where one amplifier (amplifier 1 in Fig. 1) records the potential difference (V1 - V2 in Fig. 1) between two electrodes and the other opamp (2) is used to inject current (I2 in Fig. 1) to 'clamp' the system at a particular voltage using a computerized feedback system. The potential difference is thus kept constant. As OP already mentions in the question, in Fig. 1 the charge density is locally much higher at I2, because current is injected there that dissipates across the cell (or tissue in your case) the farther it gets from its source.
Having said all that and to get to the question proper...

How should I assume my stimulator is fixing the potential difference between my electrodes

...I can only say the assumption is the mother of   all fu&% ups   many experimental failures. Instead, I advise you to either consult the device manual, or contact the distributer or manufacturer of the device to make sure what the machine is actually doing to clamp the voltage at a certain level.

Fig. 1. Voltage clamp setup. source: wikipedia

None of the three scenarios you describe are really different from another. Whatever process is used inside the amplifier, a voltage describes a potential difference between two points. It does not relate that to any other universal reference. If you have a ground connection, you could describe a different potential relative to ground, but that's not relevant here since you have no separate ground that gives an alternative electrical path to either of the contacts.
When you have a voltage between two points that are connected with less than infinite resistance, as you have in the biological environment you are stimulating in, you will get a current. That current will be exactly the same at each electrode. All that matters to determine how much current will flow is the voltage and the resistance/impedance between the contacts. You could get some differences in the stimulation duration/intensity around the two contacts if either acts like it has substantial capacitance, and the current density through the electrolyte solution surrounding each electrode can vary by the surface area of the electrode, but those are properties of the electrode, not how the voltages might compare to some unconnected ground reference.


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Is a female spider, well-fed by sexual cannibalism, less likely to mate again?
The Wikipedia page on sexual cannibalism (e.g. female spiders eating their mates) currently has a statement that sounds wrong to me, but I don't feel expert enough to edit it out:

An additional benefit to cannibalization is the idea that a well-fed female is less likely to mate again.

I can't see why that would be the case. Why not continue to seek a second, better, mate? Unless perhaps being well-fed makes you a slower, larger target for predators, so hiding for a while is a better tactic.
The reference given is to

Female hunger can explain variation in cannibalistic behavior despite male sacrifice in redback spiders. 9, 33–42 (1988)

A bit of searching suggests the author meant to include Behaviour Ecology as the journal name. I've only read the abstract, but it does not seem to support the statement. It suggests a well-fed female is less likely to consume her mate, which seems intuitive.
Am I right that this Wikipedia sentence is incorrect? If I am wrong, is there an explanation for the effect that I am missing?

It does appear that Wikipedia has not provided the most appropriate reference for that statement, but it is repeated in the article it refers to and that you link to, both in the abstract:

Male sacrifice may be adaptive because cannibalized males increase their paternity relative to those that are not eaten

and in the  body of the introduction:

Males that are cannibalized obtain paternity advantages compared to males that survive copulation

These statements do not necessarily contradict the other statement that a well-fed female is less likely to consume her mate, but there might be some nuance missing here in terms of mating versus mate consumption behaviors. However, the authors cite Andrade, 1996 (see below) for the second statement, and this seems like a more appropriate reference for the statement on Wikipedia:
Yes, a female spider who eats her mate is less likely to mate again. Andrade 1996 shows that males who are eaten during copulation mate longer, fertilize more eggs, and the females are more likely to not mate again after eating a mate.

Andrade, M. C. (1996). Sexual selection for male sacrifice in the Australian redback spider. Science, 271(5245), 70-72.

To be clear on my (prior) understanding: I accept that male sacrifice is adaptive - for example, because a well-fed mother is more likely to successfully produce offspring, but it isn't intuitive that the female wouldn't mate again. Your reference shows my intuition is wrong (which I celebrate. I learnt something!)

@Oddthinking Indeed, Andrade concludes that the mother being well-fed has little to do with it, because the male is so small relative to the female's mass and eating the mate does not result in more or larger eggs. Instead, the article suggests that the duration of copulation is probably the key factor. Feeding on the mate is occurring while copulation is still in-progress, so effectively she is distracted by the feeding into allowing longer copulation. It isn't clear to me what prevents future matings, but in some ways it is irrelevant because fertilization already occurred for many eggs.


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If post transcriptional modification happens , how can a gene code for amino acids in a particular order?
Post transcription, introns are removed and exons are rearranged randomly. If that's the case (which it is according to the book EDEXCEL SNAB A2 topic 6) then shouldn't the protein produced be different every time? Shouldn't the order of amino acids be different? And if it is, doesn't that mean that the protein produced is different?
To quote : "When mRNA is produced, its introns are removed by spliceosomes and a different number of exons is put together at different orders which changes the sequence of amino acids in proteins."
Quote from the book:

Genes contain sections that don't code for amino acids.

These sections of DNA are called introns. All the bits that do code for amino acids are called exons.
During transcription both introns and exons are copied into mRNA.
The introns are then removed by a process called splicing -- introns are removed and exons joined forming mRNA strands. This takes
  place in the nucleus.
The exons can be joined together in different orders to form different mRNA strands.

If this process happens,how can a gene code for a specific protein? This process means that exons are arranged differently, and this means that amino acids are arranged differently, and doesn't that mean that different proteins are going to be produced than the one coded for?

Can you provide a quote or something from the book? It's hard to evaluate the statement otherwise, but "exons rearranged randomly" is certainly not the usual way of business, if it happens ever (I can't think of a situation where it would). Maybe somewhere in the immune system which I am not fully familiar with.

See also https://biology.stackexchange.com/questions/5/is-exon-order-always-preserved-in-splicing

@user1136 Differential splicing isn't the same thing as "rearranging exons randomly"

@user1136 But OP doesn't seem to, and that makes your statement misleading and OP might misinterpret it as an answer to their question.

@Lia What's the context of the quote from the Edexcel book? Is it talking about a specific group of proteins? Different arrangements of exons occurs in various proteins such as antibodies but if it occurred in every protein, no receptor or enzyme would be the right shape to allow its biochemical effects. As Bryan says, it's not the usual way of business.

"then shouldn't the protein produced be different every time? Shouldn't the order of amino acids be different? And if it is, doesn't that mean that the protein produced is different?"
It is not different every single time, but it is different depending on what kind of post transcriptional modification takes place. The proteome is larger than the genome thanks to this, genes can code for many different proteins thanks to post transcriptional and post translational modification as well.
So as I understand it, gene segment = same order of nucleotides = same primary mrna
post transcriptional modification to primary mrna = different mature mrna = different order of amino acids = different polypeptide chain (then different protein later on)
Hope this helps


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Haplodiploid species that are not eusocial
Haplodiploid species need not necessarily be eusocial and eusocial species need not be haplodiploid (reference). Everywhere I look its been mentioned in general terms that some species of bees, termites and wasps are haplodiploid but not eusocial. What are some specific examples of haplodiploid species not being eusocial? I was specifically interested in bees but examples from other species are also welcomed. Thank you in advance.

https://en.wikipedia.org/wiki/Bee#Solitary_and_communal_bees

@mgkrebbs That wikipedia page doesn't mention ploidy but the wikipedia pages for the species of bees do mention their ploidy. If you can write an answer, I can accept it and close the question. Maybe you could also mention a haplodiploid non-eusocial termite and wasp too in the answer.

feel free to post your own answer with that in it; that's allowed under site rules.


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Why electroporator need a cuvette?
I have never obtain an Electroporator for my home-lab. Because it's very expensive, I'm trying to create a diy cheap version for myself. In all commercial design, I see that we need to put the sample to a 0.1cm-0.2cm cuvette to doing an electroporation, can I just replace it with an eppendorf plastic tube and put my 0.1->0.2cm alumium electrode inside?

Generally I would advise against making a home-brew electroporator: the voltage needed for electroporation is so high, that even with professional equipment you can easily get arc lightning. In an self-built device that would pose a serious fire hazard.
However even theoretically there are problems with the design you propose:
1) It is important that ALL bacterial cells in the cuvette get exposed to electrical field induced by the high voltage spike. If you use simple electrodes you will only affect the few cells directly between them, which will drastically reduce efficiency of the electroporation. For your design to work properly you would need electrodes that exactly match the dimensions of an eppendorf tube to make sure all bacteria will be squeezed between them.
2) With your device you can only do one electroporation, then you have to thoroughly clean the electrodes. This has to be done for two reasons: first you don't want any carry over bacteria (or as Chris pointed out DNA) from one batch to another. Secondly the electrodes need to be clean of any salts (or other molecules that increase conduction in a solution) to prevent arc lightning between them.

Great! Thank you very much for point out. I will buy a cuvette and be very careful making this.

It's not only bacteria. It's even more important to not carry over DNA between transfections as this can lead to unexpected results. Washing the cuvette for a short time with diluted HCl helps here. Avoid prolonged incucation in the acid as this corrodes the electrodes, so washing it afterwards is important.


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Action potential frequency presynaptic neuron comared with in post-synaptic neuron/ muscle cells
I am a physicist interested in knowing how the action potential frequency in a presynaptic neuron compares with that in
a) a post-synaptic neuron and
b) membrane depolarisation of muslce cells, and
c) how the membrane depolarisation of muscle cells quantititavely relates to muscle contraction.
From the reading I have done so far, it seems that the theory of c) is standard, and goes by the name is 'excitation-contraction coupling'. I would think that the actual relationship between the frequency of muscle cell membrane depolarisation and degree of muscle contraction- however it is quantitifed- would differ for muscle type, depletion of Ca2+ stores from the sarcoplasmic reticulum, etc. In any case, some theory is covered here for instance, although I haven't seen much mathematical modelling and quanitative comparison here.
In any case, I am then still wondering regarding a) and b). I would think that there isn't a straightforward answer; the sequence of events is action potential -> neurotransmitter release into synaptic cleft -> neurotransmitter binding -> membrane depolarisation -> hopefully an action potential.
I already see some potential sources of non-linear behaviour in the final step, and the neurotransmitter binding ->depolarisation step would prbably also be dependent on the recptor kinetics. Since we are talking on the behaviour on a temporal scale, we would have to consider the degredation rate of the neurotransmitter within the synaptic cleft, and no doubt several pathologies arise because of some dysfunction in changes in neurotransmitter degredation/re-uptake rate... Come to think of it now actually, I think differences in the extent of binding (say due to differences in the number of receptors on post-synaptic neuron membrane) are the basis- or at least one factor- in neuroplasticity. So of course they would differ. But still the question remains as to what extent. I am not sure whether for some circuits, say those in the motor system, there is little deviation between responses in people.
To give some context to my question, I am interested in technologies which actively stimulate, or disrupt stimulation, of neurons in a controlled manner, so as to achieve a desired output effect. There are several technologies and lab techniques being developed with this in mind- optogenetics on the single-neuron level, DBS and epidural stimulation for stimulating large groups of neurons for some non-specific duration of time. I would think that these techniques could be much more powerful and potent, if we knew the temporal relationship between consecutive neural firing rates on stimulation.

To be blunt, if you are interested in technologies to do what you say, you need way more information than an answer to this question, although this question is already extremely broad. I'd suggest starting with a course or textbook in neuroscience. As is, you are drifting into this territory: https://xkcd.com/793/

For example, the statement "hopefully an action potential" is a completely wrong way to think about it. Action potentials aren't an achievement that the nervous system has as a goal, they carry information. Not firing an action potential is also informative, and not nearly every input should cause an output.

@BryanKrause Hi. I am aware of this; i presume my sloppy and half-hearted phrase 'hopefully an action potential', in the context of my being a physicist, gives the impression that I have absolutely no idea about neueoscience principles. I think your comment was a bit sharp. And, if context is of any importance, I am a physicist in training- still an undergraduate- so I think my knowledge of neuroscience considering my present educational status isn't half bad. Plus, when I said 'interested in [these] technologies', I meant that literally. Not that I am trying to revolutionaluse these

Technologies now. I have read quite a bit on the fojndatiknal principles of neuroscience, but am yet to find a reference and quantitative comparison of rate of action potential firing from experiment. And besides, even if my background on this site seems pathetic, at least I am trying to find out. No point sitting like a lemon. And btw I have consulted Bear,Paradiso et al and Connors, White et al.

I only mean to suggest you should start with the biology rather than trying to figure it out from the physics. That approach might make sense if this stuff wasn't already studied, but it has been, and if you want to understand the technologies you will need to be practiced in understanding the biology. The reason that cartoon exists is because this approach is for whatever reason really common with people with a physics background, and it can be very frustrating for the biologists in the room.


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Since frogs are ectotherms and supposed to have low metabolic rate, why do they grow so fast and eat so much?
It's always emphasized in literature that endothermy enables high growth rates but requires more food.
But look at frogs, for example: bullfrogs, toads, pacman frogs etc. They would readily eat a quarter their weight a day, and they grow real fast (I used to keep pet frogs: pacmans, for example, become more that twice as big in one season). And all of that despite being ectotherms. How is that possible?

Rather than saying ectotherms can't grow fast (which is obviously false), it's probably better to think about it as a two-part argument:

Ectotherms and endotherms can grow rapidly at an optimum temperature
Ectotherms can't maintain themselves at their optimum growth temperature

If you keep ectotherms at their optimum temperature, then they can reach optimum growth. In the wild, they might not find that optimum temperature for more than a few hours per day, though in your aquarium they might be at it all day long.
There are several publications supporting this such as

Effects of temperature and volume of water on the growth and development of tadpoles of Pleurodema diplolister and Rhinella granulosa (Amphibia: Anura)
Effects of Temperature on Growth, Development and Survival in Larvae of Pelophylax ridibundus (Pallas, 1771) (Amphibia: Anura): Linking Global Warming to Amphibian Development
Thermal tolerance limits and effects of temperature on the growth and development of the green toad, Bufotes viridis

I don't see a specific reference for this but will add that ectotherm probably have greater growth potential than endotherms if they're at their optimum temperature, because endotherms have to waste energy on a whole suite of molecular machinery that's designed to maintain their body temperature.  All that extra energy can be diverted into growth by ectotherms.

Well, they don't grow slow in wild either; besides, amphibians in general prefer much lower temperatures (they don't bask like reptiles, and prefer something from 18 to 24 C). So basically, their metabolism just works differently?
"Ectotherms and endotherms can grow rapidly at an optimum temperature"
Well, the way I thought it is, in endotherms, their cells conduct reactions faster, which allows them to grow faster - and consequently, faster reactions produce more heat (basicelly, ectoterms grow faster and hence they are warmer, not the other way around).
Thanks for references!

Frogs don't bask like reptiles?  But it's common to see them out of the water, sitting on rocks & logs.

Well, some of them may have such a habit. But many don't, and many are nocturnal in the first place.


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What's the relationship between snail movement and rain?
I have a question about the relationship between snail and rain. A few days ago I found snail shells in a moist area and I brought them in for crafts work (I thought they were empty because snail usually come out if you poke them). After a few days it rained, and I found that the snails have moved from the space i put them in (but not far). My question is why did they move after it rained  outside but not when I brought them in a week before?

The movement of organisms towards water is termed hydrotaxis. 'Hydro-' refers to water and '-taxis' refers to movement. Hydrotaxis has been investigated in animals such as the nematode Caenorhabditis
elegans (Wang et al., 2016) and, closer to snails, the gastropod Littorina
littorea (Gendron, 1977). Animals may sense the water content of their surrounding environment and moisture content in the air to move where they are more comfortable.
Animals need specific amounts water in their bodies to allow effective metabolism. We can control our bodily water content by taking a drink but simpler animals aren't afforded that luxury so they need to move towards/away from water. Your snails likely moved because the water levels in their bodies dropped as they 'dried out' over the week. They could then have sensed a gradient in the moisture content of their surroundings and moved towards it. Mechanisms in animals' bodies can give animals responsive behaviour, as seen here. For instance, C. elegans uses its cGMP pathway, neurons and biochemistry to respond to water content with movement (Wang et al., 2016).
References

Wang et al. (2016). cGMP Signalling Mediates Water Sensation (Hydrosensation) and Hydrotaxis in Caenorhabditis elegans.

Gendron, R. P. (1977). Habitat selection and migratory
behavior of the intertidal gastropod Littorina
littorea. J. Anim. Ecol 46 79-92


text:
Where are the statistics for vaccine side effects?
My son told me that that during a discussion at school someone mentioned statistics about side effects of vaccines (I assume that the discussion was about standard vaccines in France). The numbers were completely off (1/100 "illness", 1/100 "death" - again, these numbers do not make sense).
I wanted to provide him facts to rationalize (quantify) the discussion but it is now an hour I am searching on French, Canadian and US official sites (as well as WHO) and I cannot find any statistics on side effects (from mild to mortal).
I understand that "side effects" and "vaccines" are general concepts but I want to start with anything to just show the error. Let's say that "side effect" is anything from "reasonably impacting" (so not an arm which hurts for 48 hours) to death, and "vaccines" is anything from the typical set a child will get.
Is there a place where such statistics are available?
Please note that I am not talking here about "vaccines cause autism" (there is plenty of information about that) or "vaccines are not useful" (plenty of comparative studies as well). I also understand that vaccination is a pro-vs-cons decision, I have a hard time finding the "cons" in the form of numbers.

(World Health Organisation, 2014. p. 2) shows the adverse effect (side-effect) rates for the MMR vaccine. For instance, fever  between the 7th to 12th day after vaccination occurs in 5 to 15% of vaccine recipients and rashes occur in 2-5% of vaccines, etc. Page 6 summarises the results in a table. As you point out, the adverse effects are variable in severity and dependent on the particular vaccine; an organisation like the WHO will take into account the risk and severity of these adverse effects before recommending the use of the vaccine. And as you point out, it is not believed by the scientific community at large that vaccines have links with autism.
References
World Health Organisation. (2014). Information sheet observed rate of vaccine reactions measles, mumps and rubella vaccines.

Thank you, this is an excellent stating point - particularly the page 6 you mention. I will translate it to French and make it available for discussion.

There are WHO information sheets on different vaccines here, and there are informative tables at the bottom of each technical report and studies cited throughout. The CDC has an extensive publications list on vaccine safety, and by accessing the "Specific Vaccines" tab at the CDC immunization safety office, you're directed to information on individual vaccines.

The CDC links for specific vaccines have products listed with links to FDA information pages. You can look through the drug package inserts for good information on adverse events.

@CKM: thank you. I have gone though the WHO site and found information about the kind of side effects but not the numbers. The specific sheets you point to in your second link are excellent - I just went though two of them and they give rates for mild effects (not for severe, but that's a start and I will dig further). I also saw the VAERS site mentioned elsewhere, but it is a technical reporting system, without statistics. Anyway - I have now plenty of information to prepare my son for the war for science :) Thanks again.

@CKM: thank you. I have gone though the WHO site and found information about the kind of side effects but not the numbers. The specific sheets you point to in your second link are excellent - I just went though two of them and they give rates for mild effects (not for severe, but that's a start and I will dig further). I also saw the VAERS site mentioned elsewhere, but it is a technical reporting system, without statistics. Anyway - I have now plenty of information to prepare my son for the war for science :) Thanks again.

@WoJ Well the statistics presented in the WHO technical documents are reported in tables as events per n doses, and so using MMR as an example, rash is reported as 5 per 100 doses or 0.05% for the measles vaccine.

Also consider that for relatively safe vaccines, serious adverse events such as grade III and IV may not have occurred or been linked to the vaccine administration, and so those weren't reported.


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Bug identifying

Can anyone help me identify this insect found in my office today?

If you could let us see the top-side of the bug, it would help us identify it.

It can help identification, if you add the approximate size and the geographical local of that bug.

That is a stink bug, order Hemiptera, family Pentatomidae. My guess is that it is a brown marmorated stink bug Halyomorpha halys, not because I can identify it as such, but rather, because this species frequently invades homes. https://en.wikipedia.org/wiki/Brown_marmorated_stink_bug


text:
Glass petri dish to replace plastic petri dish?
I never use a glass petri dish before, but I just wonder if I can use it to replace for plastic petri dish because it can reusable. The only thing I worry is , in a Fridge's user manual, it said that do not put glass container into the freezer (usually -20 oC) because it can be damaged/break and even explode. So do a glass petri dish have any special design to prevent this damage?

Glass labware is usually made of borosilicate glass which is resistant to temperature changes, so putting a glass petri dish in a -20°C freezer should not be problematic, at least with respect to glass cracking because of temperature changes. I think the warning on your freezer is probably meant to warn against closed glass containers filled with liquid; as water freezes it expands and may mechanically break the glass, but for a petri dish is should not be an issue.
I would be more cautious about heat shocks with a -80°C freezer, though; in my experience at that temperature there is still a risk if the glass is not of good quality.
On a side note, depending on what you use the petri dish for, the surface chemistry  may be different from the polystyrene of plastic petri dishes, and if you are growing cells directly in contact with the surface, switching to glass may change their behavior.

Thank you very much. I'm not sure if it was borosilicate or not. Just found it on an online store and they don't provide much info. Let me try it myself.


text:
How do seagulls know it is the 9th inning at a baseball game?
Multiple times that I’ve gone to San Francisco Giants games, the seagulls sensed when the game was ending so they could pick up food. https://youtu.be/LPra_ZfwanU

People give off many cues that are intelligible to animals: https://en.wikipedia.org/wiki/Clever_Hans

Not sure why this is receiving close votes for "opinion-based." It's not the best written question, but it's interesting and, IMHO, on topic here. The current answer should provide context for how this question can easily be answered appropriately. I hope the current answer poster provides additional resources to support his/her answer or that someone else provides some strong support for how bird behavior can be affected by human cues.

@theforestecologist how could it be better written?

Hi Austin. Typically a number of folks here don't like fun and colorful titles and prefer more strictly "scientific" language to be used both in the title and post. The post is also very short, which likely triggered it to show up in the low-quality review queue. I like fun titles (especially when relevant), but I would suggest you expand your post by 1) indicating your own research effort on the subject (show us you tried to look something up on your own), and 2) you can turn your video into a gif to provide directly here by typing "gif" between "www." and "youtube" using your video's link.

I have a seagull-level understanding of baseball, but in the linked video I can see large parts of empty sitting area empty of people but with plenty of garbage. Seagulls don't need to understand the game to see a potential for food at this moment.

Many animals, particularly some birds, are smarter than we give them credit for. Corvids, for example, are known to not only use tools, but are capable of planning and understanding some cause-and-effect scenarios that require patience.
I know practically nothing about baseball, but if it's like any other human gathering, there are probably a lot of clues that the birds learn:

Noise levels. Big events often culminate in some big fanfare with noise (cheering, music, etc.). If the game changes audibly near the end, you can bet the birds have noticed.
Motion/activity: Any large gathering I've ever gone to often has a small percentage of people leaving early because they want to avoid the crowd or traffic. I'd expect a close-scored game has fewer people leaving, but chances are good that as enough people start getting up to leave, it's another signal the birds can use.
Discarded food: Aside from getting up to leave, toward the end of an event many people will start discarding snacks and drinks. Hopefully in the correct bin, but often just on the ground (humans are messy -- which seagulls love). An increased number of people tossing garbage into bins (and missing or they start overflowing) signals a few gulls that there's scraps to be found.
Temporal.  If these events happen regularly, or even irregularly, the birds associate it with food. People filling a stadium or parking lot, playing music, buying food (birds do have a sense of smell, though not as developed as mammals), etc. The birds over time learn: Increased human activity at this location results in more food some hours later.

Gulls are very gregarious, and notice when just one bird has found a morsel. As soon as a few birds get the first discards, the rest of the flock notices and starts to mobilize; circling and calling.
I would argue that the birds don't really know when a game or event is about to end, but they are adept at reading their environment, even if it's an urban one.

Per @theforestecologist's comment, references are requested. While I do not have a reference for each specific behavior described above, the following list covers avian intelligence generally, learning and problem-solving, and physiological adaptations. Many of the described behaviors are products of associative learning and elaborate communication, traits that gulls exhibit in other activities such as dropping clams from heights.
References:

Ravens parallel great apes in flexible planning for tool-use and bartering
Can Kabadayi, Mathias Osvath
Science; 14 July 2017, Vol. 357, Issue 6347
Ecology and Conservation of Birds in Urban Environments
edited by Enrique Murgui, Marcus Hedblom
Springer Nature; 10 February 2017
Cognitive ornithology: the evolution of avian intelligence
Nathan J. Emery
Philosophical Transactions of the Royal Society of London; 7 Dec 2005, Vol. 361
Bird Sense
Tim Birkhead
Bloomsbury Publishing; 2 Feb 2012
Auditory and visual mechanisms in food-finding behavior of the Herring Gull
Hubert Frings, Mable Frings, Beverly Cox, and Lorraine Peissner
Wilson Bulletin 67; January 1955

Nice answer. However, please provide support for your claims. Thanks!

@theforestecologist I've added some references which I believe support the claims.My answer is largely based on my own ornithological studies, albeit at a non-professional level.


text:
Is an attraction to studying the philosophy of biology a good reason to pursue grad studies in the field?
I have always leaned more towards questions surrounding psychology, sociology, and philosophy but fate has me graduating with a BSc in Biology this year. Would it be smart to pursue it further more for the aesthetic beauty I find in its ability to shed light on questions beyond itself than for the science purely in itself?

Welcome to Biology SE! Your question is off-topic here, as it does not relate to how biology works or laboratory techniques in biology. Maybe Academia SE would be a better fit? In addition, a word of caution: many good questions generate some degree of opinion based on expert experience, but answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise.

I'm voting to close this question as off-topic because is not about biology in terms of SE Biology but about career choice.

In my opinion, yes and bioethics is a very interesting domain.
 First, there is a growing interest in ethics (which is a branch of philosophy) in the fast-growing field of synthetic biology ("next-generation" genetic engineering, the design of new organisms, genetic manipulations in humans etc.). In many publications (check out "synthetic biology" and "ethics" on google) and conferences, people are saying how far behind is bioethics, compared to synthetic biology. There are many burning questions such as: If we create new organisms, should we release them to the environment? Should we edit the human genome? To what extent? (Just curing illness, or maybe also to improve traits?) Should this ability be democratized?
Should a person's genetic information be used when looking for a job? Insurance? And so many more questions, not to mention the bioethics of the state healthcare (compulsory vaccinations etc.)
There are a lot of scientists that know nothing about philosophy and a lot of philosophy experts that know nothing about science. There are not enough people who know both and can help with these question.


text:
What percent of genetic disease are preventable?
I like to know what percentage of genetic disease are preventable before birth?
Also, when we can detect all of them? I heard in a TV show a doctor said about 5 years later we can prevent all genetic disease! Is this estimation true?

Five years to prevent all genetic disease is ridiculously, insanely wrong.

There is no simple answer to either of your questions.
There are many monogenic diseases where mutations in single genes result in disease phenotype.
There are far more diseases that have a genetic component where mutations in one or more gene increase the baseline risk of disease and this risk is then modified by the environment the individual encounters throughout their life-time (see Multiple Genes).
To get an overview of the functions of genes that have been so far identified, mutations within them and the diseases they have been linked to see Online Mendelian Inheritance in Man (OMIM).
If you want to get a feel for just how complex genetics is then a recently published paper on the genetics of hair colour would be worth reading...
Genome-wide study of hair colour in UK Biobank explains most of the SNP heritability

I like to know what percentage of genetic disease are preventable
  before birth?

Essentially 0%. There have been a few experimental applications of gene thereapy, but we're talking about a few thousand of people in the entire world. None are available in the context of ordinary medical care. Some genetic diseases can treated after birth with drugs that moderate the worst effects: haemophilia, PKU, and cystic fibrosis for example, but the underlying genetic problem remains.

I think this answer should clarify that it's talking about what's currently preventable, not what's theoretically preventable.


text:
Why don't primates have galactose-alpha-1,3-galactose (alpha-gal), but other mammals do?
I read in wikipedia that:

Galactose-alpha-1,3-galactose, commonly known as alpha gal, is a carbohydrate found in most mammalian cell membranes. It is not found in primates, including humans.

My question is : Why not?
In the sources for the wikipedia article about alpha gal allergy, I spotted the (pay-walled) article Evolution and pathophysiology of the human natural anti-α-galactosyl IgG (anti-Gal) antibody which has this to say in the abstract :

It is estimated that anti-Gal appeared in ancestral Old World primates less than 28 million years ago, possibly as a result of an evolutionary event which exerted a selective pressure for the suppression of α-galactosyl epitopes expression by inactivation of the gene for the enzyme α1,3 galactosyltransferase.

However this is more than a bit over my head, biology-wise.

That is because of the presence of IgE antibody. IgE response to alpha-gal causes anaphylaxis in humans. If you would like a more biological detailed mechanisms check out this article: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4600073

@m4rio Are you saying that having the IgE antibody causes us to not have alpha-gal ? If that's the case, that's just passing the buck : why do we have the IgE antibody in the first place ?

The general idea is that infectious agents use certain cell-surface proteins to enter the cell, and presumably recognize them by their particular glycoproteins. There are examples (cited in the extract below) of changes in e.g. blood group antigens in populations that are thought to convey (at least temporarily) an advantage against particular pathogens.
In this context, let me cite the rest of the section of the article that you didn’t have access to:

However, after the geographic separation of Africa and South America,
  Old World primates appear to have been subjected to a selective
  pressure for the suppression of autologous α-galactosyl epitope
  synthesis and for the subsequent production of anti-Gal. Possibly, an
  infectious agent endemic to the Old World, which was detrimental to
  primates, and which expressed α-galactosyl, or α-galactosyl like
  epitopes, exerted a selective pressure for the evolution of Old World
  primates able to suppress autologous α-galactosyl epitope expression.
  Thus, immune tolerance toward this epitope was lost and anti-Gal
  antibodies could be produced in these primates as a protective
  response to such putative pathogens.
An alternative scenario for the
  evolutionary suppression of α-galactosyl epitope expression could
  have been one in which ancestral Old World primates suppressed
  expression of these epitopes on their cell surface glycoconjugates as
  a result of exposure to a pathogen which exerted its detrimental
  effect via α-galactosyl epitopes functioning as receptors. A current
  example for such a pathogen is Clostridium difficile. Enterotoxin A
  produced by this pathogen was found to bind to the cells it damages
  through interaction with α-galactosyl epitopes on cell surface
  glycoconjugates [12, 56]. A bacterial toxin with a similar ligand
  specificity and which was detrimental to ancestral Old World primates
  could exert a selective pressure for the evolution of primates which
  suppressed the expression of α-galactosyl epitopes and, thus, lost
  the immune tolerance toward this carbohydrate structure.
[12] Clark GF, Krivan HC, Wilkins TD, Smith DF (1986) Toxin A from Clostridium difficile binds to rabbit erythrocyte glycolipids with terminal  Galα-3Galβ1-4GlcNAc sequences. Arch Biochem Biophys 257:217
  [56] Krivan HC, Clark GF, Smith DF, Wilkins DT (1986) Cell surface binding site for Clostridium difficile enterotoxin: evidence of a glycoconjugate containing the sequence Galα→3Galβ1→4GlcNAc. Infect Immun 53:573

Whatever the reason, the consequence of this was:

This also resulted in the loss of immune tolerance to the α-galactosyl epitope and the production of anti-Gal.

I presume this explains the IgE problem referred to in a comment, and I would consider this as an unfortunate side-effect of the change, and not a reason for it.


text:
What species is this gray bee?
Is this a bee at all, is it just an albino Apis mellifera?
It is roughly the same size as regular honey bees, and was pollinating lavenders along with many of the latter. There was a couple of these white ones.
Here is a photo I took. Sorry for the bad quality.

The bees were seen (and the photo taken) on December 11 (late Spring), at about 1 pm in the eastern border of Santiago, Chile (South America), at the foothills of the Andes, at about 950$\,$m of altitude.
I'm aware that it is possible that the information I provide is not enough to identify the insect. If so, any advise on how to get more meaningful information will be appreciated.
Thanks in advance

Your picture is of too low quality to be sure, but based on general habitus I would say that 1. Yes, this is a bee and 2. No, it is not Apis mellifera.


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Is studying chemical and physical properties of chemical substances that make up organisms really a task of molecular biology?
I have read in a high school textbook that (translated into English by myself): "Branch of science that concerns itself with studying chemical and physical properties of substances that make up organisms is molecular biology".
Is this statement accurate? From what I understand, molecular biology deals more with "biological processes at the molecular level", and so it would be biochemistry, or maybe even "standard" organic chemistry, that would study chemical and physical properties of such substances, not molecular biology.

If you look at the Google ngram for the term ‘Molecular Biology’ you will see that it first appears just before 1960, and it is relevant that the Journal of Molecular Biology was founded in 1959. It is not biochemistry — indeed the name was meant to indicate its difference from biochemistry, and I heard second-hand (so I cannot vouch for its truth) that Hans Krebs (Professor of Biochemistry at Oxford University at the time) referred to it as “biochemistry without a license”. What I can vouch for is that the contempt was mutual.
At the outset the term ‘molecular biology’ was used to combine two rather disparate areas of biological science that today we might refer to as Structural Biology and Molecular Genetics. The link between these was the work on the structure of DNA and proteins at this time,  and the molecular analysis of the genes that controlled the synthesis of proteins.
If you look at the definition in the short Wikipedia article, only Astbury — who worked on protein structure in Leeds — is quoted, but The Journal of Molecular Biology was initially almost the house journal of MRC Cambridge, the love-child of Crick and Perutz, as it were, with an emphasis on nucleic acid as well as protein structure, leading to the other side of the coin which was the genetic code, the lac operon and the study of bacteriophage.
Of course, terms change their meaning as science changes and what was once new and trendy becomes “yesterday’s girl”. It really doesn’t matter that much. Systems Biology anyone?

I seem to recall having written some of this previously, but I can't find where.


text:
What happens between two nodes in an evolutionary tree?
Hey guys can you help me with this one!?
What happens between two nodes (in an evolutionary tree) or a between a node and a tip?
A) at least one character changes
B) all organisms die
C) Nothing can happen between two nodes
D) Monophyly, Paraphyly, Polyphyly
E) None of the above
I came down to E) and C). Since B) doesnt even make sense, organisms don't die among two nodes- they evolve. D) it is irrelevant to the question asked A) I think that probably is wrong as well, since among a node and a tip, the organism stays the same and finally I thought C) could be the answer, but at the same time a new trait could be formed,

Thank you, I did remove them. And yes I did try to solve it my self before I post the question on the internet. I wasn't aware that I have to mention what are my thoughts.

The organism most definitely does not stay the same between internal node and tip(terminal node). the only way that can happen is if no evolution has occurred (ancestor and descendant identical) in which case you are not looking at an evolutionary tree.

The question does not make much sense and I think you've gone about as far as anyone can go.

A) at least one character changes

It depends what it means by character and it depends the detail semantic of the tree. In general, an evolutionary tree, usually called a phylogenetic tree attempts at representing time by the length of the edges in between two nodes. The goal is, in general, not to represent anything else.
In the comments, @John has argued that time can be consider as a character.  Personally, when I read the term "character" I think of a phenotypic character. While it will pretty much always be true that among two nodes some difference will exist in the phenotypic character, it is not a fundamental consequence of the concept of evolutionary tree. This is why I argued that A is false. @John takes the opposite stance in his answer. Note also, that sometimes (although quite rarely today) phenotypic states are used to build a tree and hence, in such case, it would be a direct consequence of the methodology that two nodes must necessarily differ by the value of at least one phenotypic character.
This disagreement between @John and I highlights that the question is poorly phrased and actually makes little sense.

B) all organisms die

Well, most likely enough time separate the two nodes that all organisms that were represented in the ancestral node are dead but of course they have reproduced, so that we actually have another node that descend from it.

C) Nothing can happen between two nodes

As you said, they evolve. So, things happen!

D) Monophyly, Paraphyly, Polyphyly

As you said, those terms make no sense here!

E) None of the above

If there is any intuitive answer to the question what has happened between two nodes is time has passed. I think the answer your teacher was expecting here is E but it is also possible (s)he was expecting A. Really that's a pretty poorly written question.

I know, all the given questions, are like that!!
Thank you so much for responding, Ecology and evolution is somewhere very far back in my undergrad education :)

@ANNA FYI, if you consider that the answer has answered your question you can click on the checkmark next to the answer (just below the downvote/upvote buttons). That being said, I would recommend waiting a little bit to see if other users seem to approve with this answer.

A) has to be true, because for there to be two nodes the two different nodes must represent some difference.

@John While it will pretty much always be true, it does not have to be. The only thing that must separate two nodes is time. It is also very much possible that the only change in between two nodes relate to synonymous mutations (and other mutations that has no effect on the phenotype), hence not causing a change in any character fo interest. I have clarified that in my answer.

@Remi.b Time is a character a character is part of data for a specimen, It can also be location. Characters do not need to be genetic the best ones are but they do not have to be. You are confusing a character with a characteristic.

I understood character as a phenotypic character. I very much suppose this is one was meant in the question. I doubt whoever wrote this question consider time a character

Also the question, considers that the potential answer will apply between a node and a tip. I still don't think that A is the answer ..

@remi, time can be a character however time also does not have to be considered at all, in paleontology reconstructive trees often ignore time because the spottyness of the fossil record makes it counter productive. On the other hand is a highly constrained, high preservation, time series sequence time may be a character because it is actually predictively useful then.  The only thing that has to be true is something needs to be different between two nodes (tips are nodes) for there to be two valid nodes.

@John Yes, we are here entering here the domain of the practical method used to build a tree vs the actual thing that we attempt the estimate. But I agree with you! I shall edit my answer.

Your answer is A. for one simple reason, two different nodes represent at least one notable/measurable difference between groups, so between any two nodes there must be at least one difference.
Look at this example, whether A and B represents Mammals and Birds or two subspecies of chimp, or two strains of virus the fact they are two separate nodes means there is some difference between them. When constructing a tree there has to be at least one character difference to have more than one node. A tree with no differences is just a dot by itself.
Also an organisms does not stay the same between a node an the tip (the tip is a node) to use the below example the starred node between A and B is the most recent common ancestor of A and B which is not the same thing as A or B.

Yes I understand that. But on occasion the node it could be a result of a population immigrating on a different location. That doesn't mean that a new characteristic arose... It does?!

New and arose are not part of the question nor the definition of a character. Answer A is"at least one character changes" A character change be a loss, a different numerical measurement or color, a different location or time almost anything.  A character is part of the data used to describe the specimens and that has to be a att least one character difference between nodes, nodes have to have a definable difference. without a difference the specimens will be grouped into the same node.


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Never seen a spider with this pattern before
Found this spider at work in the Leicestershire area of the United Kingdom. Never seen one with this kind of pattern on its back before so was curious as to what it is. (Size: 2-2.5 inches)

Please update with approximate size of your specimen.

Appears to be some species of Araneus (orb weaver)

It was probaly around 2inches maybe 2 and a half

The depicted spider appears to be a European garden spider Araneus diadematus. The mottling pattern that forms a cross shape is probably one of the more distinctive features, giving these the nickname cross spiders. The distribution for your locale makes sense, based on data collected on these spp: http://srs.britishspiders.org.uk/portal.php/p/summary/s/Araneus+diadematus


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Why ravens play with garbage?
Why ravens play with small plastic details and other garbage?
Could you explain how this behavior was formed by evolution for birds-scavengers?

Ravens and other corvids are among the most intelligent birds. Of note, crows and ravens are known for their ability to solve problems that require tool use, memory, and delayed rewards (patience).
Many animals play, and ravens and crows are no exception. (A study entirely on raven nestling play.) The evolutionary purpose of play activity is thought to improve coordination/dexterity, provide exercise, strengthen muscles (such as wing-flapping by young birds that have yet to fledge), and develop social skills.
As to what type of objects ravens find most interesting to play with, I'm unsure of a definitive answer. Some birds, particularly the satin bowerbird, even collect colorful objects. My hypothesis is that the choice of object is likely due to simple availability (discarded) and conspicuous nature (color). In other words, ravens more easily find such objects because they are colorful, which in turn are frequently human-manufactured.

What is specific  in "forest scavengers life style" that pushed them to become most intelligent birds?

Quite a while ago I read "Mind of the Raven" by Bernd Heinrich, an expert in ravens. If I recall correctly, he suggests that ravens will essentially investigate any object they haven't seen before. Then after learning about these objects, they don't find them as interesting anymore.

@Eff An excellent book! Indeed chapter 24 is dedicated to play. I recall the same; I think it may also have been implied that investigating objects could contribute to finding new food sources.

@JYelton "I think it may also have been implied that investigating objects could contribute to finding new food sources." That's exactly what I remember being suggested.


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How does one predict how large of an effect on antigenic drift a substitution in the amino acid sequence of a surface protein of influenza has?
I know that some amino acid substitutions are more effective in causing antigenic drift than other substitutions based on their location in the 3d structure of the HA protein (proximity to the receptor binding site).
I would like to be able to determine using a program whether a virus will be dominant based on multiple factors including genetic difference from the previously dominant virus. How can one know how much bigger of an effect one AA substitution will have on the antigenicity of a virus compared to another?
Any help is much appreciated.

Your understanding of influenza antigenic drift is, unfortunately, hypersimplified and mostly wrong. In particular, your notion that some mutations are more important for antigenic drift because of their effects on structure is at best oversimplified.
Rather than spend many paragraphs reviewing the complex patterns involved, I'd suggest you start by carefully reading papers from people who have correlated antigenic drift with sequence change, such as

Sequence-Based Antigenic Change Prediction by a Sparse Learning Method Incorporating Co-Evolutionary Information
Using Sequence Data To Infer the Antigenicity of Influenza Virus
Mapping the Antigenic and Genetic Evolution of Influenza Virus
The genomic and epidemiological dynamics of human influenza A virus
Selection of antigenically advanced variants of seasonal influenza viruses
Antibody landscapes after influenza virus infection or vaccination
Substitutions Near the Receptor Binding Site Determine Major Antigenic Change During Influenza Virus Evolution

This is a field that a lot of extremely smart people have been looking at extremely closely for many years; all the simple approaches have been tried already.


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Thermoregulatory characteristics
I have a question that probably is to obvious, or just bad wording..
The terms endorthermy, ectothermy, and heterothermy, are used to describe:
A) cold and warm individuals
B) the three layers of the skin
C) different types of body cavities
D) the source of an animals heat
E) none of the above
I think it's E) or D). My thinking process is B and C completely irrelevant.  A) i think it is very ambiguous as an answer as those three terms refer to a type of classification rather than the characteristic itself (like if their skin is cold or warm). On the other hand D) the source of an animals heat, doesn't seem very right to me. The 3 terms refer to the source of the heat that predominatly determines the body temperature, meaning that it is not THE SOURCE, but the way they exchange and regulate their temperature... That means that probably it is E?!
Thanks

Related: https://biology.stackexchange.com/questions/61444/are-homeothermic-and-endothermic-synonymous

"The 3 terms refer to the source of the heat that predominatly determines the body temperature, meaning that it is not THE SOURCE, but the way they exchange and regulate their temperature". What do you mean by this? We use heat to change our core body temperature so why does this seem wrong?

@ANNAMARIA I am not sure I understand what kind of semantic issue you are pointing to for answer D. But, in short, I don't think it is such a trick question. The answer is D.


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What is omicron squared in genetics?
Saw this equation in the conext of epidemiological genetics:

I have never seen it before and I don't know what variable it represents. Help?

Please always link to where you found this equation. It might well have been an equation that is not common enough to be recognized without the original reference. By chance, it is a very easily recognizable equation, one that has nothing to do with biology.
What your showing is an equation to compute a variance. It is not omicron but sigma ($\sigma$). In statistics, $\sigma$ is the standard deviation and hence $\sigma^2$ is the variance. $\mu$ is the mean and $n$ the number of elements from which these statistics are being computed.


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Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics?
Why are the bacteria that cause hospital-acquired infections resistant to many antibiotics, and why don't hospital acquired infections exist elsewhere ?
The infections that are caused in hospitals are usually a result of bacteria that are resistant to multiple antibiotics making them difficult to treat, but why are the bacteria resistant to all these antibiotics?
I realize that a lot of antibiotics are used in hospitals but the question that comes to my head whenever I read this is "So?".
To make my misconception clearer, I will use MRSA as an example .
I mean , for the Staphylococcus aureus bacterium to become resistant , the antibiotic has to be used on it , so how can the antibiotics used to treat different infections in difference people act as a selection pressure for  Staphylococcus aureus ( the Bacteria that causes MRSA )?

Hospital plumbing a 'vast, resilient reservoir' of superbugs. I'll make this an answer at some point...

Hospitals have certain features:

They are full of people immunocompromised in some way (old, exposed tissue, on steriods etc.)
They are full of people with pathogens
They are full of doctors who will give antibiotics to people with pathogenic infections

This is a perfect breeding ground for drug resistance in pathogens, with lots of pathogens, lots of places for them to grow (patients) and quite a lot of exposure to antibiotics.  You use Staphylococcus aureus as an example, and it is a good one.  We all have some of it on us, but it is not generally exposed to antibiotics so it does not develop resistance, and we do not generally have large areas of exposed flesh that would cause it to be pathogenic.  In hospital this is not the case, so we get it causing trouble and developing resistance.
These things do occur outside of hospitals, but it does not tend to be as common or frequent.


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Identify mystery insect found in Boston, USA
This insect is approximately 2.5mm.  It was recently observed in a Boston USA shower.  Do you know what type of insect this is?

This is a spider beetle (Coleoptera: Anobiidae: Ptininae); the focus does not let me go deeper at this time.


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What bug is this? (England)
I have found this small bug on the wall in my bedroom, and have been trying to figure it out what it is for months.
There are more of this kind. They are tiny, I can't see how they look like with bear eyes. I can only see their proper shape by zooming in. I have seen them on my wall, in my drawer and on paper tissue.
I live in England in a very humid, dumpy flat.
I have also found bites or allergic spots on my body, but don't know if this bug causes it or something else.
Any idea what it is?

This is a booklouse (order "Psocoptera"), and from the inflated hind femora likely a member of the family Liposcelidae; that family is common in domestic situations as a stored product pest, so while they may not be responsible for your skin condition, you'll still want to have them removed (look for other questions featuring domestic book- and barklice for suggestions on how to do that).


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Antigen molecular mimicry
Let us consider a situation in which the body is attacked by a microbe, and  the microbe is captured by the immune system for recognition of surface antigens.
The surface antigen recognized mimics one of our self antigens.
It is stated in textbooks that this situation results in the immune system attacking  the microbe along with the tissue containing the self antigen(auto-immunity).
(Reference: Robbins and Cotran pathologic basis of disease)
If a microbial antigen mimicks self antigen, why is the microbial antigen attacked instead of being ignored in the way that all our self antigens are ignored by our immune system?

There are different type of immune cells which falls under either innate or adaptive system.
The cells under the innate are first to respond microbial attack and are able to detect them in extracellular environment by recognizing proteins/peptides called Pathogen-associated Molecular Patterns (PAMPs) on their surfaces; these are only found on microbes.
But when the innate system fails to clear the microbes in time, the adaptive  system is kicked-in. This involves T-lymphocytes and B-lymphocytes. T-lymphocytes are trained to ignore cells that are able demonstrated that they self but B-lymphocytes which produces antibodies/immunoglobulins to the detected antigens do not have a mechanism of ignoring self cells.
So the problem lies with when the immune response gets to the point where antibodies are produced, at that point produced antibodies simply attack without discrimination.
I hope this simplified version would help you.


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Is there a mechanism of timing or delaying the expression of gap genes?
Summary

Gap genes are expressed in presence of the right combination and amount of
  transcription factors. But is there any additional mechanism of timing the expression of the gap genes to ensure that they are expressed at the right time?

Context and Detailed Question
Let's look at gap gene expression in Drosophila:

Firstly, bicoid and nanos are expressed and diffused from anterior and posterior ends respectively and form gradients;
Then, hunchback gets expressed, with bicoid acting as promoter and nanos acting as suppressor;
Then, Krüppel gets expressed, with
hunchback acting as both promoter and suppressor - meaning that there must be enough hunchback, but not too much.

(or a video: https://www.youtube.com/watch?v=uaedzlrnBGY)
Makes perfect sense, unless you look at it from dynamic, biochemical perspective:
Firstly, bicoid and nanos slowly build up in the embryo:

As soon as there's enough bicoid at the anterior region, hunchback immediately starts building up too: I mean, it can't just choose to wait for bicoid to establish its gradient or something - if there's a promoter for it, it should react accordingly.

And so it "chases" the bicoid gradient, in a manner of speaking, and will continue to chase it until it stumbles into nanos protein, which suppresses it.
All this makes sense so far.
The only problem is that at this point, there's just perfect amount of it for Krüppel at the anteriormost region, so Krüppel should start being expressed there:

Eventually, there'll  be too much hunchback at the anterior region, so Krüppel should cease to be produced - but some quantity of it should be expressed there nonetheless. The final gradient should look like this:

The only way to avoid it is if Krüppel kindly waited until the hunchback establishes its final gradient before even attempting to be expressed. But how is this possible? Is there some mechanism that prevents Krüppel from being expressed too early - and if so, then what releases it? Or maybe there's some mechanism of timing, that prevents genes from being expressed too early?
This Krüppel example is just one examples of several, when there must be some timing control in order for genes to be expressed properly.

I'm voting to close this question as off-topic because this is not the kind of precise answerable question that SE Biology is for. It is basically an argument against a model of gene expression followed by an “am I right?”.

@David 1. It's a precise answerable question (if there is a known mechanism that prevents kruppel from expressing too early, then a person who knows about it can answer).

Where did you see an argument against the existing model of gene expression?

Where did you see "am I right?" or even me proposing anything? I explained the thing about dev. biology that I don't understand and look for help. If you know the answer, you could just answer; or if you think that I misunderstood something, you could just explain where I am wrong.

OK, I'll withdraw my close vote and restrict myself to some constructive help and advice. 1. Your question is complex and very few people on this list are likely to be able to answer it. 2. They would have to read through text and 11 diagrams to get to the actual question to see if they could answer it. I think that few are likely to do so. The very least you should do is to start your question with a summary of what it is, before telling people what to consider. I have started this for you. You can delete it if you like, but I would advise you to improve on it instead. And your title.

I have absolutely now idea about drosophila embryo development, but you/your diagrams seem to assume that all these genes are - dynamically - expressed as along as their promotor is active (enough) at a given position in the embryo. I would suggest you to also look into the temporal dynamics of these genes as well - I wouldn't be surprised if these 'gap' genes only start expressing when the nanos/bicoid gradient is already fully established, maybe looking into that direction can help you find an answer.

@David, thanks. I've tried to make question and summary more clear. As you say yourself, the question is very specific and complex, and it took me two days just to formulate it properly - so I found no other way to make it clear but to include diagrams and stuff...

@Nicolai, thanks, I've found a few articles by googling temporal dynamics of gap genes, I'll see what they say. I also expect that they should wait for gradients to establish first, but I couldn't find what could be responsible for it so far. No articles that I've seen so far mention it and just say that it's all about gradients of transcription factors.

Not sure which papers you've found, but off the top of my head these address similar topics:
https://doi.org/10.1371/journal.pbio.2003174
https://doi.org/10.1371/journal.pcbi.1005285
There's also a video lecture by Johannes Jaeger in which I think he addresses similar questions/provides an overview of the above papers and previous work: https://www.youtube.com/watch?v=kVSf9Hjl9Jk
Too busy right now to read and watch these again in detail, so may not be helpful, but off the top of my head seem to address this kind of question.


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Can vaccines move from person to person?
Can someone who has been given a vaccine "infect" another person with the virus used in that vaccine? For example, let's say Bill is vaccinated against tuberculosis. If Frank is exposed to Bill, is there a chance he could "catch" the tuberculosis vaccine, and become immune?

So, A got a vaccine but still got infected by the virus (which is totally possible). And then, you are asking if A can transmit the virus to B? Is that your question?

Here are a few things that can help you clarify the question. Who is "they" in the first sentence? Does it refer to "another person" (but then it should be "he/she")? What do you mean by "contacted"? By "become immune", do you mean after the infection happen? If not, why would there be a need for the first person to be infected? Or maybe when you said "infected from viruses", you refered to the neutralized form of the viruses that were injected in the vaccine?

I think Jossie is assuming the antigen in vaccines can can be transmitted and infect other people like an ordinary pathogen.

OP, I've edited your question to try to clarify it. Feel free to roll back or further edit if I've misunderstood or missed anything.

@Jossie, in simple terms: vaccines only contain parts of "dead" pathogens that trigger an immune response to those parts inside the body of the person who was vaccinated. There's nothing to pass on (via a sneeze, cough, etc.).

A weird analogy I'm making up as I type (& as I eat): Imagine wanting to know what vanilla ice cream (IC) tastes like. You could taste vanilla extract & your taste buds would know what vanilla tastes like. You'll not have eaten vanilla ice cream, but if you ever do eat vanilla IC, your taste buds will know the IC is vanilla flavored. This is because your taste buds had previously been exposed to the parts of vanilla IC (i.e., vanilla) that could inform your brain of the sensed flavor. However, someone else could only know what vanilla tastes like if they sampled their own vanilla extract.

Most immunizations are not transmissible. A few are. To be transmissible, an immunization would have to be a live attenuated vaccine (i.e., a vaccine that can reproduce in the host, but doesn't cause disease), AND have the necessary reproduction rate and virulence factors that would allow for person to person transmission. There are many live attenuated vaccines in use today, but only one that is transmissible, Oral Poliovirus Vaccine, or OPV. OPV is currently not in use in the US, but is used in the developing world, and can circulate in communities. Some would argue that this is a good thing, as it further disseminates immune protection to the population, but it is a little problematic, because it is not without risk, including reversion to a virulent type that can cause Vaccine associated Paralytic Poliomyelitis.
On editing your question, I'm reminded that your example was of TB. I would note that BCG, the vaccination against Tuberculosis, may be a particular case, and I'm not as familiar with it except as a complicating factor in interpreting the results of a TB test in U.S. immigrants. BCG is a live attenuated strain of Mycobacterium bovis, can (rarely) produce disseminated disease itself, and the mycobacterium itself can be isolated in the blood of individuals some time after vaccination. There is also a possible report of vertical transmission of the mycobacterium (from mother to child), but these results use novel methods, and I'm unfamiliar with this group's work. Whether this would lead to immunity of the child is definitely an open question. BCG even when administered in the standard way (as in intradermal inoculation) isn't particularly good at producing immunity, though it is good at preventing meningitis and miliary TB in young children. I'm not aware of any documented case of horizontal person-to-person transmission, but wouldn't declare it impossible.


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Technical reason that specialized embryonic cells form
During the embryonic stage of human development, rapid cell division occurs and specialized cells form to build the various parts of the developing fetus.
I'm curious:

Why technically do specialized cells (such as brain cells) form?  I suspect this is due to a DNA sequence, but why chemically / mechanically should a genetic combination cause a certain specialized cell-type to form?
Have we (the international scientific community) reproduced the fundamental chemistry that causes any specialized cell-types to form?

There is indeed chemical signaling that triggers the differenciation. There are gradients of chemical species during the development. Look at https://en.wikipedia.org/wiki/Morphogen ! There are also other references there.
PS: there is a stack exchange question from today about something related Can gap genes delay their expression?


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Mild introduction to selective advantage of intelligence/nervous systems in animals?
I have a general understanding of why intelligence, i.e. nervous systems in animals, is advantageous: processing information allows an animal to adapt to its environment dynamically and perform complex sequences of actions that an animal without a nervous system could not. Larger nervous systems potentially allow for more possibilities herein.
However, I am interested in a deeper understanding of the factors that cause a species to at first develop, and increase the size of, a nervous system, and different forms of cognition:

what type of environment favors the development of a nervous system in a species?
what type of environment favors life-long learning and adaptivity (neiroplasticity?) of a species (as opposed to a fixed neural structure after development in an organism)?
what type of environment favors the development of goal-oriented planning (as opposed to simple impulse-response patterns)
what type of environment favors development of "cognitive ability" in species?

Do you know of a good book that addresses questions like this?

Look at that https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1003399

@J.A Thank you, that’s interesting. Though not precisely my question.


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Why is the Km of an enzyme half of Vmax?
Why is the Km of an enzyme half of Vmax?

We welcome new users to SE Biology, but we expect them to read the help on asking questions before posting, and to look at examples of well-presented questions. Your question, I am afraid does not come up to the mark. You have put half your question in the title, and the rest as a single line. The premise is incorrect in actual fact —  Km is the substrate concentration at Vmax/2, and I have no idea what you mean by "any other specific reason". This is why your question has been downvoted.

$K_M$ is a constant and is not $V_{\mathrm{max}}/2$ as they have different dimensions. But by the Michaelis Menten equation, $V=\frac{V_{\mathrm{max}}[S]}{K_M+[S]}$. So, when $[S]=K_M$, we have $V=\frac{V_{\mathrm{max}}[S]}{[S]+[S]}=\frac{V_{\mathrm{max}}}{2}$. Hence, $K_M$ is the substrate concentration, at which we would have $V=V_{\mathrm{max}}/2$.
Reference: Worthington Biochemical Corporation

We can also see that $K_M$ can't be identically $V_{\mathrm{max}}/2$ since $V_{\mathrm{max}}$ is dependent on the initial enzyme concentration while $K_M$ isnt.

Km is never Vmax/2. It is the substrate concentration at Vmax/2. I would sort out the question before giving an answer. In this case I would not answer the question because it is so badly presented and shows so little effort on the poster's part. See "Answer well-asked questions" in the Help on answering questions. And the suggestion that a naive user reads a "credible textbook on enzyme kinetics" is, well, incredible. Again, point him to a page online. And if you answer take the trouble to set it out in a readable manner.

[Edited] I believe your comment and my answer say the exact same thing. I've told the OP that what they've said is false. In my opinion, even if it's a low effort question, the OP deserves to know that they're wrong. If you would like the OP's question to be deleted, then please vote for that. If you take any particular issue with my formatting that suggests my answer isn't readable, please point it out.