Can one become suddenly ambidextrous? Is it possible to become ambidextrous? i'm 67 and recently and suddenly became ambidextrous about a month ago. I can write w both hands at the same time.

Normally in a right handed person the left hemisphere is considered dominant.  However, a new lesion in the left hemisphere can cause loss of this dominance so it is possible that this has occurred.

Alternatively, if the subject is now able to write using both hands concurrently but different material, it suggests that the two hemispheres are disconnected, the so called split brain syndrome which occurs with lesions of the corpus callosum.  However, ambidexterity is not described in that syndrome.

Anyway, you need to consult your physician.

You can't suddenly become ambidextrous.  You can train yourself to use objects with the opposite hand, and become use to using your other hand.

Your body learns on repetition- Repeating something over and over till it becomes a habit.  It takes time for your body to adjust to the change but you can become ambidextrous through training your body.

You just have to have the patience and the will to do it.


What is the difference between a predator and a parasite? A human encountering a tiger or a malaria plasmodium is likely to suffer, and the tiger/plasmodium is likely to gain from the transaction. Not necessarily a good example, and I am aware that a successful parasite avoids prematurely killing its host, but I can't see any fundamental difference.

Of course it's like pornography: "we know it when we see it". But is there a formal, generally-accepted distinction?

Good question.

There is no fundamental difference between parasites and predators.

Ecological Interaction

In terms of ecological interaction, they are both defined as an interaction where one species benefits and the other suffers from the interaction.

Intuition parasite vs predator

In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of

Examples when intuition don't match the above picture

Generally considered as predation but does not fit the above picture-based definition:

social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves
herbivores browsing on large trees

Generally considered as parasitism but does not fit the above picture-based definition:

indirect effect of habitat modification that would rather be considered as parasitism.
Species that take advantage of parental care of another species by mimicking babies (but being larger)
Individuals of large species stealing the habitat built by a smaller species
Batesian mimicry (see this post; Thank you @WYSIWYG and @NL_Derek for the comments)

Population culture vs science literature

In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.

A parasite may or may not kill the host. It's basic motive is to constantly derive nutrition from the host. More a sort of one time investment and as an interest you keep getting the nutrition.
Whereas a predator's motive is to kill the host to satisfy it's hunger. One kill and eat can be a taken as a case of consideration here.


During non-cyclic photophosphorylation, how does NADP+ become NADPH? I know that NADP+ gets reduced to form NADPH, but what exactly is being donated? Is it two individual electrons (from photolysis or the chlorophyll molecules) and a hydrogen ion (proton)? If this is the case, during the Calvin Cycle, do the NADPH molecules donate the same two individual electrons and hydrogen proton from the light-dependent reactions to become NADP+ again? Thanks.

Specifically during non-cyclic photophosphorylation, I know that the chlorophyll already has preexisting NADP+ molecules, water is broken to release 2 hydrogen atoms and 1 oxygen atom (two water molecules break down to form gaseous oxygen that we breath), those 2 hydrogen atoms get sent down and along the Electron Transport Chain via solar energy and then I believe one goes to a protein called ATP synthase and the other goes to photostem 1. After photostem 1 that hydrogen binds to free floating NADP+ molecules to from charged NADPH. This should be the gist of it all but I would also recommend listening to someone else's input as well.


Why upper surface of leaves is more green and shiny than the lower one? I have properly googled this and got various answers. However, those answers do not provide an answer to the "Why" part of my question. Why is it that the upper surface of leaves is more green than the lower one? Some sites suggest that it is because of the thick cuticle. Yet, that sounds weird and doesn't fully convince me. What other reasons to why the upper surface of leaves is more green and shiny than the lower one, could there be?

You can find two chlorophylls in most plant leaves, chlorophyll a and b. We'll use as a reference Leaf characteristics and chlorophyll concentration of Schyzolobium
parahybum and Hymenaea stilbocarpa seedlings grown in different
light regimes. The most important observation is that in shade-tolerant leaves, chlorophyll b dominates chlorophyll a. And the opposite is true of shade-intolerant leaves. I'll argue now that the portion of a given leaf that must tolerate more shade will have the darker green pigment due to the presence of more cholorphyll b, and that the side of the leaf that must tolerate lots of light will have the lighter pigment due to the presence of more chlorophyll a.

The light-tolerant side of the leaf is also shiny, and this is because of a thick waxy cuticle. The shade-tolerant side of the leaf also has a cuticle but if we follow it logically, the light-tolerant side of the leaf needs more protection from heat evaporation because it's always being hit by light.

So what I'd do, instead of thinking of the leaf as having a top or bottom, think of them as having a side that must tolerate excessive shade, and a side that must tolerate excessive light.

Photosynthesis is the process of trapping sunlight and converting the energy into chemical energy which is then provided as a food source.

So the sunlight is trapped through chlorophylls. This is a pigment in the organelle called the chloroplast. The upper surface of the leaf is open to sunlight where the plants have more chloroplasts containing more chlorophylls to trap the most amount of sunlight.

All these chlorophylls are green coloured and since there is an increased amount of chlorophylls in the upper surface than in the lower surface (to trap more and more sunlight), the upper surface appears to be greener than the lower surface.

Source: Grade 12 Science student.


are sperms considered living recently i got into a debate with this question on hinduism.se ,

as the link given above shows, are sperms considered as living or non-living

as far as my knowledge is concerned, sperms undergo locomotion, senescence, more over the best thing to say they are living is they contain genome, i.e. haploid sets of chromosomes

so in short are sperms living or non-living

The question of what is living is nothing but a matter of definition. We can only tell you what are the standard definitions of what is a living thing but no absolute truth exist behind these definitions. Therefore, I am afraid that all discussions here will bring anything new to your ethic or religion related discussion.

I want to argue that the @user137's answer is very misleading for two reasons. First, he based his discussion exclusively on the "reproduction ability" definition of life. Second because his definition of reproduction might be misleading as well.

Reproduction is not only cell division obviously. Following this same definition one would not consider a human to be a living things but only to be a collection of living (and non-living) things. It is important to understand that a spermatozoid is just one phase of a life-cycle. This phase yield to the next phase. That's it. It seems weird to say that a kid is not alive just because he cannot reproduce. It seems weird to say that a grandmother is not alive because it cannot reproduce. You can say however that a kid is a living thing that cannot reproduce and at another moment of its life cycle it will be able to reproduce (assuming it will survive to this age). One should not think of spermatozoids as something totally detached from the human phase as we know it. These things just form a cycle and it seems to me miseleading to say that a part of this cycle is not alive. Saying such thing would yield someone to think that two living things create non-living things that by fusion will become alive. That seems weird. But again, it is nothing but a matter of definition. I cannot say that user137 is wrong, I cannot only say that his definition seem neither useful, intuitive nor common among biologists.

You may want to have a look to life-cycle and to understand what are the haplontic and diplontic phases with a bunch of wikipedia readings.

Other concepts such as the ability to synthesize its own components, having a boundary between interior and exterior and ability to response to environmental stimulis are often used in order to define what is a living thing and what is not.

One requirement most biologists have to consider something living is the ability to reproduce. This is why viruses are generally not considered alive. They contain proteins and DNA or RNA, but require infecting a host cell and hijacking its replication machinery to reproduce itself.

Fully differentiated sperm cells cannot divide and therefore can't reproduce. Their only role is delivering DNA cargo to an oocyte and creating an embryo. An individual sperm cell is just as alive as an individual neuron or muscle cell. These require nutrients and energy, carry out metabolism, perform functions, contain DNA, but a plate of neurons won't grow into a human.


Presence of MHC on red blood cells Do red blood cells have no MHC? (I have often heard that they do not.)

If so why are they not destroyed by immune cells?

They do not, at least not normally or noticeably.  MHC I occurs on all nucleated cells, and red blood cells do not have nuclei.  If they did indeed have MHC on them, blood transfusions would be as successful and as tricky as organ donation.  There are reports of MHC detection on red blood cells, but the amount is orders of magnitude smaller than elsewhere, only present for certain MHC alleles, and often transient.

you are right.red blood cells do not have noticeable MHC 1 molecules.But rather the have high levels of CD47 markers which are recognized by the immune system as self.On the other hand red blood cells during development are nucleated they may contain small traces of MHC 1 molecules.I hope this answers your question.


What is the effect of persistent hypothermia on cardiac performance? I define persistent hypothermia in this thread about the mechanisms of persistent hypothermia.
The Graph of Katzung et al. in Pharmacology about Heart Failure:

I am thinking which parts here are critical on temperature.
Temperature has a direct effect of reaction rates of chemical reactions here, for instance NE, AII and probably chemical reactions in endothelin such as ET.

Therefore, I am thinking that the relationship between temperature and cardiac performance cannot be linear at all.
Some have said me that low temperature can decrease metabolism and oxygen consumption.
However, I started to think differently when time goes enough far that is when heart cannot anymore supply enough blood with oxygen. Thus, hypoxia can occur and asymptomatic exodus may occur.

Physiological case

Based on physiology, I can propose that the cardiac output curve shifts to the left (CO1 $\to$ CO2), due to less oxygen being supplied to the heart, similarly EDV1 (end-diastolic volume) shifts $\to$ EDV2 and SV1 (stroke volume) $\to$ SV2.
However, the venous return (VR) curve can shift much more, since I propose that the effect of temperature on smooth musculature is relatively bigger than on heart because of proportional size of tissue.
So the VR1 shifts to VR2, so EDV2 $\to$ EDV3 and SV2 $\to$ SV3.
Consequently, SV3 > SV1, while EDV3 < EDV1.
See my draft figure about this:

where EDV (End Diastolic Volume) in the x-axis and SV (Stroke Volume) in the y-axis.

In a healthy person, who have no hypertrophy of ventricles and elastic myocardium, the heart can tolerate this. So such a condition of cardiac failure as in the figure 13-3 is possible.

However, if flexibility of the myocardium, for instance, is not possible, such a pathway may not be possible.
The autonomic nervous system may enter the picture and increase vagus nerve stimulation (PS more).
However, not sure about the exact pathway.

What is the effect of temperature on cardiac performance?
How can temperature decrease cardiac performance?

Winter swimming and infarcts

The publication Long-term risks of cardiac and cerebral vascular diseases increased following winter swimming in the cold seawater which came out just some weeks ago shows a link between long-term winter swimming and CVD.
I think this is the best evidence so far about the possible link.

WYSIWYG's comment has some good general idea:

  Many processes are affected by temperature including metabolism and
  growth rates. Reaction rates increase with temperature but not in case
  of catalysed reactions where the catalyst can operate at only an
  optimum temperature.

Some related topics

temperature effect on the rate of protein degradation

So further studies

protein degradation in the heart in persistent hypothermia
...

Effect of persistent hypothermia on processes of cAF

[1]

Let's have cAF (chronic atrial fibrillation) here as an target.
Electrophysiological study shows that cAF-related remodeling is typically divided into three categories: 1) electrical, 2) contractile and 3) structural.
They cause respectively

1) shortening of both the action potential (AP) duration and effective refractory period (ERP)
2) possibly a result of impaired Ca2+ intracellular handling
3) changes of cellular level (hypertrophy, glycogen accumulation and modified mitochondrial morphology) and tissue fibrosis

cAF's processes in persistent hypothermia

I cannot say now more anything about persistent hypothermia and cAF by confidence.
Those mechanisms of Koivumäki et al are cellular processes, while the representation of the heart requires integrative analysis in the cellular, tissue and organ levels.

In cellular level

Only some catalyzed reactions can work in persistent hypothermia. TODO consider which enzymes of the heart and body work in low temperature in short-term and long-term cases. Depletion cases too.
Effect of persistent hypothermia on the outflux of Calcium (probably, slows down).

In tissue level

I can say without rigor that electrical coordination is uncoordinated in tissue fibrosis.

In organ level

I say say without rigor that the mean electrical axis should be determined and fixed in the study.
Effect of Arterial hypertension must be fixed. Sokolew-Lyon index can a starting point for the indicator but better indicator is required with higher specificity.

Persistent hypothermia from the extreme side (Sauna)

[2] Regular Sauna is with better hemodynamic function; however, the association of sauna bathing with cardiovascular and all-cause mortality is not known.

so possible effect of persistent hypothermia can be

lower hemodynamic function if no compensation mechanism
better hemodynamic function if some compensation mechanism (genetics; unknown)

Some research topics

Effect of Persistent Hypothermia on the Arterial Hypertension. This may be associated with coagulopathy, especially in the lower limb.
Effect of Persistent Hypothermia on Atherosclerosis. It would be very nice to see long-term study about the effect of regular 4-7 winter swimming on the cardiovascular risk score, SCORE and others.

Sources

In Silico Screening of the Key Cellular Remodeling Targets in Chronic Atrial Fibrillation. Koivumäki et al. Computational Biology.
Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events, here

Please, see the reference of the publication for more better view.

Both pictures you posted show that increased peripheral vascular resistance decrease cardiac output. If you are talking about someone outdoors not properly dressed in a Scandinavian winter, then their cutaneous vasculature would constrict and Also their extremities would get less blood flow. That would increase peripheral vascular resistance and thus decrease cardiac output. These articles were the first to pop up for me (http://circres.ahajournals.org/content/7/3/366 & http://www.ncbi.nlm.nih.gov/pubmed/10215232) and it seems to say that the primary cause of increased vascular resistance is actually caused by decreased cardiac output as well as local control.

This may seem contradictory to therapeutic use of hypothermia, where it is used to decrease metabolic needs (I don't know what is the mechanism for this) to help compensate for hypoxia (in cardiac tissue and the brain?). Cooling the heart would decrease it's metabolic needs (less perfusion, increased metabolic demands resulting from sympathetic input to heart. I guess the same thing probably happens when doctors prescribe a beta-blocker or non-dihydropyridine calcium channel blocker (CCB), the vascular resistance probably increases (except for the CCB diltiazem which dilates blood vessels in addition to it's effects on the heart). But the main thing is the sympathetic output to the heart, which is blocked by these drugs, and cold; this is more important than the increased peripheral vascular resistance. But remember that afterload is not identical to peripheral vascular resistance!!! The decreased cardiac output would probably decrease blood pressure and afterload, I'm guessing.

As for the slowing of reactions related to vasoconstriction (transmission of nervous signal from hypothalamus via pre ganglionic sympathetic fiber, then synapse in sympathetic chain, then transmission via post ganglionic nerve; release of NE, Epi, AT-II; rate of diffusion to receptor; effect of cold on membrane fluidity; effect on the alpha adrenergic receptor; rate of second messenger signalling cascade; effect of cAMP formation by G stimulator protein or breakdown by phosphodiesterase; effect of Ca++ release; effect on PLC mediated IP3/DAG release; effect on NO release and receptor stimulation of guanylate cyclase;  and the various other factors regulating endothelial function and smooth muscle contraction), I don't know. I also assume that an increase in viscosity (a factor included in the calculation of vascular resistance) could be another factor leading to increased vascular resistance, but even if this happens, this is less important than the decrease of the hearts metabolic rate.

Personally I'm not acquainted with the literature on therapeutic use of hypothermia, aside from the ethical debates about using Nazi hypothermia research. I'm just going at it with the same physiology knowledge you have, and relaying your confusion back at you. I'm just as lazy as you and I don't feel like spending hours delving into review articles on hypothermia research, but I agree that it is an interesting question, and it is also relevant to other very important topics in medicine (ie. use of beta blockers, non-dihydropyridine CCBs other than diltiazem).


Typical firing patterns of (some) motor neurons Since it is not so easy to imagine and visualize the behaviour of the muscles in the fingers, hand, and arm of a violinist performing a fast and accentuated trill vs. a slow and soft vibrato, I try to imagine and visualize how corresponding motor neurons do fire.

I assume there are some motor neurons that are immediately responsible for the speed and amplitude of the movement of a finger performing a fast trill, and — partly the same, partly others — that are immediately responsible for the speed and amplitude of the movement of the same finger performing a slow vibrato.

The behaviour of these motor neurons — during the trill or the vibrato — can be recorded as corresponding sequences/trains/bursts/chats of spikes.

I wonder:

  How may these spiking and/or bursting patterns look like?

Maybe like this?

fast and accentuated (= large amplitude) TRILL, each group corresponding to one movement (up-down) of the finger

slow and soft (= small amplitude) VIBRATO, each group corresponding to one movement (to-fro) of the finger

I can't answer the whole question, but what I do know:
An actionpotential can't have a small amplitude, the amplitude is always the same. If a neuron gets excited enough there will be an action potential, otherwise there won't.

"When the depolarization reaches about -55 mV a neuron will fire an action potential. This is the threshold. If the neuron does not reach this critical threshold level, then no action potential will fire. Also, when the threshold level is reached, an action potential of a fixed sized will always fire...for any given neuron, the size of the action potential is always the same. "
quoted from https://faculty.washington.edu/chudler/ap.html

Neurons have a maximum firing rate, a point where they cannot fire faster. (http://blog.eyewire.org/why-do-neurons-fire-at-a-maximum-of-about-200-hz/)
So to move faster your body can't fire faster. But it can fire more: more neurons fire if you want to move faster, and less neurons fire if you want to move slower: https://blogs.scientificamerican.com/scicurious-brain/when-you-run-fast-your-brain-runs-faster/

I do think your first row of spikes is kinda correct. Neurons fire as long as you move your hand/finger(s) in a certain direction, and as soon as these neurons stop firing and their complementairy neurons start firing you move your hand to the opposite direction.


Identify this vertebra I was walking on the beach in New Jersey (U.S.), at about 40 degrees longitude, and found this bone. It's not a fish. The long process in the front is interesting. It is likely a C2 vertebra. I looked on the web, but could not find anything aquatic that it might match. Certainly not a dolphin. It is 2 inches long (50 mm), and 2.5 inches high and wide (64 mm). I guess it need not be aquatic, and New York City (20 miles North of here) used to dump garbage in the ocean. It looks old. Can you help me identify it?

Looks like Lumbar Vertebrae or Sacral Vertebrae of a Cow like @Brian Hanson Said above.

Studying closely in laboratory can elaborate more secrets about the bones.


How many generations does it take for one species to become a new one? First lets consider that a species is a group of individuals that can reproduce by breeding fertile offsprings.

It's usually said that evolution takes a very long time. Lets say that 1000 generations are required for species A to evolve into species B.

Which species would generation 999 belong to, A or B ?
If A then it means that there was no evolution in 999 generations and that the entire evolution is going to happen in a single generation from 999 to 1000.
If B then which specie does generation 998 belong to ?
etc etc

In the end it seems to me that if there is evolution it can only be instantaneous, but that requires many improbable things, one of them being that the spermatozoids and ovules of species A contain DNA of species B !

How does that work ?

EDIT this is not a duplicate I'm not asking what a species is I'm asking what is the genetic process of evolution, how do we move up in the evolution tree.

Your question is like asking about the color spectrum. A wavelength of 530nm is green; a wavelength of 580nm is yellow. So let's say it takes 60nm of wavelength change to go from green to yellow. What color does a wavelength of 579nm have, green or yellow? If it's green, then does the color shift in a single nm difference of wavelengths? If it's yellow, what color is 578nm, etc?

The answer in this case is, 579nm is yellow; so is 578nm. 570nm is more ambiguous; some people might say it's yellow, others think it's greenish-yellow, in some contexts it might look clearly green. And so on along the spectrum; the reality is that there is no hard boundary between "green" and "yellow". There are colors that are clearly green, colors that are clearly yellow, and there is a difference between those two, but there are also plenty of intermediates that are a bit like green and a bit like yellow, and those intermediates are what you go through when you go from green to yellow. There is no definite point everybody can agree on where a single shift happens.

It is the same thing with species. A species is a group of organisms that interbreed to produce fertile offspring, but "interbreeding to produce fertile offspring" isn't a on/off thing. Organisms are more or less fertile. What if organisms from two groups interbreed and produce offspring, and only half of those offspring are fertile? Or they have half as many offspring as couples within the two groups have?

The reason species are an important concept, and can be distinguished visually as being like each other and unlike members of other species, is that within a species there is widespread sharing of genes over the generation, as individuals breed with each other, but they don't share genes with other species. Meaning species will evolve as a unit; changes that happen within a species will spread between individuals of that species, but won't spread outside of it.

But because sharing genes isn't an on/off thing, you could have 100% of genes being shared from one population to another (then they're clearly the same species), or 0% (then they're clearly not), or 90%, or 70%, or 10%... That's where you find the fuzzy boundaries. The races, strains, varieties, sub-species, all those different words to describe populations that are different but aren't outright different species. And the debates on whether different groups are different species or not in the first place, in the cases where it's really ambiguous.

And the same thing is true of evolutionary change in general. You don't have a mammalian carnivore that isn't a cat, and then bam! a cat. You have a mammalian carnivore that isn't a cat (or dog, or weasel... but kind of like any of those in various ways. Like generic carnivore-ish), then a mammalian carnivore that's a bit more like a cat or a dog (and another one next to it that's a bit more like a weasel), then a mammalian carnivore that's even more like a cat (and others that are even more like a dog, and even more like a weasel), then a mammalian carnivore that's clearly feline but isn't a cat, or a lion, or a tiger; it's a different species of feline that doesn't exist today, and also looks more generic-feline-ish than any modern feline. Then there's a feline that's more like a cat (and others around it that are more like a lion, and a tiger), but also clearly isn't a modern cat. Then there are felines that are really like cats but a bit different from modern ones and it's hard to tell, maybe we should extend the definition of "cat" to include them? And then bam! a cat. But that cat isn't clearly a Jungle Cat, or a European Wildcat, or a domestic cat, or any modern species; it's its own "archaic cat" species. And then there are cats that are more like Jungle cats, or more like domestic house cats...

Also don't confuse the creation of new species with evolutionary change in general. Over the long term they are related, because once two groups are different species then they will change through evolution in independent directions, and they will end up looking different from each other as well as from their common ancestor. But over the short term you can have speciation with very little morphological or genetic change (you just need two groups that used to interbreed, to no longer do so), or morphological/genetic change without speciation (if all the change happens within one group).

Both speciation and genetic/morphological change can happen within a single generation, but usually happen over much longer timescales. But there is no hard rule for how long that is; as far as speciation goes, if groups aren't prevented from interbreeding in some way then they will keep breeding with each other and can stay a single species indefinitely (whether individual from generation 10,000 could interbreed with individual from generation 1 is a different question, but it's not like it's a situation that happens). As far as evolutionary change goes, natural selection means species change to adapt to their environment. Once they're adapted to it, if it happens their environment never changes then natural selection will push them to stay the same as they are, again indefinitely. In the real world most environments change over time so organisms do change more often than not, but just to illustrate that the timelines are a product of circumstance, not an intrinsic feature of evolution itself.

One Generation.

The DNA you inherit from your parents provides you with a selective set of circumstances. If fostered within a confined environment, it will continue through generations with very little change.
Provide a total shift of environmental conditions, and the previously dormant DNA triggers into action, a new set of rules; some beneficial some not.The next generation will slump back to past DNA rut if the situation remains constant......or upgrade the DNA in future generations.

Such has the Industrial Revolution has dragged on from coal smoke to petroleum fumes for nearly 300 years, our DNA adjusts to the minute particles in the atmosphere; some successfully, most NOT.
You could call this a 'hiatus' in evolution.


Selection for less efficient egg transfer in Human Botfly life cycle I have heard that the Human Botfly transfers its eggs through other invertebrates, and it strikes my curiosity that if an insect could simply land on its host directly to deposit its eggs, then why have intermediate hosts?

I have speculated that the vectors may be better specialized for penetrating hosts, and that penetrating hosts may be difficult, or that approaching hosts is risky. Another speculation on my part is that the Human Botfly may be filling a niche where it does not need to compete.

In multi-host complex life cycles (CLCs), an intermediate host often aids in the dispersal of offspring.

In general terms, an animal, say a botfly, have an ultimate "purpose" or 'goal'  to spread their genetic information as much as possible. This could mean producing a large number of offspring and hoping some survive or it could mean having one offspring, investing a lot of energy and ensuring it does survive. Regardless, spreading genetic information often requires offspring to disperse (or be spread) a great distance, which may allow the individuals' genetic information to dominate an new region.

In the case of botflies, having an intermediate host means the genetic information can be spread a great distance.

If you're looking for a more thorough explanation of complex life cycles, this paper describes it well. There is also this site more specific to the botfly which is not peer reviewed, but well-researched and descriptive.

it makes sense because the mosquito which is usually the intermediate host is more "sneaky" than the bot fly. so its better for the survival of the bot fly and better for the transfer of the egg. The egg hatches upon contact with the hosts skin so its not inserted by the mosquito bite. the hatched larva diggs itself into the skin then.


Why is mammal coloration so dull? I have seen species of birds, insects and fishes with splendid colours. But when it comes to mammals (including us humans), they almost always appear in shades of brown, grey, orange, or in black and white. I don't recall seeing any pink, green and purple. Why is that so?

I don't think, there is a precise answer about the evolutionary mechanisms, but "mechanically":

mammals have principally just two types of pigments: eumelanin and pheomelanin, both of which have their color variants, but within a known range. Bird pigments, besides melanins, include carotenoids and porphyrins. Arthropods generally have carotenoids, melanins and ommochromes [and other pigments?]. E.g. carotenoids and ommochromes alone can create rather "exotic" coloration from a mammal point of view (green, pink, violet).
both birds and insects actively utilize iridescence. With fur it seems to be technically much more difficult to achieve than with feather or scales.
many (most?) mammals do not differentiate colors. Birds have much better vision abilities in this respect. From a selectionist point of view this cuts out a considerable part of selection acting upon coloration, which could otherwise produce broader spectrum of phenotypes.

The Answer is simple..EVOLUTION..
The colour of an living organisms depends on 2 things 1) attracting other sex. 2) escape from the predators.

In birds and insects: They doesn't much depend on other sex for living(except for the process of reproduction)and there is no need t exhibit  physical work for attracting other sex... For example if you take a peacock the male needs to be colourful to attract female. but there is no physical work....Let The Other example be some Insect,then if it is colourful.. a predator may not eat for its bright colour..
this made insects and birds evolute into colourful..

But in mammals. the attracting and escape both depend on physical work... a lion being handsome cannot attract lioness..  :P It need to be physically healthy to escape from predators and give an enough competition to other lions in his territory...
this made evolution for mammals much depend on their capability of body.. rather than physical attractiveness.. for example in a forest a tigress will obviously pair with a Tiger which has more territory than a more attractive handsome tiger without territory(this is not a case with insects)..


Why do cells vary in shape and function when they have the same genome and the same organelles? Why do cells vary in shape and function when they have the same genome and the same organelles. For example: why do all cells have nuclei but red blood cell's don't; why can't the cells of a eye perform the function of the tongue; and the list goes on and on. If you say it is because of gene regulation, so then how does the RNA know to transcribe the specific genes that are necessary to that particular cell?

Because cells are not only characterized by by their genetic material and other interior components, but also by the genes they express. Cells have to fulfill multiple different functions to be able to build complex multicellular organisms. Differently expressed genes lead to different proteins made in the cell, which leads to different morphology, shape or function. For example melanocytes in the skin are highly specialized cells which mostly make the pigment melanin. Plasma cells on the other are highly specialised for making antibodies.

It is all about regulation of genes. The RNA doesn't know or transcribe anything -
the DNA is trancribed into the mRNA (which is then further processed) and finally translated into proteins. Cells develop from precursors which proliferate and finally differentiate into highly specific cells. This progress is controlled and activated by specific transcription factors and growth factors. For example: pigment cells only develop, when a specific transcription factor is present. When this factor cannot be expressed, these cells do not develop at all.

This developmental process is shown schematically in the figure below (the figure is from the NIH website on stem cells):

Despite of the fact that all cells have the same genome, not all the genes contained in the cell nuclei are functional. During embryonic development, cells are subjected constantly to division and differentiation processes; this means that in the earliest stages of embryonic development, each cell of the embryo can form, by itself, a new complete body. However, these cells loose their ability of "all-forming" as the embryonic development progresses and they become able to form only certain group of tissues. Lately, they would be only able to form just one type of tissue.

All these cells have, obviously, the same genes, but what makes a cell of early stages of embryo development (stem cell) different from another of the body if they have the same genes? The answer is that although they have identical genes, differentiated cells use less genes than a stem cells would use. For this reason, only a certain number of genes of the total that a differentiated cell contains, are in use. A neuron, for example, wouldn't need a gene that produces hair protein because simply, its function isn't that, so neurons inactivate the gene of hair-producing.

There is much more to investigate and to research in this field because many questions still remain without answer such as how cells acquire certain shapes and not other or how do they form perfect 3D organized shapes (tissues and organs) and much more question in this way.


Why do we urinate more often in winter compaired to summer? I have been thinking of this question for a long time, but I do not seem to find an answer yet. Is there a hormonal change in our body during winter due to which we have to run to toilet often?

There is no 100 % sure answer for this as, obviously, nobody is that much interested in studying about urination. But there are some theories, of which the most popular and accepted one is cold diuresis.

  Cold-induced diuresis, or cold diuresis, is a phenomenon that occurs in humans after exposure to a hypothermic environment, usually during mild to moderate hypothermia.

According to this theory, what exactly happens is this (I'll explain in steps for better understanding):

When your body senses cold or low temperature of environment, it constricts the blood vessels near your skin and external organs and restricts your blood to the inner core of your body to maintain its temperature.
Thus, it causes the blood pressure to increase as there is same amount of blood in lesser volume.
This induces negative feedback on ADH (a vasoconstrictor) i.e. its secretion is reduced.
Now when blood vessels in kidney get proper amount of blood (as blood vessels aren't constricted now), they sense high blood pressure and try to reduce it as soon as possible.
So they transfer more amount of water from blood to bladder which fills the bladder more quickly and causes an urge to urinate.
Thus, we urinate more in colder climate.

There are some more theories related to it too, but they aren't as popular. According to another theory, when we are exposed to cold weather, aquaporins are inhibited around the body, making it impossible for water to be taken in by cells, leaving a lot more of it in the blood. Again, the body will try to balance that pressure, pulling water from the blood and storing it in the bladder. You can get a more frank and interactive explanation here.

I think that due to cold temperature the hormone ADH cannot function well. As in low temperature the enzymes becomes less active. So as the ADH hormone is not working well the suger concentration will increase in our blood due to which more amount of water will transfer from our cell to the blood stream. And this excess water will be removed by the kidney and result in polyurea.


Choosing PCR conditions How does one choose PCR conditions? Does it depend on the taxon, on the DNA concentration, on the primers or anything else?

You need to first build an initial protocol and then optimize it.

The most important to determine the conditions is the polymerase used. Some polymerases work at higher or lower temperatures and will work faster or slower. Find the default protocol from the polymerase seller and this will give you a good idea where to start.

The second most important is the primers used. Depending on the GC % in the primers and their length, the times or temperature of each step will change, or if you prefer will need to be Optimized.
The length of the DNA fragments will also determine the length of the cycles. Most polymerase sellers will includes steps to optimize the reaction depending on the quantity of DNA used, primer length and other parameters.

For more information:

Designing primers:

Taq DNA polymerase protocol example:

Optimizing PCR

PCR thermal profile, Deoxynucleoside Triphosphates and Primers are interesting paragraphs

According to my knowledge the main thing in annealing temperature in PCR
Primers annealing temperature should be selected by keeping in 5° less than the lower melting temperature of primers
Secondly MgCl2 working Concentration also plays a major role in PCR optimization


Why would lethal genes evolve? I've been reading through 'The Selfish Gene' by Dawkins. At a few places in the book he states that incest is damaging because it would give a very high chance of lethal recessive genes becoming active due to the high probability of both children having the gene compared to one child and one stranger from the same species.

However, this leaves me with the question why lethal genes would evolve in the first place. The only reason I can think of is that these genes have some secondary purpose and survive natural selection because of that.

Is this simply the entire story or are there things that I'm missing? It seems to me that the having possibility of getting healthy offspring from incest is beneficial to a species, if only because finding a mate would be easier, so those secondary effects would have to be pretty good.

Also I'd be curious if any research has been done which has found examples of side effects of these lethal genes that would make them preferable.

Lethal genes evolve simply because of random deleterious mutations and absence of strong selection.

Recessive lethal genes

Random mutations can make a gene product non-functional or reduce its activity. However, in diploid organisms the other fully-functional copy of the gene can compensate for the non-functional allele.

Sometimes both the alleles can carry different mutations which can lead to complementation; this would not affect the gene activity. Also see:  Explain allelic complementation at molecular level. Let's not consider this case here.

So, the fitness of the heterozygotes would not be affected and they will continue to propagate. However, if both the alleles are affected then it would lead to lethality (or lets say reduced fitness). This can happen if two heterozygotes (with the same deleterious mutation) mate and give rise to a homozygote (with both the alleles affected). Since siblings (or other close kins) are genetically related, there is a good likelihood that both of them may be carrying a copy of a non-functional allele and homozygous offspring born out of such a mating may have reduced fitness.

Dominant lethal genes

There are some cases of dominant lethal alleles. Examples include the mutated genes responsible for Huntington's disease (or similar poly-Q disorders). Other examples include a mutant allele of a proto-oncogene that leads to its hyperactivity (and therefore cancer).

Dominant lethal alleles persist in the population primarily because of their late onset. In such cases an individual with such an allele would have already mated and produced offspring before the disease kills them.

Other reasons for the persistence of lethal genes

Another possibility (applicable to the case of cancer) is that the mutations are not in the germ cells and were acquired by somatic cells because of some external agent. These mutations would not be transmitted to the next generation.

Sometimes, the deleterious nature of the allele can exert its effect only under certain conditions. Let's say someone has a mutation that causes reduced immunity. Such a person would survive well if they remain in a sterile environment. In general, we can say that there is no strong selective pressure against the mutation.

Sometimes the reduced fitness because of a mutation under a certain condition can be overwhelmed by an increased fitness caused by it under some other condition. A very well known example is that of the haemoglobin allele that causes sickle-cell anaemia. However, the RBCs in the individuals affected by this disease are resistant to infection by the malarial parasite. The mortality due to malaria is much higher than that due to sickle cell anaemia. Therefore, in regions where malaria has high incidence (like Africa) this allele is positively selected.

It would be beneficial to a population for a lethal gene to evolve in incestuous situations because genetic diversity is then promoted through natural selection. Genetic diversity is necessary for a species to evolve which would improve the chance of survival.


rapidly growing mold on flat surface For an experiment I'm conducting, I need to grow mold on a 2 foot square piece of white fiberglass. I'm in Florida, with high heat and humility, so mold already grows easily. I've seen elsewhere that mold needs organic matter to feed on, to grow rapidly. Ironically, I've seen mold grow on the side of fiberglass motor-homes and showers with no present organic matter. Any suggestions on how to grow mold rapidly on my piece of fiberglass? I thought of locating fiberglass outside, in sun. I could mist it every hour or 2 to create more moisture. Maybe there is something I could rub/spray on the fiberglass sheet to encourage rapid growth? Any other suggestions about applying moisture, light, etc?

Mold is a general name for many species of Fungi, which are heterotroph so they need organic material to feed on. You can see them grow on fiberglass because many organic material can accumulate near or on fiberglass (skin cells, plants root hairs, microbes, oils) and become substrate for the mold.
If you want to grow a specific mold you should first identify it to find the best substrate for that species and not for other. If you simply want mold you can use some kind of starch on the fiberglass and keep it moist (not wet, wetness will give you also oomycetes and bacteria). No need to spray it every 2hrs. You can close the fiberglass with a box, dark box is better (bacteria grow best with light).
You can take (with mask and gloves) some mold and put it on your fiberglass to promote the growing of that mold.
Describing your mold or posting a picture can help to identify. If you see two different colors report both of them and location (center, periphery)


What makes learning more difficult as we age? Why is it harder to adapt yourself to different cultures, places, and languages as you age? What makes breaking up with emotional patterns or ideas after years of habit more difficult?

Is there a natural process in which the neuron's synapses are set, while later in life the plasticity of the brain is nearly lost?

The answer(s) to this question can fill libraries. But I can give a few pointers here, as the question is relevant and timely, giving the tendency to an ever increasing life expectancy of the general populace in developed countries (notable exception: US).

I think your question can broadly be answered by the fact that degenerative processes in the brain slowly, but steadily, impairs all of its functions. Possible reasons for the specific decreased capability of the brain to adapt itself to new situations are:

The hippocampus plays a critical role in forming memory representations that are important for flexible cognition and social behavior (Rubin et al., 2014). Decreasing hippocampal neurogenesis during aging may impair the functioning of the hippocampus (Couillard-Despres et al., 2011)
Degenerative processes in the striatum impairs implicit learning that is necessary for mastering new tasks (Rieckmann & Bäckman, 2009);
Deficits in serotonin and dopamine neuromodulation in various brain structures due to degenerative processes during aging results in decreased learning and decision making (Eppinger et al., 2013);
Age-related altered neurosteroid levels may impair cognitive abilities (Vallée et al., 2011).

And the list goes on.

References
- Couillard-Despres et al., Gerontol (2011); 57: 559–64
- Eppinger et al., Ann N Y Acad Sci (2011); 1235: 1–17
- Rieckmann & Bäckman, Neuropsychol Rev (2009); 19(4): 490–503
- Rubin et al., Front Hum Neurosci (2014); 8: 742
- Vallée et al., Brain Res Rev (2001); 37(1–3): 301-312

There is growing evidence that loss of learning capacity is not primarily age related

Below are just a few articles on this topic... I know there's more.

The short answer is, there is growing evidence that the loss of memory and learning capabilities is NOT a foregone conclusion of aging by itself, but is, in fact, a byproduct of other health issues, specifically not controlling blood pressure and not being "heart healthy".  From a layman's view, this is because damage to the small blood vessels in the brain will slowly damage the surrounding nerve tissue.  If this occurs, you end up with all the affects that AliceD points out.

The point is:  Do not assume that loss of learning is "just a fact of aging".

References:

Protect your heart, preserve your mind?
Intensive treatment of blood pressure helps prevent memory decline in older adults
Can blood pressure drugs help reduce dementia risk?


Why are there exactly four nucleobases in DNA? Does someone know why DNA is composed of four nucleobases? In particular, is there an explanation for the number? Why four and not two, or eight?

A now deleted answer put this down to an argument based on amino-acid coding in codons but, as pointed out by Konrad Rudolph in a comment, arguments based on codons cannot be correct because the 4-base system likely pre-dates the evolution of protein translation.

So why four?

I suggest that it comes from a combination of factors which make it a 'just right' fit for RNA-based replicators: more would be bad, and less would also be bad. The four bases are able to copy with high reliability because two features combine to exclude mis-pairings: there are two size classes - meaning any purine-purine or pyrimidine-pyrimidine pairing results in incorrect separation between the strands, excluding A-G and C-U bonds; and there are two classes based on number of OH-bonds - which limits the potential for A-C and G-U bonds. More bases must, inevitably, weaken the strength of these exclusionary approaches and increase the number of mispairings. RNA world replicators will have lacked the sophisticated repair and error checking mechanisms of modern lifeforms so this increase in mispairings would likely not be corrected.

Of course, a two base system would be even more capable of reducing errors. I suggest that the advantage of the four base system is that it allows for much more complex 3-dimensional structure to form in RNA and thus enabled a broader range of catalytic capabilities. I've only considered even-numbers because only even numbered systems could use the Watson-Crick style of base pairing.

I'd also suggesting reading Eörs Szathmáry's 2003 paper on this very question.

Addendum

A group in California has just published a paper in which they successfully added a third base pair stably into DNA. I think this could shed some light on why four - you can read about it here or get the full paper here (Nature, so pay walled).

Because four is the minimum possible number. If there is no push to make a system more complex, it will never assemble.

One might then argue that a similar system could have been built only using two bases.

Fine.

Try it out.

You will miserably fail. Sure you can make a DNA strand containing adenine and thymine only. But who would be stopping guanine and cytosine from forming and joining some deoxyribose then? How would you manage information storage, preservation and transfer then?

Base pairing - no matter how complex might look - is the simplest way to safely store information at the molecular level so that it could be handled for transfer and translation somewhere else. The spatial combinations of hydrogen bonds that can be established between pyrimidine and purine derivatives are only two.

For replication purposes you need a further symmetry breaking, which leaves you with two bases, one on each strand of a DNA double helix.

Two times two is four.

P.S.: By the way, who on Earth told you that there are exactly four nucleobases in DNA? Tell them they probably forgot methylcytosine! The term "methylation" is just an excuse to avoid admitting that DNA uses five bases instead of four. Open your mind.


Why lab technicians use indirect (antibody reaction) method for diagnosing? In microbiology we have two types of microbial diagnosis. The direct method is where we detect the invader's DNA, Antigens or culture to see the exact pathogen while the second, indirect, method is the reacting the antibodies of patient's serum with different reagents.

If we use the indirect method (antibody reaction) and find that they are producing antibodies against a specific disease (let's say streptococcus A) what is the benefit of having found that they are fighting Strep A since the body is already clearly fighting it and putting up the best defence to fight the disease?

Would a doctor really prescribe antibiotics even though here is already an immune reaction against the infection?

If diagnosis and treatment are useless then why do we waste the time to do it?

Short answer: Antibiotic treatment is important because the body can't always keep up with the infection even if it has launched a response.

Background:

First, let's look at what the antibody reaction method is actually doing.

Taking a sample of blood or body fluid
Testing the sample with known pathogens - viruses, bacteria, fungi, etc.
Identifying which infection causes a reaction.

This allows us to determine which infection we are dealing with. This can be especially useful when the infection is hidden in a place we are unable to easily swab - the stomach, heart, a small wound that has already healed. Sometimes this test is just used to monitor how well you are fighting the infection, but it also allows them to evaluate what the best course of treatment is for you. (Reference 1)

Just because the body has an immune reaction doesn't mean that the body's immune system can actually finish the battle against a disease. In the example case of Strep A, you may be able to get over the infection yourself but it will take longer than if you are prescribed antibiotics against it.

See this question on the CDC:

  Q: How common is invasive group A streptococcal disease?

  A: Approximately 9,000-11,500 cases of invasive GAS (Group A Streptococcus) disease occur each
  year in the United States, resulting in 1,000-1,800 deaths annually.

Note that invasive Strep A usually infects children, elderly, and  immunocompromised people (anyone with a weaker immune system typically).

Unless you have absolutely no immune system at all, there will be an antibody response put out by your body. The NHS goes into detail about different parts of your immune system.

Recall also that Strep A (our example) could divide faster than the body can keep up with. So we would need antibiotic help to fight the disease. Using the "indirect" method we can find a hidden infection.

According to the NHS the antibiotics put a stop to growth and spread which allows the body to come in and finally finish them all off, or they disrupt a process the bacteria needs to survive and kill the infection for the body. Thereby helping the immune system (the body's best line of defence) finish off the infection when it couldn't do it on its own.

One use of indirect testing is used to test for *exposure** to organisms that we wouldn't just naturally recover from as well. One example off the top of my head is HIV. The first line of testing for this infections is simply to look for antibody responses, but because it is not effectively resolved by the patient's immune response, it is important to know about this infection.

*Also note that because we are looking at antibodies, we only know that the patient has been exposed to the organism, not that they are actively infected. The antibody test is quick and easy though, so it saves money (and probably time) to do this first.

(originally, I included TB in this answer, however it is actually a skin test - not assayed ex vivo via ELISA, so I removed it.)


Standard notation for crossings (female, male) Is there any standard for the notation of a crossing (hybrid) which tells me which part is the mother and which is the father?
Example
StrainA: egg cell
StrainB: sperm cell
Which notation is correct?
StrainA x StrainB or
StrainB x StrainA
or isn't there a rule for this?

For plants, seed (egg cell) parent is shown first and pollen (sperm) parent second.
The rule is mentioned in wikipedia,
http://en.wikipedia.org/wiki/Hybrid_(biology)
section : in plants.
Another mention of plant example:
https://www.rhododendron.org/v50n1p36.htm


What causes fruit taste enhancement? I'm not sure if this is a biology or chemistry question, maybe both? Some fruits, such as quince and quondong, taste of nothing when raw but have an extremely strong flavour when cooked. Why?

I am a little confused that does the word "cooked" means ripe？If yes, then the question will be easy to answer. Fruit has a kind of ripener, ethlyene. Ethlyene will help fructose break down and make up more glucose. That is why you may taste a strong flavour when fruit is cooked.


Why do cockroaches burst from soapy water? (careful, disturbing!)

I was experimenting with some stray cockroaches that ended up falling in my bath tub overnight (there is currently an infestation undergoing in my apartment building) and I found out that they are very easily killed by simply soaking them in soapy water.

I read that soap blocks some pores in insects' bodies which leads to suffocation, which appears to be the cause of death for my test cockroaches. But what I don't get is why about a half of them died with their innards bursting from their tail end. The water wasn't too hot to make them boil. Is it that they suffocate so hard that attempting to breathe they blow out their insides? Or is it the soap's reaction with the cockroach's bodily materials? Or is something else causing this?

I remember watching a documentary on injecting various insects with hydrogen peroxide which caused much more dramatic explosions, but it's not like I was injecting cockroaches, I just sprinkled them with soap water.

As far as I am aware, cockroaches don't burst from being sprayed with soapy water (water + some liquid dish detergent). We previously had many cockroaches in our apartment (some came back after a year of nothing!), and we regularly sprayed the cockroaches with soapy water plus some vineger (more as a disinfectant/cleaner) and they never burst. We've killed at least 30 using this method.

Having said that, what you likely witnessed was the egg sacs dislodging from the back of the female cockroach. As you didn't mention what species of cockroach you were dealing with, I am assuming you had German cockroaches as they seem to be the most common type in non-tropical/hot areas.

According to a number of biology sites, German cockroaches are particularly difficult to control and eradicate is because they carry their egg sacs with them until they are ready to hatch. At which point they drop the sac.

If you are able to catch a few that seem especially big, you will notice that they have a sac at their back.

If you don't have German cockroaches, I have not idea why they would burst...

Cockroach abdomen burst out when it sinks in soapy water. A white color thing burst out from the body which are not eggs.They lay only one big egg which will be in brown color. Cockroach lack hemoglobin(red pigmentation) in their blood. White color busting out is actually blood. So even male cockroach burst out when it is in soapy water. May be due to some soap reactions with blood it burst i guess.


Does drying meat in the sun make digesting it easier? I was looking into the relationships between man, fire, brain size, evolution, etc. and I learned about other methods of food preparation that eased digestion, but did not use fire. Then, this question popped into my head. Specifically, I am wondering how much easier is sun-dried meat to digest; how much of a benefit is gained in the amount of energy needed for the digestive process?

Various food processing methods, such as cooking, can make meat easier, that is faster, to digest. The purpose of drying meat is to extend its shelf life, not to make it more digestible. Drying removes water from the meat and somewhat physically (but not really chemically) change it.

The amount of calories used for digestion is not that high; probably less than 100 Calories per day, so meat prepared in different ways does not likely significantly affect the amount of calories burnt.

Depends on how you define digestion.

If you consider chewing to be part of digestion, then this actually makes it more difficult as dried meat ("jerky") is harder to chew (into small pieces that are easier to digest) and harder for liquid (including saliva) to permeate.

Otherwise, ease of digestion is best defined at the molecular level. Tough fibers tend to be difficult to digest; pure protein can generally be hydrolyzed except in specific cases of structures specifically designed to withstand digestion. No idea if sunlight causes significant enough structural changes to change how digestable the meat is - that would depend on if the sunlight causes chemical reactions that "tenderize" the meat.


Why is blood removed from meat? Blood is removed from meat before it is consumed. Below is, for example, how chickens are processed from Wikipedia.

Removed from transport cages
Hung by the legs on a shackle, mounted on a conveyor chain.
Stunned using an electrically charged water bath
Killed by cutting the blood vessels in the neck
Bled so that most blood has left the carcass
Scalded to soften the attachment of the feathers
Plucked to remove the feathers
Head removed
Hock cutting to remove the feet
Rehung in the evisceration room
Gutted or eviscerated to remove the internal organs
Washed to remove blood and soiling from the carcass
Chilled to prevent bacterial spoiling

Why is the blood removed? Does it just simply taste bad? This might be a stupid question but being vegetarian, I may not know.

Blood finds use in many different dishes as well as biotechnological applications. Research-grade BSA (bovine serum albumin) is derived from cow's blood, there are not special facilities, same cows go for steaks and car seats. So part answer is economical: blood can be processed further. Also it is just easier not trying to preserve liquid inside vessel already opened by slitting the throat. It also seems that blood can rot faster than other tissues, maybe, because in dead animal immune responses are deteriorated and every infection in blood will activate.

I found a forensic article that states the following:

  Because the protective agencies of the body are absent, the bacteria spread through the blood vessels using the proteins and carbohydrates of the blood as culture media.

I was unable to find anything more on this with my limited searching skill, though I plied it to the best.

There was an interesting study on the relation between decompostion of animal meat and the bacterial load though. It was a good read!


Are there verbs for "undergo mitosis" and "undergo meiosis"? From my experience on SE sites, I believe this is the right site to ask this question under "terminology".

I've been trying to find out whether English has one-word verbs for "undergo mitosis" and "undergo meiosis". I haven't been able to find confirmation on Google, but my linguistic imagination is limited, and I may have failed to google the right things.

Could you tell me if there are such verbs in common use in biology? I mean, if such verbs exist, can I find them in modern biology books or papers?

I'm actually not sure myself. If I were to use something, I would go with "Mitos'd" and "Meios'd".

However, you may not win over many fans, depending on the audience. If it's with students or maybe a professor, you could get away with shortening the processes. If it's in any formal setting, be as precise and descriptive as possible. It's not a lot of trouble to be more accurate and add "underwent" to the sentence.

Was just researching your exact same question.  Self-replicate is the closest I could find or think of... but it's a very general verb, not even biology specific.
e.g. Please don't self-replicate, I'm already having trouble with just one of you -- said the programmer to his memory gobbling AI program.
https://en.wikipedia.org/wiki/Self-replication


What Type of Mushroom is this? Recently in Eastern Pennsylvania, there has been lots of rain and heat (90's) for a couple weeks now, so lots of mushrooms are popping up.
A neighbor posted a picture of this fungus in a community group, and was wondering if it is edible.

I am no mycologist, but I think it looks like the false death cap, Amanita citrina var. alba.

I'm basing this mostly on color, size, and the universal veil remnants on the cap.  Here is a picture for comparison:

  Amanita citrina is now known to contain the toxin alpha-amanitin;
  however, if eaten in normal amounts it is considered the concentration
  is so low that it is unlikely to have any significant effect on a
  healthy adult. Of far greater risk is the possibility of confusion
  with one of the deadly Amanita species such as the Deathcap, Amanita
  phalloides, or the Destroying Angel, Amanita virosa. For this reason
  our advice is not to eat Amanita citrina, whether it is raw or cooked

Source: First-Nature

yes amanita sp. do not eat it at all. They come up in the grass after rain and hot weather.


What is this fruit / nut? These were found in a park in Pittsburgh, PA. From a distance they looked almost like plums, but they're actually hollow, paper-like covers that contain a hard pea-sized seed.

Most likely a member of the genus Staphylea. Since you are in Pittsburgh, PA, it's most likely Staphylea trifolia L., or an introduced species.

By the looks Of it,it mostly is a hop hornbeam Which are indeed found in pittsburghBut i Still cant confirm it because
they are no photos of their leaves and any twigs or the whole tree, this info would be great to identify it and do you mind mentioning the name of the park you've been to
Can you confirm whether the tree looked like this

Ostrya Virginis


What is the need for lobules in (human) testicles? While I was studying the reproductive system, the question popped up in my mind. Each testicle has lobules formed out of the tunica albuginea, in which there exist seminiferous tubules. Why is the testicle divided in these lobules? What's the point? Why isn't it one single big cavity?

The structure of the testes as with many other organs in living things has all to do with form, function, and efficiency. The testes are extremely efficient sperm producers, with on average 1,500 sperm cells being produced per minute in the average human male. If the testes were just an open space of fluid with free-floating sperm producing germ cells, it would not be as nearly an efficient design, not to mention the waste caused by an inability to sort through sperm producing cells and the cells they produced.

According to this site, each lobule in the testes contains about 1-4 seminiferous tubules, each an average of 50 cm in length. Like many structures in the human body, intestinal walls, nephrons in kidneys, etc, the complex structures and organization of the cells that have a specialized function involves increasing access to the inputs and outputs of their function and increased surface area to increase that function.

This site has a helpful graphic showing the structure of the seminiferous tubules that are wrapped up in each lobule. The germ cells which split and create sperm cells are lined along the wall and when the new sperm cell they produce have developed enough, the sperm cell is released to be moved through the tubule where it can be prepared and developed further. This complex structure allows for uniform, controlled, and efficient production of sperm, essentially, a sperm factory running with an assembly line, and is a design that nature has kept and improved upon for millions of years.


Why are mosquitoes repelled by smoke? A well known way to have a rest of mosquitoes during camping is to stand in the fire's smoke. Moreover, I learned recently that shepherds in certain regions of Africa use the same tactic for cattle. They make smoky fires and cattle gathers in smoke to get rid of mosquitoes.

Why humans and cattle can stand smoke, but mosquitoes can't? Does this technique work for other kinds of insects?

There is little hard evidence on whether smoke acts as a mosquitoe repellent. A literature review done by the WHO (Biran et al, 2008) on smoke and malaria show that evidence is mixed, at least when it comes to long term protection and protection from blood meals from firewood smoke. Their review also notes that few scientific studies have been done on the topic, and they report results from one experimental and a couple of observational studies. However, they do note that burning particular plant materials (based on traditionally used plants) may be effective (see e.g. Pålsson & Jaenson. 1999).

These results also doesn't preclude that very heavy, temporary, smoke may be effective to get rid of mosquitoes ("... during camping is to stand in the fire's smoke...") - that this can be effective is certainly my personal experience as well.

All insects have a mortal fear of smoke because it is a harbinger of flames and flames - for an insect - means instant death. They have no mechanisms at all that are capable of regulating their body temperature sufficiently to survive direct flames.

Added:

Consider a population of mosquitoes (or any flying insect for that matter) that successfully develops a smoke-avoidance response. In an environment where forest fires are common and smoke is therefore a clear precursor - would this population have a better chance of survival than another that does not? I think you could only answer yes.

It merely remains to prove that it is possible for a population I have described to develop. Well - the presence of this question on this board proves that it is possible. I realize this is a slightly weird form of proof by induction but you have to admit it works.

Sorry - no references or citations - just a "because evolution".


ID a marine creature found on a beach on the US east Coast While walking on a marshy beach, I found this creature. It has no eyes, no feet, no fin, no gills. The only thing I know is that the skin lightly contracts. I found at least three of these. It is basically carried around by water.

Found this on a Maryland beach, roughly 150 miles east of Washington D.C.

It's positively a sea anemone. It retracts the tentacles when disturbed and become quite rigid. It's hard to identify it in this condition, leave it for a whlie in a jar with sea water and you'll see.

Based on your description, it could be a sponge (but I don't think sponges have a contractile skin), a tunicate or a sea cucumber.

I would favour the last option.

The following questions might help further identification: How many holes can you spot?
If there are 2, where are they placed with respect to one another?

I hope someone can propose something more precise.

Edit:

As noted in the comments, it could also be a sea anemone. In my experience, these have a quite soft body. In that case, it should have only one opening, and the opening should let tentacles out when the animal is left quiet in the proper environment.


hummingbird feeders - is sugar water healthy for them? The top results on google for DIY hummingbird feeder suggest a white-sugar solution for the feed.  In humans we make a big deal about processed sugar vs. the sugar you get from, say, eating a piece of fruit.  Does this matter for hummingbirds?  Their metabolisms so high, it makes me wonder if this is relevant.  Maybe it is not!  But I would like to know.

Hummingbirds absolutely eat insects, and HONEY and BROWN SUGAR are a huge NO NO.
  The following is a statement from: http://wildbirdsonline.com/index.html

  Every year, as more studies are completed, we learn more about
  hummingbird life and diets. However, we find that some people think
  that hummers can survive on nectar alone. Nectar provides quick energy
  to sustain their extremely high metabolic rate and little else. This
  is important enough that the shape of the bills of hummers have
  evolved in partnership with the flower shapes that they frequent.
  Consequentially, there is a wide variety of hummingbird bill lengths
  and shapes among the more than 300 species that exist.

  There is another critical food source for the hummers. Essential
  vitamins, minerals, amino acids, proteins, oils and fats, fiber, etc.
  all come from the insects they eagerly consume, not the nectar. Their
  preferred insects include, but are not limited to: small beetles, true
  bugs, weevils, flies, gnats, mosquitoes, aphids, mites, leafhoppers,
  flying ants, and parasitic wasps. Their favorite insect food source is
  the spider and harvestmen (daddy long legs). Some ornithologists
  estimate that spiders are between 60% and 80% of their diet.

But there are lots of other resources for you to find accurate information about feeding hummingbirds.


During acid reflux and vomiting, is the burning sensation from pepsin or acid? When one's stomach contents enter one's esophagus, a burning sensation usually ensues. Is this from the enzyme pepsin breaking apart your cells or just from the acid?

It is the acid that causes the burn

Medicines like proton pump inhibitors (e.g. Prilosec), or H2 receptor antagonists (like Zantac) that reduce acid secretion reduce the burning sensation.  Medicines that neutralize the acid like calcium carbonate (e.g. Tums) also reduce the burn.  These medicines do nothing to the secretion of enzymes.

ADDENDUM. @anongoodnurse wants references.  Maybe in exchange she will remove that pesky down vote.

Cimetidine won the team that developed it the Nobel prize - the first rationally (as opposed to empirically) designed drug.  It was designed to very specifically reduce stomach acid.

https://www.acs.org/content/acs/en/education/whatischemistry/landmarks/cimetidinetagamet.html

  Smith Kline & French's multidisciplinary research team first looked at
  the physiological cause of acid secretion. They confirmed that a
  molecule found in the body called histamine triggers the release of
  acid when it binds to a specific receptor (now called the H2-receptor)
  in the stomach lining. Their aim was to find a molecule that
  successfully competed with histamine in combining with the receptor,
  but then blocked, rather than stimulated, acid release. Such a
  molecule was called a histamine H2-receptor antagonist and represented
  a new class of drugs.

This and the successor class of drugs (proton pump inhibitors) are very specifically designed to decrease acid secretion and do little else.

The fact that billions of dollars worth of these drugs are sold means that persons suffering from reflux pain / stomach ulcer perceive that their pain is reduced by a decrease in acid secretion, and so are willing to pay.

  Tagamet® was greeted with great enthusiasm by doctors and patients
  alike. Ten years after its introduction, it had achieved sales of one
  billion dollars and had become the world's number one prescription
  drug.


What is the role of hippo signalling in oral squamous cells What role do hippo signalling have on squamous cells in oral health & diseases

Mutations in the Hippo signalling pathway cause unusual organ growth in flies.  After a good deal of intensive research, its been shown that Hippo genes are responsible for suppressing organ growth in development, increasing cell death and slowing proliferation.

Given this role, its not surprising that Hippo genes are also important in cancer.  I'm not an expert in cancer, but a quick search turned up an association of cancer with the Yki (YAP in mammals) transcription activator, an oncogene from the Hippo Pathway.  YAP suppression has been linked to cancerous growth.  And its also been shown that YAP is amplified in oral squamous cell carcinoma cells.  This last is circumstantial but consistent with what we know about YAP.

Hippo Signal may affect the turnover rate of oral mucosa


Why are humans so variable in appearance Most animals look almost identical to their peers. To distinguish lions we record the spots on their face; with whales we look at the blemishes on their tail or flukes. In other words, we have to try hard to distinguish one lion from another.

In the case of dogs, we have created many different looking breeds - but within each breed they look the same: one poodle looks very much like the next one.

On the other hand, with humans we have not only the different races (cf. dog breeds), but even within one race no two people are alike. And, not only are the faces different, the body shapes vary equally much. We use face and body shape (and voice) to recognise each other. Most other animals use smell or sound.

I thought the reason for our uniqueness might be that, with civilisation, we are not constrained us to look the same. However, even in hunter-gatherer tribes each person looks different from every other one.

So what is it in human evolution that made us unique in this regard? And, are we unique? I cannot think of any other species with as much variation as ours, but are there others?

Because we as humans are really really good at picking up small differences in humans and really really bad at detecting them in anything else.

Animals are often quite good at telling each other apart, far better than humans are, birds in particular are known for this. Just because you as a human are bad at it does not mean they are.

There is a pretty strong evolutionary pressure for humans to be able to tell other humans apart and not much of an advantage for being able to tell two lions apart. We need to be able to tell mates, rivals, relatives, and strangers apart easily. We don't need to differentiating one black bird from another.

We also spend a lot of time around other humans, so we are more familiar with their differences, but the same thing happens to animal researchers whale researchers who spend a lot of time around whales can easily tell two whales apart at a glance. this is also part of the reason some people have trouble telling individuals from a different "race" apart, they are to unfamiliar and uninterested to spot differences. Or the way a car guy can spot the difference between two models at a diffrence but someone else might not.

You see the same effect chimps can tell each other apart but can't tell humans apart, unless they spend a lot of time around humans then they can. They can also match voice to face meaning the can recognize both.

Then of course you have the fact you are focusing on vision, try to tell two people apart by smell and you will likely fail but a dog will have no problem with it. likewise many monogamous song birds can identify their mates from song along, just as we recognize others by voice, penguins are another example. Humans are very visual creatures so much of our identification ability relies on vision we see the same thing in other visual species, animals tend to use whichever sense are their dominant ones. Saying organisms are more visually similar because organisms with far worse vision than humans can't tell them apart by vision alone is simply an unreasonable conclusion.

There IS in fact less difference in other species's faces than there is in humans. And you can in fact recognize subtle difference in animals as well, when they are there. The idea that we're somehow blind to very similar shape variants to human faces in other animals is absurd. You can see subtle difference in everything, you are human, you can pay attention to detail. You can do it with an object it's not very hard, how do you figure humans manage to master drawing and painting?
The reason why most animals have less diverse faces than ours is because we evolved to be easily recognizable. Since other animals can identify eachother by such things as smell or sound, they don't need distinctive facial features, factors that we're less sensitive to.


Infection treatment without anti-biotic When we have some bacterial infection, say throat infection (pharyngitis) we take antibiotics as treatment. I was wondering how throat infection was treated when there was no antibiotics at all, before 1940's I think.

Throat infection is just example, It can be post surgical operation, urinary track infection etc, basically anything where we use antibiotics currently. So in a way replacement of antibiotic tablet when antibiotic wasn't available.

Interestingly, treatment of mild pharyngitis before the advent of antibiotics wasn't too different from what it is today - it was (and still is) mostly symptomatic. First of all, viral pharyngitis, which is quite common (Hidreth et al., 2015), is not affected by antibiotics (no viral infection is), and they are not indicated in such situations. Second, mild and self-limiting bacterial infections, including pharyngitis, most often do not warrant prescription of antibiotics, as this leads to the growing problem of antibiotic resistance, which, according to the World Health Organization is "one of the biggest threats to global health." Many guidelines can be quoted, urging clinicians to prescribe antibiotics sparingly, but pharyngitis is so common (literally everyone has had it, multiple times) that one can simply turn to one's own experience - simply put, when you have a mild case of soar throat, your doctor doesn't give you antibiotics (if you even bother going to the doctor about it), most often you are advised to take only symptomatic medications (many of which are OTC). These most often include compounds with analgesic, antiseptic, and/or anti-inflammatory properties. Interestingly, such compounds were widely available long before the advent of antibiotics and even the pharmaceutical industry itself.

Menthol, for example, is a selective agonist of κ-opioid (Galeotti et al., 2002) and a modulator of GABBAa receptors (Watt et al., 2008), thereby eliciting analgesic and anaesthetic effects, respectively. Moreover, by disrupting bacterial cell membranes, menthol (and similar compounds, such as thymol, for example), elicit antibacterial activity, as well (Trombetta et al., 2005). Thus, wild mint, peppermint, and thyme are much more often indicated in cases of soar throat than antibiotics! Their use in the form of infusions and decoctions likely predates most, if not all, modern countries. Moreover, the analgesic and anti-inflammatory properties of willow bark, which are due to the salicylic acid contained therein, were known to Hippocrates (Norn et al., 2009), quite possibly dating back much earlier. Furthermore, it is known that caffeine potentiates the analgesic effects of many nonsteroidal anti-inflammatory drugs, including salicilic acid (Granados-Soto and Castañeda-Hernández, 1999). Unsurprisingly, this combination is often found in many modern drugs (many OTC), being marketed all over the world. Whether this effect was known before the advent of the pharma industry, however, is hard to say. Willow bark has been used as an analgesic and anti-inflammatory medication since ancient times, but coffee was brought to the West in the XVI century.

This is only a handful of traditional medications for pharyngitis, and I'm sure many more can be found, as well as many other treatments for many other conditions. The point is that treatments of mild pharyngitis were available before the advent of antibiotics, as a matter of fact, many of those treatments are still first-line therapy in most cases, even to this day.

Bacteriophages were used to treat infectious diseases in some places, most notably the Republic of Georgia, before antibiotics became popular. The advent of antibiotics, which many thought heralded the end of infectious diseases, unfortunately resulted in less interest in therapeutic bacteriophages.


Do organs or any structure in the human body shrink/shorten if it's function is no longer useful? Charles Darwin was one of the first scientists to theorize on the function of the appendix, which in his day had been identified only in humans and other great apes. He hypothesized that the distant ancestors of these animals survived on a diet of leaves, and so they required a large cecum, a portion of the gut that houses bacteria that can break down stubborn plant tissue. Later, he speculated, these ancestors shifted to a largely fruit-based diet that was easier to digest. A large cecum was no longer necessary, and it began to shrink...Darwin thought the appendix, which juts off of the cecum, is one of its former folds that shriveled up as the cecum shrank. Consequently, he thought it carried no function.

I recently read a source which states the above. It made me wonder that if there is some other organ/part in our body which may shrink as further evolution progresses and it's use diminishes, just like our appendix. I'd like to know if this 'theory of shrinking' applies to any organ that may become useless.

First of all, our appendix isn't 'useless'. Their is a high concentration of lymph nodes (higher than anywhere else in your gut), so it might not be needed for digestion anymore, but it's function somewhat shifted to a more immunological role.
Secondly, yes there are other organs/body parts that shrink over time. In evolutionary time, look at our tailbone. In monkeys it's still a full tail, in apes it's almost nothing, and in humans it's still present in the skeleton, but not visible on the 'outside' anymore. Probably in a few (hundred/thousand/..) years it will be completely reduced until it is no longer present in the human skeleton (because since we don't have a tail anymore, it doesn't have any function anymore).
Over a much shorter timescale it is also possible. For example the thymus expands in puberty, and afterwards it shrinks until it is almost completely gone.


Does a cell suspend or exit cell cycle at G0? In an exam, there was one question which asked whether the cell exits or suspends cell cycle at G0 phase.

I answered that it exits cell cycle but the official answer key says it suspends cell cycle.

I marked exit because a cell in G0  undergoes differentiation and maturation. Is there a difference between the two terms?

It is actually suspend and yes the words do differ. This is because the cells that enter the G0 stage is not actually exiting the cell cycle because when situation demands it will divide. It is metabolically active and therefore the word suspend suits better


How is photosynthesis observed? How is photosynthesis observed?

Say I have plants A and B, and I want to find how fast they are able to turn carbon dioxide into oxygen. How would I experiment this?
Say I have one plant A, which has two kinds of leafs B and C. I hypothesize the B-leafs produce oxygen faster than the C-leafs. What kind of experiment could I set up to test this?

Not sure, this what you need, but here you can find a detailed description of how photosynthesis efficiency can be measured in the field, with a list of modern devices. In short, it's about measuring the uptake of CO2 and release of H2O of individual leaves.

Hydrogen carbonate is an indicator commonly used for testing photosynthesis. It shows changes in carbon dioxide concentration in the air. You would set up the plant in a sealed system next to a tray of hydrogen carbonate indicator solution and observe the colour change.


Why does resting potential not become continually more negative? (Firstly, I know this is similar to other questions, but I have read those answers and they do not really cover this topic).

My understanding of resting potential: action potential is not being transmitted; by way of action potentials via Na+ and K+ pumps, for every 2K+ pumped in, 3Na+ is pumped out of the cell. This process is termed "resting potential" and the transmembrane pd roughly = -65mV.

If more Na+ are pumped out than K+ in, why does the resting potential difference remain at -65, why does it not continue to decrease (until an action potential is triggered)?

The resting membrane potential is due to internal/external differences in ion concentrations and very importantly differences in permeability to those ions.
The fact that the sodium/potassium pump does not move an equal number of ions in each direction hardly matters at all for resting membrane potential; the resting membrane potential would be almost the same if that wasn't true. What is important is just the overall concentration of the two ion species, and the permeability of the membrane to different ions (almost all of this permeability is through specialized ion channels, because ions don't otherwise flow easily through a lipid bilayer).
You can calculate the resting potential/equilibrium potential using the Goldman equation - note that nothing in this equation involves the sodium/potassium pump moving different numbers of sodium and potassium ions.
The reason the membrane potential is negative is because the membrane at rest is most permeable to potassium, and because there is more potassium inside the cell than outside. Therefore, there will be a net flow of positive ions out of the cell, until enough ions have left that there is some negative charge inside the cell to counteract that net flow.

As you mentioned, the pump will keep generating an ionic gradient (and the membrane voltage should decrease)

Nonetheless there is still open ion channels at these negative potentials. Then the resting potential will be the voltage at which the net ion Flux (ion channels + leak + pump) is zero.

Since the pump is electrogenic (generates a current) the standard Goldman equation is not applicable and has to be modified.

Here $I_{pump}$ is the current generated by the pump. This equation can also be applied when other electrogenic pumps or transporter are present

You can see the derivation in this paper.


Identify this excreta! A picture is worth a thousand words!

It's about 1.3cm (1/2") long. We rented a basement and I found this on a machine that was moved in a bit earlier.

I would like to know if there are any mice, rats, etc that could have come in.

We are on the island of Malta, in the Mediterranean sea.
The basement is below a shop that used to sell AC units and the basement was used as a storage. The walls have gaping holes where cables and pipes go in and out, etc. Clearly industrial and not made for the customer to see.

Bat is the other basement creature that comes to mind. It looks like a match as explained in this and several other videos - https://www.youtube.com/watch?v=897Fb9ndids


Has lamarckism been discredited? Lamarckism is a pre-darwinian theory according to which an organism's traits acquired to adapt to the environment are passed onto its offspring. A couple of years ago, I attended an event with Richard Dawkins and Jerry Coyne, both preeminent evolutionary biologists, in which I remember them agreeing that it is basically B.S. and that acquired traits don't get passed but instead propagate themselves through natural selection. As a non expert in biology, it does not make sense to me that acquired traits would make their way into the genotype and then get passed on, which coincides with what Dawkins was saying. But I am a non expert.

I also have read a few things about epigenetics and it sounds strangely similar to lamarckism. Steven Pinker also discusses all these things in The Blank Slate and he gives a notion that thare is some idealistic ideology behind promoting ideas that we can radically change an organism by environmental conditioning and "save" those changes into the genotype. He says that ideology is to justify government programs aimed at rapidly enhancing mankind whereas natural selection, which proponents of such ideas may deem reactionary, simply is not so optimistic.

My questions are:

Is lamarckism, or inheritance of acquired traits, been conclusively discredited?
What does lamarckism relate to epigenetics

The question is interesting at many levels. Of course, in biology and in any other science there is no absolute or 'objective' truth about some given phenomenon if we really care to look at the nuances. Lamarck seems to be vindicated mainly by a wave of empirical work on patterns of transgenerational inheritance, particularly in the field that is known as epigenetics. You can read a good intro-level review here for some recent developments, some particular examples here, or a more conceptual reading here.

As an evolutionary biologist myself, I will say that most other biologists acknowledge that epigenetics and transgenerational inheritance are important and have solid empirical support, but (for various reasons) some of them are hesitant of calling that 'Lamarckian'.

By the way, Dawkins was a very effective science popularizer, but he does not practice science nowadays, and many of his ideas lie in what is known as 'scientism', which is a blind confidence in science as an absolute truth that is inflexible. The same applies to many positions of Steven Pinker, deGrasse Tyson, etc.


Mutated and unmutated PCR product If I have a mutated colony containing the fusion protein, mCherry instead of the stop codon TAA, and an unmutated colony which does not contain the protein. Why will the PCR products of the two colonies have the same size?

I thought that since the mutated colony contains the protein instead of the stop codon, this would cause this product to be larger in size than the unmutated product. However, from experimental data it shows that both products are of same size. Could someone please explain why this is?

Thank you!

If mCherry was successfully cloned replacing the stop codon, you would indeed expect a fusion protein that is about 27 kDa larger than the original protein.
However, with a PCR you are not testing for the full length protein, but rather for a part of the target gene sequence.

The length of the PCR product very much depends on the position of your primers: If both primers are targeted at your unmutated sequence, the product size will not change by adding mCherry behind the targeted sequence. The product size of the PCR would only change, if one primer is located before or in your unmutated protein and the other one behind mCherry. This would probably result in a very large PCR product and hinder the PCR reaction from being effective.

To check for correct integration of mCherry, you would need to design a primer pair with the forward primer in your unmutated protein and the reverse primer in mCherry. This should result in a product in the fusion protein colonies, but not in the unmutated ones.

Alternatively, you could sequence your products.


Sickle-cell trait : Why is only one type of beta chain found in any one hemoglobin molecule? I was reading a textbook (iGenetics, 3rd edition page 71), and came across the following passage:

  Homozygous bS bS people make Hb-S, the defective hemoglobin, with two
  normal a chains specified by wild-type a-globin genes and two
  abnormal b chains specified by the mutant b-globin bS allele: these
  people have sickle-cell anemia. Heterozygous bA bS people make both
  Hb-A and Hb-S and have sickle-cell trait. Because only one type of b
  chain is found in any one hemoglobin molecule, only two types of
  hemoglobin molecules are possible—one with two normal b chains, the
  other with two mutant b chains.

(Emphasis mine)

My question is: Why is only one type of beta chain found in any one hemoglobin molecule? Or is this statement simply false?

I did search biology SE for similar questions, and found this one, but it is phrased poorly and the only answer does not address my question.

For one specific hemoglobin molecule, yes it's just one type of beta chain.  In the case of a heterozygote, this hemoglobin molecule could be expressing from the bS gene OR the normal beta gene.  Let's call it a 50/50 chance for each hemoglobin to be expressing bS.  Because RBCs have a ton of hemoglobin in them, this 50/50 or so expression of bS wouldn't be enough to cause RBC sickling and disease, and it also helps explain the heterozygote advantage vs malaria.