Would it be correct to state that any biological difference between the sexes has to be found in the Y chromosome? If the reason Why Men Don't Listen and Women Can't Read Maps is genetic, then one of the genes in the Y chromosome is to blame and in theory could be identified.

Correct or incorrect?

"Blame" is a strong word.  The human Y chromosome has only a few dozen protein-coding genes.  One of the most important, for males anyway, is SRY, the sex-determining region.  This is a transcription factor that is responsible for modulating the expression of other genes; those genes need not be on the Y chromosome.  SOX9 for example is itself a transcription factor, is upregulated by SRY, and is found on chromosome 11.  Most of the genes associated with maleness are found elsewhere.  Moreover, once the testes form, they can be potent secretors of hormones that cause a number of physical changes.  So is SRY to blame, or SOX9, or the testes?  It depends on how direct you want your genes to be.  If you're blaming SRY you're not wrong, but at that point you might as well blame fate.

Oh, and there are epigenetic differences between the sexes.  You could also make some arguments about the Xist gene responsible for X-inactivation in females.


When two amoeba cells form from one amoeba, does spindle fibers form? When two amoeba cells form from one amoeba, does spindle fibers form? Some sources say that spindle fibers do not form while an amoeba cell is undergoing cell division. If spindle formation does not occur, than how are the chromosomes pulled apart? Which intracellular transport mechanisms are used?

Amoebas undergo binary fission, which is a much more simplistic process than mitosis. In binary fission, the duplicated chromosomes simply separate as the cells is pulled apart.  There are no spindle fibers used in this method of cell division.


Rate of production of enzymes in human In the metabolic pathways, each of the reaction needs an enzyme(protein) in order to occur successfully. Is there any quantitative measure that can be associated to this enzyme? Like synthesis rate of enzyme, degradation rate, mRNA transcription rate, enzyme activity, amount of enzyme present per unit measure of protein in the cell and if there is rate of generation of the enzyme's product, the rate of production of this enzyme in the human body, etc? I wanted to know the list of features that can quantify enzyme activity in the cell.

Your question already answers a fundamental point: namely that there are several distinct quantitative measures that can be associated with enzymes (the list could also be extended, and you will discover more in biochemical textbooks...).
If experimentally or theoretically accessible, one additional important quantity is the formation of product over time divided by biomass ( e.g.: Jacob et Monod 1961)


I know how to solve these equations, but I'm not sure what t' represents? I am investigating the Wilson Cowan neuron population model, and I can follow most of it, but I'm not sure what is meant by t' in the equation for proportion of neurons in the refractory period. The equation of interest is below.

I figured it out, t' is just a dummy variable used to represent time over the refractory period since the integral is from t-r to t.


Difference vector target and genomic target In Pfu turbo DNA Polymerase AD information sheet (and possibly in many other) different amplification targets are divided in Genomic DNA targets, Vector DNA targets and cDNAs.
What is the difference between the first two?

Genomic DNA is a DNA that has whole set of genetic data of an organism. You usually extract it with a whole DNA extraction kit.

Vector DNA is a vector (usually a plasmid, it can also be artificial chromosome,...the type of vector depends on the species and strategy you are using) that has you desired string of DNA in it (for example a gene you want to insert in to a organism) and you are using it to get your recombinant DNA to the organism.

I hope it helps!


Parietal and Visceral epithelia If you google visceral and parietal you get: The parietal layers of the membranes line the walls of the body cavity (pariet- refers to a cavity wall). The visceral layer of the membrane covers the organs (the viscera).
but
the first image that pops up is this :

I don't understand how the inner layer is covering and the outer is lining ?

Yes, the parietal pleura is on the wall of the thorax. That picture isn't great.  Each lung has its own pleural cavity, ie its own visceral+parietal.  Another important thing is the folding over.  Imagine the parietal pleura running along the inside of the ribcage...when it gets to the middle of the chest (the mediastinum), it folds over, or "turns the corner", and is now the visceral pleural running along the surface of the lungs.  The pericardium functions similarly, and so does the peritoneum/mesentery.  Here's another diagram that could help:


Creation of healthy genetically modified crops GM crops are huge at the moment, and the noticeable 'counter movement' is for people to continue to purchase organic foods (please note I am specifically talking of GM crops and not meats, etc).

The argument as fair as I am aware is that some of the GM crops actually contain poisons to the human digestive system that cannot be broken down, and we have yet to find out their effects on long term health.

However, my question is: What can be achieved, if anything at all, in terms of creating GM crops which do not incur health issues? Is there a specific way of going about this?
EG:

Could crops be made larger?
Could crops become more pest-resistant?
Could a 'uniform shape' be created?
Would this be done with genes from other plants? Or artificially?

Thank you for your time.

Welcome to Biology.SE.

What are GMOs?

The term 'GMO' can mean a vast array of different things and there is no objective way to distinguish what most people would call GMOs from what most peopel would not call GMOs. Humans have made 'GMO' for thousands (or even tens of thousands) of years. The detailed definition of 'GMO' will not impact the answer to the question Are GMOs safe to eat?.

Are GMOs safe to eat?

Yes, GMOs are safe to eat. There is no health risk when eating GMOs. Every scientist agree on that. Arguments saying that GMOs cause health risks have no foundation and are not based on evidence. Have a look at the Skeptics.StackExchange.com > Is Genetically Modified food safe to consume?.

Note that I am not saying that there is no discussion or debate to have around GMOs. I am only saying that these discussions have no reason to be around health risks for the consumer.

Your questions

  Could crops be made larger?

Yes. We already did that.

  Could crops become more pest-resistant?

Yes. We already did that.

  Could a 'uniform shape' be created?

I do not understand what you mean.

  Would this be done with genes from other plants? Or artificially?

The term 'artificially' has no good definition and it makes your question unclear. Most would consider pretty 'artificial' to take a gene from a species and insert it into another species (even though it occurs in nature).


Why don't we hear ultrasonic sounds as aliased versions of the original signals? The upper limit of hearing is approximately 15 kHz, dependent on age and other factors. According to the principles of digital signal-processing, such an upper limit would mean that the auditory system samples at least at 30 kHz or more.

Now suppose an ultrasonic signal, say a 40-kHz acoustic frequency - why would I hear nothing, instead of that signal aliased at a 30 kHz sampling rate?

Short answer
The cochlea is a tonotopic map with certain physically determined boundaries that determine the range of frequencies perceived. Ultrasonic soundwaves simply do not have a correlate on this map.

Background
The cochlea is a frequency analyzer that basically translates acoustic frequencies into a place-map. High frequencies are encoded basally (up to 20 kHz), low-frequencies apically (down to 20 Hz or so). Hence, it is pretty much a Fourier analyzing system (Fig. 1). This way of analyzing sounds is referred to as the place-coding theory of pitch. The place where a frequency is encoded is mainly dependent on physical characteristics of the basilar membrane in the cochlea. Every part is sensitive to a slightly different frequency then the next. This is caused by gradual variations in the stiffness and width of the basilar membrane, among other less important factors like hair cell length and so forth. The specific physical characteristics determine what specific resonant frequency a particular part of the basilar membrane has. Hence, incoming sounds are torn apart with standing waves, where each frequency results in a standing wave at a particular spot in the cochlea.

Fig. 1. Tonotopic map of the inner ear. source: Ternopil State Medical University

The frequencies mentioned are physical wavelengths of the acoustic air pressure differences entering the outer and middle ear. The cochlea translates these into fluid-based pressure differences. Hair cels in the cochlea pick up these fluid pressure differences and tranlate them into potential gradient differences.

The sampling rate of hair cells is pretty much infinite, as they work on a continuous membrane voltage, i.e., they are analogue.

The secondary neurons, the spiral ganglion cells, translate these voltage differences into neural spikes and lead them through the auditory nerve to the brain.

Neural spiking follows the acoustic frequencies up to, say 1 kHz (frequency following response). This phenomenon is referred to as the temporal code of pitch hearing. After that, the refractory characteristics cause single fibers to fire only to one in a few wavelength periods. So at the upper limit of hearing, say 20 kHz, a ganglion cell may only fire once every 20 wavelengths or so. No problem, as many others do the same thing. Stochastics cause the wavelength to be nicely encoded in a population of responsive fibers. Furthermore, the auditory cortex contains a tonotopic map, meaning that high frequencies are processed elsewhere then lower frequencies. In other words, the auditory nerve doesn't need to faithfully encode the incoming wave.

A nice example in this are cochlear implants; they stimulate the auditory nerve with electrical currents. The place of the electrodes determines the pitch, not their pulse rate (although it can have an effect).

Now why are you not hearing ultrasounds? Simply because the basilar membrane does not contain regions sensitive to frequencies above 20 kHz or so. This is referred to as the Greenwood map, which depends on species.


Is sexual selection evolutionarily advantageous? Our biology teacher says that peacocks will soon become extinct because of bigger and bigger (and heavier and heavier) tails. Why natural selection did not eliminate sexual selection?

What does "evolutionary advantageous" mean?

First note that is sexual selection evolutionarily advantageous? is a question that makes no sense. An allele or a trait can be evolutionarily advantageous if it increases the fitness of its carrier. If an allele, an evolutionary process or an environmental change decreases the risk of extinction for a species, then you cannot talk about evolutionary advantage. Selection (whether natural, sexual, artificial or whatever) does not (necessarily) minimize the risk of extinction of species.

This post is very related to your question and is definitely worth reading.

I hope your teacher didn't really say that! Assuming he did say that, then know that it is really not as easy as he's suggesting.

There are a number of studies that address the question on whether Sexual Selection (SS) and Natural Selection (NS) have opposite or antagonist effects. The subject is not easy and as SS is not my field of expertise my answer will not be complete. I will talk about two possible hypotheses for explaining the existence of SS and what they mean in terms of probability of extinction.

Good Genes

Under the "Good Gene" hypothesis, females' preference (we'll assume that females are choosy but there are many species where males are choosy) of some traits evolve because those traits are correlated with the global health of the male. In consequence, by choosing a male carrying some trait, the female makes sure that her offsrping will receive good genes from their father. This hypothesis assumes that poor males cannot produce fancy phenotype, while good males can. This is called Zahavi's Handicap Principle.

Under this hypothesis, if a trait become too costly for a given male, the male will just die, therefore limiting the evolution of secondary sexual traits. As a result, the population will no get extinct. Furthermore, under this hypothesis, SS may actually increase the effect of NS making sure that only the best male reproduce. In results the mean absolute fitness of the population should increase faster in a population where "Good gene"-SS occurs.

Sexy Son

Females preference for some trait may also evolve because mating with a sexy male means having sexy sons. This is called the "sexy son" hypothesis.

Under this hypothesis, again if a sexy male has a low enough survival, then a female has better to mate with a less sexy male (even though her offspring won't be very sexy) so to increase the survival of her offspring. After a bunch of generations, all females will end up preference mating with non-sexy male, changing the concept of what we call sexy in this population and therefore reversing the effects of SS.

You may also want to read about Fisher's runaway processes.

Just an article among others

Aneil Agrawal has some nice articles on SS that may interest you. This article for example discusses how sexual antagonist genes influence whether SS has an antagonist or parallel effect to NS.

Is SS really different from NS?

Your question Why natural selection did not eliminate sexual selection? assumes that NS and SS are two different things! This is a very old-style point of view. Charles Darwin coined these two terms thinking of two, unrelated processes. Today, most authors see SS as being part of NS (if a chestnut tree is a type of tree, SS is a type of NS). And many of the processes that are termed SS has actually not much to do with "competition to access a mate" but only has to do with NS. For example, many people talk about SS when talking about sexually antagonist genes or sexual conflicts. In short, the concepts are kind a mixed up. You may want to read about the work of Hannah Kokko about the semantics of terms related to SS.


About the plight of Elephants and efforts to conserve them? Poachers are only after the ivory horns right? I read this story from the New York Times ( I think) of saving a Rhinocerous by some Park Rangers and a Vet. ( forgive spelling) ; they tranquilized the Rhino and took its horn off so it wouldn't be killed. I know Rhinos need their horns so maybe a hard plastic 'prosthesis' could be put in its place. Maybe the 'prosthesis' could be colored yellow or have some markings on it so any poacher would know it's fake. Of course this could all be done for the elephant too.

Could this be a feasible way to save Elephants or Rhinos??

Dehorning of rhinos has been tried with limited success. Poachers have killed dehorned rhinos anyway, either out of spite or to avoid tracking worthless prey in the future. There is the problem of anesthesia (always a risk) and the fact that rhino horns are usually not destroyed but saved in the event of decriminalization. But at least horn grows back.

Considering the strength of horn and ivory, and the force applied in their use, plastic would not be of much use to them (especially elephants with long tusks).

  They are used for digging for water, salt, and roots; debarking or marking trees; and for moving trees and branches when clearing a path. When fighting, they are used to attack and defend, and to protect the trunk. - Wikipedia

To detusk elephants would be akin to declawing a lion, though much more dangerous and painful. Though this might help prevent poaching, the future of these animals lies in prevention.


Why are plant buds called 'eyes'? I was reading the etymology of the Latinate English verb 'inoculate' which contains the following part that generated the question entitled above:

  [...] inoculare "graft in, implant a bud or eye of one plant into another," from in- "in" (see in- (2)) + oculus "bud," originally "eye" (see eye (n.)).

The OED confirms 'eye' as a synonym of 'bud,' but I doubt that 'potato buds' generated this meaning because it already existed in Classical Latin that (I am assuming) South Americans did not speak in the 1500s when they introduced potatoes to the Spaniards.

Just take a look at a potato and observe each of its eyes. You will see that each of them has two parts:

1) An "eyebrow" : this is a vestigial leaf

2) A small bud in the axil of that leaf

Thus, the two of them together form an eye + eyebrow

The eyes are not evenly distributed in a potato plant. One side may have just one or two but the other side will have lots of them. This is because that is the growing spot!

Examples:


Why have certain plants evolved to contain psychoactive compounds? Plants such as marijuana (Cannabis) and kratom (Mitragena speciosa) contain compounds that affect the human brain. Why have these plants evolved to incorporate substances like THC and mitragynine into their leaves/flowers?

The evolutionary history of different plants expressing psychoactive compounds can vary, and in many cases it's difficult if not impossible to pinpoint a particular origin. However, we can make some general observations:

Homology across wide ranges of species

Despite the differences between, say, a human versus a locust, animals share a lot of their physiology. Mammals and insects tend to use different neurotransmitters for different purposes, for example, but the actual neurotransmitters and their receptors are often homologous. A plant could therefore develop a compound that acts as a neurotoxin in certain insects, but also has some psychoactive effects in a human. Nicotine is an example of a psychoactive compound that has insecticidal effects: not only does nicotine protect a tobacco plant, but humans have even used nicotine as an insecticide. Plants could of course also develop toxins to protect them from other mammals, and those would be even more likely to have effects in humans.

There is even homology across kingdoms, such that plants could make compounds to prevent growth of competing plants, act as antibiotics/antifungals, etc, and all have a possibility to act on some homologous proteins that humans have.

Artificial selection

Once humans are aware of a plant's psychoactive or other medicinal properties, that plant can be cultivated and selected for desirable properties. In the case of a compound like THC, there is good evidence that this has occurred recently. In the case of plants that produce opiate compounds, many have been cultivated by humans for thousands of years, so they are a lot more prevalent than they would be if humans had not chosen to do so.

Selection bias

Maybe I should have opened with this one, because I think it's very very important to be aware of. I'm not talking about selection in evolutionary terms here, but in terms of cognitive biases. Selection bias happens when you focus on certain outcomes and not others. There are innumerable compounds produced by plants that can potentially have some biological activity in humans: thousands and thousands. Some do have psychoactive effects, others have effects on other body systems, and many have little effect at all besides dietary contributions. You notice all of the plants that do produce something "interesting" but ignore those that are benign or simply toxic.


How did parasitoid wasps evolve their life cycle? I know there are a variety of wasps with various strategies for acquiring and controlling hosts. Do these form a rough picture of how these life cycles could have developed in the first place? What is the most recent speculation?

This is similar to the seahorse problem, in that it requires a distinctly non-mammalian perspective. Parasitoid Wasps, Natural Enemies of Insects provides a more in-depth explanation.

Existing wasp strategies may illustrate the possible transitional forms. It is not a linear transition: all of these have branched off and there are multiple parasitic strategies.

Solitary wasp, captures prey to feed to its larvae
Ectoparasitoid wasp, which lays its egg directly on prey that is paralyzed or otherwise unable to resist as the larvae eats it alive
Endoparasitoid wasp, which has formed a symbiotic relationship with a virus that disables the prey's immune system thus allowing eggs to be laid inside the prey
Hyperparasitoid wasp, which preys on other parasitoid wasps


How to operate a microtome? In the picture above (Source: Amazon.com, United Scientific MCT001 Hand Microtome) we can see a microtome. How is it operated?

The imnstrument is shown here upside down. If it is turned around, it looks like this:

The glass disc are placed around the middle tube. The operation principle can be seen in this image:

The specimen is placed in the tube in the middle and pushed out by turning the knob at the bottom. The minimal increment for this kind of microtome is 10 micrometers. The razor knife is used to cut the slices of the specimen.
An operation manual can be found here.


Collecting virgin fruit flies Suppose that you place P generation wild type males and mutant virgin females in a vial and allow them to mate. You leave this vial undisturbed in the incubator for 12 days. Could you collect F1 flies for your inter se cross out of this vial? Why or why not?

The answer depends which species (melanogaster, simulans, yakuba etc.), strain/population (e.g. Canton S, DGRP), mutant line (e.g. eb, CiD), food substance, larval density, and incubator settings (temperature, humidity etc.).

The rough answer is no, but if you clear the already hatched flies from the vial in the morning (~1 hour before lights on) and collect flies within a few of hours they should be virgin. Day 12 will likely be too late to collect many as most will have hatched at 25 degrees, at 18 degrees this may slow development but you should be certain that it will not affect your experiment, and report it properly in the methods. You could also collect and store them for a few days in single sex vials (all males or all females), then check the food that you store them in for larvae before using them, this helps to ensure virgins are actually virgins. If you find lots of eggs or even a single little larvae then throw the vial away. This also allows the females to mature properly, allowing them to eat some yeast and they will be more willing to mate when needed.

An experienced fly handler should be able to sort consistently enough to have just a few back up vials. If it is a beginner then make many vials with few flies in, this reduces the damage if a male slips through, it's much nicer to throw away a vial of 10 females than a vial of 100!

(Answer based on >7 years practical experience with D. simulans and D. melanogaster, collecting tens to hundreds of thousands of virgin flies in that time).


Lateral, axional and temporal resolutions for imaging in vivo What are the spatial (lateral and axional), and temporal resolutions that one is expected to get with the following optical imaging techniques?

Optical Bioluminiscence Imaging (BLI)
Optical Fluorescence Imaging (FLI)
Multiphoton Microscopy (e.g. 2-photon microscopy)

Are they any better than the  others in providing higher resolutions?

The lateral and axial resolution depends on the numerical aperture of your objective (lateral = lambda/2NA; axial = 2lambda/NA^2). You can improvee the axial resolution with FLI by using a confocal approach or with 2-photon microscopy (2PM). In 2PM you need absorption of two infrared photons to get emission. The probability of 2 infrared absorption depends quadratically on the excitation intensity. Therefore, fluorescence is restricted where the illumination beam is focused which give a better sectioning. An advantage of 2PM is the higher penetration depth and reduce phototoxicity. Indeed you can use 2 infrared photons to excite fluorophore which required visible excitation.

Temporal resolution depends on the area you want to measure and the integration time.

Resolution is limited by the diffraction. In the best case with the 3 imaging techniques you mentioned you can get ~200-300 nm in lateral resolution and 500 - 800 nm in axial resolution
Higher resolution can be achieved by using super resolution techniques. They are separated in two groups. The first one exploid the photo-physical properties of the fluorophore to excite and de-excite it. This allows to resolve sub-diffraction areas. This is the case STED (Stimulated emission depletion) microscopy or SSIM (saturated structured illimination microscopy). The second group use the fluctuation of the fluorophore emission to localize it better. It includes techniques such as STORM (STochastic Optical Reconstruction Microscopy, PALM (Photo-Activated Localization Microscopy) and SOFI (super-resolution optical ﬂuctuation imaging).


How long human can survive with just drinking water everyday Can humans live without eating food, just by drinking water?  How long can we survive just by drinking water everyday?

About 52 to 74 days according to hunger strike wiki page.

This wiki page bases its data on 8 persons who died due to hunger strike:
Days survived by each person: 66, 59, 61, 61, 61, 46, 71, 73, 62, 60.


Translate DNA to Protein Assuming the sequence shown is read left to right, what is the sequence of the protein produced?

sequence: 5’-ATGTACTTCCATCTGGAATAG-3’

MY ATTEMPT: I know RNA is synthesized 5 to 3.  This is throwing me off because if we read the above sequence from left to right then we are going to synthesize 3 to 5.  If I ignore this for now, I get an mRNA of 3'-UACAUGAAGGUAGACCUUAUC-5'  from this i could easily get the protein looking at a mRNA to protein chart.  Is this correct?

Since the sequence starts with an initiation codon and ends with a stop codon I think it's safe to conclude that this is the coding strand.  The coding strand has the same sequence as the transcribed RNA (except T>U). This is because it is the other strand of the DNA that is the template for the synthesis of an RNA. The RNA is indeed made 5'>3', but the template it uses has to run in the opposite direction.

5’-ATGTACTTCCATCTGGAATAG-3’
3'-TACATGAAGGTAGACCTTATC-5' template strand

5'-AUGUACUUCCAUCUGGAAUAG-3’ mRNA transcript
3'-TACATGAAGGTAGACCTTATC-5' template strand (read from left to right by the polymerase)

and the sequence of the protein is MetTyr...etc


Antibody production in secondary immune response Can IgG antibodies be produced in the secondary immune response without the help of T cells?

Is the affinity of antibody for antigens higher during secondary immune response?

1)  The secondary response requires CD4+ T cells to activate memory B cells.  That first paper actually gives some evidence that some of the rapidity could arise because T cells and memory B cells are in very close proximity to each other in germinal centers.

2) Yes.  The affinity of antibodies increases during the initial infection, both through isotype switching and affinity maturation, producing far superior antibodies.  Upon reactivation, memory B cells can undergo further somatic hupermutation.


What exothermic reaction distinguishes warm blooded animals? I would appreciate an answer specifically in the form of an exothermic chemical reaction. Namely, the one primarily responsible for generating heat in warm blooded animals that does not take place in cold blooded animals.

Brown adipose tissue or brown fat is one of the primary ways of generating body heat, and it is only found in warm-blooded animals. It is brown due to the high numbers of mitochondria, and heat is generated by uncoupling the electron transport chain from ATP synthesis by oxidative phosphorylation.

In the typical (ATP-producing) mitochondria, an energy gradient is formed by storing protons within the inter-membrane space, and these then flow through the ATP synthase to power the generation of ATP from ADP and phosphate. In brown fat mitochondria, Uncoupling Protein 1 (UCP1 or thermogenin) forms a pore in the inner membrane, allowing the proton/electron ratio to reach equilibrium and robbing ATP synthase of its motive power. This is what generates the heat.

From Wikipedia


In a skeletal muscle contraction, what happens after ACh binds to the nicotinic iontropic receptors on sarcolemma? Does the bound ACh becomes unbound and then gets hydrolysed by acetylcholinerase?

Acetyl choline, which is released at the neuromuscular junction is continuously broken down by the enzyme acetylcholineesterase into acetate and choline. Choline is once again taken up by the neuron through choline carriers to regenerate acetylcholine. This process continues as long as an the neuron is stimulated.
Source:
Wikepedia


Can a lizard shed a regrown tail again? Some lizards are famous for their ability to voluntarily shed their tail to elude predators (Autotomy). After a while, the tail will be regenerated, though with slightly different qualities, as visible in this photograph:

(source)

My question: Can this regrown tail be discarded again voluntarily, or is it a one-time feat?

Short answer: many species can drop a regrown tail again and again again, however a few can only drop it once, while some lizards cannot drop their tails at all. It all depends on the species.

Background information:

According to this site the tail will only be able to be shed above the site it originally broke off. Although according to UCSB there are a few species of lizard that only have their tail grow back once.

Every site I've visited has said that the tail is nearly a completely different structure than the one it originally had. The original tail has "score marks" (fracture planes) which were studied by Sanggaard et al. (there are a few figures that you can see in their paper).

However, according to W. N. F. Woodland, D.Sc. (Lond.), there is no apparent limit to the amount of times a Gecko can drop its tail, "save the longevity of the animal". His paper goes into great detail, and has a lot of information about autotomy (limb dropping) of the gecko. I highly recommend going through it if you're interested.

So tail re-dropping looks like it primarily depends on the lizard that you're studying.


Why do yeast ferment Equal sweetener I had my students conduct a fermentation experiment manipulating sugar amounts (number of sugar packets in solution) and measuring CO₂ production via capture in a balloon and measuring circumference (very common HS lab experiment). I also had them conduct a trial with two packets of Equal sweetener. To everyone's surprise two packets of the "zero calorie" sweetener produced as much CO₂ as four packets of sugar. Can anyone shed light on why this would have occurred? Equal contains maltodextrin and dextrose in addition to the aspartame. I'm assuming that yeast are able to metabolize one or more of these substances, but I haven't been able to find a more detailed explanation.

Your sugar substrate was sucrose. Yeast cells metabolise this by secreting an enzyme, invertase, which splits the disaccharide into glucose and fructose both of which can be fermented by yeast to produce CO2.
According to this site

Equal Original (blue packaging)  is a zero calorie sweetener that contains aspartame and acesulfame potassium as its sweetening ingredients along with a bulking agent.
Equal Original PACKETS:
dextrose with maltodextrin, aspartame, acesulfame potassium

This agrees with what you say - that the sweetener that you used contained dextrose - and leaves me very confused. Dextrose is another name for glucose so how can this contain zero calories?
The answer lies in the legal definition of zero calories  = less than 5 calories per serving (presumably per package in this case.) So let's assume that by adding two packs you were adding 8 calories equivalent of glucose.
Calorie content of carbohydrate = 4 calories per gram
Two packs could contain 8 calories = 2 g glucose.
The molecular weight of glucose = 180
therefore 2 g = 2/180 moles
if completely fermented to CO2 each mole -> 6 moles CO2
12/180 moles CO2 = 0.75 litres of CO2.
I conclude that there is enough glucose in two packets of Equal to generate a reasonable amount of CO2.
Yeast cannot ferment maltodextrins. It is possible that aspartame (aspartyl-phenylalanine-methyl ester) could be metabolised, but I think the dextrose/glucose solution is the best explanation.
EDIT:
I meant to say, just to illustrate that this is a significant amount of glucose, standard rich yeast medium is 2 g glucose /100 ml (2 % w/v).
EDIT #2 My back-of-an-envelope calculation has a fundamental error in it, but luckily I am the first to spot it. If glucose is being used fermentatively, then only one third of the carbon will end up in CO2, with the remainder going to ethanol. This means 0.25 litres instead of 0.75 litres. Yeast is so oriented towards fermentation that even in the presence of oxygen the fermentative pathway will dominate.


Can children restore brain cells? By "children" I mean young people at the age of 10 or lower.

I know that the adult brain cannot restore brain cells, but what about children? I mean, the brain must develop from a few cells to a 90 billion cells somehow, when do we lose this ability?

I'm also interested in cases when a child gets hit into the head (concussion). Can the damage  be fixed over time?

I am not an expert in neurobiology, but this is what I have been able to find:

In general, the PNS (peripheral nervous system) does have remarkable neuroregeneration capabilities. However, the CNS (central nervous system), which includes the brain, has extremely limited neuroregeneration abilities. However, there are some interesting examples of CNS recovery:

  Children under six who undergo, unfortunately, a hemiectomy, whereby one half of their brain is taken out, are able to regain almost normal function because of the brain’s ability to rewire and literally take over the functions of the missing other half of the brain.

I am guessing one thing that can explain this is that in children, the CNS is still developing, and so if there is damage, the CNS can just entirely replace damaged parts (this might be different than "fixing" which is required in adults).

Again, I am not an expert on this and would be glad to hear a neurobiologist's opinion.


Why do we breath oxygen? I like this contradiction. But seems like my Biology teacher doesn't.

If oxygen oxidates us, why do we breath it? Why can't we evolve into a new kind of human being that breaths other component of air? Following the need of all species to survive longer.

When life evolved, first came heterotrophs that obtained their organic molecules from their environment. Then came autrotrophs who made their own organic lecyles. The most important autotrophs are photosynthetic organisms. These photosynthetic organisms lived in the water and made glucose from CO2 and H2O. A byproduct of this reaction was O2.

Now, O2 killed off many of the species since it is very reactive. But the remaining species used the O2 for cellular respiration. Before, the cellular respiration was done anaerobically, without oxygen. The way this wroked was that the glucose was oxidated and the electrons from the glucose was used to make ATP, the main source of cellular energy. Once those electrons were used, they were deposited in a highly electronegative element compound, such as Nitrogen containing compounds. When plants produced O2, instead organisms doing anaerobic respiration, since oxygen is an extremely electronegative element, organisms deposited the electrons in the oxygen molecule. This is aerobic respiration. This from of respiration was more efficient and advantageous for land organisms. That is why we use oxygen.

Lungs and breathing is one of the many ways organisms obtain oxygen for delivering to cells to do cellular respiration. Fishes use gills. Most mammals use lungs. Many single celled organisms just obtain their oxygen through diffusion.


What is "non-immune immunoglobulin"? From a short introduction to immunohistochemistry controls:

Isotype Control
This control can be utilized when working with monoclonal primary antibodies. The sample is incubated with antibody diluent, supplemented with a non-immune immunoglobulin of the same isotype (for example, IgG1, IgG2A, IgG2B, IgM) and concentration as the primary monoclonal antibody. The sample is then incubated with the secondary antibody and detection reagents. These steps will help ensure that what appears to be specific staining was not caused by non-specific interactions of immunoglobulin molecules with the sample. Background staining should be negligible and not resemble specific staining.

I googled and found out that some pathological agents can bind immunoglobulins in a non-immune fashion, i.e. by binding to their Fc regions. But that still leaves me in the dark on "non-immune IGs".
Maybe it is an IG with which the secondary antibody will not bind?
Or maybe it's an IG that has no activity against the target antigen?

The term "non-immune immunoglobulin" is both confusing and non-standard in the immunology field - "pre-immune" is sometimes used, but not always accurate. A negative control is as they describe - the same diluents and components of the sample incubated with the antibody of interest, only they use a non-specific antibody of the same isotype that is not expected to bind to any targets in an "immune-dependent" manner - the "usual" way you think of an antibody binding to a target antigen. However, antibodies can bind samples in an immune-independent manner, via protein-protein interactions (the sample was insufficiently blocked) or to Fc receptors, for example.

The non-specific antibody can be from several sources - a pre-immunization bleed from the animal that generated a polyclonal primary antibody, an antibody to a target not expected to be present in the sample, such as KLH or GFP, or a monoclonal antibody engineered or screened to not bind to anything.


What's the simplest set-up to demonstrate soiless plant growth to middle school students? I'm looking for a simple, inexpensive way to demonstrate that soil is not needed for plant growth to middle school students.  I plan to germinate bean seeds in cotton, but where do I take it from there?

You can take a glass mason jar, a bean seed, and a moist paper towel. Place the seed between the paper towel and the glass. If you press the paper towel so that it lines the inside of the glass jar, the seed with grow and the students can see this process through the glass.


How big is the change in proteins due to alternative splicing? How different can the proteins be that are coded from the same DNA-sequence but undergoe alternative splicing?

What I am trying to wrap my head around is why we are so fixated with the DNA-sequences and what they are coding for, if the outcome can differ a lot due to alternative splicing.

For your first question, They can vary dramatically.

I did not originally post as a formal answer because my statement below is hard to cite a source and would therefore be somewhat subjective, although I am pretty confident in the assertion. It is based on my own experience in both GWAS and EWAS literature reading. My research concerns methods for analysis of such data.

To answer your second question, the main focus has shifted from genetic variation (still done though) to expression variation and epigenetic variation. The expression research focuses exactly on the type of issue you are discussing with alternative splicing, and this is largely possible because of the decrease of the cost of RNAseq. We aren't as fixated on sequence anymore; the advent of GWAS, once thought to be a panacea for the explanation of disease susceptibility has only ended up explaining a fraction of genetic heritability estimates. Not to say it isn't focused on, just in the context of other types of variation and environmental exposures.


Confusion about read counts distribution in RNA-seq While reading old DESeq paper (Anders and Huber 2010) I came across following line.

  If reads were independently sampled from a population with given,
  fixed fractions of genes, the read counts would follow a multinomial
  distribution, which can be approximated by the Poisson distribution.

I am unable to grasp this line. Why would read counts follow multinomial distribution? My guess would have been Gaussian distribution. Can anyone explain this?

Textbook example of multinomial distribution is multiple dice toss. The fair dice has following probabilities:

side 1: 16,66666666%
side 2: 16,66666666%
side 3: 16,66666666%
side 4: 16,66666666%
side 5: 16,66666666%
side 6: 16,66666666%

Lets roll a typical fair dice n = 20 times:

6 5 1 1 3 5 4 3 1 2 4 4 6 6 2 2 5 6 5 2

So this particular outcome of above multinomial variable is:

side 1: 3 rolls
side 2: 4 rolls
side 3: 2 rolls
side 4: 3 rolls
side 5: 4 rolls
side 6: 4 rolls

Multinomial distribution is not restricted to fair dice - the probabilities can be rigged. It also is not restricted to 6 sides - there can be any number of categories. Another textbook example of multinomial distribution is puling colored balls from wery (infinitely) large bag. Probabilities correspond to proportions of colored balls in the bag:

Blue: 53.283%
Green: 19.956%
Orange: 8.336%
Purple: 5.213%
Red: 4.374%
Silver: 3.920%
White: 2.751%
Yellow: 2.167%

Lets simulate n = 200 balls pulled from such a bag in R:

sample(c("B","G","O","P","R","S","W","Y"), replace = T, size = 200, prob = c(0.53283,0.19956,0.08336,0.05213,0.04374,0.03920,0.02751,0.02167))
B S O B B G G P B O B B P G B B G G G G B P G B B P B G B G B S W B B O O G B B O G G B S B O G B B B B B O O O B O B B B B B B O O G B B Y B R G B B B G P W Y G B P W B S R B W G Y B W B G O G B R B B G B B B B B B P R G P B B B G Y G S B B B G P B B B B B G B O G P B G B G P B B G B R B P R B G W B B B B O P G B B B B B B B B G B G G R W B B G G B G O B B B B B G B B B P B B B O R G B B B O B G

So this particular outcome multinomial variable is:

Blue: 102 balls
Green: 42 balls
Orange: 18 balls
Purple: 14 balls
Red: 8 balls
Silver: 5 balls
White: 7 balls
Yellow: 4 balls

In RNA-seq we are "pulling" reads (balls) out of a large set of suitable cDNA molecules fragments in a sample (bag). Each read belongs to a gene (color). We assume fixed fractions of genes in a sample:

gene 1: 0.05217%
gene 2: 0.00319%
gene 3: 0.00073%
...

But what we get from RNA-seq (n = milions of reads) are integer counts of reads:

gene 1: 492 reads
gene 2: 44 reads
gene 3: 5 reads
...

To comment on your idea of using Gausian distribution: Gausian distribution is continuous so using it we would assume we can get fractions of reads per gene which is not the case.


What is this giant mosquito-like insect? I found this bug in my kitchen in this morning, in a suburb of Houston Texas, about 30 miles Northwest of downtown. It was on the wall, and when I went in for a closer look, it quickly flew away - up towards the light, then crash landed behind the refrigerator where I hit it with bug spray.
It looks sort of like a mosquito, but much much larger.
Everything I find online about "giant mosquitoes" points to the Crane fly or "mosquito hawk" - which I've seen plenty of (very common here). I'm no expert, but this doesn't look like a cranefly.
I also read that giant mosquitoes are known to hatch after hurricanes, and there was just a huge one <200 miles from me. But those accounts speak of smaller insects (albeit, still very large for a mosquito).
For example, this article about "gallinippers" in North Carolina, speaks of mosquitoes only the size of a penny.
I did not think to put a coin in the shot for reference, but based on the size of the paper towel underneath it, it must be at least the size of a quarter.
Is this even related to a mosquito? What could it be?

The better entymologists among us may need to correct me, but I believe you are looking at a robber fly, especially based on the characteristic long, tapering abdomen, as well as the proboscis that reminded you of a mosquito and the large size.
I see a couple people posting images from Texas that look a bit like yours (especially the all-black body) on Google images but none of these mention a genus/species for me to dig further on. Bromley, S. W. (1934). The robber flies of Texas (Diptera, Asilidae). Annals of the Entomological Society of America, 27(1), 74-113. may be useful but is a bit too deep for me to dig into for you.


Does the 1:1 sex ratio at birth apply to every human pregnancy or is it a statistical average? Are there genetic factors that biase the sex ratio of offsprings for each person but average to 1:1 for the entire human population, or does the 1:1 ratio apply to every single fertile person?

The ratio you are referring to is indeed computed aggregating multiple observations and thus it is a "statistical average".

Any individual (or couple, in this case) can have a specific ratio that differs from the average one. Many factors may affect sex ratio, among which sperm/egg viability, chromosomal aberrations, and hormones misbalance are the ones usually affecting the fertility of a couple and they can also bias the sex ratio.

Many other factors can play a role.
Different populations have slightly different sex-ratio and even smoking can skew the sex ratio!


What are these stars in my microscopic image? I see this very curious patterns on the sun-facing side of a jasmine (probably) leaf - visible with a makeshift microscope (about 50x)

What are them? Pores? Are there other plants with similar textures?

The microscope is made out of a webcam, as described here

Despite low resolution, I'd say those are trichomes. Jasminum is genera that produce essential oils, so it have glandular hairs and other trichomes wich help to rettain the oil layer.

Source: http://cms.herbalgram.org/herbalgram/issue53/article2207.html?ts=1376643526&signature=b4349f7f3ca6f6a47823f4754237eaac

The image displayed above shows glandular and non-glandular trichomes in lavander shown by scanning electron microscopy. I'm afraid I couldn't find anything about Jasminum in particular, but I think it must be the same kind of structure.


Do cats produce DMT? Edit: If somebody (anybody) wants to add an answer so the bounty won't go to waste, please do so! The comments have already introduced me to the Kegg metabolism database, some interesting papers, and an amazing chapter on the biochemistry of cats. Thus, this question has been useful to me (and hopefully, to the community as well).

  There is a question on Skeptics.SE that asks if "cats have a chemical in their brains that resembles LSD." I haven't found any similar claim online, but started wondering:

 1. Do cats produce (natural) compounds that structurally resemble LSD?
 2. Do cats produce (natural) compounds that functionally resemble LSD?

Quickly glancing at the structure of LSD, it contains an indole ring. Hovering over the various indoles here found one substance that occurred in animals and was consumed as a psychedelic drug.

There is a paper that writes:

  N,N-Dimethyltryptamine (DMT) is an indole alkaloid widely found in plants and animals. It is best known for producing brief and intense psychedelic effects when ingested. Increasing evidence suggests that endogenous DMT plays important roles for a number of processes in the periphery and central nervous system, and may act as a neurotransmitter.

The paper also proposed the role of DMT as a neurotransmitter. However, I haven't been able to confirm DMT is naturally produced by cats.

Do cats produce DMT? If so, what is the purpose of DMT in the cat?

Yes! Many mammals, including cats and humans, produce DMT in small amounts.
DMT has been detected in blood and urine and is produced by the enzyme indolethylamine N‐methyltransferase (INMT). These do bind to serotonin receptors. Serotonin receptors are actually expressed in multiple tissues outside of the brain. However, DMT does cross the blood-brain barrier (ref), so it's possible that endogenous DMT has some neuroactive effect (I really don't know). Good question.
This 2016 paper states (referring to a 2012 review) that it was identified in urine, blood, and CSF:

A review by Barker in 2012 assessed 69 studies that reported endogenous DMT detection and quantities reported in urine (29 studies), blood (11 studies), and cerebrospinal fluid (4 studies) from 1955 – 2010 primarily comparing detection levels within healthy controls and schizophrenic patients. DMT in urine was examined in 861 individuals (635 patients), 276 patients and 145 controls were positive for DMT.

I think that's the most direct answer to you question I could find.
I didn't find anything on cats specifically, but that's likely to be similar.
This earlier 2004 paper states that it was only found in urine, but the previous study refers to studies before 2004, so I don't know why these two seem to contradict:

In mammals, endogenous bufotenine and DMT have been identified only in human urine. The DMIAs bind effectively to 5HT receptors and their administration causes a variety of autonomic effects, which may reflect their actual physiological function. Endogenous levels of bufotenine and DMT in blood and a number of animal and human tissues were determined using highly sensitive and specific quantitative mass spectrometric techniques.

Here's the entry for INMT on Kegg, and the Human Protein Atlas lists where INMT is expressed. Weirdly, that enzyme is highly expressed in the human lung.


Hypothalamic breakdown and effect of temperature on membrane lipids I'm in my last year of high school and doing a research assignment on thermoregulation. In the excellence level exemplar for the standard, a student made the statement:

  Once the body's internal temperature is well above the optimum range, important enzymes start to denature, phospholipids start to destabilise, and cell membrane lipids begin to dissolve. As a result of this, important organs in the trunk of the body are unable to carry out important metabolic processes. If the temperature continues to rise it causes tissue damage which could cause disability depending on its severity. It also causes the hypothalamic thermostat to break down, meaning the body can no longer have control of the core temperature.

However, I have been unable to find any sources which mention destabilisation of phospholipids or the dissolving of membrane lipids. I have also not found anything on tissue damage or the cessation of the hypothalamic thermostat.

Are these things true? And if so, could someone please direct me to a reliable source which states this?

If you supply heat to a system, the entropy increases which results in destabilization of order. This is a general thermodynamic principle and you can refer any basic book on that topic. However, it is not essential that all molecules would be affected equally. There are heat-stable enzymes in thermophiles such as Thermus aquaticus which are resistant to heat. Also the membranes in these organisms are made up of stronger and more rigid isoprenoid lipids.

Even in mesophiles, lipid membranes with higher content of cholesterol are rigid and more resistant to thermal movements.

On Breakdown of thermostat:
The body can regulate the temperature only in a certain range; at higher temperatures these mechanisms will fail as well.


Can't identify this fish caught off NC coast It was caught approximately 35 miles off the coast of North Carolina. I've been a charter fisherman for more than 25 years and never seen anything like it. Thanks for your help!

i think this is a frogfish. there is multiple types of this fish. i think this is an Ocellated frogfish. frogfishes related to anglerfishes. memorizing animals by classification eventually helps with identification. little google search and using fishbase site about information helps. this sites very helpful about finding fishes.

fisbase frogfishes

frogfish site

this link says it can be found on North Carolina


Why is the body cooled during cardiac surgery? When undergoing cardiac surgery, the heart is disconnected from the blood circulation and blood is passed through a heart-lung machine and cooled so that the body temperature of the patient is reduced.

I understand that this would slow down metabolic processes but how exactly does slowing down these processes benefit the patient?

Thanks for answering!

As you mention, hypothermia is routinely induced during cardiac surgery. There is a blog post including a photo of a heart being cooled with ice chips here: https://www.heart-valve-surgery.com/heart-surgery-blog/2010/10/17/ice-cardioplegia-open-heart-surgery/

The primary therapeutic benefit of deliberate hypothermia was long thought to be, as you say, the slowing-down metabolic processes, which reduces the amount of oxygen needed by the brain and other vital organs (source). Cooling the blood during open heart surgery therefore allows the operation to be performed more slowly (2-4 hours).

However, according to this open-access article on the benefits of therapeutic hypothermia for cardiac surgery:

  the widely held notion that hypothermia protects because lower
  temperatures slow metabolism is not completely accurate. Recent
  research has shown that hypothermia can alter a plethora of cell death
  and cell survival pathways including gene regulation resulting in the
  inhibition of apoptosis and inflammation and the up-regulation of
  anti-apoptotic or trophic factors.

So basically it does slow down the metabolic processes but it also reduces inflammation and cell death.

After surgery, rewarming needs to be done slowly to maximise the chances of recovery (source).


Bacterial division and mutation rate When a bacteria A divides it produces two cells A', A''. Each of them receives a copy of the chromosome/plasmids. Now, DNA replication occurs way before division in a semiconservative manner. That is, each new chromosome has an 'old' strand and a 'new' strand. Since the polymerase is error prone, my belief is that both genomes can potentially have mutations. Now when people refer to the mutation rate/genome/replication, e.g. 3x10-4 , Does this mean that:

Only one of the resulting genomes have this mutation rate? (according to me not likely).
The mutation rate takes into account the total number of mutations in both new genomes.
Each of the genomes can potentially have independently as many mutations as the mutation rate specifies.

Your question comes down to the definition of the units you state in your question - mutations genome-1 generation-1. In my opinion the answer is your choice (2).

How are mutation frequencies measured? Usually it is a case of scoring the appearance of a mutant phenotype as an indicator of underlying mutational events (see Drake,JW (1991)A constant rate of spontaneous mutation in DNA-based microbes. Proc. Natl. Acad. Sci. USA 88:7160-7164 for a detailed explanation.) Since, as you say, DNA replication is semi-conservative, the two daughter cells of a bacterial cell division each inherit one old DNA strand and one new DNA strand and so have the same probability of sustaining a given mutation. The overall mutational frequency has to be an aggregate of what has happened in both of them (and in all other cells in the population) since there is no way of distinguishing between them. In terms of your question the answer is (2) and this is why the mutation rate is normalised per genome.

In practice this figure is arrived at as follows. Suppose that you study a 1 kb gene, gene X, and measure the rate of spontaneous mutation in that gene (by some convenient assay) as 1 mutation per 107 cell divisions (again see the Drake reference for details). Assume also that the bacteria have a genome size of 2 x 106 bp.  Since each cell division equates to the creation of one new genome we get:

mutations per gene X per generation = 1 x 10-7

mutations per bp per generation  = 1 x 10-7/1000 (because it is a 1000 bp gene)

mutations per genome per generation = 1 x 10-7 * 2 x 106/1000

mutations per genome per generation = 0.0002

Now this is an underestimate because not all mutations will create a detectable change in phenotype. Drake uses a correction factor of 3.12 for this.

true mutations per genome per generation = 0.0002 * 3.12 = 0.0006 or 6 x 10-4

These were made-up numbers. See review in Drake JW et al.(1998) Rates of spontaneous mutation. Genetics 148: 1667-1686 for real examples.


Properties of berries that are not shared by strawberries What are examples of properties that (all) berries (from a botanical point of view) have and that strawberries do not have? This does not need to be the exact reason, why strawberries are not counted as berries. I'm more looking for properties that emphasize the difference.

Since I'm not a biologist, I'd be happy about simple examples. Thanks a lot!

Botanically a berry is something quite different from what is commonly termed a berry in English.

From that Wikipedia page:

  a berry is a fleshy fruit without a stone produced from a single flower containing one ovary

...

  Berries so defined include grapes, currants, and tomatoes, as well as cucumbers, eggplants (aubergines) and bananas

On the other hand, many things called "berries" (including strawberries) are actually aggregate fruits, which are

  a fruit that develops from the merger of several ovaries that were separate in a single flower

Therefore, the botanical difference is the originating tissue of the fruit: a single flower/one ovary, versus a collection of ovaries grouped together.

These botanical groupings don't have much relevance to practical use (i.e., cooking/nutrition) and there aren't other properties that are definitive for what a berry is and is not. For that reason, there is nothing wrong with referring to strawberries, raspberries, etc, as "berries" in cooking: berry simply has different meaning in botany and culinary fields, just like the many culinary "vegetables" that are botanically "fruits."


Activity driven model threshold So I am trying to figure out a threshold for an activity driven model. That is described in this paper: https://www.nature.com/articles/srep00469

That is I don't see how the researchers got R0 to be between 0.2 and 0.5 (page 6). If they are using gamma=-2.1 and epsilon=10^-3 and threshold is defined in equation 4, my calculations give me threshold of 2.020396043515874.

Now if the power law distribution (activity) is a random number i.e. this:
http://mathworld.wolfram.com/RandomNumber.html

this yields average activity of 0.005489691793543477 using this equation:

((1-gamma)/(2-gamma))*((1-(epsilon**(2-gamma)))/(1-(epsilon**(1-gamma))))

so then following equation 4, the threshold is 2.020396043515874, but that's not what Figure 4 (B) is showing so I'm very confused.

I would really appreciate if someone could clear this out for me.

(A little too long for a comment, and maybe useful)

Assuming that a is supposed to represent the degree of a node, and
using the formulas from Wikipedia for the Pareto distribution, I have

mean (which I'm assuming is <a>)  =  gamma*epsilon/(gamma-1)

and
variance (equal to <a^2>-<a>^2, or <a^2>= mean^2  + var) = epsilon^2*gamma/((gamma-1)^2*(gamma-2))

Translating into R code (rather than doing the algebra):

pmean <- function(gamma=2.8,epsilon=0.001) {
    gamma*epsilon/(gamma-1)
}
pvar <- function(gamma=2.8,epsilon=0.001) {
    epsilon^2*gamma/((gamma-1)^2*(gamma-2))
}
prms <- function(gamma=2.8,epsilon=0.001) {
    sqrt(pvar(gamma=gamma,epsilon=epsilon)+ pmean(gamma=gamma,epsilon=epsilon)^2)
}

When I use the value of gamma=2.1 in the figure caption and feed it into equation (4):

2*pmean(gamma=2.1)/(pmean(gamma=2.1)+prms(gamma=2.1))

I get 0.588 (still not right, but closer ... ??)


Enzyme inhibitors, reversible or irreversible? So far, I know about competitive, non-competitive inhibitors and allosteric inhibitor. Which ones are reversible and which ones are irreversible?

These modes of inhibition are reversible. They describe a particular modification of the working of the enzyme (change of affinity, of maximum velocity, of both) due to the reversible binding of an inhibitor to a particular site.

On the other hand irreversible inhibition stops the enzyme from working through an inhibitor that binds irreversibly : no more transformation of substrate occurs after that. One cannot define a velocity, affinity, or IC50, for a non-working enzyme, thus "competitive", "non-competitive", "uncompetitive" are not useful concepts in that case.


Why we need an egg cell donor and a surrogate mother in an organism cloning process? Could a whole set of artificial organism-cloning process only be operated on the  somatic nuclear donor ,which means for example ,can we extract the somatic nuclear from animal "A" and put it into the egg cell plasma also from animal "A"  then implant it into the animal"A"'s uterus to clone "A" ?

Could a whole set of artificial organism-cloning process only be
  operated on a somatic nuclear donor?

No, this would not be possible. Single-cell reprogramming would enable you to reset the potency status of that cell up, yielding an embryonic stem cell (ESC). However, ESC do not have the ability to generate extra-embryonic structures (e.g. placenta), which are known to be required for providing oxygen and nutrients to the embryo, amongst other relevant functions.

Theoretically, it could be possible to replicate the embryological environment, and I think this is the second part of your statement. Nevertheless, in practice this is not possible... the amount of signals and parameters that one would need to control simultaneously is far too extensive.

I don't quite see the point of having an enucleated egg and performing somatic cell transfer, when you're not really interested in implantation in utero. Somatic cell reprogramming would be sufficient (see iPSC)


What defines a microbial species? I know that microbes are not capable of sexual reproduction, thus sorting them into species according to "groups that can interbreed and generate fertile offspring" should not apply.

Your question is relative to the species concept that you are using. Mayr's biological species concept (BSC) is based on the ability to interbreed; a process-based definition. Most biologists use it, but most taxonomists, who are the people who actually describe species, use some variation of the phylogenetic species concept. The phylogenetic species concept is not based on process, but on fixed differences. Fixed differences are evidence of a lack of interbreeding, but the concept is not explicitly based on reproduction. Fixed morphological differences have been used to classify microbes, most often in culture. But currently, microbes are most often classified with a combination of morphological and genetic characters. The small subunit rRNA is sequenced and put through an algorithm for estimating species based on genetic distances. In short, your question depends a lot on which species concept you are using, and whether you would accept a distance-based DNA definition. But species need not be defined reproductively.


Why do human eyes glow red on a photo and dog's eyes green? Previous Research

I know that cameras sometimes come with an anti "red eye" functionality that involves two flashes, presumably the second flash coincides with the shutter opening.

Question

Why do camera flashes sometimes lead to photos of humans with red eyes? And why do dog's eyes appear green?

Related

The reason for the green dog's eyes has been answered quite shortly under the question "why-do-dogs-eyes-glow-green-on-a-photo", but that question does not answer my specific question: Why do humans have red eyes on flashed photos and why are dog's eyes  green?

Short answer
In humans it is basically the red choroid plexus in the back of the eye you are seeing on a flashed photo, while it is the green-reflecting tapetum lucidum in dogs.

Background
The red-eye effect in humans was explained nicely by Yale Scientific Magazine, and I adapted the following text from that source:

The human eye can effectively adjust to different light conditions, but this adaptation is also what leads to the red-eye effect. The eye regulates the amount of entering light by contracting or expanding the pupil. At night, your pupils will accordingly enlarge to extract more light from their surroundings. However, this dilation also leaves your eyes unprepared for the sudden burst of light from a camera flash.

When light from the flash enters your eyes under these conditions, your pupils are unable to contract fast enough (full constriction takes a few seconds) to prevent the light from reflecting back, off of the red blood vessels of the choroid. The choroid plexus nourishes the retina, and therefore contains ample blood supply. As a result, the camera will pick up the red reflection, resulting in the red-eye effect. Interestingly, due to their increased “dark adaptation,” children more commonly have red eyes in photographs.

The amount of melanin, a light-absorbing pigment in the eye, also has a role in the red-eye effect. Individuals with lower levels of melanin will absorb less and thus reflect more light, explaining the high incidence of the red-eye effect in albinos.

Though the cause of this effect is wired in the biology of the eye, some cameras can reduce red-eye by sending a few preliminary flashes before the final flash to give the pupils enough time to contract and adapt to the increased-light conditions. Another way to reduce the effect is to avoid looking directly into the camera lens, which will reduce the reflection of light. Finally, if all else fails, modern image editing software, such as Photoshop, can remove the red discoloration.

With regard to why dogs and other animals may not have red-eyes but other colors, this was indeed answered in your linked question: some animal species have a tapetum lucidum, which is situated in front of the choroid and reflects light back onto the retina thereby increasing light sensitivity. In dogs it is green, as aptly shown in the linked question's answer. The following figure shows the anatomy and the position of the tapetum in front of the choroid. It was adapted from Pets.SE with the related question "Should I be concerned that my dog's right eye is reflecting green in the dark when his left eye doesn't?"

Hence, the reason why animals with a tapetum lucidum have another eye color is that light does not reach the choroid in these species, giving rise to green-eye effects in dogs and cats (picture taken from Ask Nature):


Does a theory exist for the formation of thylakoid structure? I'm interested in how the structure of the thylakoid forms into its characteristic highly rugose stacks of grana. What causes the thylakoid to invaginate and self-associate, albeit with what appear to be fairly large gaps in between folds?

I think I found a reference.  Most of these papers are behind paywalls - its a pretty obscure topic in biology, though not because it isn't interesting...

For those not familiar with the question, the thylakoid membranes are an organelle structure in the chloroplast, which contains all the photosynthetic machinery in the plant cell.  The chloroplast is though to be a symbiotic cyanobacterium captured to make eukaryotic plants.  Like mitochondria, the chloroplast maintains its own chromosome and some ribosomal machinery.

The stack (grana) and extended (stromal lamallae) structures of the thylakoid no doubt help optimize light/energy capture by distributing the light gathering proteins in an advantageous way.  It was previously believed that the electrostatic charge of the thylakoid membrane helped make the stacks, but this Trends in Plant Science review article (Allen and Forsberg, 2001) discusses how the distribution of photosystem (PS) I and II are more concentrated in the stroma and grana respectively.

They put forth that Light Harvesting complex II (LHC II), which gathers photons for PSII tends to cluster in a trans fashion - forming contacts with LHCII in membranes above it, specifically forming the grana stacks enriched in PSII.


What are the obstacles to "refitting" the human body's metabolism? As a layman, I understand the problem of rising obesity like this:

In the old times, humans could never get enough food, thus they would eat whatever they could get. This "program" is encoded in our genes.
At least in industrial countries, the ubiquity of energy-rich food makes some of us get obese, at least partial because we follow this old "program".

I hope I didn't get it too wrong. Now my question is this:

Would it be possible to somehow "rig" the human body to change the metabolism and make it fit to a rather sedentary lifestyle?

For example: Instead of storing surplus food / energy within the body, it could be excreted, thus keeping humans at their weight even when eating a lot more than they need.

Could this be possible? Which organs/hormones control the utilization of food within the human body and can they be influenced in such a way?

Yes, you got it right. The theory you're referring to is called the thrifty gene hypothesis. There have been several attempts at "rigging" metabolism to reduce the amount of surplus calories stored as fat, as you suggest, and some of them have gone all the way to approved drugs.

One strategy is to block intestinal absorption of nutrients, so that excess food is simply excreted. Perhaps the most well known example is Orlistat, a prescription drug that prevents fat absorption by inhibiting lipases secreted by the pancreas. This has been proven (somewhat) effective in clinical trials, but also causes gastrointestinal problems like oily stool. Most drugs of this type, preventing the gut from doing normal digestion, will probably have this limitation.

There are also ideas about increasing metabolism of absorbed nutrients to "burn" more calories. Generally, utilization of nutrients in the body does not happen on its own; it is a consequence of activating other energy-demanding processes, like muscle contraction, brain activity, immune system function, and so on. And any attempt to increase metabolism, regardless of mechanism, will end up generating more heat. So in order to increase metabolism, it is necessary to turn on some heat-generating function (other than exercise :) Some research groups are experimenting with increasing energy expenditure in brown fat (a type of fat that normally oxidized nutrients to generate heat) to burn off excess nutrients. This is still a long way from medical use though.


Why are centrioles aligned at 90 degree with each other? The centrioles are aligned at 90 degree with each other. What is the function of this?

As far as I know, the function is not truly known, although there are some seriously interesting guesses.  Part of the problem seems, from scanning the literature, to be that it's not easy or obvious to disrupt centriole orientation.  This paper in PLoS Biology presents some really interesting results, in particular two piece of evidence:

Centriole orientation, to some degree, is dictated by the "mother" centriole during centriole division and is thus passed on from cell to (daughter) cell.
Defects in centriole orientation can result in organelle localization defects in the cell (e.g. nuclear orientation), and at least some of these defects are genetic.

So it seems that orientation is, in some part, a product simply of centriole division, but that there are some gene products that do help determine orientation and localization.  This paper puts forth the hypothesis that centriole orientation determines the axis of cell division which can affect embryo orientation, whereas this suggests that external environmental factors could translate into altered centriole, and therefore cellular, orientation.


What biotechnology can be used to treat lazy eye, and possibly cure lazy eye? I tried very hard researching and finding the root cause of amblyopia. It is mainly because of imbalance in eye muscle. But, there are a lot more complicated causes of this disease. Thus, I need some help in finding a biotechnology for treating lazy eye.

In order to treat amblyopia you first have to treat the initial problem with the eyes that caused it, which is a medical issue and probably not what you are asking anyway. However, as wikipedia states, "after the underlying cause is fixed, vision is not restored right away, as the mechanism also involves the brain."

As a rule of thumb anything related to brain functions (in humans) is so complex that we don't really have the (bio)technology to just cure it. Sure, their are some advancements in a few areas, but especially if you want biotechnology to do this, you'll probably have to wait at least 10+ years for a medically save and readily usable method.


Why does an autoclave need to pressurize steam? I've looked this up on other sites and they say that an autoclave needs high pressure in order to raise the boiling point of water so that you can achieve steam of a higher temperature.

If you look at this diagram though, it seems to me as if it would be much simpler to further heat the steam at the ambient pressure of the autoclave room. Does the pressure of the chamber play some role that I am unaware of? Thanks in advance for clearing this up!

An autoclave can sterilize both solids and liquids, whereas an oven with no pressure control is typically not suitable to sterilize liquids.

Not only do you need to heat the chamber to 121°C, but you also need to make sure that the things you are trying to sterilize are not degraded by the treatment.

For dry objects (e.g. glassware) you could heat the chamber up to 121°C at ambient pressure. In that case, the instrument you're using is called a "dry heat sterilizer" rather than an "autoclave" (REF)

So why use an autoclave at all, and not just a dry heat sterilizer? Quite often the things you would put in an autoclave are water-based solutions (for example, LB broth or buffers).
If you do not increase the pressure and try to heat to 121°C, the liquid in your bottles will first boil around 100°C until all the aqueous solvent is in the gas state (i.e. your solutions are going to evaporate) and then the temperature will increase to 121°C. However if the pressure is raised to stay at the liquid-gas phase transition, then the gas and the liquid are in equilibrium, therefore you neither lose or gain any volume in your solution.

So in theory, if you autoclave 1L of medium, then you get 1L back at the end. Note that in real life, the temperature and pressure of the autoclave are set based on the diagram for water, but for concentrated solutions these settings may be slightly off, meaning that the volume in the bottle at the end of the cycle is sometimes a little different from what you put in there at the beginning. See this illustrative diagram of how a solution behaves differently from the pure solvent:

(Copyright: Lumen Learning)


How do T-cells determine which cells they've already inspected? From what I understand, T-cells are constantly traveling in the body, inspecting cells by looking for antigens. If they're self antigens, then the T-cell doesn't attack, whereas if they're non-self, they attack. My question is how does a T-cell know when it just inspected a cell? Does the T-cell leave something behind on the cell to mark it as checked or does the cell itself present something on its surface to indicate that it has just been checked? If there is no such system, then what prevents the T-cells from being stuck in a loop, and just inspecting the same cell over and over?

Your question spans two activities of T-cells that are related to each other: migration and activation. T-cells that usually stay in lymphoid organs migrate to non-lymphoid organs with different mechanisms for each T-cell subtype. When migrated to non-lymphoid organ, the T-cells move through the organ looking for infected cells.

Migration

As you can see in the image below, there are many mechanisms for moving T-cells across the endothelial layer.

The main idea for all three mechanisms is that the tethering of the T-cell to the endothelial layer is weak. Because of the weak interaction, the blood flow causes the T-cell to move across the endothelial layer while still being attached to the endothelial layer. This is known as rolling. Other stimuli (usually chemokines) such as CCL21, CCL25, or ICAM 1 are needed to induce T-cell to migrate across the endothelial layer. This is important because these chemokines are expressed where there is inflammation. For example, there is a correlation between CCL25 level in the gut and inflammation in the area.

T-cells express α4β7 integrin or CCR7 that bind T-cell to the endothelial layer. Central memory T-cells and naive T-cells express CCR7 and CD62L and thus reside preferentially within the secondary lymphoid organs. Effector memory T-cells bind to gut endothelium with α4β7 integrin, CCR9, and LFA-1.

CCL21 is expressed by both stromal cells of lymph node paracortex and endothelium of lymphatic vessels to assist migration of activated dendritic cells and naive and central memory T-cells to lymph node respectively. Dendritic cells are professional antigen-presenting cells (APCs) that migrate to lymph node where it can interact with T-cells more efficiently.

T-cell activation

One important concept to take away from T-cell activation is that there needs to be direct contact between MHC complex and T-cell receptor (TCR).

T-cells that have moved into the lymph node interact with dendritic cells, which have high MHC complex concentration on their cell surface. This leads to subsequent activation of the T-cell leading to release of cytokines such as IL-2 leading to proliferation of activated T-cells.

The activated T-cells now are able to freely move across the endothelial layer of non-lymphoid organs to infiltrate and look for infected sites. (Naive T-cells enter endothelial layer of non-lymphoid organs as well but this is chemokine independent nad thus not a reaction to inflammation).

Sources:

Difference between naive T-cells and memory T-cells: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782715/

Dendritic cell's role in immune response: http://lab.rockefeller.edu/steinman/dendritic_intro/immuneResponse

Memory vs naive T-cell migration:
http://www.nature.com/icb/journal/v86/n3/full/7100132a.html

Dendritic cell and role of CCL21:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078419/

Naive T-cell non-lymphoid organ infiltration: http://onlinelibrary.wiley.com/doi/10.1002/eji.200535539/full

CCL25 and inflammation relation:
http://www.sciencedirect.com/science/article/pii/S0896841116300014


Thrombus and Embolii Can treatment of thrombus cause embolism, in case of very high blood pressure, that may even lead to a heart attack ?

As the very high Blood pressure may cause some of the enzymes not act completely on the thrombus and release emboli in the blood stream ?

Yes, treatment of thrombus can cause embolism. Hypertension favors hemorrhagic complications.

Thrombolytics:

Yes, they can cause paradoxical embolism, although it is a rare complication [1]. The most fearful complication of thrombolytic medication is major hemorrhage. And hypertension favors bleeding [2].

Catheter-directed thrombolysis:

Hypertension (more than 180 mmHg and associated with congestive heart failure) was found to increase hemorrhagic complications [3].

Angioplasty:

Angioplasty produces some embolic particles [4]. However, using embolic protection is disputed [4, 5].

References:

Liu YF, Bayliss M. Paradoxical embolism: a rare complication of thrombolysis. Emerg Med J. 2008 Mar;25(3):180-1. doi: 10.1136/emj.2007.053934. PubMed PMID: 18299379.
Meneveau N, Vuillemenot A, Bassand JP. [Complications of thrombolytic therapy in pulmonary embolism]. Arch Mal Coeur Vaiss. 1995 Nov;88(11 Suppl):1769-76. PubMed PMID: 8815838.
Agle SC, McNally MM, Powell CS, Bogey WM, Parker FM, Stoner MC. The association of periprocedural hypertension and adverse outcomes in patients undergoing catheter-directed thrombolysis. Ann Vasc Surg. 2010 Jul;24(5):609-14. doi: 10.1016/j.avsg.2009.12.011. PubMed PMID: 20413257.
Malik RK, Landis GS, Sundick S, Cayne N, Marin M, Faries PL. Predicting embolic potential during carotid angioplasty and stenting: analysis of captured particulate debris, ultrasound characteristics, and prior carotid endarterectomy. J. Vasc. Surg. 2010 Feb;51(2):317-22. doi: 10.1016/j.jvs.2009.08.063. PubMed PMID: 20006918.
Divani AA, Berezina TL, Zhou J, Pakdaman R, Suri MF, Qureshi AI. Microscopic and macroscopic evaluation of emboli captured during angioplasty and stent procedures in extracranial vertebral and internal carotid arteries. J. Endovasc. Ther. 2008 Jun;15(3):263-9. doi: 10.1583/07-2326.1. PubMed PMID: 18540698.


What is the name of this beautiful white trees? I found this beautiful white trees in an unknown video.

If you do a Google Image search with the picture in the question, you'll see the screenshot is from the 2000 movie The Patriot starring Mel Gibson. The movie's filming locations were mainly scattered around South Carolina, on the southern East Coast of the United States. I've spent a lot of time in the region, and the gray-ish fluffy stuff hanging off the branches is almost certainly Spanish moss (Tillandsia usneoides), which is very common in the area.

While it is more difficult to identify the tree, as the bark and leaves are not clearly visible up close, a good educated guess based on the size and shape of the tree would be live oak (Quercus virginiana), which also happens to be one of the primary hosts of Spanish moss.


What is the name of this flower with purple leaves and orange inner part in NYC? I've photographed this flower a few days ago in New York City:

Does anybody know the name of it? (and how is the orange part called?)

It's Echinacea. I've linked to one site but if you run an images search with Echinacea as the search term you'll see lots of examples.

And here is the WP page.

Supplementary

Echinacea are members of the Compositae. The flower (the head) in your picture is actually made up of lots of individual smaller flowers (i.e. it is a composite flower). The petals are formed by ray flowers, and the central part, the disc is made up of disc flowers. More details at the WP page I have linked to for Compositae.


What does it mean for a species to be ancient? When we say that a species like cockroaches is ancient, what does it mean exactly?
Does that mean that cockroaches haven't evolved for a long time? But isn't evolution always occurring? So is that because they haven't evolved as much and are very similar to their ancestors, ie they had a "very slow rate of evolution"?

It depends on the context.

first "cockroaches are ancient" is different than a species being ancient, cockroaches are not a species but a group of species with a similar morphology and ancestry (similar to a clade).

It can mean they are mrophologically similar to their ancestors. Which is very different than saying they have not evolved. It means the pressures on the linage have not favored much in the way of morphological change. Some shapes just work well,(or reach equilibrium) and once you reach it the morphology don't change much even when other things are changing.
It often means that the split between the lineage in question and other groups is old. example, you could say mammals are ancient for instance because the mammal lineage split off the rest of the amniotes 275 millions years ago. They have changed a great deal since then but the groups as a whole goes back a long time. the issue here is these splits are minor when they occurred, like any other specialization event, but look big due to human constructed categories.
But it can also mean that the lineage has not undergone a specification event for a long time, It has changed but has not left behind any offshoots, this is the rarest case but can happen.

Note however this is a phrase the media like to throw around when it doesn't have a solid scientific definition, it is a qualitative contextual statement. They often have little understanding of its meanings. They also often fail to clarify which they mean, and often fail to properly define the "thing" being ancient.


Radial Basis Function Network (RBF Network) In the Wikipedia article on radial basis function network, I didn't understand what was meant by "center vector for neuron i", in other words "center of the RBF units called also prototype".

In RBF networks each neuron in the hidden layer applies a computation that is related to its "center vector".

First consider the set of input neurons as a vector $\mathbf{x}$, and that each hidden layer neuron receives the complete input vector as its own input.

Second, each hidden layer neuron $i$ is parametrised through a vector (center vector) $\mathbf{c_i}$ of equal dimension than $\mathbf{x}$.

The computation of each hidden layer neuron $i$ consists of:

Evaluate the distance (according to a metric, which may or may not be Euclidean) between the input $\mathbf{x}$ and the center vector $\mathbf{c_i}$. When the input is equal to the center vector, the output for that neuron will be maximal (see 2).
Evaluate a Gaussian function that decays with increasing distance between the vectors. That's the output of each hidden layer neuron. In the following equation, $\beta$ is a parameter that specifies the decay rate of the Gaussian (converse to the standard deviation in a regular Gaussian distribution).

\begin{equation}
\rho_i(\mathbf{x})=\exp{[-\beta\Vert\mathbf{x}-\mathbf{c_i}\Vert^2]}
\end{equation}

Now combine linearly the output of all hidden layer neurons to obtain the total neural network output. For that, you need an additional set of parameters or weights $a_i$ (one $a_i$ for each hidden layer neuron, but the $a_i$ values are scalars while each $\mathbf{c_i}$ is a vector).

The final equation, that yields the total network output (a scalar value), is:

\begin{equation}
\varphi(\mathbf{x}) = \sum_{i=1}^N a_i \rho(||\mathbf{x}-\mathbf{c}_i||)
\end{equation}

And that's it.


What animal does this skull belong to? This skull was found in Greece, about 40 years ago, possibly in the island of Euboea (there is uncertainty about the area it was found).

The length from nose to the end of horns is 67 cm. The skull's length without the horns is 42 cm. Just for reference, the floor tiles in the pictures have a side of 33cm.

What could this animal be? It does not have to be native to Greece, even though a native animal would be more probable.

Update:
The size of the skull points to an animal larger than a goat. It looks more like an antelope, a gazelle, or even a deer.  Only deers are native to Greece, however the horns look nothing like deer.

I believe the horns are the key to unlock this mystery.

Its definitely a bovid, most likely an african antelope specifically a Hartebeest or Alcelaphus buselaphus . There are several sub-species but those horns are a dead giveaway. The the horn do vary a bit by sub-species. The Neumann's or Tora hartebeest might be your best bet but I can't be 100% sure. They are all popular hunting trophies since forever and are even kept in some european game reserves so it is not that hard to find there skulls in private hands. Search "hartebeest skull" and you'll find a million of them so you can try for a more exact match.


Ribosomal DNA references sequences I'm having a bit of trouble with searching for this piece of information. I'm doing a study related to phylogenetic susceptibility of hosts to pathogens (based on a recent Nature publication), specifically to flu. This requires knowing the reference 18S ribosomal DNA sequence for chickens, wild ducks, horses, pigs and humans (amongst others). Is there a resource that enables us to easily download these?

For birds you can start by searching 18s in http://birdgenenames.org/cgnc/

But generally NCBI Nucleotide database, should provide you with all information and accession numbers. See this broad search: http://www.ncbi.nlm.nih.gov/nuccore/?term=18S+ribosomal+RNA+gene

Adding species specification and other parameters, you might find what you are looking for. For example, see chicken 18S ribosomal RNA gene


In the life-cycle of the HIV virus, how does the created DNA enter the nuclear membrane? I am in a high school biology class, so I cannot truly attest to how accurate the information I am given is, but as far as I know only RNA and very small molecules can enter the nuclear membrane through the pores on it (thus excluding DNA). Furthermore, I am fairly sure that the reverse-transcriptase used in the process of reverse transcription of the viral RNA must be used outside of the nuclear membrane, in the cytosol. My question is: How does the viral RNA, after it is reverse transcripted, enter the nuclear membrane?

My teacher and I have come to the conclusion that it probably creates the provirus sometime during mitosis, as the nuclear membrane dissolves, but this is more of an educated guess.

Thanks in advance!

Some proteins are transported from cytoplasm to nucleus by the importin family through nuclear pore. These proteins have a specific sequence called Nuclear Localization Sequence (NLS) and the importin family recognizes NLS to import them. Recently it has been clear that the accessory protein vps which is translated from viral RNA and composes pre-integration complex (PIC) with viral DNA has atypical sequence like NLS.
So. it has been thought that DNA from HIV is imported into host nucleus by importin family with PIC.


growth limit on muscle Is there any biological limit on muscle growth in human body, one can keep pushing body and keep growing more and more muscle but somewhere it must become diffcult for body to sustain those cells right?

Natural athletes have to deal with MSTN gene.

  The MSTN gene provides instructions for making a protein called myostatin.

  This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

Just look at the top natural athletes. There are a lot of them who train for 20+ years and still can't be as large as those athletes who take steroids. Here are some examples of professional natural athletes(Bobby Pandour, Georg Hackenschmidt)

With steroids you can exceed all natural limits up until your body meets its boundaries, often accompanied by serious health issues.


Can anti-aging cream work? I have a friend who told me that anti-aging cream cannot work to reduce wrinkles as it only penetrates x amount of skin layers and can never make a long term effect. Me not knowing much about how penetrative skin actually is, I was wondering if anyone knows if this is true and if anti-aging products are only working like a temporary moisturiser?

Since there are different formulations for anti-aging creams, it would be helpful to focus on the specific compound or combination of compounds.

According to a comprehensive literature review done in 2007, certain compounds (Vitamin C, alpha-hydroxy acids, Vitamin A, Vitamin B derivatives, and botanicals) have had varied success in literature demonstrating anti-aging efficacy with Vitamin C and alpha-hydroxy acids being the better candidates.

Vitamin A/retinols have been shown to reduce wrinkles in some studies but no large studies have been conducted to show efficacy, Vitamin C has been shown to be the most effective (statistically significant improvement in texture, wrinkling, etc.) and alpha-hydroxy acids have been shown to increase collagen density, for example among other improvements.  A lot of these and other compounds have had positive or encouraging results replicated in literature, on mostly animal and human cell models so whether they actually have a significant effect on a large group of people needs to be looked at but to assess whether or not they actually "work" depends on what issues of skin damage as a result of aging one is targetting, the severity, the age at "treatment" and whether you're referring to over the counter or prescription-strength.

Huang, C. K. and T. A. Miller (2007). "The truth about over-the-counter topical anti-aging products: a comprehensive review." Aesthet Surg J 27(4): 402-412; quiz 413-405.


How to learn molecular biology through pubmed research articles? Instead of using a textbook, is there an alternative curriculum, that simply lists a set of pubmed research articles for each topic covered in a typical undergrad molecular biology course?

I am currently learning molecular biology by reading a textbook.  Different chapters focus on different topics such as Cells and Genomes, Cell Chemistry, Proteins, DNA, Gene Expression, etc...  However, I'd prefer to learn these topics directly from research papers on pubmed.

For example, I would imagine the DNA "chapter" of such a curriculum would include the Watson Crick paper on DNA.

As another example, searching for "Protein" in pubmed reveals a ton of research papers, but which subset of them cover the topics taught in an intro molecular biology course?

Note: The pubmed articles don't have to be free or open access, I'm ok with getting the papers through my university library.  Also if an alternative curriculum such as this doesn't exist, maybe there is a supplemental one?  Or maybe you can recommend a set of papers that you'd include in such a curriculum?

Tom Silhavy would use a similar method in the first year graduate Molecular Biology course.

His text was basically a set of papers bound into a book "The power of bacterial genetics: a literature based course".  I'm not sure its in print anymore, but a used copy can be had.  If you find a copy you can just fetch the papers if you like.

You can't do much better than finding excellent papers to read.

Briefly, the class covered the development of selection for mutations and mapping them onto genes - use of bacteriophage and replicate plating.  The papers started in the 40s and went on from there to the heyday of molecular biology.

It was an awesome course to take... an awesome baptism of fire.

As they say... Whatever doesn't kill you, will select you for a distinguishing phenotype.


Are RNA cleavage sites always polyadenylated? During RNA processing (including both mRNA and non-coding RNAs), is the end of 3'UTR always polyadenylated after cleavage?

I could not find the answer to my question in the Wikipedia entry for polyadenylation.

If a recent reference could be provided, that will be great. I've done quite a bit search and hasn't found a good source yet.

Some background to this question: we are developing bioinformatics tools to predict potential cleavage sites, we need to understand this problem better in order to design a suitable algorithm

This answer attempts to cover only the question of mRNA processing. It does not address the polyadenylation of non-coding RNAs.

As far as I can see from the recent review by Neve et al. (2017) cleavage and polyadenylation are tightly coupled. It is interesting, in this regard, that histones mRNAs which lack polyA tails, have a different structure, lacking the canonical AAUAAA, at their 3ʹ ends (see review by Marzluff et al.).

As distinct enzyme activities are involved in cleavage and polyadenylation, it would, I imagine, be possible (either genetically or chemically) to disrupt the protein complex responsible for polyadenylation and hence prevent it occurring (this has probably been done). However this would not be physiologically relevant.

There is an earlier review by Tian and Graber (2007) of the sequence requirements of the cleavage site which makes no distinction between cleavage and polyadenylation.

However this is not my field, so others may have additional information I have missed.


Colourful aquatic animal identification Of what species is the following creature?

I expect it would be a Cephalopod living in not too deep water with a tropical climate (Brazil?). However, I can not find any information about what species it actually is.

This is the Sarcastic fringehead fish (Neoclinus blanchardi). [Source2]


Why is male balding so common in comparison to female balding? I have heard that over 30% of men will be bald by 30, and that 60% will be bald by 50. However, I hardly ever see a bald woman unless it is a story about a cancer survivor or someone going through cancer, meaning that they lost their hair through chemotherapy rather than natural balding. I do not understand why this is. I do know that women tend to have longer hair than men, so maybe their follicles are more active, preventing them from going bald. If someone could correct my explanation, that'd be appreciated.

Let's start off by saying that "baldness" is a very broad term... it includes not only hair loss but also miniaturization, which accounts for the majority of the phenotypic "baldness" associated with alopecia areata.  While alopecia areata is not the only cause of baldness, it accounts for 4 out of 5 cases in men, whereas in women it only accounts for half.
The reason that it's more frequent in males is the presence of 5α‐reductase in the sebacious glands and the dermal papilla - this enzyme mediates the metabolism of testosterone into dihydrotestosterone.  Dihydrotestosterone, in its turn, binds to androgen receptors and affects gene expression, speeding up the anogen phase.  Consequently more hairs are in the telogen phase, and the hair is shorter. In severe cases, miniaturization can become actual hair loss.
Because males higher levels of androgens, there is more testosterone available to be metabolized in the follicles. Therefore, the incidence of alopecia areata (and consequently baldness) is higher in men than in women.

References

Piraccini BM, Alessandrini A. Androgenetic alopecia. G Ital Dermatol Venereol. 2014 Feb;149(1):15-24. PMID: 24566563.

Randall VA, Thornton MJ, Messenger AG. Cultured dermal papilla cells from androgen-dependent human hair follicles (e.g. beard) contain more androgen receptors than those from non-balding areas of scalp. J Endocrinol. 1992 Apr;133(1):141-7. doi: 10.1677/joe.0.1330141. PMID: 1517703.


Workspace preparation and cleanup for DNA work What steps should be taken in a molecular lab environment to help ensure that DNA samples/stocks are not contaminated, or contaminate other objects in the lab?

From the comment section:

Mostly segregation of PCR-amplified DNA from non-amplified DNA. Typically no DNA or sample should ever enter a specific room designed to prepare the MasterMix for PCR (this is true for diagnostic labs, in the research one I never saw that). For the rest, following good laboratory practices (google that) should be enough.